Ultimate Podiatry Review Manual

The

Ultimate Podiatry Interview Review Manual

© 2010 OZ

Ingredients:

AJM Prism Manual – 100 pages, the best one out there Crozer-Keystone 2nd edition – Another really good ones Surgery Review book (OCPM/SCPM) – Simple and easy to read Classification manual (CCPM) – Quick overview of classifications to know cold Radiology Review notes (SCPM) – Some topics are over-detailed for the interviews Mangold manual – Abx, Labs, Pain management, Surgery procedures, EKG (SCPM) Sean Pimp List – Excellent list of Q and A OZ manual Hershey – 1 of 2 classic 1000+ notes Presby – 1 of 2 classic 1000+ notes Residency Review manual – Good for some classic articles, lots of pages but a quick read Trauma manual – Didn’t read this one before interviews ABPS questions – Good practice run Qs NBPME 2 questions – Some what easy Qs Scholl Misc Manual – Sample cases to work up Classic Articles



The AJM

PRISM And Externship Guide. A 100-page Podiatric Residency Interview Study Manual. This 2009 First Edition was edited by RC.

David Hockney’s Mount Fuji and Flowers

Introduction: Preparing for externships and the residency interview is one of the most challenging tasks facing the podiatric medical student. It can be a completely overwhelming exercise unless you are efficient about the way you approach the process. If you are reading this introduction, then you are already aware that in order to be fully prepared for residency interviews and externships, you need to study a lot more than what you got from classes and clinic in school. You should have a strategy going into the residency interview, just as your interviewers should have a strategy about how to evaluate you. One of the most important ways to prepare is to think about the interview process from the other side of the table. The interviewers only have a given amount of time to spend with you; no more than 30 minutes in most cases. This is not a lot of time. What do they really want to know about you? What information can they get from you in 30 minutes that tells them about what kind of doctor you are going to be? Remember that the attendings of a program are essentially hiring you to help handle their patients, and at the interview they want to know if they can trust you with this responsibility. Asking inane, esoteric questions during the academic interview doesn’t really give them this information. On the other hand, asking basic “work-up” based questions does. These questions allow the interviewer to see how you will be approaching their patients in the future. It gives them information about how your mind works when dealing with patients on an everyday level. If you were an attending on the other side of the table, would you rather know if the student can take you through the clotting cascade, or how they are going to handle your patient in the ED with a suspected post-operative infection? Another thing to think about is that the interviewers need to compare your answers to the other people you are going against for the program, and they don’t have a lot of time to do this. They should have some standardized way of quantitatively grading your performance against the performance of others. I like to think of this as “check marks”. Think of the interviewers asking the same exact questions to each student and then having a form or a list in front of them. There are certain “buzz words” that they want you to say and certain questions that they want you to ask during the work-up. The more things you get correct, the more “check marks” you get on their form. And at the end of the day, they add up all the “check marks” and see who got the most. Your goal during a 30-minute interview should be to get as many “check marks” as possible. This manual was put together based on the way that I studied for interviews. There is certainly no shortage of material to study, and this manual in no way can replace or even rival some of the other study guides that are out there. The goal of the PRISM is simply to help you be as efficient as possible with the process and to think about the interview from the other side of the table. My goal with coming up with the following sheets was to take a given topic and fit everything that could be asked about that topic during an interview onto a single sheet of paper. Realize that it is not all the information on a given topic, but all the information that is likely to be asked during an interview. There’s a big difference there. Your goal heading into the interview process should be to have a standardized way of handling every question or situation that you are presented with, and to get as many “check marks” as possible. Think about it. The easiest way for the interviewers to answer the questions they have about you is to present you with a clinical scenario, and see how you work-up that situation. Therefore, the most efficient way to study for interviews is to take a given topic, and then “work-up” a patient in that situation. I made all of the AJM Sheets with this thought in mind (see “Gout” example on next page). Also included in this manual are AJM Lists. Studying is by nature a passive exercise, but the interview process involves actively answering questions and talking out loud. The Lists allow you to actively think about a topic like you will be expected to do during the interview. It takes a broad, clinical situation/subject and asks you to come up with as many answers as possible. I hope that they help you realize that there is not always one answer to a question, but possibly many different answers that can all be considered correct. The more answers that you can come up with for a given List, the more “check marks” you get during the interview. Again, this manual is far from complete and absolutely does not contain all of the information you will be asked during an interview. It simply hopes to change the way that you think about the interview process and highlight some of the information that you are most likely to be asked. I limited it to 100 pages of the most commonly asked information and the kind of stuff that I’m going to ask if I’m a residency director someday. It is not in any way meant to be overwhelming. I also want this to be a “living” document. It is not intended to be commercial and should never be sold. I’m going to take it with me when I graduate from residency, leave it with the Inova program, and distribute it electronically to anyone who wants it. Feel free to change/update it in any way that you think would be helpful, but please keep it to exactly 100 pages. In other words, if you think something is important and should be included, you also have to decide what isn’t as important and should be taken out. It will be interesting to see how it evolves over the years! Good luck and please do not hesitate to contact me if there is any way that I can be of service to you.

[email protected] 2

AJM Sheet Example: Gout -Subjective CC: Pt classically complains of a “red, hot, swollen joint”. Typical patient is a male in the 6th decade (as much as a 20:1 M:F ratio). HPI: -Nature: Intense pain out of proportion with swelling/pressure. -Location: Single or multiple joints. Unilateral or bilateral. Most common is 1st MPJ, but can occur in any joint. -Acute, abrupt onset; more commonly at night. -Aggravating Factors: Pressure, WB, diet (red wine, organ meat, lard, seafood). -History: Recurrent gouty attacks are very common PMH: -Genetic enzyme defects, obesity, lead poisoning, tumor, psoriasis, hemolytic anemia may all be underlying causes. -Renal disease (renal disease is 2nd most common complication of gout). -Kidney stones Meds: -Diuretics, low dose ASA, TB meds, warfarin may exacerbate. SH: -Diets high in red wine, organ meat, lard and seafood may exacerbate. All/FH: -Usually non-contributory ROS: -May be associated with fever.

-Objective Physical Exam -Derm: -Erythema, Calor, Edema present at affected joint -May see tophi sticking out of skin -Vasc: -Non-pitting edema at affected site -Neuro: -Intense pain out of proportion -Ortho: -Decreased PROM/AROM at affected joint with guarding. Imaging -Plain Film Radiograph:

-Increased soft tissue density with joint effusion. Tophi may be visible in soft tissue. -Fine striated pattern of periosteal reaction along the cortex adjacent to tophi -Lace pattern of osseous erosion -Round osseous erosion with a sclerotic margin (“rat bite erosion” or “punched-out lesion”). -Martel’s sign: Expansile lesion with an overhanging osseous margin.

Laboratory -Joint aspirate is mandatory for diagnosis of gout: -Needle-shaped monosodium urate crystals -Negatively birefringent (bright yellow) when viewed under polarizing light microscope parallel to axis of lens. -Blue when perpendicular to axis of lens. -Serum uric acid levels > 7.5mg/dl (non-diagnostic) -Elevated ESR -Synovial fluid analysis: Elevated leukocytes with a predomination of neutrophils -Generalized increased white cell count

-General Information -Definition: Metabolic disorder secondary to the build-up of monosodium urate crystals and supersaturated hyperuricemic extracellular fluids in and around joints and tendons causing the clinical manifestations of a red, hot, swollen joint. -It is the most common cause of inflammatory arthritis in men over the age of 30.

-Classification -Primary: Elevated serum urate levels or urate deposition secondary to inherent disorders of uric acid metabolism. -Uric Acid Overproduction (Metabolic Gout): 10% of patients -Excessive amounts of uric acid excreted into the urine -Occurs secondary to an enzyme defect, tumor, psoriasis, hemolytic anemia, etc. -Dx: Uric Acid Level >600mg in a 24-hour urine collection -Uric Acid Undersecretion (Renal Gout): 90% of patients -Relative deficit in the renal excretion of uric acid. -Secondary: A minor clinical feature secondary to some genetic or acquired process

-Treatment -Symptomatic Pharmacology (relieves symptoms, but doesn’t attack underlying pathophysiology) -Indomethacin: 50mg PO q8 -Colchicine: 0.5-1.0mg PO initially, then 0.5mg PO q1 hour until symptoms (GI) or pain relief Then around 0.5mg PO qday as prophylaxis -Active/Physiologic Pharmocology (attacks underlying pathophysiology and prevents recurrence) -Allopurinol: 100-600mg PO qday as single or divided doses. -Blocks uric acid production by inhibition of the enzyme xanthine oxidase. -Probenecid: 250mg PO bid for one week; then 500mg PO bid -Increases uric acid removal from urine (decreases reabsorption) -Surgical Intervention (if you get rid of the joint, then you get rid of a potential site for gout to attack!) -I&D/Washout -Arthroplasty -Arthrodesis

-Further Reading -Roper RB. The perioperative management of the gouty patient. J Amer Podiatry Assoc. 1984 Apr;74(4):168-72. -Schlesinger N. Management of acute and chronic gouty arthritis: present state-of-the-art. Drugs. 2004;64(21):2399-2416. -Keith MP. Updates in the management of gout. Am J Med. 2007 Mar;120(3):221-4.

3

Table of Contents:

AJM Lists [Pages 5-29] -5: Introduction and Proposed Schedule -Surgery

Lists…………………....……….6-10

-6: HAV Procedures with Indications -7: Risks and Complications of Surgery -8: Measurement of Radiographic Angles -9: Radiographic Review -10: Surgical Layers of Dissection

-Medicine Lists…………………….……11-15 -11: -12: -13: -14: -15: -Trauma -16: -17: -18: -19: -20:

Post-Op Fever Etiology Lab Infection Diagnosis Imaging Infection Diagnosis Labs and Why they are important Vascular and Neurologic Assessment

Lists…………………………...16-20 Ankle Fx DDx Synthes Chart with Screw Anatomy Methods of Fixation Hardware Insertion Classifications

-Anatomy -21: -22: -23: -24: -25: -Social

Lists……………………….…21-25

Ossification of Lower Extremity Bones 5th Metatarsal Anatomy Dorsal Arterial Anastomosis Variations Lower Extremity Peripheral Nerve Blockade Dermatomes with Spinal Levels

Interview Lists……………....….26-29

AJM Sheets [Pages 30-100]: -Diabetic Foot Infections……………….30-50 -30: Introduction and Contents -31: Diabetic Foot Infection History -32: Diabetic Foot Infection Physical Exam -33: Wound Classification Systems -34-35: Diabetic Foot Infection Laboratory Results -36: Common Infective Agents -37: Diabetic Foot Infection Imaging Studies -38: Diabetic Foot Infection Pathogenesis -39: Functional Diabetic Foot Infection Anatomy -40: Osteomyelitis -41: Osteomyelitis Classifications -42: Charcot Neuroarthropathy -43: Charcot Classifications -44: Differentiating Charcot vs. Osteomyelitis

-45: Common Situational Bugs -46: Empiric Antibiotic Choices -47: IDSA Empiric Recommendations -48-49: Bugs with Drug of Choice -50: Antibiotic Dosing Guide

-Trauma…………………………………51-68 -51: Introduction and Contents -52: The Trauma Work-Up -53-54: General Trauma Topics -55: Digital Fractures -56: Sesamoid Trauma -57: Metatarsal Fractures -58: 5th Metatarsal Fractures -59: Metatarsal Stress Fractures -60: LisFranc Trauma -61: Navicular Trauma -62: Talar Fractures -63: Calcaneal Fractures -64-65: Ankle Fractures -66: General Tendon Trauma -67: Achilles Tendon Work-up -68: Achilles Tendon Treatment

-Peri-Operative Medicine and Surgery….69-99 -69: Introduction and Contents -Peri-Operative Medicine -70: Admission Orders -71: Electrolyte Basics -72: Glucose Control -73: Fluids -74: Post-Op Fever -75: DVT -76: Pain Management -General Surgery Topics -77: AO -78: Plates and Screws -79: Suture Sheet -80: Surgical Instruments -81: Power Instrumentation -82: Biomaterials -83: External Fixation -84: Bone/Wound Healing -Specific Surgery Topics -85: How to “Work-Up” a Surgical Patient -86-87: Digital Deformities -88: Lesser Metatarsals -89: 5th Ray -90-91: HAV -92: HAV Complications -93-94: HL/HR -95-96: Pes Plano Valgus -97-98: Cavus -99: Equinus

-Page 100: “Can you give me some good articles to read?” 4

Lists Schedule: AJM Lists were originally created to be done during an externship. Students often have a lot of down time during the day while the residents are doing work that doesn’t need assistance. The lists give the students something to do during this time and make it look like they’re busy instead of just standing around doing nothing (in front of the attendings and residents). It also encourages students to collaborate, and shows the residents/attendings that they can work well with each other and in groups. When I was a resident, I would give the students one list and a related article each day, and then we would try and get together once a week to go over them. It usually generated a great deal of good discussion. If you are using these lists to study on your own, get together with a group of friends to go over them and talk about your answers out loud. The way you know if you really understand a topic is if you can intelligently discuss it and explain it to your peers. Again, studying is by nature a passive exercise, but at the interview you will be expected to actively answer questions out loud. Only about half of what the interviewers appreciate from your answer is the actual content, the other half is how you say it. Remember that the interviewers are probably asking the same question to every student that walks through the door, so they’ve probably heard the same answer several times before you even sit down. What they haven’t heard is how you’ve said it! In other words, you should also be studying “how to say it”. See the following suggested schedule: Mondays: Surgery -HAV Procedures with Indications (page 6) -Risks and Complications of Surgery (page 7) -Measurement of Radiographic Angles (page 8) -Radiographic Review (page 9) -Surgical Layers of Dissection (page 10) Tuesdays: Medicine -Post-Op Fever Etiology (page 11) -Lab Infection Diagnosis (page 12) -Imaging Infection Diagnosis (page 13) -Labs and Why they are Important (page 14) -Vascular and Neurologic Assessment (page 15) Wednesdays: Trauma -Ankle Fx DDx (page 16) -Synthes Fill-in Chart with Screw Anatomy (page 17) -Methods of Fixation (page 18) -Hardware Insertion (page 19) -Classifications (page 20) Thursdays: Anatomy -Ossification of Lower Extremity Bones (page 21) -5th Metatarsal Anatomy (page 22) -Dorsal Arterial Anastomosis Variations (page 23) -Lower Extremity Peripheral Nerve Blockade (page 24) -Dermatomes with Spinal Levels (page 25) Fridays: Social Questions -Social Question Sheets: Part I (pages 26-27) Part II (pages 28-29) Part III (page 30)

5

AJM List: HAV Procedures and Indications Clinical Scenario: You are a first year resident scheduled to be in a “bunion procedure” at a surgery center tomorrow. You are working with the attending for the first time and want to appear as prepared as possible. Name as many “bunion procedures” as you can. Student Goal: Name 20 HAV procedures from distal to proximal. What are the specific clinical and radiographic indications for each?

6

AJM List: Surgical Complications Clinical Scenario: You are a first year resident at a surgery center. The attending isn’t there yet, and you aren’t exactly sure of the specifics of the case, but you want to have all the paperwork filled out for when the attending gets there (including the consent). Student Goal: Name as many risks and complications of a generic foot and ankle surgery as possible. What are some specific complications associated with some specific surgeries? How would you handle these complications in the post-op period?

7

AJM List: Measurement of Radiographic Angles Student Goal: Name as many foot and ankle radiographic measurements as possible. What are the normal values? What clinical information is this giving you?

8

AJM List: Radiology Review Clinical Scenario: There is a big difference between describing and diagnosing a radiograph. During an interview, you need to be able to describe the findings you are seeing before you diagnose the pathology. You also need to be able to do this out loud during the interview process. Student Goal: Out loud, using as many terms as possible, and in a systematic manner, intelligently describe the following radiographs before making a diagnosis.

Note: RC and I found it very helpful to practice for interviews by picking up random podiatry textbooks, and alternating through the pictures describing the radiographs out loud.

9

AJM List: Surgical Layers of Dissection Student Goal: Identify the 5 surgical planes and 3 surgical intervals of dissection. What structures will you see in each plane/interval for a standard HAV procedure? For a standard digital procedure?

10

AJM List: Post-operative Fever Clinical Scenario: On call, you are paged at 3am by a nurse to report a fever in a patient POD#2 of 101.6°F. Student Goal: Name as many potential causes of fever as possible. How would you diagnose and work-up each one?

11

AJM List: Laboratory Infection Diagnosis Clinical Scenario: A patient enters the Emergency Department with a suspected lower extremity infection. Student Goal: Name as many laboratory tests that you can order to help diagnose an infection. What clinical information is each test really telling you about the situation?

12

AJM List: Imaging Infection Diagnosis Clinical Scenario: A patient enters the Emergency Department with a suspected lower extremity infection. Student Goal: Name as many imaging tests that you can order to help diagnose an infection. Exactly what are you looking for with each test?

13

AJM List: Routine Lab List Student Goal: Identify routine labs, their normal values, and what information they are giving you about the patient. Which labs should be drawn when an infection is suspected and why? Which should be done in the pre-operative work-up of a patient?

14

AJM List: Vascular and Neurologic Assessment Student Goal: Name as many subjective and objective vascular and neurologic assessments as possible while performing a lower extremity examination.

15

AJM List: Ankle Fracture Clinical Scenario: A patient arrives in the ED exclaiming that they “broke their ankle”. Obviously you will take an x-ray, but what exactly are you looking for on the radiograph? Student Goal: Name as many possible fractures that can occur following an ankle sprain.

-Bonus: What do the “Ottawa Ankle Rules” say about getting a radiograph following an ankle sprain?

16

AJM List: Screw Games Thread Diameter

Spheric Head Diameter

Screwdriver: Hex or Cruciate?

Core Diameter

Drill bit Thread Hole

Drill bit Gliding Hole

Tap Diameter

Mini Frag Set 1.5mm 2.0mm 2.7mm Small Frag Set 3.5mm 4.0mm PT 4.0mm FT Large Frag Set 4.5mm 4.5mm Mall Screw 6.5mm PT 6.5mm FT Hint: pg 76 McGlam’s

-Pitch on a cortical screw?: -Pitch on a cancellous screw?:

-Draw a screw labeled with as many anatomic landmarks identified as you can (eg. Head, major diameter, pitch, etc):

17

AJM List: Methods of Fixation Student Goal: Name as many methods as possible to fixate an osteotomy.

18

AJM List: Hardware Insertion Technique Student Goal: Describe standard AO lag screw insertion technique. What is the purpose of each step? Why are they done in that particular order? What is compromised technique? Splintage?

-Bonus: What is the quantitative measurement of “two-finger tightness?”:

-What are some strategies for hardware extraction?:

19

AJM List: Classifications Student Goal: Name as many different trauma classifications as you can that cover the foot and ankle from distal to proximal.

20

AJM List: Ossification Dates Student Goal: Name every bone in the lower extremity in order of ossification date.

21

AJM List: 5th Metatarsal Anatomy Student Goal: Name as many structures as you can that attach to the 5th metatarsal.

22

AJM List: Dorsal Arterial Anastamosis Variations Student Goal: Draw out as many different variations as possible for the arterial supply to the dorsum of the foot.

How does this apply to the angiosome principles? (hint: read Dr. Attinger’s work)

23

AJM List: Local Anesthesia and Peripheral Nerve Blockade Student Goal: Identify as many named foot and ankle peripheral nerve blocks as possible. Which specific nerves are being anesthetized with each block?

-Toxic Dose of Lidocaine?:

-Toxic Dose of Marcaine?:

-How and why does epinephrine influence the toxic dose of a local anesthetic?

-What are the reversing agents for local anesthetic toxicity?

24

AJM List: Dermatomes Student Goal: Draw a lower extremity with all of the dermatomes illustrated with associated spinal levels and landmarks.

-Bonus: How are dermatomes different than sclerotomes?

25

AJM List: Social Questions Part I: General Questions Personal: Strengths: Be prepared to give at least 3 personal strengths and why they will make you a good resident. -Strength #1: -Why it will make you a good resident: -Strength #2: -Strength #3: Weaknesses: Be prepared to give at least 3 weaknesses, and more importantly, how you are remedying them. -Weakness #1: -Remedy: -Weakness #2 -Weakness #3: Goals: Be prepared to give professional and personal goals, and how you will go about accomplishing them. Another form this question could take is where you see yourself in a given number of years. -Professional Goals: -Goal #1: -Goal #2: -Goal #3: -Personal Goals: -Goal #1: -Goal #2: -Goal #3:

-Where do you see yourself in: -5 years?: -10 years?: -25 years?:

Program Specific: For each program that you apply to, you should have a list of strengths and weaknesses for that program. Obviously be careful with weaknesses, and always have a way that you can improve the situation. You should be able to answer why you personally are a good fit for that program. I found it helpful to have a list of priorities that I was looking for in the different programs, and then described how that particular program fit into my priorities. -Program #1: -Strength #1: -Strength #2: -Strength #3: -Weakness #1: -Weakness #2:

-What you are able to bring to the program: -Favorite attending and why: -Least favorite attending and why: -Favorite resident and why: -Least favorite resident and why: -Best case you saw at the program:

Here’s my list of priorities that I used based on what was important to me. Everyone’s list can (and really should) be different, this is just to provide an example: 1. Surgery/Academics -How is this program going to make you a better doctor? You’re going to learn surgery and do some academic events at any program in the country, is there anything special about this particular program that sets it apart? Do they really care about academics, or are they just done to meet a requirement? (Hint: a good way to tell this is to see how often attendings are excited to show up to and be involved in meetings). Although the quantity of surgery is important (you have be able to get your “numbers”), also consider the quality and variety of the surgeries at a program. 2. Outside Rotations -All programs have the same set of “core” rotations that everyone has to do. Is there anything unique about this particular program that shows that they really care about your complete education and want you to have outstanding quality and variety to your residency experience? 3. Location: -This one kind of speaks for itself, but you should consider if you are going to be completely at one hospital versus traveling to different hospitals and different surgery centers (there are pros and cons to each). Also consider what the presence is of the program within the hospital. Is the podiatric surgery department intricately involved in the hospital, or is it more of an afterthought? 4. Independence -I’m an independent guy who likes to come up with and pursue my own projects and ideas. Other people really like structure and would prefer to get an exact schedule for the next three years on day 1 of their residency. So this was something that I was really looking for, but someone else may want exactly the opposite. 5. The Future -How is this program going to help you accomplish your professional goals now and after you graduate?

26

AJM List: Social Questions Part II: Personal Questions Personal Questions: These questions are hard to answer and often irrelevant, but you should have answers ready to go (even if they are made up). Answer as specifically as possible to give the interviewer something tangible to grab onto about yourself. Always answer “Why?” before they have the chance to ask you. “Why?” may be the most important question you get during the interview process. -What do you like to do with your free time? -Answer #1: -Answer #2: -Answer #3: -What professional accomplishments are you most proud of?: -What personal accomplishments are you most proud of?: -What was your hardest/most trying experience? What did you learn from this?: -What is your most embarrassing moment?: -Name three things that you would bring with you to a deserted island: -#1: -#2: -#3: -Tell me a joke: -#1: -#2: -#3: -Favorite Movie: -Favorite Book: -Last movie you saw: -Something you liked about it: -Something you didn’t like about it: -Last book you read: -Favorite Band/Kind of Music: -Last concert you went to: -Tell me about the craziest patient you have ever had to deal with: -What is your funniest medical story?: -What animal would you be and why?: -What tree would you be and why?: -Favorite TV show: -Favorite actor: -Favorite actress: -Favorite surgical instrument: -Do you have any pets?: -Favorite pet: -If you could take a vacation anywhere in the world, where would it be?: -Tell me something about yourself that few people know: -Who’s the most important person in your life (real and/or fictional) that you have never met?:

-And of course, “Tell me a little about yourself”: -Important Note: You should be able to spout off both a 30-second and a 5-minute answer to this question at the drop of a hat.

-Note: These questions are very easy to answer if you think about them, but you don’t have time to think during the interview. You don’t want to show any hesitation during this process, especially questions about yourself. The worst answer you can give to a specific personal question is “I don’t know.” What is that saying about you? ***Practice answering all of these questions out loud to yourself in the time leading up to interviews! You may feel silly talking to yourself, but it is undoubtedly the best way to prepare for this line of questioning.***

27

AJM List: Social Questions Part III: Academic and Ethical Social Questions Academic Social Questions: These are hidden academic questions, but ones you can’t study for in any book. Please plan these questions out because it is very easy to get trapped in your answer if you lie. -What journals do you read? Which is your favorite?: -What was the last good journal article you read? (be able to cite it!): -What was the last thing you built with your hands?: -Favorite class in school?: -Least favorite class in school?: -Favorite teacher in school?: -What types of things does the field of podiatric surgery need to do to improve in the future?: -What is something you learned about the field of podiatric surgery since you started school/externships?: -Have you participated in any research projects? Why or why not? What was your role in this project?: -What would you do with your life if you couldn’t be a surgeon/physician?:

Ethical Questions: The key to answering an ethical question is to take a step back from the situation. Pretend that someone else is in the situation and you are going to give that person advice. Don’t pretend that you are in the situation; it actually makes it more difficult to think through the process. Remember the concept of chain-of-command and also remember that there is a real patient involved. Something else that really helped me out was having a clear order of my priorities. Everyone’s can be different, but mine are: 1. Responsibility to the patient as a physician 2. Responsibility as an employee of a hospital 3. Responsibility as a resident of the residency program 4. Responsibility for my own education 5. Responsibility for the education of junior residents/students So whatever ethical situation I was put into, I would make decisions based upon this order of priorities. Remember that usually there is no right or wrong answer when it comes to ethical situations. Like George Costanza said about beating a lie detector test: “It’s not a lie (wrong), if you believe it.”

The Semistructured Conversation: Many residency programs (and especially general medicine or general surgery residency programs) have reevaluated the way that they have traditionally selected residents, and have moved away from a structured academic interview. They have instead moved onto what’s called a “semistructured conversation” that tries to evaluate if the applicants have the “knowledge, skills and attitudes deemed necessary for the practice of medicine”. The questions are a kind of mix of academic and ethical questions that can develop into more of a conversation. So while these are not purely academic questions, they can lead into a conversation about specific academic topics. There’s actually a couple articles about it (Neitzschman HR, Neitzchman LH, Dowling A. Key Component of Resident Selection: The Semistructured Conversation. Acad Radio. 9: 1423-29; 2002.), and I’ve put together a long list of these type questions on the next List.

28

AJM List: Social Questions Part IV: The Semistructured Conversation Interview Questions -Tell me about a patient care situation in which podiatric surgery altered the management of the patient. -Describe a critical clinical situation and how you communicated with the family. -Tell me about something you learned during one of your externships. -How would you respond to a patient who asks, “Am I going to die?” -Can you recall any time when you disagreed with a patient’s diagnosis or treatment? -Tell us about the biggest argument/controversy you were involved with in podiatry school. -Give us an example of a situation when you were pivotal in the resolution of a conflict between two other people. -Suppose you’re in charge of the call schedule. You need to fill a slot with one of two people, one of whom has told you he has to be out of town as best man in a wedding, and the other has to present a paper at a meeting. How would you resolve the conflict? -Describe a time when you were in a position to give someone a bad evaluation. How did you handle it? -What features would you add to a medical school curriculum that you think might better prepare you for a podiatric career? -Can you recall a time when you received an evaluation with which you disagreed? -If a referring physician insists that you perform a study on a patient and you believe that study could be harmful to the patient, how would you handle the situation? -Describe a patient for whom you felt very little empathy but you knew you should. -What would you do if you saw a senior resident make a mistake that might harm a patient if not corrected promptly? -A patient acquires your pager number and home phone number and calls several times per day. How do you handle this patient’s needs? -A consulting physician asks you a question, and you are not sure of the answer. How do you handle it? -Tell me about a negative interaction you had during medical school with anyone from a transporter to an attending and how the two of you dealt with it at the moment and afterwards. -What do you see as the most challenging aspects of a podiatric residency? -How would you handle a situation when you know one of your fellow residents has a problem with drugs or alcohol? -For what reasons do you want to come this particular geographic area? -You are on call and someone else asks you a question on a subject you know nothing about. How do you gather information about the topic expeditiously? -What resources did you use for researching residency programs? -Outside of the structured lecture, what other formats did you find most helpful as learning tools? -Describe for me how you deal with a colleague who is exhibiting evidence of substance abuse. -Describe your response to an episode of someone cheating on the Gross Anatomy final examination. -How would you decide (and what factors would you consider), as an HMO executive, whether to immunize 2,500 children at $100 each or provide one liver transplant at $250,000 each? -In what ways do you maximize your own health and well-being? -How would you deal with a fellow resident who is not “pulling their own weight” in their work? -What personal questions most helped you during medical school? -Tell me about a patient from whom you learned something. -How would you like to see podiatric surgery develop over the next 5 years? -How do you see yourself changing between now and the end of residency? -Tell me about your experience in using online resources, library resources, and internet resources. -Did you ever feel as a medical student that you were not part of the clinical team? How did you address the situation in order to optimize your learning experience? -Can you recall an experience that made you decide to choose podiatry as a profession? -Describe one of your most challenging cases during your externships. -Tell me about an experience in medical school where you felt particularly competent. -What particular skill do you feel you have that makes podiatric surgery the best specialty for you. -As you examine different programs, what characteristics are you looking for that we might offer you? -What diseases or topics have fascinated you in medical school and why? -What topics interest you that you haven’t had time to explore yet? -Tell me about an experience when you took a risk that ended up being successful. -Can you tell me about a patient who had an impact on you? -Can you recall a time in medical school when you had some doubt about the professional path you have chosen? What did you do? -A number of residents (15-20%) leave general surgery residency. What do you think influences their choice? -How would you rate yourself in terms of your ability to establish rapport and maintain healthy relationships with other health professionals?

29

AJM Sheets: Diabetic Foot Infection Work-Up The Diabetic Foot Infection work-up is arguably the most important concept that you can study during the interview process because it is the one topic that you are almost guaranteed of being asked at some point. My thought process during interviews was that if I’m certain that I will be asked about it, I’m going to spend extra time and energy knowing everything possible on the subject. Every student at interviews is going to get something along these lines; therefore it’s important to be the most prepared and best able to “wow” the attendings when asked. So I put together a collection of AJM Sheets (totaling about 20 pages) that goes through an in-depth work-up of a diabetic foot infection. This topic is also a classic example of hitting as many “check marks” as possible during the interview by having a standardized way of going through a work-up. The way this situation is often presented at interviews is for them to simply ask you: “There is a diabetic patient in the ED with a suspected foot infection. What do you want to know about the patient, and what do you want to do?” By having a standardized way of going through this work-up (or any work-up), you will seem more prepared during the interviews, hit more check marks, and won’t stumble about thinking what to ask next. The basics of this work-up can be applied to any clinical situation. This work-up also highlights taking an active approach and going on the offensive during the interview process. Take control of the interview from the interviewers. Do not simply ask if the patient has diabetes; ask specific questions about the patient’s knowledge, management and known complications of diabetes. This will show that you really understand the concepts and pathogenesis of the disease process. This section has a lot of the same information presented in a number of different ways, giving you a couple ways to study. While there is certainly no shortage of material to study this information from, my favorite article on the topic is a must-read: Lipsky BA, et al. Diagnosis and Treatment of Diabetic Foot Infections. IDSA Guidelines. CID 2004; 39: 885-910. You also certainly should read: Frykberg RG, et al. Diabetic foot disorders. A clinical practice guideline (2006 revision). J Foot Ankle Surg. 2006 Sep-Oct; 45(5 Suppl): S1-66. And finally, the June 2006 Supplement of Plastic and Reconstructive Surgery is a fantastic resource covering a wide variety of diabetic foot issues, mostly from the Georgetown perspective. Contents: -Diabetic Foot Infection History (page 31) -Diabetic Foot Infection Physical Exam (page 32) -Wound Classification Systems (page 33) -Diabetic Foot Infection Laboratory Results (pages 34-35) -Common Infective Agents with Gram Stain Characteristics (page 36) -Diabetic Foot Infection Imaging Studies (page 37) -Diabetic Foot Infection Pathogenesis (page 38) -Functional Diabetic Foot Infection Anatomy (page 39) -Osteomyelitis (page 40) -Osteomyelitis Classifications (page 41) -Charcot Neuroarthropathy (page 42) -Charcot Classifications (page 43) -Differentiating Charcot vs. Osteomyelitis (page 44) -Common Situational Bugs (page 45) -Empiric Antibiotic Choices (page 46) -IDSA Empiric Recommendations (page 47) -Bugs with Drug of Choice (pages 48-49) -Antibiotic Dosing Guide (page 50)

30

AJM Sheet: Diabetic Foot Infection Subjective History Subjective CC: Pt’s can present with a wide variety of complaints ranging from the systemic signs of infection to increased ulcer drainage to a change in mental status. Infection should always be in your differential diagnosis dealing with any situation. Ask the patient at least the following questions: -NLDOCAT of chief complaint -Systemic signs of infection: Nausea, vomiting (quantity and quality), fever, chills, night sweats, ague, loss of appetite, change in mental status, diarrhea (quantity and quality), constipation, change in sleep patterns, headache, shortness of breath, chest pain, etc. -Local signs of infection: Patient reported increases in pain, erythema, swelling, temperature, drainage (quantity and quality), odor, etc. -Ulcer specific questions if applicable: Duration of ulcer, changes in size/depth/color, dressing changes, dressing change schedule, wound care products, last formal evaluation, primary wound care specialist, previous treatments, any history of hospitalization for infection, etc. HPI:

-Remember: The patient probably knows their ulcer better than you!

-It is extremely important to get an antibiotic history from the patient. Are they taking any antibiotic therapy currently (including dosage and last dose)? When was the last time they were prescribed an antibiotic?, etc. This information can provide useful information with respect to the development of resistant organisms. Specific risk factors include antibiotic use in the last 6 months, any fluoroquinolone use, and hospitalization in the last 6 months. -Richard et al. Risk factors and healing impact of multidrug-resistant bacteria in diabetic foot ulcers. Diabet Metab. 2008 Sep. -Hartemann-Heurtier et al. Diabetic foot ulcer and multidrug-resistance organisms: risk factors and impact. Diabet Med. 2004 Jul. -Kandemir et al. Risk factors for infection of the diabetic foot with multi-antibiotic resistant microorganisms. J Infect. 2007 May.

-Tetanus Status -NPO Status PMH: -DM: Complete DM history including length of disease, previous complications, glucose monitoring schedule, normal glucose readings, HbA1c values, medications, last podiatric evaluation, last internal medicine evaluation, implemented preventative measures, evaluation of patients level of understanding of pathogenesis of disease, evaluation of patients role in self-treatment, etc. -Any known complications of diabetes with interventions/treatment: cardiac disease, peripheral vascular disease, hypertension, retinopathy. -Specifically ask about renal disease and liver disease (antibiotic implications). -Any other immuno-compromising conditions. -Any other PMH issues. PSH: -Specifically any previous amputations, foot/ankle surgeries and diabetes-related surgeries. Meds: -Detailed list of drugs, dosages, and patient compliance to schedule. All: -True allergies and reactions to drugs, food, products, etc. -Very important and not to be overlooked. -Work: line of work, quantity of WB and ambulation, hours, ability of the patient to take time off or take it easy, worker’s compensation issues, etc. -Diet and exercise. -Home support network. Includes assessment of patient compliance and family understanding/education/compliance. -Smoking, alcohol, drug use. -House structure: stairs, bathrooms, pets. -Other wound contamination risk factors.

SH:

FH: ROS:

-Anything applicable. -Anything applicable.

***Diabetic foot infections are one of the most challenging aspects of podiatric surgery that will take up a lot of your time, energy, and stress if you dedicate yourself to the side of limb salvage. Taking a complete history will give you an idea of how compliant you can expect the patient to be and how actively involved you can expect the patient to be in their care.

31

AJM Sheet: Diabetic Infection Objective Physical Exam Objective -Vital Signs: -Temperature: Hyperthermia is a non-descript sign of infection. It is important to monitor temperature on a regular basis, and follow both current and maximum temperatures. Keep in mind however that Armstrong has documented that 82% of patients admitted for osteomyelitis were afebrile on admission (JFAS.1996 Jul-Aug; 35(4): 280-3). It has been suggested that diabetic patients, particularly those with ESRD, are not able to mount an effective immunologic response to the invading pathogen. -Blood Pressure: Hypotension is a sign of sepsis and non-descript measure of infection. -Heart Rate: Tachycardia is a sign of sepsis and non-descript measure of infection. -Respiratory Rate: Increased respiratory rate is a sign of sepsis and non-descript measure of infection. -Pain Level: Important to document and follow. Has been deemed the “5th vital sign” by JCAHO. -Glucose Levels: AJM considers blood glucose level the “6th vital sign” and can be one of the most important quantitative measurements of infection and response to therapy. Research indicates that the immune system is significantly impaired and essentially not working at levels as high as 150-175 ml/dL. (The Portland Diabetic Project is a good place to start reading about this. Also see Inzucchi SE. Management of Hyperglycemia in the Hospital Setting. NEJM. Nov 2006. 355;18: 1903-11). Also see the Sheet on “Glycemic Control” on page 72. -Ins and Outs: Important in patients with renal compromise. -Physical Exam -Derm: -Wound Characteristics: There are several classification systems you need to know for describing wounds including: -Wagner Classification -University of Texas Health System Classification -PEDIS Classification used by the Infectious Disease Society of America -Liverpool Classification used by the Musculoskeletal Infectious Disease Society -Acronym 3D MOBB (depth, diameter, drainage, measure, odor, base, border) -Regardless of classification, you absolutely must document certain wound characteristics: -Base: -Exact length, width and depth; consistency (ranging from red/granular to yellow/fibrotic to black/necrotic. Estimate percentages for mixed bases). -Depth—Probe to bone? [Grayson JAMA 1995. 89% positive predictive value for OM]. Also… -Lavery LA. Probe-to-Bone Test for Diagnosing Diabetic Foot Osteomyelitis. Reliable or relic? Diabetes Care. Feb 2007; 30(2): 270-274.

-Wound Edges:

-Consider hyperkeratotic, macerated, necrotic, clean, bleeding, epithelial, etc. -Undermining? Tunneling? -Drainage: -Consider serous, sanguinous, purulent (describe color), combination, etc. -Mild, moderate, severe/heavy -Describe any odor (This is probably Dr. Attinger’s most important variable in infection assessment!) -Periwound skin: -Consider normal, erythematic (document/draw extent), streaking, stasis changes, trophic changes. -Vascular: -Describe extent (anatomic level) and nature (pitting vs. non-pitting) of any edema. -Pulses (DP, PP, PT, Pop, and Fem every time) -Always doppler if nonpalpable at each level -CFT, Pedal Hair -ABI: -Values >0.9 associated with good healing potential -Values 0.5-0.9 associated with PVD and delayed healing -Values <0.5 associated with ischemia and problematic healing -Be wary of elevated values secondary to vessel calcification -TcPO2: -Values >30mmHg associated with good healing potential [Mars M. Transcutaneous oxygen tension as a predictor of success after an amputation. JBJS-Am. 1988; 70(9): 1429-30.]

-Values <20mmHg associated with microcirculatory problems and delayed/problematic healing. -Absolute Pressures: -Should have 40mmHg at ankle and 20mmHg at the digits for healing potential. -Absolute/Relative skin temperature: compare B/L (normal around 94° F). -Any other relevant vascular testing. -Neurologic: -Include testing for sensory, motor and autonomic neuropathy -Sensory testing: -Posterior column: Vibratory, Proprioception -Anterior column: Light touch (5.07 SWMF) -Lateral column: Pain and temperature -Motor testing: -Expect intrinsic weakness with advanced neuropathy -Manual Muscle Testing -Spinal Reflexes (Achilles, Patellar, Babinski) -Autonomic: -Increase in skin temperature -Lack of sweating leading to xerosis -Any other relevant neurologic tests (you should have an awareness of Dellon’s work and the PSSD). -Orthopedic: -Document any/all foot deformities, especially osseous prominences. -Expect intrinsic muscle weakness leading to digital deformities. -Overall foot type -Equinus

32

AJM Sheet: Specific Wound Classification Systems -Wagner Classification: [Wagner FW: The dysvascular foot: a system of diagnosis and treatment. Foot Ankle 2: 64–122, 1981] 0: Pre-ulcerative area without open lesion 1: Superficial ulcer (partial/full thickness) 2: Ulcer deep to tendon, capsule, bone 3: Stage 2 with abscess, osteomyelitis or joint sepsis 4: Localized gangrene 5: Global foot gangrene Modified with the following risk factors: A: Neuropathic B: Ischemic C: Neuroischemic -So an infected ulcer with localized gangrene and bone exposure on a fully sensate, ischemic foot is: Wagner 4B.

-University of Texas: [Lavery LA, Armstrong DG, Harkless LB: Classification of diabetic foot wounds. J Foot Ankle Surg 35:528–531, 1996] 0:

1:

2:

3:

A:

No open lesion

Superficial Wound

Tendon/Capsule

Bone/Joint

B:

With infection

With infection

With infection

With infection

C:

Ischemic

Ischemic

Ischemic

Ischemic

D:

Infection/Ischemia

Infection/Ischemia

Infection/Ischemia

Infection/Ischemia

-So an infected ulcer with localized gangrene and bone exposure on a fully sensate, ischemic foot is: UT-3D.

-Liverpool Classification System: -Primary:

-Neuropathic -Ischemic -Neuroischemic

-Modified with: -Uncomplicated -Complicated (cellulitis, abscess, OM, etc.)

-PEDIS System: [Lipsky BA, et al. Diagnosis and Treatment of Diabetic Foot Infections. IDSA Guidelines. CID 2004; 39: 885-910]. -Recommended by the Infectious Disease Society of America. -PEDIS is an acronym standing for perfusion (measure of vascular supply), extent/size, depth/tissue loss, infection, and sensation. -Each of the 5 categories is graded from 0 (minimal) to 2 (severe). -Based on10-point scale with 10 being most serious ulcer with greatest difficulty in treatment.

33

AJM Sheet: Diabetic Infection Objective Laboratory Results: Basic -Complete Blood Count (CBC) with Differential: -Total Leukocyte Count (~4-10 x 10^3 leukocytes/ul) -Leukocyte is a generalized term for any WBC including neutrophils/granulocytes, monocytes, lymphocytes, eosinophils and basophils. So an increased leukocyte count can indicate a rise in any or all of these. This is the reason why a differential is so important. -Neutrophils/Granulocytes (Usually ~54%; increased >85%) -Part of the humoral system. -Phagocytic cells in the inflammatory process. -Normally take 8-14 days to mature. Functionally last 1-2 days. Half-life 6 hours. -Would be increased in an inflammatory state. -PMNs: Mature neutrophils that you would expect to see in an infection. -Band cells: Immature neutrophils. Presence indicates active, ongoing infection. -A left shift is an increased neutrophil percentage in the presence of band cells. -Monocytes (Usually ~6%) -Phagocytic, bacteriocidal macrophages in the humoral system. -Accumulate after neutrophils in acute infection. -Presence indicates post-inflammatory state or chronic infection. -Lymphocytes (Usually ~37%) -Part of the cellular system. -Produce immunoglobulins and express cellular immunity (T and B cells). -Not normally increased in bone/soft tissue infections. -Possibly increased in a foreign body reaction. -Eosinophils (Usually ~2%) -Part of the cellular system. -Generally involved in allergic and immune responses. -Develop in the same line as lymphocytes. -Increased with acronym NAACP -(Neoplasm, Allergy, Addison’s, Collagen vascular disorder, Parasites) -Basophils (Usually ~0.5%) -Part of cellular immunity. -Involved with acute allergic responses and histamine release. -Leukocytosis is an increased WBC. The absolute count tells you very little, but trending can be very important. An increased leukocyte count indicates an increased level of inflammation, not necessarily infection. Keep in mind that there are many other causes of leukocytosis besides infection. -Drugs: Lithium, Corticosteroids -Leukopenia is a decreased WBC. This could lead to a normal WBC in the presence of infection. -Drugs: Methotrexate, Phenybutase, Dilantin, Salicylates -[Armstrong DG. Leukocytosis is a poor indicator of acute osteomyelitis of the foot in DM. JFAS 1996 Jul-Aug; 35(4): 280-3.]

-Chem-7/Metabolic Panel -Little information about specific infection, but insight into general health of patient. -Generally: -General increased concentrations: Dehydrated state -Acidosis: Non-descript finding in infection -Increased BUN: Dehydrated state -BUN/Cr: Renal function which has antibiotic consequences -Minerals (Ca, Mg, P) -Abnormal in renal dysfunction with long term vascular consequences. -Glucose, HbA1c -Long-term effects of hyperglycemia discussed in pathogenesis section. -HbA1C: Measure of glycosylated hemoglobin and long-term glucose control: -1% equals approximately 20 glucose points (7% equals ~140ug/ul) -Note that the stress of infection will probably cause a hyperglycemic state. -H&H, Coags -Essential to know if you are planning surgery.

34

AJM Sheet: Diabetic Infection Objective Laboratory Results: Advanced -Erythrocyte Sedimentation Rate (ESR) -Normal: <20mm/hr Moderate elevation: 20-60mm/hr Severe elevation: >60mm/hr -Analyzed using the Westergren method, which measures the distance erythrocytes fall in one hour in a vertical column of anti-coagulated blood under the influence of gravity. -Sensitive, but not specific for infection as it is increased in any inflammatory state with increased fibrinogen. -Also elevated in: Pregnancy, DM, ESRD, CAD, CVD, Malignancy, Age, etc. -[Karr JC. The diagnosis of osteomyelitis in diabetes using ESR. JAPMA 2002 May; 95(5): 314.] -[Lipsky BA. Bone of contention: diagnosing diabetic foot osteomyelitis. Clin Infect Dis. 2008 Aug; 47(4): 528-30.]

-C-Reactive Protein (CRP) -Normal: 0-0.6mg/dl -Measures a liver protein only present in acute inflammation (not normally found at all). -Sensitive, but not specific for infection. -Also elevated in: RA, Malignancy, MI, SLE, Pregnancy, etc. -More expensive and technically difficult to perform. -[Jeandrot A. Serum procalcitonin and CRP concentrations to distinguish mildly infected from non-infected diabetic foot ulcers: a pilot study. Diabetologia. 2008 Feb; 51(2): 347-52.]

-Nutrition Analysis -Albumin: -Normal Value: 3.6-5g/dl -Value decreased with inflammation and malnutrition. -Transport protein in liver with important functions in catabolism. -Pre-albumin -Normal Value: 19-36 mg/dL -Not covered well in PRISM, but check out [Arnold M. Nutrition and Wound Healing. Plast Reconstr Surg. 2006 Jun; 117(7 Suppl): 42S-58S.]

-Wound Culture and Sensitivity -Wound cultures are still a hotly debated topic because of controversies regarding contamination, colonization and defensive medicine. Suffice to say that swab cultures are easily contaminated by normal cutaneous flora, so should be taken as deeply as possible without surface contamination. The ideal situation is a deep wound specimen (not just a swab) following incision and drainage with pulse lavage before beginning antibiotic therapy. -Gram Stain (results usually within 24 hours) -PMNs if present: Do not overlook! Presence indicates inflammation. -Presence of any organism: essentially irrelevant. -Preliminary (results usually within 48 hours) -Gram stain nature (positive/negative) and shape (cocci/bacillus) of any organism -See chart of common organisms on next page -Clues you into organism -Continue Abx unless you are really off-base -Final (results usually within 72 hours) -Should always get sensitivities. -Allows for conclusive Abx planning. -Blood Cultures -Should be drawn from 2 sites; 20 minutes apart. -Indicates bacteremia/septicemia -Bone Biopsy -Gold standard for diagnosis of osteomyelitis (discussed further later) -Consider EKG and CXR if patient is a surgical candidate.

35

AJM Sheet: Gram Stain Results with Common Infective Agents: -Aerobic Gram Positive Cocci Staph aureus MRSA Staph epi MRSE Enterococcus VRE

Strept pyogenes (Group A) Strept agalactiae (Group B) Strept bovis (Group D) Strept Viridans

-Anaerobic Gram Positive Cocci Peptostreptococcus -Aerobic Gram Positive Rods Bacillus anthracis Corynebacterium diphtheriae Listeria Monocytogenes -Anaerobic Gram Positive Rods Clostridium perfringens Clostridium difficile Clostridium tetani -Aerobic Gram Negative Rods Pseudomonas E. coli Enterobacter Proteus Vibrio Y. pestis

Shigella Salmonella Klebsiella Serratia E. Corrodens P. multicide

-Anaerobic Gram Negative Rods Bacteroides fragilis -Aerobic Gram Negative Cocci Neisseria -Spirochetes Treponium pallidum Borrelia burgdorferi

36

AJM Sheet: Imaging in Diabetic Foot Infections -Plain Film Radiographs -Soft Tissue: Infection characterized by radiolucent area. One should be able to see a soft tissue deficit if an ulcer is present. It is very important to rule out emphysema (gas in the tissues) with a plain film. Can also appreciate soft tissue edema. -Osseous Tissue: -Early Osteomyelitis signs: No reliable ones. Possible rarefaction and periostitis. -Subacute OM signs: Brodie’s abscess (lytic lesion surrounded by sclerotic rim). -Chronic OM: Lysis, Malformation, Involucrum, Cloaca, Sequestra. -Plain film radiographs are 67% specific, 60% sensitive for OM (Termaat, JBJS 2005) -MRI -Cellulitis:

T1: Diffuse and infiltrative decreased signal intensity as inflammation replaces fat. T2 and STIR: Increased signal intensity.

-Abscess:

T1/T2/STIR: Homogeneous increased signal intensity. -Note that pus/necrotic tissue has a decreased intensity compared to inflammatory fluid.

-OM:

T1: Decreased signal intensity, cortical lysis and intramedullary changes. -Increased signal intensity in known OM indicates healing as fat infiltrates. T2: Increased signal intensity, cortical lysis, and intramedullary changes. -Rim sign: thin layer of active infection surrounding normal bone. -60% Specificity, 85% sensitivity per Termaat. -Bone Scans -A radio-isotope is injected into the patient and imaged at specific intervals. -Phases: -Immediate Angiogram (1-3sec): Essentially an arteriogram. -Blood Pool (3-5min): Demonstrates blood pooling in capillaries and veins. -Delayed (2-4 hours): Increasingly specific to activity patterns and pathology. -4th Phase: Increasingly specific to activity patterns and pathology. -Technetium-99 Bone Scan -Binds to calcium hydroxyapatite and measures osteoblast/osteoclast activity. -Half-life: 6 hours -Excreted through kidneys which will show homogenous control signal. -Mucomyst 600mg PO q12 day before and of surgery as renal ppx. -Cellulitis: Focal uptake in blood pool; Negative in delayed phase. -OM: Diffuse uptake in blood pool; Hot increased uptake in delayed phases. -45% Specificity; 86% sensitivity per Termaat. -WBC Scans -Same principles and phases as bone scan, but WBCs are tagged and followed instead. -Gallium-67 Citrate -Uptake by siderophore complex (direct bacteria) and lactoferrin (protein-released by bacteria) -Scan taken 48-72 hours after injection or done in triphasic manner. -Has longer half-life -42% Specificity; 80% Sensitivity per Termaat. -Indium-111 Oxime -WBCs isolated from blood sample, labeled and re-injected. -Scan at 24 hours. Half life: 67 hours. -Predominantly uptaken by neutrophils, so it demonstrates acute infections better than chronic infections. -Technetium-99m HMPAO -WBCs isolated from blood samples, tagged and re-injected. Scan at 3 hours. -Tagged molecule is HMPAO (hexamethylpropyleneamine oxime) -Technically easier with less radiation than indium. -Technetium-99m Sulfur Colloid Marrow Scan -Specific for bone marrow and neutrophil production -Has shown promise in differentiating OM from Charcot -Combination Sequential Technetium-Gallium Scans -Scan at 4 hours, then at 48-72 hours. Based on half-lives. -Increased specificity for infection if gallium has higher uptake then technetium. -Can use any other combination. -Computed Tomography (CT scans) -Radiograph altered by computer to highlight specific “windows”. You can isolate soft tissue or different aspects of bone, for example. -Soft tissue infection: Exact locations and anatomy of abnormal soft tissue density. -OM: Increased density in the marrow. -CT scans can be combined with contrast. -Positron Emission Tomography (PET scans) -A tracer is injected/inhaled into the patient which releases radioactive positrons. The positrons collide with electrons and produce gamma rays. ->90% Sensitivity and Specificity per Termaat (best in study).

37

AJM Sheet: Diabetic Foot Ulcer Pathogenesis -The pathogenesis of the diabetic foot ulcer can be described via three mechanisms: neuropathy, trauma and impaired healing. -Neuropathy -30-50% of diabetics have some form of sensory, motor and/or autonomic neuropathy. -Sorbitol accumulation in Schwann cells leads to hyperosmolarity of the nerve cells leading to swelling and cellular lysis. This leads to decreased nerve signal conduction. Microvascular damage to the nerve (described later) also impairs healing of the damaged nerve. -Sensory Neuropathy -Loss of light touch/protective sensation (anterior spinothalamic tract) -Loss of vibratory/proprioception mechanisms (posterior tract) -Loss of pain/temperature sensation (lateral tracts) -The patient has no warning of current, developing or impending trauma. -Motor Neuropathy -“Intrinsic Minus” foot-type with wasting of the intrinsic muscles and extensor substitution. -Undetected excess plantar pressures develop. -Autonomic Neuropathy -Damage occurs in the sympathetic ganglion -AV shunting occurs with global LE edema not relieved by diuretics or elevation. -Increased skin temperature predisposes to ulceration (Armstrong) -Decreased sweating leads to xerosis and fissuring (portal for infection) -Trauma leading to Ulceration -Abnormal anatomy: extrinsic and intrinsic abnormalities secondary to motor neuropathy and glycosylation. -Decreased joint mobility: secondary to non-enzymatic glycosylation and excess collagen cross-linking of tendons, ligaments, joint capsules (especially at the STJ and the MTPJ). -Equinus: Increased cross-linking of collagen in the Achilles tendon (leads to increased forefoot pressures). -Skin stiffness: secondary to glycosylation of keratin. -Intrinsic skin weakness: trophic changes associated with PVD. -All lead to increased plantar pressures, which is the driving force behind ulceration. -Impaired Wound Healing -Can be thought of as increased inflammation, decreased vasculature and decreased catabolism. -Increased Inflammation -The inflammatory phase of the healing process actually lasts longer than necessary. -Inflammation initially not as effective due to decreased leukocyte adhesion and morphologic changes to the macrophages. -Prolongation occurs due to decreased chemotaxis of growth factors and cytokines. -MMPs increase their activity and continue to produce an “inflammatory soup.” -All contribute to a wound “stuck” in the inflammatory phase. -Decreased Vasculature -Macroangiopathy: Atherosclerotic obstructive disease of large vessels due to LDL oxidation. -Microangiopathy: Thickened basement membrane decreases diffusion at capillary level. -Mechanism behind neuropathy, nephropathy and retinopathy -Think of it in terms of a decreased TcPO2 -Endothelial dysfunction: -Decreased NO and prostaglandin to promote vasodilation -Decreased smooth muscle cell relaxation to promote vasodilation -AV shunting secondary to autonomic neuropathy -Decreased vasodilation and membrane permeability in response to trauma/damage/inflammation: -Usually regulated by substance P and vasomodulators from damaged cells and nociceptors. -Overall leads to a “sluggish” vasculature with decreased inflow, diffusion, outflow and angiogenesis. -Decreased Catabolism -Decreased collagen synthesis, both in peptide production and post-translational modification -Morphologic changes to keratinocytes -Decreased angiogenesis Further Reading: -Shaw JE, Boulton AJ. The pathogenesis of diabetic foot problems: an overview. Diabetes. 1997 Sep; 46 Sep; Suppl 2:S58-61. -Rathur HM, Boulton AJ. The diabetic foot. Clin Dermatol. 2007 Jan-Feb; 25(1): 109-20. -Boulton AJ, et al. The global burden of diabetic foot disease. Lancet. 2005 Nov 12; 366(9498): 1719-24.

38

AJM Sheet: Diabetic Foot Infection Functional Anatomy From: Essential Questions for Surgical Intervention of Diabetic Foot Infections (http://www.podiatrytoday.com/article/8134)

Dedicating yourself to the side of limb salvage in the fight against diabetic foot disease is a demanding and personally challenging enterprise. In the face of infection, it often seems as though all variables are against the surgeon and the patient as together, you struggle against proximal amputation and limb loss. In fact, it often appears as though the only constant is the unpredictability of the disease progression. But one constant always on the side of the surgeon is anatomic knowledge. The infection can only work with the anatomy that it is given, and this is certainly something that can be used to your advantage. Your expert knowledge in lower extremity anatomy is one of the most valuable tools that you have in your fight. It is a constant, and it is predictable. There are different anatomic paradigms that must be considered in terms of the evaluation of the infection source. Certainly depth is one of these paradigms. Absolute depth measurements offer very little clinical information when compared to a functional view of depth from the surgical layers of dissection. An infection should be evaluated in terms of whether it extends through the dermis, superficial fascia, deep fascia, musculotendinous structures or to the level of bone (Table 1). From this general information, specific anatomic structures can then be identified as being within the path of the infection. Infections tend to develop and travel along the path of least resistance. This implies that an infection will stay within the potential space of a given surgical layer or plantar compartment before extravasation into another layer or compartment. Often, this involves proximal extension along the relatively avascular tendon sheaths or fascial planes between muscular layers. The studies that have been used to define the number and boundaries of plantar foot compartments have also given information about relatively consistent fascial clefts where communication between different layers and compartments is likely. These have involved pressurized injection imaging studies where a known compartment is infiltrated with a contrast medium and the extravasation into other compartments can be mapped. The findings of these studies are summarized in Table 2. These communications are obviously numerous and complex. The important concept to realize is that an infection is likely to initially develop within the potential space of a single layer or compartment. There is a tendency for the infection to move proximally before communicating with another layer or compartment. Note however, that patterns of communication are present along known anatomic structures such as tendons and neurovascular structures to each of the other compartments, as well as the dorsum of the foot and plantar superficial fascia. Intra-operative investigation of an infection should focus on these structures to trace the extent of plantar involvement. Also note the majority of these communications are found in the forefoot around MPJ level, so distal infections have an increased likelihood of multicompartment involvement. Table 1: Surgical Layers of Dissection Used for Diabetic Ulcer Depth Measurement Skin Superficial Fascia -First Dissection Interval containing superficial neurovascular structures Deep Fascia -Second Dissection Interval containing muscular and deep neurovascular structures Periosteum -Third Dissection Interval Bone

Table 2: Intercompartmental Communications Medial Compartment To Central Compartment via: -Adductor Hallucis tendon -Flexor Hallucis Longus tendon -Peroneus Longus tendon -Neurovascular structures penetrating the medial IM septum To Distal Deep Leg via: -Flexor Hallucis Longus tendon Lateral Compartment: To Central Compartment via: -Long flexor tendon to 5th digit -Short flexor tendon to 5th digit -Lumbrical muscle to 5th digit -Plantar interosseous muscle to 5th digit -Peroneus Longus tendon -Neurovascular structures penetrating lateral IM septum To Dorsal Structures To Plantar Superficial Fascia

Central Compartment To Medial Compartment via: -Adductor Hallucis tendon -FHL Tendon -PL Tendon -NV structures penetrating medial IM septum To Lateral Compartment via: -Long flexor tendon to 5th digit -Short flexor tendon to 5th digit -Lumbrical muscle/tendon to 5th digit -Plantar interosseous muscle to 5th digit -PL tendon -NV structures penetrating lateral IM septum To Distal Deep Leg via: -FHL tendon -FDL tendon To Dorsum of Foot via: -Interosseous muscles -MPJ communications To Plantar Superficial Fascia

39

AJM Sheet: Osteomyelitis General -Osteomyelitis is a complicated issue dealing with diabetic foot infections both in diagnosis and treatment. However, there are several definitions, classification systems, diagnostic modalities and treatment tenets that you should be aware of. -Definitions per Resnick: -Periostitis: Inflammation of the periosteum -Osteitis: Inflammation of the cortex -Osteomyelitis: Inflammation of the medullary canal -Sequestrum: piece of dead bone floating in pus/inflammation -Involucrum: sheath of bone surrounding pus/inflammation -Cloaca: tract through an involucrum -Brodie’s Abscess (1832): Chronic abscess in bone surrounded by sclerosis -Sclerosing OM of Garre: low grade inflammatory condition -Waldvogel and Lew [Osteomyelitis. NEJM. 1997; 336(14): 999-1007.] -The classic Waldvogel and Lew article is NOT a classification, rather a serious of definitions. However, it can be turned into a stratified classification based on their definitions. -Acute Osteomyelitis: Systemic clinical signs of infection -Chronic Osteomyelitis: Subacute clinical signs of infection -Contiguous/Direct Extension: spread of infection to bone from exogenous source or adjacent tissue. This can be described as an “outside-in” spread invading the cortex and proceeding to the medullary canal. -Hematogenous Spread: Infective agent reaches medullary canal of bone from the vascular supply. This can be described as an “inside-out” infection invading the medullary canal first and spreading to the cortex. -Vascular Impairment: Decreases the effectiveness of the inflammatory response and Abx delivery. -Others have done a little better job of differentiating acute vs. chronic OM: -Weiland: Describes chronic OM as lasting > 6months. -Schauwecker: Describes chronic OM as lasting > 6 weeks and one failed episode of tx. -AJM has turned these definitions into a classification system that made more sense to him: -Acute Osteomyelitis -Contiguous/Direct Extension -No PVD -PVD -Hematogenous Spread -No PVD -PVD -Chronic Osteomyelitis -Contiguous/Direct Extension -No PVD -PVD -Hematogenous Spread -No PVD -PVD -Cierny-Mader-Penninck Classification [A clinical staging system for adult osteomyelitis. CORR. 2003; (414): 7-24.] -This is described as a classification, but doesn’t make much sense to AJM. -Anatomic Stage 1: Medullary: infection of only the medullary canal (Stage 1) 2: Superficial: infection of only the superficial cortex (Stage 2) 3: Localized: infection of only the cortex (Stage 3) 4: Diffuse: infection of both the cortex and medullary canal (Stage 4) -Physiologic Stage A: Normal Host Bs: Compromised Host with systemic risk factors (eg DM) Bl: Compromised Host with local risk factors (eg smoking) C: Treatment worse than the disease -So a smoking DM patient with infection of only the superficial portion of the cortex is: 2Bs -Obviously much more work needs to be done on the topic of osteomyelitis classification.

40

AJM Sheet: Osteomyelitis Diagnosis and Treatment -Subjective Findings (See Diabetic Infection Work-up) -Objective Findings (Diabetic Infection Work-up) -Probing to bone 89% positive predictive value (Grayson JAMA 1995). -Gold Standard: Bone biopsy. This is ideally performed when the patient has been free of antibiotics for 2 weeks. -Imaging Studies: -Review plain films, MRI, Bone Scans, WBC scans, CT, PET in Diabetic Infection Imaging Sheet. -These all add evidence, but are rarely exclusively diagnostic. -Blood Cultures: Hematogenous OM diagnosed with positive BCx and positive bone scan. Treatment -There is much controversy regarding long-term Abx (PO vs. IV vs. PMMA) vs. Surgical Debridement. -The Cierny-Mader Classification makes some general recommendations: -CM Stage 1: 2 weeks IV + 2-4 weeks PO Abx -CM Stage 2: Surgical Debridement + 2 weeks IV -CM Stage 3&4: Surgical Debridement + 4-6 weeks IV Abx -Antibiotic administration options -Long-term Abx (4-8 weeks) is a conservative option because many people believe you can never cure OM and that it can reactivate at any time for years to come. -PO -Doxycycline and Ciprofloxacin are reputed to have the best bone penetration. -Most ID docs would never substitute coverage for bone penetration. -Your Abx choices should be culture driven. -IV -Culture driven -Access options: IV, PICC, Infusion pump, etc. -PMMA beads -PMMA: polymethylmethacrylate -PMMA is a combination of monomer (liquid) and polymer (powder). -Comes in 20, 40 and 60g packets. -7% elusion in the first 24 hours with activity noted for 14 days. -Demonstrates exponential release. -Cierny proposes a 1:5 ratio of Abx:PMMA. Another common standard is 4-8g:40-60g. -Increased Abx means increased elution, but decreased bead hardening. -Smaller beads means increased surface area and increased elution. -The Abx must be heat-labile -Gentamycin, Tobramycin, Vancomycin, Ticarcillin, Cefazolin, Moxalactam, Cefotaxime

41

AJM Sheet: Charcot Neuroarthropathy -Definition: Neuropathic osteoarthropathy first described by Musgrave in 1703 and named for JM Charcot in 1868. -Pathogenesis: -Neurovascular/French Theory/Theory of Charcot -Trophic centers in the anterior horn of the spinal cord maintain nutrition to joints. -Trauma to these trophic centers leads to increased blood flow and osteoclastic activity. -Evidence for the Neurovascular Theory: -Autonomic neuropathy in DM leads to increased AV shunting, edema and skin temperature. -Boulton: Increased PO2 in venous system of Charcot pts (63mmHg vs. 46mmHg) -Shows increased perfusion in neuropathic diabetics -Edmonds: Increased blood velocity in neuropathic diabetics -Young: Decreased bone density in patients with decreased nerve conduction velocities -Cundy: Decreased bone density in Charcot patients -Gough: Increased osteoclastic activity in Charcot patients -Neurotraumatic/German Theory/Theory of Virchow and Volkmann -Repeated trauma from biomechanical stresses during ambulation on an insensate foot. -Evidence for the Neurotraumatic Theory: -Eloesser and Johnson: Trauma is the necessary predisposing factor, and not underlying bone weakness, to create Charcot changes in a neuropathic limb. -Common sense -Two opposing, fighting theories? Probably a little bit of both. -Etiology: Anything that causes neuropathy! -First described: Tabes Dorsalis (Charcot 1868) -Most common: DM -3 most common: DM, Syringomyelia (longitudinal cavities lined by dense tissue), and Tabes Dorsalis -C: Myelomeningocele, Spina Bifida, CMT, MS, CP, Syringomyelia, Congenital insensitivity M: DM, Alcoholic neuropathy, Uremia, Pernicous Anemia I: Tabes Dorsalis, Polio, Leprosy, TB N: Tumors in brain, spinal cord, peripheral nerve T: Trauma to brain, spinal cord, peripheral nerve D: Indomethacin, Intra-articular corticosteroids, phenylbutazone -DDx: OM, AVN, inflammatory arthritis, PVS, septic arthritis, CPPD, neoplasm, etc. -Clinical Findings: -Presents similar to infection -Red, hot, swollen, deformed foot +/- pain -Neuropathic -Readily available pulses (often described as bounding) -Radiographic Findings: -Atrophic:

-With osteopenia, pencil&cup deformities, resorption of bone ends -Without osteophytes, sclerosis, fragmentation, soft tissue debris -Hypertrophic: -With joint space narrowing, fractures, fragmentation, ST debris, periosteal rxn, subluxation -Without osteoporosis -Be aware of both types.

-Classification Systems (described in detail on next page) -Eichenholtz Classification (1966) -Brodsky Classification -Schon Classification -Treatment -Acute: -Strict and immediate NWB and immobilization for 12-16 weeks. -Edema control (Jones cast, ACE inhibitors, Diuretics, Posterior splint, Elevation, Ex Fix, etc.) -Education and family support -FXR every 4-6 weeks with relatively few cast changes -Transition: -Transition to WB (CAM walker, CROW, Bracing, MAFO, Shoes, etc.) -Permanent: -Surgical correction of underlying deformity -Consider TAL, Arthrodesis, Wedging osteotomies, Amputation -Adjunctive: -Bone stimulators -Bisphosphonates: -Pamidronate (Aredia): 60-90mg over 24h. 3 doses in 2 weeks. -Alendronate (Fosamax): 5mg PO q24h.

42

AJM Sheet: Charcot Classifications -Eichenholtz Classification (1966) -Based on plain film radiographic findings -Originally described Stages 1
3, but Stage 0 added later (Yu given credit, but really Schon). -[Yu GV, Hudson JR. Evaluation and treatment of stage 0 Charcot’s neuroarthropathy of the foot and ankle. JAPMA. 2002; 92(4): 210-20.] -Stage 0: High risk pre-Charcot -Radiograph: Unremarkable. Maybe increased ST density, bone flecks or change in foot architecture. -Clinical: Sudden onset of non-pitting edema, erythema, calor, +/- pain, bounding pulses, intrinsic atrophy. -Normal skin temp: 94°F; can increase by 12° -Uptake in all three phases of Tc-99 bone scan -Stage 1: Acute/Developmental -Radiograph: Capsular distention, fragmentation, debris, subluxation -Clinical: Red, hot, swollen foot with joint laxity -Stage 2: Coalescence -Radiograph: Sclerosis, resorption of debris, fusion -Clinical: Subjectively decreased red, hot, swollen -Stage 3: Reconstruction -Radiograph: Decreased sclerosis (with increased vascularity) and remodeling -Clinical: Decreased joint mobility with increased stabilization -Brodsky Classification (1992) -Describes location of deformity -Type 1: Lisfranc joint (27-60% incidence) -Type 2: Chopart’s joint and STJ (30-35% incidence) -Type 3A: Ankle joint (9% incidence) -Type 3B: Posterior calcaneus -Type 4: Multiple combinations of above -Type 5: The forefoot -Schon Classification [Charcot neuroarthropathy of the foot and ankle. CORR. 1998; 349: 116-131.] -Describes location and severity of condition I: Lisfranc Pattern -A
C with increasing deformity to medial rockerbottom and ulceration. II: Naviculocunieform Pattern -A
C with increasing deformity to lateral rockerbottom and ulceration. III: Perinavicular Pattern -A
C with lateral rockerbottom, Talar AVN and ulceration. IV: Transverse Tarsal Pattern -A
C with increasing deformity to central rockerbottom and ulceration.

43

AJM Sheet: Differentiating Osteomyelitis from Charcot -Please keep in mind that these are not mutually exclusive and both can be present! -These are just general guidelines and many people will vehemently argue them. -The gold standard is a bone biopsy which would show infection in OM and not in Charcot. Subjective -OM: Constitutional signs and symptoms of infection, infectious risk factors, history of infection. -Charcot: Uncontrolled DM, history of Charcot, history of recent trauma. Objective -OM: Necrosis, pustular drainage, elevated white count, cultures, positive bone biopsy. -Charcot: Increased joint laxity, non-pitting edema, bounding pulses, rockerbottom deformity, negative bone biopsy. Imaging -Not enough evidence yet, but some believe that OM is positive on bone scans and WBC scans for greater than 24 hours whereas Charcot neuroarthropathy is only positive during the first 24 hours. -The Tc99 Sulfur Colloid scan would also theoretically be positive for infection, but not for Charcot. -Not too much here, but check out some further reading: -Soysal N, et al. Differential diagnosis of Charcot arthropathy and osteomyelitis. Neuro Endocrinol Lett. 2007 Oct; 28(5): 556-559. -Shank CF, Feibel JB. Osteomyelitis in the diabetic foot: diagnosis and management. Foot Ankle Clin. 2006 Dec; 11(4): 775-89. -Ledermann HP, Morrison WB. Differential diagnosis of pedal osteomyelitis and diabetic neuroarthropathy: MR Imaging. Semin Musculoskelet Radiol. 2005 Sep; 9(3): 272-83. -Berendt AR, Lipsky B. Is this bone infected or not? Differentiating neuron-osteoarthropathy from osteomyelitis in the diabetic foot. Curr Diab Rep. 2004 Dec; 4(6): 424-9. -Yu GV, Hudson JR. Evaluation and treatment of stage 0 Charcot’s neuroarthropathy of the foot and ankle. J Am Podiatr Med Assoc. 2002 Apr; 92(4): 21020. -Schon LC, et al. Charcot neuroarthropathy of the foot and ankle. Clin Orthop Relat Res. 1998 Apr;(349): 116-31. -Berendt AT, Peters EJ, et al. Diabetic foot osteomyelitis: a progress report on diagnosis and a systemic review of treatment. Diabetes Metab Res Rev. 2008; 24(S1): S145-S161.

44

AJM Sheet: Common Situational Bugs -Cellulitis with an open wound:

-SA (if no streaking present) -Strept (with streaking and palpable border) -Usually monomicrobial

-Infected ulcer in Abx naïve pt:

-SA -Strept -Usually polymicrobial -SA -Strept -Enterobacter -Usually polymicrobial

-Chronically infected ulcer in Abx naïve pt:

-Macerated infected ulcer:

-Pseudomonas -Usually polymicrobial

-Chronic, non-healing ulcer with prolonged Abx therapy:

-SA -MRSA -Staph epi -Enterococci -VRE -Diptheroids (Corynebacterium) -Enterobacter -Pseudomonas -Extended GNR -Usually polymicrobial

-Fetid Foot with necrosis and gangrene:

-Resistant Gram positive cocci -Mixed GNR -Anaerobes -Polymicrobial

-Osteomyelitis with hemodialysis:

-SA -Enterobacter -Pseudomonas

-Osteomyelitis with IVDA:

-SA -Enterobacter -Pseudomonas

-Osteomyelitis with Decubitus Ulcer:

-Gram Negatives

-Osteomyelitis with hemoglobulinopathy:

-Salmonella

-Human mouth pathogens (HACEK):

-Haemophilus, Actinobacillus, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae

-Water exposure:

-Vibrio -Aeromonas hydrophila -Mycobacterium -Pseudomonas

-Puncture through a shoe:

-Clostridium

-Any dirt/soil: -Cat bite:

-Pasteurella multocida

-Immunocompromised pt: -Septic bursitis:

-Dog bite:

-Strept viridans, Capnocytophaga canimorsus

-Gram negatives -SA

-Gas gangrene:

-Clostridium

-Foul smelling discharge:

-Anaerobes

-White discharge:

-Staph epi

-Post-op infection following implant: -Staph epi -Fruity odor/green hue:

-Pseudomonas

-Creamy yellow discharge: -SA

45

AJM Sheet: Empiric Antibiotic Choices Generalized Gram Positive Coverage: -2nd Generation PCN -4th Generation PCN -1st Generation Cephs -2nd Generation Cephs -Carbapenems -Tetracyclines

-2nd Generation Quinolones -Macrolides -Bactrim -Vancomycin -Clindamycin -Zyvox

-Synercid -Rifampin

Generalized MRSA Coverage: -Vancomycin -Clindamycin -Zyvox

-Synercid -Bactrim/Rifampin -Cubicin

Generalized Gram Negative Coverage: -3rd Generation PCN -4th Generation PCN -Carbapenems -Tetracycline -Aztreonam

-2nd Generation Quinolones -3rd Generation Quinolones -4th Generation Quinolones -Bactrim

Generalized Pseudomonas Coverage: -Cephalosporins x 3 (Fortaz, Cefobid, Maxipime) -PCN x 2 (Zosyn, Timentin) -Aminoglycosides -Primaxin -Quinolones -Aztreonam

Generalized Anaerobes: -4th Generation PCN -1st Generation Cephs -2nd Generation Cephs -3rd Generation Cephs -4th Generation Cephs

-Aminoglycosides -Carbapenems -4th Generation Quinolones -Clindamycin -Flagyl

46

AJM Sheet: IDSA Empiric Recommendations -from Lipsky BA, et al. Diagnosis and Treatment of Diabetic Foot Infections. IDSA Guidelines. CID 2004; 39: 885-910. -Uninfected Wound -Definition: No purulence, inflammatory manifestations, or systemic manifestations -Empiric Therapy: None -Mildly Infected Wound -Definition: -2+ Manifestations of Infection (purulence, induration or erythema/pain/warmth) -<2cm of erythema -Limited to skin and subcutaneous tissue -No systemic complaints -Empiric Therapy Recommendations: -2-PCN -Clinda -Keflex

-Bactrim -Augmentin -Levo

-Moderately Infected Wound -Definition: -As above, in a systemically/metabolically stable patient PLUS ->2cm cellulitis OR streaking OR involvement of deep tissue -Empiric Therapy Recommendations: -Bactrim -Augmentin -Levo -2-Ceph -3-Ceph -Daptomycin + Aztreonam -Zyvox + Aztreonam

-Invanz -Ceftin + Flagyl -Timentin -Zosyn -Levo + Clinda -Cipro + Clinda

-Severely Infected Wound -Definition: -Infection as above in a patient with systemic toxicity and metabolic instability -Empiric Therapy Recommendations: -Primaxin -Zosyn -Cipro + Clinda -Levo + Clinda -If MRSA is likely: -Zyvox -Zyvox + Aztreonam -Daptomycin -Daptomycin + Aztreonam

-Vanco + Fortaz -Vanco + Fortaz + Flagyl

-Vanco + Fortaz -Vanco + Fortaz + Flagyl

-To cover all bases: -Vanco + Aztreonam + Flagyl

47

AJM Sheet: Common Infective Agents with DOC: DOC

Alternatives

-Aerobic Gram Positive Cocci Staph aureus MRSA Staph epi MRSE Enterococcus VRE Strept pyogenes (Group A) Strept agalactiae (Group B) Strept bovis (Group D) Strept Viridans

1-Ceph Vanco 2-PCN Vanco 3-PCN Linezolid 3-PCN 3-PCN 3-PCN 3-PCN

Vanco, Clinda, Azithromycin Bactrim, Cubicin, Zyvox, Clinda 4-PCN, 1,2-Ceph, Vanco Zyvox, Cubicin, Synercid Vanco, Tetracyclines, Quinolones Macrobid, Cubicin, Chloramphenicol 4-PCN, 1,2-Ceph, Vanco, Clinda 4-PCN, 1,2-Ceph, Vanco, Clinda 4-PCN, 1,2-Ceph, Vanco, Clinda 4-PCN, 1,2-Ceph, Vanco, Clinda

-Anaerobic Gram Positive Cocci Peptostreptococcus

Clinda

3-PCN, 4-PCN, Carbapenems

-Aerobic Gram Positive Rods Bacillus anthracis Corynebacterium diphtheriae Listeria Monocytogenes

Cipro Macrolide 3-PCN

3-PCN, Vanco, Clinda Clinda, Vanco, Bactrim, Carbapenems

-Anaerobic Gram Positive Rods Clostridium perfringens Clostridium difficile Clostridium tetani

Ertapenam Flagyl Clinda

Vanco, Clinda, 4-PCN, Tetracyclines Vanco Flagyl

-Aerobic Gram Negative Rods Pseudomonas E. coli Enterobacter Proteus Vibrio Y. pestis Shigella Salmonella Klebsiella Serratia E. Corrodens P. multocida

Zosyn 3-Ceph Bactrim 3-PCN Tetracyclines Aminoglycosides Cipro Cipro 3-Ceph 3-Ceph Augmentin Doxycycline

1,2-Quin, Aztreonam, Primaxin 4-PCN, Bactrim, Quinolones Quinolone, Aztreonam, Carbapenems 3-Ceph, 4-PCN, Bactrim, Quinolones Bactrim, Cipro Bactrim, Cipro Bactrim, Amp, 4-PCN 3-PCN, 4-PCN, Bactrim 4-PCN, Bactrim, 2-Quin, Aminoglycosides Zosyn, Bactrim, Aztreonam, Quin Tetracyclines Bactrim, 3-PCN

-Anaerobic Gram Negative Rods Bacteroides fragilis

Ertapenam

Clinda, Flagyl

-Aerobic Gram Negative Cocci Neisseria

Rocephin

3-PCN, Quinolones

-Spirochetes Treponium pallidum Borrelia burgdorferi

1-PCN 1-PCN

Tetracyclines, Macrolides Amox, Macrolides

48

AJM Sheet: Antibiotics/Drugs of Choice 1.

2.

Staph Aureus -PO: Keflex Clindamycin Zithromycin -IV: Ancef Vancomycin Clindamycin

-500mg PO tid or 750mg PO bid -300mg PO qid -500mg PO day 1, 250mg PO days 2-5 -1g IV q8 -1g IV q12 -600mg IV q8

Streptococcus -PO: Keflex Clindamycin -IV: Ancef Vancomycin Clindamycin

-500mg PO tid or 750mg PO bid -300mg PO qid -1g IV q8 -1g IV q12 -600mg IV q8

3.

MRSA -IV: Vancomycin -1g IV q12 -PO: Bactrim -1 tablet PO bid Rifampin 300mg + Minocycline 100mg PO bid

4.

Enterococcus -PO: Amoxicillin Augmentin Zyvox -IV: Vancomycin Zyvox

-250-500mg tid -875mg bid or 500mg tid (or bid) -600mg PO bid -1g IV q12 -600mg IVq12

VRA/VRE -PO: Zyvox -IV: Zyvox Synercid

-600mg PO bid -600mg IV q12 -7.5mg/kg/hr over 1 hour q12

Pseudomonas -PO: Ciprofloxacin -IV: Ciprofloxacin Fortaz Aztreonam

-250-750mg PO bid -400mg IV q12 -2g IV q12 -1g IV q8

E.coli, Proteus -PO: Keflex Cipro Levaquin Tequin -IV: Ancef Cipro Levaquin Tequin

-500mg PO tid or 750mg PO bid -250-750mg PO bid -500mg PO qday -400mg PO qday -1g IV q8 -400mg IV q12 -500mg IV qday -400mg IV qday

5.

6.

7.

49

AJM Sheet: Antibiotic Dosing Guide Penicillins 1st Generation: 2nd Generation: 3rd Generation: 4th Generation:

-Pen V: -Pen G: -Dicloxacillin: -Oxacillin: -Nafcillin: -Amoxicillin: -Ampicillin: -Augmentin: -Unasyn: -Zosyn: -Timentin:

Cephalosporins 1st Generation: -Keflex: -Duricef : -Ancef: 2nd Generation: -Ceftin: -Zinacef: -Mefoxin: 3rd Generation: -Omnicef: -Vantin: -Rocephin: -Fortaz: -Cefobid: 4th Generation: -Maxipime: Quinolones 2nd Generation: 3rd Generation: 4th Generation:

500mg q6 PO 250,000 units/kg/day IV 250mg q6 PO 1-2g q4 IV 1-2g q4 IV 500mg q8 PO 1g q4-6 IV 875mg q12 PO 3g q6 IV 4.5g q6 IV 3.1g q6 IV

500mg q8 PO or 750mg PO bid 2g q24 PO 1g q8 IV 500mg q12 PO 1.5g q8 IV 1g q6 IV 300mg q12 PO 400mg q12 PO 1g q24 IV 1g q8 IV 2g q12 IV 2g q12 IV

-Ciprofloxacin: -Levofloxacin: -Tequin: -Avelox:

750mg q12 PO/400mg q12 IV 500mg q24 PO/IV 400 q12 PO/IV 400 q24 PO

Macrolides

-Biaxin: -Ketek: -Zithromax: -Erythromycin

500mg q12 PO 800mg q24 PO 500 q12 IV/ 500mg PO Day 1; 250 mg PO Day2-5 500mg q6 PO

Carbapenems

-Invanz: -Primaxin: -Merrem

1g q24 IV 500mg q8 IV 1g q8 IV

Aminoglycosides -Amikacin: -Tobramycin: -Gentamycin:

1500mg/day 3-5mg/kg/day 3-5mg/kg/day

Tetracyclines

-Minocycline: -Doxycycline: -Tetracycline:

100mg q12 PO/IV 100mg q24 PO 500mg q6 PO

Misc

-Bactrim DS: -Aztreonam: -Vancomycin: -Clindamycin: -Zyvox: -Cubicin: -Synercid: -Flagyl: -Rifampin: -Tygacil:

160/800mg q24 PO 1g q8 IV 1g q12 IV 600mg q8 IV; 300mg q6 PO 600mg q12 PO/IV 4mg/kg q12 IV 7.5mg/kg q8 IV 500mg q8 PO 300mg q12 PO/IV 100mg loading dose; then 50mg q12 IV

50

AJM Sheets: Trauma Trauma is another area that is often highlighted during the interview process. This section first details a trauma-specific work-up, and then goes through some specific traumatic conditions. In terms of the interview, you generally will be expected to work-up, diagnose and classify based on radiographs, CTs and MRIs. While you should certainly have an understanding of treatment interventions and protocols, this will probably be less emphasized than diagnosis and classification. A lot of these classifications are very visual (and I don’t have room for that in 100 pages), so I’ve tried to include a lot of specific references with pictures of the classifications (mostly to McGlamry’s and Gumann’s texts). I’ve also tried to include a lot of references to “classic” articles and review articles. Textbooks with good trauma information for additional reading include specific ones (Gumann’s, Scurran’s, Rang’s, etc), but also general ones (McGlamry’s, Myerson’s, Hansen’s, etc). I said that while I was studying for the Diabetic Foot Infection work-up, I tried to learn as much as possible on the topic and really tried to “wow” the attendings at the interview. However, my strategy was different when dealing with trauma and the specific surgical work-ups. Here I tried to demonstrate “competence” as opposed to “mastery” of the material. With specific surgeries, you’re really not supposed to have strong, pre-formed opinions as a student or as an intern. That’s what your residency is for; developing surgical opinions. If you already know what to do in every surgical situation, then what’s the point of doing a residency? So while on externships and at the interview, you should really try to walk a fine line between: 1. Displaying competence in knowledge of the baseline material 2. Displaying that you still have a lot to learn, and that you are eager to learn it Contents: -The Trauma Work-Up (page 52) -General Trauma Topics (pages 53-54) -Digital Fractures (page 55) -Sesamoid Trauma (page 56) -Metatarsal Fractures (page 57) -5th Metatarsal Fractures (page 58) -Metatarsal Stress Fractures (page 59) -LisFranc Trauma (page 60) -Navicular Trauma (page 61) -Talar Fractures (page 62) -Calcaneal Fractures (page 63) -Ankle Fractures (pages 64-65) -General Tendon Trauma (page 66) -Achilles Tendon Work-up (page 67) -Achilles Tendon Treatment (page 68)

51

AJM Sheet: Trauma Work-up -The Trauma Work-up is very similar to the regular patient work-up, but with a few things added. You still need to go through the HPI, PMH, PSH, Meds, Allergies, SH, FH, ROS and complete physical exam in that order. In addition, there are three other topics that you need to address on every trauma patient for every work-up: 1. ABCDE’s of the Primary Survey -Airway: Three common forms of airway obstruction are cervical spine injury, swollen tongue and facial fracture. -Breathing: Note how this is different than an established airway. Someone can have an airway, but still not be breathing. -Circulation: Assess vascular status in all four extremities. Two large-bore (18-gauge) IV’s should be started immediately if fluid replacement is considered necessary. -Deficits (Neurological): There are two ways to assess this. -AVPU -Alert, responds to Verbal stimuli, responds to Painful stimuli, or Unresponsive -Glasgow Coma Scale -Based upon three criteria: eye opening, verbal response, motor response. -Based on scale of 0-15 with a higher score indicating a better prognosis. -13+ associated with a good prognosis; 7- associated with a poor prognosis. -Exposure: Complete exposure of the patient to evaluate further, unknown damage. -Secondary Survey: This is when you go through a normal history including HPI, PMH, etc. and a comprehensive physical exam. 2. Tetanus Status -Clostridium tetani is a racquet-shaped gram-positive bacillus. It releases an exotoxin causing a pre-sympathetic blockade. -Triad of tetanus symptoms: Trismus, Risus Sardonicus, and Aphagia. -Characteristics of a tetanus-prone wound: greater than 6 hours old, clinical signs of infection, deep, devitalized tissue, contamination, traumatic mechanism of injury, etc. -Basic Tetanus Algorithm: -Unknown tetanus status:

-Clean wound: -Tetanus-prone wound:

Give the toxoid; Hold the TIG Give the toxoid; Give the TIG

-Incomplete tetanus status: (No booster within 5 years)

-Clean wound: Give the toxoid; Hold the TIG -Tetanus-prone wound: Give the toxoid; Give the TIG

-Complete tetanus status: (Booster within 5 years)

-Clean wound: -Tetanus-prone wound:

-Dosages:

Hold the toxoid; Hold the TIG Hold the toxoid; Hold the TIG

-Toxoid: 0.5ml -TIG (tetanus immunoglobulin): 250-300 units

3. NPO status -All trauma patients are potential surgical candidates, so get this information for the weenie anesthesiologists. -Traditional guidelines recommend: -Nothing by mouth after midnight the night before elective surgery -Nothing by mouth within 6-8 hours of any type of surgery -These strict guidelines are in the process of changing however, particularly with regard to allowing the ingestion of small amounts of clear liquids up to the time of surgery. If interested, please read: -[Brady M, Kinn S, Stuart P. Preoperative fasting for adults to prevent perioperative complications. Cochrane Database Syst Rev. 2003; (4): CD004423.] -[Murphy GS, et al. The effect of a new NPO policy on operating room utilization. J Clin Anesth. 2000 Feb; 12(1): 48-51.]

52

AJM Sheet: General Trauma Topics -In addition to having a good trauma work-up, there are a few other things that are helpful to know regarding foot and ankle trauma. 1. Podiatric Surgical Emergencies -Infection with emphysema (gas gangrene) -Open fracture/dislocation -Compartment syndrome -Necrotizing Fasciitis -General Neurovascular compromises 2. Mangled Extremity Severity Score (MESS) -[Helfet DL, et al. Limb salvage versus amputation. Preliminary results of the Mangled Extremity Severity Score. CORR 1990; 256: 80-6.] -[Bosse MJ, et al. A prospective evaluation of the clinical utility of the lower-extremity injury-severity scores. JBJS-Am 2001; 83(1): 3-14.] -Based on 4 criteria: Skeletal/Soft Tissue Injury, Limb Ischemia, Age, and Shock -Based on a scale from 1-11 with a higher score leading to an increased incidence of amputation. -A score of 7+ has an increased likelihood of amputation. 3. Open Fractures -Note that 30% of lower extremity open fractures are associated with polytrauma. -Mainstays of treatment: Aggressive incision and drainage with copious lavage. -It is generally recommended to never primarily close an open fracture until devitalized soft tissue has demarcated, but this certainly isn’t always the case in practice. In fact, the Ortho Trauma service at INOVA routinely primarily closes open fractures following I&D with ORIF. -Gustilo-Anderson Classification of Open Fractures [Gustilo RB, Anderson JT. Prevention of infection in the treatment of one thousand and twenty-five open fractures of long bones: retrospective and prospective analyses. JBJS-Am. 1976; 58(4): 453-8.] I. Clean Wound <1cm in diameter -Abx choice: 1st generation cephalosporin (Ancef) II. Wound 1.0-5.0cm in diameter with minimal soft tissue damage -Abx choice: Ancef, Clindamycin III. Wound >5cm in diameter with extensive soft tissue damage -Abx choice: Ancef (or high dose PCN), Clindamycin and Aminoglycoside -IIIA: Adequate soft tissue coverage -IIIB: Extensive soft tissue damage with periosteal stripping and massive contamination -IIIC: Arterial damage requiring primary repair 4. Fracture Blisters -Location: Subepidermal -Note that the fluid is sterile. Fracture blisters are histologically similar to 2nd degree burns. -Most common LE etiology? Secondary to high-energy trauma such as ankle fx, calcaneus fx or Lisfranc injury. -2 Common Types of Fracture Blisters -Clear fluid: Most common (75%). Very tense in appearance. -Hemorrhagic: Most severe. Roof is flaccid. Takes longer to re-epithelialize. -Treatment is controversial, but the conservative approach is to never incise through a fracture blister and to delay surgery until re-epithelialization. -[Strauss EJ, et al. Blisters associated with lower-extremity fracture: results of a prospective treatment protocol. J Orthop Trauma. 2006 Oct; 20(9): 618-22.]

5. Shock -Signs/Symptoms of Shock: Tachycardia, Tachypnea, delayed capillary refill, decreased pulse pressure, change in mental status, decreased systolic pressure, decreased urinary output and decreased H&H. -Types of Shock: -Hypovolemic: most common; defined as the acute loss of circulating blood. Treatment is aggressive fluid replacement. -Cardiogenic: induced by myocardial dysfunction. -Neurogenic: secondary to decreased sympathetic tone from head and spinal cord injuries. -Septic: shock secondary to infection. -Goal of Treatment: restore organ perfusion.

53

AJM Sheet: General Trauma Topics -Foreign Bodies/Puncture Wounds -When should a foreign body be removed? -Clinical signs of infection, known contaminated object, pain, object close to NV elements, intra-articular -Recommended imaging studies for a foreign body? -Plain film radiography (no oblique views!), fluoroscopy, CT, MRI, US -How will wooden objects appear on US? -hyperechoic with a hypoechoic dark shadow -How large must a glass foreign body be to be visible on plain film radiography? Does leaden matter? -A piece of glass, regardless of whether it is leaden, must be >5mm to be visible. -Classification for foreign bodies? -Resnick Classification [Resnick CD. Puncture wounds: therapeutic considerations and a new classification. J Foot Surg. 1990 Mar-Apr; 29(2): 147-53.]

-I. Superficial/cutaneous: usually visible without signs of infection. -II. Subcutaneous or articular without signs of infection. -IIIA. Subcutaneous or articular with signs of infection. -IIIB. Bone penetration without signs of infection. -IV. Bone penetration with known osteomyelitis. -Patzakis Classification [Patzakis MJ. Wound site as a predictor of complications following deep nail punctures of the foot. West J Med. 1989 May; 150(5): 545-7.]

-Zone 1: Toe to met head (50% incidence of osteomyelitis in this limited study.) -Zone 2: Midfoot (17% incidence of osteomyelitis in this limited study.) -Zone 3: Calcaneus (33% incidence of osteomyelitis in this limited study.) -Puncture wound common bugs -Most common? Staph Aureus -2nd most common? Beta-hemolytic strept -Puncture through shoe gear? Pseudomonas -Puncture involving soil or a farm? Clostridia -Human bites? Eikenella corrodens -Cat bites? Pasteurella multocida -Dog bites? Enterobacter, Pseudomonas, Staph, Bacillus -Mainstays of foreign body/puncture wound treatment? -Tetanus status, antibiotics, aggressive I&D with copious lavage

-Gun Shot Wounds -High velocity GSWs are characterized by speeds >2500 ft/s. This is significant because high velocity GSWs have a tendency to yaw and tumble leading to increased cavitation. -Cavitation: Large wound is created under a situation of negative pressure. This negative pressure “sucks” outside contaminants into the wound.

-[Holmes GB. Gunshot wounds of the foot. CORR. 2003 Mar; (408): 86-91.] -Compartment Syndrome -First described by Volkmann. Myerson has good articles/chapters on this topic. -[Perry MD, Manoli A. Foot compartment syndrome. Orthop Clin North Am. 2001 Jan; 32(1): 103-11.] -[Myerson M, Manoli A. Compartment syndromes of the foot after calcaneal fractures. Clin Orthop Relat Res. 1993 May: 142-50.]

-Results when interstitial pressure exceeds capillary hydrostatic pressure, so the microcirculation shuts down. -The foot has anywhere from 3-11 compartments depending on who you read: -Intermetatarsal Compartments X 4: contains the interossei muscles -Medial Compartment: Abductor Hallucis -Lateral Compartment: Abductor digiti minimi -Superficial Central Compartment: FDB -Deep Central Compartment: Adductor Hallucis -Calcaneal Compartment: Quadratus Plantae and lateral plantar artery -Dorsal Compartment: EHB and EDB -P’s of Compartment Syndrome (These are very generalized.) -Pain out of proportion and not controlled by analgesics -Paralysis -Pain with passive dorsiflexion of the toes -Pulselessness -Paresthesia -Pressure -Pallor -Diagnosis -Normal compartment pressure? 0-5mm Hg -When do you start getting worried? 20-30mm Hg -When do you consider surgical intervention? >30-40mm Hg -How is diagnosis made? Wick or slit catheter to measure compartment pressures -Treatment -Decompression via fasciotomy, debridement of necrotic tissue, copious lavage and delayed closure -Incision approaches: Consider dorsal vs. medial approaches -Complications: permanent loss of function with structural deformity (Volkmann contractures), myoneural necrosis, sensory loss, chronic pain

54

AJM Sheet: Digital Fractures -Even suspected digital fractures should be worked up according to a standard, full trauma work-up during the interview if the case is presented as a trauma. The following describes unique subjective findings, objective findings, diagnostic classifications and treatment. Subjective -History of trauma. “Bedpost” fracture describes stubbing your toe while walking at night. Also common are injuries from dropping objects on the foot. Objective -Edema, erythema, ecchymosis, open lesions, subungual hematoma, and onycholysis should all be expected. -Any rotational/angulation deformities should be identified on plain film radiograph. Diagnostic Classifications -Rosenthal Classification [Rosenthal EA. Treatment of fingertip and nail bed injuries. Orthop Clin North Am. 1983; 14: 675-697.] -Zone I: Injury occurs with damaged tissue completely distal to the distal aspect of the phalanx. -Zone II: Injury occurs with damaged tissue completely distal to the lunula. -Zone III: Injury occurs with damaged tissue completely distal to the most distal joint (IPJ in hallux; DIPJ in lesser). Treatment -Zone I Injuries -If injury involves no exposed bone and a total tissue loss less than 1cm squared, then: -Allow to heal in by secondary intention. -If injury involves a total tissue loss greater than 1cm squared, then: -A STSG or FTSG should be used depending on weight-bearing position. -Zone II Injuries -Flaps and Skin Grafts generally employed: -Atasoy flap: plantar V
Y advancement -[Atasoy E. Reconstruction of the amputated fingertip with a triangular volar flap. JBJS-Am 1970; 52: 921-926.] -Kutler flap: biaxial V
Y advancement -[Kutler W. A new method for fingertip amputation. JAMA 1947; 133: 29-30.] -Zone III Injuries -Usually requires distal amputation (Distal Symes amputation) Miscellaneous Notes -Hallux fracture is regarded as the most common forefoot fracture. -Digital fractures without nail involvement and displacement/angulation/rotation can be treated conservatively with immobilization. -If a subungual hematoma is present, then there is a 25% incidence of underlying phalanx fracture. -If a subungual hematoma covers >25% of the nail, then the nail should be removed. -Only 1mm squared of free space from onycholysis is necessary for hematoma development. -For proper nail function and adherence, there should be no onycholysis within 5mm of the lunula. -A Beau’s line is a transverse groove often associated with nail trauma.

55

AJM Sheet: Sesamoid Trauma -The following describes unique subjective findings, objective findings, diagnostic classifications and treatments. Subjective -History of trauma is very important in this case. You want to differentiate between acute and chronic conditions involving the sesamoids. Be careful to elicit any neurologic complaints that could be present. Objective -Expect edema, erythema, ecchymosis and open lesions. Take the time for proper palpation. -Joplin’s neuroma is irritation of the medial plantar proper digital nerve. -Associated with rigidly plantarflexed first metatarsals, anterior cavus, etc. -One of the most difficult things to differentiate is an acute sesamoid fracture from a bipartite sesamoid. There are several generic plain film radiographic characteristics found in acute fractures: -Jagged, irregular and uneven spacing -Large space between fragments -Abnormal anatomy -Bone callus formation -Comparison to a contra-lateral view -Also useful are: -HISTORY of acute incident -Bone scan (would show increased osteoblastic/osteoclastic activity with acute fracture). Diagnostic Classifications -Jahss Classification [Jahss MH. Traumatic dislocations of the first metatarsophalangeal joint. Foot Ankle. 1980 Jul; 1(1): 15-21.] -Type I -Mechanism: Dorsal dislocation of the hallux -Intersesamoid ligament: Intact -Fracture?: No sesamoid fracture -Treatment: Requires open reduction -Type IIA -Mechanism: Dorsal dislocation of the hallux -Intersesamoid ligament: Ruptured -Fracture?: No sesamoid fracture -Treatment: Closed reduction/Conservative Care -Type IIB -Mechanism: Dorsal dislocation of the hallux -Intersesamoid ligament: Ruptured -Fracture?: Fracture of at least one sesamoid -Treatment: Closed reduction/Conservative Care -Type II Variant -Mechanism: Dorsal dislocation of the hallux -Intersesamoid ligament: Ruptured -Fracture?: Separation of a bipartite sesamoid -Treatment: Closed reduction/Conservative Care Treatments -Conservative -Immobilization (NWB SLC, PWB SLC, Surgical Shoe, CAM Walker, etc.) -Dancer’s Pad -Surgical -Excision of the fractured fragment or entire sesamoid Miscellaneous Notes -Ilfeld’s Disease: Agenesis of the fibular sesamoid -[Ilfeld FW, Rosen V. Osteochondritis of the first metatarsal sesamoid. CORR 1972; 85: 38-41.] -Incidence of Bipartite Sesamoid in Population: -As much as Kewenter: 35.5% -As few as Inge: 10.7% with 75% of cases being unilateral

56

AJM Sheet: Metatarsal Fractures -The following describes unique subjective findings, objective findings, diagnostic classifications and treatments. -Subjective and Objective -All will point to some form of traumatic injury. Common injuries leading to metatarsal fracture include direct trauma, blunt trauma, shearing, ankle sprains, etc. -Most important in your work-up will be how you read the plain film radiographs. Remember that at least two views are necessary to accurately describe displacement/angular/rotational abnormalities. -Metatarsal Head/Impaction Fractures -MOI: Direct or indirect trauma -Radiographic findings: -Examine for evidence of displacement/angulation/rotation -Expect a shortening mechanism -Examine for intra-articular nature of fracture -Treatment: -Conservative -Closed reduction generally unsuccessful -Surgical -ORIF with fixation of K-wire, screws or absorbable pins - immobilization for 4-6 weeks and NWB -Follow-Up -Early PROM suggested -Subsequent arthrosis is a common complication -Metatarsal Neck Fractures -MOI: Shearing forces or direct trauma -Radiographic findings: -Expect elements of shortening, plantarflexion and lateral displacement of the distal segment. -Treatment: -Conservative -Closed reduction generally unsuccessful -Surgical -ORIF effective in restoring and maintaining alignment with K-wires, IM pinning and plates. -Follow-up -NWB in SLC for 4-6 weeks -General Information: -Metatarsal neck fractures often involve multiple metatarsals due to the mechanism of injury. Multiple fractures are very unstable due to loss of function of the deep transverse metatarsal ligament, which usually prevents displacement. -Vassal Principle: Adjacent fractures generally improve alignment after reduction of the initial fracture because soft tissue structures are returned to their normal position through traction. -Midshaft Metatarsal Fractures -MOI: Result of direct, blunt or torsional injuries -Radiographic findings: -Expect oblique fracture line, but transverse, spiral and comminuted are all possible. -Expect elements of shortening, plantarflexion and lateral displacement of the distal segment. -Treatment: -Based on displacement and fracture type: -Non-displaced fractures: NWB SLC 4-6 weeks -Fractures with >2-3mm of displacement and >10 degrees of angulation: ORIF -Transverse displaced fractures -Consider buttress plate, compression plate, IM percutaneous pinning, crossed K-wires -Long oblique or spiral fractures -Consider screws, plates, IM pinning, cerclage wiring -Comminution -Consider screws, plates, cerclage wiring, K-wires and external fixation -Metatarsal Base Fractures -MOI: Direct trauma (MVA, fall from height, etc.) Usually associated with Lisfranc’s trauma. -Radiographic findings: -Generally remain in good alignment/angulation because of surrounding stable structures. -Treatment: -Conservative -NWB SLC 4-6 weeks with good alignment -Surgical -ORIF with displacement/alignment/angulation -First Metatarsal Fractures -MOI: Direct trauma (MVA, fall from height, crush, etc.) and indirect trauma (torsional, twisting, avulsions, etc.) -Radiographic findings: -Variable -Examine for distal intra-articular fractures -Examine for avulsion-type fractures -Treatment: -Conservative -SLC 4-6 weeks with non-displaced fractures -Be wary of closed reduction because extrinsic muscles may displace after apposition. -Surgical -Various ORIF techniques detailed above -Percutaneous pinning and cannulated screws are option in first metatarsal -ORIF should be utilized if intra-articular fracture involves >20% of articular surface

57

AJM Sheet: 5th Metatarsal Base Fractures -The following describes unique subjective findings, objective findings, diagnostic classifications and treatments. Subjective and Objective -All will point to some form of traumatic injury. Common injuries leading to metatarsal fracture include direct trauma, blunt trauma, shearing, ankle sprains, etc. -Most important in your work-up will be how you read the plain film radiographs. Remember that at least two views are necessary to accurately describe displacement/angular/rotational abnormalities. Diagnostic Classifications Stewart Classification -[Stewart IM. Jones fracture: Fracture of the base of the fifth metatarsal bone. Clin Orthop. 1960; 16: 190-8.] -Type I: Extra-articular fx at metaphyseal-diaphyseal junction (True Jones Fracture) -MOI: Internal rotation of the forefoot while the base of 5th met remains fixed -Radiographic findings: -Usually oblique or transverse fx at metaphyseal-diaphyseal junction -Treatment: -NWB SLC 4-6 weeks for non-displaced fractures -ORIF with displacement >5mm -Misc: -Fracture first described by Sir Robert Jones in 1902 from injuring himself while ballroom dancing. [Jones R. Fracture of the base of the fifth metatarsal bone by indirect violence. Ann Surg. 1902; 35(6): 776-82.] -Very unstable fracture with high incidence of non-union/delayed union secondary to variable blood supply. Remember that the diaphysis and metaphysis are generally supplied by two different arterial sources. -[Smith JW. The intraosseous blood supply of the fifth metatarsal: implications for proximal fracture healing. Foot Ankle. 1992 Mar-Apr; 13(3): 143-52.]

-Type II: Intra-articular avulsion fracture -MOI: Shearing force caused by internal twisting with contracture of peroneus brevis tendon -Radiographic findings: -1 or 2 fracture lines -Intra-articular in nature -Treatment: -NWB SLC 4-6 weeks for non-displaced fractures -ORIF with displacement >5mm -Type III: Extra-articular avulsion fracture -MOI: Reflex contracture of peroneus brevis with ankle in plantarflexed position -Radiographic findings: -Extra-articular; Involvement of styloid process -Treatment: -NWB SLC 4-6 weeks for non-displaced fractures -ORIF (pins, screws, tension-band wiring) for displacement >5mm -Consider excision of fragment and reattachment of peroneus brevis tendon -Type IV: Intra-articular, Comminuted fracture -MOI: Crush injuries with base of 5th met stuck between cuboid and the external agent -Radiographic findings: -Multiple fragments; joint involvement -Treatment: -NWB SLC 4-6 weeks for non-displaced fractures -ORIF with displacement -Consider bone grafting and fragment excision with severe comminution -Misc: -High rate of non-union/delayed union -Type V: Extra-articular avulsion fractures of the epiphysis -MOI and treatment similar to Type II and III fractures -Note that this can only occur in children (similar to a Salter-Harris Type I fracture) Torg Classification [Torg JS, et al. Fractures of the base of the fifth metatarsal distal to the tuberosity. JBJS-Am. 1984; 66(2): 209-14.]

-Radiographic classification of Jones fractures describing potential for non-union development. -Type I: Acute injuries -Radiographic findings: Narrow fracture line without intra-medullary sclerosis -Type II: Delayed Union -Radiographic findings: Widened fracture intersurface with evidence of IM sclerosis -Type III: Non-Union -Radiographic findings: Complete sclerotic obliteration of the IM canal

58

AJM Sheet: Stress Fracture Work-up Also called: March fx, Hairline fx, Fatigue fx, Insufficiency fx, Deutschlander’s dz, Bone exhaustion, etc.

-Subjective -CC: Patient presents complaining of a diffuse foot and ankle pain. Classic patient is a military recruit or athlete. -HPI: -Nature: Pain described as “sharp with WB” or “sore/aching.” May have element of “shooting” pain. -Location: Described as diffuse, but can be localized with palpation. Common areas include dorsal metatarsal or distal tib/fib. -Course: Subacute onset. Usually related to an increase in patient’s physical activity. -Aggravating factors: Activity -Alleviating factors: PRICE -PMH: -Look for things that would weaken bone (eg. Osteoporosis) -SH: -Look for recent increases in physical activity or a generally active patient -PSH/Meds/All/FH/ROS: Usually non-contributory

-Objective Physical Exam -Derm: -Generalized or localized edema -Ecchymosis is rare -Vasc/Neuro: Usually non-contributory -Ortho: -Painful on localized palpation (positive pinpoint tenderness) -Possible pain with tuning fork

-Imaging -Plain Film Radiograph: -Localized loss of bone density and bone callus formation are hallmark signs -Note that there must be a 30-50% loss of bone mineralization before radiographic presentation of decreased bone density. This generally takes 10-21 days in a stress fracture. -Bone Scan: -Increased uptake in all phases regardless of time of presentation

-General Stress Fracture Information -Somewhere between 80-95% of all stress fractures occur in the LE with the most common sites being the metatarsals (20% with 2nd metatarsal most commonly involved [11%]) and the distal tibia/fibula. -Stress fractures can occur via two mechanisms: -Chronic strain upon a normal bone -A chronic, normally benign strain upon a weakened bone

-Treatment -Conservative treatment is mainstay: -Immobilization and NWB for 4-6 weeks (SLC, Unna boot, surgical shoe, etc.) -Be certain of anatomic position with no angulation/rotation/displacement (very uncommon)

59

AJM Sheet: Lisfranc Trauma -History -Dr. Jacques Lisfranc was a French gynecologist who was called into the service of Napoleon’s army where he served as a trauma surgeon in the 1820’s and 30’s. He also served under Dr. Dupuytren during this time. -Del Sel first described Lisfranc dislocations following equine injuries (JBJS 1955). -Anatomy -Tarsometatarsal joint: 9 bones, ~13 joints, 7 weak dorsal ligaments, 7 strong plantar ligaments, the Lisfranc ligament -Myerson described three functional columns of the Lisfranc joint. Ouzounian and Shereff described the sagittal plane motion of each of these columns. -Medial Column: 1st met and medial cuneiform: 4mm of motion in the sagittal plane. -Central Column: 2nd/3rd mets and central/lateral cuneiforms. 1mm of motion in sagittal plane. -Lateral Column: 4th/5th mets and cuboid. 10mm of motion in the sagittal plane. -Mechanism of Injury -Accounts for 0.2% of all traumatic injuries. Most common in MVA and sports injuries. -Occurs either by direct crushing (i.e. dropping something on the foot) or indirectly (usually a plantarflexed and abducted foot). -Diagnosis -Clinical -Midfoot pain and tenderness. Possibly exacerbated with pronation, abduction or plantarflexion. -Plantar ecchymosis -Be wary of compartment syndrome! Always check neurovascular status. -Imaging -Plain Film Radiography -Pathognomonic “fleck sign” representing an avulsion fx in the 1st IM space. -Look for deviations from normal in the AP, MO and Lat views. Normal is: -AP: Medial border of the 2nd met continuous with the medial border of the central cuneiform. Lateral border of the medial cuneiform continuous with the medial border of the central cuneiform. -MO: Medial border of the 4th met continuous with the medial border of the cuboid. Lateral border of the 3rd met continuous with the lateral border of the lateral cuneiform. -Lat: No sagittal displacement. Look for lateral column shortening with a “nutcracker fracture” of the cuboid. -“Lisfranc variant” is fracture damage extending proximally into the cuboid-navicular region. -Consider stress radiographs with the foot in plantarflexion or abduction. -CT, Bone Scan, MRI could all be utilized. -Classifications -Classification originally described by Quenu and Kuss, then modified by Hardcastle, then modified by Myerson. The Myerson Classification is listed with the Quenu and Kuss equivalent in parentheses. -Type A: Total incongruity in any plane (QK: Homolateral) -Type B: Partial incongruity (QK: Isolateral) -B1: 1st met goes medial -B2: Lesser mets go lateral -Type C: Divergent (QK: Divergent) -C1: Partial (only 1st and 2nd mets involved) -C2: Total (all mets involved) -Treatment -Literature strongly favors ORIF with any displacement (>2mm between the 1st and 2nd mets). Exact anatomic reduction is the key to prognosis. -Non-operative -If plain film and stress radiographs show no displacement, then NWB SLC for 6 weeks with films q2 weeks looking specifically for displacement. -Operative -Goal: Reduction and stabilization of the medial and central columns. You must reduce the lateral column, but it is usually left unfixed because of the pronating mobile adapter mechanism. The medial and central columns do not have as much sagittal plane motion, but you still don’t want excess compression with associated chondrolysis to develop. -Fixation: -1st met to medial cuneiform, 2nd met to central cuneiform, and 3rd met to lateral cuneiform with crossed 0.062” K-wires (removed at 8 weeks), cannulated cancellous screws (removed at ~12 weeks) or 3.5mm corticals. Consider putting a notch 1.5cm distal to the joint for screw to prevent stress risers. Drill the hole for the screw in the superior aspect of the notch and not the base to prevent splitting the base. -Consider 4th met to cuboid and 5th met to cuboid with a single 0.062” K-wire -Lisfranc Screw: Medial cuneiform to 2nd met base, screw in a lag fashion -Length of the lateral column must be restored following a “nutcracker fracture.” Consider using an H-plate or external fixation. -Incisions: -Longitudinal over the 1st IM space (provides access to 1,2,3) and longitudinal over the 4th IM space (provides access to 3,4,5). -Longitudinal in the 1st IM space, 3rd IM space and lateral to the 5th met. -Post-Operative -NWB SLC for 8 weeks transitioned to PWB SLC for 4 weeks transitioned to rehab. High impact activity can usually be resumed at 6 months. -Complications -ARTHRITIS! Essentially everyone develops post-traumatic arthritis to some extent. Additional Reading: -[Myerson M. The diagnosis and treatment of injuries to the Lisfranc joint complex. Orthop Clin North Am. 1989; 20(4): 655-64.] -[Hardcastle PH, et al. Injuries to the tarsometatarsal joint. Incidence, classification, and treatment. JBJS-Br. 1982; 64(3): 349-56.] -[Desmond EA, Chou LB. Current concepts review: Lisfranc injuries. Foot Ankle Int. 2006; 27(8): 653-60.]

60

AJM Sheet: Navicular Trauma -Suspected navicular trauma should be worked up with a primary and secondary survey. The following describes unique subjective findings, objective findings, diagnostic classifications and treatments. Subjective -History of trauma ranges from contusions to ankle sprains to forced abduction/plantarflexion of the forefoot. Objective -MMT of the posterior tibialis tendon is important in these cases. -Multiple view plain film radiographs are extremely important because of the possible obliquity of some fractures. CT scans and MR images may also be necessary for complete visualization and analysis of stress fractures. Relevant Anatomy -The navicular is surrounded by a number of joints of varying stability. The TNJ proximally is very mobile, while the distal NCJ and lateral NCJ are very stable. The navicular is also very stable medially because of the insertion of the PT tendon. -Vascular anatomy to the navicular can be extremely important as described by Sarrafian: -It has been demonstrated that the central 1/3 of the navicular is relatively avascular. -The dorsalis pedis artery adequately supplies the dorsal and medial aspects. -The medial plantar artery adequately supplies the plantar and lateral aspects. -The central 1/3 has variable, radially-projecting branches from anastomosis of these arteries. Diagnostic Classification -Watson-Jones Classification -Type I: Navicular Tuberosity Fractures -Occur secondary to eversion and posterior tibialis contracture -Watch for associated “nutcracker fracture” of cuboid and anterior calcaneal process fractures -Must be differentiated from accessory navicular -Treatment: -Displacement <5mm: -Conservative immobilization -Displacement >5mm consider: -Excision of fragment with reattachment of tendon -ORIF with a cancellous screw -Type II: Dorsal Lip Avulsion Fractures -Occur secondary to plantarflexion/frontal plane mechanisms. -Must differentiate from os supranaviculare and os supratalare accessory ossicles. -Generally intra-articular -Generally treated with conservative immobilization -Type III: Navicular Body Fractures. Described by Sangeorzan. -[Sangeorzan BJ, et al. Displaced intra-articular fractures of the tarsal navicular. JBJS-Am. 1989; 71(10): 1504-10.] -IIIA: Coronal Plane Fracture with no angulation -~100% successful reduction usually achieved -IIIB: Dorso-lateral to Plantar-medial fracture with adduction of the forefoot -67% successful reduction usually achieved -IIIC: Comminution with abduction of the forefoot -50% successful reduction usually achieved -Principles of ORIF for Type III fractures: -Must achieve 60% reapproximation of proximal joint space -Incision placed dorsal-medial, between the TA and TP -Complications involve post-traumatic arthritis and/or AVN -Fixation Options using 3.5mm Cortical Screws: -Two screws directed lateral to medial -Two crossed screws directed proximal to distal -One screw directed proximal-medial to distal-lateral into the middle cuneiform -Consider FDL transfer in the presence of a weakened PT tendon -Type IV: Stress Fracture of the Navicular -Generally occurs secondary to running -Torg describes typical stress fracture occurring in central 1/3 of body in the sagittal plane. -DDx: Tibialis anterior tendonitis -Usually plain films, CT and bone scans are necessary to diagnose

61

AJM Sheet: Talar Fractures -Talar fractures are generally associated with high energy trauma, and a standard evaluation with primary and secondary surveys should precede any specific talar evaluation. The following describes unique subjective findings, objective findings, diagnostic classifications and treatment considerations. Subjective -History of trauma with a high incidence of MVC. The classic description of a talar neck fracture comes from a forced dorsiflexion of the foot on the ankle (“aviator’s astragulus”). Talar fractures account for approximately 1% of all foot and ankle fractures. Objective -Important to verify neurovascular status, and rule out dislocations and compartment syndromes. -Imaging: -Canale View: Plain film radiograph taken with the foot in a plantarflexed position. The foot is also pronated 15 degrees with the tube head orientated 75 degrees cephalad. This view allows for evaluation of angular deformities of the talar neck. -CT scan is essential for complete evaluation and surgical planning. Relevant Anatomy -An intimate knowledge of the vascular supply to the talus is essential with regard to avascular necrosis (AVN): -Dorsalis Pedis: Supply the superior aspect of the head and neck (artery of the superior neck) -Anastomoses with the peroneal and perforating peroneal arteries -Artery to the sinus tarsi: supplies the lateral aspect of the talar body -Forms an anastomotic sling with the artery of the tarsal canal -Posterior Tibial Artery: -Deltoid branch: medial aspect of the talar body -Artery of the canalis tarsi: majority of the talar body -Forms an anastomotic sling with the artery of the tarsal sinus -Also sends branches to the posterior process -Peroneal/Perforating Peroneal Artery: supplies posterior and lateral aspects of the talar body -Anastomoses with the dorsalis pedis artery branches Classifications/Named Fractures: Hawkins Classification: Talar neck fractures Type I: Non-displaced (~13% incidence of AVN) Type II: Displaced fracture with STJ dislocation (~50% incidence) Type III: Displaced fracture with STJ and ankle dislocation (~95%) Type IV: Displaced fracture with STJ/ankle/TN dislocation (>95%) -(Type IV added by Canale and Kelly)

Berndt and Harty: Talar dome fractures Type 1: Chondral Depression Type 2: Partial chondral fracture, seen on MRI Type 3: Nondisplaced complete osteochondral fracture Type 4: Displaced complete osteochondral fracture

Sneppen: Talar body fractures Type 1: Osteochondral fracture Type 2: Sagittal, Coronal, Transverse body fracture Type 3: Lateral process fracture Type 4: Posterior tubercle fracture Type 5: Crush fracture

Modified Hawkins: Lateral process fractures Type I: Simple bipartite fracture Type II: Comminuted fracture Type III: Chip fracture of anteroinferior lateral process

Others: -Shepherd’s fracture: Acute fracture of posterolateral talar process -Cedell’s fracture: Acute fracture of the posteromedial talar process -Snowboarder’s fracture: lateral process fractures Treatment -NWB in SLC 6-8 weeks versus ORIF depending on nature of fracture and degree of displacement. -Titanium hardware may be used so that MRI evaluation may be used in post-operative period to evaluate for AVN! -Hawkins sign: radiolucency of the talar body noted at 6-8 weeks after fracture. This sign is indicative of intact vascularity. However, the absence of this sign does not indicate that osteonecrosis and talar collapse are eminent. Additional Readings: -Talar fractures are relatively uncommon in the medical literature. Most studies are case reports or small retrospective reviews leading only to Level IV or V evidence. -[Ahmad J, Raikin SM. Current concepts review: talar fractures. Foot Ankle Int. 2006 Jun; 27(6): 475-82.] -[Golano P, et al. The anatomy of the navicular and periarticular structures. Foot Ankle Clin. 2004 Mar; 9(1): 1-23.] -[Berndt A, Harty M. Transchondral fractures of the talus. JBJS-Am. 1959; 41: 988-1020.] -[Canale ST, Kelly FB. Fractures of the neck of the talus. Long-term evaluation of seventy-one cases. JBJS-Am. 1978 Mar; 60(2): 143-56.]

62

AJM Sheet: Calcaneal Fractures -The standard trauma work-up again applies with primary and secondary surveys. The following describes unique subjective findings, objective findings, diagnostic classifications and treatment considerations. Subjective -Demographics: Men>Women; Age range generally 30-60; account for ~2% of all fractures; 2-10% are bilateral; 10% associated with vertebral fracture (most commonly L1); 1% associated with pelvic fracture and urethral trauma. -Common mechanisms of injury: Direct axial load, vertical shear force, MVC, gastroc contraction, stress fracture, ballistics, iatrogenic surgical fracture Objective -Physical Exam: -Pain with palpation to heel -Mondor’s Sign: characteristic ecchymosis extending into plantar medial foot -Short, wide heel -Hoffa’s sign: less taut Achilles tendon on involved side -Inability to bear weight -Must rule out compartment syndrome -Imaging: -Plain film Imaging: -Bohler’s Angle: normally 25-40 degrees (decreased with fracture) -Critical Angle of Gissane: normally 125-140 degrees (increased with fracture) -Both demonstrate loss of calcaneal height -Broden’s View: 2 oblique views to view the middle and posterior facets -Isherwood Views: 3 oblique views to highlight all facets -Calcaneal Axial View: demonstrates lateral widening and varus orientation -CT Scan: -Gold standard for evaluation and surgical planning -The coronal view forms the basis of the Sanders Classification Classifications Sanders Classification: Uses widest view of posterior facet on semicoronal CT cut -Type I: Non-displaced articular fx -A, B and C further describe the fx (lateral
medial) -Type II: Two-part posterior facet fx -A/B: divide posterior facet into equal 1/3’s -Type III: Three-part posterior facet fx -C: divides posterior facet from sus tali -Type IV: Four-part/comminuted fx -See page 1845 of McGlam’s, or 224 of Gumann’s for actual pictures. -[Koval KJ, Sanders R. The radiographic evaluation of calcaneal fractures. CORR. 1993 May; 290: 41-6.] -[Sanders R. Displaced intra-articular fractures of the calcaneus. JBJS-Am. 2000 Feb; 82(2): 225-50.]

Rowe Classification: -Type I: -Type IA: Plantar tuberosity fractures (medial more common than lateral) -Type IB: Sus tali fracture (remember FHL: pt will have pain with hallux PROM) -Type IC: Anterior process fractures (remember your anatomy: bifurcate ligament) -further divided into three parts by Degan Classification -Type II: -Type IIA: Extra-articular “beak” fracture of posterior-superior calcaneal body -Type IIB: Intra-articular “tongue-type” Achilles avulsion fracture -Type III: Extra-articular calcaneal body fracture -Type IV: Intra-articular joint depression fracture -Type V: Intra-articular comminuted fracture -See page 1830 of McGlam’s or page 223 of Gumann’s for pictures. -[Rowe CR, et al. Fractures of os calcis: a long term follow-up study of one hundred forty-six patients. JAMA 1963; 184: 920-3.] -[O’Connell F, Mital MA, Rowe CR. Evaluation of modern management of fractures of the os calcis. CORR 1972; 83: 214-23.] Essex-Lopresti [Essex-Lopresti P. The mechanism, reduction technique, and results in fractures of the os calcis. Br J Surg 1952; 39: 395-419.]

-Differentiated between extra-articular (~25%) and intra-articular (~75%) fractures and further sub-divided intra-articular fractures into tongue-type and joint depression fractures (both with the same primary force, but different secondary exit points).

Zwipp [Rammelt S, Zwipp H. Calcaneus fractures: facts, controversies and recent developments. Injury 2004; 35(5): 443-61.] -Assigns 2-12 points based on: -Number of fragments -Number of involved joints -Open fracture or high soft tissue injury -Highly comminuted nature, or associated talar, cuboid, navicular fractures Treatment -Appreciate the debate in the literature between cast immobilization vs. percutaneous reduction vs. ORIF vs. primary arthrodesis. [Barei DP, et al. Fractures of the calcaneus. Orthop Clin North Am. 2002 Jan; 33(1): 263-85.]

-Goals of therapy are to restore calcaneal height, decrease calcaneal body widening (reduce lateral wall blow-out), take it out of varus, and articular reduction. -Review the lateral extensile surgical approach [Benirschke SK, Sangeorzan BJ. Extensive intraarticular fractures of the foot. Surgical management of calcaneal fractures. CORR. 1993 Jul; 292: 128-134.]

-Complications: Wound healing, arthritis, lateral ankle impingement, malunion, nonunion, etc.

-[Benirschke SK, Kramer PA. Wound healing complication in closed and open calc fractures. J Orthop Trauma. 2004; 18(1): 1-6.] -[Cavadas PC, Landin L. Management of soft-tissue complications of the lateral approach for calcaneal fractures. Plast Reconstr Surg. 2007; 120(2): 459-466.]

63

AJM Sheet: Ankle Fracture Evaluation -The standard trauma work-up again applies with primary and secondary surveys. The following describes unique subjective findings, objective findings, diagnostic classifications and treatment considerations.

-Residents and attendings love to ask questions about ankle fractures for whatever reason, so this is certainly a subject where you should know the classification systems cold, and do a lot of the additional readings. We’ll keep it brief here. -Relevant Anatomy to Review (not just for this topic; think lateral ankle instability, peroneal tendonopathy, sprains, etc.): -Ankle Ligaments: -Lateral: ATFL, CFL, PTFL -Medial: Superficial Deltoid: superficial talotibial, naviculotibial, tibiocalcaneal ligaments Deep Deltoid: anterior talotibial and deep posterior ligaments -Syndesmotic Ligaments: -AITFL, PITFL (and inferior transverse tibiofibular ligament), Interosseous ligament -Classifications: -Ottawa Ankle Rules [Stiell IG, et al. A study to develop clinical decision rules for the use of radiology in acute ankle injuries. Ann Emerg Med. 1992; 21(4): 384-90.]

-Developed by ED docs to minimize unnecessary radiographs following ankle sprains. X-ray only required if: -Bone tenderness along distal 6cm of posterior edge of fibula or tibia -Bone tenderness at tip of fibula or tibia -Bone tenderness at the base of the 5th met -Bone tenderness on the navicular -Inability to bear weight/walk 4 steps in the ED -Lauge-Hansen Classification -First submitted as a doctoral thesis [Lauge-Hansen N, Anklebrud I. 1942]. Co-authored with a guy named “Ankle”-brud! -[Lauge-Hansen N. Fractures of the ankle: analytic, historic survey as the basis of new experimental roentgenologic and clinical investigations. Arch Surg 1948; 56: 259.]

Stage I

Stage II

Stage III

Stage IV

Supination Adduction Pronation Abduction

Lateral collateral ligament tear/ avulsion fibular fx (Weber A) Transverse avulsion fx medial malleolus/deltoid rupture (Muller B)

Near vertical medial malleolar fx (Muller D)

NA

NA

AITFL syndesmotic rupture or avulsion of its insertion

NA

Supination External Rotation Pronation External Rotation Pronation Dorsiflexion

AITFL syndesmotic rupture or avulsion of its insertion

Spiral lateral malleolus fracture (Weber B) Long, posterior spike on lateral radiograph

Short, oblique lateral malleolus fracture (Weber B) Transverse on lateral radiograph PITFL syndesmotic rupture or avulsion of its insertion

Transverse avulsion fx medial malleolus/deltoid rupture (Muller B)

AITFL syndesmotic rupture or avulsion of its insertion

Oblique or spiral fibular fracture suprasyndesmotic (Weber C)

PITFL syndesmotic rupture or avulsion of its insertion

Transverse avulsion fx medial malleolus/deltoid rupture (Muller B)

-The problem with the Lauge-Hansen classification: This was an experimental/laboratory study looking at the result of forced talar movement on a fixed tibia-fibula. But most ankle fractures in real-life occur when a moving tibia-fibular acts on a fixed foot. -Danis-Weber/AO Classification for lateral malleolar fractures (From AO Group) AO Type A: Type B: Type C: Infrasyndesmotic Transyndesmotic Suprasyndesmotic 1

Isolated

Isolated

Simple diaphyseal fibular fx

2

With medial malleolar fx

Complex diaphyseal fibular fx

3

With posterior-medial fx

With medial malleolar fx or deltoid rupture With medial lesion and posteriorlateral tibial fx

Proximal fibular fx

-Mueller Classification for medial malleolar fractures (From AO group) A B C D Avulsion Transverse at level Oblique Near vertical of mortise

64

AJM Sheet: Ankle Fracture Treatment -Additional named fractures associated with the ankle: -Tillaux-Chaput fx: AITFL avulsion from the anterolateral tibia -Wagstaff fx: AITFL avulsion from the anteromedial fibula -Volkmann fx: PITFL avulsion from the posterior-lateral tibia -Bosworth fx: PITFL avulsion from the posterior-medial fibula -Maisonneuve fx: Weber C-type proximal fibular fracture that occurs within 10cm of the fibular neck -Pott’s fx: Generic term for a bimalleolar ankle fracture -Destot fx: Generic term of a trimalleolar ankle fracture -Dupuytren fx: At least a bimalleolar fracture when the talus gets lodged up between the tibia and fibula -Posterior Malleolar Fractures: Different than an avulsion fracture of the PITFL; this is a true fx involving a portion of the tibial plafond cartilage. CT is usually done to estimate a percentage of the involved joint space. The rule of thumb (although certainly not proven) is that fractures involving >25-30% of the joint space require ORIF. -Principles of Fixation: -This is one area where there is a lot of controversy in the medical literature. There are certainly some things you want to accomplish besides the generic concept of “anatomic reduction”. I can’t get too much into it in this limited space, but I will try and give you a couple sides of the argument and some reading to do. The question you are really trying to answer is: “How reduced is reduced enough?” Then we’ll briefly cover some specific aspects of the surgeries themselves. One thing to appreciate is that most of these arguments are made about SER fractures (because they are the most common): -Restore fibular length -Most people agree that the fibular fracture is the dominant fracture. In other words, if you adequately reduce the fibula, then the other fractures and dislocations more or less fall into line because of the soft tissues (poor man’s definition of the Vassal Principle). It doesn’t mean that the other fractures don’t require fixation, but it means there’s no real sense in fixating the other fractures unless you have the dominate fracture fixated (or at least reduced). -The other concept is that a fixed fibula is essentially acting as a buttress, keeping the talus within the ankle mortise. -The fibula is generally shortened in ankle fractures, so you want to get the full length back with your reduction (generally visibly seen by reduction of the posterior spike on a lateral view). -[Yablon IG, et al. The key role of the lateral malleolus in displaced fractures of the ankle. JBJS-Am. 1977; 59(2): 169-173.]

-Restore the ankle mortise (medial clear space and the syndesmotic gap) -This goes back to the fibula keeping the talus in the ankle mortise. The classic article you need to know is Ramsey and Hamilton that showed a 42% decrease in the tibiotalar contact area when the talus was displaced 1mm laterally. From this, people inferred that if the talus isn’t perfectly reduced back into the mortise, then gross instability occurs. -This is assessed by: -Medial clear space (from the talar shoulder): Should be ~4mm or less after reduction -Tib-Fib Overlap: Approximately >10mm on AP view at 1cm superior to the joint line -Talar Tilt: <10 degrees absolute, or <5 degrees compared to other side -[Ramsey PL, Hamilton W. Changes in tibiotalar area of contact caused by lateral talar shift. JBJS-Am. 1976; 58(3): 356-7.] -[Park SS, et al. Stress radiographs after ankle fracture: the effect of ankle position and deltoid status on medial clear space measurements. J Orthop Trauma. 2006; 20(1): 11-18.]

-Fix the syndesmosis? -Another area of controversy where there is no clear answer is when and how to fixate the syndesmosis with internal fixation. One point is clear: the purpose of placing internal fixation across the syndesmosis is to stabilize the fibula against the tibia to prevent lateral migration of the talus and instability. If the fibula is stable against the tibia with all of your other fixation, then you don’t really need any additional fixation. How can you tell? Radiographic findings and the Cotton hook test for instability intra-operatively. -Other questions where people have opinions, but no clear answers are: What type of screws? How many screws? How many cortices? How far above the ankle? Temporary vs. permanent fixation? Weightbearing? etc. -Lateral Malleolus: -Fracture is primarily reduced and fixated with a single 2.7mm cortical screw with interfrag compression. -Then a generic 1/3 tubular plate or a specialized contoured plate is used for buttress stabilization. -Attempt for 6 cortices proximal to fracture with 3.5 bicortical screws -Get as many distal screws as you can. 3.5 bicortical if above the ankle joint. 4.0 unicortical if not. -Proximal fibular fractures still amendable to 1/3 tubular plating, but may need to double-stack the plates. -Should appreciate the concept of lateral vs. posterior anti-glide plating. -Medial Malleolus: -Several options including 4.0 cancellous, K-wires, plating, cerclage, etc.

-Additional Reading: -[Mandi DM, et al. Ankle fractures. Clin Podiatr Med Surg. 2006 Apr; 23(2): 375-422.] -[Mandracchia DM, et al. Malleolar fractures of the ankle. A comprehensive review. Clin Podiatr Med Surg. 1999 Oct; 16(4): 679-723.] -[Kay RM, Matthys GA. Pediatric ankle fractures: evaluation and treatment. J Am Acad Orthop Surg. 2001; 9(4): 269-78.] -[Jones KB, et al. Ankle fractures in patients with diabetes mellitus. JBJS-Br. 2005; 87(4): 489-95.] -[Espinosa N, et al. Acute and chronic syndesmosis injuries: pathomechanics, diagnosis and management. Foot Ankle Clin. 2006 Sep; 11(3): 639-57.]

65

AJM Sheet: General Tendon Trauma -Mechanism of Injury -Tendon is actually the strongest part of the muscle-tendon-insertion system. It is much more likely for the complex to fail at the myotendinous junction or at the tendinous insertion, but acute tendon injuries do occur. They are usually the result of direct trauma, or overload on an intrinsically weakened tendon. -Tension overload on a passive muscle -Eccentric overload on an actively contracting muscle -Laceration -Blunt Trauma -Factors which can intrinsically weaken tendons -Increased age: -increased cross-linking of collagen fibrils decreases tendon elasticity -decreased reaction time and muscular contraction speed -decreased vascularity -Sex: -M>F -Systemic inflammatory process: -RA, SLE, Gout, etc. -Underlying endocrine dysfunction: -Xanthoma (hyperbetalipoproteinemia), DM, Hyperparathyroidism secondary to renal failure, hyperthyroidism, infection, intratendinous calcifications, etc. -Medications: -Fluoroquinolones, Corticosteroids -Tendon Healing -As with most tissue, there is a generalized inflammation, reparative and remodeling phase. -Week 1: Severed ends fill in with granulation tissue -Weeks 2-3: Increased paratenon vascularity; collagen fibril alignment -Week 4: Return to full activity without immobilization -Imaging in Diagnosis of Acute Tendon Injury -Plain Film Radiograph: -May see avulsions, soft tissue swelling, accessory bones/calcifications -Tenograph:

-Radiopaque dye injected into tendon sheath and viewed on plain film radiograph -Technically difficult with many false positives and negatives

-Ultrasound:

-Tendon normally appears hyperechoic to muscle on US. -Look for discontinuity of fibers, possible alternating hyperechoic/hypoechoic bands, and an area of intensely hyperechoic hematoma. -It is very important that the US head is held perpendicular to the long axis of the tendon.

-CT:

-Tendon normally appears as a homogenous, well-circumscribed oval surrounded by fat on CT. It normally has a higher attenuation than muscle. -Will be able to appreciate discontinuity on CT with injury.

-MRI:

-T1: Tendons normally have a uniform low-intensity (very black). Will be uniform with variable high-intensity signal with injury. -T2: Tendons are normally relatively low-intensity. Will light up with high-intensity signal with injury. -Remember the magic angle phenomenon. Any MRI signal shot at 55 degrees to the course of the tendon will show a false-positive damage signal. Very common in the peroneals. -[Mengiardi B, et al. Magic angle effect in MR imaging of ankle tendons: influence of foot positioning on prevalence and site in asymptomatic patients and cadaver tendons. Eur Radiol. 2006 Oct; 16(10): 2197-2206.]

-Principles of Repair -It is possible, but rare to get acute tendon injury to any of the long tendons of the leg. An Achilles tendon work-up will be featured in another AJM sheet, but realize there are some basic principles that apply to any tendon. -One is generally able to primarily repair the tendon. Non-absorbable suture is preferred. -Special attention should be paid to vascular supply. Remember that the majority of a tendon’s vascularity comes from the mesotenon, and therefore should be preserved as much as possible. -If primary repair is not possible, consider using lengthening tendon slides, tendon grafts, tendon transfers and biomaterials such as Graft-Jacket (allograft dermal tissue matrix) or Pegasus (equine pericardium) to restore the integrity of the tendon. -The goal of treatment should be to allow early PROM without gapping of the tendon.

66

AJM Sheet: Achilles Tendon Rupture Work-Up Subjective: CC: Typical complaint is pain, weakness and swelling in the back of the leg following an acute injury. The typical patient is the “weekend warrior” type. This is a 30-50 y/o male participating in a strenuous athletic activity after a generally inactive lifestyle. HPI: Nature: Pain, weakness and swelling. Pain is surprisingly non-intense allowing the patient to ambulate. The patient may relate an audible “pop” or “snap”. They may also relate feeling like they were “kicked or shot” in the back of the leg. Location: Distal posterior leg. The left leg is more affected. Some people theorize that this has to do with the majority of people having right-handedness and a greater strength and proprioception of the RLE. Duration, Onset, Course: Acute onset with gradually progressive increase in swelling and edema. Mechanism of Action: -Three classic MOA are described: -Unexpected dorsiflexion with triceps contraction -Pushing off during WB with the leg extended (tennis lunge) -Violent dorsiflexion on a plantarflexed ankle -Also consider lacerations and blunt trauma Previous History: obviously more likely to re-rupture PMH: -Inflammatory conditions: RA, SLE, Gout -Endocrine dysfunction: DM, Renal failure with hyperparathyroidism, hyperthyroidism, Xanthoma (hyperbetalipoproteinemia) -Infection: Syphilis Meds: -Corticosteroid injection -Fluoroquinolone use SH: -Smoking -Sedentary lifestyle with weekend activity Objective: Derm: -Posterior, Medial and Lateral Ecchymosis -Open lesion associated with laceration Vasc: -Posterior, Medial and Lateral edema Neuro: -Sural Neuritis Ortho: -Palpable gap (“hatchet strike defect”) -Positive Thompson test -Negative Jack’s test -Pain in the area -Increased PROM ankle dorsiflexion -Decreased AROM ankle plantarflexion -Retraction of proximal gastroc belly -Apropulsive gait Other specific tests: -Mattles test: Foot should be in plantarflexed position with patient prone and knee at 90° -Simmonds’ test: Foot should be in plantarflexed position with patient prone -Various needle tests (O’Brian, Cetti) -Toygar’s skin angle: Normally 110-125 degrees. Increases to 130-150 degrees with rupture. Imaging: -Plain film:

-r/o Rowe Type IIB avulsion fracture -Radiodense gap -Obliteration of Kager’s triangle -Soft tissue edema -US: -Alternating hyperechoic and hypoechoic bands -Hyperechoic hematoma -MRI: -TI: -Ill-defined low-intensity with mixed high-intensity signal -T2: -High-intensity signal from hematoma

67

AJM Sheet: Achilles Tendon Rupture Treatment -Anatomy Review -Muscles of the Triceps Surae (origins, insertions, NV supply, action) -Plantaris (origins, insertions, NV supply, action) -Segmental Blood Supply of Tendon -“Twisting” of tendon -Specific Information regarding the Watershed Area -Lagergren and Lindholm -Used microangiographic technique on human cadavers -Found decreased vascularity 2-6cm proximal to insertion -Theorized this was secondary to atrophy from inactivity -Conflicting information from laser Doppler flowmetry studies -Found uniform vascularity throughout tendon -Found decreased vascularity with age and in men -Found decreased vascularity with physical loading/stress of tendon, specifically at insertion -Leadbetter -Found increased stress/strain at the watershed area regardless of vascularity -Kuwada Classification of Achilles Tendon Ruptures [Kuwada GT. Classification of tendo Achilles repair with consideration of surgical repair techniques. J Foot Surg. 1990; 29(4): 361-5.] -Type I: Partial tear involving <50% of tendon. Note that in a partial Achilles tear, the posterior fibers are torn first. So the direction of the tear/rupture is from posterior to anterior. -Type II: Complete tear with <3cm deficit -Type III: Complete tear with a 3-6cm deficit -Type IV: Complete tear with a >6cm deficit -Puddu Classification of Chronic Achilles Pathology -Peritendonitis: Inflammation of the surrounding tissues, not the tendon itself. This pain will remain stationary as the tendon is taken through a range of motion. -Tendonosis: Intra-tendinous degeneration. This pain will move proximally and distally as the tendon is taken through a range of motion. -Peritendonitis with tendonosis: combination of the two pathologies.

-The podiatric surgeon is faced with three options: do nothing, cast immobilization and surgical repair. There’s a lot of information out about this in the medical literature now, particularly with open repair vs. immobilization and when to start weight-bearing/PT. -Do nothing -Gap will eventually fill in with fibrotic scar tissue -Usually requires later surgical intervention -Cast Immobilization -AK cast versus SLC -Schuberth is proponent of AK casting -Knee should be in a 20 degree flexed position -General recommendations: -Gravity equinus cast x 4 weeks -Reduction of 5 degrees every 2 weeks to a neutral ankle position (~4-6 weeks) -Heel lift and PT until normal ankle PROM -Return to full activity at approximately 6 months -Surgical Repair -Surgical approach -Midline to medial incision to avoid superficial neurovascular structures -Pt in a prone or supine frog-legged position -Use full-thickness flaps with emphasis on atraumatic technique -Primary Open Repair -Keith needles with non-absorbable suture (or fiberwire) with absorbable sutures to reinforce -There are three common stitches used: -Bunnell: Figure of 8 or weave stitch -Krakow: Interlocking stitch -Kessler: Box stitch -Augmented Open Primary Repair -Lynn: Plantaris is fanned out to reinforce -Silverskoild: 1 strip of gastroc aponeurosis brought down and twisted 180 degrees -Lindholm: Utilizes multiple strips of gastroc aponeurosis -Bug and Boyd: Strips of fascia lata are used to reinforce
Y lengthening of the proximal segment with primary repair -V
-Reinforcement with FHL -Graft Jacket, Pegasus, etc. -Percutaneous Primary Repair -Ma and Griffith described a percutaneous Bunnell-type approach -May be associated with high re-rupture rates -Post-Op Treatment -SLC in gravity equinus with gradual reduction over 6-10 weeks

68

AJM Sheets: Peri-Operative Medicine and Surgery Contents: Peri-Operative Medicine -Admission Orders (page 70) -Electrolyte Basics (page 71) -Glucose Control (page 72) -Fluids (page 73) -Post-Op Fever (page 74) -DVT (page 75) -Pain Management (page 76) General Surgery Topics -AO (page 77) -Plates and Screws (page 78) -Suture Sheet (page 79) -Surgical Instruments (page 80) -Power Instrumentation (page 81) -Biomaterials (page 82) -External Fixation (page 83) -Bone, Bone Healing and Wound Healing (page 84) Specific Surgery Topics -How to “Work-Up” a Surgical Patient (page 85) -Digital Deformities (pages 86-87) -Lesser Metatarsals (page 88) -5th Ray (page 89) -HAV (page 90-91) -HAV Complications (page 92) -HL/HR (pages 93-94) -Pes Plano Valgus (pages 95-96) -Cavus (pages 97-98) -Equinus (page 99)

This particular section is intended to be more general, as opposed to a specific surgical study guide. It is ridiculous to think that you could learn foot and ankle surgery in 100 pages, especially with only 15 pages dedicated to specific deformities. In other words, you should absolutely not be doing all of your specific surgical preparation for externships and interviews from the PRISM. Many of the Sheets from the Specific Surgery Topics section are simply summarizations of the 3rd edition of McGlamry’s chapters for example. This may be an area where you feel the PRISM could be updated in the future. Again, I said that while I was studying for the Diabetic Foot Infection work-up, I tried to learn as much as possible on the topic and really tried to “wow” the attendings at the interview. However, my strategy was different when dealing with trauma and the specific surgical work-ups. Here I tried to demonstrate “competence,” as opposed to “mastery” of the material. With specific surgeries, you’re really not supposed to have strong, pre-formed opinions as a student or as an intern. That’s what your residency is for, developing surgical opinions. If you already know what to do in every surgical situation, then what’s the point of doing a residency? So while on externships and at the interview, you should really try to walk a fine line between: 1. Displaying competence in knowledge of the baseline material 2. Displaying that you still have a lot to learn, and that you are eager to learn it. Page 85’s “How to Work-Up a Surgical Patient” gets into this concept a little deeper.

69

AJM Sheet: Admission Orders/ADC VANDILMAX (Note: If I wanted to be mean during an interview, I would have you write out a set of admission or post-op orders as I was asking you other questions.)

Admission: Pt is admitted to the general medical floor on the Podiatric Surgery Service under Dr. Attending. Most patients on the podiatric surgery service are admitted to the general medical floor or a surgical floor. Any pts admitted to a critical care unit or telemetry unit will probably be on a medicine service with a podiatric surgical consult. Diagnosis: Infection of bone of right 2nd toe Always use terminology that everyone in the hospital can understand, but also be as specific as possible. Condition: Consider: -Stable -Fair -Guarded -Critical Podiatric surgery pts will generally always be in stable or fair condition. Vitals: Vitals recorded q8 hours per nursing. Always designate how often you want them recorded. Also common is “q-shift.” Consider neurovascular checks to the affected limb if indicated. Ambulatory Status:

Consider:

-CBR (Complete bed rest) -As tolerated -NWB -OOB to chair -PWB Always designate which leg the order is for. Be specific with PWB status (“toe-touch” or “heel-touch”). If order is for CBR, consider DVT ppx and a bed pan order. If the order is OOB, specify # of times and length per day. Also consider Physical Therapy and/or Occupational Therapy orders here. Nursing Instructions:

Consider:

-Accuchecks (how often and when?) -Bedside Commode -Wound Care -Drain management -Spirometry

-Regular diet -Renal diet -Decreased Na

-ADA 1800-2200 calorie -Cardiac diet -Decreased K+

Diet:

Consider:

Ins/Outs/IVs:

Consider:

-Ice and elevation -Dispense Post-op shoe/Crutches -Dressing Instructions -Off-loading instructions

-Mechanically soft -NPO

-Measurement and recording of Ins and Outs (especially dialysis pts) -Foley -IV Fluids

-CBC with diff -Chem-7/Met Panel -Coags -Type and Screen -Wound cultures -Blood cultures -D-Dimer -HbA1c -CRP -ESR Always detail when the labs should be done. For example, initial CBC and Chem-7 should be taken “upon arrival to the floor.” Additionally, 2 sets of blood cultures should be taken from 2 different sites. Labs:

Consider:

-Write out all at-home medications in full -Pain medication -Antibiotics -Insomnia -Anti-emetics -DVT ppx -Constipation -Diarrhea -SSI -Fever -Throat lozenges -Anti-pruritic Be as specific as possible. SSI needs to be written out in full. Many medications require hold parameters. For example, fever medications should not be given unless the temperature reaches 101.5° F. Anti-HTN agents should be held if the blood pressure or heart rate drops too low.

Medications:

Consider:

Ancillary Consults:

Consider:

-General Medicine -Vascular Surgery -PT/OT -Pulmonary -Renal -Home Care

X-rays/Imaging:

Consider:

-Plain film radiographs -MRI -Vascular Studies

-Infectious Disease -Cardiology -PM&R -GI -Social Work -Case Manager -CT scans -CXR -EKG

-US Doppler -Bone Scans

70

AJM Sheet: Electrolyte Basics

-Sodium: -Hyponatremia -Manifestations: Primarily neurologic, lethargy, headache, confusion, obtundation -Restrict water intake and promote water loss -Correct underlying disorder -Treatment: -Replace Na+ deficits -Hypernatremia -Manifestations: Change in mental status, weakness, neuromuscular irritability, focal neurologic deficits, coma, seizures -Replace water loss and promote sodium excretion -Treatment: -Water deficit = ([Na+]-140)/140 x Total Body Water in liters -Rapid correction of either of these disorders is dangerous due to rapid shifts of water in and out of brain cells. It should therefore be corrected slowly over 48-72 hours. Aim correction at 0.5 mEq/L/hr with no more than a 12 mEq/L correction over the first 24 hours.

-Potassium: -An abnormal potassium level is a major reason a surgery will be cancelled and/or delayed. You should have a specific understanding how to raise and lower potassium levels in the peri-operative setting. -Hypokalemia -Manifestations: Fatigue, myalgia, muscular weakness, cramps, arrhythmia’s, hypoventilation, paralysis, tetany -Treatment: -Minimize outgoing losses -Treat underlying cause -Correct K+ deficit via oral or IV means (K+ riders added to fluid, oral KCL, etc.) -Hyperkalemia -Manifestations: Cardiac toxicity (peaked T waves, prolonged PR, torsades de pointes), muscle weakness, paralysis, hypoventilation -Treatment: -Increase cellular uptake of K+ -Insulin (10-20 units) with 50 g IV glucose -IV NaHCO3 (3 ampules in 1L of 5% dextrose) -Albuterol (5-10mg nebulized over 30-60 minutes) -Increase K+ excretion -Loop diuretic, Thiazide diuretic -Kayexalate (cation exchange resin) (25-50mg mixed with 100ml 20% sorbitol to prevent constipation) -Dialysis -Calcium Gluconate (10ml of 10% solution over 2-3 minutes emergently to reduce membrane excitability)

-Chloride and Carbon Dioxide: -Not going to talk much about this, but you should have a basic understanding of Acid-Base Regulation. -Equation for determining Anion Gap: Anion gap (all units mmol/L) = (Na + K) - (Cl + [HCO3-]) -Normal gap (~8-20mmol/L) -Negative/lowered gap (<8mmol/L): Alkalotic state -Positive/elevated gap (>20mmol/L): Acidotic state -MUDPILES algorithm: methanol/metformin, uremia, diabetic ketoacidosis, propylene glycol, infection, lactate, ethanol, salicylate/starvation

-BUN and Creatinine: -Measures of kidney function and hydration status -BUN (Blood Urea Nitrogen): Protein metabolism waste product eliminated by the kidneys. This can be increased if your kidneys aren’t eliminating it properly, or in a dehydrated state where it’s a relatively high concentration. -Creatinine: A more direct measure of kidney function from elimination of this skeletal muscle waste product. -Creatinine clearance and estimated glomerular filtration rate (GFR) with the Cockcroft-Gault Equation: [(140-Age in years) x Weight in kg] / [72 x Serum creatinine] x 0.85 if female -GFR < 60 ml/min indicates chronic kidney disease; < 15 indicates kidney failure -Antibiotics and other drugs should be dosed appropriately in these situations -Renal protective agents are utilized prior to procedures that are known to affect the kidneys in patients with kidney disease. A common example of this is an angiogram with dye to evaluate the vascular status of a patient with diabetic foot disease. -Pre-procedural hydration -Mucomyst (N-acetylcysteine) (also used for acetaminophen OD) -Sodium Bicarb Protocols -[Lawlor DK. Prevention of contrast-induced nephropathy in vascular pts. Ann Vasc Surg. 2007 Sep: 593-7.]

-Glucose covered in another AJM sheet

71

AJM Sheet: Blood Glucose and Glycemic Control -The importance of in-patient management of blood glucose cannot be overstated. This is an area however where medicine tends to be very passive with regard to intervention. Rigid control of blood glucose in the in-patient setting has been definitively shown to: -Reduce mortality -Reduce in-patient complications -Reduce infection rates -Decrease length of stay -Reduce hospital costs -Specifically with regards to diabetic foot disease, a single blood glucose level higher than 150-175mg/dl significantly limits the function of the immune system for a period of days, particularly cytokine activation and recruitment. -My favorite article of the 2006-7 academic year was Inzucchi SE. Management of Hyperglycemia in the Hospital Setting. NEJM. Sep 2006; 355: 1903. It is a must-read on this topic. I also strongly recommend obtaining a FREE copy of the Yale Diabetes Center Diabetes Facts and Guidelines 2006. They will mail it to you (FOR FREE!) by calling 203 737-1932 or emailing [email protected]. An online version is also available at http://info.med.yale.edu/intmed/endocrin/yale_diab_ctr.html. You are a complete sucker if you don’t take advantage of this resource. And if you are really interested in this topic, research the work of the Portland Diabetic Project. Oral Agents -Sulfonylureas: Bind to β-cell receptors stimulating insulin release -Glyburide (Micronase) -Glipizide (Glucotrol) -Biguanides: Decrease production of glucose in the liver -Metformin (Glucophage) -Thiazolidinediones: Increase peripheral cellular response to insulin -Rosiglitazone (Avandia) -Pioglitazone (Actos) -α-glucosidase inhibitors: Reduce intestinal carbohydrate absorption -Acarbose (Precose) -Miglitol (Glyset)

-Glimepiride (Amaryl)

Insulins Type Rapid Acting Lispro (Humalog) Aspart (Novolog) Short Acting Regular Intermediate Acting NPH Lente Long Acting Glargine (Lantus) Detemir (Levemir) Combinations 70/30 (70% NPH/30% Regular)

Onset

Peak

Duration

10-15 minutes 10-15 minutes

1-2 hours 1-2 hours

3-5 hours 3-5 hours

0.5-1hr

2-4 hours

4-8 hours

1-3 hours 2-4 hours

4-10 hours 4-12 hours

10-18 hours 12-20 hours

2-3 hours 1 hour

None None

24+ hours 24 hours

0.5-1 hour

2-10 hours

10-18 hours

In-patient Recommendations -There is increasing data that sliding scales are completely inefficient at in-patient glucose management. Sliding scales are passive, reactionary scales that compensate after a hyperglycemic incident occurs. Inzucchi recommends the following, instead of a sliding scale: -Basal Rate: Lantus or other long acting -Start 0.2-0.3 Units/kg/day; then increase 10-20% q1-2 days prn -Prandial Coverage: Novolog or other rapid acting -Start 0.05-0.1 Units/kg/day; then adjust 1-2 Units/dose q1-2 days prn Diabetic NPO Recommendations -Type 2 DM: -1/2 the normal dose of long acting if they get any -BG checks q6 hours with short acting agent available for coverage -D5W or D5-1/2NS at 50-75cc/hr while NPO -Type 1 DM: - Strongly consider an insulin drip -1/2 – 2/3 normal dose of long acting agent - BG checks q6 hours with short acting agent available for coverage - D5W or D5-1/2NS at 75-100cc/hr while NPO

72

AJM Sheet: Fluids -Fluid management is a difficult topic to cover because it can be used for a variety of different problems/purposes. It can be used to maintain fluid balance in a patient who is NPO, correct electrolyte disturbances, and/or provide glucose to name just a few examples. This sheet will cover the basics of short-term maintenance therapy and show differences in electrolyte concentrations between the most common fluids. -Maintenance therapy for the NPO patient -An NPO patient is still losing water that needs to be replaced to ensure homeostasis. Sources of water loss include: -Urine output: At least 500ml/day -Insensible water losses (Skin and Respiration): At least 500ml/day -This can increase by 150ml/day for each degree of body temperature of 37°C. -Gastrointestinal losses: Extremely variable -Direct blood volume loss from the surgery itself -Electrolytes are also lost to varying degrees. In the short term, it is usually only necessary to replace Na+, K+ and glucose. The other electrolytes usually do not need replacement until around 1 week of parenteral therapy. -Pediatric Considerations -Pediatric patients should be aggressively rehydrated after a surgical procedure for two reasons: -They will lose a higher percentage of their total fluid volume during a procedure. -They have a tendency to “third space” and shift fluid balances in the perioperative period. -To determine the total intravascular volume of a pediatric patient: -The first 10kg of body weight account for about 80ml/kg. -So a 7kg kid would be (7x80) = 560ml -The next kg’s account for about 70ml/kg -So a 25kg kid would be (10x80 + 15x70) = 1850ml -General Recommendations: -At the very least you should replace fluid to account for water loss. This is at least 1L/day, but you can certainly increase this and lose the excess through the urine. -It is also recommended to provide some electrolyte supplementation: -Na+: 50-150 mEq/day -K+: 20-60 mEq/day -Glucose: 100-150g/day to minimize protein catabolism and ketoacidosis -Common parenteral solutions: IV Solution

Osmolality (mOsm/kg)

Glucose (g/L)

Na+ (mEq/L)

D5W 278 50 0 D10W 556 100 0 D50W 2778 500 0 0.45% NaCl 154 (5% available) 77 0.9% NaCl 308 (5% available) 154 3% NaCl 1026 0 513 Lactated Ringer’s 274 (5% available) 130 -LR also contains 4 mEq/L K+, 1.5 mEq/L Ca2+, and 28 mEq/L lactate

Cl- (mEq/L) 0 0 0 77 154 513 109

-Common administrations: -Normal adult: NS or 1/2 NS or LR at 75-120ml/hr +/- 20mEq KCl -Diabetic patients: D5-1/2NS at 50-100ml/hr +/- 20mEq KCl while NPO There usually isn’t a need to deliver extra glucose (D5) to diabetic patients while they are PO. -The key to fluid management is an understanding and knowledge of exactly why you are giving fluids in the first place, what you hope to accomplish, what substances you are giving in the fluid and how much you are giving. -Obvious care needs to be taken with diabetic patients, those with renal pathology, and those with CHF. Additional Reading: -[Grocott MP, et al. Perioperative Fluid Management and Clinical Outcomes in Adults. Anesth Anal. 2005 Apr; 100(4):1093-106.] -[Paut O. Recent developments in the perioperative fluid management for the paediatric patient. Curr Opin Anaesthesiol. 2006 Jun;19(3):268-77.]

73

AJM Sheet: Post-Op Fever -General Information -When dealing with a fever work-up, always note what the baseline temperature of the patient is and the method of measurement. -Fever in most institutions is defined as greater than 101.5° F. -Temperatures between 98.6-101.5° are low-grade fevers. -Intra-operative causes of fever -Inflammatory process of the surgical procedure itself -Pain -Transfusion Reaction -Malignant Hyperthermia -Pre-existing Sepsis -The 5 “W’s” of Post-Operative Fever -Wind: Atelectasis, aspiration pneumonia, PE -Wound: Surgical site infection, thrombophlebitis (IV site), pain -Water: UTI, dehydration, constipation -Walk: DVT -Wonder Drugs: Virtually any drug can cause fever, but the most common are antimicrobials and heparin. -Timeline General Guide -0-6 hours post-op: Pain, anesthesia rxn, rebound from cold OR, endocrine causes (thyroid crisis, adrenal insufficiency) -24-48 hours post-op: atelectasis, aspiration pneumonia, dehydration, constipation -72+ hours: infection (3-7 days), DVT, UTI, drug allergy, thrombophlebitis -Temperature General Guide (in degrees F) -107: Anesthetic Hyperthermia -106: -105: Blood transfusion reaction -104: Closed abscess -103: Atelectasis; pneumonia; drug reaction; liver disease -102: Wound infection -101: Draining abscess -100: Benign post-op fever; post-anesthesia overshoot -General Knowledge -Usually only two infectious agents can cause a fever within a few hours of surgery: -Group A Strep (GAS) -Clostridium perfringens -Dialysis patients typically run approximately 1 degree F cooler than the normal population, so a fever for HD patients wound be defined as 100.5° F. This is hypothesized to be due to a resetting of the hypothalamic set point. -The majority of causes of fever are non-infectious. AJM always carries with him a copy of the DDX of fever copied from Harrison’s text (it’s 2 pages long!). Common non-infectious causes of post-op fever include: -Surgical site inflammation -Seroma -Hematoma -Pain -The purpose of any fever work-up is to find the source! -If you are thinking infection, then infection from where: Surgical site? Pulmonary? Urine? Blood? Does the patient have any peripheral vascular access lines?

74

AJM Sheet: Deep Vein Thrombosis (DVT) -Signs and Symptoms -Pain -Homan’s Sign: Pain in calf with dorsiflexion of the ankle -Pratt’s Sign: Pain with compression of the calf -Edema -Fever -SOB -Calor -Palpation of clot -Risk Factors -Virchow’s Triad: -Hypercoagulable state -Immobilization -Vessel Wall Injury

-History of DVT -Collagen Vascular Dz -Family History of DVT -Trauma -Pregnancy -Infection -Oral Contraceptives -Post-partum -Age > 75 -Hormone Replacement Therapy -Malignancy -Obesity -HIV/AIDS -There is also the acronym I AM CLOTTED: Immobilization, Afib/CHF, Malignancy/MI, Coagulopathy, Longevity (age), Obesity, Trauma, Tobacco, Estrogen/BCP/HRT, DVT/PE history. -Diagnosis -Compression Ultrasound: can actually visualize the clot -D-Dimer > 500ng/ml: Not sufficient as a stand alone test -Consider full coagulation work-up for hypercoagulable states -Contrast venography -Impedance plethysmography -Treatment -Goals of Treatment:

1. 2. 3.

Prevent pulmonary embolism Prevent clot extension Prevent recurrence

-Immediate Anti-Coagulation -IV Unfractionated Heparin -Law of 8018 -Initial Dose 80mg/kg IV bolus and then 18mg/kg/hour -PTT should be checked q6 until it stabilizes at 1.5-2.5X normal (46-70s) -Goal is to get PTT in this range -LMWH may also be used -Enoxaparin (Lovenox): 1mg/kg subcutaneous q12 -Heparin Dosing Guide -Initial Dose: Law of 8018 with PTT checks q6 -If PTT <35s: 80 units/kg IV bolus, then increase infusion rate by 4 units/kg/hr -If PTT 35-45s: 40 units/kg IV bolus, then increase infusion rate by 2 units/kg/hr -If PTT 46-70s: No change to dosing. Continue with 18mg/kg/hour infusion rate -If PTT 71-90s: Decrease infusion rate by 2 units/kg/hr -If PTT >90s: Hold infusion for 1 hour, then decrease infusion rate by 3 units/kg/hr -Continued Anti-Coagulation -Warfarin (Coumadin) -Load at 10mg or 7.5mg PO qdaily for 2 days -Decrease/adjust dose to a target INR=2.5 -DO NOT stop heparin infusion until INR reaches 2.5 -INR should be maintained at 2.5 for 3-12 months -Consider placement of IVC filter (inferior vena cava) -Pulmonary Embolism (PE) -PE occurs when a clot from a peripheral location embolizes to the pulmonary vasculature - <25% of deep vein thromboses distal to the iliac veins go on to develop PE. -The more proximal the clot, the more likely it is to develop into a PE. -“Classic Triad” of signs and symptoms of a PE: Dyspnea/SOB, Chest Pain, Hemoptysis -Please note that less than 14% of patients experience the classic triad -Diagnosis of a PE -Gold standard: Pulmonary Angiography, spiral CT -V/Q study -CXR -Treatment of PE -Thrombolytic Therapy: -Urokinase: 4400units/kg IV over 10 min, then 4400units/kg/hr for 12 hours -Streptokinase: 1.5 million units IV over 60 minutes -Pulmonary Embolectomy -Various filters

75

AJM Sheet: Pain Management -Pain Management is a subject that you will be dealing with a lot during residency, but something that you won’t receive much formal education on. Honestly, you probably won’t get many interview questions about it either, but it’s something that I think is important. This is a shameful plug, but Clinics in Podiatric Med and Surg had a whole edition to the subject (July 2008) that is worth reading. Specifically for the residency interview, read Articles 1, 5 and 8. I also wrote the “Perioperative Pain Management” chapter in the 4th edition of McGlam’s. -The “attack points” are a concept that AJM made up to promote an active approach to multimodal pain management. -Acute Operative Pain Physiology “Attack Points” (In Clinics: The Physiology of the Acute Pain Pathway) Attack Point Physiology Intervention Stimulus: Noxious stimuli resulting in Resolution/Limitation of Stimulus Stimulus tissue damage to superficial and deep -Prevention of secondary aggravation somatic structures. Anti-Inflammatory Pharmacologics Transduction: Nociceptor activation by -NSAIDs chemical, mechanical or thermal means. Carboxylic Acid Derivatives Proprionic Acid Derivatives Post-Injury Inflammatory Response: Acetic Acid Derivatives Normal response to cellular damage with Fenamates the chance to develop into the Enolic Acid Derivatives pathophysiologic mechanism of peripheral Naphthylkanones sensitization. COXII Selectives -Non-NSAIDs -Anti-histamines -Topical Agents -Local Anesthetics Anti-Inflammatory physiotherapeutics Transmission

Modulation

Peripheral sensory afferents carrying the action potential of the noxious stimulus from the periphery to the CNS. -Normally controlled by myelinated Adelta and unmyelinated C fibers. -Allodynia is a pathophysiologic state of sensitization when A-beta fibers transmit light touch as painful. Spinal Cord Dorsal Horn -Peripheral Excitatory Signals -Peripheral Inhibitory Signals -Central Excitatory Signals -Central Inhibitory Signals

Local Anesthetics Sodium Channel Blockers

Opioids Calcium Channel Blockers NMDA Receptor Antagonists Beta-adrenergics Anti-Inflammatories

Perception

Ascending Central Processes Descending Central Processes Patient Emotional Response

Anxiolytics Anti-Depressants Patient Education

-Multimodal Approach to Active Pain Management A passive unimodal therapy like Percocet has very little total effect on the physiology of pain. Opioids and acetaminophen influence small portions of the modulation attack point, but essentially do not influence any of the other attack points. A multimodal approach actively intervenes at several attack points with several therapies to interrupt the known physiologic and pathophysiologic mechanisms. -Pre-emptive Analgesia (In Clinics: Perioperative Pain Management) -The concept of pre-dosing pain medications before surgery to interrupt pain pathways before they start

76

AJM Sheet: AO -AO: Arbeitsgemeinschaft fur Osteosynthese fragen -History -Plates and screws for fx fixation first described by Alain Lambotte in 1907. -Robert Danis (Belgium surgeon) published “The Theory and Practice of Osteosynthesis” in 1949. -Described use of compression plate called a coapteur. -Maurice Mueller, a pupil of Danis, founded AO with other Swiss surgeons in 1959. -Principles of AO 1. Accurate and precise anatomic reduction of fracture fragments (especially in joints). 2. Atraumatic surgical technique with emphasis on preservation of blood supply. 3. Rigid/Stable fixation 4. Early mobilization -The “Guide to Internal Fixation” by the AO group is a great book that reads fairly quickly. You should also read the text “Internal Fixation of Small Fractures” and “AO Principles of Fracture Management” from the AO group. General notes from these books are included throughout the following sheets dealing with specific traumatic fractures. -General Principles of the Lag Technique -Why? Generates compression. So? Compression leads to lack of motion and therefore primary bone healing. Motion disrupts angiogenesis, decreases oxygen tension levels and inhibits osteogenesis. So, it is the lack of motion and NOT the compression that is osteogenic. -Orientation of the screw 90° to the fracture line obtains optimal compression. ->20° displacement from perpendicular is significant -Weakest in translation from axial loading -Orientation of the screw 90° to the long axis optimally prevents displacement with axial loading. -Weak in compression -Ideal screw placement for a long, oblique fracture: -One central anchor screw 90° to the long axis -One proximal and one distal compression screw 90° to the fracture line -Principles of Insertion -AO Recommendations: Overdrill, Underdrill, Countersink, Measure, Tap, Screw -Some underdrill before overdrill -Some don’t overdrill until after tapping -Two finger tightness = 440-770lbs. -To prevent thermal necrosis: -Sharp tip -Fast advancement (2-3mm/sec) -Slow drill speed (300-400rpm) -Firm force (20-25lbs) -Screw Pull-out -Directly proportional to screw diameter, screw length and bone strength (cortical nature). -Indirectly related to pilot hole diameter. -To increase screw pull-out, maximize bone-screw contact. -Fairly Irrelevant Definitions -Stress: pressure on a material -Strain: measurable deformation following a given stress -Stress-Strain Curve/Load Deformation Curve -Elastic Range: -Non-permanent strain/deformation with a given stress -Proportional stress and strain (Hook’s Law) -Slope of the line is the stiffness (Young’s Modulus of Elasticity) -Yield Point: -Past the yield point, a given stress causes a non-proportional increase in strain. -Plastic Range: -Permanent deformation past the yield point -Ultimate Failure Point -Fatigue Failure: failure from repetitive cyclic loading -Creep: temperature dependant permanent deformation of a metal -Stress Shielding: Internal fixation absorbs physiologic stress from bone and results in bone resorption per Wolff’s Law.

77

AJM Sheet: Screws and Plates Screws -Screw Anatomy/Definitions -Head: more efficient hexagonal vs. cruciate -Land: underside of the head which contacts the near cortex. Want as much land-bone contact as possible to reduce stress at any one location. This is the same principle as washers and countersinking. -Shank: unthreaded portion of the screw -Run-out: junction between the shank and the threads. Represents the weakest portion of the screw. -Thread diameter: diameter of threads + core (major diameter) -Core diameter: diameter without the threads (minor diameter) -Pitch: distance between threads -Tip: can be round, trocar or fluted -Axis: central line of the screw -Rake Angle: thread to axis angle -Thread Angle: angle between the threads -Cortical and Cancellous Screws -Please memorize Table 1, page 76 in McGlamry (Also AJM List: page 17) -Cortical: tighter pitch designed for hard cortical bone -Cancellous: higher pitch designed for metaphyseal and epiphyseal bone -Self-Tapping Screws -Fluted tip that clears debris as it is advanced -Require larger pilot holes, have decreased thread-bone contact and have the ability to cut its own path different from the underdrill -Cannulated Screws -Classically 3.0, 4.0, and 7.3mm, but really have just about any size available now -Advantages: self-drilling, self-tapping, good for hard to visualize fractures, avoids skiving of cortical bone on insertion and has definite co-axial nature with K-wire. -Disadvantages: hollow core, decreased thread-core ratio, decreased pull-out strength -Herbert Screws -Proximal and distal threads separated by a smooth shaft. Headless. -Leading threads have increased pitch, so it draws the trailing threads. -Does generate interfragmental compression, but not a lot. -Interference Screws -FT, headless screw -prevents axial displacement. Does not generate compression. -Malleolar Screws -Essentially a self-cutting, PT cortical screw.

Plates -General: -Quarter Tubular Plate: For use with screws from the mini fragment set -One-Third Tubular Plate: For use with screws from the small fragment set -Many other shapes and sizes of plates are available that specifically fit just about any bone/situation. -General Plate Characteristics: -Dynamic Compression (DCP): Wider/Deeper holes that allow for eccentric drilling and axial compression -Limited Contact (LC): Essentially grooves on the underside of the plate that limit periosteal contact -Locking: see -Miranda MA. Locking plate technology and its role in osteoporotic fractures. Injury. 2007 Sep; 38 Suppl 3:S35-9. -Egol KA, et al. Biomechanics of locked plates and screws. J Orthop Trauma. 2004 Sep; 18(8): 488-93.

-General Plate Functions: -Neutralization -Buttressing

-Interfragmentary Compression -Tension Band

-AO Basic Stabilization Rule: Ideally you want 3 or 4 cortical threads in each main fragment distally, and 5 or 6 proximally.

78

AJM Sheet: Suture Sheet -Suture materials are best classified as to whether they are absorbable vs. non-absorbable, synthetic vs. natural, and monofilament vs. multifilament. 1. Absorbable (usually used for deep closure) A. Natural -Pig collagen, sheep intestine, cow intestine or cat gut -May be chromic (treated with chromic salts to increase strength and decrease hydrolysis) -Digested by lysosomal enzymes in 20 days B. Synthetic 1. Vicryl (Polyglactin 910) -Braided. May be coated (polyglactin 370 or calcium stearate) -65% tensile strength at 14 days -Hydrolyzed (to CO2 and H20) in 80-120 days -Vicryl Rapid: Hydrolyzed in 42 days; loses strength in 7-10 days -Vicryl Plus: Coated with broad spectrum antibiotic Triclosan (also found in toothpaste) 2. Dexon (Polyglycolic acid) -Braided. May be coated (polycaprolate 188) -Hydrolyzed in 100-200 days 3. PDS (Polydiaxonone) -Monofilament -70% tensile strength at 14 days -Hydrolyzed in 90 days 4. Maxon (Polyglyconate) -Monofilament -Hydrolyzed in 180 days; Longest lasting absorbable (“Max”-imum) 5. Monocril (Poliglecaprone) -Monofilament -20-30% tensile strength at 14 days -Hydrolyzed in 90-120 days 2.

Non-absorbable (usually used for superficial closure/skin sutures) -It can be argued that all sutures are eventually absorbable! A. Natural 1. Silk -Made from silk worm -Actually very slowly absorbed (hydrolyzed in 1 year) -Very low tensile strength 2. Cotton/Linen -Weakest suture B. Synthetic 1. Nylon (Ethilon, Surgilon) -Both monofilament and braided available -Highest “knot slippage” rate: monofilaments are at a higher risk of knot slippage 2. Polypropylene (Prolene, Surgilene) -Monofilament -Can be used in contaminated/infected wounds (Nonabsorbable, synthetic, monofilaments best in this situation). This is the least reactive suture. 3. Polyester (Ethibond, Dacron) -Strong suture. May be used for tendon repair. -Braided. May be coated with silicone. 4. Fiberwire (polyethylene multifilament core with a braided polyester jacket) 5. Stainless Steel -Monofilament or braided (braided is called Flexon) -Strongest suture with longest absorption rate -Used for bone fixation and tendon repair, but may corrode bone at stress points

Other Notes: -Sutures are also classified according to size. They can range from 0-0 (very thick) to 9-0 (extremely thin). -Surgeon’s choice is extremely variable and you usually just work with what you are used to, but here are some safe bets: -Capsule closure: 2-0 or 3-0 Vicryl -Subcutaneous tissue closure: 3-0 or 4-0 Vicryl -Skin: 4-0 Nylon or Prolene -Skin sutures are removed at 10-14 days because at this point the tensile strength of the wound equals the tensile strength of the suture. -This was the very first AJM sheet!

79

AJM Sheet: Podiatric Surgery Instrumentation This sheet is simply a summary of the first chapter of McGlamry’s text by Dr. Malay.

-General Information -Surgical Instruments are composed of stainless steel which itself is composed of several different metals: -Carbon: gives instrument “hardness” -Chromium: chromium oxide layer prevents corrosion of instrument -Tungsten Carbide: extreme “hardness” for grasping surfaces (teeth of needle drivers) -Nickel -Molybdenum -There are two different series of stainless steel depending on how it is manufactured: -300 series Austenitic: Implants and internal fixation. Resists corrosion with resilience. -400 series Martenitic: Cutting instruments. Hardness maintains sharp edges and jaw alignments. -Categories of Instruments ***Know how to appropriately handle each instrument if handed it during an interview. ***Be able to identify each instrument if handed it or shown a picture during an interview. 1. Surgical Blades -Most common: 10, 15, 11, 62 on a minihandle -Purpose: Sharp (blade) and blunt (handle) dissection -Cutting edge width: 0.015” 2. Scissors -Most common: Tissue: Metzenbaum, Mayo, Iris, Crown&Collar (Sistrunk) Non Tissue: Suture, Utility, Bandage -Purpose: Dissection 3. Hemostats -Most common: Mosquito (Halsted), Kelly, Crile -Purpose: Grasping and holding 4. Pick-ups -Most common: 1-2 (Rat tooth), Adson-Brown, Atraumatic (Potts-Smith) -Purpose: Grasping and Holding 5. Retractors -Most Common: Hand Held: Skin Hooks, Senn, Ragnell, Malleable, Army-Navy, Volkmann Rake, Meyerding Self-retaining: Weitlaner, Holzheimer, Heiss -Purpose: Retraction and exposure 6. Elevators -Most Common: Freer, Sayre, Key, Crego, McGlamry, Langenbeck -Purpose: Dissection 7. Rasps -Most Common: Joseph, Maltz, Bell, Parkes -Purpose: Cutting 8. Miscellaneous -Osteotomes -Chisels -Gauges -Mallets -Bone-Cutting Forceps -Rongeurs -Trephine -Curettes -Bone Handling Clamps -Reduction Forceps (Lewin, Lane, Lowman, Verbrugge) -Needle Holders (Mayo-Heger, Sarot, Ryder, Halsey, Webster) -Suction-Tip (Frazier)

80

AJM Sheet: Power Instrumentation General Information This sheet is simply a review of McGlamry’s Chapter 2 by Dr. Alfred Phillips. -General Information -Hardest material in the human body? Teeth Enamel -Power instrumentation developed by which medical field? Dentistry -Power Sources (3) 1. Pneumatic -Advantages: Delivers high power and torque, does not overheat, cheap -Disadvantages: Does not operate at slow speeds, bulky, burdensome, cords prone to contamination -General: -Most commonly driven by compressed nitrogen -Tank pressure > 500 psi -Dynamic instrument pressure: 90-110 psi 2. Electric -Advantages: Light, quiet, small, good for office use -Disadvantages: Prone to overheating, expensive -General: -Utilizes an alternating current drive 3. Battery -Advantages: No cords -Disadvantages: Loses power quickly, bulky handling -General: -Utilizes direct current -Brands: Stryker, Hall-Zimmer, Microaire -Definitions -Torque: Measurement of power and force. Units: Newtons/cm^2 -Cortical bone requires more torque to cut through than cancellous bone. -Speed: Distance per time -Pod procedures usually require 20,000 rpm. -Decrease risk of thermal necrosis by decreasing torque and increasing speed. -Collet: Distal end of a saw where the saw blade attaches -Stroke: One arc of excursion for a saw blade -Oscillation: One back and forth motion of a saw blade. (Two strokes equal one oscillation). -Power Saws -Types -Sagittal Saw: Cuts in the same plane as the instrument -Better for longer and deeper cuts -4° arc of excursion -Blade may be positioned anywhere within a 160-180° arc. -Oscillating Saw: Cuts in plane perpendicular to instrument -7° arc of excursion -Blade may be positioned anywhere within a 360° circle. -Blades -Vary by cutting depth, width, thickness, shape and number of teeth -Shapes: straight (most commonly used), inward flair, outward flair -The angulation of the teeth and NOT the thickness of the blade determine the thickness of a cut. -Blades may contain holes which collect debris, thereby decreasing heat and friction. -Wire Drivers -K-Wires (Kirshner wire) -Sizes: 0.028”, 0.035”, 0.045”, 0.062” -Threaded vs. Non-threaded. Note that the direction of the driver only matters with threaded wires. -K-Wires provide splintage (stability, but no compression) -Steinman Pins -Sizes: 5/64”-3/16” -Rotary Cutting -Power Drill Bit Sizes: 1.1, 1.5, 2.0mm -Burrs -Shapes: Round, Barrel, Straight, Straight-tapered -Definitions: -shank vs. shaft vs. head -flute vs. blade -edge angle vs. clearance angle vs. rake angle -Surgical Skills Section -Surgical skills are something best learned by practice, practice, practice. A few hints are listed below: -The surgeon’s hands provide 3 functions when operating power instrumentation: -Control of power of the instrument -Control of direction of the instrument -Stability between the instrument and the surgical site -Review concepts of: -Axis guide -Reciprocal planing -With a saw or K-wire, always divot perpendicular to the cortex, and then redirect. -The spin of a burr should be parallel to the grain of the cortex or parallel the ridge of bone to be removed. -Poor man’s ways to practice handling and control of surgical instruments: -K-wire through a Nerf ball -Sagittal saw through a wine cork or wood blocks

81

AJM Sheet: Biomaterials Summary of McGlamry’s Chapter 3 by Dr. Cicchinelli.

-Properties of the ideal implant material: clinically inert, no inflammatory or foreign body response, noncarcinogenic, nonallergenic, structurally stable, capable of sterilization, capable of fabrication in desired forms, serve as a scaffold for new bone growth and gradual biodegradation. -Host Response to Implant -Cellular Response (Acute) -Immediately after implantation, implants are covered with a coat of proteins that denature and elicit an inflammatory response. Denatured fibrinogen accumulates neutrophils and macrophages. -Detritic Synovitis: Foreign body reaction to shards of silicone materials in the lymphatic system. -Environmental Stress Cracking: Surface defects on polyetherurethane implants secondary to chronic inflammation. Chronic inflammation results from fragmentation and leads to intracortical lysis and cyst formation. -Tissue Remodeling Response: Normal for implants to have fibrous capsule formation. -Infection Potential -Susceptible to S. Aureus and S. Epidermidis infections -Malignancy and Type III hypersensitivity reactions extremely rare -Biomaterials -PLLA (Polylactic-L-Acid: L is enantiomer) -Degrades to lactic acid via hydrolysis -Retains strength 36 weeks and degrades in 2-3 years -Available in FT 2.0, 2.7, 3.5 and 4.5mm screws -PGA (Polyglycolic Acid) -Degrades to glycolic acid and glycine -Elliptical. Provides compression secondary to shape. -Brittle and rigid -Highest likelihood of FB rxn or complication (<4%) -PDS (Poly-para-dioxanone) -Tapered form swaged on metallic wire. Provides compression secondary to shape. -Flexible and malleable -Increased degradation times are good because it decreases the load the body has to clear. -These screws don’t “bite” like metal screws, but swell 2-4% in the first 48 hours. -Advantages: decreased stress shielding, no second operation for removal. -Disadvantages: more expensive than metallic screws, but are cheaper in the long run if you remove >31% of metallic screws in your practice. -Metallic Implants -Surgical Stainless Steel -316LVM (low carbon vacuum remelting) -Iron, 17-25% chrome, 10-14% nickel, 2-4% molybdenium, 1% carbon -Nickel most commonly causes reaction: allergic eczematous dermatitis. -Titanium -Very inert, integrates into surrounding bone, resists corrosion, decreased capsule formation -Addition of 6% aluminum and 4% vanadium increases the strength similar to steel -Nitrogen implantation forms a stable oxide layer -Black metallic wear debris is often seen. No toxicity or malignancy associated with this. -Cobalt Chrome and Alloys -30% cobalt, 7% chromium, <0.034% moly/carbon -Used in joint replacement prostheses -Corrosion: breakdown of metallic alloys because of electrochemical interactions within the environment

82

AJM Sheet: General External Fixation -Selected History -377BC: Hippocrates with wood from a cornel tree -1904: Codvilla (Italy) used unilateral fixator for limb lengthening -1951-1991: Ilizarov (Siberia, Russia). Father of modern ex-fix and developer of external ring fixator for WWII vets from old bus parts. -General Principles -Tension-Stress Effect (Ilizarov) -Distraction performed at proper rate and in the proper area leads to tissue growth similar to hormone-mediated growth at adolescent growth plates. -Too fast: Stretching and traction injuries -Too slow: Bone callus consolidation preventing future distraction -An important principle is that all tissues (bone, skin, muscle, NV structures, etc.) become mitogenically active and grow. They proliferate as opposed to “stretching”. Much of this has to do with the distraction serving as a mechanical stimulus for growth factor release (such as osteoblastic growth factor) and dramatic increases in vascularity. -Tension-Stress Effect Influences: -Stability: increased stability leads to increased osteoblastic activity -Rate: Ideal is 1mm/day in 4 increments -Bone Cut: Best to keep medullary canal and as much periosteum intact as possible. Best technique is a percutaneous subperiosteal corticotomy with a Gigli saw or osteotome/mallet. -Location of Bone Cut: Metaphysis found to be superior to other areas -Behrens Principles of External Fixation -Avoid and respect neurovascular structures -Allow access to injured area for future fixation -Meet mechanical demands of the patient and the injury -Tajana’s Stages of Callus Development -Colloidal (0-2 weeks): formation of microreticular network -Fibrillar (2 weeks-1 month): collagen organization -Lamellar (1 month-years): formation of compact lamellar tissue and calcification -Advantages of Ex-Fix -Decreased soft tissue dissection -Immobilization of multiple regions -Allows for post-operative adjustment -Skin grafting and wound debridement available -Early ROM and WB

-Complications of Ex-Fix -Pin tract infection vs. irritation -Pain -Cage rage -Non-unions -Fracture -NV injury

-Anatomy -Knowledge of cross-sectional anatomy is essential for the application of external fixation. There are numerous manuals and tests available demonstrating proper pin and wire placement in a given location. -The key is to have solid bone with avoidance of neurovascular structures. -As a general rule, the medial and anterior aspects of the tibia are safe locations. -Types of External Fixators -Unilateral Fixators -EBI Dynafix and Orthofix -Can be straight (uniplanar) or articulated (multiplanar) -Allow for compression/distraction in a single plane only -Attached to bone via half-pins -Rigidity and stiffness determined by half-pins/bone interface. Want pins spread over a large area. -Weak in the sagittal plane -Circular Fixators (Multi-lateral) -Smith&Nephew -Generate compression/distraction in multiple planes -Tensioned wires generate stability; half-pins generate rigidity. -Best if these are located 90° to each other for optimal stability -Can be formulated to allow for immediate WB -Hybrid Fixators -Orthofix, Dynafix, Smith&Nephew, Rancho -Combination of unilateral and circular fixators -Taylor Spatial Frames -Smith&Nephew -Allows for reduction of triplanar complex deformities -Brief Indications -Limb Lengthening/Distraction -Percutaneous metaphyseal subperiosteal corticotomy with Gigli saw or osteotome/mallet -Apply fixation before corticotomy -Distraction begins 7-14 days after corticotomy at 1mm/day -Angular Deformities -CORA principle (center of rotational angulation) -Double Taylor spatial frame -Dynamization: release of tension from wires and loosening of half-pins to allow bone a period of introductory WB -Fracture -Ligamentotaxis: pulling of fracture fragments into alignment with distraction -Arthrodesis

83

AJM Sheet: Bone, Bone Healing and Wound Healing -Bone Properties/Variables -Bone is a two component system consisting of minerals (increases the yield and ultimate strength of bone) and collagen (mostly Type II). -Variables: -Porosity. Increased porosity leads to increased compressive strength of bone. Cortical bone has <15% porosity and cancellous bone has ~70% porosity. -Strength. Strength is defined as the amount of force a material can handle before failure. Bone can handle a 2% increase in length before failure. Bone is has the greatest strength in compression, followed by tension and is weakest in shear. Strength is affected by collagen fiber orientation, trabecular orientation, age, presence of defects and osteoporosis. -Stiffness. Cortical bone has 5-10 times the stiffness of cancellous bone. -Vascular Supply to Bone -Blood supply to bone comes from two sources. A nutrient artery feeds the endosteal and medullary vessels and supplies the inner 2/3-3/4 of bone. The periosteal vessels supply the outer 1/3 of bone from muscle and tendon attachments. -The amount of vascular disruption following a fracture depends on the force/displacement of the fracture and which vascular systems are disrupted. -Phases of Bone Healing -Inflammation (10%) -Hematoma fills the area with fibrin, RBCs, neutrophils, platelets, macrophages, fibroblasts (from PMNs). -Mesenchymal cells from the cambium layer differentiate into osteoblasts and chondrocytes. -Chemotaxis by growth factors (transforming growth factor beta, platelet derived, and macrophage derived) -Reparative/Regenerative (40%) -Soft callus forms and is replaced by bone. -Cartilage, fibrocartilage, collagen and hydroxyapatite deposition -Cartilage replaced by bone like endochondral ossification -Remodeling (70%) -Callus completely replaced by bone -Vascular network is normalized -Remodels according to Wolff’s Law -Piezoelectric Effect: appearance of electrical potentials within bone in response to the application of an external force -Compression side: electronegative leading to bone production -Tension side: electropositive leading to bone resorption -Types of Bone Healing -Direct Osseous Repair (Primary Intention, Direct Healing) -No callus formation; no motion -Cutting cone: Osteoclasts in the front, osteoblasts in the back. Travels across the fx line (Schenk and Willinegger). -Gap Healing: Bone deposition at 90° to the orientation of bone fragments -Indirect Osseous Repair -Callus formation -The literature has demonstrated that cyclic loading and dynamization have resulted in decreased healing times, decreased stiffness, increased torque and increased energy absorption in rabbit and dog bones. A practical means to accomplish this in human subjects hasn’t been perfected yet.

Wound Healing Additional Readings: -[Broughton G, Janis JE, Attinger CE. Wound healing: an overview. Plast Reconstr Surg. 2006 Jun; 117(7 Suppl): 1S-32S.] -[Broughton G, Janis JE, Attinger CE. The basic science of wound healing. Plast Reconstr Surg. 2006 Jun; 117(7 Suppl): 12S-34S.] -[Hunt TK, Hopf H, Hussain Z. Physiology of wound healing. Adv Skin Wound Care. 2000 May-Jun; 13(2 Suppl): 6-11.] -[Lawrence WT. Physiology of the acute wound. Clin Plast Surg. 1998 Jul: 25(3): 321-40.] -[Falanga V. Wound healing and its impairment in the diabetic foot. Lancet 2005; 366: 1736-43.]

Phases of Wound Healing: 1. Substrate/Lag/Inflammatory Stage (Days 1-4) -Inflammation characterized by edema/erythema/calor/dolor -PMNs start out dominating, but are eventually taken over by macrophages 2. Proliferative/Repair Phase (Days 3-21) -Collagen proliferation and macrophages -Myofibroblasts also begin working 3. Remodeling/Maturation Phase (Day 21+)

84

AJM Sheet: How to “Work-Up” a Surgical Patient With regard to specific surgery and the interviews, it’s always important to “know your program”. In other words, programs tend to have favorite procedures that they routinely do. For a given bunion deformity, one program may primarily do Austin-Akins, whereas other programs may never do an Akin, and still others may always do a Lapidus in the exact same situation. Some people may feel very strongly in favor of the lateral release, while others may never do it for any situation. This could even happen between two attendings at the same program in the same room during your interview! If you give a hard, definitive answer for a procedure choice, one attending may completely agree with you while another may think it’s completely the wrong choice. So if you are asked what type of procedure you would do for a given situation, be as general as possible, but always give the reason/specific indications why you are choosing that procedure or group of procedures. Name a couple different similar procedures instead of sticking by your guns with one procedure. Additionally, your interviewers may not expect you to know for sure what procedure to choose, but they will definitely expect you to be able to completely work-up the patient and know which procedures are acceptable for which indications. The two work-ups that you should have down cold are the HAV and flatfoot work-ups. Practice, practice, practice working through these situations out loud, and practice, practice, practice going through the radiographic analyses of these deformities out loud. Again, RC and I found it helpful while studying for interviews to pick up random podiatry textbooks and just flip through the pages, alternating our description of the radiographs out loud. There are of course many, many radiographic angles that you can use to describe during either of these work-ups, so focus the majority of your energy on those that will have the most impact on your treatment choice. Here’s the way that I think about these deformities. This certainly isn’t the “right” way; it’s just the way that helped me as I first started doing this out loud: HAV: I simply use the radiographic angles to define two aspects of the deformity: -Where is the deformity? -In which bone or bones, and/or which joint or joints is there deformity? -Is the deformity mild, moderate or severe? Once you have successfully answered these questions in your mind, then the remainder of the radiographic work-up falls into place. For example, if you identify a deformity at the first metatarsal-phalangeal joint, then you can use your radiographic angles to define it: “In the area of the patient’s presenting complaint I see a (mild, moderate, or severe) hallux abductovalgus deformity at the level of the metatarsal-phalangeal joint as defined by a (mildly, moderately, or severely) increased intermetatarsal angle, (mildly, moderately, or severely) increased hallux abductus angle, and approximate tibial sesamoid position of (1-7). The PASA and DASA of this joint appear (within normal limits or deviated). There (does or does not) appear to be a hallux interphalangeus deformity as defined by the (increased or normal) hallux interphalangeus angle. The overall length of the first metatarsal appears (normal, shortened, or long) compared to the remainder of the lesser metatarsal parabola on the AP view. On the lateral view the first metatarsal appears (dorsiflexed, plantarflexed, or normal) compared to the second metatarsal using Seiberg’s index. There (is or is not) an underlying metatarsus adductus as defined by the metatarsus adductus and Engle’s angles. Generally, the rearfoot appears (rectus, pronated, or supinated) as defined by…” Now that you have defined the location and severity of the deformity with your angles, suggest procedures based on these specific abnormal findings. For every abnormality that you described, suggest a procedure (or group of procedures) to correct it. “I would consider doing a distal metatarsal osteotomy in this case to laterally translate and plantarflex the capital fragment of the first metatarsal to decrease the intermetatarsal and hallux abductus angles in addition to reducing the sesamoids.” If you described the DASA and interphalangeus angles as normal, then don’t suggest an Akin procedure! If you described a mild deformity, then don’t suggest procedures that are indicated for moderate to severe deformities! I also use the above questions to classify each and every surgical procedure. For each surgical procedure I think: This procedure will correct for a (mild, moderate, or severe) deformity of this bone or at that joint. Flatfoot: Here I use a similar approach, but think of it in terms of planal dominance: -In which plane does the deformity present? “Consistent with the patient’s presenting complaint we see a (mild, moderate, or severe) pes planovalgus deformity. In the sagittal plane I see a (decreased or increased) calcaneal inclination angle, talar declination angle, talar-calcaneal angle, first metatarsal inclination angle, Meary’s angle, and medial column fault on the lateral view. I would also evaluate the patient for equinus using the Silfverskiold test to determine a sagittal plane deformity. In the transverse plane I see a (decreased or increased) talar-calcaneal angle, cuboid abduction angle, talar head coverage, talar-first metatarsal angle, metatarsus adductus angle on the AP view. In the frontal plane we can see the Cyma Line is (anteriorly displaced, posteriorly displaced or normal) on the lateral view, and that the subtalar joint alignment, ankle joint alignment and calcaneal position are (normal or abnormal) on the long leg calcaneal axial views.” Now that you have defined the deformity on your own terms, you can now suggest how to fix it using the same tools. “I would consider performing a (Gastroc recession, TAL, Cotton osteotomy, medial column arthrodesis, etc.) to correct for the sagittal plane deformity, a (Evans osteotomy, CC joint distraction arthrodesis, etc.) to correct for the transverse plane deformity, and a (medial calcaneal slide, STJ implant, etc.) to correct for the frontal plane deformity.

This is a little philosophic, but radiographic angles aren’t real. They only come into reality if you use them, so only use them as tools to your advantage. You can use them to first define the deformity on your own terms, and then to show that your intervention was successful.

85

AJM Sheet: Digital Deformity Work-Up Subjective -CC: Pt can complain of generalized “corns, calluses and hammertoes.” -HPI: -Nature: “Sharp, aching and/or sore” type pain. May have a “tired feeling” in the feet. -Location: Usually dorsal PIPJ/DIPJ of the toes or submetatarsal -Course: Progressive onset and course. -Aggravating factors: WB, shoe gear (especially tight shoes) -Alleviating factors: NWB, wide shoebox, sandals -PMH/PSH/Meds/Allergies/SH/FH/ROS: Usually non-contributory Objective Physical Exam -Derm: -Hyperkeratotic lesions can be seen submetatarsal, dorsal PIPJ or DIPJ of the lesser digits, distal tuft of the lesser digits, or interdigitally. All can have erythema, calor and associated bursitis. -5th digit is usually dorsolateral at the PIPJ, DIPJ or lateral nail fold (Lister’s corn). Hyperkeratotic lesion of the adjuvant 4th interspace may also be present (heloma molle). -Vasc/Neuro: Usually non-contributory -Ortho: -See discussion on pathomechanics -Positive Coughlin test: Vertical shift of >50% of the proximal phalanx base on the met head. Also called the “draw sign” or Lachman’s test. -Kelikian push-up test: Differentiate between a soft-tissue and osseous deformity -Specific to the 5th digit: -Toe usually has a unique triplanar deformity (dorsiflexion, adduction and varus). -Bunionette, splay foot and equinus may be present -The 5th digit is in the most susceptible position in terms of a muscular imbalance deformity because the FDL has such an oblique pull on the 5th digit as opposed to the relatively axial pull of the other digits. Imaging -Plain film radiograph: “Gun barrel” sign Specific Deformities -Hammertoe: Extension at MPJ level; flexion at PIPJ level, neutral/extended DIPJ -Mallet toe: Neutral at MPJ and PIPJ level; flexion at DIPJ level -Claw toe: Extension at MPJ level; flexion at PIPJ and DIPJ level -Curly toe: Claw/hammertoe deformity with an additional frontal plane component -Digitus Adductus: Digital deformity with adduction in the transverse plane -Digitus Abductus: Digital deformity with abduction in the transverse plane -Heloma Molle: Generally occurs in the 4th interspace with a curly toe deformity of the 5th digit. Using this example, the head of the proximal phalanx of the 5th digit abuts the base of the proximal phalanx of the 4th digit causing a hyperkeratotic lesion in the proximal 4th interspace. Pathomechanics -Digital deformities are thought to occur via one of three potential mechanisms. Each involves a muscular imbalance at the digital level. -The way AJM thinks of digits is from distal to proximal. During weight-bearing, the toes cannot function in propulsive gait to aid in load transfer if the most distal segment is not stabilized. The distal phalanx is stabilized by the long flexor tendons holding it solidly against the weight-bearing surface. With the distal phalanx stabilized, the short flexor tendon can hold the middle phalanx against the weight-bearing surface. With the middle phalanx stabilized, the lumbrical muscles hold the proximal phalanx against the ground. The lumbrical muscles must work against the extensor tendon complex, but this complex is usually not actively firing to extend the MPJ during propulsion. The interosseous muscles also stabilize the proximal phalanx in the transverse plane. When the proximal phalanx has been effectively stabilized against the weight-bearing surface, the head of the metatarsal can effectively move through its range of motion and transfer load across the metatarsal parabola. Any disruption in the stabilization process will lead to abnormal biomechanics and deformity. -Flexor Stabilization: -Most common origin of hammertoe deformity -Occurs when the PT muscle is unable to effectively resupinate the midtarsal and subtalar joints at the beginning of propulsion. To compensate, the FHL and FDL fire earlier, longer and with greater force to resupinate the foot. This puts too much force on the distal and middle phalanges causing the toe to “buckle” in a dorsiflexed position at the MPJ. This retrograde buckling puts the PIPJ in a vulnerable dorsal position and also pushes the metatarsal head plantarly. -Flexor Substitution: -Occurs when the triceps surae muscle group is unable to effectively plantarflex the foot during propulsion for whatever reason. To compensate, the muscles of the deep posterior compartment (PT, FHL, and FDL) again fire earlier, longer and with greater force leading to the same type of deformity. -Extensor Substitution: -Can occur in two ways -One way is when the TA is unable to dorsiflex the foot through the swing phase. In this case the EDL and EHL fire earlier, longer and with greater force than normal and are actually actively extending the MPJ. This easily overpowers the lumbricals and leads to retrograde buckling. -The other way is in a situation with anterior cavus where the EDL is actually at a mechanical advantage over the lumbricals. Passive stretch of the EDL, rather than active contraction, overpowers the lumbricals and leads to deformity.

86

AJM Sheet: Digital Deformity Treatment Conservative -Do nothing: Digital deformities are not a life-threatening condition and can be ignored if the patient is willing to put up with it. -Palliative care: Periodic sharp debridement of hyperkeratotic lesions -Splints/Supports: -Metatarsal sling pads -Silicone devices -Toe crests -Orthotics: -Cut-outs of high pressure areas -Metatarsal pads to elevate the metatarsal heads -Correction of the underlying deformity Surgical Options -Two approaches to remembering digital surgical options are the acronym HEECAT, and an anatomic approach thinking of procedures moving from superficial to deep. -HEECAT -Head arthroplasty: Post procedure (1882) -Extensor hood and PIPJ capsule release -Extensor tendon lengthening -Capsulotomy (MPJ) -Arthrodesis (PIPJ) -Tendon transfer (flexor longus tendon transfer to function in MPJ plantarflexion) -Anatomic Approach -Percutaneous tenotomy -Both the extensor and flexor tendons can be transected through a percutaneous approach -Extensor Tendon lengthening -Done proximal to MPJ level with a Z-lengthening -Capsulotomy -Of the PIPJ and MPJ -Remember the “J” maneuver for release of the collateral ligaments -Extensor hood release is also usually performed -Some use the McGlamry elevator in this step to free plantar attachments -PIPJ Arthroplasty -Post procedure 1882 -Resection of the head of the proximal phalanx at the surgical neck -PIPJ Arthrodesis -Fusion of the PIPJ using a variety of techniques: table-top, V, peg-in-hole, etc. -Fusion maintained with K-wire crossing the MPJ extending into the distal 1/3 of the metatarsal -Flexor Tendon Transfer -Transfer of the FHL tendon dorsally to act as a more effective plantarflexor of the proximal phalanx -Girdlestone-Taylor technique: Tendon is bisected, crossed and sutured on the dorsal aspect. -Kuwada/Dockery technique: Tendon is re-routed through a distal drill hole -Schuberth technique: Tendon is transferred through a proximal drill hole -Syndactyly -Soft tissue fusion of one digit to a normal adjacent digit to help “bring it down” -Interposing skin is removed and the digits are sutured together -You should be able to go through the steps of a Post procedure for an interview. -Please also review the neurovascular elements for each digit and be able to recite which cutaneous nerves supply which corner of each digit. 5th digit skin incisions -It is possible to alter your skin incision to incorporate a derotational element to your skin closure. While the osseous work can be accomplished using a longitudinal or lazy “s” incision (proximal medial to distal lateral), those are really best for uniplanar deformities. 5th digit HT is usually a triplanar deformity. -Two semi-elliptical incisions directed proximal lateral to distal medial. -The more oblique the incision is, the greater transverse plane correction. -The more longitudinal the incision is, the greater the frontal plane correction.

87

AJM Sheet: Lesser Metatarsal Deformity Work-up Subjective -CC: Pt presents complaining of “pain in the ball of my foot.” -HPI: -Nature: Generalized pain (aching, sharp, sore, etc.) -Location: Submetatarsal. Can usually be localized to an exact metatarsal. -Course: Gradual and progressive onset. “Has bothered me for years.” -Aggravating factors: WB for long periods, shoe gear, etc. -PMH/PSH/Meds/All/SH/FH/ROS: Usually non-contributory Objective: Physical Exam Derm: -Diffuse or focal hyperkeratotic lesions submetatarsal Vasc/Neuro: Usually non-contributory Ortho: -Many of the same signs/symptoms as HT digital deformity. HT often present. -Anterior displacement of the fat pad -Hypermobility of the first ray -Anterior Cavus foot type -Hypermobility of the fifth ray -Equinus Objective: Imaging -Plain film radiograph:

-Look for irregularities of the metatarsal parabola -Look for excessively plantarflexed or dorsiflexed position on lateral/sesamoid axial views

General Information -Lesser metatarsalgia has several possible etiologies: -Retrograde force from hammertoes. Please see AJM Sheet: Digital Deformities. -An excessively long and/or plantarflexed metatarsal leads to increased load bearing under that particular metatarsal. -An excessively short and/or dorsiflexed metatarsal can lead to increased load bearing on the adjacent metatarsals. -Hypermobility of the first ray leads to increased load bearing under at least the second metatarsal. -Hypermobility of the fifth ray leads to increased load bearing under at least the fourth metatarsal. -Anterior cavus and equinus deformities lead to increased pressures across the forefoot. -Before a surgical option is considered, it is extremely important to understand where the increased load is coming from. The goal of treatment should be to restore a normal parabola and weight-bearing function to the foot. Failure to correct the underlying deformity will dramatically increase the rate of recurrence and transfer lesions. Treatment: Conservative -Do nothing: Lesser metatarsal deformities are not a life-threatening condition. -Palliative care: Periodic sharp debridement of hyperkeratotic lesions -Splints/Supports: -Metatarsal sling pads -Toe crests -Silicone devices -Orthotics: -Cut-outs of high pressure areas -Metatarsal pads to elevate the metatarsal heads -Correction of the underlying deformity Treatment: Surgical -Structural correction of lesser metatarsals -Distal metatarsal procedures -Duvries: plantar condylectomy on both sides of the MPJ -Jacoby: “V” shaped cut in the metatarsal neck to allow for dorsiflexion of the head -Chevron: “V” shaped cut similar to a Jacoby, but with removal of a wedge of bone to obtain metatarsal shortening as well. -Dorsiflexory wedge osteotomy: similar to a Watermann of the first metatarsal -Weil: Distal dorsal to proximal plantar oblique cut to allow for distal metatarsal dorsiflexion and shortening. Can be made in several planes to obtain desired dorsiflexory/shortening effects. -Osteoclasis: Through and through cut through the metatarsal neck allowing the distal head to find its own plane. -Metatarsal shaft procedures -Cylindrical shortening -Giannestras step-down procedure: Z-shaped cut which can allow for shortening and distal dorsiflexion. -Metatarsal base procedures -Dorsiflexory wedge: (1mm of proximal dorsal shortening equivalent to ~10 degrees of dorsiflexion) -Buckholtz: Oblique dorsiflexory wedge which allows for insertion of a 2.7mm cortical screw Complications -By far, the most common complications are floating toe, recurrence and transfer lesions caused by undercorrection and overcorrection. While you can evaluate the parabola and transverse plane in the OR with a C-arm, you really can’t appreciate the sagittal plane. -Studies have demonstrated that osteoclastic procedures allowing the distal segment to find their own plane without internal fixation have the least occurrence of recurrence and transfer lesions, but they also have a higher rate of malunion, delayed union and non-union. -[Derner and Meyr. Complications and Salvage of Elective Central Metatarsal Osteotomies. Clinics Pod Med Surg. Jan 2009.]

88

AJM Sheet: 5th Metatarsal Deformity Work-up Also called: Tailor’s Bunion or Bunionette Deformity Subjective/Objective -Very similar to work-ups for lesser metatarsal deformities and digital deformities. Pts may complain of pain related to the lateral column in general, 5th digit, plantar 5th met head, lateral 5th met head or 4th interspace heloma molle. Imaging -Plain Film Radiograph: -4-5 Intermetatarsal Angle > 9 degrees (Normal is 6.47 degrees per Fallat and Buckholtz) -Lateral Deviation Angle > 8 degrees (Normal is 2.64 degrees per Fallat and Buckholtz) -[Fallat LM, Buckholtz J. J Am Podiatry Assoc. 1980 Dec; 70(12): 597-603.]

-Splay Foot Deformity -Plantarflexed 5th metatarsal position -Structural changes to 5th metatarsal head General Information -Etiology -Numerous authors have chimed in on the etiology of the 5th Metatarsal Deformity: -Davies: incomplete development of deep transverse metatarsal ligament -Gray: malinsertion of adductor hallucis muscle -Lelievre: forefoot splay -Yancey: congenital bowing of metatarsal shaft -Root: abnormal STJ pronation -CMINT, etc, etc, etc.

Treatment Conservative -Do nothing: 5th metatarsal deformities are not a life-threatening condition. -Palliative care: Periodic sharp debridement of hyperkeratotic lesions -Splints/Supports: -Shoe gear modification with large toe box -Derotational tapings -Orthotics: -Cut-outs of high pressure areas -Metatarsal pads to elevate the metatarsal heads -Correction of the underlying deformity Surgical -Exostectomy: Removal of prominent lateral eminence from 5th met head -Arthroplasty: Removal of part/whole of 5th met head -Distal Metatarsal Osteotomies: -Reverse Hohmann -Reverse Wilson -Reverse Austin -Crawford: “L” shaped osteotomy allows for insertion of cortical screws -LODO (Long Oblique Distal Osteotomy): similar to Crawford but simply oblique -Read [London BP, Stern SF, et al. Long oblique distal osteotomy of the fifth metatarsal for correction of tailor's bunion: a retrospective review. J Foot Ankle Surg. 2003 Jan-Feb;42(1):36-42.] Especially if externing at Inova! -Medially-based wedge -Proximal Osteotomies: -Transverse cuts -Oblique cuts -Medially based wedges

89

AJM Sheet: HAV Work-up Subjective CC: “Bump pain,” “Big toe is moving over,” Typical patient is female although it is unclear whether there is a higher incidence among females, or if there is a higher complaint incidence among females. HPI: -Nature: Throbbing, aching-type pain -Location: Dorsomedial 1st MPJ is most typical presentation. Pain could also be more medial (suggesting underlying transverse plane deformity such as met adductus) or dorsal (suggesting OA of 1st MPJ). -Course: Gradual and progressive -Aggravating Factors: Shoe wear, WB PMH: -Inflammatory conditions (SLE, RA, Gout, etc.) -Ligamentous Laxity (Ehlers-Danlos, Marfan’s, Downs syndrome) -Spastic conditions (40% incidence of HAV among those with CP) PSH: -Previous F&A surgery FH: -Hereditary component (63-68% family incidence among general population, 94% with juvenile HAV) -Johnston reports an autosomal dominant component with incomplete penetrance Meds/All: Usually non-contributory ROS: Usually non-contributory Objective: Physical Exam Derm: -Dorsomedial erythema +/- bursa -Submet 2 lesion -Nail bed rotational changes -Pinch callus Vasc/Neuro: Usually non-contributory

Ortho: -Dorsomedial eminence -Varus compensation -Underlying met adductus -PROM 1st MPJ -Tracking vs. Track-bound 1st MPJ

-Pes plano valgus -Equinus -Hypermobile 1st ray -LLD

Objective: Radiographic Evaluation Plain Film Radiographs: -Increased soft tissue density -In first met head: subchondral bone cysts, osteophytes, hypertrophy of medial eminence -Overall metatarsal parabola -1st MPJ joint space: ~2mm of clear space; Congruent vs. Deviated vs. Subluxed Angular deformities: -Met Adductus (<15 degrees) -Meary’s Angle -Engle’s Angle (<24 degrees) -Seiberg’s Angle -IMA (<8 degrees) -TDA -HAA (<15 degrees) -CIA -HIA (<10 degrees) -Cyma Line -Tibial sesamoid position (1-7) -Calcaneal-Cuboid Angle -PASA (<8 degrees) -Talar Head Uncovering -DASA (<8 degrees) -Talar Axis -Met protrusion distance (<2mm) -Kite’s Angle HAV Dissection and Capsule Procedures -Anatomic Dissection -1st incision is through epidermis and dermis -Incision is planned along the dorsomedial aspect of the 1st MPJ, just medial to EHL and lateral to the medial dorsal cutaneous nerve. -From midshaft of 1st metatarsal to just proximal to the hallux IPJ -Subcutaneous tissue is dissected to deep fascia/capsular layer -NV structures: Superficial venous network, medial dorsal cutaneous nerve -Be wary of the anterior resident’s nerve (Extensor capsularis)! -Lateral Release -Sequence of events: -Release of adductor hallucis tendon from base of proximal phalanx and fibular sesamoid -Release of fibular metatarsal-fibular sesamoid ligament and lateral capsule -Tenotomy of the lateral head of the FHB between the fibular sesamoid and the proximal phalanx -Optional excision of the fibular sesamoid -Medial Capsulotomies -Linear -Washington Monument: Strongest medial capsulotomy allowing for both transverse and frontal plane correction -Lenticular (Elliptical): Allows for transverse and frontal plane correction with removal of redundant capsule -Inverted L: Transverse plane correction with removal of redundant capsule -Medial T: Transverse plane correction with removal of redundant capsule -Medial H: Transverse plane correction with removal of redundant capsule

90

AJM List: HAV Procedures and Indications Distal Phalanx 1. Medial Nail Bed Rotation: Corrects soft tissue mal-alignment Hallux IPJ 2. Amputation of the distal phalanx: Permanent correction of abnormal Hallux Interphalangeus Angle (HIA) 3. IPJ Fusion: Corrects abnormal HAI Proximal Phalanx 4. Distal Akin: Corrects abnormal HAI with a medially-based wedge osteotomy at distal proximal phalanx 5. Central Akin: Corrects for long proximal phalanx seen with concurrent HL/HR 6. Oblique Akin: Corrects for distal articular set angle (DASA) midshaft proximal phalanx 7. Proximal Akin: Corrects for DASA of the proximal phalanx 8. Keller Arthroplasty: Corrects for abnormal Hallux Abductus Angle (HAA) and with concurrent HL/HR 9. Keller-Brandis Arthroplasty: Same as the Keller, but with removal of 2/3 of the proximal phalanx 10. Bonney-Kessel: Dorsiflexory osteotomy with concurrent HL/HR with modified forms correcting for abnormal DASA 11. Distal Hemi-Implant: Corrects for abnormal HAA or DASA with concurrent HL/HR 12. Regnauld: Allows for correction of DASA and abnormal proximal phalanx length in presence of HL/HR 13. Sagittal Z: Corrects for DASA and abnormal proximal phalanx length in presence of HL/HR MPJ 14. 15. 16. 17. 18. 19. 20. 21.

Total Implant: Correction of HAA in presence of HL/HR McKeever arthrodesis: Allows for permanent correction of DASA, PASA and HAA McBride: Soft tissue reconstruction for correction of HAA Modified McBride: Bone and soft tissue reconstruction for correction of HAA and medial eminence Silver: Correction of medial eminence Hiss: Modified McBride with Abductor hallucis advancement External Fixation: Double Taylor frame for gradual soft tissue realignment Hallux Amputation: Permanent correction of abnormal HAA

Distal 1st Met 22. Proximal Hemi-Implant: Correction of PASA and HAA with concurrent HL/HR 23. Mayo: First met head resection for correction of HAA with HL/HR 24. Stone: Mayo with sesamoid articulation left intact 25. Reverdin: Correction of PASA. Incomplete osteotomy. 26. Reverdin-Green: Correction of PASA with incomplete osteotomy and plantar shelf 27. Reverdin-Laird: Correction of PASA and IMA with complete osteotomy and plantar shelf 28. Reverdin-Todd: Correction of PASA, IMA and sagittal plane deformity (elevatus) 29. Youngswick: Correction of IMA and elevatus 30. Austin: Correction of IMA 31. Bicorrectional Austin: Correction of IMA and PASA 32. Tricorrectional Austin: Correction of IMA, PASA and elevatus 33. Mitchell: Rectangular osteotomy with lateral spicule to correct for IMA, elevatus and metatarsal length. Perpendicular to first met axis. 34. Roux: Wedged Mitchell to also correct for PASA 35. Miller: Mitchell with osteotomy oblique to first met axis for further correction of IM and length 36. Hohmann: Transverse through and through cut to correct for IMA and sagittal plane 37. Wilson: Oblique through and through osteotomy to correct for IMA and metatarsal length 38. Distal L: Similar to a Reverdin-Green without correction of PASA 39. Kalish: Austin with a long dorsal arm to allow for screw internal fixation 40. Mygind: Mexican hat procedure of distal first metatarsal for correction of IM and length 41. Off-set V/Vogler: Proximal Kalish 42. Peabody: Proximal Reverdin 43. Short-arm Scarf: Correction of IMA 44. Percutaneous DMO: Percutaneous Hohmann 45. DRATO (Derotational Abductory Transpositional Osteotomy): Can be used to correct frontal plane, IMA, sagittal plane and wedged for PASA 46. Distal Crescentic: Correction of IMA 47. Distal Crescentic with a shelf: Correction of IMA with greater stability Central 1st Met 48. Scarf: Correction of IMA 49. Ludloff: Correction of IMA. Dorsal-proximal to distal-plantar cut. 50. Mau: Correction of IMA. Distal-dorsal to proximal-plantar cut. Proximal 1st Met 51. Cresentic: Correction of IMA 52. Cresentic Shelf: Correction of IMA with greater stability 53. OBWO: Correction of IMA 54. Trethowan: OBWO using medial eminence for graft 55. CBWO (Loison-Balacescu): Closing base wedge proximal osteotomy. Corrects IMA. 56. Logroscino: CBWO with Reverdin. Corrects IMA and PASA. 57. Juvara: Oblique CBWO 58. Proximal Austin: Correction of IMA 59. Lambrinudi: Plantar CBWO to correct for sagittal plane 1st Met-Cunieform 60. Lapidus with internal fixation 61. Lapidus with external fixation 62. Cotton: OBWO of the cuneiform to correct for transverse plane 63. Westman: OBWO of the cuneiform to correct for sagittal plane 64. Cotton-Westman: OBWO of the cuneiform to correct for transverse and frontal plane Misc. 65. 66.

2nd digit amputation EHL lengthening

91

AJM Sheet: HAV Complications -Recurrence -Early (<1 year) -Usually due to wrong procedure choice, surgical error, or a post-operative complication. -As little as 1% and as much as 14% rate reported (Kitaoka on 49 feet). -Late (>1 year) -Usually due to an unrecognized underlying deformity (such as met adductus, Ehlers-Danlos, equinus, 1st met hypermobility, etc.) -Symptoms usually worse than initial presentation -Treatment: Distal soft tissue procedures or a proximal osteotomy usually indicated -Hallux Varus -Defined as a purely transverse plane adduction -Hallux Malleus: extension at MPJ with flexion at IPJ -Etiology -Underlying causes:

-Iatrogenic causes:

-Treatment:

-Long 1st metatarsal -Round 1st metatarsal head -1st MPJ hypermobility -Staking of the 1st metatarsal head -Overcorrection of the IM angle -Overzealous medial capsulorraphy -Fibular sesamoidectomy -Over extensive lateral release -Overcorrection of the PASA -Overzealous bandaging

-Soft tissue rebalancing (medial releases and lateral tightenings) -EHB tendon transfer -Reverse distal osteotomies -Ludloff/Mau -Resection arthroplasty, implant, arthrodesis

-MalUnion/Delayed Union/Non-Union -Malunion -Consolidated osteotomy with an angular or rotational deformity -Most common is sagittal plane abnormality (“dorsal tilting”) -Must be corrected with an osteotomy -AVN

92

AJM Sheet: HL/HR Work-up Subjective CC: Pt will generally complain of a “painful big toe.” HPI: -Nature: Aching, Dull, Throbbing -Location: Dorsal 1st MTPJ and within the joint -Course: Usually gradual and progressive. May follow an acute traumatic event. -Aggravating Factors: Shoe gear, WB -Alleviating Factors: Ice, NSAIDs, Rest PMH: -Inflammatory Condition: RA, SLE, Gout PSH: -Past 1st MTPJ surgery Meds/Allergies/SH/FH: Non-contributory ROS: Non-contributory Objective: Physical Exam Derm: -Hyperkeratotic lesions: Plantar hallux IPJ, Medial pinch callus hallux IPJ, Submet 2 -Erythema, Calor, Dorsal 1st MTPJ bursa Vasc/Neuro: Non-contributory -Varus Deformity Gait: Ortho: -Decreased PROM 1st MTPJ -Dorsal eminence 1st MTPJ -Plantar Contracture -Dorsal eminence 1st Met-Cun -Equinus -Hypermobile 1st ray Objective: Imaging Plain Film Radiographs:

-Osteophytes at 1st MTPJ -Irregular Joint Space Narrowing -Lateral view: dorsal flag sign, dorsal lipping -Loose bodies (joint mice) -Square-shaped 1st met head

-Early Heel-off -Apropulsive Gait -Abductory Twist

-Long 1st met -Long hallux proximal phalanx -Elevated 1st met -Osteophytes at hallux IPJ, 1st met-cun

General HL/HR Information -Definitions -Hallux Limitus vs. Hallux Rigidus -This is a progressive deformity, so what defines rigidus from limitus? Bony ankylosis and sesamoid immobilization. -Functional HL is defined as a decreased PROM with the foot loading and in a neutral position, and normal PROM when the foot is unloaded. Dannanberg first defined functional HL. -Flexor Stabilization of the hallux: Essentially a hammertoe of the hallux with extension at the MTPJ and plantarflexion at the IPJ. -Axis of rotation of the 1st MTPJ: Normally found in the center of the metatarsal head allowing for a gliding motion of the hallux up and over the first metatarsal head. In a HL/HR deformity the axis of rotation moves distally and plantarly leading to dorsal jamming of the joint. -Met Primus Elevatus: Dorsiflexed position of the 1st metatarsal. -Primary: Structural. Distal segment is dorsiflexed compared to proximal segment. -Secondary: Global. Due to some extrinsic variable. This can be measured by Meary’s Angle on a lateral plain film radiograph or using the Seiberg technique comparing the 1st and 2nd metatarsal positions. -What stimulates osteophyte production in and around the joint?: Loss of functional cartilage. -1st MTPJ ROM -Normal PROM of the 1st MTPJ is classically described as 65-75 degrees of dorsiflexion of the hallux referenced to the weight-bearing surface (same as 85-95 degrees of dorsiflexion referenced to the 1st met shaft). Plantarflexion is 30 degrees to the weight-bearing surface. -Hetherington contradicts this somewhat by finding an average ROM of 31degrees of dorsiflexion during pain-free gait in asymptomatic patients. -Compensation Patterns for Lack of Motion -Distal: Hallux IPJ leading to OA and plantar hyperkeratotic lesions -Lateral: Lesser metatarsalgia -Proximal: 1st met-medial cuneiform joint increased motion and OA -Gait patterns: Abductory twist with roll-off; early heel-off; apropulsive gait -HL/HR Etiology -Many people have reported potential causes of HL/HR including Root, Lapidus and Nilsonne: -Acute Trauma -Chronic degenerative trauma -Pes planus with 1st met hypermobility -Long first metatarsal -Short first metatarsal with hallux gripping -Long hallux proximal phalanx -Iatrogenic -Compensated varus deformity -Neuromuscular imbalance -Plantar contracture -Spastic conditions -Square first metatarsal head shape -Met primus elevatus -No single characteristic has been shown to reliably lead to HL/HR except acute trauma -Coughlin (FAI 2003) performed a retrospective analysis and seemed to demonstrate that there are no reliable underlying indicators for development of HL/HR. -Classification Systems -Numerous exist; usually in the mild, moderate, severe format: -Mild: Mild pain; Normal PROM; Radiographic evidence of osteophytes -Moderate: Increasing pain; Decreasing PROM; Osteophytes and irregular joint space narrowing on radiograph -Severe: Increasing pain; Decreasing PROM; Osteophytes, irregular joint space narrowing, subchondral sclerosis on radiograph. -Rigidus: Increasing pain; Absent PROM; Sesamoid immobility -Examples of classifications include the Regnauld, Hanft and KLL.

93

AJM Sheet: HL/HR Treatment -Conservative -Do nothing -Activity modification -Orthotics: First ray cut-out, Morton’s extension, rocker-bottom sole -Meds: PO NSAIDs, Intra-articular corticosteroid injections -Surgical -Surgical options are always divided into joint-sparing and joint-destructive procedures, and further divided into whether the correction occurs at the proximal phalanx, at the MTPJ, or at the first metatarsal. -Joint Sparing -Proximal Phalanx -Bonney-Kessell -Regnauld -Vanore -Sagittal “Z” -Central Akin -1st MTPJ -Cheilectomy -1st Metatarsal -Youngswick -Watermann -Watermann-Green -Jacoby -Hohmann -Derner -Dorsal OBWO -Lambrinudi -Westman -Joint Destructive -Proximal Phalanx -Keller -Keller-Brandis -Distal Hemi-Implant -1st MTPJ -Total Implant -McKeever arthrodesis -Valenti -1st Metatarsal -Mayo -Stone -Lapidus

94

AJM Sheet: Flatfoot Work-up -This is a lot of information to cover in 2 pages, so these sheets will focus on clinical and radiographic signs, as well as indications for specific surgeries. Also, will try and include a good amount of additional readings. Subjective -Wide range of presenting ages and complaints. -Always think about posterior tibialis tendon dysfunction when someone complains of “medial ankle pain.” Objective -Underlying Orthopedic Etiologies:

-Compensated forefoot varus -Forefoot valgus -Rearfoot valgus -Equinus -Compensated and uncompensated ab/adduction deformities -Muscle imbalances (PTTD) -Ligamentous laxity -Tarsal coalitions -Planal dominance -Normal STJ axis: 42° from transverse/16° from sagittal -Normal MTJ-O: 52° from transverse/57°from sagittal -Normal MTJ-L: 15° from transverse/9° from sagittal

-Clinical findings: -“Too many toes” sign (forefoot abduction) -Evaluation for flexible versus rigid deformity -Single and double heel raise

-Hubscher maneuver -RCSP -Subjective gait analysis

-Radiographic evaluation: -Lateral: -Decreased calcaneal inclination angle -Increased talar declination angle -Increased first metatarsal declination angle -Calcaneal-cuboid “break”

-Anterior break in Cyma line -Meary’s Angle -Midfoot “breaks” or “incongruity”

-AP:

-Increased talo-calcaneal angle -Cuboid-abduction angle -Talar head coverage -Look for “skew foot” deformity

-Talar-first metatarsal axis -Intermetatarsal angle -Forefoot adduction angle or Engle’s Angle

-Harris-Beath: Evaluation of tarsal coalitions -Long-Leg Calcaneal Axial Views: Evaluation of structural rearfoot deformities Classifications -Johnson and Strom [Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. CORR. 1989; 239: 196-206.] -Later modified by Myerson who added Stage IV (he does that a lot): -[Myerson MS. Adult acquired flatfoot deformity: treatment of dysfunction of the posterior tibial tendon. JBJS-Am. 1996; 78: 780-92.] -[Bluman EM, et al. Posterior tibial tendon rupture: a refined classification system. Foot Ankle Clin. 2007 Jun; 12(2): 233-49.]

-Stage I: Tenosynovitis with mild tendon degeneration; flexible rearfoot; Mild weakness of single heel raise and negative “too many toes” sign -Stage II: Elongated tendon with tendon degeneration; flexible rearfoot; Marked weakness of single heel raise and positive “too many toes” sign -Stage III: Elongated and ruptured tendon; Rigid valgus rearfoot; Marked weakness of single heel raise and positive “too many toes” sign -Stage IV: Same as Stage III with a rigid ankle valgus -Funk: Classification based on gross intra-operative appearance -[Funk DA, et al. Acquired adult flatfoot secondary to posterior tibial tendon pathology. JBJS-Am. 1986; 68: 95-102.]

-Type I: Tendon Avulsions -Type III: In-continuity tears -Type II: Complete midsubstance rupture -Type IV: Tenosynovitis -Jahss or Janis Classifications: There are several MRI classifications generally along the lines of: -[Conti S, Michelson J, Jahss M. Clinical significance of MRI in preoperative planning for reconstruction of posterior tibial tendon ruptures. Foot Ankle. 1192; 13(4): 208-214.] -[Janis LR, et al. Posterior tibial tendon rupture: classification, modified surgical repair, and retrospective study. JFAS. 1993; 31(1): 2-13.]

-Type I: Tenosynovitis, increased tendon width, mild longitudinal splits -Type II: Long longitudinal splits with attenuated tendon -Type III: Complete rupture Additional Reading: -[Mendicino RW, et al. A systemic approach to evaluation of the rearfoot, ankle and leg in reconstructive surgery. JAPMA. 2005; 95: 2-12.] -[Lamm BM, Paley D. Deformity correction planning for hindfoot, ankle and lower limb. Clin Podiatr Med Surg. 2004 Jul; 21(3): 305-26.] -[Greisberg J, Hansen, Sangeorzan. Deformity and degeneration in the hindfoot and midfoot joints of the adult acquired flatfoot. Foot Ankle Int. 2003 Jul; 24(7): 530-4.] -[Weinraub GM, Saraiya MJ. Adult flatfoot/posterior tibial tendon dysfunction: classification and treatment. Clin Podiatr Med Surg. 2002 Jul; 19(3): 345-70.]

95

AJM Sheet: Flatfoot Treatment -Again, this is a lot of information to cover, so we’ll just focus on organizing general procedures and indications, but supplement it with some additional reading. -Conservative Treatments -Not going to be discussed here, but try reading: -[Elftman NW. Nonsurgical treatment of adult acquired flatfoot deformity. Foot Ankle Clin. 2002 Mar; 7(1): 95-106.] -[Marzano R. Functional bracing of the adult acquired flatfoot. Clin Podiatr Med Surg. 2007 Oct; 24(4): 645-56.]

-Johnson and Strom/Myerson Classification: -In addition to describing the deformity, this classification system (discussed on a previous sheet) also makes general treatment recommendations: -Stage I: Conservative treatment; Tenosynovectomy; Tendon Debridement -Stage II: Tendon transfer; Rearfoot arthrodesis -Stage III: Isolated rearfoot arthrodesis; Triple arthrodesis -Stage IV: TTC arthrodesis; Pantalar arthrodesis -General Surgical Procedures/Indications: -Keep in mind that it is very common to do combinations of these procedures. Soft Tissue Procedures: -FDL Tendon Transfer: FDL is sectioned as distal as possible (consider anastomosis of stump to FHL) and either attach proximal FDL to the PT, within the PT sheath or into the navicular under tension. -Cobb: Split TA tendon, transfer to the PT or into the navicular -Young’s Tenosuspension: TA rerouted through navicular -Anastomosis of PB and PL: Removes PB as deforming force -STJ implant (arthroeresis) -TAL -Gastroc recession Rearfoot Osseous Procedures: -Evans Osteotomy (1975): opening wedge calcaneal osteotomy -Silver (1967) is a more proximal (and less common) Evans-type opening wedge -[Sangeorzan BJ, et al. Effect of calcaneal lengthening on relationships among the hindfoot, midfoot and forefoot. Foot Ankle. 1993; 14(3): 136-41.] -[Raines RA, et al. Evans osteotomy in the adult foot: an anatomic study of structures at risk. Foot Ankle Int. 1998 Nov; 19(11): 743-7.] -[Weinraub GM. The Evans osteotomy: technique and fixation with cortical bone pin. JFAS. 2001; 40(1): 54-7.] -[DeYoe BE, Wood J. The Evans calcaneal osteotomy. Clin Podiatr Med Surg. 2005 Apr; 22(2): 265-76.]

-Medial Calcaneal Slide (Koutsogiannis - 1971): medial translation of posterior calcaneus -[Weinfeld SB. Medial slide calcaneal osteotomy. Technique, patient selection and results. Foot Ankle Clin. 2001 Mar; 6(1): 89-94.] -[Catanzariti AR, et al. Posterior calcaneal displacement osteotomy for adult acquired flatfoot. JFAS. 2000; 39(1): 2-14.]

-Double Calcaneal Osteotomy: Evans with a medial calcaneal slide -[Catanzariti AR, et al. Double calcaneal osteotomy: realignment considerations in eight patients. JAPMA. 2005; 95(1): 53-9.] -[Nyska M, et al. The contribution of the medial calcaneal osteotomy to the correction of flatfoot deformities. Foot Ankle Int. 2001 Apr; 22(4): 278-82.]

-STJ arthrodesis -Triple arthrodesis -Tibiotalocalcaneal arthrodesis -Pantalar arthrodesis -Closing wedge of the medial calcaneus: Essentially the opposite of an Evans but with more NV structures -Dwyer (1960) -Slakovich: opening wedge behind the sus tali -Baker-Hill: opening wedge osteotomy with graft horizontally under the posterior calcaneal facet Midfoot/Forefoot Osseous Procedures: -Cotton: opening wedge osteotomy with graft in medial cuneiform -Kidner: advancement and reattachment of PT tendon (+/- resection of portion of navicular) -TN arthrodesis: called a Lowman when wedged and combined with TAL -Medial column arthrodeses -Miller: NC and 1st met-cun arthrodesis -Lapidus (1931/1960): 1st met-cun arthrodesis -Hoke: arthrodesis of navicular with 1st/2nd cuneiforms -Any other combinations -[Greisberg J, et al. Isolated medial column stabilization improves alignment in adult-acquired flatfoot. CORR. 2005 Jun; 435: 197-202.]

-Additional Reading: -[Hix J, et al. Calcaneal osteotomies for the treatment of adult-acquired flatfoot. Clin Podiatr Med Surg. 2007 Oct; 24(4): 699-719.] -[Mosier-LaClair S, et al. Operative treatment of the difficult stage 2 adult acquired flatfoot deformity. Foot Ankle Clin. 2001 Mar; 6(1): 95119.] -[Roye DP, Raimondo RA. Surgical treatment of the child’s and adolescent’s flexible flatfoot. Clin Podiatr Med Surg. 2000 Jul; 17(3): 515-30.] -[Toolan BC, Sangeorzan, Hansen. Complex reconstruction for the treatment of dorsolateral peritalar subluxation of the foot. JBJS-Am. 1999 Nov; 81(11): 1545-60.] -[Weinraub GM, Heilala MA. Adult flatfoot/posterior tibial tendon dysfunction: outcomes analysis of surgical treatment utilizing an algorithmic approach. J Foot Ankle Surg. 2001 Jan-Feb; 40(1): 54-7.]

96

AJM Sheet: Cavus Foot Work-up -The cavus foot work-up is one of the most feared in the residency interview process because of its complex nature. The most important technique during this work-up is to use a standardized system to identify several specific variables which will let you best identify the deformity and decide on a treatment course: -Underlying Etiology of the Deformity (Spastic vs. Progressive vs. Stable) -Forefoot vs. Rearfoot driven deformity (Anterior Cavus vs. Posterior Cavus) -Plane of the Deformity (Sagittal vs. Frontal vs. Transverse vs. Combination) -Rigid vs. Flexible -Underlying Etiology of the Deformity (Spastic vs. Progressive vs. Stable) -Obtained through a good PMH and physical exam -Brewerton of the Royal Hospital in London identified 75% of 77 patients seen at his pes cavus clinic to have an underlying neuromuscular disorder. -Common Congenital Conditions leading to neuromuscular dysfunction: -Spina bifida -Charcot-Marie-Tooth -Myelodysplasia -Friedreich’s Ataxia -Cerebral Palsy -Roussy-Levy syndrome -Muscular Dystrophy -Dejerine-Sottas -Poliomyelitis -Etc, etc, etc. -Also consider MMT, clonus, deep tendon reflexes, EMG studies and nerve conduction studies during your physical exam. -Forefoot vs. Rearfoot Driven Deformity -Anterior Cavus: plantar declination of the forefoot in relation to the rearfoot. Subdivided based on apex of deformity: -Metatarsus Cavus: Apex at Lisfranc’s joint. Generally more rigid. -Lesser Tarsus Cavus: Apex in the lesser tarsus area -Forefoot Cavus: Apex at Chopart’s joint -Combined Cavus: Combination of any of the above -The apex of the deformity can be found several different ways: -Intersection of Meary’s lines (longitudinal axes of talus and first met) -Intersection of Hibb’s Angle (longitudinal axes of calcaneus and first met) -Dorsal boney prominences -Joint space gapping -Posterior Cavus: Dorsiflexion of the rearfoot in relation to the forefoot -Generally defined as an increased calcaneal inclination angle (>30 degrees) and a varus positioning. -Usually the result of an anterior cavus; rarely presents as separate entity. -An anterior cavus and a posterior cavus can be defined based on radiographic evidence and a physical exam measure called the Coleman Block Test. In this test the forefoot, or the medial and lateral portions of the forefoot, are suspended off of a block. If the calcaneus returns from a varus to a normal position, the deformity is forefoot driven. A deformity is rearfoot driven only if the varus positioning of the calcaneus remains after all forefoot elements are removed. -Biomechanical compensation for a sagittal plane cavus deformity: -Digital retraction: HT deformity where EDL gains mechanical advantage and uses a passive pull. -MPJ Retrograde buckling: As per above -Lesser Tarsal Sagittal Plane Flexibility: The lesser tarsus “absorbs” some of the dorsiflexion. They can be clearly seen when comparing NWB and WB lateral views of an anterior cavus foot. -Pseudoequinus: Occurs when the ankle joint must dorsiflex because the lesser tarsus cannot “absorb” all of the dorsiflexion. Limits the amount of “free” dorsiflexion available during gait. -Plane of the Deformity: -Sagittal Plane:

-Transverse Plane: -Frontal Plane:

-Anterior Cavus (Global, Medial Column, or Lateral Column) -Posterior Cavus -Muscular Cavus (Gastroc Equinus, Gastroc-Soleus Equinus) -Osseous Equinus (Tibiotalar exostosis) -Met adductus (measured via met adductus angle or Engle’s angle) -Met abductus (measured via met adductus angle) -Forefoot Varus -Forefoot Valgus -Rearfoot Varus -Rearfoot Valgus

-Rigid vs. Flexible Deformity -Flexible deformities can be manipulated out during the physical exam and are obvious comparing NWB and WB lateral radiographs. -Rigid deformities show no compensation with manipulation of weight-bearing. -Defining each of these variables during your work-up will give you a clear enough understanding of the deformity to recommend a treatment option.

97

AJM Sheet: Cavus Foot Treatment -Basic principles of treatment based on definition of deformity: -Underlying Etiology: -Progressive/Spastic conditions are generally treated with osteotomies and arthrodeses. -Stable conditions are generally treated with soft tissue procedures and osteotomies. -Forefoot vs. Rearfoot Driven: -Forefoot driven conditions are treated with manipulation of the bones and soft tissue of the forefoot. -Rearfoot driven conditions require rearfoot osteotomies and arthrodeses. -Plane of the Deformity: -Procedures are chosen by which plane you want correction in. -Rigid vs. Flexible: -Rigid deformities are generally treated with osteotomies and arthrodeses. -Flexible deformities can usually be managed with soft tissue procedures and tendon transfers. -Soft Tissue Releases: Reduces contracture of the plantar fascia seen with long standing disease. -Subcutaneous Fasciotomy: Cuts the plantar fascia at its insertion. -Steindler Stripping: Removes all soft tissue from the plantar surface of the calcaneus. -Plantar Medial Release: Releases plantar musculature and ligaments from the plantar-medial foot. -Tendon Transfers: Used to treat flexible conditions based upon plane of the deformity. -Jones Suspension: Transfer of EHL through the first metatarsal head. -Heyman Procedure: Transfer of EHL and EDL tendons through each of the respective metatarsal heads. -Hibbs Procedure: Transfer of EDL into lateral cuneiform; EHL into first metatarsal; EDB into sectioned tendons. -STATT: Tibialis anterior is split and sutured into peroneus tertius. -Peroneus Longus Transfer: Peroneus longus is split and anastomosed to the TA and peroneus tertius tendons. -Peroneal Anastomosis: Increases the eversion power of the foot. -PL/PT transfer to calcaneus: Tendons are attached into the calcaneus via bone anchors to aid weak Achilles tendon. -Osseous Procedures: Reduction of rigid deformities. Can be used to correct multi-planar deformities. -Cole Procedure: Dorsiflexory wedge is removed from Chopart’s joint. -Japas Procedure: “V” shaped osteotomy through the midfoot (apex proximal) to dorsiflex forefoot. -Jahss Procedure: Essentially a Cole procedure performed at Lisfranc’s joint. -Dorsiflexory Metatarsal Osteotomies -Dwyer Osteotomy: Closing wedge osteotomy out of lateral calcaneus to reduce rigid rearfoot varus. -Dorsiflexory Calcaneal Osteotomy: Must be used with caution -Arthrodesis Procedures: Used as last resort to correct rigid deformities in the face of progressive disease. -Hoke: STJ and TNJ arthrodesis -Ryerson (1923): Triple arthrodesis -Additional Reading: -[Younger AS, Hansen. Adult cavovarus foot. J Am Acad Orthop Surg. 2005 Sep; 13(5): 302-25.] -[Statler TK, Tullis BL. Pes Cavus. JAPMA. 2005; 95: 34-41.]

98

AJM Sheet: Ankle Equinus -This sheet is not a work-up because equinus rarely presents as a chief concern, but rather as a concomitant and underlying deformity. It may be seen and deemed correctable in the following deformities: -Charcot arthropathy -Digital deformities -Pes plano valgus -Met primus elevatus -HAV -Plantar fasciitis -Medial column hypermobility -Diabetic foot ulcerations -Etc. -History -First TAL: Paris on Achilles in the “Iliad” -First medically documented procedure: Stromeyer on Dr. Charles Little. Dr. Little was a prominent physician suffering from cerebral palsy (CP) who then became an advocate for surgical correction of equinus. -Anatomy -Review the origins/insertions/course/action/NV supply of the gastroc and soleus. -Review the concept of the “twisting” fibers within the Achilles tendon. -[White JW. Torsion of the Achilles tendon: its surgical significance. Arch Surg 1943; 46: 784-7.]

-Definitions -Muscular Equinus -Spastic vs. Non-Spastic -Gastroc Equinus -Gastroc-Soleal Equinus -Osseous Equinus -Tibio-talar exostosis -Pseudoequinus -Combination equinus -Biomechanic Compensation for Equinus (proximal to distal) -Lumbar lordosis -STJ pronation -Hip flexion -MTJ pronation -Genu recurvatum -Forefoot abduction -No compensation (toe walking) -Medial column hypermobility -Testing for Equinus -Silfverskiold test -Stress dorsiflexion plain film radiographs -WB wall test Treatment -Conservative Treatment -Stretching -Heel Lifts (?) -Casting -Physical Therapy -Neuromuscular blockage injections (Botox) -Surgical Correction -Gastroc Equinus -Neurectomy of motor branches of tibial nerve -Proximal recession (Silfverskiold procedure) -Release of muscular heads of gastroc +/- reattachment to tibia +/- neurectomy -Distal aponeurotic recession -Vulpius&Stoffel (1913): Inverted “V” shaped incision without suture reapproximation -Strayer (1950): Transverse incision with proximal dissection and suturing (absorbable) -Baker (1956): Tongue and groove with suturing (two incisions distal) -Fulp&McGlamry: Inverted tongue and groove with suturing (two incisions proximal) -Endoscopic recession -Gastroc-Soleal Equinus -Sagittal plane “Z” lengthening: equal medial and lateral portions -Frontal plane “Z” lengthening: equal anterior and posterior portions -Hoke Triple Hemisection (1931): 2 medial cuts/1 lateral cut -White slide technique -Percutaneous -Similar to the Hoke procedure -1cm
3cm
3 cm

Additional Reading: -[Pinney SJ, Hansen, Sangeorzan. The effect on ankle dorsiflexion of gastrocnemius recession. Foot Ankle Int. 2002 Jan; 23(1): 26-9.] -[Pinney SJ, Hansen, Sangeorzan. Surgical anatomy of the gastrocnemius recession. Foot Ankle Int. 2004 Apr; 25(4): 247-50.] -[Lamm BM, Paley, Herzenberg. Gastrocnemius soleus recession: a simpler, more limited approach. JAPMA. 2005; 95: 18-25.] -[Graham HK, Fixsen JA. Lengthening of the calcaneal tendon in spastic hemiplegia by the White slide technique. A long term review. JBJB-Br. 1988 May; 70(3): 472-75.]

99

AJM Sheet: Page 100

One of the most frequent questions asked by students and externs is “Can you give me some good articles to read?”

-I tried to do this by incorporating current and historical articles throughout this edition. All referenced articles (as well as other suggested readings) can be found on the Inova Pubmed page:

-www.pubmed.com -My NCBI link on the left -User Name: INOVA -Password: resident -Although this was specifically designed for the use of externs and residents at the Inova program, the collection of articles on this page can be used by anyone. Additionally, anyone is welcome and encouraged to update these collections with articles they feel are valuable.

----------------------------------------------------------------------------------------------------------------------------------

In conclusion, this PRISM was not designed to help you pass the boards or even to directly make you a better physician; it simply hopes to make you better prepared and more efficient as you approach externships and the residency interview. Use, change, and pass this guide along as you see fit, keeping in mind the general goal of selfless education of the next generation. Good luck, and please don’t hesitate to contact me if there is any way that I can be of service to you. [email protected]

100

CROZER-KEYSTONE RESIDENCY MANUAL SECOND EDITION

Original Author Brett Chicko, DPM

Second Edition Sandi Pollard, DPM Hubert Lee, DPM

Table of Contents Introduction

William Urbas, DPM ................................................................................. i Brett Chicko, DPM ................................................................................... ii

Chapter 1

Anatomy ......................................................................................................1

Chapter 2

Antibiotics ...................................................................................................7

Chapter 3

Bugs and Drugs ........................................................................................19

Chapter 4

Labs ...........................................................................................................25

Chapter 5

Medicine ....................................................................................................29

Chapter 6

Clinical Podiatry ......................................................................................51

Chapter 7

Biomechanics ............................................................................................59

Chapter 8

Surgery ......................................................................................................67

Chapter 9

Trauma......................................................................................................85

Chapter 10

Bone Tumors ............................................................................................91

Chapter 11

Wound Care .............................................................................................97

Chapter 12

Classifications Forefoot ..........................................................................................99 Rearfoot........................................................................................106 Other Classifications ....................................................................121

Chapter 13

Special Studies ........................................................................................127

Chapter 14

Name That Surgery! ..............................................................................131

Chapter 15

Special Surgical Section Introduction ..................................................................................149 Achilles Tendon Achilles Tendon Repair ...................................................150 Delayed Repair of the Achilles Tendon ...........................152 Excision of Calcification of Achilles Tendon ..................154 Murphy Procedure ...........................................................155

Arthrodesis Ankle Arthrodesis ............................................................156 Tibio-Calcaneal Arthrodesis ............................................158 Subtalar Arthrodesis.........................................................160 Talo-Navicular Arthrodesis .............................................161 Triple Arthrodesis ............................................................163 Calcaneal Osteotomy Calcaneal Slide Osteotomy ..............................................164 Evans ................................................................................165 Tendons Peroneal Brevis Tendon Repair and Reconstruction .......166 Posterior Tibial Tendon Repair-Substitution ...................167 Posterior Tibial Tendon Transfer .....................................169 Split TA Tendon Transfer (STATT) and Tibialis Anterior Tendon Transfer (TATT) .....................170 Trauma Ankle Fracture Weber A ..................................................171 Ankle Fracture Weber B ..................................................173 Medial Malleolar Fractures ..............................................177 Posterior Malleolar Fracture ............................................180 Syndesmotic Repair .........................................................181 ORIF Calcaneus ...............................................................183 ORIF Talus Neck .............................................................185 Tibial Periarticular Fracture Reduction & Fixation .........188 Other Surgeries Ankle Arthroscopy ...........................................................190 Arthroereisis.....................................................................192 Arthrosurface 1st Metatarsal Implant ...............................193 Brostrom-Gould ...............................................................195 Fibular Derotational and Lengthening Osteotomy ..........196 Ilizarov Method................................................................197 Osteochondral Lesions of the Talus .................................198 Tarsal Tunnel Release ......................................................199 Chapter 16

Case Studies Case 1 ..........................................................................................201 Case 2 ..........................................................................................203

Chapter 17

The Interviews ........................................................................................205

Introduction Dear Student: In the pages that follow is useful information that will help make your externships, interviews and transition from student to resident a little bit easier. This information contained within is not the end all on the subject, but the tidbits that need to be on your “Mind’s Fingertips”. This booklet is a useful guide on the need-to-know, need-to-keep information. Please use it as it was intended--a guide on the ever-changing world of medical information. My thanks go out to the Podiatric Surgical Residents at Crozer-Keystone Health System for the formation of this manual. Sincerely,

William M. Urbas, DPM Crozer-Keystone Residency Director

i

Author’s Introduction This manual is NOT meant to replace “McGlamry’s”, the “Presbyterian Manual”, the “Podiatry Institute Manual” or any other reference source. Those manuals are excellent resources and should be used to continue to learn the information. To this day, I still use those texts for information and reference. This manual is based on questions I came across as an extern or a resident, either from my own questions or questions from a superior. I would write these questions down and after I looked up the answers, I would keep the questions with their answers in a log. Later, as a resident, I was quizzing a student in order to get her ready for her interviews. The student asked me, “Why can’t there be a book of these questions?” After that I started to put together the manual. I also added some additional items to complete the manual. In no way, shape or form do I claim that the answers written here are the only answers possible, nor do I even claim that they are all 100% correct. These answers are the ones that I came up with when I researched the questions. It is up to you to go to the true references--not only to make sure that the answers are correct, but also to make sure that you understand why. Therefore, the purpose of this manual is so that the reader can have some questions and answers so that he or she can go to the sources and really learn podiatry. I am not able to provide all of my sources because when I started writing down the answers, I had no idea of turning it into a manual. However, my major sources are, “The Comprehensive Textbook of Foot Surgery”, “The Presbyterian Manual” and “The Podiatry Institute Manual”. A special thank you to my attendings and co-residents at the Crozer-Keystone Health Systems in Springfield, PA, especially Dr. Urbas our residency director, mentor and friend.

Good Luck and Happy Studying,

Brett Chicko, DPM

ii

Anatomy How many bones are in the foot? 26 (not including sesamoids) How many joints are in the foot? 35 Name the accessory ossicles Os Intermetatarsium Os Vesalianum Os Tibiale Externum Os Supranaviculare Os Peroneum Os Calcaneus Secondarius Os Sustentaculi Os Trigonum Os Subtibiale Os Subfibulare

Between 1st cuneiform and 1st and 2nd metatarsal bases Proximal 5th metatarsal base Accessory navicular Dorsal aspect of navicular Sesamoid bone in PB tendon Dorsal, anterior process of calc Posterior aspect of sustentaculum tali Posterior aspect of talus (Steida process) Distal to medial malleolus Distal to lateral malleolus

Name the avascular necroses Renandier Tibial sesamoid Trevor Fibular sesamoid Theiman Phalanges Freiberg Metatarsal heads Iselen 5th metatarsal base Buschke Cuneiforms Kohler Navicular Lance Cuboid Diaz Talus Severe Calcaneus Blount Proximal, medial tibial epiphysis Osgood-Schlatter Tibial tuberosity Legg-Calve-Perthes Femoral epiphysis What attaches periosteum to bone? Sharpey fibers What are the different types of coalitions? Syndesmosis – fibrous Synchondrosis – cartilaginous Synostosis – osseous

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

1

What is the difference between a coalition and a bar? Coalition – intra-articular fusion of two bones Bar – extra-articular fusion What is the most common coalition in the foot? Distal and middle phalanx of 5th digit What is the most common coalition in the rearfoot? Talocalcaneal What is a Steida process? Enlarged Os Trigonum What is the only bone in the foot without any muscle origin or tendon insertion? Talus What are the plantar muscle layers of the foot from superficial to deep? 1. Abductor hallucis, flexor digitorum brevis, abductor digiti minimi 2. Quadratus plantae, 4 lumbricals 3. Flexor hallucis brevis, adductor hallucis, flexor digiti minimi 4. 3 plantar interossei, 4 dorsal interossei What layer of the foot does FDL run? 2nd layer – it is the origin of the lumbricals and the insertion of QP What deformity will result from cutting QP? Digits 4 and 5 will become adductovarus How is EDL attached to the proximal phalanxes? Sling wraps around capsule which attaches to plantar plate, DTML, and flexor tendon sheath thus attaching to plantar proximal phalanx. No direct insertion to proximal phalanx. What is the origin and insertion of the capsularis tendon? Origin – extensor hallucis longus muscle or tendon Insertion – first metatarsophalangeal joint capsule What is the Master Knot of Henry? Fibrous connection between FHL and FDL tendons What structures attach to the fibular sesamoid? Plantar metatarsal-phalangeal ligament Lateral metatarsal-sesamoidal ligament Intersesamoidal ligament Phalangeal-sesamoidal ligament FHB tendon ADH tendon 2

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Are the sesamoids capsular or extra-capsular? Capsular What is the Lisfranc ligament? Attaches lateral aspect of medial cuneiform to medial base of 2nd metatarsal What structures in the Lisfranc joint are not connected by ligaments? 1st and 2nd metatarsals What is the spring ligament? Plantar calcaneonavicular ligament What ligaments compose the bifurcate ligament? Dorsal calcaneonavicular and calcaneocuboid ligaments Which is stronger – the lateral ankle ligaments or the deltoid ligament? Deltoid ligament What are the components of the deltoid ligament? Superficial – tibionavicular, tibiocalcaneal, posterior tibiotalar Deep – anterior tibiotalar What tendons pass over the deltoid ligament? Tibialis posterior and FDL What are the lateral ankle ligaments? Anterior talofibular, calcaneofibular, posterior talofibular What angle do the ATFL and CFL create? 105° What is the strongest lateral ankle ligament? Posterior talofibular Which ankle ligaments are extra-capsular? Which are capsular? Calcaneofibular ligament is extra-capsular, all others are capsular What tendons pass over the lateral ankle ligaments? Peroneus brevis and longus What ligaments support the ankle syndesmosis? Anterior-inferior tibiofibular ligament Posterior-inferior tibiofibular ligament Interosseous tibiofibular ligament

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

3

What is the Bassett ligament? Anterior-inferior tibiofibular ligament What is another name for the flexor retinaculum? Laciniate ligament What is another name for the superior extensor retinaculum? Transverse crural ligament What is another name for the inferior extensor retinaculum? Cruciate crural ligament Where does plantaris insert? Medial aspect of tendo-Achilles into the calcaneus What is the incidence of peroneus quartus? 7% What is the Hoke tonsil? Fibrous, fatty plug within the sinus tarsi What is pes anserinus? Insertion of sartorius, gracilis, and semitendinosus (anteromedial aspect of proximal tibia) where bursa may cause knee pain (pes anserinus bursitis) What is a Bakers cyst? Swelling of the bursa between the tendons of the medial head of the gastrocnemius and the semimembranosus muscles What is a fabella? Sesamoid bone occasionally found in tendon of lateral head of gastrocnemius What nerves form the sural nerve? Medial sural cutaneous nerve – branch of the tibial nerve Sural communicating branch – branch of the lateral sural cutaneous nerve, which originates from the common peroneal nerve Does a neuroma lie dorsal or plantar to the deep transverse intermetatarsal ligament? Plantar Where do these muscles run in relation to the deep transverse intermetatarsal ligament? Interossei – dorsal Lumbricals – plantar

4

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What layers of the foot do the plantar nerves run? Medial plantar nerve – in the 1st layer (between FDB and abductor hallucis) Lateral plantar nerve – between the 1st and 2nd What is the innervation to the plantar muscles of the foot? Blood supply? (Never LAFF at A FAD) N – medial plantar Nerve L – 1st Lumbrical A – ABH F – FHB F – FDB (innervated by both medial and lateral plantar nerves) A – medial plantar Artery F – FDB A – ABH D – 1st Dorsal interossei What are the branches of the femoral nerve? Nerve to femoral artery Small muscular branch to pectineus Anterior division (cutaneous)  Anterior femoral cutaneous  Nerve to sartorious  Intermediate femoral cutaneous nerve  Medial femoral cutaneous nerve Posterior division (muscular)  Saphenous nerve  Infrapatellar branch  Medial crural cutaneous nerve  Nerve to rectus femorus  Nerve to vastus medialus  Nerve to vastus intermedialus  Nerve to vastus lateralus What are the branches of the femoral artery? Superficial epigastric artery Superficial circumflex iliac artery Superficial external pudendal artery Deep femoral (profunda femoris) artery Medial femoral circumflex artery Lateral femoral circumflex artery Descending genicular artery Femoral artery continues as the popliteal artery

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

5

Trace the path of a drop of blood from left ventricle to the hallux Ascending aorta → aortic arch → descending aorta → thoracic aorta → abdominal aorta → common iliac artery → external iliac artery → femoral artery → deep femoral artery → popliteal artery → anterior tibial artery → dorsalis pedis → 1st dorsal metatarsal artery → 1st dorsal common digital artery → 1st dorsal proper digital artery What are the sources of blood supply to the talus? Essentially the 3 major blood supplies to the foot  Superior surface of head and neck – artery of sinus tarsi and branch from anterior tibial artery or dorsalis pedis  Medial side of body – artery of tarsal canal and posterior tibial artery  Lateral turbercle – anastamosis of branch of peroneal artery with medial calcaneal branch What are the sources of blood supply to tendons? Myotendinous junction, paratenon, and at the insertion to bone

6

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Antibiotics What should you always consider before starting an antibiotic?  What is the most likely infecting organism?  Have a gram stain and C&S been done? What are the results?  Allergies?  Kidney function (check BUN and Cr)? Many antibiotics are renally metabolized so it is imperative to make sure the kidneys are functioning properly.  What medications is the patient currently taking? Be concerned of possible drug interactions.  Any other reason you may or may not want to give the antibiotic?

Name That Drug Augmentin Zosyn Unasyn Timentin Zyvox Invanz Cubicin Tygacil Bactrim Rocephin Avelox Zithromax Primaxim Synercid Cleocin Flagyl

amoxacillin/clavulonic acid piperacillin/tazobactam ampicillin/sulbactam ticarcillin/clavulonic acid linezolid ertapenem daptomycin tigecycline trimethoprim/sulfamethoxazole (TMP/SMX) ceftriaxone moxifloxacin azithromycin imipenem/cilastatin dalfopristin-quinupristin clindamycin metronidazole

Augmentin What is the dose? 500 or 875 mg PO BID How much clavulonic acid is in Augmentin 500 mg? Augmentin 875 mg? Both have 125 mg What is the indication? PO antibiotic for outpatient therapy of polymicrobial infections What is the spectrum of activity? Staph (not MRSA), Strep, Enterococci, Gram negatives, anaerobes

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

7

Does it cover Pseudomonas? No

Zosyn What is the dose? 3.375 g IV q6h Renal dose – 2.25 g IV q6h Alternate dose – 4.5 g IV q6h What is the indication? Approved for use in adults for the treatment of moderate to severe diabetic foot infections What is the spectrum of coverage? Staph (not MRSA), Strep, Enterococci, Gram negatives, anaerobes Does it cover Pseudomonas? Yes

Unasyn What is the dose? 3.0 IV q6h Renal dose – 1.5 g IV q6h What is the indication? Empiric therapy for polymicrobial diabetic foot infections What is the spectrum of activity? Staph (not MRSA), Strep, Enterococci, Gram negatives, anaerobes Does it cover Pseudomonas? No What is an alternative for a patient with a PCN allergy? Clinda/Cipro Levaquin (there are others)

Timentin What is the dose? 3.1 g IV q4-6h What is the indication? Broad spectrum antibiotic for polymicrobial infections

8

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What is the spectrum of activity? Staph (not MRSA), Strep, Gram negatives, anaerobes Does it cover Pseudomonas? Yes What should you watch for? Increased Na+ load (5.2 meq/gram)

Penicillins Which cover Pseudomonas? (4th and 5th generations) piperacillin, Zosyn ticarcillin, Timentin carbenicillin, mezlocillin, azlocillin What are IV alternatives for PCN allergic patients? clindamycin, vancomycin, Levaquin, Bactrim How are PNC’s excreted? All are renally excreted except mezlocillin, azlocillin, piperacillin (the ureidopenicillins are 2030% renal) What concern is there of a patient on both PCN and probenecid? Probenecid will increase duration of serum levels of PCN and most cephalosporins

Cephalosporins What is the cross-reactivity of cephalosporins and PCN? 1-10% (depending on whom you talk to) Are cephalosporins contraindicated for a patient with a PCN allergy? Many people will say yes, and according to Dr. Warren Joseph, ―Cephalosporins should be avoided entirely in patients with a history of anaphylaxis to penicillin.‖ However, he states that if there is a questionable allergy history (rash or upset stomach), ―Cephalosporins can be used with little worry.‖ Personally, I will give a cephalosporin to a patient with a PCN allergy if all he or she had was an upset stomach and I document this. How to treat serious hospital acquired Gram negative infections? 3rd generation cephalosporins, aminoglycoside (i.e. Rocephin, gentamycin) What is the coverage of cephalosporins for each class? 1st Generation Gram positive – Staph (not MRSA) and Strep Gram negative – Proteus, E. coli, Klebsiella, Salmonella, Shigella (PECKSS) Anaerobes – not Bacteroides

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

9

2nd Generation Gram positive – similar to 1st gen Gram negative – more coverage, H. influenza, Neisseria, Proteus, E. coli, Klebsiella, Salmonella, Shigella (HEN PECKSS) 3rd Generation Gram positive – less than 1st and 2nd gen Gram negative – expanded coverage, ceftazadime covers Pseudomonas 4th Generation Gram positive – similar to 1st gen Gram negative – similar to 3rd gen, including Pseudomonas No anaerobic coverage Name a couple cephalosporins for each generation 1st Generation – cefazolin (Ancef), cephalexin (Keflex) 2nd Generation – cefaclor (Ceclor), cefuroxime (Ceftin) 3rd Generation – ceftriaxone (Rocephin), ceftazidime (Fortaz), cefdinir (Omnicef) 4th Generation – cefepime (Maxipime) How are they excreted? Renally except for ceftriaxone (renal/hepatic) and cefoperazone (hepatic)

Vancomycin What is the main indication? MRSA What is its spectrum of activity? All Gram positives, including MRSA and MRSE What is the dose? 1 g IV q12h with slow infusion When are levels drawn? Peak taken 30 min after the 3rd dose Trough taken 30 min before the 4th dose What should the peaks and troughs be? Peak 15-30 mg/mL Trough <10 mg/mL How do you adjust the dose? If the peak is too high, decrease the dose If the peak is too low, increase the dose If the trough is too high, increase the interval between doses If the trough is too low, decrease the interval between doses

10

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What happens when you infuse too quickly? Red Man syndrome – erythema and pruritis to the head, neck, and upper torso. It is caused by an anaphylactoid reaction where histamine is released by mast cells. (A different Red Man syndrome is associated with excessive Rifampin that causes a bright reddish-orange pigmentation of the skin.) How can you decrease the risks of Red Man syndrome? Slow infusion over one hour How do you treat Red Man syndrome? Antihistamines (Benadryl 25-50 mg IV q2-4h) until symptoms resolve Symptoms are self-limiting What are other side effects? Ototoxicity and nephrotoxicity Does the duration a patient has been on vancomycin increase the risks of side effects? Yes. Vancomycin has a reservoir effect: the more often a patient receives vancomycin, the higher the chance of getting either ototoxicity or nephrotoxicity. Therefore, use vancomycin carefully; it is a powerful drug with severe side effects. When should PO vancomycin be used? Treatment of Pseudomembranous colitis (125 mg PO q6h)

Bactrim What is the dose? One tab PO BID How much is in the single strength tablet? Double strength? Single strength – TMP 80 mg / SMX 400 mg Double strength (DS) – TMP 160 mg / SMX 800 mg How does it work? Trimethoprim and sulfamethoxazole inhibit folate synthesis in bacteria which prevents DNA replication What is the spectrum of activity? Broad spectrum covering Gram positives (MRSA) and Gram negatives Does it cover Pseudomonas? No What allergy should be avoided? Sulfa

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

11

What are the side effects? Hemolytic anemia, hypersensitivity What are the contraindications? Patient on oral hypoglycemic or with G6PD deficiencies

Zithromax What is the dose? 250 mg PO, two tabs on the first day then one tab for the next four days What is the spectrum of activity? Staph, Strep, and some anaerobes (but not bacteroides) Can you give it to a patient with a PCN allergy? Yes What is the half-life? 68 hours

Primaxin What is the dose? 500 mg IV q6-8h (most common) or 1 gm IV q6-8h What is the spectrum of activity? Very broad spectrum including most Gram positive, Gram negative, and most anaerobes Does it cover MRSA? Pseudomonas? No and no What is a side effect? Seizure in patients with history of seizures 1% risk with 500 mg dose, 10% risk with 1 g dose How does it work? imipenem – antibiotic cilastatin – renal dehydropeptidase inhibitor, which prevents imipenem from being metabolized by the kidneys Which antibiotic is nicknamed ―Gorillamycin‖? imipenem (because of its very broad of spectrum activity)

Invanz What is the dose? 1 g IV q24h

12

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What is the indication? Approved for use in adults for the treatment of moderate to severe diabetic foot infections What is the spectrum of activity? Gram positive, Gram negative, and anaerobes Does it cover Pseudomonas? No What class is Invanz? It is a structurally unique 1-β-methyl-carbapenem related to β-lactams

Zyvox What is the dose? 400-600 mg PO/IV q12h What is an indication? Oral Zyvox may be used for outpatient treatment of MRSA infections What is the spectrum of activity? All Gram positives, including MRSA and VRE What is a major side effect? Thrombocytopenia (check CBC) Why isn’t it used more often? It is expensive

Quinolones What are some common quinolones? ciprofloxacin (Cipro), levofloxacin (Levaquin), moxifloxacin (Avelox) What is the dose of Cipro? 250-750 mg PO q12h 200-400 mg IV q12h What is the dose of Levaquin? 250-500 mg PO/IV q24h What is the dose of Avelox? 400 mg PO/IV q24h What is the spectrum of activity? Gram negative, including Pseudomonas Cipro – limited Gram positive Levaquin and Avelox – better Gram positive CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

13

What are side effects? Tendonitis and tendon ruptures Who should not be given quinolones? It is contraindicated in children with open growth plates. Risk of cartilage degeneration.

Aztreonam What is the dose? 1-2 g IV q8h What is the spectrum of activity? Gram negative aerobes and pseudomonas (its main indication) What are the major side effects? None Why isn’t it used more often? It is expensive

Aminoglycosides What are some major aminoglycosides? Gentamycin, Tobramycin, Amikacin What is the spectrum of activity? Gram negative aerobes What are the side effects? Ototoxicity – irreversible Nephrotoxicity – reversible Neuromuscular blockade – prevented by slow infusion What are the doses, peaks, and troughs? Dose Gent and Tobramycin 3-5 mg/kg q8h Amikacin 15 mg/kg q8h

Peak (µg/mL) 6-10 20-30

Trough (µg/mL) 2 <10

How to dose gentamycin? 1. Loading dose is 2 mg/kg for Gent and Tobra (7.5 mg/kg for Amikacin) 2. Determine creatinine clearance (CC) CC = (140 - Age) x Weight (in kg) 72 x Serum Creatinine For females, multiply the CC by 0.85 3. Maintenance dose is adjusted for CC (e.g. If the CC is 0.75, then the patient has 75% kidney function. Give 75% of a normal dose.)

14

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Clindamycin What is the dose? 600-900 mg IV q8h or 150-300 mg PO BID What is the spectrum of activity? Most Gram positive and most anaerobes What is a side effect? Pseudomembranous colitis How is clindamycin metabolized? Liver

Flagyl What is the dose? 500 mg PO TID What is the spectrum of activity? Some Gram positive anaerobes and most Gram negative anaerobes

MRSA What antibiotics cover MRSA? PO – linezolid, Minocycline, Cipro/rifampin, Bactrim/rifampin IV – vancomycin, linezolid, minocycline, Cipro/rifampin, Bactrim/rifampin, Synercid, tigecyclin, telavancin Topical – Bactroban What are the only FDA-approved drugs for treating MRSA? vancomycin linezolid daptomycin tigecyclin telavancin (Vibativ)

VRE How do you treat VRE? linezolid or dalfopristin-quinupristin What is the only PO therapy for VRE? linezolid

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

15

Pseudomonas What drugs cover Pseudomonas? Aztreonam Aminoglycosides – gentamycin, tobramycin, amikacin Cipro Ceftazidime, cefepime Timentin Zosyn

Polymicrobial Infections What are some empiric therapies for polymicrobial foot infections? Vanco/Zosyn, Clinda/Cipro, Vanco/Invanz What are the only FDA-approved drugs for treating diabetic foot infections? (The 3 Z’s) Zosyn Zyvox Invanz

Antibiotic-Associated Diarrhea What are two main causes of antibiotic-associated diarrhea? Pseudomembranous colitis – Clostridium difficile Non-specific colitis – Staph aureus How to you test for Clostridium difficile? Order ―check stool for C diff‖ What is the most common cause of Clostridium difficile colitis? clindamycin (though any antibiotic can cause it) How do you treat Clostridium difficile colitis? Vanco 125 mg PO q6h Flagyl 500 mg PO TID

Miscellaneous What antibiotics are metabolized by the liver? (3 C’s and 1 E) Clindamycin Cefoperazone Chloramphenicol Erythromycin Can antibiotics affect PT/INR? Yes. Antibiotics can affect normal flora, which alters Vitamin K. Therefore, the PT/INR can increase. 16

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What can β-lactams cause? Leukopenia What is the MOA of aminoglycosides? Macrolides? Aminoglycosides bind to bacterial 30s ribosomes inhibiting protein synthesis Macrolides bind to bacterial 50s ribosomes inhibiting protein synthesis (A boy at 30 does not become a Man until 50) What antibiotics can be safely used with PMMA beads? Vancomycin, gentamycin, tobramycin, cefazolin The curing of PMMA is exothermic, therefore the antibiotic must be not be heat-labile What open fractures should be treated with antibiotics? Grades 2 and 3

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

17

18

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Bugs and Drugs Gram Positives What are Gram positive, catalase positive cocci in clusters? Staphylococcus aureus DOC for Staph? Keflex or Ancef Alternative for Staph? clindamycin, Levaquin, Vancomycin, Azithromycin, dicloxacillin, nafcillin Alternative for Staph if PCN allergy? clindamycin, Levaquin, Vancomycin, Azithromycin What if the organism is resistant to methicillin? MRSA (methacillin-resistant Staph aureus) DOC for MRSA? Vanco IV, Bactrim PO (if sensitive) Alternative for MRSA? Synercid or linezolid Topical DOC for MRSA? Bactroban DOC for Strep? Keflex or Ancef What are Gram positive, catalase negative cocci that are in pairs or chains? Streptococcus DOC for Strep? Keflex or Ancef Alternative for Strep? clindamycin, Levaquin, vancomycin Alternative for Strep in PCN allergy? clindamycin, Levaquin, vancomycin DOC for Enterococcus? amoxicillin or vancomycin CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

19

Alternative for Enterococcus? Augmentin, linezolid What if the organism is resistant to vancomycin? VRE (vancomycin-resistant Enterococcus) DOC for VRE? linezolid or Synercid DOC for Diptheroids? vancomycin

Gram Negatives What is a short, Gram negative rod? Escherichia coli DOC for E. coli? Keflex or Ancef Alternative for E. coli if PCN allergy? Cipro or Levaquin DOC for Proteus? Keflex or ampicillin Alternatives for Proteus if PCN allergy? Cipro or Levaquin DOC for E/C/S/M group? Quinolone (Cipro or Levaquin) Alternatives for E/C/S/M group? 3rd generation cephalosporin, Aztreonam, Bactrim What is a small Gram negative rod with pili and polar flagella? Pseudomonas aeruginosa DOC for Pseudomonas? Cipro Alternative for Pseudomonas? 3rd gen cephalosporins, Aztreonam, Zosyn, Timentin How does Pseudomonas typically present? blue-green purulence with grape-like odor

20

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What Gram negative spirochete causes Lyme disease? Borrelia burgdorferi DOC for Lyme disease? doxycyline or Rocephin Alternative for Lyme disease? amoxicillin

Anaerobes DOC for Bacteroides? Augmentin, Zosyn, Unasyn, Timentin Alternatives for Bacteroides if PCN allergy? clindamycin/Cipro, Primaxin, Flagyl What is a large, Gram positive, anaerobic, ―racquet-shaped‖ rod that forms spores? Clostridium perfringens DOC for Clostridium? Penicillin, imipenem, clindamycin, tetracycline What are two soft tissue clinical manifestations caused by Clostridium? Anaerobic cellulitis and gas gangrene Why is gas gangrene a surgical emergency? It rapidly progresses to shock and renal failure and is fatal in 30% of cases

Less Common Organisms DOC for Aeromonas? Cipro PO/IV Alternative for Aeromonas? Bactrim DOC for Pseudomonas cepacia? Bactrim Alternative for Pseudomonas cepacia? Ceftazidime DOC for Necrotizing Fasciitis? Primaxin DOC for superficial thrombophlebitis? Timentin CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

21

DOC for Gonorrhea? Ceftriaxone or PCN if sensitive DOC of Cutaneous Larva Migrans? Promethia under occlusion

Miscellaneous What organisms may form gas in soft tissue? Gram positive – Clostridium perfringens, Staphylococcus, Streptococcus, Peptostreptococcus Gram negative – Bacteroides, E. coli, Klebsiella, Serratia What are some anaerobes? Gram positive – Actinomyces, Clostridium, Peptostreptococcus Gram negative – Bacteroides, Fusobacterium What is the drug of choice (DOC) for a patient with diabetes and a PCN allergy? clindamycin DOC for severe limb-threatening infection? Primaxin What are most common organisms of bite wounds? Human – Eikenella corrodens Cat and dog – Pasteurella multocida What is Gram negative rod is associated with dog bites? DF-2 DOC for cat and dog bites? Augmentin What are the most common organisms causing cellulitis? Staph and Strep Which type of Strep can cause impetigo, cellulitis, and erysipelas? Group A Strep What is the difference between cellulitis and erysipelas? Cellulitis – confined superficial infection Erysipelas – superficial infection that extends into the lymphatics What is the most common organism that causes acute hematogenous osteomyelitis? Staphylococcus aureus (adults), Gram negative rods (elderly) What is the most common organism that causes osteomyelitis following a puncture wound? Pseudomonas aeruginosa 22

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What is an anaerobic Gram positive filamentous bacteria? Actinomyces What organism may be found following a puncture wound in the ocean? Vibrio vulnificus What type of bacteria is gonorrhea? Gram negative diplococci What is gonorrhea cultured on? Chocolate agar What is the treatment for gonorrhea? Ceftriaxone If a patient is currently on an antibiotic, how long should it be stopped before taking a wound culture? At least 48 hours (if possible)

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

23

24

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Labs CBC What is in a CBC? WBC, hemoglobin, hematocrit, platelets What are normal lab values for CBC? Note: normal values vary between labs WBC 4.8-10.8 k/µL Hemoglobin ♂ 14.0-18.0 g/dL, ♀ 12-16 g/dL Hematocrit ♂ 42-52%, ♀ 37-47% Platelets 145-400 k/µL With an infection, what is expected to happen to the WBC count after surgery? Eventually it should go down, but in post-op days 1-2, the WBC may actually increase a bit. This is may occur because surgery activates the body's reaction to the infection. What should be done if the patient’s WBC is over 10? First, decide if the patient has an infection  If there is an infection, then antibiotics and possible incision and drainage (I&D) should decrease the WBC count  If there is not an infection, then the cause must be determined. Is the increase acute or chronic? Is there another source of infection (other than the foot)? Is the patient on corticosteroids? Is there a combination of medical conditions causing this? What to do if platelets are low (under 150-350 k/mL)? Can transfuse platelets, but this is not commonly done What are the minimum levels for hemoglobin and hematocrit for elective surgery? Hemoglobin 10 gm/dL and Hct 30% What should be done if the Hemoglobin/Hematocrit (H/H) is below 10/30? If necessary, transfuse 1-2 units of packed red blood cells (PRBC) What is the condition called? Anemia What are causes of microcytic, hypochromic anemia? Iron deficiency, thalassemias, lead poisoning What are causes of macrocytic, megaloblastic anemia? Vitamin B12/folate deficiency

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

25

Following a transfusion of PRBC, when will changes in the H/H be seen? Approximately 3 hours. Therefore, order new labs to be drawn 4 hours after last unit given.

BMP What is in a BMP? Sodium, potassium, chloride, carbon dioxide, BUN, creatinine, glucose What is in a CMP? BMP with ALP (alkaline phosphatase), ALT (alanine amino transferase, also called SGPT), AST (aspartate amino transferase, also called SGOT), bilirubin, albumin, total protein, calcium What are normal values for BMP? Note: normal values vary between labs Sodium 135-146 mmol/L Potassium 3.5-5.1 mmol/L Chloride 96-106 mmol/L CO2 24-32 mmol/L BUN 10-20 mg/dL Creatinine 0.7-1.3 mg/dL Glucose 70-110 mg/dL What do Na+, K+, Cl and CO2 tell you? These electrolytes indicate nutritional status What should be done if Na+ is low? Give NSS or regular salt What should be done if K+ is too low? Hypokalemia may cause cardiac arrhythmias, muscle weakness, paresthesias, cramps Manage hypokalemia  Give K-Dur (potassium chloride supplement)  Give potassium-rich foods (i.e. banana) What should be done if the K+ is too high? Hyperkalemia may cause cardiac arrhythmias, lethargy, respiratory depression, coma Order EKG Manage hyperkalemia  Calcium gluconate  Sodium bicarbonate  Dextrose with insulin  Kayexalate What do BUN and creatinine indicate? Renal function

26

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What should be done if the creatinine is too high? Consult renal if creat is over 1.5 for a couple of results Note: creat may be increased after muscle breakdown or loss Which is a more important indicator – BUN or creatinine? Creat is more important, because BUN is influenced by hydration state. If the BUN is high but creat is normal, then the patient is most likely dehydrated and rehydration should correct the BUN. However, if both BUN and creat are high, then the patient most likely has renal damage.

PT/PTT/INR What do PT/PTT/INR tell you? The coagulable state of the patient. If the levels are high, it will take longer for the patient to develop a clot and stop bleeding. It requires blockage of only one pathway to anticoagulate the patient. What are normal values for PT/PTT/INR? Note: normal values vary between labs PT 11.7-14.5 sec INR 0.9-1.1 PTT 23-36 sec What can cause an elevated PT/INR? Coumadin Malnutrition Alcoholism Antibiotics Vitamin K disorders What does INR stand for? Why was it developed? International Normalized Ratio There are different methods to determine PT, and thus each lab has a different normal value for PT. INR was devised to standardize all the results. If the patient is on Coumadin for anticoagulation, what should the INR be? Intense anticoagulation 2-3 What causes the PTT to be high? Heparin Which pathway does PTT check? Intrinsic (―PITT‖) Which pathway does PT check? Extrinsic (―PET‖)

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

27

28

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Medicine What are reasons for post-op fever? Wind (12-24 h)  Atelectasis (from muscle relaxers)  Post-op hyperthermia Water (~24 h)  UTI Walk (~48 h)  DVT  PE Wound (~72 h)  Post-op infection Wonder drug (anytime)  Drug fever What are treatments of post-op fever? Wind  Encourage incentive spirometer  Chest x-ray Water  Straight catheter  Urine analysis (UA) with Gram stain, culture and sensitivity  Treat with antibiotics if necessary Walk  Heparin or Lovenox protocol  Use SCDs, TEDs, or get patient out of bed Wound  X-ray, Gram stain, culture and sensitivity, blood cultures  Begin antibiotic Wonder drug  D/C drug  Give reversal drug if necessary When do fever peaks occur? Between 4-8 pm What part of the brain regulates the body's temperature? Hypothalamus What is malignant hyperthermia? A side effect of general anesthesia – tachycardia, hypertension, acid-base and electrolyte abnormalities, muscle rigidity, hyperthermia CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

29

What is the treatment for malignant hyperthermia? Dantrolene (for muscle relaxation) 2.5mg/kg IV x l, then 1 mg/kg IV rapid push q6h until symptoms subside or until max dose of l0 mg/kg If a risk of malignant hyperthermia is suspected, what pre-operative test may be performed? CPK – elevated in 79% of patients with malignant hyperthermia

Anesthetics What is the mechanism of action for local anesthetics? Block Na+ channels and conduction of action potentials along sensory nerves What is the toxic dose of lidocaine (Xylocaine)? 300 mg plain (4.5 mg/kg) 500 mg with epi (7.0 mg/kg) What is the toxic dose of bupivacaine (Marcaine)? 175 mg plain (2.5 mg/kg) 225 mg with epi (3.2 mg/kg) How to convert percentage of solution to mg/mL? Move decimal point of percentage one place to right (e.g. 1% solution has 10 mg/mL) What are the side effects of lidocaine and bupivacaine associated with systemic exposure? CNS effects – initial excitation (dizziness, blurred vision, tremor, seizures) followed by depression (respiratory depression, loss of consciousness) Cardiovascular effects – hypotension, bradycardia, arrhythmias, cardiac arrest What can be given to help reverse local anesthetic-induced cardiovascular collapse? Intravenous fat emulsion (Intralipid) Is there a risk with intra-articular injections of bupivacaine? Studies have shown chondrocyte death following prolonged exposure to bupivacaine In what age group should bupivicaine be avoided? Children <12 year of age How are amides (lidocaine and bupivacaine) metabolized? Liver How are esters (Novocain) metabolized? Plasma pseudocholinesterase What is the only local anesthetic with vasoconstriction? Cocaine 30

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

How is cocaine metabolized? Plasma pseudocholinesterase (just like other esters) Can local anesthetics cross the placental barrier? Yes What does MAC (as in MAC with local) stand for? Monitored anesthesia care For anesthesia, what cannot be given to a patient with an egg shell injury? propofol (Diprivan)

Pain Medications Pain management with a codeine allergy? (STUD or STTUUDDD-N) S – Stadol T – Toradol T – Talwin U – Ultram D – Darvon D – Darvocet D – Demerol N – Nubain First choice for oral? Darvocet N-100 one tab PO q4-6h prn pain First choice for non-narcotic oral? tramadol (Ultram) 50 mg one to two tabs PO q4-6h prn pain, max daily dose of 400 mg per day First choice for non-narcotic IV? Toradol 30-60 mg IV Choice narcotic IV pain med? Demerol Note: many hospitals, including our own, do not use Demerol due to its side effects Name two non-narcotic analgesics ketoralac (Toradol), tramadol (Ultram)

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

31

Drugs and Usual Doses What schedule are these drugs? Percocet II high potential for abuse – requires narcotic script Vicodin III moderate potential for abuse Tylenol #3 III moderate potential for abuse Darvocet IV low potential for abuse Percocet 5/325? oxycodone/acetaminophen (5 mg/325 mg) 1-2 tabs PO q4-6h prn pain Roxicet? oxycodone/acetaminophen (5 mg/325 mg/5 mL) Essentially a liquid form of Percocet that is good for pediatric patients What is the difference between Percocet and Percodan? Percocet has 325 mg of acetaminophen and Percodan has 325 mg of ASA Vicodin 5/500? hydrocodone/acetaminophen (5 mg/500 mg) 1-2 tabs PO q4-6h prn pain Tylenol #3? codeine/acetaminophen (30 mg/300 mg) 1-2 tabs PO q4-6h Darvocet-N 100? propoxyphene/acetaminophen (100 mg/650 mg) 1 tab PO q4h prn pain Ultram? tramadol 50 mg 1-2 tabs PO q4-6° prn pain Toradol? ketorolac 10 mg 30 mg IV q6h 1 tab PO q4-6h prn pain An NSAID not to be used more than 5 days due to possible significant side effects Darvon? propoxyphene 1 tab PO q4h prn pain OxyContin? oxycodone extended release 32

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Morphine sulphate? 2-4 mg IV q2-6h prn mod-severe pain For very painful dressing change or bedside debridement – 2 mg IV x one dose MS Contin? morphine sulfate extended release (15-30 mg) 1 tab PO q8-12h prn pain Dilaudid? hydromorphone 2-8 mg PO q3-4h prn severe pain 1-4 mg IV q4-6h prn severe pain This drug is very strong Demerol? meperidine Our hospitals do not use this due to its side effects

Acetaminophen What therapeutic effects are seen with acetaminophen? Analgesic and anti-pyretic What is the maximum daily dose? 4g

NSAIDs What therapeutic effects are seen with most NSAIDs? Analgesic, anti-pyretic, and anti-inflammatory What pathway do NSAIDs work on? Cyclooxygenase (COX) NSAIDs nonselectively inhibit both COX-1 and COX-2 pathways What is the most common side effect of NSAIDs? GI disturbance (except with COX-2 inhibitors, because COX-1 protects the stomach lining) What is the only FDA-approved COX-2 inhibitor? celecoxib (Celebrex) Others were withdrawn due to increased risk of heart attack and stroke Which NSAIDs only have anti-inflammatory effects? indomethacin, tolmetin Do NSAIDs decrease joint destruction? No, they only decrease inflammation

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

33

Do NSAIDs affect bone healing? NSAIDs and COX-2 inhibitors may inhibit bone healing via their anti-inflammatory effects What NSAID causes irreversible inhibition of platelet aggregation? aspirin What NSAID does not inhibit platelet aggregation? The COX-2 inhibitor, Celebrex What is the only IV NSAID? ketorolac (Toradol) Which NSAID is often given during surgery or immediately post-op to decrease pain and inflammation? Toradol 30 mg IV What are the NSAIDs with the least nephrotoxicity? Celebrex, Relafen, Lodine What is the effect of NSAIDs on asthma? Can increase symptoms of asthma What are the safest NSAIDs for a patient with asthma? Diclofenac, ketoprofen Which NSAIDs treat collagen vascular disease? Ibuprofen, sulindac, tolmetin Which NSAIDs are not renally cleared? Indomethacin, sulindac What are the cardiovascular effects of NSAIDs? Can cause vasoconstriction and increase blood pressure Which NSAIDs have the least cardiovascular effects? Diclofenac, ketoprofen Which NSAIDs are the most hepatotoxic? Ibuprofen, naproxen, diclofenac What should be given for an indomethacin overdose? Benadryl – decreases serotonin and histamine release What is Arthrotec? diclofenac/misoprostol – an NSAID with protection for the stomach

34

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What is the anti-inflammatory dose of ibuprofen? 1200-3200 mg/day in divided doses What NSAIDS work on both the lipooxygenase and cyclooxygenase pathways? Ketoprofen and diclofenac What is the difference between Cataflam and Voltaren? Cataflam is diclofenac potassium and has an immediate release Voltaren is diclofenac sodium and has a delayed release What are the only pro-drugs for NSAIDs? nabumetone and sulindac What is the only nonacidic NSAID? nabumetone Which NSAIDs have fewer pulmonary problems? ketoprofen and diclofenac What are some once a day NSAIDs? celecoxib (Celebrex), piroxicam (Feldene), oxaprozin (Daypro), nabumetone (Relafen), others What drugs do NSAIDs interact with and what are the effects? Coumadin – increases action of Coumadin Sulfonylureas – increases action of sulfonylureas Corticosteroids – increases GI risk Anti-epileptics – increases anti-epileptic toxicity Antihypertensives – antagonizes antihypertensive meds Digoxin – increases digoxin’s effect Methotrexate – decreases methotrexate’s clearance Lithium – decreases lithium’s clearance Probenecid – increases concentration of NSADs

Anticoagulation What are causes of acute arterial occlusion? Embolism – detached thrombus, air, fat, or tumor Thrombus – occlusion of vessel by plaque or thickened wall Extrinsic occlusion – traumatic, blunt, penetrating What is the triad of pulmonary embolism? Dyspnea Chest pain Hemoptysis (although tachycardia is more common)

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

35

What tests can be ordered to diagnose a PE? Chest X-ray Ventilation perfusion scan Pulmonary angiography What is Virchows triad? Venous stasis – tourniquet, immobilization Endothelial wall damage/abnormality – surgical manipulation, trauma, smoking Hypercoagulability – birth control, coagulopathy, history of DVT What does the Virchow triad predict? Risk of DVT Previous DVT is #1 risk factor for having another DVT What are risks factors for DVT? (I AM CLOTTED) I – immobilization A – arrhythmia M – MI (past history) C – coagulable states L – longevity (old age) O – obesity T – tumor T – trauma T – tobacco E – estrogen D – DVT (past history) How is a DVT diagnosed clinically? Pain, heat, swelling, erythema of unilateral limb Positive Pratt sign – squeezing of posterior calf causes pain Positive Homan sign – abrupt dorsiflexion of foot causes calf pain Pulmonary embolism What tests can be ordered to diagnose a DVT? Doppler ultrasound Venogram D-Dimer For long term DVT prophylaxis, what drugs can be ordered? Why? Heparin – works right away Coumadin – takes 3-5 days and causes an initial transient hypercoagulable state What are treatments for a DVT? Thrombolytic agents Heparin 5000 Units IV bolus, then 1000 Units IV q1h and monitor PTT 36

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

How to dose Heparin for perioperative DVT prophylaxis? 5000 units SC 2h prior to surgery 5000 units SC q12h until patient ambulates What is the half-life of heparin? 1.5 hour How does heparin work? Intrinsic pathway Potentiates antithrombin III 100-fold, which inhibits the serine protease in the clotting cascade How is heparin reversed? Protamine sulfate 1 mg per 100 units of heparin What is enoxaparin (Lovenox)? Low molecular weight heparin How to dose Lovenox for perioperative DVT prophylaxis? 30 mg SC q12h for 7-10 days (adjust dose to q24h for renal patients) What is the half-life of Lovenox? 4.5 hours What are the advantages of using Lovenox vs. regular Heparin? Disadvantages? Advantages – Lovenox has longer plasma half-life with significant anticoagulation in trough Disadvantages – increased post-op complications when used with spinal/epidural anesthesia How do you check Lovenox? There is no test for the effects of Lovenox How is Lovenox reversed? Recombinant Factor VII How to dose Coumadin? 5-10 mg PO daily for 3-4 days then adjust for INR What is the half-life of Coumadin? 20-60 hours How long before Coumadin is therapeutic? 3-5 days How does Coumadin work? Extrinsic pathway Interferes with clotting factors II, VII, IX, X

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

37

How is Coumadin reversed? Vitamin K Fresh frozen plasma What are the INR values? Normal l Intense anticoagulation 2-3 What are levels of heparin and Coumadin for DVT/anticoagulation prophylaxis? Heparin – maintain 2-3 times normal PTT Coumadin – maintain 2 times normal INR What nonpharmacologic measures are used for perioperative DVT prophylaxis? Early ambulation – most important TEDs – thromboembolic deterrent stockings SCDs – sequential compression devices What is a surgical treatment for a patient with prior DVTs or recurrent PEs? Greenfield filter What level of the body is a Greenfield filter inserted? Inferior vena cava below the renal veins What is Pletal? cilostazol What is Trental? pentoxifylline What is an indication for Pletal or Trental? Intermittent claudication

CRPS What is CRPS? Complex regional pain syndrome (previously known as RSD – reflex sympathetic dystrophy) is a progressive disease of the autonomic nervous system causing constant, extreme pain that is out of proportion to the original injury What are the different types and causes of CRPS? CRPS Type I (reflex sympathetic dystrophy)  Nerve injury cannot be immediately identified  Spontaneous pain not limited to single nerve distribution  Abnormal response in sympathetic nervous system  Abnormal reflex leading to vasomotor instability and pain

38

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

CRPS Type II (causalgia)  Distinct, "major" nerve injury has occurred o Trauma o Peripheral nerve injury o Drugs – anti-TB, barbiturates, cyclosporine  Continued pain not necessarily limited to injured nerve distribution What are the stages of CRPS? 1. Acute – early (0 to 8-20 weeks)  Constant pain out of proportion (intense burning)  Possible edema, muscle wasting  Hyperhidrosis  Pain increased by light touch, movement, emotion 2. Dystrophic – mid (2-6 months, possibly up to 1 year)  Increased edema that is indurated (brawny edema)  Constant pain by any stimulus  Skin is cool pale and discolored  X-ray shows diffuse osteoporosis 3. Atrophic – late (over 6-12 months)  Intractable pain spreads proximally to involve entire limb  Decreased dermal blood flow causing cool, thin shiny skin  Fat pat atrophy  Joint stiffen, may proceed to ankylosis What are radiographic findings of CRPS? Periarticular, mottled, irregular bony demineralization (30-60% of cases) and cortical thinning What are bone scan findings of CRPS? The 3-phase bone scan has sensitivity of 96% and specificity of 98%. A normal scan does not exclude the diagnosis. The findings of the bone scan are based on the phase. 1. Acute  Increased flow and blood pool activity in the affected extremity  Increased activity particularly in a periarticular distribution on delayed images 2. Dystrophic  Flow and blood pool abnormalities begin to normalize  Increased activity on delayed images persists 3. Atrophic  Flow and blood pool activity can be normal or decreased (in about 1/3 of patients)  Normal or decreased activity is commonly seen on delayed images, however, persistent increased delayed activity has been reported (up to 40%)  Decreased flow in advanced stages may be related to disuse, which is a common feature of post-hemiplegic CRPS

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

39

What are treatments of CRPS? Anti-inflammatory drugs Antidepressant drugs Local peripheral nerve blocks Paravertebral sympathetic ganglion blocks Physical therapy

Diabetes For diabetic patients, who gets diabetic ketoacidosis and who gets diabetic coma? Type I (IDDM) – DKA Type II (NIDDM) – coma What are signs of hypoglycemia? Nervousness, tachycardia, diaphoresis, nausea, headache, confusion, tremor, seizures, coma What are signs of hyperglycemia? Polyuria, polydipsia, weight loss What is the function of a biguanide? Antihyperglycemic (not hypoglycemic) What is a typical supplemental insulin scale? BG (mg/dL) Low Medium <120 0 0 121-150 1 2 151-180 2 4 181-210 3 6 211-240 4 8 241-270 6 10 271-300 8 12 301-350 10 14 351-400 12 16 >400 call physician What are the only FDA-approved drugs for treating diabetic neuropathy? duloxetine (Cymbalta) pregabalin (Lyrica)

Osteoarthritis What are clinical findings of OA?  Pain relieved with rest  Stiffness aggravated with activity  Crepitus with motion  Asymmetric joint swelling

40

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What are radiographic findings of OA?  Asymmetric joint space narrowing  Broadening and flattening of articular surfaces  Osteophytes at joint margins  Subchondral sclerosis

Gout What is the most common inflammatory arthritis in men over 30? Gout What are the stages of Gout? 1. Asymptomatic hyperuricemia 2. Acute gouty arthritis 3. Intercritical gout 4. Chronic tophaceous gout What are clinical findings of gout?  Asymmetrical, monoarticular arthritis  Sudden onset of red, hot, and swollen joint  Excruciating pain with acute attack  Tophaceous deposits  Most commonly affects 1st MPJ What are radiographic findings of gout?  Radiographic findings appear late in the disease after multiple attacks  Bone lysis in acute stages  Periarticular swelling with preserved joint space  Tophi at joint margins  Rat bite – punched-out, periarticular erosions  Cloud sign – tophaceous material  Martel sign – periarticular overhanging shelves of bone What are laboratory tests for gout?  Uric acid – males >7 mg/dL, females >6 mg/dL, though may be normal during attack  Synovial fluid analysis provides a more accurate diagnosis What would a joint aspirate of gout show? Needle-shaped monosodium urate crystals that are negatively birefringent under polarized light (CPPD are rhomboid-shaped and positively birefringent) What is a martini sign? Histology showing a PMNC engulfing a crystal If gout is suspected, what should a specimen be sent in? One in formaldehyde (dissolves gouty tophi) and one in alcohol (does not dissolve gouty tophi) CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

41

How to treat acute and chronic gout? Acute  Colchicine  NSAIDS – indomethacin  Corticosteroids  ACTH Chronic  Colchicine (prophylactically)  Allopurinol  Uricosurics – probenecid, sulfinpyrazone What is the dose colchicine? 0.6 mg PO q1h until symptoms resolve, GI side effects occur, or max dose of 6 mg reached What is the max daily dose of colchicine? 6 mg Can allopurinol, probenecid or sulfinpyrazone be used for acute gout? No, because they may cause an initial hyperuremia How to determine if patient is an overproducer or underexcretor? Take a 24 hour uninalysis Which is more common – to be an overproducer or an underexcretor? Underexcretors make up approx 90% What medication should be given if the patient is an overproducer? Underexcretor? (Over-Achieving, Under-Paid) Overproducer → Allopurinol Underexcretor → Probenecid

Rheumatoid Arthritis What are clinical findings of RA?  Symmetric, progressive, polyarticular, and degenerative inflammatory arthritis  Age of onset between 3-4th decades  Females > males  Pain first thing in morning  Stiffness after rest and reduced with activity  Rheumatoid nodules (25%)  Nail fold infarcts, splinter hemorrhages  Swan neck deformities – flexed DIPJ and extended PIPJ  Boutonniere deformities – extended DIPJ and flexed PIPJ  Other – bullous dermatosis, Raynaud phenomenon, vasculitis

42

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What are laboratory findings of RA?  Rheumatoid factor – positive  RBC – slight to moderate anemia  WBC – elevated in acute cases and normal to decreased in chronic  ESR & CRP – moderate to marked elevation  Synovial fluid analysis – elevated WBCs with cloudy fluid What are radiographic findings of RA?  Clinical symptoms may present several years prior to radiographic findings  Peri-articular edema  Periosteal elevation and ossification  Marginal erosions  Subluxation and contractures (Swan neck deformities)  Fibular deviation of digits  Osteoporosis  Symmetric joint space narrowing and destruction (late stage finding) What causes the fibular deviation of digits? Erosive changes of medial plantar metatarsal heads compromises the integrity of medial collateral ligaments leading to lateral deviation of digits What is pannus? Granulation tissue that secretes chondrolytic enzymes which break down articular cartilage

Psoriatic Arthritis What are clinical findings of PA?  Polyarthritis including DIPJ involvement  Sausage digits  Psoriatic skin changes  Nail lesions What are laboratory findings for PA?  HLA-27 – positive  Rheumatoid factor – negative What are radiographic findings of PA?  Erosions with bony proliferation  Symmetric narrowing of joint space  Increased periosteal activity  Pencil-in-cup appearance  Osteopenic changes

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

43

Reiter Syndrome What are clinical findings of RS?  Polyarticular, asymmetric arthritis of lower extremity (mostly affects small bones of feet, ankle, knee, SI joint)  Most affects males  Capsulitis with digital edema  Bony erosions  Reiter Syndrome Triad (can't see, can't pee, can't climb a tree) o Conjunctivitis o Urethritis o Arthritis o Also keratoderma blenorrhagicum What are laboratory findings for RS?  HLA-27 – positive  Rheumatoid factor – negative  ESR – elevated  Synovial fluid analysis – Pekin cells What are radiographic findings of RS?  Fluffy periosteal reactions  Large, bilateral heel spur formation  Inflammation and widening of Achilles tendon insertion  Deossifications

Ankylosing Spondylitis What are clinical findings of AS?  Mostly males affected  Bilateral sacroiliitis – low back pain and stiffness  Heel pain  Peripheral joint pain What are laboratory findings for AS?  HLA-27 – positive  Rheumatoid factor – negative What are radiographic findings of AS?  Irregular joint widening with erosions  Reactive sclerosis  Bony ankylosis  Sacroiliac joint fusion  Bamboo spine

44

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Septic Arthritis What are clinical findings of SA?  Painful, hot, swollen joint  Systemic signs of fever, N/V, tachycardia, confusion What are laboratory findings for SA?  WBC – elevated with left shift  ESR – elevated  CRP – elevated  Blood cultures – positive  Synovial fluid analysis – elevated WBC with cloudy white or gray color What are radiographic findings of SA?  Normal in early stages  Joint effusion  Juxta-articular osteopenia What are etiologies of SA? Contiguous, hematogenous, direct implantation, surgical contamination What is the most common offending organism of SA? All ages – Staphylococcus aureus Neonates – Streptococcus and Gram negatives Children – H. influenza Teenagers – Neisseria gonorrhea Puncture wounds – Pseudomonas aeruginosa Adults with sickle-cell – Salmonella What is the treatment for SA? Needle drainage of joint Open arthrotomy if osteomyelitis, joint implant, or chronic infection Initial joint immobilization followed by passive ROM Appropriate IV antibiotics for 2 weeks followed by 2-4 weeks of oral antibiotics

Other Diseases What is brachymetatarsia? Premature closure of epiphyseal plate of metatarsal resulting in a short metatarsal Usually the 4th metatarsal is affected What are some conditions associated with brachymetatarsia? Downs syndrome Turners syndrome Cri du chat Pseudo- or pseudopseudohypoparathyroidism May be idiopathic CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

45

What is the maximum length that a metatarsal may be acutely lengthened for correction of brachymetatarsia? 1 cm graft allows acceptable stretching of neurovascular structures If more than 1 cm of lengthening is required, what procedure may be performed? Callus distraction with Mini-Rail fixation How much lengthening is typically achieved with callus distraction? 1 mm per day (0.25 mm q6h) What is achondroplasia? Dwarfism – all bones short with tibia undergrowth and fibular overgrowth causing genu varum What is fibular hemimelia? Aplasia or hypoplasia of the fibula What is DISH? Diffuse Ideopathic Skeletal Hyperostosis – characterized by multiple ossifications at tendinous or ligamentous insertions What is Apert syndrome? Multiple bony coalitions What is Paget disease? Osteitis deformans – abnormal bony architecture caused by increased osteoblastic and osteoclastic activity. More common in elderly. What malignant bone degeneration may be seen with Paget disease? Osteosarcoma What are the stages of Paget? 1. Destructive – osteolytic 2. Mixed – osteolytic and osteoblastic 3. Sclerotic – osteoblastic What are the stages of Charcot? 1. Acute or destructive 2. Coalescence 3. Remodeling What conditions are associated with positive HLA-B27? Ankylosing spondylitis, Reiter disease, psoriatic arthritis, reactive arthritis, enteropathic arthropathies

46

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What are components of CREST syndrome? Calcinosis Raynauds phenomenon Esophageal dysmotility Sclerodactyly Telangiectasias What is the treatment of cutaneous larva migrans? Promethia under occlusion What is the treatment for Lyme disease? Doxycycline 100 mg PO daily or Rocephin l g IV daily DOC for necrotizing fasciitis? Primaxin 250-1000 IV q6-8h (most commonly 500 mg IV q8h) What is Felty syndrome? Rheumatoid arthritis, splenomegaly, leukopenia What is mycosis fungoides? Cutaneous T-cell lymphoma that can resemble eczematoid or psoriasis What is erythrasma? Chronic, superficial infection of intertriginous skin caused by Corynebacterium minutissimum. Interdigital lesions appear as maceration. What is ecthyma? Ulcerative pyoderma of the skin often caused by Streptococci. Infection extends into dermis and is characterized by ulcers with overlying crusts. What is cellulitis? Acute spreading infection of dermal and subcutaneous tissue commonly caused by group A Strep or Staph aureus. Affected area is erythematous, warm, edematous, and tender. What is erysipelas? Superficial infection that extends into the lymphatics. Lesions are erythematous, indurated with sharply-demarcated margins, and have erythematous, ascending streaks. What is lymphangitis? Inflammation of the lymphatics as a result of a distal infection What is psoriasis? Hereditary disorder with chronic scaling papules and plaques in areas of body related to repeated minor trauma. Positive Koebner phenomenon and Auspitz sign. Also present are joint pain and nail changes including pitting, beau lines, oil spot, subungual hyperkeratosis, and discoloration.

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

47

What is lichen planus? Inflammatory dermatosis involving skin or mucous membranes with pruritic, violaceous papules clustered into large, flat-topped lesions with distinct borders. Lesions possibly covered with Wickham striae (white streaks). Ridges, onycholysis, subungual hyperkeratosis, and discoloration. What is another name for menopausal lipoma? Juxtamalleolar lipoma What is the main screening test if AIDS is suspected? ELISA (Enzyme Linked Immunosorbent Assay) What test should be performed to confirm the diagnosis of AIDS? Western blot

Miscellaneous Drugs What are some effects of steroids? Anti-inflammatory  Decreases production of prostaglandins, cytokines, and interleukins  Decreases proliferation and migration of lymphocytes and macrophages Metabolic  Decreases osteoblast activity What are differences between phosphate and acetate-based steroids? Phosphate-based – soluble with shorter half-life  Minimize inflammatory reaction and edema Acetate-based – insoluble with longer half-life  May delay inflammatory process or healing and can mask infection What is a common complication following steroid injection? Steroid flare – hypersensitivity reaction. Apply ice. How are glucocorticoids metabolized? Metabolized in the liver and secreted in urine What is diazepam? Valium, a benzodiazepine, is an anxiolytic/anticonvulsant/muscle relaxant How to reverse diazepam? Flumazenil (Romazicon) for benzodiazepine reversal 0.2 mg IV over 15 seconds, then 0.2 mg IV prn over 1 minute up to 1 gram total

48

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What are drugs for insomnia? (BE HARD) B – Benadryl E – estazolam H – Halcion A – Ambien R – Restoril D – Dalmane Most commonly used are Benadryl 25 mg PO qhs or Ambien 5 mg PO qhs What drugs leave a metallic taste in the mouth? Flagyl, Lamisil What is given for a Tylenol overdose? acetylcysteine (Mucomyst) What can cause Gray Baby Syndrome? Chloramphenicol What is chloramphenicol? An antimicrobial

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

49

50

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Clinical Podiatry What are the clinical patterns of tinea pedis? What are common infecting organisms? Chronic (moccasin or papulosquamous)  Trichophyton rubrum Acute (interdigital or vesicular)  Trichophyton mentagrophytes Ulcerative  Trichophyton mentagrophytes with Pseudomonas or Proteus What are the clinical patterns of onychomycosis? What are common infecting organisms? Distal subungual onychomycosis (DSO) ~ 90%  Most common  Trichophyton rubrum Proximal subungual onychomycosis (PSO) ~ 1%  Seen in immunocompromised patients  Trichophyton rubrum Superficial white onychomycosis (SWO) ~ 10%  Trichophyton mentagrophytes Candidal onychomycosis  Candida albicans What test confirms tinea pedis or onychomycosis? Potassium hydroxide (KOH) preparation of skin or nail specimen Septate hyphae confirms diagnosis Who does Lamisil work? Inhibits ergosterol synthesis What is phenol? Carbolic acid During a P&A procedure, why is alcohol used after phenol? Phenol is soluble in alcohol, and the alcohol will irrigate excess phenol from the nail groove For a nail avulsion, what can be done for anesthesia if the patient is allergic to all local anesthetics? Saline block (pressure induced block) Pressure cuff Benadryl block (blocks histamine release)

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

51

In evaluating a bunion, what does the position of the tibial sesamoid indicate? Why isn’t the fibular sesamoid evaluated? The tibial sesamoid indicates the abnormal affects of the adductor and flexor brevis tendons. Once the fibular sesamoid reaches the intermetatarsal space, it travels in the frontal plane (as opposed to transverse), therefore the tibial sesamoid is a more reliable indicator of deformity. What are some causes of hallux varus? Congenital  Clubfoot  Metatarsus adductus Traumatic  MPJ dislocation  Fracture Iatrogenic  Overcorrection of intermetatarsal angle  Excessive resection of medial eminence or staking the head  Fibular sesamoidectomy  Overaggressive capsulorrhaphy  Bandaging too far into varus What is staking the head? Excessive resection of the 1st metatarsal head with cutting into the sagittal groove may lead to hallux varus Describe the types of hammertoes Flexor stabilization  Most common  Stance phase  Flexors overpower interossei  Pronated foot Extensor substitution  Swing phase  Extensors overpower lumbricals  Anterior cavus, ankle equinus, anterior compartment muscle weakness Flexor substitution  Least common  Stance phase  Deep compartment muscles overpower interossei  Supinated, high arch foot or weakened Achilles What is the result of accidentally severing the quadratus plantae? Adductovarus deformity of digits 4 and 5 as the pull of FDL is unopposed

52

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What are differences between flexible, semi-rigid, and rigid deformities? Flexible – reducible when NWB and WB Semi-rigid – reducible when NWB only Rigid – non-reducible What is a Haglund deformity? Pump bump What x-ray measurements evaluate a Haglund deformity? Parallel pitch lines Fowler & Philip Total angle What is the Silfverskiöld test? Determines gastroc vs. gastroc-soleus Positive test  Dorsiflexion of the foot to neutral or beyond with the knee in flexion  Gastroc equinus Negative test  Lack of dorsiflexion of the foot to neutral with knee in flexion and in extension  Gastroc-soleus equinus What is the Lachman test? Determines if there is a plantar plate tear or rupture. While stabilizing the metatarsal, a dorsal translocation of the proximal phalanx greater than 2 mm is suggestive of rupture. What is the Mulder sign? Identifies a Morton neuroma by a palpable click when compressing metatarsal heads and palpating the interspace What is the Sullivan sign? Separation of digits caused by a mass within the interspace What is Q angle? Angle between the axis of the femur and the line between the patella and tibial tuberosity What to do if patient has edema with a cast? If edema goes down in AM → gravity edema → normal If edema does not go down in AM → abnormal What is Raynaud phenomenon? Recurrent vasospasm of digits usually in response to stress or cold

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

53

What are the stages of Raynauds Phenomenon? White → blue → red  Pallor – spasm of digital arteries  Cyanosis – deoxygenation of blood pools  Rubor – hyperemia What is an ABI? Ankle Brachial Index – compares ankle to arm pressures Normal 1 Intermittent claudication 0.6-0.8 Rest pain 0.4-0.6 Ischemic ulcerations <0.4 What may falsely elevate the ABI? Vessel calcifications/non-compressible vessels What other tests are typically performed with an ABI? Segment pressures  Measured at high thigh, above the knee, below the knee, ankle, midfoot, and toe  Normal 70-120 mm Hg  Drop between segments >30 mm Hg indicate disease in vessel above Pulse volume recordings (PVRs)  Normal waveforms are triphasic  Waveforms are widened and blunted with severe disease What is the most common type of skin cancer? Basal cell carcinoma – found on sun-exposed parts of the body What skin cancer may appear cauliflower-like? Squamous cell carcinoma – found on sun-exposed parts of the body What is the most common type of melanoma? Superficial spreading melanoma – found on any part of the body Most malignant? Nodular melanoma – may be misdiagnosed as pyogenic granuloma Most benign? Lentigo melanoma – typically found on back, arms, neck, and scalp Typically found on the palms, soles, and nail beds? Acral lentiginous melanoma What is a Hutchinson sign? Pigment changes in the eponychium seen with subungual melanoma

54

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What is the most common vascular proliferation? Hemangioma What vascular malignancy appears as red-blue plaques or nodules and has a high incidence in AIDS? Kaposi sarcoma What conditions may be associated with plantar fibromatosis? Ledderhose disease Dupuytren contracture Peyronie disease What is another name for congenital convex pes valgus? Vertical talus What are radiographic findings of CCPV? Calcaneus in equinus, plantarflexed talus, dorsally dislocated navicular, increased talo-calc angle What additional radiographic study should be obtained for neonates with CCPV? Lumbosacral films

Coalitions What are three coalitions of the rearfoot? Talocalcaneal, calcaneonavicular, and talonavicular What percentage of tarsal coalitions are bilateral? 50% Which is most symptomatic? C-N Asymptomatic? T-N Which is most common? T-C > C-N > T-N Which T-C facet is most commonly fused? Medial > anterior > posterior What are the ages of fusion? T-N (3-5 years) C-N (8-12 years) T-C (12-16 years)

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

55

What are clinical symptoms of tarsal coalitions? Pain Limited ROM of STJ and possibly MTJ Peroneal spastic flatfoot What are radiographic findings of tarsal coalitions?  Rounding of lateral talar process  Talar beaking due to increased stress on talonavicular ligament  Asymmetry of anterior subtalar facet  Narrowing or absence of middle and posterior subtalar facets  Halo sign – circular ring of increased trabecular pattern due to altered compressive forces  Anteater sign – C-N coalition in which calcaneus has elongated process on lateral view  Putter sign – T-N coalition in which neck of talus unites with broad expansion of navicular The anterior facet is best seen by which radiographic views? Medial oblique, Ischerwood The middle and posterior facets are best seen by which radiographic view? Harris Beath What are treatments for symptomatic tarsal coalitions?  Orthotics or supportive therapy  Immobilization  NSAIDs  Badgley – surgical resection of coalition or bar with interposition of muscle belly  Isolated fusion or triple arthrodesis

Clubfoot What are the 3 components of clubfoot? FF adductus, RF varus, ankle equinus What ligaments/capsules are contracted? Posterior  Posterior tib-fib  Posterior talo-fib  Lateral calcaneofibular  Syndesmosis Medial  Superficial deltoid  Tibionavicular  Calcaneonavicular  Talo-Navic, Navic-Cunei, and Cunei-1st MT joints  Spring ligament

56

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What muscles/tendons are contracted? Posterior  Achilles tendon  Plantaris tendon Medially  PT, FDL, and FHL  Abductor hallucis Anteriorly  Tibialis anterior What is the technique for correction of clubfoot called? Ponseti technique  Serial casting  First correct the FF and RF deformities, and then correct ankle equinus  During manipulation, pressure is applied to the head of the talus (not the calcaneus)  4-8 casts, percutaneous Achilles tenotomy (last cast for 3 weeks), occasional TA transfer, and D-B bar brace until age 3 y/o to prevent relapse What is the most accepted theory about clubfoot? Germ plasma defect-malposition of head and neck of talus What is the Simon rule of 15? For clubfoot, children <3 years → talo-navicular subluxation T-C angle is <15° and talo-1st metatarsal angle is >15°

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

57

58

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Biomechanics 1st Ray/Bunion Evaluation Hallux interphalangeal angle Normal 0-10° DASA (distal articular set angle) Normal 7.5° PASA (proximal articular set angle) Normal 7.5° Types of joint deformities Congruent – joint lines are parallel Deviated – joint lines intersect outside joint Subluxed – joint lines intersect inside joint Types of bunion deformities Structural  Bony deformity  Abnormal PASA and DASA  PASA + DASA = HA Positional  Soft tissue deformity with subluxed or deviated joint  Normal PASA and DASA  PASA + DASA < HA Combined  Elements of both structural and positional with subluxed or deviated joint  Abnormal PASA and DASA  PASA + DASA < HA Hallux abductus angle Normal 10-15° IM angle (intermetatarsal angle) Normal 8-12° Head procedure if mild 10-13° Shaft procedure if moderate 14-17° Base procedure if severe 18-21° Lapidus procedure if hypermobile 1st ray Metatarsus adductus angle Normal <20° CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

59

True IM angle True IM angle = (metatarsus adductus angle - 15) + IM angle 1st Metatarsal protrusion distance Normal +/- 2 mm compared to the 2nd metatarsal Tibial sesamoid position Normal 1-3 ROM 1st MPJ Normal 65-75° dorsiflexion and 40° plantarflexion 1st Metatarsal-medial cuneiform angle Normal 22° 1st ray ROM Normal 5 mm dorsiflexion + 5 mm plantarflexion = 1 cm total ROM

5th Ray/Tailor Bunion Evaluation Fallat & Buckholz 4th IM angle Angle between bisection of 4th metatarsal and proximal-medial cortical border of 5th metatarsal Normal 6° Pathologic 8.7° Fallat & Buckholz Lateral Deviation angle (lateral bowing) Angle of line bisecting head and neck of 5th met and line adjacent to proximal-medial cortex Normal 2.64° Pathologic >8°

Metatarsals/MPJ Metatarsal length Longest 2 > 3 > 5 > 4 > 1 shortest Metatarsal protrusion Longest 2 > 3 > 1 > 4 > 5 shortest Lesser MPJ dorsiflexion/plantarflexion 30-40° Dorsiflexion and 50-60° plantarflexion Metatarsal declination angle Normal 21° Metatarsal abductus angle Normal 0-15°

60

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

IM angle of 2nd and 5th metatarsals Normal 14-18°

Splayfoot IM angle of 1st and 2nd metatarsals Pathologic >12° IM angle 4th and 5th metatarsals Normal 4-5° Pathologic >9° (Schoenhause says normal 4th IMA is 8°) Splayfoot 1st IM angle >12° and 4th IM angle >8° With metatarsus primus adductus, there is a high predilection of splayfoot

Talus Talar neck angle Long axis of head and neck with long axis of the body Birth 130-140° Adult 150-165° Talar head and neck Plantarflexed 25-30° Medially aligned 15° to body Talar torsion angle Head is laterally rotated on the body Fetus 18-20° Childhood 30° Adult 40° Note: this motion brings the supinated foot in utero to a more pronated adult position Talar declination angle Normal 21° Pronation – increases Supination – decreases Meary angle – Lateral view Intersection of longitudinal axis of talus and 1st metatarsal Normal 0° Increases with either pronation or supination Pronation – moves axis of the talus plantar to 1st metatarsal Supination – moves axis of the talus dorsal to 1st metatarsal

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

61

Cyma line S-shaped line formed by the articulation of T-N and C-C joints Pronation – moves line anteriorly Supination – moves line posteriorly Talo-navicular joint Normal 75° coverage Pronation – decreases coverage Supination – increases coverage Forefoot abductus Normal 8° (0-15°)

Calcaneus Calcaneal inclination angle Normal 21° Pronation – decreases Supination – increases Hibb angle – Lateral view Intersection of longitudinal axis of calcaneus and 1st metatarsal Fowler & Philip angle Angle formed from the intersection of a line along the anterior tubercle and the plantar tuberosity and another line along the posterosuperior prominence at the Achilles tendon insertion Normal <70° Haglunds deformity >75° Total angle of Ruch Fowler & Philip angle + calcaneal inclination angle Normal 90° Haglunds deformity >90° Calcaneal-cuboid abduction Normal 0-5° Increases with pronation Kite angle (Talocalcaneal) – AP view Infant 30-50° Adult 20-40° Pronation – increases Supination – decreases Talocalcaneal angle – Lateral view Normal 25-50° (does not change with age)

62

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Rearfoot Angles Subtalar joint axis direction STJ goes through 1st ray in neutral, 2nd ray in supination, and is medial to 1st ray in pronation STJ axis of motion Lateral, posterior, plantar → medial, anterior, dorsal 48° from frontal plane 42° from transverse plane 16° from sagittal plane STJ ROM From neutral, 2/3 motion in inversion (20°) and 1/3 in eversion (10°) Longitudinal midtarsal joint 75° from frontal plane 15° from transverse plane 9° from sagittal plane Oblique midtarsal joint 38° from frontal plane 52° from transverse plane 57° from sagittal plane Bohler angle Angle formed by the intersection of a line from the superior aspect of the anterior process to superior aspect of the posterior facet and another line from the superior aspect of the posterior facet to superior point of the calcaneal process Normal 25-40° Decreases with intra-articular calcaneal fracture Gissane angle Angle formed by the intersection of a line along the posterior facet and another line along the middle and anterior facets Normal is 125-140° Increases with intra-articular calcaneal fracture Toyger angle Line drawn down posterior aspect Normal should be a straight line (180°) Decreases with Achilles rupture

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

63

Ankle Dorsiflexion/plantarflexion Normal 10-20° dorsiflexion and 20-40° plantarflexion Axis Lateral, posterior, plantar → medial, anterior, dorsal

Tibia Tibial torsion Birth 0° 6 years 13-18° Adult 18-23° Tibial varum/valgum Compare distal 1/3 of tibia to ground Birth 5-10° varum >2 years 2-3° valgum

Femur Angle of inclination 1 year 146° 4 years 137° Adult 120-136° (avg 127°) Angle of declination (antetorsion angle) 1 year 39° 10 years 24° Adult 6° Angle of anteversion Birth 60° Adult 10-12°

Lower Extremity Joint ROM Hip flexion/extension with knee extended Normal flexion 90-100° Normal extension 10-20° Hip flexion with knee flexed Normal flexion 120-130° Rotation of hip Internal rotation External rotation 64

Adults 35-40° 35-40°

Children 20-25° 45-50°

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Hip abduction/adduction Abduction 24-60° (avg 36°) Adduction <30° Knee flexion/extension Flexion 130-150° Extension 5-10° Knee rotation with knee flexed Medial rotation 40° Lateral rotation 40° Knee valgum/varus (bow leg, knock knee) Birth 15-20° (genu varum) 2-4 yrs 0° (straight) 4-6 years 5-15° (genu valgum) 6-12 years 0° (straight) 12-14 years 5-10° (genu valgum) > 14 years 0° (straight)

Clinical Tests What is the Ortolani test? Test for congenital hip dislocation in newborns. With newborn supine and hip and knees flexed, the hips are adducted while pressing downward and abducted while lifting upward. An unstable hip will dislocate when adducted and reduce when abducted. Barlow test? Test for a hip that is dislocatable but not dislocated in infants. With infant supine and hip and knees flexed, push posteriorly in line with the shaft of femur. An unstable femoral head will dislocate posteriorly from acetabulum. Galeazzi (or Allis) sign? Sign of unilateral congenital hip dislocation in infants. With infant supine and hip and knees flexed, the knees should be level. If a knee is lower, that hip is dislocated. Trendelenberg test? Test for weak hip abductors. As patient stands on affected limb, pelvis drops to opposite side.

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

65

66

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Surgery Surgical Prophylaxis What are indications for the use of antibiotics?  Implants (joint or internal fixation)  Prolonged surgery (>2 h)  Trauma surgery  Revisional surgery  Immunocompromised patient  Extensive dissection required  Intra-operative contamination  Endocarditis (SBE) What antibiotics are most commonly used? Ancef Clindamycin if PCN allergy Vancomycin if concerned about MRSA

Peri-operative Management What pre-op orders are needed for an in-house patient?  NPO after midnight, except AM meds with sips of water  Hold all AM hypoglycemics and cover with SSI (if patient with DM)  Accu-Check on call to OR (if patient with DM)  Begin ½NSS @ 60 mL/h at 0600 (D5W½NSS if patient with DM)  Labs – CBC with diff, PT/PTT/INR, BMP  Chest X-ray, EKG (if necessary)  Consult medicine for medical clearance (if not already done)  Anesthesia to see patient (if necessary) What are indications for ordering a chest X-ray? >40 years of age, smoker, any history of cardiac or pulmonary disease What are indications for ordering an EKG? >40 years of age, any history of cardiac disease What is the most common time for post-operative myocardial infarction? Day 3 How long should elective surgery be delayed following an MI or CABG? 6 months

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

67

How to calculate daily fluid input requirements? First 10 kg x 100 = 1000 mL/day Second 10 kg x 50 = 500 mL/day Remaining kg x 20 = ___ mL/day (e.g. 70 kg patient requires 1000 + 500 + 1000 = 2500 mL/day) How to calculate IV fluid input rate? ―421 Rule‖ calculates IV mL/h First 10 kg x 4 = 40 mL/h Second10 kg x 20 = 20 mL/h Remaining kg x 1 = ___ mL/h (e.g. 70 kg patient requires 40 + 20 + 50 = 110 mL/h) What other factors should be considered prior to surgery? Is the patient on any insulin, anticoagulants, steroids, or anything else that might put them at risk Note: any non-routine orders should be cleared with patient's primary service What is the perioperative management for patients with diabetes?  NPO after midnight  Start D5W½NSS in AM  Accu-Check  If insulin-controlled, hold regular insulin, give ½ NPH dose, and cover with SSI  If oral-controlled, hold oral meds and cover with SSI  If diet-controlled, cover with SSI What should be obtained prior to surgery on a patient with rheumatoid arthritis? Cervical spine x-ray What are effects of a long-term, high-dose course of steroids? Long-term therapy suppresses adrenal function  Risk of poor or delayed wound healing. Decreased inflammatory process.  Risk of infection. Low WBC may mask infection. What is the perioperative management for patients on long-term, high-dose steroids? Peri-op IV steroid supplementation Hydrocortisone 100 mg IV given the night before surgery, immediately prior to surgery, and then q8h until postoperative stress relieved What is the perioperative management for patients at risk for gout? Begin colchicine 0.6 mg PO daily 3-5 days pre-op and continue 1 week post-op What is the perioperative management for patients with hypertension? If the patient has been on long-term diuretics (e.g. HCTZ, Lasix), check for hypokalemia Avoid fluids high in sodium; may use ½NSS at low rate

68

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

When should aspirin be discontinued prior to surgery? 7 days due to irreversible binding to platelets When should NSAIDs be discontinued prior to surgery? 3 days due to reversible binding to platelets When should heparin be discontinued prior to surgery? 8 hours (monitor PTT) When to Coumadin be discontinued prior to surgery? 3-4 days (monitor PT/INR) What should the INR be for elective surgeries? <1.4 What should be done if the INR is >1.4? If necessary, transfuse Fresh Frozen Plasma (FFP) One unit of FFP will decrease INR by approximately 0.2 Vitamin K can be given but is slow-acting When should a patient with an INR >1.4 be allowed to proceed to surgery?  If the risk of not doing surgery outweighs the risk of excessive bleeding (i.e. if it is an emergency surgery and you have anesthesia's approval)  If the patient has PVD and the surgery is a simple debridement or amputation. Note: if the patient has PVD, make sure you have Vascular Surgery's approval for surgery. In this case, it is acceptable for the patient to bleed a little extra. If a patient with a high INR undergoes surgery, what labs should be carefully monitored? Hgb and Hct When should a RBC transfusion be given? If Hgb <8 or Hct<24, consider transfusing 1-2 units PRBC One unit of PRBC will increase Hct by approximately 3 percentage points What should be done if the patient is thrombocytopenic? Order a six pack of platelets, which is a concentration of six pooled platelet units, and consult hematology

Plastic Surgery How are relaxed skin tension lines (RSTL) oriented? Perpendicular to the long axis of the leg and foot Should a skin incision typically be made parallel or perpendicular to the RSTL? Parallel incisions will remain approximated and heal better while perpendicular incisions may gap apart due to increased transverse forces

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

69

What is an anti-tension line? S-shaped or zig-zagged incision when exposure needed is not parallel to RSTL To close a lesion with minimal tension, what should the ratio of length to width be? 3:1 length:width How much lengthening can be achieved with a 60° Z-plasty? 75% To correct a skin contracture, how should the Z-plasty incisions be oriented? The central arm of the ―Z‖ should be parallel to the contracture To correct a 5th digit adductovarus rotation, how should the skin incision be oriented? Distal medial to proximal lateral What is the order of wound graft closure? 1. Direct closure 2. Graft 3. Local flap 4. Distant flap What are the stages of skin graft healing? 1. Plasmatic 2. Inosculation of blood vessels 3. Re-organization 4. Re-innervation What are Blair and Humby knives? Knives for harvesting skin grafts What device is more commonly used to harvest skin grafts? Dermatome What is the most common complication of skin grafts? Seroma/hematoma How do you prevent it? Mesh or pie crust graft and apply compressive dressing What are advantages of using a split-thickness skin graft? Donor site heals spontaneously May cover large wounds

70

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What are disadvantages? Grafts are fragile Contraction of graft during healing May be abnormally pigmented What are advantages of using a full-thickness skin graft? Minimal contraction of graft Better appearance What are disadvantages? More difficult to take Must close donor site What is an advantage of using a muscle flap? It brings immediate increased blood supply to donor site

Fixation Devices AO principles of internal fixation (2002)  Anatomic articular reduction, adequate shaft reduction  Stable/biologic fixation  Preservation of blood supply  Early ROM AO principles (1958)  Anatomic reduction  Rigid internal fixation  Preservation of blood supply  Early ROM What are the steps to inserting a fully threaded screw? 1. Overdrill near cortex 2. Underdrill through far cortex 3. Countersink 4. Measure 5. Tap 6. Screw How much of a screw should pass the far cortex? 1 ½ threads What is the purpose of tapping? Creates a path for the screw threads Why do you countersink a screw? Prevents stress risers and soft tissue irritation Provides even compression from screw head (land) CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

71

Describe mini fragment screws Screw sizes of 1.5, 2.0, 2.7 – all fully threaded, cortical screws What is the screwdriver handle made out of? Pressed linen What are the differences between cortical and cancellous screws? Cortical has smaller pitch Cortical has smaller rake angle Cortical has smaller difference between thread diameter and core diameter Describe a malleolar screw For fixation of medial malleolus, partially threaded, same thread profile and pitch as cortical screw, trephedine self-cutting tip What screw has a fluted tip? Self-tapping What are the screw sizes? What are their underdrill sizes? Overdrill? Countersink? Mini Fragment Sizes Overdrill Underdrill Countersink

1.5 1.5 1.1 1.5

2.0 2.0 1.5 2.0

2.7 2.7 2.0 2.7

All are fully threaded

Small Fragment Sizes Overdrill Underdrill Countersink

3.5 3.5 2.5 3.5

4.0 fully threaded 4.0 2.5 4.0

4.0 partially threaded 4.0 2.5 4.0

Large Fragment Sizes Overdrill Underdrill Countersink

4.5 4.5 3.2 4.5

4.5 malleolar 4.5 3.2 4.5

6.5 partially threaded 6.5 3.2 6.5

What sizes are in the Synthes modular hand screw system? 1.0, 1.3, 1.5, 2.0, 2.4, 2.7

72

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

6.5 fully threaded 6.5 3.2 6.5

What are the cannulated screw sizes? For Synthes 3.0, 4.0 For Smith & Nephew 4.0, 6.5, 5.5 and 7.0 What are the steps for inserting a 4.0 cannulated screw? 1. Insert 1.3 mm guide pin to far cortex 2. Measure 3. Drill near cortex with 4.0 cannulated bit (optional) 4. Drill far cortex with 2.7 cannulated bit (unnecessary for soft bone) 5. Tap (unnecessary with self tapping screws) 6. Countersink 7. Screw What is a Herbert screw? Headless screw – can be inserted through articular cartilage. Threaded portion proximally and distally and smooth in between. Proximal portion has tighter pitch for compression. What is a Reese screw? Headless – create compression through arthrodesis. Proximal threads run clockwise, and distal threads run counterclockwise. Smooth in between. What are the K-wire sizes and widths in millimeters? Size 0.028 0.035 0.045 0.062 Width (mm) 0.6 0.9 1.2 1.6 Why is there a question about K-wires in a screw set section? K-wires can be used for the underdrill if the situation arises (e.g. underdrill bit is missing or it fell on the floor) The 0.062 can be used for the 1.5 underdrill (for the 2.0 screw) The 0.045 can be used for the 1.1 underdrill (for the 1.5 screw) What are the K wire sizes and their appropriate caps? 0.028 0.035 0.045 0.062 Yellow Blue White Green (young boys wear green) What are the sizes of Steinman pins? Every one from 5/64 to 12/64 except for 11/64 What are the different types of plate fixation? Compression  Provides axial compression of fracture  Pre-bend plate  Eccentric drilling of hole adjacent to fracture; remaining holes drilled centrally  Place plate on tension side of bone

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

73

Neutralization  Protects against shear, bending, and torsional forces at the fracture site  Interfragmental compression obtained by lag screws  All holes drilled centrally Anti-glide  Neutralization plate placed on the posterior aspect of the fibula Buttress  Maintains alignment of unstable fracture fragments  No interfragmental compression Should a plate be placed on the tension or compression side of a fracture? Tension Is the tension side of a metatarsal on the dorsal or plantar aspect? Plantar What is a locking plate? Plate in which threaded screws are secured in to threaded plate holes Does not rely on the bone for stability but rather forms a fixed-angle construct Good for osteoporotic, comminuted fractures, or revision surgeries What is the Hooke law? For a material under load, strain is proportional to stress What is the Young modulus? After a load is removed, the material will spring back to its original shape, the resulting slope represents the stiffness of a material or the Young modulous

Suture and Absorbable Fixation Devices What is a Keith needle? Straight needle What are some common needle point configurations? Taper point – for soft, easily penetrated tissue (subcutaneous tissue, fascia) Cutting – cutting edge on inner curve (skin) Reverse cutting – cutting edge on outer curve for tough, difficult to penetrate tissue What is orthofix? Polyglycolic acid (same as dexon) How long for orthofix to lose strength/absorb? Loses strength in 6-12 weeks Absorbed in 1-3 years What is orthosorb? PDS (PDS=orthosorb) 74

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

How long before PDS loses its strength? When is it absorbed? Loses strength in 4-6 weeks Absorbed in 3-6 months What are the two sutures that are the least reactive to tissue? Stainless steel (least reactive), Prolene What is Vicryl? Polyglactin 910 (a copolymer of 90% glycolide and 10% lactide) How is Vicryl broken down? Hydrolysis How long does it take to absorb Vicryl? Tensile strength 75% @ 2 weeks 50% @ 3 weeks 25% @ 4 weeks Absorbed completely in 10 weeks Should you use Vicryl with an infection? Avoid it if possible, since Vicryl is too reactive

Arthroscopy Who first describe arthroscopy? Takagi Who were the first podiatrists to describe a podiatric use for arthroscopy? Heller & Vogel (1982) What are the different scope techniques? Scanning – side to side, up and down Pistoning – in and out Rotation – 360° What are a few indications for an ankle scope? Synovitis Osteochondral lesion/fracture Soft tissue impingement Osteophytes Loose bodies What are other uses for arthroscopy? Endoscopic plantar fasciotomy (EPF) or endoscopic gastroc recession Ankle fusion Arthroscopy of STJ or 1st MPJ CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

75

What is the most common complication following an EPF? Lateral column instability → calcaneal-cuboid joint pain

1st Ray Surgery What is the most common indication for a Lapidus? Hypermobile 1st ray What is the order of the lateral release for a McBride? 1. Extensor hood 2. ADH tendon release 3. Fibular sesamoid ligament 4. Lateral collateral ligament 5. FHB 6. Fibular sesamoid excision (if performing) What is the difference between a Vogler, Kalish, and Youngswick? Vogler – offset V (apex at metaphyseal-diaphyseal joint) Kalish – long-arm Austin with angles of approximately 55° for screw fixation Youngswick – Austin with a slice taken dorsally to allow decompression and plantar flexion What procedures correct PASA? Reverdin Peabody Biangular Austin DRATO Offset V with rotation What procedure corrects DASA? Proximal Aikin What procedure corrects hallux interphalangeous? Distal Aikin What are complications associated with a Keller? Diminished propulsion of digit, loss of hallux purchase, stress fracture of 2nd metatarsal What should be done if the capital fragment falls on the floor? 1. Rinse with saline 2. Bacitracin soak for 15 minutes 3. Rinse with saline 4. Bacitracin soak for 15 minutes 5. Rinse with saline 6. Document and inform patient

76

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Post-Op White and Blue Toes What are causes of a white toe post-operatively? Arterial in nature, usually acute Signs – pain, pale, parasthesia, pulselessness What are treatments for a white toe?  D/C ice and elevation  Loosen bandages  Place foot in dependent position  Rotate K-wire  Apply warm compresses proximally  Apply nitroglycerine paste proximally  Local nerve block proximally  Avoid nicotine  Consult vascular surgery What are causes of a blue toe? Poor arterial inflow – toe is cold and doesn't blanch with pressure Poor venous outflow – toe is warm and will blanch with pressure What are treatments for blue toe due to arterial insufficiency?  (Treat like white toe)  D/C ice and elevation  Loosen bandages  Place foot in dependent position  Rotate K-wire  Apply warm compresses proximally  Apply nitroglycerine paste proximally  Local nerve block proximally  Avoid nicotine and caffeine  Thermostat controlled heat lamp, not to exceed 90°  Vasodilators  Consult vascular surgery What are treatments for blue toe due to sluggish venous outflow?  D/C ice (but not elevation)  Loosen bandages  Avoid dependency  Don’t attempt to increase vascular perfusion  Consult vascular surgery

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

77

Rearfoot Surgery Describe a Keck & Kelly procedure? For Haglund deformity with cavus foot and high calcaneal inclination angle. Remove wedge from posterior-superior aspect of calcaneus. The posterior superior prominence is moved anteriorly. What are treatments for equinus? Stretching/exercises Night splints Gastroc recession  Strayer  Vulpius  Baker  McGlamary & Fulp Tendoachilles lengthening  Open/closed Z  Hauser  White  Hoke  Sgarlato  Stewart What is the Murphy procedure? Achilles advancement for spastic equinus Name surgical procedures for pes planus Transverse  Evans  Kidner  C-C distraction arthrodesis Sagittal  Cotton  Young  Lowman  Hoke  Miller  Cobb Frontal  Koutsogiannis  Dwyer  Chambers  Gleich  Baker-Hill  Lord

78

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Name surgical procedures for pes cavus Tendon  Jones  Hibbs  STATT  PT Bone  Dorsiflexory osteotomy of 1st metatarsal  Cole  Japas What is an arthroereisis? A surgical procedure to limit joint mobility (i.e. MBA implant in sinus tarsi) Typically want 2-4° of STJ eversion with implant What is the Valente procedure? STJ block using a polyethylene plug with screw threads. Allows 4-5° of STJ pronation. Who first described the triple arthrodesis? Ryerson What order do you resect and what order do you fixate the joints in a triple arthrodesis? Resection 1. Midtarsal joints (T-N, CCJ) 2. Subtalar joint (T-C) Fixation (opposite order) 1. Subtalar joint 2. Midtarsal joints What are some types of fixation for a triple arthrodesis? 6.5-7.0 mm interfragmental compression screws, staples, plates What are FDA-approved total ankle implants? Two-component devices  Agility  Eclipse  INBONE  Salto Talaris Three-component devices  STAR  (Not FDA-approved – Buechal-Pappas, TNK, HINTEGRA)

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

79

Bone Healing What are the stages of bone healing? Bone heals either primarily or secondarily Primary healing – no motion and no callus formation 1. Inflammation 2. Induction 3. Remodeling Secondary healing – micro-motion with callus formation 1. Inflammation 2. Induction 3. Soft callus 4. Hard callus 5. Remodeling What are some factors that negatively affect bone healing? Smoking, antimetabolite or steroid therapy, anemia, osteoporosis Name the types of non-unions Hypertrophic  Elephant foot  Horse hoof  Oligotrophic Atrophic  Torsion wedge  Comminuted  Defect  Atrophic What study can distinguish between a hypertrophic and an atrophic non-union? Bone scan – positive for a hypertrophic and negative for an atrophic (avascular) non-union What is a pseudoarthrosis? Type of non-union in which fibrocartilaginous tissue forms between fracture fragments What are indications for bone stimulators? Non-union, failed fusion What are contraindications for bone stimulators? Pseudoarthrosis, gap greater than ½ bone diameter What are the stages of avascular necrosis? 1. Avascular – loss of blood supply, epiphyseal growth ceases 2. Revascularization – infiltration of new blood vessels, new bone deposited on dead bone, flattening or fragmentation of articular surface 3. Repair and remodeling – bone deposition replaces bone resorption 4. Residual deformity – restoration of epiphysis, sclerosis, deformed articular surface 80

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What is the best study for evaluating avascular necrosis? MRI – decreased signal intensity within medullary bone in both T1 and T2 images

Bone Grafts What are the different types of bone grafts? Osteogenic – able to synthesize new bone  Mesenchymal stem cells from autologous bone or bone marrow aspirate Osteoinductive – contains factors that induce host tissue to form new bone  Demineralized bone matrix  Bone morphogenic protein  Platelet-derived growth factors Osteoconductive – provides scaffold for host tissue to propagate new bone  Allografts  Hydroxyapatite  Calcium phosphate  Calcium sulfate What type of bone graft is osteogenic, osteoinductive, and osteoconductive? Autograft What are the stages of bone graft healing? 1. Vascular ingrowth 2. Osteoblastic proliferation 3. Osteoinduction 4. Osteoconduction 5. Graft remodeling What is an early radiographic finding of bone graft healing? Initial radiolucency of the graft due to increased osteoclastic activity which is followed by osteoblasts laying down new bone What is creeping substitution? Process in which the host’s cutting cone (osteoclasts followed by osteoblasts) invade bone graft

Miscellaneous What is the ASA classification for general anesthesia? Class 1 – healthy Class 2 – mild systemic disease Class 3 – severe systemic disease Class 4 – incapacitating systemic disease that is a threat to life Class 5 – moribund patient who is not expected to live without surgery Emergency

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

81

What is the maximum tourniquet time? 90-120 minutes After that, allow 5 minutes of perfusion for every half hour over What are contraindications to using a tourniquet? Infection Open fracture Sickle cell disease Peripheral vascular disease Recent arterial graft Previous DVT Hypercoagulability Skin grafts application where bleeding must be distinguished According to Seddon, what are the different types of nerve damage? Neuropraxia – nerve contusion resulting in conduction block that recovers promptly Axonotmesis – interruption of axons with distal Wallerian degeneration. Supporting connective tissue sheaths remain intact allowing regeneration. Neurotmesis – complete severance of the nerve that is irreversible What is the difference between an incisional and excisional biopsy? Incisional – only a portion of the lesion is removed Excisional – the entire lesion is removed What are different biopsy techniques? Punch, shave, curettage, surgical excision How does a bone stimulator work? Piezoelectric principle – side under compression makes a negative charge that leads to bone growth. Therefore, placing a cathode in a non-union site will stimulate growth. What is the direction of the cut for reverse Wilson of the 5th metatarsal? Distal lateral to proximal medial Who was the first to describe an arthrodesis? Soule What is the order for hammertoe surgery? Note: Perform a Kelikian push-up test to determine if the next step is required 1. PIPJ  Tendon  Dorsal capsule  Collaterals  Plantar capsule  Arthroplasty

82

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

2. MPJ     3. PIPJ 

Hood Tendon Capsule Plantar plate Arthrodesis

Why are joint implants used? Maintain space between bony surfaces Relieve pain What is the lag time for presentation of osteomyelitis on an X-ray? 10-14 days How to culture osteomyelitis? Take one culture from the infected bone, and take a second culture proximal to the clearance margin to ensure remaining bone is not infected What is a Brodie abscess? What is the treatment? Subacute osteomyelitic lesion usually found in children. It is a well-circumscribed, lytic lesion with sclerotic borders found in the metaphysis, epiphysis, and rarely diaphysis. Painful with periods of exacerbation and remission. Tx: curettage and packing with autologous bone What is in antibiotic beads? PMMA or Poly(methyl methacrylate). Gentamycin or tobramycin are often used since they are heat stable with good diffusion coefficiencies. Vancomycin and cefazolin may also be used.

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

83

84

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Trauma What should be done when assessing a patient with trauma? Primary survey (ABCDE)  Airway  Breathing  Circulation with hemorrhage control  Disability – assess neurologic status  Exposure of patient and environmental control Secondary survey  Full history – medical and drug  Thorough examination o Evaluate tenderness and stability as well as neurovascular status of each limb o Is there injury to joint above or below?  X-rays and/or CT of all suspected fractures What should always be asked with a break in the skin? Tetanus status Name the appropriate classification Distal phalangeal/nail 1st Metatarsophalangeal 5th Metatarsal base Lisfranc joint Navicular Posterior tibial tendon Talar neck Talar body Talar dome Calcaneus Anterior process calcaneal fracture Ankle sprains Physeal ankle fracture Epiphyseal fracture Ankle fracture Pilon fracture (distal tibia metaphysis) Achilles rupture Open fracture Non-unions Frostbite

Rosenthal Jahss Stewart Quenu & Kuss, Hardcastle Watson Jones Conti (based on MRI findings) Hawkins Sneppen Berndt-Hardy, Fallot & Wy Rowe, Essex-Lopresti, Sanders Degan O'Donoghue, Leach, Rasmussen Dias & Tachdjian Salter-Harris Lauge-Hansen Ruedi & Allgower, Dias & Tachdjian Kuwada Gustillo Weber & Cech Orr & Fainer, Washburn

What is a clinical test for a fracture? Point tenderness over fracture site

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

85

What are common fracture patterns? Transverse, greenstick, torus, oblique (spiral), comminuted Which is the most stable pattern? Transverse is most stable What is the weakest region of the physis? Zone of cartilage maturation What is the Vassal principle? Initial fixation of the primary fracture will assist stabilization of the secondary fractures What are possible complications of fractures? Delayed union Non-union Pseudoarthrodesis OA AVN What is the most common cause of non-healing for a bone fracture? Improper immobilization Who was Lisfranc? He was a field surgeon in Napoleon's army Are dorsal or plantar Lisfranc dislocations more common? Dorsal – the plantar ligaments are stronger than dorsal What are the Ottowa Ankle Rules? A series of ankle X-ray films is required only if there is any pain in the malleolar zone and any of the following findings:  Bone tenderness at posterior edge or distal 6 cm of lateral malleolus  Bone tenderness at posterior edge or distal 6 cm of medial malleolus  Inability to bear weight both immediately and in ED A series of foot X-ray films is required only if there is any pain in midfoot zone and any of the following findings:  Bone tenderness at base of 5th metatarsal  Bone tenderness at navicular  Inability to bear weight both immediately and in ED

Talar Fractures What is the classification for talar dome lesions? Berndt & Hardy What stages of Berndt & Hardy are often associated with lateral ankle ligament ruptures? II, III, IV 86

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What are the common locations of talar dome lesions and their mechanisms of injury? (DIAL a PIMP) Dorsiflexion Inversion – Anterior Lateral (unstable, shallow, wafer-shaped lesion) Plantarflexion Inversion – Medial Posterior (deep, cup-shaped lesion) What is Hawkins sign? Presence of subchondral talar dome osteopenia seen 6-8 weeks after talar fracture signifying intact vascularity. Absence of the sign implies AVN. What is the Sneppen classification? Talar body fractures What percentage of fractures of the talus involve the calcaneus? 60% Of these fractures, how many involve the joint? 75%

Calcaneal Fractures What is a Mondor sign? Plantar, rearfoot ecchymosis that is pathognomonic for calcaneal fractures How is the Bohler angle affected by a calcaneal fracture? Decreases with intra-articular calcaneal fracture How is the Gissane angle affected by a calcaneal fracture? Increases with intra-articular calcaneal fracture What fractures are commonly associated with calcaneal fractures? Vertebral fractures, especially L1 Femoral neck Tibial plateau What is the mechanism of injury for an anterior process fracture? Inversion with plantarflexion

Ligamentous Ruptures What are tests for ankle ligament pathology? Anterior drawer test Calcaneofibular-stress inversion Abduction stress Ankle arthrogram Peroneal tenography

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

87

Describe the anterior drawer test 5-8 mm drawer → rupture of ATF 10-15 mm drawer → rupture of ATF + CF >15 mm drawer → rupture of ATF + CF + PTF Describe the talar tilt test >10° → rupture of CFL Describe the stress inversion test 5° inversion → rupture of ATF 10-30° inversion → rupture of ATF + CF

Achilles Tendon Ruptures What are clinical symptoms of an Achilles tendon rupture? Pain with history of ―pop‖ Weakness or loss of function Palpable dell in area of ruptured tendon Inability to perform single leg rise Increased ankle dorsiflexion What is the Thompson test? A positive test results when squeezing of the calf muscle does not plantarflex the foot What is the Hoffa sign? Increased dorsiflexion compared to the contralateral side along with the inability to perform a single leg rise test What is a radiographic finding of an Achilles tendon rupture? Disruption of Kagers triangle Where is the most common location for the Achilles tendon to rupture? 1.5-4 cm proximal to the calcaneal insertion

Ankle Fractures Name the fractures Pott Bimalleolar fracture Cotton Trimalleolar fracture Tillaux-Chaput Avulsion fracture of anterior, lateral tibia from AITFL Wagstaff Avulsion fracture of anterior, medial fibula from AITFL Volkman Posterior tibial malleolar fracture from PITFL Cedell Fracture of posterior medial process Shepard Fracture of posterior lateral process Foster Entire posterior process Bosworth Lateral malleolar fracture with ankle displacement Maisonneuve Proximal fibular fracture

88

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What is the most common mechanism of injury (MOI) causing an ankle fracture? SER What is the MOI causing a transverse lateral malleolar fracture? SAD I What is the MOI causing a short, oblique medial malleolar fracture? SAD II What is the MOI causing a short, oblique lateral malleolar fracture (AP view)? PAB III What is the MOI causing a spiral, lateral malleolar fracture with a posterior spike (AP and Lateral views)? SER II What is the MOI to the ankle with a high fibular fracture? What is this fracture called? PER III Maisonneuve fracture What is a Lauge-Hansen Type V? Pronation dorsiflexion 1. Vertical tibial malleolar tip fracture 2. Anterior tibial lip fracture 3. Supramalleolar fibular fracture 4. Transverse posterior tibia fracture level with proximal aspect of anterior tibial fracture When should a posterior malleolar fracture be fixated? ORIF when fragment is greater than 25% of the posterior malleolus What direction should transsyndesmotic screws be inserted? Approximately 30° from the sagittal plane from posterior-lateral to anterior-medial Should transsyndesmotic screws be inserted using a lag technique? No. Fully-threaded cortical screws are placed across both cortices of the fibula and the lateral cortex of the tibia. The goal is stabilization rather than compression. What do you test clinically test via Jack Toe Test? Foster fracture – a fracture of the entire posterior process What is the Thurston-Holland sign? Epiphysis is separated from the physis with the fracture extending into the metaphysis resulting in a triangular fracture fragment (AKA Flag sign)

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

89

90

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Bone Tumors What are the different patterns of bone destruction? Geographic – well-defined, short zone of transition → benign or low-grade malignancy Moth-eaten – more aggressive, intermediate zone of transition → benign or malignant Permeative – poorly-defined, wide zone of transition → malignant What are the different patterns of periosteal reactions? Single layer – benign but sometimes malignant Onion skin – malignant, multiple layers of periosteum Sunburst – spiculated rays Hair on end – parallel rays Codman triangle – triangular elevation of periosteum Name benign bone tumors of the foot (FOG MACHINES) F – fibrous dysplasia O – osteochondroma G – giant cell tumor M – myeloma A – aneurysmal bone cyst C – chondroblastoma, chondromyxoid fibroma, clear cell H – hemangioma I – infection N – non-ossifying fibroma E – eosinophillic granuloma, enchondroma, epidermal inclusion cyst S – solitary bone cyst Name malignant bone tumors of the foot Chondrosarcoma Osteosarcoma Periosteal sarcoma Ewings sarcoma Fibrosarcoma Multiple myeloma What is the most common, benign, primary bone tumor? Osteochondroma What is the most common, malignant, primary bone tumor? Multiple myeloma

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

91

What primary bone tumors are more frequent in females? Giant cell tumor ABC Parosteal osteosarcoma What are the most common cancers that metastasize to foot? Breast, prostate, lung, kidney What bone tumors do not form matrix? Bone cysts Ewings sarcoma Giant cell tumor What are bone tumors typically located? Epiphysis  Chondroblastoma  Giant cell tumor (forms in metaphysis) Metaphysis  Enchondroma (also diaphyseal)  Osteochondroma  Nonossifying fibroma  Unicameral bone cyst  Aneurysmal bone cyst  Giant cell tumor (extends into epiphysis)  Medullary osteosarcoma  Parosteal osteosarcoma  Chondrosarcoma Diaphysis  Osteoid osteoma  Osteoblastoma  Enchondroma (also metaphyseal)  Ewings sarcoma (also meta-diaphysis)  Periosteal osteosarcoma Centrally located  Enchondroma  Unicameral bone cyst Eccentrically located within medullary canal  Giant cell tumor  Chondrosarcoma  Osteosarcoma Cortical  Osteoid osteoma  Nonossifying fibroma

92

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Periosteal  Osteochondroma  Periosteal osteosarcoma What are characteristics of an osteoid osteoma?  Benign, osteolytic lesion with central nidus (<1 cm) that may have calcifications  1st to 2nd decades of life  Dull pain, worse at night, relieved with ASA What are characteristics of an osteoblastoma?  ―Giant osteoid osteoma‖  Benign tumor that may become malignant  Osteolytic lesion with well-circumscribed nidus (>1.5 cm) that may have multiple calcifications  2nd to 3rd decades of life  Less symptomatic than osteoid osteoma, pain not relieved by ASA What are characteristics of an enchondroma?  Benign, well-defined, intramedullary, cartilaginous lesion  Geographic lesions with punctuate calcified matrix  3rd to 4th decades of life  Painless swelling unless pathologic fracture What is Ollier disease?  Multiple enchondromatosis  May become malignant  1st decade of life What is Maffuccis disease?  Multiple enchondromas with soft tissue hemangiomas  Most become malignant  1st decade of life What are characteristics of a chondroblastoma?  Benign, geographic, osteolytic, lesion with sclerotic margins  2nd to 3rd decade of life  Pain and joint effusion What are characteristics of an osteochondroma?  Most common benign primary bone tumor  Cartilage-capped, hyperplastic bone pointing away from the joint  2nd to 4th decades of life  Suspect malignant transformation with growth after skeletal maturity, pain, or cap >2 cm

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

93

What are characteristics of nonossifying fibromas?  Benign connective tissue lesion with fibrous replacement of bone  Expansive, radiolucent, medullary lesions  1st to 2nd decades of life  Lesions typically resolve with age  Do not biopsy What are characteristics of a fibrous dysplasia?  Benign, geographic, fibro-osseous lesion with ground glass matrix  Presents with deformity  Sometimes painful 2° to fracture What are characteristics of a unicameral bone cyst?  Benign, geographic, medullary lesion that is fluid-filled  Commonly found in calcaneus  Fallen fragment sign – pathologic fracture in which cortex lies within lesion  1st to 2nd decades of life  Asymptomatic until fracture What are characteristics of an aneurysmal bone cyst?  Benin, expansile, lytic lesion with blood-filled cavities  May extend into soft tissue  Fluid-fluid levels seen on MRI  1st to 3rd decades of life  More common in females  Painful, especially with pathological fractures What are characteristics of a giant cell tumor?  Benign but locally aggressive, lytic lesion with ground glass, ―soap bubble‖ appearance  May destroy cortex and have soft tissue mass  More common in females  3rd to 4th decades of life  Painful What are characteristics of a multiple myeloma?  Most common primary malignant bone tumor  Punched out lesions or diffusely osteopenic with hair-on-end radiating spicules  Affect 45-80 y/o  Painful with weakness or neurologic symptoms  Bence-Jones protein found within urine

94

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What are characteristics of an osteosarcoma?  Most common primary malignant bone tumor  Sunburst periosteal reaction with Codman triangle and cloud-like, dense bone formation  2nd to 3rd decades of life  Dull aching pain  Medullary o Poor prognosis  Parosteal o More common in females o Better prognosis than medullary  Periosteal o Slightly better prognosis than medullary What is the most common bone tumor associated with Paget disease? Osteosarcoma What are characteristics of a Ewings sarcoma?  Common, malignant, primary bone tumor  Aggressive, permeative, lytic lesion with hair-on-end, Codman triangle, and onion skin (wings and onion rings)  May have large soft tissue mass  Usually under 20 y/o  Painful with fever, weight loss, and elevated ESR  Poor prognosis What are characteristics of a chondrosarcoma?  Common, malignant, moth-eaten, lesion with medullary and soft tissue calcifications  May arise from malignant transformation of enchondromas or osteochondromas  5th to 6th decades of life  Painful What study is most useful in searching for metastatic bone disease? Total skeletal bone scan Malignant lesions will show increased uptake

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

95

96

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Wound Care What are the stages of wound healing? 1. Inflammatory (lag) phase  Days 1-4  Initial vasoconstriction (minutes) followed by vasodilation (days)  Neutrophils and macrophages are recruited 2. Proliferative (repair) phase  Days 3-21  Collagen synthesis provides tensile strength of wound  At 14 days, tensile strength of would equals that of suture 3. Remodeling (maturation) phase  Days 21 up to one year In what stage of healing do chronic wounds stop progressing? Proliferative What is Santyl? collagenase – an enzymatic debrider that digests collagen in necrotic tissue What is Regranex? PDGF-1 (platelet derived growth factor) Where is Regranex made? Puerto Rico (I was really asked this once) What is a normal value for serum albumin? 3.4-5.0 g/dL What is a low serum albumin level (<3.5 g/dL) associated with? Decreased wound healing Edema Impaired cellular immunity Decreased collagen synthesis Decreased fibroblast proliferation What minimum ABI is necessary for wound healing? Non-diabetic patient – 0.35 Diabetic patient – 0.45 Using transcutaneous oximetry, what minimum pressure is necessary for wound healing? Non-diabetic patient – 30 mm Hg Diabetic patient – 40 mm Hg

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

97

How does negative pressure wound therapy (e.g. Wound VAC) assist wound closure? NPWT applies mechanical shear stress to the wound site. This is believed to promote granulation by decreasing bacterial bioburden, reducing edema, and inducing capillary budding. How does hyperbaric oxygen therapy assist wound closure? HBOT increases the partial pressure of O2 in arterial circulation, which increases diffusion of O2 at the wound site. This is believed to increase growth factors promoting angiogenesis and collagen synthesis.

Bioengineered Tissue What is Integra? Bilayer graft composed of bovine tendon collagen with chondroitin-6-sulfate and a silicone layer to control moisture loss Oasis? Extracellular graft matrix derived from porcine, small intestine submucosa Apligraf? Bilayer graft derived from neonatal foreskin with dermal and epidermal layers GraftJacket? Extracellular graft matrix derived from human tissue with intact vascular channels TissueMend? Acellular collagen matrix derived from fetal bovine dermis

98

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Classifications Note: Although all of the classifications are important, the ones in bold and capitalized (i.e. LAUGE-HANSEN) are the most commonly used.

Forefoot Hallux Valgus Stage 1  Excess pronation causes hypermobility of 1st ray. Tibial sesamoid ligament gets stretched & fibular sesamoid ligament contracts.  Lateral subluxation of proximal phalanx occurs Stage 2  Hallux abductus progresses, touches against 2nd digit  FHL & FHB gain lateral mechanical advantage  Crista starts to erode Stage 3  Further subluxation at 1st MPJ, formation of IMA  IMA increases secondary to retrograde forces from abductor hallucis Stage 4  Hallux subluxes & dislocates on 1st metatarsal  Increased crista erosion

Hallux Limitus REGNAULD (Foot, 1986) Grade 1 – functional hallux limitus with dorsal spurring  Intact sesamoids with no associated disease  Joint enlargement but joint space narrowing and arthrosis  <40° dorsiflexion and <20° plantarflexion Grade 2 – broad flat metatarsal head with structural elevatus and significant spurring  Pain at rest  Osteochondral defects in metatarsal head and sesamoidal hypertrophy  Joint space hypertrophy and narrowing  75% decrease in total ROM Grade 3 – ankylosis and articular hypertrophy with extensive peri-articular osteophytes  Osteochondral defect with joint mice and extensive 1st metatarsal-sesamoid disease  Severe loss of joint space or collapse of joint → bone on bone  FDL contracture

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

99

MODIFIED REGNAULD/OLOFF (ACFAS, 1994) Stage 1 – functional hallux limitus  Limited dorsiflexion with weightbearing but normal ROM with non-weightbearing  No DJD changes on x-ray  No pain on end ROM Stage 2 – joint adaptation  Flattening of metatarsal head with small dorsal exostosis  Pain on end ROM Stage 3 – joint deterioration  Severe flattening of metatarsal head with non-uniform joint space narrowing, osteophytes, and subchondral sclerosis/cysts  Crepitus on ROM Stage 4 – ankylosis  Obliteration of joint space with osteophyte fragmentation  Minimal to no ROM Drago, Oloff, and Jacobs (J Foot Ankle Surg, 1984) Grade 1 – pre-hallux limitus  Pain on end ROM  X-Rays: plantar subluxation of proximal phalanx, met primus elevatus, minimal DJD  Joint preservation/reconstruction surgery Grade 2 – flattening of metatarsal head  Pain on end ROM, limited ROM  X-Rays: small dorsal exostosis, osteochondral lesion, flattened met head  Joint preservation/reconstruction surgery Grade 3 – severe flattening of the metatarsal head  Pain on full ROM, crepitus  X-Rays: large dorsal exostosis, marked flattened met head, osteophytic production, nonuniform joint space narrowing  Joint preservation/reconstruction surgery Grade 4 – obliteration on joint space with joint mice  <10° ROM  May be asymptomatic if ankylosed  X-Rays: loss of joint space, loose bodies  Joint destructive surgery Hanft (J Foot Ankle Surg, 1993) Grade 1 – metatarsus primus elevatus, mild dorsal exostosis, and sclerosis around MPJ Grade 2 – Grade 1 with flattening of metatarsal head, joint space narrowing, and dorsal/lateral osteophytes Grade 3 – Grade 2 with DJD findings (osteophytes, subchondral sclerosis, and cysts) Grade 4 – Grade 2 with severe flattening and sesamoid hypertrophy Grade 5 – Grade 3 with DJD findings

100

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Ktavitz, Laporta, Lauton (1994) Stage 1 – normal to mild flattening of the head Stage 2 – minimal narrowing Stage 3A – irregular joint space narrowing with dorsal spurring and cysts Stage 3B – minimal joint space with loose bodies and large dorsal flag Stage 4 – no joint space with sesamoid fusion and large exostosis formation

1st Metatarsal Dislocations JAHSS (condensed) Type l – dorsal dislocation of proximal phalanx and sesamoids with intact intersesamoid ligament Type 2 – dorsal dislocation of proximal phalanx and sesamoids 2A – intact sesamoids with ruptured of intersesamoid ligament 2B – transverse fracture of sesamoid with intact intersesamoid ligament JAHSS (Foot Ankle, 1:15, 1980) * Secondary to extreme dorsiflexion Type 1 – dorsal dislocation of proximal phalanx and sesamoids with intact intersesamoid ligament  Tx: requires ORIF Type 2A – dorsal dislocation of proximal phalanx and sesamoids with ruptured intersesamoid ligament  Tx: closed reduction and surgical shoe or BK walking cast Type 2B – dorsal dislocation of proximal phalanx and transverse fracture of sesamoid with intact intersesamoid ligament  Tx: closed reduction and surgical shoe or BK NWB cast or excision of the fractured sesamoid

5th Metatarsal Fractures Stewart (condensed) Type 1 – extra-articular fracture at metaphyseal-diaphyseal junction (true Jones fracture) Type 2 – intra-articular avulsion fracture of 5th metatarsal base Type 3 – extra-articular avulsion fracture of styloid process of 5th metatarsal base Type 4 – intra-articular comminuted fracture of 5th metatarsal base Type 5 – extra-articular avulsion of epiphysis in children Stewart (Clin Ortho, 1960) – Stewart described only the first 4 types Type 1 – transverse fracture at the metaphyseal-diaphyseal junction of 5th metatarsal base approximately 1 cm from the articular cartilage. This is due to rotation of the forefoot with the base of the 5th metatarsal remaining fixed.  True Jones fracture (Sir Robert Jones 1902-4 fractures his own)  This type of injury has a high propensity for non-union  MOI: internal rotation, PF ankle, and adduction of forefoot  Tx if non-displaced: BK NWB cast for 4-6 weeks  Tx if displaced: ORIF CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

101

Type 2 – intra-articular avulsion fracture of the 5th metatarsal base (styloid process)  MOI: shear force. Resulting from contraction of the peroneus brevis.  Tx if reducible: BK NWB cast for 4-6 weeks  Tx if non-reducible: ORIF Type 3 – extra-articular avulsion of the 5th metatarsal base  ―Tennis fracture‖  Most common is 5th metatarsal fracture  MOI: contraction of PB with DF of ankle  Tx if reducible: BK NWB cast for 4-6 weeks  Tx if non-reducible: ORIF (possibly tension band wiring) Type 4 – intra-articular, comminuted fracture of the 5th metatarsal base  MOI: crush  Tx: BK NWB cast for 4-6 weeks  Tx if severely displaced: bone graft and ORIF Type 5 – extra-articular, avulsion fracture of the epiphysis (in a longitudinal direction)  Seen in children with open growth plates  Risk of Iselin AVN  AKA Salter-Harris type 1  Tx: BK NWB cast 4-6 weeks Lawrence – Review Article (Foot Ankle, 1993) Confusion of 3 fracture  Jones fracture  Diaphyseal stress fracture  Tuberosity avulsion fracture Shereff (Foot Ankle, 1991) Spalteholtz tech. of 5th blood supply/nutrient artery proximal and medial 1/3 shaft On X-ray, fracture heals medially to laterally Fixation: tension band wire, low profile plate, screws, cross K-wires, 4.5 malleolar screw Complications: sural nerve entrap Apophysis fuses at 9-12 years of age Torg (JBJS, 1984) Type 1 – acute Jones fracture Type 2 – delayed union of a Jones fracture or diaphyseal stress fracture Type 3 – non-union of a Jones fracture or a diaphyseal stress fracture Champman Type 1A – Jones fracture Type 1B – displaced Jones fracture with possible comminution Type 2 – delayed or non-union of a Jones fracture Type 3A – avulsion fracture of the styloid Type 3B – intra-articular fracture of the styloid

102

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Nail Injuries ROSENTHAL (Ortho Clinics NA, 14(4):695, 1983) Zone 1 – distal to bony phalanx Zone 2 – distal to lunula  Tx: V-Y advancement Zone 3 – proximal to distal end of lunula  If nail bed is lacerated, it is considered an open fracture  Tx: amputation

Metatarsal Head Freiberg Infarction Type 1 – metatarsal head dies but heals by replacement. Articular surface preserved. Type 2 – head collapses but articular surface remains. Peripheral osteophytes (dorsal). Type 3 – head collapses with articular cartilage loosening. Joint is destroyed. Type 4 – multiple heads involved

Lisfranc Dislocations QUENU & KUSS (Rev Chir, 39:281-336,720-91,1093-134, 1909) Convergent homolateral  All metatarsals subluxed laterally  All 5 metatarsals displaced laterally in the transverse plane Isolateral  1st metatarsal subluxed medially or metatarsals 2-5 subluxed laterally  1 or 2 metatarsals displaced laterally in the transverse plane Divergent  1st metatarsal subluxed medially and metatarsals 2-5 subluxed laterally  Displacement in both sagittal and transverse planes HARDCASTLE (JBJS, 64B:349, 1982) Type A – total incongruity A1 – homolateral A2 – homomedial Type B – partial incongruity Bl – partial medial displacement  1st metatarsal displaced medially and/or in combination with metatarsals 2-4 B2 – partial lateral displacement  Lateral displacement of one or more lesser metatarsals Type C – divergent Cl – partial displacement  1st metatarsal displaced medially with any combination of metatarsals 2-4 displaced laterally C2 – total displacement  1st metatarsal displaced medially with metatarsals 2-5 displaced laterally

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

103

Treatment Options  Cast immobilization (sprains 3-5 weeks)  Closed reduction and percutaneous pinning  ORIF Reduction Sequence 1. First realign 2nd metatarsal on middle cuneiform. Once stabilized, lesser metatarsals will follow. 2. Next stabilize 1st metatarsal and then lateral metatarsals Post-op Care  BK casting for 6 to 12 weeks  Initial NWB for 6-8 weeks  Partial WB approximately 6 weeks  Begin ambulation in stiff-soled shoe  PT ASAP  Accommodative orthotics Complications  Majority – post-op DJD  Serious – circulatory compromise Myerson (Foot Ankle, 6(5):225, 1986) Type A – total displacement in any plane or direction Type Bl – medial displacement of 1st metatarsal Type B2 – lateral displacement affecting 1 or more lesser metatarsals Type C1 – partial displacement with medial 1st metatarsal and lateral lesser metatarsals Type C2 – total displacement with a divergent pattern and total incongruity

Navicular Fractures WATSON-JONES (condensed) Type 1 – navicular tuberosity fracture Type 2 – dorsal lip fracture Type 3 – transverse body fracture 3A – fracture of body without displacement 3B – fracture of body with displacement Type 4 – stress fracture WATSON-JONES (Fracture and Joint Injuries, Watson & Jones, 5th ed, p 1200) Type 1 – navicular tuberosity fracture  Usually an avulsion fracture by tibialis posterior tendon  24% of navicular fractures  Nutcracker fracture – displaced fracture with compression fracture of the cuboid between 4th and 5th metatarsal bases and calcaneus  MOI: forceful eversion w/medial avulsion of the PT off the tuberosity or 104

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

 MOI: direct blow to the tuberosity  Need to D/Dx Os Tibiale Externum vs. true fracture,  Best viewed on AP and lateral oblique films  TX: BK cast with partial WB for 4 weeks Type 2 – dorsal lip fracture  Most common  Tx: BK cast with partial WB for 4-6 weeks Type 3 – transverse navicular body fracture 3A: without displacement o Tx: BK walking cast for 6-8 weeks 3B: with displacement o Tx: ORIF and BK NWB cast for 6-8 weeks Type IV – stress fracture of the navicular  Tx if non-displaced: BK NWB cast for 4-6 weeks  Tx if displaced: ORIF followed by BK NWB x 6-8 weeks

Accessory Navicular – Os Tibiale Externum Geist (1914), first described by Bahin (1605) Type l – sesamoid in tendon Type 2 – articulating os center (Sella Clin Ortho, 1986, Foot Ankle, 1987) 2A – synchondrosis acute angle 2B – synchondrosis obtuse angle Type 3 – fused accessory os center

Navicular Classifications Wilson Chip, comminuted, and crush Watson Jones Tuberosity, dorsal lip, and transverse DePalma Dorsal lip, avulsion, tuberosity, and fracture dislocation Rockwood & Green Body fracture with/without dislocation, chip, and tuberosity Goldman Chip, tuberosity, body, displaced, and osteochondral fracture

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

105

Rearfoot Calcaneal Fractures ROWE (condensed) Type 1 1A – fracture of plantar tuberosity 1B – fracture of sustentaculum tali 1C – fracture of anterior process Type 2 2A – ―beak fracture‖ 2B – avulsion fracture of Achilles insertion Type 3 3A – simple oblique fracture of body not involving STJ 3B – comminuted oblique fracture of body not involving STJ Type 4 – intra-articular fracture involving STJ Type 5 – intra-articular, comminuted, depression fracture with STJ involvement Note: Rowe is primarily used for extra-articular fractures. Intra-articular fractures (Rowe 4 & 5) are usually replaced by Essex & Lopresti. ROWE (JAMA, 184:98-101, 1963) Type 1 1A – fracture of the plantar tuberosity due to inverted or everted foot  Tx of non-displaced: CR and BK WB cast for 6 weeks  Tx of displaced: ORIF 1B – fracture of the sustentaculum tali due to twist on a supinated foot  Tx of non-displaced: CR and BK cast for 6 weeks  Tx of displaced: ORIF 1C – fracture of the anterior tubercle due to plantarflexion on a supinated foot  Most common type 1 fracture  Most common in females  Tx: CR and BK WB cast for 6 weeks. If symptoms persist, excise the fragment Type 2 2A – ―beak fracture‖ without Achilles insertion involvement  Tx: NWB BK cast for 6 weeks in plantarflexion 2B – avulsion fracture of the Achilles tendon  Tx: ORIF or attempt percutaneous pinning Type 3 3A – simple oblique fracture of body not involving STJ 3B – comminuted oblique fracture of body not involving STJ  Most common extra-articular  Tx of non-displaced: NWB AK cast with knee flexed  Tx of displaced: ORIF Type 4 – intra-articular fracture involving STJ Type 5 – intra-articular, comminuted, depression fracture with STJ involvement 106

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

ESSEX-LOPRESTI (condensed) Type 1 – tongue fracture (vertical fracture line) without STJ involvement Type 2 – joint depression fracture (horizontal fracture line) with STJ involvement ESSEX-LOPRESTI (Br J Surg, 39:395-419, 1952) Type 1 – tongue type fracture with a primary fracture line running superior to inferior with a secondary fracture line exiting the posterior aspect of the calcaneus without STJ involvement 1A – tuberosity fracture 1B – calcaneal-cuboid joint involvement Type 2 – joint depression fracture with a primary fracture line running superior to inferior with a secondary fracture line involving STJ 2A – non-displaced secondary fracture line exits posteriorly 2B – displaced secondary fracture line exits dorsally 2C – gross comminution ** 75% of all calcaneal fractures are intra-articular Treatment of Intra-articular Fractures Essex-Lopresti Technique Percutaneous pinning technique placing a Steinmann pin into the tuberosity. The tongue fragment is reduced, and a pin is placed into the anterior calcaneus or cuboid. No cast required, and motion is performed immediately. The pin is removed in 8-10 weeks and WB is begun. Indicated for Sanders 2C (87% success rate). Closed reduction Used if <2 mm displacement ORIF Incisional Approaches  Medial Approach: Burdeaux  Combined Approach: Stephenson  Extended Lateral Approach: Benirschke Procedure  Goal is to restore the STJ and C-C articulation  Perform surgery within 6-8 hours of the injury or wait until the swelling is reduced  Reduction is performed by placing a Steinmann pin through the tuberosity fragment to restore the STJ posterior facet. Once aligned, the tuberosity fragment is fixated to the constant fragment (sustentaculum fragment). Various plates can be used as a buttress.  Before arthrodesis is performed, CR or ORIF should be attempted DEGAN (J Bone Joint Surg, 64:519, 1982) Type 1 – non-displaced fracture of the anterior process Type 2 – extra-articular, displaced fracture of the anterior process Type 3 – intra-articular, displaced fracture of the anterior process involving C-C joint

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

107

SANDERS (Clinics Ortho, 290:87-95, 1993)  Used for CT evaluation from coronal and axial views  Classified by number of pieces  Lines A and B divide the inferior portion of the posterior talar facet into 3 equal portions. Line C separates the medial and posterior facets. A – lateral B – midline C – medial (at sustentaculum tali) 1 – any number of fracture lines  All non-displaced, extra-articular fractures 2 – one fracture line  Two-part fracture of posterior facet  Use one letter (2A, 2B, or 2C) 3 – two fracture lines  Three-part, intra-articular fracture of posterior facet with depressed central fragment  Use two letters (3AB, 3AC, or 3BC) 4 – three fracture lines  Four-part, intra-articular fracture of posterior facet and sustentaculum fragment with high degree of comminution

Anterior Calcaneal Process Fractures Hannover (Clinics Ortho, 290:76-86, 1993) CT scan evaluation based on fragments involved and number of joint fractures 1 – sustentaculum 2 – tuberosity 3 – STJ 4 – anterior process 5 – anterior STJ * Most common is the 5 fragment/2 joint fracture

Talar Neck Fractures HAWKINS (condensed) Type 1 – vertical fracture of talar neck that is nondisplaced Type 2 – vertical fracture of talar neck with STJ dislocation/subluxation Type 3 – vertical fracture of talar neck with STJ and ankle dislocation/subluxation Type 4 – vertical fracture of talar neck with STJ, ankle, and T-N dislocation/subluxation HAWKINS (J Bone Joint Surg, 60A:143-156, 1978) MOI: hyperdorsiflexion of the foot on leg Type 1 – vertical fracture of talar neck without displacement  Disruption of 1 blood vessel with 12% risk of AVN  Tx: BK cast immobilization for 8-12 weeks, NWB for 6-8 wks  Must have trabeculation across fracture site prior to weightbearing Type 2 – vertical fracture of talar neck with STJ displacement (ankle joint remains aligned)  Disruption of 2-3 blood vessels with 42% risk of AVN 108

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION



Tx: attempt closed reduction by pushing backward on plantarflexed foot while pulling forward on the distal tibia. If successful, percutaneous pinning is performed. Cast in equinus for 4 wks with subsequent casts bringing the foot out of equinus. Requires 3 months of NWB casting.  Tx: after one unsuccessful attempt at closed reduction, ORIF is indicated. Avoid multiple attempts at closed reduction. Longitudinal anteromedial incision along the neck of the talus, just medial to the TA. 6.5 mm cannulated cancellous screws. Use titanium screws to facilitate the later use of MRI to monitor the progress of osteonecrosis. Type 3 – vertical fracture of talar neck with STJ and ankle displacement  Disruption of 3 blood vessels with 91% risk of AVN  25% are open fractures  Tx: during ORIF, it is important not to dissect off deep fibers of deltoid ligament which may remain attached to the talar body (osteotomize the medial malleolus rather than reflect the deltoid) Type 4 – vertical fracture talar neck with STJ, ankle joint and talonavicular joint displacement  Disruption of 3 blood vessels with 91% risk of AVN  Tx: ORIF 10% incidence of calcaneal fractures associated with talar neck fractures 19-28% incidence of medial malleolar fractures associated with talar neck fractures X-rays to provide best view of talar neck  Ankle in maximum equinus  Foot on cassette pronated 15°  X-ray tube directed 75° from horizontal Sclerotic (apparent increase in density) appearance due to surrounding bones becoming osteoporotic due from disuse and acute hyperemia Osteonecrosis is the most common complication associated with this injury Rates of osteonecrosis  Type 1 (0-13%)  Type 2 (20-50%)  Types 3, 4 (83-100%) MRI can define the presence and extent of osteonecrosis in the talar body as early as 3 weeks Hawkin sign – presence of subchondral talar dome osteopenia seen 6-8 weeks after talar fracture signifying intact vascularity. Absence of the sign implies AVN. Up to 36 months are required for complete creeping substitution of the body after union has occurred. Protect the patient from WB until complete revascularization occurs. A patellar tendon brace may partially relieve the load on the talar dome once WB is initiated.

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

109

Blair fusion – if the talar dome collapses, excise the avascular talar body and place a sliding corticocancellous graft from the anterior distal tibia into the residual, viable talar head and neck Subchondral fenestration to increase vascularity and fibrocartilage production

Talar Body Fractures SNEPPEN (condensed) Type 1 – compressive fracture of the talar dome usually involving medial or lateral aspect Type 2 – shearing fracture of the talar body 2A – coronal shearing force 2B – sagittal shearing force 2C – horizontal shearing force Type 3 – fracture of the posterior tubercle Type 4 – fracture of the lateral process Type 5 – crush fracture SNEPPEN (Acta Ortho Scand, 45:307, 1974) Type 1 – transchondral or compression fracture of the talar dome (including osteochondritis of the talus) Type 2 – coronal, sagittal, or horizontal shearing fracture involving the entire body 2A – coronal shearing force 2B – sagittal shearing force 2C – horizontal shearing force  MOA: unknown but thought to be forced dorsiflexion with the foot locked, combined with axial compression  Fractures displaced >2-3 mm at trochlear surface require ORIF  75% incidence of OA of STJ Type 3 – fracture of the posterior tubercle of the talus  Shepherd fracture – posterior lateral tubercle fracture  Sometimes confused with os trigonum. Bone scan can differentiate.  MOA: hyperplantarflexion or avulsion of posterior talofibular ligament  Tx: short leg NWB cast with foot in mild equinus. If pain persists, excise fragment. Type 4 – fracture of the lateral process of the talus  "Snowborder's ankle"  MOA: dorsiflexion with inversion  Tx: 6 weeks of NWB cast immobilization in slight equinus. Large fragments can be internally fixated. Type 5 – crush fracture of the talar body  Poor prognosis  Primary arthrodesis after 2-3 weeks due to risk of soft tissue envelope if performed immediately 23% of open talar fractures go on to osteomyelitis and may result in future talectomy

110

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Boyd & Knight (South Med J, 35:160, 1942) Type 1 – coronal or sagittal shear fracture 1A – non-displaced 1B – fracture with displacement of talo-crural joint 1C – Type 1B with displacement of the STJ 1D – fracture with total displacement of the talar body Type 2 – horizontal shear fracture 2A – non-displaced 2B – displaced

Talar Dome Fractures BERNDT & HARDY (condensed) Stage 1 – nondisplaced compression of talar dome Stage 2 – partially detached osteochondral lesion Stage 3 – completely detached, nondisplaced osteochondral lesion Stage 4 – completely detached, displaced osteochondral lesion BERNT & HARDY (J Bone Joint Surg, 41A:988-1020, 1959) Mechanism: – DIAL A PIMP Stage 1 – nondisplaced, subchondral compression of the talar dome  Tx: conservative, off-loading patellar tendon brace Stage 2 – partially detached, nondisplaced osteochondral fracture  Tx: conservative, off-loading patellar tendon brace Stage 3 – completely detached, nondisplaced osteochondral fracture  Tx medial lesion: conservative, off-loading patellar tendon brace  Tx lateral lesion: surgical excision of the fragment, saucerization of crater, and fenestration to increase vascularity and fibrocartilage production Stage 4 – completely detached, displaced osteochondral fracture  Tx: surgical excision of the fragment, saucerization of crater, and fenestration to increase vascularity and fibrocartilage production Mechanism of Injury: DIAL a PIMP DIAL – Dorsiflexion and Inversion → Anterior-Lateral lesion  Wafer-shaped lesion, associated with trauma PIMP – Plantarflexion and Inversion → Posterior-Medial lesion  Small, deep, round cup-shaped fragment, 80% not associated with trauma Stages 2-4 require lateral ankle ligament disruption to occur Treatments  Tx of Stages 1, 2, and medial 3: NWB Short leg cast for 6-12 wks  Tx of lateral stage 3 and 4: surgical excision of the fragment, saucerize the crater, and

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

111

Lateral Talar Process Fractures Hawkins (J Bone Joint Surg, 47A:1170, 1965) Type 1 – simple fracture of lateral process that extends from talofibular articular surface down to posterior talocalcaneal articular surface of the STJ Type 2 – comminuted fracture of lateral process that involves both fibular and posterior calcaneal articular surfaces of the talus and the entire lateral process Type 3 – chip fracture of anterior and inferior portions of posterior talar articular process

Posterior Lateral Talar Process Fractures Dobas & Watson (Arch Pod Med Foot Surg, 3:17, 1976) Stage 1 – normal posterior lateral process; no clinical significance Stage 2 – enlarged posterior lateral process Stage 3 – non-fused os trigonum Stage 4 – synchondrosis of the os trigonum to the talus McGougall (J Bone Joint Surg, 37B:257-265, 1955) Stage 1 – line of cleavage occurs at impingement point Stage 2 – posterior lateral process begins to separate from the main body of the talus Stage 3 – complete separation of the posterior lateral process from the talar body

STJ Dislocations Buckingham Type 1 – medial STJ dislocation (FF moves medially and talar head moves laterally) Type 2 – lateral STJ dislocation Type 3 – anterior and posterior STJ dislocation

Tarsal Coalitions DOWNEY (JAPMA, 81:187-197, 1991) Juvenile (Osseous Immature) Type 1 – extra-articular coalition A – no secondary arthritis  Tx: Badgley procedure B – secondary arthritis  Tx: resection or triple Type 2 – intra-articular A – no secondary arthritis  Tx: resection, isolated arthrodesis, or triple B – secondary arthritis  Tx: triple Adult (Osseous Mature) Type 1 – extra-articular A – no secondary arthritis  Tx: resection or triple

112

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

B – secondary arthritis  Tx: triple Type 2 – intra-articular A – no secondary arthritis  Tx: isolated or triple B – secondary arthritis  Tx: triple

Chopart Fractures Main & Jowett (JBJS, 57B:89, 1975) Classification based on direction of deforming force and resulting displacement Medial force Type A – flake fracture of dorsal talus or navicular and of the lateral calcaneus or cuboid Type B – medial displacement of forefoot with medial disassociation of T-N and C-C joints Type C – forefoot rotates medially around interosseous talocalcaneal ligament, with T-N disassociation and intact C-C joint Longitudinal force Type A – maximally plantarflexed ankle giving a characteristic pattern of through and through navicular compression fracture Al – force through the 1st ray crushes medial 3rd with tuberosity displaced medially A2 – force through the 2nd ray crushes middle 3rd with middle 3rd and tuberosity displaced medially A3 – force through the 3rd ray crushes lateral 3rd with medial 2/3rd and tuberosity displaced medially Type B – submaximally plantarflexed ankle resulting in dorsal displacement of the superior navicular and crush of the inferior portion Lateral forces Type A – forefoot forced into valgus with resulting fracture of the navicular tuberosity or dorsal talus and a compression fracture of the C-C joint (Nutcracker Fracture) Type B – T-N joint displaces laterally with comminution of the C-C joint Plantar forces Type A – avulsion fracture of the dorsal navicular to talus and the anterior process Type B – impaction fracture of the inferior C-C joint

Ankle Fractures LAUGE-HANSEN 1st word – position of the foot with respect to the leg 2nd word – motion that causes fracture pattern (how talus moves with respect to tibia/fibula) * indicates hallmark sign Supination-Adduction (SAD) – No tib-fib diastasis Stage l – rupture of lateral collaterals or * transverse fracture of lateral malleous below level of ankle joint Stage 2 – * vertical fracture of medial malleolus CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

113

Pronation-Abduction (PAB) Stage 1 – rupture or deltoid ligament or transverse avulsion fracture of medial malleolus Stage 2 – rupture of anterior and/or posterior distal tib-fib ligaments Stage 3 – * short fibular fracture (oblique on AP, trans, on lateral) at level of ankle joint Supination-Eversion (SER) – most common Stage 1 – disruption of anterior tib-fib ligament with either a tibial avulsion (Tillaux-Chaput) or a fibular avulsion (Wagstaffe) Stage 2 – * spiral oblique fracture of the fibula at level of ankle joint Stage 3 – rupture of posterior tib-fib ligament or tibial avulsion (Volkmann) Stage 4 – ruptured of deltoid or transverse fracture of medial malleolus Pronation-External Rotation (PER) Stage 1 – rupture of deltoid ligament or transverse avulsion of med malleolus Stage 2 – disruption of anterior tib-fib ligament with rupture of interosseous ligament and Tillaux-Chaput or Wagstaffe avulsions Stage 3 – * high fibular fracture above level of ankle joint (Maisonneuve fracture) Stage 4 – Posterior tib-fib ligament or Volkmann fracture Pronation-Dorsiflexion (Arch Surg, 67:813-820, 1953) Describes pilon fracture Stage 1 – rupture of deltoid ligament or fracture of medial malleolus (oblique or transverse) Stage 2 – fracture of anterior lip of tibial plafond Stage 3 – fracture of fibula above the level of the syndesmosis Stage 4 – transverse fracture of the distal tibia at the same level as the proximal margin of the large tibial fracture DANIS WEBER (condensed) Describes location of fibular fracture Type A – transverse avulsion fracture below the level of the ankle joint (corresponds with Lauge-Hansen SAD) Type B – spiral or oblique fracture at the level of the ankle joint (corresponds with Lauge-Hansen SER and PAB) Type C – fracture above the level of the ankle joint (Maisonneuve fracture) (corresponds with Lauge-Hansen PER) DANIS-WEBER (Ortho Clinics of NA, 661, 1980) Type A – transverse avulsion fracture of fibula below the level of ankle mortise  MOI: SAD  Tx: K-wire w/ tension band for fibular fracture and 2 interfrag screws for the med malleolus Type B – fracture at the level of ankle mortise  MOI: PAB or SER  Tx: interfrag screws and/or plate, repair ATFL

114

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Type C – fracture above the level of ankle mortise  MOI: PER  Tx: interfrag screws and plate, repair ATFL and interosseous membrane

Pilon Fractures Lauge-Hansen Pronation-Dorsiflexion (Arch Surg 67:813-820, 1953) Stage 1 – deltoid ligament rupture or medial malleolar fracture (oblique or transverse) Stage 2 – fracture of the anterior lip of the tibial plafond Stage 3 – fibular fracture above the level of the syndesmosis Stage 4 – transverse fracture of distal tibia at level of proximal margin of the large tibial fracture RUEDI & ALLGOWER condensed Pilon fractures – distal tibial metaphyseal fracture Type 1 – non-displaced tibial fragments Type 2 – intra-articular tibial fracture without comminution Type 3 – comminution and disruption of tibial articular surface Ruedi & Allgower (Clin Ortho, 138:105-110, 1979) Type 1 – mild displacement, no comminution, without major disruption of ankle joint Type 2 – moderate displacement, no comminution, with significant dislocation of ankle joint Type 3 – "explosion fracture", severe comminution, with displacement of distal tibial metaphysis Femoral distractor – brings tibia out to length before fixation If Type 3 fracture, fix tibia first 40-80% failure of ankle fusion Maale and Seligson (Orthopedics, 3:517-521, 1980) Modification of Ruedi & Allgower Type 1 – distal tibial compression fracture Type 2 – external rotatory fracture with a large posterior fragment Type 3 – spiral fracture extending from the articular surface into the metaphysis Ovadia and Beals (J Bone Joint Surg, 68A:543-551, 1986) Modification of Ruedi & Allgower Type II Type 1 – non-displaced articular fracture resulting from rotational forces Type 2 – minimally displaced fracture resulting from articular forces Type 3 – displaced articular fracture with several large fragments due to compressive forces Type 4 – displaced articular fracture with multiple fragments including a large metaphyseal fragment resulting from compressive forces Type 5 – severe comminution due to compressive forces

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

115

AO System (Ankle Fractures) Type A – extra-articular Type B – partially articular Type C – completely articular All 3 can involve:  No comminution or impaction in the articular or metaphyseal surface  Impaction involving the supra-articular metaphysis  Comminution and impaction involving the articular surface with metaphyseal impaction Destot System Subgroup 1 – posterior marginal tibial fracture Subgroup 2 – anterior marginal tibial fracture Subgroup 3 – explosive tibial fracture Subgroup 4 – supra-articular tibial fracture with extension into the ankle joint Kellam and Waddell (J Trauma, 19:593-601, 1979) Type A – rotational pattern consisting of two or more large tibial articular fragments, minimal or no anterior cortical comminution, and a transverse or short oblique fibular fracture at the level of the tibial plafond Type B – compressive fracture pattern with multiple tibial fragments and marked anterior tibial cortical comminution Mast (Clinics of Ortho, 230:68-82, 1988) Type 1 – malleolar fracture with significant axial load at the time of the injury producing a large posterior fragment Type 2 – spiral extension fracture Type 3 – centrally compressive injury divided into A, B and C

Medial Malleolar Fractures Muller Type A – avulsion of the tip of the medial malleolus, horizontal orientation Type B – avulsion fracture at the level of the ankle joint, horizontal orientation Type C – oblique fracture Type D – vertical fracture

Fibular Avulsion Fractures Pankovich: Wagstaffe-LeFort Fracture (Clinics Ortho Rel Res, 143:138, 1979) Type 1 – avulsion fracture maintaining attachment to both the anterior talofibular and anteriorinferior tib-fib ligaments Type 2 – avulsion fracture associated with an oblique fracture of the fibula originating distal to the anterior-inferior tib-fib ligament. Spiral fracture of the fibula with a proximal fibular spike and a transverse fracture associated with the avulsion fragment. Type 3 – avulsion fracture of the anterior tibial tubercle followed by a Type 2

116

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Lateral Ankle Trauma Leach 1st Degree – rupture of the ATF 2nd Degree – rupture of the ATF and CF 3rd Degree – rupture of the ATF, CF, and PTF O'Donoghue (condensed) Grade 1 – partial ATF tear Grade 2 – complete ATF tear Grade 3 – complete ATF and CFL tear O'Donoghue (Northwest Med, 1277, 1958) Grade 1 – partial ATF tear with mild tenderness and swelling  No loss of function or instability. Pt can walk, play. Grade 2 – complete ATF tear with moderate pain, swelling, ecchymosis  Some loss of function and moderate instability. Pt limps after injury. Grade 3 – complete ATF and CFL tear of with severe pain, swelling, and ecchymosis  Unable to bear weight and severe instability. Pt cannot walk after injury. Dias (J Trauma, 19:266-269, 1979) Grade 1 – partial rupture of the CFL Grade 2 – rupture of the ATF Grade 3 – complete rupture of the ATF, CF, and/or PTF Grade 4 – rupture of all lateral collateral ligaments and partial failure of the deltoid ligament

Posterior Tibial Malleolar Fracture Volkmans Type A – large intra-articular fracture (>25% of surface area) with displacement Type B – small intra-articular fracture (<25% of surface area) with impaction Type C – small fracture with minimal impaction and articular damage Type D – avulsion of posterior-inferior tib-fib ligament without articular involvement

Physeal Injuries Salter-Harris Classification of Fractures Site – epiphysis, metaphysis, diaphysis Extent – complete vs. incomplete Configuration – transverse, oblique, spiral, comminuted Position – rotated, angulated, distracted, impacted, overriding, lateral shift Environment – open, closed

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

117

SALTER-HARRIS (SMACK – Same, Metaphysis, Articulation, Continuous, Krush) (SALTR – Same, Above, Lower, Through, Really bad) 1 – fracture through physis 2 – fracture through physis into metaphysis 3 – intra-articular fracture through physis into epiphysis 4 – intra-articular fracture through epiphysis, physis, and metaphysis 5 – crush injury SALTER-HARRIS (Skeletal Rad, 6:237-253, 1981) Type 1 – complete transverse separation of the epiphysis from the metaphysis through the physis  Epiphysis separates from the metaphysis without any bone fragments  Germ cells remain with epiphysis  Common in infants  Shearing force seen in pathologic fractures  Growth is not disturbed unless there is associated avascular necrosis or premature closure of the physis  Tx: closed reduction if within 7 days of injury, followed by 3-4 weeks of casting Type 2 – fracture through the physis extending into the metaphysis  Thurston-Holland sign  Tx: closed reduction if within 7 days of injury, followed by 3-4 weeks of casting Type 3 – intra-articular fracture extending from the physis through the epiphysis  Tillaux fragment Type 4 – continuous, intra-articular fracture extending from the epiphysis into the physis and metaphysis Type 5 – comminuted fracture from impaction of the epiphysis into the physis and metaphysis  Tx of Types 3-5: attempt closed reduction, but usually requires anatomic reduction of the physis. Fixation should be kept within metaphysis. Rang Type 6 – perichondral injury produced by shearing force resulting in a cup-shaped fragment of epiphyseal, physeal, and metaphyseal bone with possible degloving  Tear of the ―ring of Lacroix‖ Ogden Type 7 – intra-epiphyseal fracture not involving the physis Type 8 – transverse fracture of the metaphysis only Type 9 – diaphyseal growth injury resulting in periosteal elevation and possible degloving of the periosteum Poland Type 1 – separation of the epiphysis from the metaphysis Type 2 – partial separation of the epiphysis from the metaphysis with fracture of the diaphysis  Thurston-Holland sign Type 3 – partial separation of epiphysis from the metaphysis with fracture of the epiphysis Type 4 – complete separation of the epiphysis from metaphysis with fracture of the epiphysis 118

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Peterson (J Ped Ortho, 14:439, 1994) Type 1 – transverse fracture of the metaphysis with extension to the physis by longitudinal compression (15.5%) Type 2 – separation of part of the physis with a part of the metaphysis attached (53.6%)  Thurston-Holland sign  Salter-Harris Type 2 Type 3 – separation of the epiphysis from the diaphysis through the physis (13.2%)  Salter-Harris Type 1 Type 4 – separation of a portion of the physis with extension of a fracture into the joint (10.9%)  Salter-Harris Type 3 Type 5 – fracture involving the metaphysis, physis, and epiphysis (6.5%)  Salter-Harris Type 4 Type 6 – fracture involving a missing portion of the physis.  Often caused by open fractures, lawn mowers, farm machinery, or other power equipment Weber Type A – extra-articular Al – separation of the epiphysis and metaphysis A2 – fragments in the epiphysis or metaphysis Type B – intra-articular Bl – fracture within the physis extending into the epiphysis B2 – fracture through the epiphysis, physis, and metaphysis

MRI Rupture CONTI Stage 1 – 1-2 fine, longitudinal tears Stage 2 – intramural degeneration, variable diameter Stage 3 – diffuse swelling

Achilles Tendon Ruptures KUWADA Type 1 – partial tear <50%  Tx: cast with foot plantarflexed Type 2 – complete tear with <3 cm defect after debridement  Tx: end-to-end attachment Type 3 – complete tear with 3-6 cm defect after debridement  Tx: end-to-end attachment and tendon flap Type 4 – complete tear with >6 cm defect after debridement  Tx: end-to-end attachment, recession, or graft

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

119

Radio-opaque Lesions of Achilles Tendon Morris & Giacopelli (J Foot Surg, 1990) Type 1 – opacities at the Achilles insertion with calcifications within tendon and partially attached to the calcaneus Type 2 – opacities l-3 cm proximal to insertion with lesions separate from calcaneus Type 3A – opacities > 3 cm proximal to insertion with partial tendon calcification Type 3B – opacities > 3 cm proximal to insertion with total tendon involvement

Peroneal Tendon Subluxations Eckert & Davis (J Bone Joint Surg, 58A:670, 1976) Grade 1 – retinaculum and periosteum ruptures from the cartilaginous lip and lateral malleolus Grade 2 – distal edge of fibrous lip elevated with retinaculum Grade 3 – thin fragment of bone with fibrous lip avulsed from deep surface of peroneal retinaculum and deep fascia

Posterior Tendon Ruptures MUELLER 1 – direct injury 2 – pathologic rupture (RA) 3 – idiopathic 4 – functional abnormality

Posterior Tibial Tendon Dysfunction Johnson & Strom Stage 1 – normal tendon length with mild degeneration  Medial foot and ankle pain Stage 2 – supple flatfoot with attenuation or PT rupture  ―Too many toes‖ sign  Abducted forefoot, increased talar-1st metatarsal angle, and uncovering of talar head Stage 3 – rigid flatfoot with complete PT rupture  Fixed calcaneal valgus with decreased STJ ROM Stage 4 – rigid flatfoot  Valgus tilt of talus/ankle mortise leading to lateral tibial/talar degeneration Wilson (J Bone Joint Surg, 54B:677, 1972) Inversion Injury Stage 1 – lateral dislocation of 4 lesser metatarsals with divergent diastasis Stage 2 – Stage 1 with dorsolateral dislocation of 1st metatarsal and other metatarsals Eversion Injury Stage 1 – medial dislocation of 1st metatarsal Stage 2 – dorsolateral dislocation of lesser 4 metatarsals with divergent diastasis

120

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Other Classifications Open Fractures GUSTILLO & ANDERSON (condensed) Type 1 – wound l cm without extensive soft tissue damage Type 3 – extensive skin, soft tissue, muscle, and neurovascular damage 3A – adequate tissue coverage, high energy trauma 3B – periosteal stripping, massive comminution 3C – arterial injury GUSTILLO & ANDERSON (J Bone Joint Surg, 58A:453, 1976) Type 1 – open fracture with wound <1 cm without extensive soft tissue damage  Simple, transverse or short oblique fracture with little comminution  No crush involved Type 2 – open fracture with a laceration >1 cm without extensive soft tissue damage  Slight or moderate crushing injury with moderate comminution  Moderate contamination  Minimal foreign material Type 3 – open fracture with extensive soft tissue damage >5 cm  Severe comminution associated with high velocity injury  High degree of contamination  Significant foreign material  Gunshot wounds, farm injuries, arterial injuries, motor vehicle accidents 3A – adequate soft tissue coverage 3B – extensive soft tissue loss/damage with periosteal stripping and bone exposure requiring local or free flap 3C – any open fracture associated with arterial injury requiring repair. Amputation rate of 25-90%.

Non-Union of Fractures WEBER & CECH Hypertrophic – hypervascular (90%)  Elephant foot  Horse hoof  Oligotrophic Atrophic – avascular (10%)  Torsion wedge  Comminuted  Defect  Atrophic

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

121

Ulcerations WAGNER (Foot Ankle, 2:64-122, 1981) Grade 0 – no open lesions but bony prominence and/or structural deformity present Grade 1 – superficial ulcer without penetration to the deep layers Grade 2 – deep ulcer penetrating to tendon, joint capsule, or bone Grade 3 – Grade 2 depth with the presence of infection Grade 4 – gangrene of the forefoot Grade 5 – gangrene of the entire foot Wound, Ostomy and Continence Nurses Society (formerly I.A.E.T., Standards of Care, 1987) Stage 1 – nonblanchable erythema of intact skin Stage 2 – partial thickness loss of skin involving epidermis, dermis, or both.  Ulcer is superficial and presents clinically as a blister or shallow crater with erythema and induration Stage 3 – full-thickness tissue loss involving damage to or necrosis of subcutaneous tissue that many extend down to, but not through underlying fascia  Ulcer presents clinically as deep crater often with undermining, erythema, and drainage Stage 4 – full-thickness tissue loss with extensive destruction, tissue necrosis, or damage to muscle, bone or supporting structures (e.g. tendon, joint capsule)  Undermining and sinus tracts often associated University of Texas at San Antonio – UTSA (J Foot Ankle Surg, 35:528-531, 1996) Grade 0 – completely epithelialized pre- or post-ulcerative lesion Grade 1 – superficial wound not involving tendon, capsule, or bone Grade 2 – wound penetrating to tendon or capsule Grade 3 – wound penetrating to bone or joint Within each grade, there are 4 subtypes: A – non-ischemic, clean wound B – infected wound C – ischemic wound D – infected and ischemic wound

Diabetic Foot Ulcers Meade & Mueller (Med Times, 96:154-169, 1968) Type 1 – diffuse, inflammatory infection of soft-tissue Type 2 – deep plantar space infection Type 3 – mal perforans neuropathic foot ulcers (subclassed by Wagner and USATHC)

Charcot Sanders & Freykberg 1 – IPJ, phalanx, MPJ, and metatarsals 2 – Lisfranc 3 – C-N, T-N, and C-C 4 – ankle 5 – calcaneus 122

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Osteomyelitis Waldvogel Hematogenous – spread via blood starting inside the bone and working out towards the cortex  Seen most commonly in metaphyseal region of children with open growth plates Direct extension – secondary to trauma or surgery first affecting periosteum, then cortex, and then marrow  Proteolytic enzymes destroy Sharpey fibers Contiguous – spread of infected soft tissue to underlying bone Vascular insufficiency – PVD Cierny & Mader Anatomic Type Medullary Superficial Localized Diffuse Physiologic Type A-Host – good immune system and delivery  Normal immune response  Normal metabolic reserve  Good vascular supply B-Host – compromised locally or systemically  Metabolic compromise  Nutritional compromise  Immunologic compromise  Impaired vascularity  Systemic illness C-Host – no treatment because treatment is worse than disease  Minimal disability  High morbidity  Poor prognosis for cure Buckholz (J Foot Surg, 26(1):17, 1987) Type 1 – wound induced osteomyelitis 1A – open fracture with complete incontinuity 1B – penetrating wound of injury 1C – post-op infections Type 2 – mechanogenic osteomyelitis 2A – implants and internal fixation 2B – contact instability as bone-to-bone appositional movement Type 3 – physeal osteomyelitis Type 4 – ischemic limb disease Type 5 – combination osteomyelitis, Types 1-4 as acute bone infections Type 6 – osteomyelitis with septic arthritis Type 7 – chronic osteomyelitis CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

123

Medicare PVD Classification Class A A1 – nontraumatic amputation of foot or integral portion thereof Class B B1 – absent posterior tibial pulse B2 – advanced trophic changes such as (3 required) 2a – hair growth diminished or absent 2b – nail changes (thickened) 2c – pigmentary changes 2d – skin texture (thin, shiny) 2e – skin color (rubor, redness) B3 – absent dorsalis pedis pulse Class C C1 – claudication C2 – temperature changes (cold feet) C3 – edema C4 – parathesias C5 – burning

Soft Tissue Injuries Tscheme & Gotzen Grade 0 – little or no soft tissue injury Grade 1 – significant abrasion or contusion Grade 2 – deep, contaminated abrasion with local contusion to skin or muscle Grade 3 – extensive contusion or crushing of skin or destruction of muscle

Malignant Melanoma Clark (Cancer Res, 29:705-727, 1969) Based on histological level of invasion Level 1 – located within epidermis or epidermal-dermal junction Level 2 – located within papillary dermis Level 3 – located within papillary-reticular junction Level 4 – located down into reticular dermis Level 5 – located within subcutaneous tissue Breslow (Ann Surg, 172:902-908, 1970) Based on thickness Level 1 – <0.75 mm (99% cure) Level 2 – 0.76-1.5 mm Level 3 – 1.51-4.0 mm Level 4 – >4.0 mm

124

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Polydactyly Blauth & Olason Radiographic and morphological presentation of the deformity Describes position of duplication in both the longitudinal and transverse planes Longitudinal Type – describes degree of duplication of the ray from distal to proximal with a division into 5 types:  Distal phalanx  Middle phalanx  Proximal phalanx  Metatarsal  Tarsal Transverse Type – indicates which rays are involved in the duplication  Classification in Roman numerals starting with the 1st ray and ending with the 5th ray Temtamy & McKusick Preaxial – located on the medial side of a line that bisects the 2nd digit (15%) Postaxial – located on the lateral side (80%) Type A – fully developed Type B – vestigial duplication involving soft tissue Venn & Watson Based on degree of differentiation  Wide metatarsal head  T-metatarsal  Y-metatarsal  Complete duplication

Syndactyly Davis & German Type 1 – Incomplete webbing between two digits Type 2 – Complete webbing to ends of digits Type 3 – Simple with no phalangeal involvement Type 4 – Complex with abnormal phalangeal bones

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

125

126

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Special Studies Bone Scan What are the phases of bone scan? When is each phase done? Phase 1 – Immediate, early, blood flow, or angiogram (it goes by all these names)  2-3 seconds Phase 2 – Blood pool  2-3 minutes Phase 3 – Delayed  2-3 hours Phase 4 – Fourth phase  24 hours What do each of the phases of the bone scan test for? Immediate – Blood flow Pool – Soft tissue Delayed – Bone activity Fourth phase – Bone uptake for patient with PVD What normally lights up on a bone scan? Epiphysis of a growing child Fracture Tips of scapula Bladder Sternum Intercostals (ribs) What is the half-life of Technetium-99? 6 hours What does it mean if the bone scan lights up in Phases 1-2 but not in 3? Cellulitis most likely Name a way to test between Charcot disease and osteomyelitis Ceretec scan or Indium-111 What does Indium-111 tag? WBC’s (as does the Ceretec scan) What does Indium-111 test for? Highly sensitive and specific for acute soft tissue and osseous infections What does Gallium-67 test for? Acute inflammation and infection CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

127

How long does it take for a Gallium-67 test to work? 2-3 days Note: it’s expensive Why would you use a Technetium-99 scan with a Gallium-67 scan? Acute Osteo Chronic Osteo Septic Arthritis Tech-99 + +/+++ Phase 1 ++ + +++ Phase 2 +++ +++ +/Phase 3 Positive focal uptake Negative Positive focal uptake Gallium-67 Positive Negative Positive Indium-111

Tech-99 Phase 1 Phase 2 Phase 3 Phase 4 Gallium-67 Indium-111

Fracture

Acute Cellulitis

Charcot

+++ +++ +++

+++ ++ +

Negative Negative

Positive diffuse uptake Positive

+/+/+++ ++/+++ Negative Negative

MRI What causes increased signal intensity on a T1 image? Fat What causes increased signal intensity on a T2 image? Fluid, Infection, Inflammation, Tumor (F.I.I.T.) For MRI, what are the main indications for STIR imaging? It is useful for evaluation of edema in high lipid regions, such as bone marrow. It is also useful for evaluating cartilage. What is fat saturation used for? Evaluation of fat…c’mon, that’s obvious What is Gradient Echo also known as? Steady State Magnetization What is Gradient Echo used for? Joint imaging

128

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

What are 2 uses for Gadolinium? Intravenously  It will be distributed to places with increased vascularity, such as neoplasms and inflammation  Cellulitis and walls of abscesses will enhance, but the pus will not. Intra-articular  Tests cartilage integrity What will a stress fracture show up as on MRI? T1  Linear zone of decreased signal intensity surrounded by a less defined area of signal intensity T2  Linear zone of decreased signal intensity surrounded by an increased signal intensity due to edema STIR  Increased signal intensity because fatty bone marrow is suppressed How will osteomyelitis show up on MRI? T1  Break in cortex, decreased signal in the bone marrow T2  Break in cortex, increased signal in the bone marrow How will AVN show up on MRI? T1 and T2  Decreased signal intensities STIR and Long T2  Double rim sign: Inner margin will show an increased signal intensity (this represents granulation tissue). Outer margin will show decreased signal intensity (this shows mineralization). What does MRA stand for? Magnetic Resonance Angiography What is MRA used for in the LE? PVD, DVT, neoplasm and anatomic studies Most commonly ordered by a vascular surgeon for further description of occlusions/stenosis

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

129

CT What are the 3 planes of a CT Scan? Coronal Axial Sagittal Which of these planes is computer reconstructed? Sagittal What does the coronal plane of a CT scan represent? Frontal plane (Memorization tip! 1st vowel in coronal and frontal is ―O‖) What does the axial plane of a CT scan represent? Transverse plane (Memorization tip! 1st vowel in transverse and axial is ―A‖)

Miscellaneous What must you D/C before an A-gram? Glucophage because patient may develop metabolic acidosis What are some tests for sickle cell anemia? Microscope and observe Hemoglobin electrophoresis How many phases in a Ceretec scan? One! What does HMPAO stand for? Hexylmethypropyleneamineoxime (a.k.a. Ceretec scan) What does MDP stand for? Methyldiphosphate

130

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Name That Surgery! Note: This section has a variety (but incomplete list) of surgeries with some indications and brief descriptions to help you sift through the vast amounts of procedures that are named after their creators. If you’re going to interview or rotate with a program that has an attending in which a procedure is named after, please know more than what is listed here! Asterisks are next to the most common procedures you should know.

1st Ray & Tailor Bunion Procedures * Akin Indications:

Procedure:

Large DASA → Proximal Akin Long proximal phalanx → Central Akin High hallux abductus angle >15° → Distal Akin Medially based wedge osteotomy of the proximal phalanx

* Austin (a.k.a. Distal Chevron Osteotomy) Note: If you don’t know this one, stop reading this book and find a paper bag to cover your head in shame. Indications: HAV (IMA 12°-14°) Procedure: V-shaped osteotomy with the apex in the center of the metatarsal head and the arms forming a 60° angle * Cheilectomy Indications: Hallux limitus Procedure: Removal of the dorsal bone spur and dorsal ⅓ of the 1st metatarsal head OPTIONAL – Removal of bony prominences from proximal phalanx base * Closing Base Wedge Osteotomy (CBWO, a.k.a. Louisan-Balaceau) Indication: HAV (high IMA) Procedure: Closing wedge osteotomy straight across the base of 1st metatarsal (difficult to fixate) * Crescentic (a.k.a. Weinstock or Arcuate) Indication: HAV (IMA >13°) Procedure: Crescentic osteotomy, (with crescentic blade) concavity directed proximally DRATO Indications: Procedure:

Large 1st IMA + Abnormal PASA + Valgus rotation of 1st metatarsal Derotational osteotomy of the 1st metatarsal head (vertical cut through metatarsal head, cartilage is rotated for realignment, very unstable)

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

131

Hohmann Note: Reverse Hohmann used for Tailor’s bunion Indications: HAV Procedure: Through and through transverse osteotomy at the metatarsal neck (unstable osteotomy) * Juvara Indications: Procedure:

* Kalish Indications: Procedure:

HAV (IMA >15°) Oblique CBWO (apex prox-med, wedge laterally with the base ending in mid ⅓ of the metatarsal, direction allows for better fixation) HAV (IMA ≤15°) Similar to Austin but with a long dorsal arm for screw fixation (angle reduced to 55° between arms)

* Keller Note: Used in patients >50-55 years old Indications: HAV (IMA 16° or less) + Hallux limitus/rigidus Procedure: Resection of the proximal ¼ to ⅓ base proximal phalanx (⅓ more commonly, cut perpendicular to long axis of bone), and cheilectomy with capsular tissue sewn into 1st MPJ space Kessel-Bonney Indication: Hallux limitus Procedure: Removal of a pie-shaped dorsiflexory wedge of bone from proximal phalanx Lambrinudi Indication: Hallux limitus Procedure: Plantarflexory wedge osteotomy of 1st metatarsal base * Lapidus Indication: Procedure:

HAV + 1st ray hypermobility Fusion of 1st metatarsal base to medial cuneiform (with the resections of bone angled to correct the deformity)

Logroscino Indications: HAV (IMA ≥15° in rectus foot, 13° with adductus) + Abnormal PASA Procedure: 1. CBWO (or Crescentic) → to correct HAV 2. Reverdin (or Peabody) → to correct cartilage orientation Loison Indications: Procedure:

132

HAV Transverse CBWO

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Ludloff Note: Opposite orientation to Mau Indication: HAV Procedure: Oblique bone cut diagonally (dorsal-prox to plantar-dist) through the 1st metatarsal. Transpositional osteotomy. Mau Note: Opposite orientation to Ludloff Indication: HAV Procedure: Oblique bone cut diagonally (dorsal-dist to plantar-prox) through the 1st metatarsal. Rotational osteotomy. * McBride Indication: Procedure:

Mild HAV (does not truly correct the HAV deformity) Silver plus soft tissue, capsular releases/tightening

* McKeever (a.k.a. 1st MPJ Arthrodesis/Fusion) Indications: HAV with dislocation Hallux limitus/rigidus Polio, CP, previous joint surgery Procedure: 1. Removal of cartilage on 1st metatarsal head and base of proximal phalanx 2. Remodel the opposing sides to be a matching cone-in-cup shape Hallux Position: Abducted 5°-10° (or parallel to lesser digits) DF 5°-10° off WB surface Mitchell Indication: Procedure:

HAV Distal metaphyseal osteotomy with rectangular block of bone removed and preservation of lateral cortical ―spur‖ (width of spur varied depending on amount of correction needed) that hangs over shaft when transposed.

* Opening Base Wedge Osteotomy (OBWO, a.k.a. Trethowan) Indication: HAV Procedure: Opening base wedge osteotomy (osteotomy across base of 1st metatarsal, then insert a pie-shaped piece of bone graft into the side of the 1st metatarsal cut) Peabody Indication: Procedure: * Reverdin Indications: Procedure:

Abnormal PASA Reverdin done in the 1st metatarsal neck

Mild HAV + Abnormal PASA Medially based wedge (proximal cut perpendicular to long axis 1st metatarsal and distal cut parallel to articular cartilage surface) resection in 1st metatarsal head

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

133

* Reverdin-Green Indications: Mild HAV + Abnormal PASA Procedure: Reverdin osteotomy but in an L-shape (or trapezoidal) to preserve sesamoid articulation * Reverdin-Laird Indications: Moderate HAV + Abnormal PASA Procedure: Reverdin-Green with lateral shift of capital fragment to correct IMA Reverdin-Green-Laird-Todd Indication: Hallux limitus + HAV Allows for correction in 3 planes Procedure: Triangle-shaped wedge removed from both the top and side of the distal 1st metatarsal * Scarf Indication: Procedure: Silver Indications:

HAV (IMA 12°-18°) Z-type osteotomy through the shaft of the 1st metatarsal

Procedure:

Medial 1st MPJ pain Mild HAV (but does not correct the true HAV deformity) Isolated resection of medial eminence of 1st metatarsal head

Stamm Indication: Procedure:

HAV OBWO in medial cuneiform (wedge of graft inserted into medial cuneiform)

Valenti Indication: Procedure:

Hallux limitus Removal of angled (usually 45°) dorsal wedges from the 1st metatarsal and proximal phalanx to increase ROM

* Vogler (a.k.a. Offset-V) Indication: HAV Procedure: V-osteotomy made in the neck of the 1st metatarsal (similar to Kalish but more proximal) Watermann Indication: Hallux limitus Procedure: Removal of closing wedge of bone from 1st metatarsal head to DF capital fragment Watermann-Green Indications: Hallux limitus Procedure: Watermann osteotomy but with a plantar shelf to preserve sesamoid articulation 134

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Wilson Note: Reverse Wilson can be done for Tailor’s bunion Indication: HAV (IMA 12°-14°) HAV + Long 1st metatarsal Procedure: Oblique (dist-med to prox-lat) through and through osteotomy at the 1st metatarsal neck, capital fragment slides laterally on shaft (unstable and slow healing) * Youngswick Indications: HAV + DF 1st metatarsal HAV + Hallux limitus Procedure: Austin but with an extra slice taken out on the dorsal arm to allow the head to drop plantarly and decompress the 1st MPJ Gerbert Indication: Procedure:

Mercado Indication: Procedure:

Tailor’s bunion Wedge osteotomy (transverse or oblique) at 5th metatarsal base. K-wire or screw fixation. Tailor’s bunion Oblique wedge osteotomy at 5th metatarsal neck

Reverse Austin (or Reverse Chevron) Indication: Tailor’s bunion Procedure: Transverse plane V-osteotomy in distal 5th metatarsal with medial transposition and impacted on shaft for fixation (or pin fixation) Reverse Hohmann Indication: Tailor’s bunion Procedure: Transverse osteotomy in distal metaphysis of 5th metatarsal with medial transposition of capital fragment. Fixation not usually used. Reverse Wilson Indication: Tailor’s bunion Procedure: Osteotomy from dist-lat to prox-med to shorten the 5th metatarsal and medial transposition of metatarsal head. Fixation not usually used. Yancey Indication: Procedure:

Tailor’s bunion Oblique or transverse (most stable) wedge osteotomy at 5th metatarsal prox middiaphyseal area. Fixation used.

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

135

Metatarsus Adductus Procedures Bankart Indications: Procedure:

Met adductus + Age 8 years or older Congenital absence of medial cuneiform Excise cuboid (to balance out lack of medial cuneiform)

Brown Indications: Met adductus + Ages 2-6 years old Procedure: 1. Transfer TP into navicular 2. Medial capsulotomy of nav-cun joint Chondrotomy by Johnson Indications: Met adductus + Ages 6-8 years old Procedure: 1. Resect 2.5 mm lateral based wedges (apex medial) of cartilage in metatarsals 2-5, enlarge bases medially 2. Lateral base wedge osteotomy distal to epiphysis of 1st metatarsal 3. Lengthen ABductor hallucis Fowler See Clubfoot Procedure section * Berman & Gartland Note: Most popular osseous procedure for met adductus Indications: Met adductus + Age 6 years or older Procedure: 1. Panmetatarsal base wedges dome-shaped or crescentic osteotomies a. Optional – rearfoot procedures to correct combined deformities 2. Manipulate foot into corrected position, use pin fixation in all metatarsals and cast for 6 weeks Ghali Indications: Met adductus + Ages 2-6 years old Procedure: 1. Heyman, Herndon & Strong procedure 2. PLUS ant-medial release of naviculocuneiform joint * Heyman, Herndon & Strong (a.k.a. Tarsometatarsal soft tissue release) Indications: Met adductus + Ages 2-6 years old Procedure: 1. 3 dorsal incisions (originally one dorsal transverse incision) 2. Capsulotomies and ligament releases of all tarsometatarsal joints (metatarsals 1-5) a. Keep plantar lateral ligaments and joint capsules intact (modification from original to prevent dorsal subluxation)

136

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

b. Optional – syndesmotomy of naviculocuneiform joint and release of TA tendon, also could use K-wires to maintain corrected positions 3. Manipulate metatarsals and foot into rectus position and cast for 3 months Lange Indications: Procedure:

Met adductus + Ages 2-6 years old Capsulotomy of 1st metatarsal-cuneiform, followed by serial casting

Lepird Indications: Met adductus + Age 8 years or older Procedure: 1. 3 dorsal incisions 2. Transverse plane osteotomies in bases of metatarsals 2-4 from dorsal-dist to plantar-prox, parallel to WB surface of foot, fixated with compression screws 3. Oblique base wedge osteotomies of 1st and 5th metatarsals, fixed with compression screws Lichtblau Note: Same name as procedure for clubfoot Indications: Met adductus + Ages 2-6 years old To release abductor hallucis Procedure: Sectioning of abductor hallucis through a small medial incision McCormick & Blount Indications: Met adductus + Age 8 years or older Procedure: 1. Arthrodesis of 1st metatarsal-cuneiform joint 2. Osteotomy of bases metatarsals 2-4 Peabody & Muro Indications: Met adductus + Age 8 years old or older Procedure: 1. Excise bases of metatarsals 2-4 2. Osteotomy of 5th metatarsal 3. Mobilize and reduce subluxation of 1st metatarsal -cuneiform joint 4. Correction of any abnormal insertion of TA tendon 5. Optional – Hoke triple arthrodesis to realign rearfoot when necessary Steytler & Van der Walt Indications: Met adductus + Age 8 or older Procedure: Oblique V-osteotomy (apex of ―V‖ toward rearfoot) of all metatarsal bases Modified from original to include fixation

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

137

Thompson Indications:

Procedure:

Met adductus + Ages 2-6 years old + hallux varus (a.k.a. hallux abductus, severe contraction of abd hallucis) To release abductor hallucis Resect abductor hallucis

Achilles Tendon Procedures * Baker Indication: Procedure:

Bauman Indication: Procedure:

Achilles tendon lengthening Tongue-in-groove cut in aponeurosis with the tongue distal, facing upward Suture aponeurosis bands to one another in retracted position

Gastroc equinus Isolated gastroc recession in the deep interval between soleus and gastroc muscles

Hoke Indication: Achilles tendon lengthening Procedure: 1. Incision 5 cm in length over medial aspect of tendon 2. Triple hemisection of Achilles tendon a. Cut Achilles in half in 3 sections: posteriorly in proximal and distal aspects of incision and anteriorly in central portion of incision b. Modification – cuts med/lat instead of ant/post, can be percutaneous 3. Forcibly DF the foot to allow for sliding into lengthened position Lindholm Indication: Procedure:

Achilles tendon ruptures Two flaps taken proximally from Achilles and reflected distally to fill defect

Lynn Indication: Procedure:

Achilles tendon ruptures End-to-end reapproximation of ruptured Achilles (may reinforce with plantaris)

Fulp & McGlamry Modification (of Baker’s technique) Indication: Achilles tendon lengthening Correction of non-spastic gastroc equinus Procedure: Tongue-in-groove cuts in aponeurosis with the tongue distal, facing downward (inverted version of Baker’s technique) Silfverskiöld Note: Makes a 3 joint muscle into a 2 joint muscle Indication: Achilles tendon lengthening Procedure: 1. Release the gastroc heads at their attachments to the femoral condyles (above knee joint) 2. Reinsertion into the posterior proximal tibia area (below knee joint) 138

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

* Sliding ―Z‖ Lengthening Indication: Achilles tendon lengthening Procedure: Cuts most commonly done in frontal plane but can be in sagittal plane Usually percutaneous, recommended open in McGlamry DF the foot after cutting to separate and lengthen ends of the tendon If open procedure, suture ends of ―Z‖ together in lengthened position Strayer Indication: Gastroc equinus Procedure: 1. Distal recession with the complete transverse cutting of gastroc aponeurosis 2. Proximal retracted portion of gastroc is sutured into the deeper soleus * Vulpius & Stoffel Note: Originally a transverse cut in aponeurosis Indications: Gastroc equinus Procedure: Distal resection of gastroc aponeurosis using an inverted ―V‖ But DON’T suture to soleus White Indication: Achilles tendon lengthening Procedure: 1. Section anterior ⅔ of distal Achilles and medial ⅔ of Achilles (5-7.5 cm proximal to this point) 2. This lengthens the gastroc in relation to its twisting before its insertion

Pes Planus and PTTD Procedures Baker & Hill Indications: Pes planus (to restore alignment of STJ and reduce heel valgus and excess pronation) Cerebral palsy Procedure: Horizontal osteotomy inferior to posterior facet of STJ (in calcaneus, medial cortex intact as hinge) and a wedge-shaped graft inserted Chambers Indication:

Flexible pes planus (more often in children, <8 years old) Rarely performed anymore

Procedure: 1. TAL 2. Bone graft under sinus tarsi (similar to location of arthroereisis to block translocation of talus on the calcaneus)

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

139

Chiappara Indication: Pes planus Procedure: 1. Silver (opening wedge calc osteotomy from lateral side) with TP advancement 2. TA tenodesis to TP Cobb Note: Good procedure because FDL preserved Indications: PTTD Pes valgus Procedure: 1. Hemi-section of TA (more medial portion released, other half left intact at insertion near ankle level) 2. Lay released portion of TA along TP tendon and suture together * Cotton Indications:

Pes planus PTTD Medial column repair (to get structural PF of medial column)

Procedure: 1. Medial (and sometimes intermediate cuneiforms) osteotomy dorsal to plantar (maintaining plantar cortex intact) 2. Triangular shaped bone graft (base measuring 4-7mm) inserted in osteotomy. No fixation necessary. * Dwyer Indication: Procedure:

Pes planus To produce calcaneal varus Closing wedge osteotomy from medial side (difficult due to possible nerve entrapment)

* Evans Calcaneal Osteotomy Note: Same name as procedures indicated for clubfoot and lateral ankle instability Indications: Pes valgus foot deformity To lengthen calcaneus Procedure: 1. Incision over C-C joint, reflect EDB 2. Osteotomy of calcaneus parallel and 1-1.5 cm (dist ⅓) prox to C-C joint 3. Wedge of graft inserted into osteotomy (lateral side of graft up to 1 cm in kids and max 7 mm in adults) Gleich Indication: Procedure:

140

Pes valgus foot deformity (especially frontal plane dominant) Oblique calc osteotomy (posterior calc osteotomy) displaced anteriorly (to ―restore the normal angle of the long axis of the calc to the floor‖)

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

* Hoke Arthrodesis Note: Not to be confused with the Hoke Achilles procedure Indication: Pes planus Medial column repair Usually done in conjunction with ankle equinus correction and calcaneal osteotomies or arthroeresis Procedure: 1. TAL 2. Fusion of navicular to medial and intermediate cuneiforms * Kidner Indications:

Pes planus Kidner foot type (accessory navicular and/or enlarged navicular) Medial column repair

Procedure: 1. Detach TP from navicular medially 2. Resect accessory navicular and/or bump from navicular 3. Reattach TP to navicular more plantarly (tendon bone anchors commonly used) * Koutsogiannis (nickname ―Kouts‖) Note: Sometimes combined with Evans osteotomy for PTTD Indication: Pes valgus foot deformity Restores heel valgus, less so in restoring medial longitudinal arch. Also shifts the functional insertion of the Achilles medially. Procedure: 1. Medial displacement of an oblique osteotomy of calcaneus from lateral incision a. Posterior portion of calcaneus ―slides‖ medially ⅓ to ½ the width of calcaneus until it sits just below sustentaculum tali 2. K-wire, Steinmann pins, or lag screw fixation Lord Indication: Procedure:

Lowman Indications:

Pes planus A Gleich (oblique calcaneal osteotomy) displaced anteriorly, medially, and inferiorly

Pes planus Medial column repair

Procedure: 1. TAL 2. Talo-navicular wedge arthrodesis 3. Reroute TA under navicular and suture into spring ligament 4. Tenodesis of medial arch by taking slip of TA and reflect downward (leave its insertion to the calcaneus intact) along medial arch

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

141

Miller Indications:

Pes planus (more often appropriate in adults than children) Medial column repair

Procedure: 1. TAL 2. Medial column fusion (navicular to medial cuneiform to 1st metatarsal) 3. Resect hypertrophy of navicular (use as bone graft for fusion sites) 4. Advance medial soft tissues Peroneus Brevis Tendon Transfer (PBTT) Indication: Type 1 vertical talus Severe pes planovalgus Procedure: Detach PB and reroute dorsally to talar neck ALT – Detach PB and transfer to lateral cuneiform or 3rd metatarsal Selakovich Indication:

Flexible pes planus + Ages 5-9 years old Congenital vertical talus (flexible/supple deformity) + Ages 5-9 years old

Procedure: 1. Osteotomy and grafting of sustentaculum tali a. Osteotomy performed midway between interosseous talocalcaneal ligament and post margin of sustentaculum tali b. Wedge bone graft inserted to redirect the middle and anterior facets 2. Tightening of medial structures (tightening redundant spring ligament and repositioning of the TP) 3. Reroute half or all of TA into navicular Silver or Opening Wedge Dwyer Indication: Pes planus Procedures: 1. Opening wedge calcaneal osteotomy from lateral incision a. Oblique osteotomy from just post to post facet inferiorly to just prox to C-C joint b. The more proximal and anterior the osteotomy, the greater correction 2. Graft insertion into osteotomy a. Average wedge size ¼ inch, no fixation needed * STJ Arthroereisis Indication: Flexible pes valgus + patient not yet at skeletal maturity (or if arthrodesis not appropriate in older patient) Procedure: 1. Incision 2-4 cm long parallel to relaxed skin tension lines over sinus tarsi. Incise deep fascia to expose lateral talar process, post facet and sinus tarsi floor. 2. Further steps of dissection depend on the specific device you are using a. MBA (Maxwell-Brancheau Arthroereisis) implant, STA-peg device

142

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Young Tenosuspension Note: Often done in conjunction with other procedures Indications: Pes planus + Age 10 years or older Patients with navicular-cuneiform fault but no DJD yet Helps to PF 1st ray (takes away TA antagonist action against PL) Procedures: 1. TAL 2. Reroute TA through keyhole in navicular (do not detach TA from insertion) a. Alternate – detach TA from insertion and reattach after passing through a trephine hole in navicular 3. TP reattachment beneath navicular (creates a powerful plantar navicular-cuneiform ligament)

Lateral Ankle Instability Procedures * Brostrom-Gould (or just Brostrom) Note: Common procedure used, see Special Surgery Section for details Indication: Lateral ankle instability For primary repair Procedure: 1. Incise lateral ankle capsule 2-3 cm distal to lateral malleolus 2. Evert foot and tighten capsule including ATFL and CFL in pants over vest fashion with non-absorbable suture 3. Mobilize extensor retinaculum, pull it over capsule and suture down * Christman & Snook Note: Could use PL instead of PB for this procedure Indication: Lateral ankle instability To reinforce ATFL and CFL Procedure: 1. Detach half of PB from its insertion 2. Reroute it through a drill hole in the talar neck and distal lateral malleolus (through widest part, anterior to posterior). Suture graft tendon to periosteal flap at level of CFL. 3. Distal half of PB then sutured to proximal half Elmslie Indication: Procedure:

Lateral ankle instability To reinforce ATFL and CFL Tensor fascia lata routed through calcaneus, then lateral malleolus, then talus, back through lateral malleolus and back through calcaneus

Evans Note: Same name as osteotomies indicated for pes planus and clubfoot. Similar to Nilsonne but with an osseous tunnel instead of subperiosteal tunnel. Indication: Lateral ankle instability Reinforces ATFL only (this does not reconstruct ATFL or CFL anatomically)

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

143

Procedure: 1. PB is detached proximally 2. Reroute it through fibular drill hole (anterior-most and distal-most → post-prox location). PB secured posteriorly at prox aspect of superior peroneal retinaculum. 3. Prox PB is attached to PL Hambly Indication:

Lateral ankle instability Reinforces ATFL and CFL

Procedure: 1. Split PL 2. Reroute into talus (or attached through it), through a lateral malleolus drill hole (anterior to posterior), through calcaneus and attached to the other half of the PL Kelikian Indication:

Lateral ankle instability Reinforces ATFL and CFL

Procedure: 1. Isolate the plantaris tendon 2. Reroute it from the calcaneus into lateral malleolus through a drill hole (posterior to anterior), back through the calcaneus then sutured on itself Lee Indication:

Lateral ankle instability Reinforces ATFL only

Procedure: 1. PB detached proximally 2. Reroute it through lateral malleolus drill hole (post → ant) and sutured upon itself (peroneal anastomosis) 3. Periosteal flap from dist fibula reinforces new ligament 4. Prox PB attached to PL Nilsonne Indication:

Lateral ankle instability Reinforces ATFL only

Procedure: 1. PB detached proximally at musculotendon junction 2. Reroute it through subperiosteal groove through fibula (post-superior → ant-inferior), CFL primarily repaired if necessary 3. PB secured in subperiosteal tunnel (this approximates ATFL course) 4. Prox PB attached to PL Seeburger Indication:

144

Lateral ankle instability Reinforces ATFL and CFL

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Procedure: 1. Use a hemi-section of PL 2. Reroute it from talus into lateral malleolus and into calcaneus Watson-Jones Indication: Lateral ankle instability Reinforces ATFL only Procedure: 1. PB detached proximally 2. Reroute it through lateral malleolus (drill hole posterior to anterior ~2 cm from distal tip of fibula) into talar neck (vertical drill hole dorsal to plantar), then back through lateral malleolus (along ATFL course) and sutured on itself posterior to fibula 3. Proximal PB attached to PL Whinfield Indication:

Lateral ankle instability Reinforces ATFL and CFL

Procedure: 1. PB detached proximally while maintaining distal attachment 2. The detached portion is rerouted through a lateral malleolus drill hole (anterior to posterior) and inserted into calcaneus

Clubfoot Procedures Baja Project Indication: Clubfoot Procedure: 1. Cuboid decancellation procedure 2. Laterally based triangular wedge of bone removed from cuboid and lateral cuneiform * Dwyer Note: Indicated also for pes planus but wedge done laterally instead of medially (calcaneus goes into varus) Indication: Clubfoot Cavus foot deformity Procedure: Opening wedge medial calcaneal osteotomy Calcaneus goes into a more valgus position * Evans Note: Same name as procedures indicated for pes planus and lateral ankle instability Indication: Clubfoot Procedure: Shorten lateral column by calcaneal-cuboid fusion

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

145

Fowler Note: Often done in conjunction with other procedures, especially if more rigid deformity Indications: Residual clubfoot deformity Cavovarus deformity Met adductus + Age 8 years or older Procedure: Bone graft inserted into medial cuneiform with opening wedge osteotomy to lengthen medial column Modification – closing wedge osteotomy of cuboid and lateral cuneiform, then use this bone as the graft for the opening medial cuneiform osteotomy. Good with ages 3-10 years old, residual adduction, or varus deformity in forefoot/midfoot. Lichtblau Note: Same name as a procedure for met adductus Indication: Clubfoot Procedure: Closing base wedge osteotomy of anterior calcaneus (base of wedge lateral, shortens lateral column) Lund Indication:

Clubfoot (neglected or arthrogryphotic neuromuscular type) + Ages 2-5 years old (ideally, occasionally in adults)

Procedure: Talectomy (foot posteriorly displaced allowing for correction in sagittal and frontal planes) Optional – portions of navicular and fibula may need to be resected. Also may use midfoot wedges adjunctively. Often multistaged. Fixation with Steinmann pin from calc to tibia for pseudojoint space. Long leg casting for 1 month to BK cast for 4 months.

Miscellaneous Procedures Hibbs Indication: To decrease MPJ buckling and increase DF Procedure: 1. EDL is detached from insertion and reattached to lateral cuneiform or 3rd metatarsal 2. Distal stubs of EDL are attached to EDB at metatarsal head area * Hoffman Note: Often done with Keller arthroplasty Indications: MPJ subluxation secondary to rheumatoid arthritis and fat pad atrophy Procedure: Resection of metatarsal heads 2-5 Hoffman-Clayton Indications: MPJ subluxation secondary to rheumatoid arthritis and fat pad atrophy Procedure: Resection of metatarsal heads 2-5 and bases of proximal phalanxes

146

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

* Jones Indications:

Cock-up hallux Weak TA (procedure enhances DF)

Procedure: 1. EHL is detached and inserted into 1st metatarsal head via a med → lat drill hole 2. IPJ fusion 3. Stump of EHL is attached to EHB Murphy Indication: Procedure:

Spastic equinus Anterior transfer of TA into calcaneus Modification – route under FHL

OATS (Osteoarticular Transfer System) Indication: Posterior medial talar dome osteochondral lesion Procedure: 1. Take a plug of bone with articular cartilage from the knee 2. Through a trans-tibial approach, insert it into the talus (matching the contours of cartilage on graft to dome of talus) Peroneus Longus Tendon Transfer (PLTT) Indication: Drop foot Anterior muscle weakness Flexible cavus deformity Procedure: 1. Cut PL near PB insertion site, suture distal PL to PB 2. Reroute it dorsally to 3rd cuneiform Silver & Simon Indication: Spastic equinus Procedure: 1. Proximal release of gastroc without reinsertion of heads 2. Neurectomy of tibial branches to medial head of gastroc * Split Tibialis Anterior Tendon Transfer (STATT) Note: Same as TATT but only half the tendon is used. See Special Surgery Section for details. Indications: To increase true ankle DF and decrease long extensor swing phase To decrease adductovarus forefoot Procedure: 1. Detach half of TA from its insertion 2. Reroute and insert it into peroneus tertius (or cuboid, if peroneus tertius isn’t present) Stoffel Indication: Procedure:

Correction of spastic muscular forms of ankle equinus Selective denervation of tibial nerve

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

147

Tachdjian-Grice Note: Grice procedure = STJ arthrodesis Indications: Congenital convex pes planovalgus (vertical talus!) + Ages 4-6 years old Procedure: 1. First stage: TAL with posterior ankle and STJ capsular release 2. Second stage: (3 weeks later) STJ extraarticular arthrodesis Tibialis Anterior Tendon Transfer (TATT) Note: The STATT is slightly preferred due to fewer complications. See Special Surgery Section for details. Indications: To decrease forefoot supinatory twist To increase true ankle DF Procedure: 1. TA is detached from its insertion 2. Reroute and insert it into lateral cuneiform or 3rd metatarsal (or inserted into peroneus tertius if present) Tibialis Posterior Tendon Transfer (TPTT) Note: See Special Surgery Section for details. Indications: Drop foot To eliminate flexor substitution Procedure: 1. TP is detached at its insertion site on the navicular 2. It is then rerouted through the interosseous membrane of the tibia and fibula, brought anteriorly and then inserted into the lateral cuneiform

148

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Special Surgical Section This section is based on my notes on how to do a select few rearfoot and ankle cases. Basically, the outlines are a combination of McGlamry’s, Coughlin’s, and Kitoaka that I used in my third year to prepare for the cases. Obviously, my notes are only one of many ways to do the cases. I have included my notes here as a quick outline reference. As always, it is up to the reader to go to the original sources to learn the material. --Brett

We also used McGlamry and Coughlin & Mann to prepare for cases. We have included a few additional notes that we found helpful. --Hubert & Sandi

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

149

Achilles Tendon Rupture   





 



150

Frequently in ―Weekend Warriors‖ men 30-50 yrs old Location of tear usually occurs in the ―watershed area‖ (2-6 cm proximal to the Achilles insertion) though avulsions and myotendinous junction ruptures are also possible Clinical Exam o Patient can PF because of posterior tibialis but can’t do a one-legged heel raise o Positive Thompson test (squeezing the calf reveals an absence of ankle plantarflexion) o Palpable gap, although this may be less obvious with edema after 24 hours Surgery vs Conservative Tx o Younger people tend to do better and recover faster with surgery over conservative methods o Older, non-active people tend to do better with conservative methods Conservative Treatment o PF cast for 2 weeks NWB o Increase DF (but still PF) for 2 more weeks. Continue NWB. o At 4 weeks, if can cast in neutral, pt can WB o At 8 weeks, D/C cast and use CAM boot for 4 more weeks. A 2-2.5 cm heel lift can be put in shoes. Begin passive ROM. o At 12 weeks, start active exercises in regular shoe (with ¼‖ to ½‖ heel lift) Pre-op Tx o Jones compression dressing with mild PF of foot Procedure o Patient set-up  Prone  General or spinal  Thigh tourniquet 1. Incision: medial aspect of the Achilles tendon from just above the myotendinous junction to insertion on calcaneus. Incision is down to paratenon. a. Use very careful dissection as this area is very avascular b. Watch out for: i. Plantaris medially ii. Sural nerve perforates the Achilles tendon centrally at the myotendinous junction and then courses laterally iii. Lesser saphenous vein may also run with the sural nerve 2. Incise the paratenon. The paratenon should be opened as part of the full thickness flap. Get good exposure to the tendon. For End-to-end or mid-tendon ruptures 3. Irrigate, debride the mop-top ends of tendon 4. Reapproximate using Bunnel, Kessler or Krackow type of suture using 3-0 or 2-0 Ethibond or other non-absorbable polyester suture 5. Reinforce site with 1-0 or 2-0 Vicryl in a circumferential stitch. Irrigate again. 6. Close paratenon with 3-0 Vicryl, subcutaneous, then skin

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION







For Myotendinous junction ruptures (Reverse Lindholm’s technique) 3. Rather than inverted strips of tendon being raised from prox → dist (as in Lindholm’s technique), go dist → prox 4. Weave inverted tendon into place 5. Suture with Bunnel, Kessler or Krackow technique, similar to end-to-end repair 6. Reinforce with Vicryl circumferential suture, close subcutaneous and skin For Avulsion ruptures 3. Extend incision distally past insertion of Achilles onto calcaneus 4. Debride calcaneus of fibrous tissue, debride down to cancellous bone 5. Make 2 drill holes longitudinally to each other and put non-absorbable suture in tendon (i.e. half a Kessler) bring suture through drill holes and tie over itself or (more commonly now) use suture bone anchors 6. Close Post-op o Jones compression dressing for 7-10 days o NWB BK cast for 2-3 weeks  Cast in 20° PF for avulsion and mid-tendon ruptures  Cast in neutral for myotendinous ruptures o After the PF cast, cast in neutral position (have the patient rest foot on a footrest for 1520 min to gently allow the foot to go to neutral or close). WB BK cast for 2-4 weeks or CAM boot (removable walking cast) here instead. Pt may also start passive ROM. o After casts, return to regular shoes with a 1‖ heel lift o Aggressive walking may begin around 10 weeks post-op o Return to sports at 14-16 weeks post-op o Note: Pt may not be able to get full DF of foot for 3-6 months

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

151

Delayed Repair of Achilles Tendon 



 



152

Clinical Presentation o At time of rupture, pt feels as if struck in the back of the calf o Pt complains of weakness in PF o If pt has progressive degenerative changes to Achilles tendon, insidious onset o Often rupture is not palpable o Tendon tends to be thicker as it progressively gets longer Areas of Ruptures o At tendon 2-6 cm from insertion o At myotendinous junction o Calcaneal avulsion Conservative Treatment o Heel lifts, lace up shoes, MAFO, braces o BUT…these won’t restore normal push-off Indications for Surgery o Restore normal push-off power o Take X-rays and MRI  If >3 cm defect and >3 months → end-to-end suture (as in Acute Achilles repair) Procedure o Patient set-up  Prone  General or spinal  Thigh tourniquet o For mid-tendon tear 1. Posterior medial incision over Achilles from just above myotendinous junction to past calcaneal insertion. Make full thickness incision to paratenon. 2. Incise paratenon, reflect with full thickness flap 3. Irrigate, clean up mop-handle like edges o If >3 cm tear 4. Kessel, Bunnel or Krackow type suture with 3-0 Ethibond 5. Reinforce ends circumferentially with 2-0 or 3-0 Vicryl o If gap is approx 3 cm → inverted V-Y advancement is done 4. Inverted V-Y – leaving underlying muscle attached to the paratenon 5. Advance the distal flap distally 6. Close the defect via Kessel, Bunnel, or Krackow with 3-0 Ethibond 7. Reinforce ends circumferentially with 2-0 or 3-0 Vicryl o If gap is much greater than 3 cm → V-Y advancement, close end-to-end, reinforce with FHL  Inverted V-Y will have to be done at an acute angle and will make the tendon very thin…which is why you have to reinforce with FHL  FHL Transfer 1. Incision is on medial border of midfoot, from the navicular to head of 1st metatarsal, just above the level of the abductor muscle (approximately where plantar skin meets regular skin) CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

2. Dissect down to the layer of the abductor hallucis fascia. Reflect the muscle downward. Retract with Weitlaner. 3. FHB is reflected plantarly 4. Identify the FHL (medial) and FDL a. These are usually covered by a fatty layer b. Flex the IPJ of the hallux, and the FHL can be identified 5. Section the FHL as distally as possible, generally at midshaft of 1st metatarsal 6. Tag prox part of FHL. Suture distal FHL to FDL with the toes in neutral position. o Posterior Medial Incision 1. Posterior medial incision over Achilles from just above myotendinous junction to past calcaneal insertion. Make full thickness incision to paratenon. 2. Incise paratenon, reflect with full thickness flap 3. Irrigate, clean up mop-handle like edges 4. Incise the fascia overlying the FHL. By pulling on the suture from the FHL, you can identify the muscle. 5. Retract the tendon through post-medial incision 6. Make transverse drill hole into posterior calcaneus just distal to insertion of calcaneus halfway from medial → lateral 7. 2nd drill hole goes from prox → dist to intercept the holes in calcaneus. A large towel clip is used to connect the 2 holes. 8. A suture passer is inserted in the dist-medial hole upward. The FHL is attached to it and the FHL tendon is passed from prox → dist-medial. 9. The FHL is then woven into the Achilles tendon from dist → prox and repeated to use the full length of FHL tendon. 10. The tendon is secured with Ethibond 11. Repair paratenon, then close in layers 

Post-op o Jones compression dressing and plaster splints with foot in 15° PF until first post-op visit (7-10 days) o BK cast with foot in 15° PF for 4 weeks o Cast foot in neutral with BK walking cast or removable cast boot for 4 weeks  Put foot on footrest with hip flexed. Allow foot to passively go to neutral. o At 8 weeks post-op, begin strength training and ROM exercises o Patient remains in removable cast boot until the 10° of DF and 4/5 PF strength is achieved o Half-inch heel lift is added to their shoe. Home exercises are performed at this period. o Athletic activity restricted for 6 months

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

153

Excision of Calcification of Achilles Tendon  Procedure o General or spinal o Prone is ideal o Thigh tourniquet  Have Mitek anchor or other kind of anchor in room 1. Incision: from the superior-medial of the Achilles tendon (can go 1 cm medial to tendon and 3-4 cm proximal to spur or tuberosity)lateral (2-3 cm distal to spur or tuberosity), with the horizontal part over the spur a. Note: can go the other direction which may keep away from sural nerve 2. Dissect in layers, tag paratenon 3. Incise Achilles tendon longitudinally (Lateral ½ = Medial ½). Keep distal attachments of Achilles, if possible. a. If total resection of Achilles tendon must be performed, remove all bony prominences and treat it like a ruptured Achilles tendon i. Can drill holes and use non-absorbable suture (ie fiberwire) or Mitek bone-tendon anchor 4. Reflect Achilles tendon side to side, remove any intra-tendon calcification 5. Deepen incision—remove retrocalcaneal bursa 6. Release any paratenons fibrosing or scaring a. Expose any posterior calcaneal exostosis b. Can resect calcaneal exostosis with an osteotome 7. Repair Achilles tendon with 2-0 Vicryl in running suture 8. Close  Post-op o 3-6 weeks NWB in cast (if necessary) o 3-6 weeks in a WB boot

154

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Murphy Procedure – Achilles Tendon Advancement 

Indication o Spastic equinus o Plantarflexory force of gastroc-soleus complex at ankle joint is weakened with minimal decrease of toe-off force



Procedure 1. Incision 5 cm slightly medial to midline of Achilles tendon 2. Dissect down to deep fascia and paratenon. Incise and tag the paratenon. Do not dissect in layers because this will lead to soft tissue necrosis. 3. Detach TAL from its insertion to the calcaneus a. If child, careful not to disturb the calcaneal apophysitis 4. Reroute the TAL under the FHL (if desired) 5. Divide the fat over the calcaneus, then resect a 0.5 cm wedge of bone from calcaneus just posterior to posterior facet 6. From that wedge, make 2 drill holes, one exiting medially, one exiting laterally 7. Use a Bunnell technique to the distal end of the TAL with either an absorbable (1-0 Vicryl) or non-absorbable (1-0 Ethibond) suture 8. Bring one of the loose end strands through the medial drill hole, and bring the other strand laterally 9. With the foot in neutral, guide the tendon into the wedge and tie the sutures over the dorsal surface of the calcaneus, anterior to Achilles tendon 10. Close, cast in AK cast with knee slightly flexed, foot in neutral

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

155

Ankle Arthrodesis 

Ideal position o Ankle neutral (no DF or PF) o 5° valgus o External rotation equal to opposite limb



Procedure o Patient set-up  Prone with sandbags  Thigh tourniquet  General or spinal



Lateral approach 1. Incision is curved starting approx 10 cm proximal to fibula to base of 4th metatarsal a. Avoid sural and intermediate dorsal cutaneous nerves 2. Create skin flaps 3. Strip periosteum from fibula (reflect anteriorly and posteriorly) 4. Incision is carried down to expose posterior facet of STJ and sinus tarsi 5. Use a periosteal elevator to strip the tibia, ankle joint and prox talar neck (med → lat) a. Do NOT dissect talar neck except for prox portion. You don’t want to strip off the blood supply to the talus! 6. Osteotomize the fibula approx 2 cm prox from ankle joint a. Bevel the cut proximal-lateral to distal-medial so you don’t leave a sharp edge b. Remove distal portion of the fibula c. Reflect peroneal tendons posteriorly 7. Make incision through deep fascia at post tibia. With a periosteal elevator, strip the soft tissues off the tibia. a. This is visualized after fibula is removed 8. The initial cut in the tibia is with the short wide blade, then complete with the long wide blade a. Cut is perpendicular to long axis of bone b. Remove as little bone as possible c. Stop cut where the tibia curves for the medial malleolus



Medial approach 1. Incision is 4 cm over the anteromedial aspect of the medial malleolus and directed slightly inferior so that the medial tip of the medial malleolus can be exposed 2. Strip soft tissue anteriorly a. Do as little damage to deltoid ligament as possible 3. With a size 10 osteotome, cut along the medial malleolus to finish the initial tibial cut while freeing up the initial portion

156

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION



Lateral incision 1. With a broad osteotome, wedge out the tibial cut using gentle levering 2. In the talus, cut 3-4 mm from the superior surface 3. Check alignment and remove more bone if needed



Fixation 1. Temporary fix with 0.062 K-wire a. Check position relative to patella b. Place two 3.2 drill bits, one in sinus tarsi and one just above lateral process c. Check position 2. Insert two 6.5 mm screws from lat-distal → med-prox a. Note: There are multiple specialty plates available specifically for this procedure that may change the way you do your fixation 3. Be sure to engage medial cortex of tibia 4. If soft bone, use a washer a. Check rigidity of arthrodesis site b. Optional – Can put 3rd screw through medial incision c. Optional – Fixation of fibula with 4.0/4.5 mm cancellous screw 5. Closure a. Use a drain b. Deep closure, etc. c. Administer marcaine block d. Compression dressing and splint

 Post-op 1. Leave post-op dressing in place for 10-12 days, change and remove stitches 2. Put patient in BK cast, NWB 3. Do not use removable cast because they don’t provide enough support 4. At 6 weeks, X-ray. If healing begins to appear, use BK WB cast. 5. At 12 weeks, if satisfactory healing, can WB 6. Avg fusion time: 14 weeks 7. Avg shortening: 9 mm

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

157

Tibial-Calcaneal Arthrodesis 

Procedure o Patient set-up  Supine with bump under ipsilateral hip  Thigh tourniquet  General or spinal



Lateral Approach (similar to lateral approach in Tibiotalar arthrodesis) 1. Incision 10 cm proximal to tip of lateral malleous across the tip of the lateral malleolus and toward the 4th metatarsal base a. Watch out for sural nerve and superficial peroneal nerve 2. Strip the periosteum from the anteroposterior aspect of the fibula, the lateral aspect of the talus, and the calcaneus 3. The distal portion of the fibula is removed approx 1.5 cm above the level of the distal tibia 4. Dissect over the anterior portion of the tibia to the medial malleolus 5. An incision is made over the posterior aspect of the tibia, and the periosteal elevator is passed along the back of the tibia to the level of the calcaneus a. The entire lateral aspect of the ankle joint and talus is now exposed 6. Using a saw, cut the talar neck, from lat → med just distal to the dorsal articular cartilage of the talus 7. Remove the talus body a. The calcaneal articular surface can now be visualized 8. Remove the articular cartilage of the tibia perpendicular to the long axis of the tibia a. Starting approximately 2 mm above the cartilage, remove as little bone as possible 9. With the foot in plantargrade position, remove the dorsal aspect of the calcaneus. This creates a flat surface for the arthrodesis. a. This includes the posterior and middle facets but leaves the sinus tarsi intact b. Do not violate the C-C joint or the anterior process of the calcaneus



Medial approach 1. Incision over the anteromedial aspect of the joint and carry it out distally past the tip of the medial malleolus for about 2cm to the TN joint 2. Strip the periosteum from the medial malleolus (the portion uncut from the osteotomy) 3. Remove this portion of the medial malleolus, usually by osteotome a. Be careful of the neurovascular bundle at the posterior medial portion of tibia



Remember your alignment (5° of dorsiflexion and 5° of valgus) 1. If necessary, remove bone from tibia or calcaneus to achieve it 2. The fusion site should be posterior enough for normal posterior curvature of the heel 3. Make cut in anterior aspect of the tibia parallel to the cut made in the talar neck 4. Drill surfaces of arthrodesis sites

158

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION



Internal Fixation 1. Use 0.062 K-wires for temporary fixation a. Check alignment 2. Insert 7.0 or 7.3 cannulated screws from posterior calcaneus to anterior portion of tibia a. If possible, insert two screws b. The screws are more plantar than in a subtalar arthrodesis, even if this means you are on a WB surface c. Can throw a third screw from tibia to calcaneus post → ant or apply a blade plate 3. Fixate the talus to tibia with two 4.0 screws 4. Note: There are multiple specialty plates available specifically for this procedure that may change the way you do your fixation 5. Check alignment with C-arm 6. Close

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

159

Subtalar Arthrodesis 

Procedure o Patient set-up  Prone  Thigh tourniquet 1. Lateral incision over sinus tarsi from tip of lateral malleolus to 4th metatarsal base 2. Free the EDB from its attachment to calcaneus 3. Incise the fatty plug longitudinally 4. Retract the peroneals plantarly 5. With lamina spreader, spread the sinus tarsi. 6. Remove articular cartilage with rasp, curette, osteotome or rongeur a. Preserve the shape and contour of the bones b. Be careful not to violate the tibio-talar joint 7. Make a stab incision. Put guide wire in calcaneus. 8. Put heel in 5˚-10˚ of valgus a. After the heel is in good position, advance wire into talus b. X-ray and advance 7.0 mm cancellous screw with 16 mm thread length 9. Test strength of fusion 10. Optional – 2nd screw through same incision. 11. If not stable, remove hardware and insert a screw through talar neck into calcaneus. 12. If bone graft is needed, you can take part of the anterior process of calcaneus. Or use Grafton.



Post-op o First 48˚ Jones compression dressing with splint o Then BK cast NWB for 6 weeks (remove stitches at 3 weeks) o BK WB cast for 4-5 weeks until radiographic evidence of healing o Eventually rehab with or without PT

160

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Talo-Navicular Fusion  Good results in low activity patients  High demand patients should probably add a C-C fusion (double arthrodesis)  Indications o Primary arthrosis secondary to trauma or rheumatoid arthritis (main indication) o If instability secondary to PT dysfunction or collapse of TNJ from rupture of spring ligament, isolated T-N fusion is indicated (but Coughlin usually does triple)  Procedure o Ideal position of foot  5° valgus  TNJ in neutral  Forefoot 0-5° varus o Patient set-up  General or spinal  Thigh tourniquet  Patient supine 1. Incision just distal to medial malleolus to 1 cm beyond the navicular-cuneiform joint, curved slightly dorsal (especially if large dorsal osteophyte is present) 2. Strip joint capsule with periosteal elevator or sharp osteotome 3. Remove osteophytes with rongeur or osteotome 4. Identify articular surfaces, remove with curette or osteotome a. Can use towel clip in medial navicular for exposure b. Visualization can be improved with lamina spreader if bone is hard c. Difficult to see laterally, but this must be exposed and debrided 5. Joint surfaces are heavily feathered and foot is manipulated into anatomic alignment 6. Stabilize calcaneus and place STJ in 5° valgus a. Manipulate midtarsal joint into a few degrees abduction b. Forefoot into a plantigrade position that is perpendicular to long axis of tibia c. Forefoot should not have a residual of more than 7-10° varus or valgus 7. Internal fixation—can use two 4.0 or 4.5 mm canulated cancellous screws. For large person, can use 7.0 mm screw. If bone is soft, can use multiple staples. 8. Hold foot in corrected alignment, drive guide pin into navicular starting at navicularcuneiform joint and drill obliquely across navicular into head and neck of talus 9. Check alignment of foot, C-arm 10. Add second guide wire, C-arm 11. Overdrill navicular, insert 40 to 50 mm long threaded cancellous screw. Screw threads must pass the intended fusion site. If soft bone, use washer. C-arm 12. Check stability of foot 13. If bone is soft or the fusion is not stable, use staples. This is also useful if there is a fracture of the navicular. 14. Close 15. Marcaine at the end

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

161

 Post-op o Compressive dressing with two splints o NWB for at least 6 weeks o Add cast on 1st visit o After sutures are removed, place patient in short leg removable cast o After 6 weeks, and x-rays look good, patient can ambulate with short leg cast o 3 months after surgery, if x-rays ok, patient can d/c the short leg cast  Complications o Non-union—Rate is higher than in CCJ or STJ probably because of inadequate exposure to joint. Also because navicular is avascular. o Flatfoot—Results from placing the STJ in too much valgus and forefoot in too much abduction  Correct with a triple arthrodesis  Items needed for surgery o Periosteal elevator, osteotome, curettes o Possible saggital saw o Wire driver o Towel clips o Lamina spreader o 4.0, 4.5 or 7.0 canulated cancellous screw (probably 40-50 mm) o Possible washers o Possible staples o 3-0, 4-0 Vicryl, 5-0 Monocryl or 4-0 prolene o Splints for stirrup/posterior split

162

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Triple Arthrodesis 

Procedure o Patient set-up  Prone  Thigh tourniquet  General or spinal 1. See Subtalar Arthrodesis for subtalar steps 2. Lateral incision a. Incise over sinus tarsi from lateral malleolus to base of 4th metatarsal i. Avoid superficial peroneal nerve and peroneal tendons b. Reflect EDB off calcaneus c. Longitudinally incise sinus tarsi fat plug d. Find bifurcate ligament → this will show you the entry point to debride the talonavicular (TNJ) e. Spread with lamina spreader f. Mobilizing the soft tissues is necessary for reducing the pes planovalgus articulation 3. Calcaneal-Cuboid joint (C-C joint) a. From the above incision, reflect down to the C-C joint b. Distract with a Hohmann spreader c. Reflect the soft tissues 4. Talonavicular joint a. Find the bifurcate ligament and resect it b. Resect the soft tissues of the TN joint 5. After all the soft tissues are released, the deformity can be corrected → minimally resect the articular cartilage of the joints a. Resect TN joint, then C-C joint, then the talocalcaneal joint 6. Dorsomedial incision a. Incision is centered over TNJ and extends proximally up talar neck b. Resect the soft tissues and then the cartilage 7. Fixation: Order TC → TN → CC a. From talar neck aimed post-lat, a 6.5 mm partially threaded cancellous screw i. Avoid placing the screw too far posteriorly into the talar neck because it will cause ankle impingement ii. Could also go from calcaneus into talus. b. A 4.5 mm cortical screw is placed from the navicular to talus i. Screw should measure less than 40 mm c. C-C joint is fixated with a 4.5 mm cortical screw placed from calcaneus to cuboid i. Screw should measure less than 40 mm

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

163

Calcaneal Slide Osteotomy  Can slide medially for flatfoot, or laterally for ankle instability  Procedure o Patient set-up  General or spinal  Supine  Thigh tourniquet  Bump hip 1. Incision is1 cm posterior to fibula and 2 cm proximal to superior aspect of calcaneous (behind peroneal tendons and anterior to Achilles tendon). Stay posterior to peroneal tendons. Ends at junction of plantar and lateral skin at level of peroneal sulcus. 2. Sharp dissection down to bone, careful of peroneal tendons and sural nerve. 3. Bone cut: perpendicular to calcaneous. From the midpoint of tuberosity to 1 cm past the plantar weight bearing portion of the calcaneous. ***Careful about cutting too far medial because your nerves and arteries are over there. a. Score your cut first b. Get a wider, longer blade than usual. c. May have to finish with osteotome. 4. Displace tuberosity: a. If laterally so that midaxis of tibia is slightly medial to the midpoint of the calcaneus. The lateral wall of calc should be just lateral to the lateral malleolus. b. If medially, displace approx 1 cm. c. Can displace with an osteotome or lamina spreader without teeth. 5. If needed, can use a Dwyer wedge for added valgus. A Dwyer wedge is generally 1 cm laterally. 6. Fixation: angled plate, one (or two) 6.0 or 7.0 partially threaded cannulated screws, or two 4.0 partially threaded screws. a. For the screws: insert just off the heel pad posteriorly (about 1.5 cm above plantar surface). If sliding medially, insert screw just laterally. If sliding laterally, insert just medially. b. C-Arm for position. 7. Marcaine post-op block 8. Close.  Post-op o Posterior splint in OR, compression dressing o Cast application after 1st visit for 5 weeks. o Removable cast: ROM exercises until osteotomy site is healed.

164

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Evans Calcaneal Osteotomy  Mark out tendons and CC joint before surgery  Procedure o Patient set-up  General or spinal  Supine  Thigh tourniquet 1. Get bone graft in saline and starting to reconstitute. 2. Incision is oblique over distal half of calcaneous (cut will be 1-1.5 cm from CCJ) 3. Dissect to bone. Careful of Intermediate Dorsal Cutaneous Nerve (Dorsal) Sural N and Peroneal Tendons (Plantar) 4. Expose to osteotomy site 1-1.5 cm from CCJ 5. Free up EDB 6. Pass a probe thru the anterior and middle facets. 7. Make cut with sagital saw parallel to CCJ, aimed slightly distal to emerge in between the anterior and middle facets. Don’t go too far medially or you may damage vital soft tissues medially. Can use osteotome to finish the medial cut 8. Lamina spreader is put in place of the osteotomy site. 9. The osteotomy site is opened by loading the fifth met and putting foot in adduction. Load until the hind foot valgus is corrected as well as the forefoot varus. 10. Insert bone graft. Bone graft is probably going to be twice as wide on the outside as the medial side. Most likely the graft will be about 1cm in width at the widest side (maximum). Don’t forget to keep the cortical sides with the other cortical sides. 11. Can fixate with staple, or screw. Screw is placed distal dorsal to proximal plantar. a. Very often no fixation is used.  Post-op o NWB BK cast. For adults 6-8 weeks, for adolescents 5-6 weeks.

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

165

Peroneal Brevis Tendon Repair and Reconstruction  Non-operative management—BK cast in neutral to slight inversion for 6 weeks. o Associated with 30-40% rate of redislocation.  Procedure o Pt supine o Sandbag under hip or lateral decubitous. o General or spinal o Thigh tourniquet 1. Incision-curvilinear, approx 5-7 cm behind the fibula, inline with the peroneal tendons. Half of incision above malleolus, half below. 2. Full thickness flaps, identify superior peroneal retinaculum 3. Inspect peroneal tendons for subluxations, partial or complete tears and tenosynovitis 4. Retract PL anteriorly to visualize PB and often reveals a central split and subluxation over posterior ridge of fibula a. If PB tear is found and degenerative tissue is <50% of tendondebride degenerative tissue. Then tubularize the remaining tissue using a running, absorbable suture. b. If peroneus tertius or low-lying muscle belly is presentexcise it. c. If lateral ligament instabilityuse Brostrom or Chrisman-Snook d. If PB tear is >50% then resect the whole tendon (not sure about this personally) and attach to PL. 5. Inspect floor of peroneal groove. If too shallow make larger groove (pg 303) 6. Use rongeur to prepare fresh-bleeding fibular bed, then reattach the superior peroneal retinaculum through drill holes in lateral ridge. Go from deep thru holes to dorsal. Suture the rest of superior peroneal retinaculum with pants over vest style.  Post-op o NWB splint for 1 week o BK walking cast for 4-6 weeks

166

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Posterior Tibial Tendon Repair-Substitution  Stages o I: Normal length with tendonitis or peritendonitis  Surgical options: Debridement or repair o II: PT is elongated, but RF is still flexible  Surgical options: FDL transfer o III: PT is elongated, RF rigid  Surgical options: Triple arthrodesis  Tendon is usually worse than you thought  Always try conservative first-rest, arch supports, PT, oral anti-inflamatories, immobilization with cast or brace  Steroid injections are contraindicated.  Procedure o Almost always done with an osseous procedure 1. Incision is 10 cm proximal to tip of tibial malleolus and 1 cm posterior down behind the medial malleolus to the navicular tuberosity’s plantar portion. (Follows the TP tendon) 2. At the upper end of the incision, the deep fascia is incised and the TP is exposed. a. The TP lies very close to the posterior margin. Trace the tendon distally to its insertion while leaving a 2 cm pulley just posterior to medial malleolus at the level of the tibial plafond. 3. Determine the length of the TP tendon. a. If TP is normal length, it’s stage Ithen do tendon debridement, tenosynovectomy and sheath resections are done and close wound b. If tendon is elongated, it’s stage II and FDL transfer is needed. 4. For debridement of tendon: a. If fraying—smooth edges leaving major portion of tendon intact b. If bulbous enlargement just tip of medial malleolus-an ellipse is removed from bulb and tendon is sutured burying the knot c. If longitudinal split exists-clear inner side of tendon of scars and approximate scars 2. Tenosynovectomy—the outer portion of the tendon sheath distal to the pulley is removed to prevent a possible reformation of stenotic tendon sheath 3. Inspect tendon for area of tear. Proximal to the region involved, the tendon will be dull and white if the tear is old. Sometimes there is a transverse tear. 4. Transfer of the FDL: Detach FDL distal to the crossover area of FDL and FHL. Cut the FDL under direct vision. a. Optional: Suturing of distal end of FDL to FHL 5. Tag FDL with strong, non-absorbable suture in zigzag suture 6. Identify tuberosity of navicular and expose the inferior and superior surfaces of the tuberosity 7. With 0.25 or 0.375 inch drill bit, a drill hole is done from superior to inferior. The drill hole should come out inferior to the main surface of the PT 8. Leave FDL in its own sheath. Bring FDL into navicular drill hole from inferior to superior. Pull through as tightly as possible with foot PF and supinated. CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

167

9. Suture the FDL with its non-absorbable suture into the capsule dorsally. Reinforce the tendon by suturing the inferior portion of FDL (under navicular) into the TP tendon. 10. Assess the proximal TP muscle. Often the muscle will become fibrotic and stiff after a TP dysfunction. Test the muscle by pulling on the proximal portion of the tendon. a. If there is some elasticity (the muscle still has some function)—then do a side-toside suturing of FDL to TP with non-absorbable sutures, buried knot. b. If the muscle is stiff—don’t suture the two muscles together. 11. Optional: Advancement of the spring ligament and the TN capsule 12. Alternative method: TP tendon repair with side-to-side suturing. a. Limitations-cannot restore significant flatfoot deformity to normal alignment, but it should relieve pain and improve function b. Identify and resect the diseased section of the TP tendon. Suture tendon ends together with non-absorbable suture c. Then do a side-to-side repair with the FDL with non-absorbable suture.  Post-op o Without FDL transfer  Jones compression cast with foot in PF and inversion for 1-2 days  BK WB cast for 3 weeks  Post op shoe and gradually move into shoe. May take months o With FDL transfer  Jones compression cast with foot in PF and inversion for 1-2 days  NWB BK with foot in adduction and inversion for 3 wks.  Remove sutures, NWB BK with foot in neutral for 3 more weeks  Progress to WB as tolerated, PT

168

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Tibialis Posterior Tendon Transfer (TPTT) 

Procedure o Patient set-up  Prone  Thigh tourniquet  General or spinal o Four incisions  One at TP insertion site on navicular  One at middle distal 1/3 of leg, medial to tibial crest  One at middle distal 1/3 of leg, 1 cm lateral to tibial crest  One at lateral cuneiform-3rd metatarsal insertion site 1. First incision – at TP insertion on navicular a. Release the TP from its insertion on navicular 2. Second incision – at middle distal 1/3 of leg medial to tibial crest a. Pull TP up through this incision 3. Third incision – at middle distal 1/3 of leg 1 cm lateral to tibial crest a. Separate TA from tibia b. Expose interosseous membrane and make a window in it c. Compress the posterior muscle mass. This will expose TP 4. Gently pull TP from medial incision through window in interosseous membrane with blunt curved Kelly forceps and moist sponges a. Be careful of NV bundle which lies under TP b. Often there are muscle fibers attached distally from the window → gently pull them free 5. Fourth incision – over lateral cuneiform or 3rd metatarsal a. Insert tendon passer, Bozeman forceps or uterine packing forceps into insertion site incision and retrograde up extensor sheath. Grab TP and retrograde. b. Fixate TP to lateral cuneiform with foot in neutral position

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

169

Split Tibialis Anterior Tendon Transfer (STATT)/ Tibialis Anterior Tendon Transfer (TATT) STATT  Procedure o Patient set-up  Prone  Thigh tourniquet  General or spinal 1. Three incisions a. One over TA insertion of medial cuneiform-1st metatarsal b. One over anterior surface of leg just proximal to transverse cruciate ligament c. One over peroneus tertius insertion i. If the peroneus tertius is not present, the tendon can be inserted to cuboid or sutured to the PB 2. Split the tendon with umbilical tape with a tendon passer in leg incision through to TA insertion 3. Cut the lateral ½ of the TA tendon and retrograde that through to the proximal window 4. Insert to peroneus tertius tendon TATT  Procedure o Patient set-up same o Note: Usually with TATT, the 3rd incision is over the lateral cuneif-3rd metatarsal and the TA is transferred to this bone. However, it is possible to transfer the TA all the way to the peroneus tertius sheath. 1. Three incisions a. One over TA insertion of medial cuneiform-1st metatarsal b. One over anterior surface of leg just proximal to transverse cruciate ligament. c. One over lateral cuneiform 2. Tendon is separated from its insertion 3. Tendon is drawn up through insertion onto leg incision 4. With a tendon passer, bring tendon up through peroneus tertius sheath (same as the EDL tendon sheath) a. Be sure to be under extensor retinaculum 5. Insert TA into lateral cuneiform via hole and button

170

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Note: These sections on Ankle Fractures are based on my notes from my personal experiences, the texts I have previously referenced and from my lectures from the AO course in Davos, Switzerland. The first thing they stated at the AO Course in Fracture Management was that they used the Weber Classification and not the Lauge-Hansen system because the Lauge-Hansen was too complicated. Therefore, the surgical choices are broken down by the Weber Classification. However, you still want to learn the Lauge-Hansen system because that is what you will most likely be quizzed/tested. -Brett

Weber A Surgical Procedures 

Screw Placement o Patient set-up  Supine with bump under hip  Thigh tourniquet  General or spinal 1. Small incision at tip of lateral malleolus a. Expose tip of malleolus by splitting calcaneofibular ligament longitudinally b. Avoid tilting lateral malleolus toward the talus 2. Insertion point for medullary fixation is at lateral surface of malleolar tip a. 4.0 cancellous screw (or malleolar screw) is inserted across fracture into the proximal medial cortex of fibula above the fracture site b. Insertion of a long screw (4.0 mm) across the fracture line into the medullary canal of the proximal fragment 3. Avoid rotation or displacement of distal fragment as screw is inserted a. K-wire can be added as temporary fixation b. Note: Since the medullary device (screw) is straight, the lateral malleolus may be inadvertently tilted toward the talus – this will result in narrowing of ankle mortise and reduced motion 4. Close



Tension Band Wiring o Patient set-up  Supine with bump under hip  Thigh tourniquet  General or spinal 1. Skin incision vertical and parallel to long axis of tibia directly over lateral malleolus a. Note: A straight incision is often used because it can be extended. Try to avoid Jshaped incision because they cannot be extended. 2. Dissect sharply down to bone a. If undermining is necessary, do it just over periosteum

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

171

3. With a periosteal elevator or #15 blade, elevate the periosteum 2-3 mm proximal and distal to the fracture line a. Remember, be good to the soft tissues 4. Curette and irrigate fracture fragments to remove all hematoma 5. Inspect joint 6. Reduce fracture with towel clip on fracture fragment and guide it with periosteal elevator 7. Insert two 0.045 or 0.062 K-wires. Insert from dist → prox from tip of lateral malleolus across the fracture line, up the diaphysis of the fibula. a. Insert at right angles to the fracture (this is pretty vertical) b. Be careful not to violate the joint 8. 20-gauge wire is then passed through a transverse drill hole above fracture site and placed in a figure-8 fashion around bent tips of protruding K-wires. The fragment should be well-aligned and held securely in place with the wires. a. Twist the 20-gauge wire and trim the excess wire off and make sure the twisted tips lie flat against the bone b. Note: Instead of a transverse drill hole above the fracture site, a screw may be placed at the same level above the fracture line with a washer and tightened down after the figure-8 of wire is wrapped around it. 9. Close

172

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Weber B Surgical Choices  Fixation Options o 2 lag screws o Posterior anti-glide plate o Lateral plate with lag screw  Weber B Ankle Fracture Characteristics o Fracture at the joint line o Corresponds with PAB or SER  Lateral Malleolus Anatomy o PB and PL posterior to fibula o Superficial Peroneal Nerve anterior/medial to fibula o Sural Nerve and Short Saphenous Vein is posterior and plantar to fibula o FHL is posterior and mainly muscular at this level o Proximally incision is between peroneus tertius (anteriorly) and PL and PB (posteriorly) o Generally safe with an incision centered over fibular fracture site  Fixation With 2 Lag Screws o Indications to use 2 Lag Screws  If fibular fracture is spiral (2x diameter of bone) + not comminuted + not osteoporotic → then sufficient fixation can be achieved with only 2 lag screws o Advantages  Allows for a smaller incision  Hardware is not prominent and usually does not have to be removed  Will not interfere with syndesmotic screws (if they are needed) o



Procedure 1. Incision is made slightly anterior to midline of fibula a. Incision is down to bone without too much layered dissection 2. Irrigate and clean up wound edges 3. Restore fibular length a. Hold with reduction clamps b. Check with C-arm 4. Insert two 3.5 screws (or 2.7 if small pt) from ant → post using AO lag techniques a. C-arm to confirm position 5. Close

Lateral Plate and Anterior-to-Post Lag Screw o Most common surgical approach for Weber B fibular fracture o Ideally, you want to cross 5 cortices of fixation proximally and distally. If using a buttress plate, only unicortical screws are used and most likely only 3 cortices will be fixated distally.

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

173

o Procedure  Patient set-up  Supine with lateral bean bag/bump  Thigh tourniquet  General or spinal 1. Incision directly over fibular fracture site. May make incision slightly anterior to midline. (If posterior malleolus fracture is present, then make it posterior.) a. Do not do too much dissection. Make incision down to periosteum preserving soft tissues. Any undermining should be done at the periosteum level. 2. Elevate periosteum 2-3 mm from the fracture line. The full anterior and posterior portions of the fracture line must be exposed. 3. Curette and irrigate fracture fragments and hematoma 4. Explore talus for any osteochondral defects 5. Reposition fracture (increase deformity, distract, reposition) using towel clip and periosteal elevator to assist 6. Hold fracture in anatomical position with bone clamps 7. Reassess anatomical position a. Can use bone clamps, lobster claw, or K-wire across fracture to stabilize it b. Note: Keep in mind the next step with the lag screw, your clamp will most likely be in the way, so position it thoughtfully! c. Can use posterior spike of fracture as guide for adequate reduction d. C-arm for verification of position 8. Insert lag screw (3.5 mm cortical) ant → post, as perpendicular as possible across the main fracture line a. Screws must engage posterior cortex, but should not extend so far as to disrupt the peroneal tendon sheath 9. Apply ⅓ semi-tubular plate laterally a. Bend plate to appropriately contour of fibula b. Plate size is based on the number of screws around fracture site and position on fibula i. 3 proximally (3.5mm cortical screws) ii. 2-3 distally 4.0 cancellous screws iii. Run distal screws short so to avoid violating fibular-talar joint 10. C-arm to check position 11. Close 

174

Posterior Antiglide Plate o Advantages  Achieves strong fixation even in osteoporotic bone  Hardware generally does not cause symptoms or wound necrosis (or at least less than a straight lateral plate would)  Does not interfere with syndesmotic screw insertion  Distal screws obtain better purchase, because they engage a thicker part of distal fibula

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION



Engage 2 cortices without risk of joint penetration (essentially no risk of intraarticular screw insertion because of plate placement)  Biomechanically, this construct is stronger than lateral plate fixation, especially in osteoporotic bone (i.e. good in elderly!)  Loss of fixation is rare due to the stability of the construct  Posterior plate provides better fixation with posterior comminution  Posterior incision allows access to the posterior malleolus, when direct fixation is required o Disadvantages  Technically more challenging  May irritate peroneal tendons in minority of patients, but this often spontaneously resolves in 4-8 weeks  Peroneal tendon subluxation  Should not be a problem is the tendon sheath is left intact o Procedure  Patient set-up  Supine with lateral bean bag/bump  Thigh tourniquet  General or spinal 1. Incision is made along the most posterior border of the fibula at fracture level a. The plate often lies slightly posterolaterally (rather than directly post), thus the incision will be away from the plate b. Incision is carried down to peroneals, but does not violate the peroneal sheath c. Incision proceeds over the lateral edge of peroneals which are usually retracted posteriorly 2. Some of proximal retinaculum may need to be released to expose distal fibula a. Clear periosteum off fibula 3. Fracture reduction – Ideally, anatomic reduction should be achieved prior to plate application a. Reduction can be held with a single K-wire or lag screw b. Apply lag screw from ant → post so not interfere with plate application 4. Plate application – ⅓ tubular plate is applied to posterior surface of the fibula a. 4-hole plate – Classically b. 6-hole plate – More recently c. Because posterior surface of fibula is straight, contouring of the plate is usually not necessary d. Due to the lateral bow of fibula, the plate sits best posterolaterally 5. Proximal screw insertion a. 1st 3.5 mm cortical screw is placed proximally, through the plate, 2 mm above posterior fracture line b. Plate helps prevent proximal gliding of the distal fragment c. If anatomic reduction is achieved, the proximal screw can be tightened down

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

175

6. 7.

8.

9.

176

d. If anatomic reduction has not been achieved, then do not fully tighten the screw yet i. Apply bone clamps to both fracture fragments and distract out to length ii. Apply slight internal rotation to distal fragment iii. Proximal screw is now tightened, and fragment should be properly aligned Remaining proximal 3.5 mm cortical screws are inserted Lag screw insertion a. Lag screw is then inserted post → ant through the first plate hole which is distal to the posterior fracture line i. Because the posterior cortex is thin, lag screw must be inserted through plate (which serves as solid posterior cortex) b. The screw must be angled slightly proximally in order to be perpendicular to the fracture site i. Remember to remove initial lag screw (inserted ant → post) if used c. Note: Lag screws improve fracture reduction but do not significantly improve anti-glide strength d. Okay to leave screw slightly long because screw is directed away from the peroneal tendons e. If possible, a 2nd lag screw can be inserted using the same technique Optional – Insert distal screws: Technically the more distal screws are not necessary, but 4.0 mm cancellous screws may be inserted. Because there is no risk of joint penetration, longer screws can be used to get a better hold on bone. Close

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Medial Malleolar Fractures  Fixation Options o 2 Lag Screws o Medial Plate o Tension Band Wiring  Patient set-up for all types o Supine o General or spinal o Thigh tourniquet  Two Lag Screw Procedures o Two methods  Two Screw Fixation either open or percutaneous (a.k.a. two stab incision)  Lag Screws: True lag screws are used to counteract and neutralize a tension failure on the medial side  Brett Chicko Note: I prefer to do an open procedure over a stab incision because with a fracture of the medial malleolus, there usually is some soft tissue inbetween the fracture fragments  Two Stab Incision Procedure (Percutaneous) o Most common procedure for medial malleolus fracture 1. Two stab incisions at tip of medial malleolus 2. Blunt dissect (with hemostat) 3. K-wire from distal tip across fracture line at right angles into proximal section a. Aim somewhat vertically to avoid the ankle joint b. C-Arm to check position 4. Insert two 4.0 mm cancellous partially-threaded cannulated screws a. C-Arm to check position 5. Close  Open Procedures (Screw/Plate or Tension Band) o Indications  For plate insertion  For two screw insertion with better visualization  Comminuted fractures  Difficulty in reduction with percutaneous method o For Screw Fixation or Plate Insertion 1. Incision – vertical and parallel to with long axis of tibia directly over medial malleolus a. A straight incision is often used because it can be extended. Try to avoid Jshaped incision because they cannot be extended. 2. Dissection sharply down to bone. If undermining is necessary, do it just over the periosteum.

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

177

3. With a periosteal elevator or #15 blade, elevate the periosteum 2-3 mm from the fracture lines a. Remember to be good to the soft tissues! 4. Curette and irrigate fracture fragments to remove all hematoma 5. Inspect joint 6. Reduce fracture with towel clip and guide it with periosteal elevator 7. Stabilize with 2 K-wires a. Insert from distal → proximal from tip of malleolus across the fracture b. Insert at right angles to the fracture (this is pretty vertical) with care not to violate the joint 8. Insert two 4.0 mm cancellous bone screws a. Cannulated screws may be used b. If not cannulated, remove K-wire and insert screw in K-wire hole 9. If using a plate, insert with 3.5 mm cancellous screws. Run the proximal screws short so they don’t violate the ankle joint. a. Other options: ⅓ semi-tubular, DCP, T, Clover Leaf b. Note: For a "push off" (shear) fracture, the purpose of the plate is to provide an anti-glide or a buttressing effect 10. Close o Tension Band Wiring  This can be used for the very small medial malleolar fragments or comminuted  Studies differ onto effectiveness of tension band  Tension bands are rarely used now for medial malleolus  If you always place two screws, you are going to comminute a few medial malleoli and you’ll to be very unhappy. Then you will need this tension band technique for salvage.  Also, pts hate these wires. Anytime you do a tension band wire and leave a wire long (in an area where there is movement) patients will hate you a lot. 1. Incision – vertical and parallel to with long axis of tibia directly over medial malleolus a. A straight incision is often used because it can be extended. Try to avoid Jshaped incision because they cannot be extended. 2. Dissect sharply down to bone. If undermining is necessary, do it just over the periosteum. 3. With a periosteal elevator or 15 blade, elevate the periosteum 2-3 mm from the fracture lines a. Remember to be good to the soft tissues! 4. Curette and irrigate fracture fragments to remove all hematoma 5. Inspect joint 6. Reduce fracture with towel clip on fracture fragment and guide it in with periosteal elevator 7. Two parallel K-wires (0.045 inch or 0.062) are inserted at distal end of fibula and engage the proximal medial cortex above fracture site

178

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

8. 20-gauge wire is then passed through transverse drill hole (or a cortical screw may be placed instead at this level, which you would wrap the wire around and tighten the screw down after the wrapping) above fracture site and placed in a figure-8 fashion around bent tips of protruding K-wires a. Twist end of wire and trim. Make sure to bend it so it sits close to bone. 9. Let the first year close

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

179

Posterior Malleolar Fracture 

When to do an ORIF? o When > 25% of posterior articular surface is involved as seen on lateral view o Fracture is displaced >2 mm o There is posterior subluxation of talus o If fracture prevents reduction of tibia



Procedure o Patient set-up  Use a posterior lateral approach (similar to the one used for a fibular antiglide plate)  Lateral or prone  General or spinal  Thigh tourniquet 1. Incision is at posterior border of fibula, if fibula needs to be reduced, do that first a. Hold with temporary fixation b. Brett Chicko Note: According to Coughlin – Do the definitive fixation of fibula after the post malleolus because of lack of exposure after fibula is fixated. However, I have seen the fibula fixated first and then the post malleolus was addressed. 2. Bluntly dissect between the PB/PL and the FHL (muscular at this level) to the posterior surface of the tibia. Must get exposure of entire fracture fragment. 3. Reduce fracture a. The fracture reduction is determined by palpation and visualization of extraarticular fracture line and C-arm. Cannot directly visualize the intra-articular joint because talus is in the way. b. Note: Reduction of fibular fracture most likely will reduce the posterior malleolus because of firm attachment of post tibiofibular ligament. Ligamentotaxis! c. If difficulty reducing fracture, DF foot may give slack to ligaments and posterior capsule 4. Hold reduction with large reduction clamp 5. Insert 2 K-wires to the fragment in place (for 4.0 mm partially threaded cancellous lag cannulated screws) 6. Insert screws post → ant a. Insert at right angles to the fracture 7. Alternate fixation: Stab incision anteriorly, insert 4.0mm cortical screw ant → post a. Check C-arm for position 8. Let the 1st year close



Post-op o NWB until union is solid. This may take up until 3-4 months.

180

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Syndesmotic Repair    









After every ankle fracture repair, evaluate the syndesmosis with intra-op stress exam Syndesmotic separations are unstable and should be stabilized Remember the AO principle of stable fixation if non-articular Indications for Syndesmotic Fixation o Irreparable medial joint injury w/ disruption of syndesmosis o High fibular (Weber C) fracture >15 cm above the joint line o Medial ligament injury, syndesmotic disruption, talar shift w/o fracture of fibula o Widening of the tibiofibular "clear space" as a result of disruption of the syndesmosis. The clear space is normally < 5 mm wide. Injury Patterns o Isolated o Syndesmotic injury with fibular fracture o Syndesmotic injury with medial injury Choices of Syndesmotic Screws o 4.5 mm screw (most common) x2 or 3.5 mm screws in smaller patients o Bioabsorbable fixation (polylevolactic acid) o Fiberwire (Tightrope or others like this…technique as per manufacture’s guidelines) Proper level for a Syndesmotic Screw o Screws should be parallel to joint line o 1 cm prox to syndesmosis or 4 cm prox to ankle joint o If too low, can pass through distal tib-fib articulation causing pain o If too high, may cause tip of fibula to go outward Procedure o Patient set-up  Prone with hip bump  General or spinal  Thigh tourniquet 1. Stabilize the fibular fracture before the syndesmosis a. Use a plate on the fibula b. Fibula should be reduced posteriorly into the tibial sulcus c. The syndesmosis should be reduced before the screw(s) are inserted 2. Dorsiflex foot 5° 3. Stab incision on fibula a. Use C-arm to find correct level: 1cm proximal to syndesmosis and/or 4 cm prox to ankle joint 4. Insertion of screw (4.5 mm cortical fully-threaded) a. Because fibula is posterior to tibia, aim screw through posterior-lateral fibula to anterior-medial tibia at an angle of 25-30° anteriorly b. Perpendicular to long axis of bones, parallel to the ankle joint c. Engage 3 cortices or 4 (depending on doctor preference) d. Do not lag! Do not over-tighten!

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

181



182

Post-op o Screws generally will not loosen or break if the ankle does not dorsiflex past neutral o Patients are allowed to WB after 6 weeks in a short leg cast or walking boot o Routine removal of screw 8-12 weeks after surgery

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

ORIF Calcaneus 







Indications o Injuries that would do poorly without surgery, such as severely displaced intraarticular, widening of heel, horizontally oriented talus, severe soft tissue injury, and high-energy mechanism Contraindications o Severely comminuted o Impaired vascularity o Infection o Severe neuropathy Essex-Lopresti Classification o Primary fracture line runs from ant-lat → post-med through the STJ (mostly through the posterior facet). As the primary fracture line progresses, this will lead to lateral wall blowout and decrease in calcaneal height. o Both Essex-Lopresti types start with the primary fracture line o Type 1 – vertical force will lead to tongue type o Type 2 – more horizontal force will lead to joint depression Procedure o Patient set-up  Lateral decubitus position  General or spinal  Thigh tourniquet o General order of reduction  Anterior process  Medial wall  Posterior facet  Lateral wall 1. Incision is curved behind the lateral malleolus. The proximal portion is halfway between the anterior portion of the Achilles and the peroneal tendons. The line progresses distally, around the lateral malleolus, and then runs parallel to the bottom of the foot, ending up roughly at the C-C joint. a. Watch out for sural nerve and peroneal tendons 2. Sharply dissect down to bone, create a flap with the CFL and the peroneals and flap that anterior-superiorly 3. Insert two 0.062 K-wires into the talus and bend K-wires upward to hold this flap up 4. Expose STJ, remove hematoma and small fracture fragments via irrigation and rongeur 5. Identify the fracture lines in the anterior calcaneus that extend medially a. Determine if the fracture line progresses to the C-C joint 6. The anterior process is typically elevated. Therefore, the anterior process needs to be retracted plantarly. Use a retractor or lamina spreader between the talus and the anterior process. Fix with K-wire. 7. Identify the fracture line progressing from ant-lat → post-med (the primary fracture lines), separating the posterior facets from the anterior and middle facets

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

183

8. The posterior facet is usually PF. With the use of a periosteal elevator, lift up the posterior facet. Hold with K-wire directed from the anterior process laterally to the posterior facet medially. a. The lateral part of the posterior facet is retracted laterally or removed. This allows visualization of the medial posterior facet 9. A 4.0 Shantz pin is inserted into the tuberosity fragment from post → ant (from the back of the heel into the posterior tuberosity). This is used as a lever to reduce the fragment plantarly, medially, and into slight valgus. 10. When the medial wall of the tuberosity lines up with the medial wall of the facet fragment, it is held with two 0.062 K-wires. The K-wires are inserted from the posterior aspect of the tuberosity and directed to the sustentaculum tali (be careful not to damage articular cartilage). Use C-arm for this. 11. After the anterior process and the medial wall are reduced, the posterior facet is reduced. Match the lateral fragment to the medial fragment. Insert 0.062 K-wires into the anterior and posterior margins. 12. Get intra-op X-rays. If alignment is good, insert a 2.7 mm cortical lag screw below the subchondral surface. a. Reconstruct the lateral wall if necessary. Bend and insert plate. b. Best bone for a plate is subchondral bone deep to the C-C joint, the subchondral bone near Achilles tendon insertion, and the dense bone of the sustentaculum tali c. May need to fill in deficit with bone chips, Grafton or other bone substitute 13. Insert drain and close 

Post-op o Course depends on the amount of damage o If minimal displacement, 6-8 weeks ROM exercises and NWB o If severe displacement, >12 weeks ROM exercises and NWB



Complications o Relatively common o Infection o Delayed wound healing o Sural nerve o Tibial nerve problems (more likely from injury rather than surgery)

184

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

ORIF Talar Neck Fractures 

ORIF should be done even if Hawkins type II was close reduced because this type of fracture will inevitably develop an equinus contracture that happens with prolonged casting in PF



Talar neck fracture WITHOUT dislocation o Procedure  Patient set-up  Supine with bump under ipsilateral hip  Have C-arm ready 1. Anterior-medial incision – made from anterior aspect of the medial malleolus to the dorsal aspect of the navicular tuberosity a. Dissect carefully down, go dorsal to TP tendon. Don’t disrupt deltoid ligament because this might disrupt some of the vasculature to the talus. 2. Remove hematoma. Don’t dissect the soft tissues off the talus dorsally and plantarly because this might disrupt the blood supply to the talar neck. 3. Anterior-lateral incision – starting from anterior margin of lateral malleolus to the base of the 3rd or 4th metatarsals a. This allows confirmation of the reduction of the talar neck b. It also permits removal of foreign bodies 4. Incise inferior retinaculum 5. Retract EDL and peroneus tertius. Retract EDB dorsally. 6. Remove all fragments. Probe STJ blindly for fragments. 7. Reduce the fracture a. Careful not to have comminution or reduce into varus position. 8. Insert two 2.5mm titanium screws (can be used with MRI). Do not lag! A lag screw might send talus into varus.



Talar neck fracture is displaced (as in Hawkin’s Type III – STJ and Ankle joint) o Procedure 1. Anterior-medial incision – extend the incision over the medial malleolus and the distal aspect of the tibia 2. Go into the space between tibia and Achilles. The body of the talus will be visualized. 3. A femoral distractor may be needed. Put pins in the tibia and calcaneus. 4. Manually place the body of the talus back into mortise a. If the talus will not return to the mortise, a medial malleolar osteotomy will have to be done i. For medial malleolar osteotomy 1. Identify the ankle joint for tibia 2. Make 2 retrograde 2.5 mm drill holes in the medial malleolus across the osteotomy site 3. Release the anterior portion of the capsule off the deltoid ligament as well as a portion of the TP sheath. Protect the TP tendon. 4. Incise the periosteum about 5-10 mm superior to the ankle joint CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

185

5. With oscillating saw, cut the transverse portion, then the 2 vertical portions 6. Reflect the medial malleolus distally. Don’t damage the deltoid ligament. 7. Manually place the talus back into its place 5. Anterior-lateral incision – as above a. Fix medial malleolus with two 4.0 mm cancellous titanium screws 

Post-op o Post-splint or boot o Do not do ROM exercises until wound healing is done o NWB for 8-12 weeks until trabeculae cross the fracture



Complications o AVN o Arthrofibrosis o Malunion, nonunion o Skin necrosis

186

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Tibial Periarticular Fx Reduction & Fixation  Indications o Pilon or Tibial Plafond fractures o Articular displacement of >2mm or unacceptable axial alignment o Open fractures o Neurovascular injury due to fracture  Pre-op planning o Check NV, compartment syndrome, soft tissue injury o Radiographs: AP, Lat, MO o Whole tibial shaft o Foot radiographs o CT can be useful  Procedure o Staged surgery—First part immediate once the patient has stabilized (usually 12-18 hours) with ORIF of fibula and external fixator for tibia. Kitaoka recommends EBI or Orthofix o 1st Stage 1. Fibular incision-slightly posterior-laterally to increase the width of the skin bridge with the later anterior incisions. 2. Do not do calcaneal skeletal traction- (even with a Bohler-Braun frame) this pulls patient out of bed and displaces foot posteriorly 3. Fix Fibula fracture 4. Apply Ex-Fix onto tibia 5. When the soft tissue edema has subsided (usually 10-21 days), ORIF can be performed o 2nd Stage  Patient set-up  Pt supine  General or spinal  Thigh tourniquet  Take frame off tibia but don’t remove the pins. Have circulator sterilize the frame. This may be used later in the case for distraction.  Anterior-medial incision 1. Locate the fracture fragment. If the fragment is anterior-medial: incision begins just lateral to the medial crest of tibial shaft. Extend the incision distally across the ankle joint, staying just medial to tibialis anterior 2. Identify the anterior tibia tendon sheath. Once identified, create a full thickness flap by incision the tendon sheath and the extensor retinaculum. Bring this incision down to bone/joint down to the periosteum. Do not strip the periosteum or remove any fat unnecessarily 3. Identify fracture ends, debride and irrigate. Remove all clots 4. Reduce the fracture. This incision works well with a medial pilon plate

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

187

 Anterior Midline Incision  Use this incision when the fracture is a pure anterior crush injury. This injury gives good exposure and will allow for easy placement of low profile anterior tibial plate 1. Incision is made between the TA and the EDL a. Identify the superficial peroneal nerve, the artery and the deep peroneal nerve. Retract all of this laterally  Anterior-Lateral Incision  Use this with large lateral fragments, such as the Tillaux-Chaput avulsions. Careful with this incision because it may jeopardize the skin from the fibular incision.  This is why you usually use a posterior lateral incision for the fibula. 1. Incision starts proximal to the ankle joint and slightly medial to Chaput’s tubercle and extends distally in a strait line toward the base of the 3rd and 4th mets. a. Superficial peroneal nerve is protected 2. Incise through the superior and inferior extensor retinaculum 3. Mobilize the peroneus tertius and EDL, the deep peroneal nerve and the anterior tibial/DP artery 4. Distally the EDB is seen and can be retracted laterally or detached 5. Protect the lateral branch of deep peroneal nerve and the lateral tarsal artery  Fixation o Fix the jigsaw puzzle, then use reduction clamps followed by 1.6 mm k-wire o Canulated screws are rarely used o If a piece is small, a bioabsorbable pin can be used o Once the screws are in place, a cancellous graft can be used o Apply plate. Options are:  Medial pilon plates for rotational and varus valgus injuries  Anterior pilon plate for anterior crush plates. Note Dr Lutz states to always use an anterior plate.  Supplemental washer plates may be needed. Ex: spider washer plate  Closure o Small drain, close etc.  Post-op o Jones compression dressing and splint o At 1 week change to compression stocking and removable boot and start ROM. o Pt is to wear the boot at all times, even sleeping or the patient may develop equinus deformity o Start formal PT about 4-6 weeks, only after the wounds have healed o WB at 3 months if radiographic evidence of healing o Outcome is based on the fracture at presentation

188

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

 Technical Pearls o Joint surface should be reconstituted first because anatomical malalignment is not acceptable. The ankle will accept some axial malalignment, but not articular. o Shaft reconstruction is performed second o Reconstruct the joint with isolated lag screws followed by neutralization plate of the metaphyseal-diaphyseal component o Joint surface needs to be anatomic reconstructed. If there are centrally depressed pieces, the perimeter fragments need to be retracted and the central ones need to be elevated  Technical Pitfalls o Doing definitive surgery too soon because fracture patterns are not clear with all of the soft tissue swelling o Unstable EX-FIX o Failure to stabilize the fibula  Complications o Infection o Wound complications o Malunions o Post-traumatic complications at 1-2 years

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

189

Ankle Arthroscopy 

Portals o Most commonly used – Ant-med, ant-lat, and post-lat o Anterior-medial port  Medial to TA  Lateral to saphenous vein and nerve o Anterior-lateral port  Lateral to Peroneus Tertius  Medial to intermediate dorsal cutaneous nerve o Posterior-lateral port  Lateral to Achilles tendon, 1-2 cm distal to anterior ports o Anterior-central port  Just lateral to FHL  Medial to DP and deep peroneal nerve, medial dorsal cutaneous nerve crosses over FDL at this level and may be lateral  Due to all of the potential complications, this port is usually contraindicated o Posterior-medial port  Medial to Achilles tendon  Also in this area: FHL, FDL, posterior tibial nerve and artery, calcaneal artery  Due to all of the potential complications, this port is usually contraindicated o Posterior-central port  A.k.a. ―trans-Achilles‖ because it is through the Achilles  This is usually contraindicated…

 

Procedure Insertion of scope 1. Mark anatomic landmarks (medial and lateral malleolus, superficial peroneal nerve, TA and peroneus tertius, if this is not present use EDL) 2. Use 2.7 or 4.5 scope  For Anterior-medial and Anterior-lateral ports 3. Find the ankle joint, insert 18-gauge needle into joint. Fill the joint with 20 cc of NSS or Lactated Ringers 4. Incise the skin only, use blunt dissection down to the capsule 5. Insert cannula and blunt obturator. Insert scope. 6. With direct vision of scope, insert 18-gauge needle into lateral port, find the needle with the scope (―Triangulate‖ your position!). Be careful of the superficial peroneal nerve. 7. Incise the skin over the 2nd port hole, blunt dissect and use obturator to complete the port  For Posterior-lateral port 8. Go lateral to Achilles tendon approx 1-2 cm distal to anterior port levels (this will be just distal to posterior syndesmotic ligament) 9. Cannula is used for dedicated inflow

190

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

 Joint examination 10. Look for anterior joint synovitis and shave with 2.9 or 3.5 shaver 11. Always remember to do a good irrigation, often times this may be all that is needed  Anterior ankle exostosis approach 12. Reflect the capsule by putting the shaver against the osteophyte and lifting the capsule off of it 13. Use a 4 mm burr from the ant-lat port while viewing from ant-med port. You may also use a rongeur or osteotome. 14. Switch portals and do lateral portion 15. C-arm or intra-op radiographs may also be used  Anterior medial exostosis approach at tip of medial malleolus 16. Make secondary port approx 1-2 cm medially and slightly distal to ant-medial port 17. Be sure to suture close all ports used

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

191

Arthroereisis  Procedure o Patient set-up  General or spinal  Thigh tourniquet  Pt heel is resting over edge of bed 1. Incision over sinus tarsi 2. Blunt dissect to sinus tarsi 3. Insert guide pin so it abuts the anterior aspect of the body of talus. Advance pin until it tents the skin medially. Can C arm here, or at any step. a. Axis: distal lateralprox medial. Proper insertion of probe should cause the distal aspect of the probe to exit just superior to the tibialis post tendon and anterior and slightly inferior to medial malleolus—this is the direction you’re aiming 1. The torpedo shaped probe is inserted until it tents the skin. Make incision. 4. Rotate probe clockwise and counterclockwise to dilate the tarsal canal. 5. The guide pin is then placed within sinus tarsi. 6. Most often the 8 and 10 mm implants will be used. Use the sizers, the correct size should allow 2-4° of subtalar eversion. 7. Next, use the trial implant of the above size. Check ROM, and clinical correction are assessed. Use C-arm at this point. 8. Now use actual implant on screw driver with nose cone. Apply over guide pin. Screw in clockwise. Insert no more than 1 cm medial to calcaneal wall and no more than ½ way across talus 9. Once inserted, the implant should be resting on floor of sinus tarsi. Take x-ray 10. When satisfied, remove guide pin and inserter. Irrigate with NSS. Re-valuate motion, close in layers.  Post-op o WB in cast for 2 weeks, gradual return to shoe gear.

192

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Arthrosurface 1st Metatarsal Head Implant  

Indications o Hallux limitus/rigidus + Good bone stock! o Also a good procedure if arthrodesis is not an option Contraindications o Significant bone demineralization or inadequate bone stock o Inadequate skin, musculotendinus or NV system status o Inflammatory, rheumatoid arthritis, sepsis, infection and osteomyelitis o Pts known to have sensitivity to metal alloys typically used in prosthetic devices



Simple Technique Guide Steps o Step 1 – Drill Guides, match with Articular Component o Step 2 – Cannulated Pin, Drills o Step 3 – Tap o Step 4 – Driver o Step 5 – Tap Cleaner o Step 6 – Trial Cap o Step 7 – Centering Shaft o Step 8 – Contact Probes o Step 9 – Circle Cutter and Surface Reamer o Step 10 – Sizing Trial o Step 11 – Implant Holder, insert Articular Component and Impactor o Size is usually 15



Procedure 1. Dissect down and expose 1st metatarsal head (similar to an exposure for a bunion) 2. Use Drill Guide to locate the axis normal to the articular surface and central to the defect a. Be sure to choose a Drill Guide where the diameter circumscribes the defect 3. Confirm Articular Component diameter by matching it to the Drill Guide 4. Place Guide Pin through the Drill Guide into bone a. Make sure its central to defect b. It is very important to verify that Drill Guide is seated on the curved articular surface such that four points of contact are established. A normal axis and correct Articular Component diameter are necessary for proper implant fit. 5. Place Cannulated Drill over Guide Pin and Drill until the proximal shoulder of drill is flush to the articular surface 6. Tap hole to etched depth mark on tap a. Optional – insert bone cement into pilot hole 7. Place Driver onto the Taper Post over the guide pin and advance until the line on the Driver is flush with the height of the original articular cartilage level a. Optional – advance the Driver further to decompress the joint 8. Remove guide pin 9. Clean taper in Taper Post with Taper Cleaner

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

193

10. Place Trial Cap into taper post to confirm correct depth of Taper Post a. The peak height of the trial cap must be flush or slightly below the existing articular cartilage surface to avoid the articular component from being place above the surface of the defect i. Adjust depth using the driver to rotate the taper post (clockwise to advance) 11. Place Centering Shaft into Taper Post 12. Place Contact Probe over Centering Shaft and rotate around Centering Shaft. Read contact probe to obtain offsets at four indexing points. a. Superior/inferior and medial/lateral b. Select appropriate Articular Component using Sizing Card 13. Remove Centering Shaft and replace with Guide Pin. Advance Circle Cutter back and forth. a. Don’t bend guide pin b. Score articular cartilage down to subchondral bone 14. Choose appropriate Surface Reamer based on the offsets. Drill Surface Reamer over Guide Pin until it contacts the top surface of Taper Post. a. Begin rotation of Surface Reamer prior to contacting bone to avoid chipping articular rim 15. Remove Guide Pin and clean Taper Post to remove any debris from implant bed 16. Place the Sizing Trial into the defect that matches the offset profile selected a. Confirm that the Sizing Trial is equal or slightly recessed to edge of articular cartilage b. If the Sizing Trial is proud at the edge of articular cartilage, ream with the next appropriate sized reamer and matching Sizing Trial 17. Use the Implant Holder (attached to suction wall tubing) and align the Articular Component on the holder with appropriate offsets 18. Insert implant into Taper Post 19. Tap the Impactor gently against the implant to seat it against the bone. 20. Check ROM of 1st MPJ and close in appropriate layers

194

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Brostrom-Gould Repair  Indications o Chronic ankle instability unresponsive to conservative treatment o Athlete with ankle instability  Contraindications o Fixed varus heel type (need to correct with Dwyer) o People over 200-225 lbs (use Evans with PB repair) o Peroneal weakness (i.e. CMT)  Procedure o Patient set-up  Supine with bump (to internally rotate leg)  Thigh tourniquet  General or spinal  Optional – Bump under foot 2. Incision curvilinear over anterior border of fibula, stop at peroneal tendons a. Be careful of sural nerve, intermediate dorsal cutaneous nerve, peroneal tendons b. You will may have to ligate lesser saphenous branch of nerve 3. Dissect down to capsule, incise it from 2-3 mm from border of fibula a. Leave a cuff for later attachment 4. Find CFL by reflecting peroneals and incise it 5. Put foot in neutral DF and slight eversion 6. Resect necessary capsule, reapproximate using 0 or 2-0 absorbable (or non-absorbable) suture starting with the CFL then ATFL (extend incision if necessary) 7. Test for full range of DF and PF (gently) 8. Identify extensor retinaculum (should be distal), its fibers run perpendicular to ATFL and CFL (extend incision if necessary) 9. Mobilize extensor retinaculum. Pull it over the repaired capsule and attach to the tip of the fibula using 2-0 absorbable suture. 10. Check again for ROM and stability 11. Close  Post-op o Posterior splint 3-5 days o BK walking cast for 3-4 weeks o Air-type stirrup for an additional month with ROM exercises

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

195

Fibular Derotational and Lengthening Osteotomy  General o Tramatic displacement of talus is associated with displacement of lat malleolus o Malalignment is characterized by distal fibular shortening, lateral shift or malrotation o Increases pressure in mid-lateral and posterolateral quadrants of the talar dome o Goal of Fibular Derotational and Lengthening Osteotomy is to restore the sensitive WB area to normal anatomic relationship  Radiographs (Can also use CT and MRI) o Abnormalities of talar position is seen on x-rays. Check for (compared to other side)  Widening of medial joint space  Talar tilt  Fibular shortening o Mortise View—Check for:  Equidistant and parallel joint space with no medial widening  Shenton’s line of the ankle  A dense subchondral supporting bone creates a radiographic line that can be followed over the syndesmotic space from tibia to fibula (Kitoaka pg. 501)  This should be even and continuous between the two bones  Unbroken curve between the lateral part of the articular surface of the talus and the distal fibular recess  Talar tilt.  This should be parallel or within 3° of parallel  Abnormal seating of fibula in the incisura fibularis of the tibia. (Pg. 501)  Normal is less than 6mm as measure 1 cm above tibial plafond  If internal fibular rotation-increase in this measurement  If external rotation of fibula-measurement is normal or decreased. This is more common  Check for DJD o If no DJD—Fibular Derotational and Lengthening Osteotomy o If severe DJD-ankle arthrodesis  Contraindications o Infection o Neuropathy  Surgical choices o Oblique osteotomy—can only gain 3-5 mm in length o Transverse osteotomy of fibula, uses iliac bone graft, with plate and syndesmotic screws through plate

196

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Ilizarov Method 





Insertion of wires 1. Place wire with the frame already built 2. Make stab incision 3. Blunt dissection (with a hemostat) 4. Wire is inserted via safe tract via clamp 5. Remember to pulse the drill to avoid overheating 6. Use a wet Ray-Tec sponge to keep wire cool and stabilized Positioning the frame o Proximal: 2 fingers between the frame and tibia o Distally: 3 fingers (to allow for swelling) o Frame should be 2-3 cm from the surface of the ground to allow for WB Tibial wire insertions 1. Break the tibia into 6 segments (1st being most proximal and probably out of our scope of practice) 2. At the 2nd segment a. Put half pin perpendicular to subcutaneous surface of tibia (pretty much the general rule for insertion of half pin at the tibia) b. For the wire, try to engage the widest portion of the tibia. This means inserting the wire slightly oblique to the transverse plane of the tibia, thus exiting a little more ant-medial when compared the plane of tibia. 3. At the 3rd and 4th segment a. Similar to 2nd segment 4. At the 5th segment a. Wire is inserted almost perpendicular to frontal plane of tibia. i. Note: Often the tibial wires will be parallel so that the frame can be slid both medial and lateral th 5. At the 6 segment a. Wire options i. Directly med → lat ii. More ant-lat → post-med iii. Through fibula and into tibia

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

197

Osteochondral Lesions of the Talus  

Conservative treatment indicated for Stage 1-2 and Stage 3 medial lesions Surgery indicated for Stages 3 lateral and Stage 4 lesions



Procedure o Patient set-up  Supine  Thigh tourniquet  General or spinal 1. Get scope portals 2. Use 2.7 mm scope, both 30˚ and 70˚. Examine the joint. 3. With a probe, evaluate the articular cartilage. Look for any loose bone fragments beneath articular surface and the extent of the lesion over the talar dome. 4. Type of surgery is dependent on type of osteochondral defect a. Acute fracture is usually ant-lat, more substantial bone base and better for internal fixation b. Chronic post-med lesion is more likely to have fragmented necrotic bone and poor articular cartilage. These lesions must be removed. c. In young patients without skeletal maturity, simple drilling may be enough if articular cartilage remains intact 5. For drilling, use 0.062 K-wire to depth of 1-1.5 cm  For post-med lesion o Old method was to use trans-tibial approach. o New method is to use a guide and go through sinus tarsi into post-med portion  For articular cartilage that is fragmented, loose and necrotic 1. For post-med lesions, use post-lat port for 70˚ scope 2. Use probe to lift cartilage 3. Remove cartilage with forceps 4. Use angled cervical curette to debride lesion to healthy, bleeding bone a. Stopping the inflow will demonstrate bleeding 5. If good bleeding, just remove all remaining bone fragments 6. If not good bleeding, drill as previously described  For bone grafting o If cartilage is good and intact, but either there is a viable bone fragment or there is only edema of the underlying cancellous bone o Insert in the trans-talar approach (like drilling through subtalar) o OATS Procedure  For post-med lesion  Take a plug of bone with articular cartilage from knee and through a trans-tibial approach, insert into the talus

198

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Tarsal Tunnel Release  Most often occurs in the fibro-osseous tunnel (bound by lacinate ligament), most often at the distal edge of the ligament.  Division of nerve of medial and plantar nerve occur deep to lacinate ligament in 93% of people, and proximal in the other 7%  The nerve is in the third channel (Tom, Dick and A Very Nervous Harry.)  Need ―peanuts,‖ posterior splint, and Penrose drain.  Procedure o Patient set-up  General or spinal usually  Thigh tourniquet, deflate before closure.  Don’t esmarch the foot, just elevate it. 1. Incision 10 cm proximal to the tip of the medial malleolus and 2 cm posterior to the tibia. After the medial malleolus, gently curve plantar to the level of the talonavicular joint (plantar to TNJ). This should be about the midpoint of the abductor hallucis a. McGlamry—2cm proximal to superior edge of lacinate ligament and gently curving to the proximal margin of the abductor hallucis. 2. With hemostats, blunt dissect the SubQ. A moistened 4x4 can be used. When in the SubQ, be careful of the medial branch of the nerve as it punctures the lacinate ligament. 3. When at the lacinate ligament, feel for the pulse of the PT artery. Also palpate for the tendons of the PT and FDL. The FHL (4th compartment) can be palpated by moving the big toe. 4. From proximal to distal, make incision of the roof of the third canal. May want to use hemostats and split them, or may use groove channeler/director. 5. Isolate the Tibial Nerve and all 3 branches (medial and lateral plantar nerve, and the calcaneal branch) of its branches from all tissues. 6. Remove any neoplasm. Be careful! 7. Move varicose veins. Ligate veins if necessary, but make sure that you aren’t ligating an artery. 8. Follow nerve distally through the abductor canal. Section the abductor canal stricture. 9. Go proximal and follow nerve upwards. 10. Deflate tourniquet. 11. Closure—but don’t reapproximate the lacinate ligament (McGlamry says only partially reapproximated) and the subQ and skin are closed. If a lot of ooze, then use a drain. 12. Marcaine at the end  Post-op o Below the knee compression dressing is applied. o NWB or partial WB for two weeks. o Begin DF and PF of ankle after 2 weeks.

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

199

200

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Case Study 1 A 23 y/o male presents to the ED with foot trauma. What should you do first? Obtain a quick history and check neurovascular status HPI – patient had foot run over at work. He complains of 10/10 pain and that his toes feel cold and numb. PE – pulses are present. Toes feel cold. Patient cannot feel you touching his toes. Toes are changing color (purple or white). Patient cannot move his toes. What is your diagnosis? Compartment syndrome What is compartment syndrome? Condition with increased tissue pressure within a limited space which compromises the circulation and function of the tissues. It can lead to ischemia of the tissues. Is this a surgical emergency? Yes. Compartment syndrome is a clinical diagnosis, according to the AO Principles course. It is better to get the patient up to surgery than to find an instrument to measure the pressure. What are some causes of compartment syndrome? Fractures, crush injuries, prolonged limb compression, post-ischemic swelling. Practically any injury can result in compartment syndrome. What are the signs of compartment syndrome?  Pain out of proportion (most important)  Paresthesia  Pallor  Pulses present  Poikilothermia  Paralysis What are some techniques for measuring pressure? Wick catheter, slit catheter, Synthes catheter, needle technique, continuous infusion technique. But as stated before, this should be a clinical diagnosis. What is the treatment? Fasciotomy of the compartment. In the leg, surgical access should be made to all four compartments. To do a leg fasciotomy, make one incision medial to the tibia and one lateral. From the medial incision, open the superficial and deep posterior compartments. From the lateral incision, open the anterior and lateral compartments.

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

201

What are some absolute indications for a fasciotomy?  Tissue pressure above 30 mm Hg (normal 4 ± 4 mm Hg)  Sensory and motor loss  Pain out of proportion

202

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Case Study 2 A patient who you prescribed pain medications has wheels, hives, itching, and trouble breathing after taking the medication. What is most likely going on? Anaphylaxis What is anaphylaxis? Rapid, generalized immunologically-mediated event that occurs after exposure to foreign antigen substances in previously sensitized persons. This syndrome can affect any organ in the body, but it most commonly affects the pulmonary, circulatory, cutaneous, neurologic, and GI systems. What are the clinical symptoms of anaphylaxis? Mild (common)  Urticaria, weakness, dizziness, flushing, angioedema, congestion, sneezing Severe  Upper respiratory tract obstruction, hypotension, vascular collapse, GI distress, cardiovascular arrhythmias, cardiac arrest What is the difference between anaphylaxis and anaphylactoid reaction? Clinically, they present the same, but anaphylactoid reaction is not mediated by the IgE antibody and does not necessarily require previous exposure to the inciting substance What is the treatment for anaphylaxis? Stop the offending agent, and if necessary, D/C all meds If the patient is having life-threatening problems, get them to the ED Treat the symptoms  Airway – bronchospasm o O2 40-100% o Epinephrine 0.3-0.5 mL 1:1000 soln SC or IM q15min o Albuterol 0.5 mL 0.5% in 2.5 mL NS nebulized q15min o Benadryl 50 mg PO q4-6h o Methylprednisolone 2-60 mg PO daily  Cardiovascular – hypotension o IV fluids 1 L q20-30min prn o Maintain systolic pressure >80-100 mm Hg o Epinephrine 1 mg 1:1000 in 500 mL D5W IV at rate of 0.25-2.5 mL/min o Norepinephrine 4mg in 1 L D5W IV at 0.5-3 mL/min o Benadryl 50 mg PO q4-6h  Cutaneous reactions o Epinephrine 1:1000 0.3-0.5 mL SC or IM q15min o Benadryl 50 mg PO q4-6h Document offending agent and educate patient on future avoidance CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

203

What is the best way to prevent anaphylaxis? Thorough history and elimination/avoidance of the offending substance

204

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

The Interviews For some people, the social interview is harder than the academic interview. In my opinion, the reason that it is harder is because people don’t prepare for the social interview. After sitting through 2 years of interviews, I’m amazed at how some people don’t seem ready for the social questions. Many of these ideas are from my past as a salesperson on a job interview. Essentially that is what you are…a person selling themselves for a job. -Brett Chicko

The amount of Social vs. Academic Interviewing will vary from program to program. Some will only ask social questions (but pimp you when you rotate with them) and some may ask only one social question and a battery of academic questions. Review this section so you have some baseline answers for common social questions and review the rest of the book for common academic questions. Overall: be yourself and relax! -Hubert & Sandi

Hint #1 – Look and dress appropriate!  Men o Wear a pressed shirt, tie, and suit. (Suggest a dark suit with a blue or white shirt.) o Hair should be neat and combed and facial hair clean cut.  Women o Wear a conservative suit. Keep the skirt length and shirt neckline appropriate. o Hair should be neat and combed.  Sitting in the interview chair o When you sit in the chair, sit back with good posture. NO SLOUCHING! o Your hands should be in your lap (when you’re not talking to them). o Keep your feet flat on the floor for men or legs crossed for women. o Do not lean your arms on the table in front of you…you’re not at your desk at home! Hint #2 – Proper entrance/exit from interviews  Do not be late for your interview!  When you enter the room, sit in the chair and give a proper greeting. o Say hello at least. o Say ―nice to see everyone again‖ or something similar if you’ve rotated with the program.  Make sure to make eye contact with everyone in the room and SMILE! (But don’t be too cheesy about it.) CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

205

 

When you leave the room, it is appropriate to only shake hands with the director unless the other members of the room offer to shake their hands. Thank the interviewers for their time.

Hint #3 – Do your homework  At the end of many interviews, the host will ask the interviewee if he/she has any questions. o Brett says: You should not. ―You should have done your homework by this point. Why would you spend your money and time to interview at a place you don’t have any information about (other than what is in the CASPR book)? To ask questions in the interview that should’ve been asked on a visit makes you look unprepared and uninterested. o Hubert & Sandi say: It is okay to ask any burning questions you may have about the program (rumors about taking 4 residents instead of 3, or hearing a program may be closing next year). Avoid simple questions that may be answered by reading a program’s handbook or website.  By the time of your interview, you should have visited the program (and in theory asked all your questions at that time) o If you live and attend school near a program you’re interviewing with by golly you BETTER HAVE VISITED there by the time of the interview! o If you live too far away (airplane ride distance) then a phone call to one of the residents will work (track down a resident’s pager number or contact info through the number given in the handbook for each program)  During this phone call, get your questions answered.  As always, be prepared and have a good list of questions for the resident.  If any questions do arise after the visit/phone call then it is perfectly acceptable to call or re-page or email the resident.  A good response to this question: ―Do you have any questions about our program?‖ o ―No Sir/Ma’am, all of my questions were thoroughly answered by Dr. So-and-So on my visit (or phone call). I feel as if I have a good understanding of the opportunities of your program.‖ Hint #4 – Ask for the program  Brett says: o I know some people feel that by showing up for the program their presence alone means they want the program. I still feel like one should go the extra yard and ask for the program. I do not mean suck up to them, but state to the interviewers that you want the program in a mature and professional manner. o By asking for the program or stating that you want the program it shows the program that you want to be there and that this is not a practice interview o I know personally that if there are 2 women I want to date, the one who expresses an interest me versus one that is indifferent, I will always choose the one who expresses an interest o Proof? All the interviews I’ve been a part of, only 4 people asked for the program (over a 3 year span) and all 4 have gotten the program.

206

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION



Hubert & Sandi say: o Getting a good program’s spot (like Crozer’s) is highly competitive, and many students have learned to sneak in ―I love your program‖ or ―I definitely want to come here‖ as many opportunities as they can. o Proof that this doesn’t always work? Since this book was written, the occasional student who has said they wanted the program has turned in to more like 60-75% of the students coming through with visits or externships that ―ask for the program.‖ Trust us, your actions speak way louder than your words… o But if it makes you feel better to say this as a parting goodbye, you wouldn’t be the first or the last!

Hint #5 – Be enthusiastic  Don’t be one of those people that walk around looking like they have a hangover or just took a sleeping pill.  Get a good night’s rest so your tiredness from studying/drinking doesn’t overcome your alertness and enthusiasm.  But don’t be a cheeseball or act unnaturally. Hint #6 – Act like someone you would want to work with  If you’ve rotated with the program for a whole month, no matter how you act in the interview, they already know your personality. But acting like a big goof can hurt your chances.  Continuing on Hint #5 and think about #7, be like a mature, responsible adult, or at least act like one.  If you’re picked, you’d be the one representing the program so you need to show you’re a good person to work with. Hint #7 – Remember you’re in a formal interview  Even if you joked around a lot on a visit or on a rotation, especially when answering academic questions, keep the ridiculously silly answers to yourself.  Although you may have spent a month at a program, not everyone at the interview may have met or remember you. Make sure your first impression with them a positive one.  You want to do well because sometimes a good or bad interview makes or breaks your chances with a program. Hint #8 – Prepare for the social interview  Go over some of the sample social questions and formulate some answers for a couple of them. Go over these answers with a classmate, a resident you’re working with or are friends with, your mom, anyone really.  Practice, practice, practice…  Be creative, but please read your answers out loud to another human being so your creativity is not interpreted wrong or sound ridiculous.  Don’t ignore this part because you have a thousand other things to study for the academic portion!

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

207

Hint #9 – Have fun  Seriously, this is the only way to get through these types of questions.  This will show the program you are applying to a part of your personality and how you’re handling the stress of interviewing. Hint #10 – Don’t over think things  With nerves and anywhere from 2 to 15 people interviewing and watching you, even the most confident person can show some nervousness.  With a few exceptions of certain known hard-core academic programs, most programs just want to see your scope of basic knowledge and reasoning when working up a case study or working through the questions.  If it looks like a dog, smells like a dog...it’s probably a dog. Meaning, if you think you know the answer, you probably do!  And if you hear hoofbeats, think horses – not zebras… Hubert & Sandi’s Bonus Tips  The Match for students with programs is designed to work in favor of STUDENTS NOT PROGRAMS  Rank programs the way YOU want them. Don’t let rumors influence how you rank your programs. (Ex: If you rank a program you really want and they don’t end up picking you, it just bumps you down to your #2 pick, but at least this way, if you’ve put them #1 you’ve given yourself the strongest chance of matching with your first pick!) After all, no one knows how you ranked programs except YOU (or the people you tell…).  When evaluating a residency program, in addition to making sure you’d get the cases and experience you’re looking for, evaluate the senior resident class and how they’re performing. Think about it...if they’re good, that’s how you would be if you graduated that program! (Ex: Are they excellent surgeons who are confident doing a variety of cases? Are they getting skin-to-skin cases? Are they having trouble getting their numbers? Are they knowledgeable? Are they happy they went there??)

Sample Social Questions Tell us about yourself  Keep this one short. Three sentences is a good length (i.e. who you are, what you are and what you like to do).  Keep this to the point and under 15 seconds. Who is your hero?  Obviously, besides ―Jazzy‖ Jeff Lehrman, DPM (Crozer attending extraordinaire and graduate of the Crozer program).  It’s probably not wise to say someone in your class or a cartoon superhero…but anything else is probably appropriate. Why did you pick podiatry? Foot fetish is NOT okay. 208

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

Why should we take you over the other applicants? Just don’t personally call out any of the other applicants when answering this. What do you know about our program? What did you learn on your externships? What is your favorite externship and why? Yup, what you’re thinking is correct…it is not wise to name a different program than the program that asks this silly question. Did you visit our program?  If yes, what did you learn (or like) about our program?  If no, why didn’t you visit our program? o If you live close to the program (i.e. Temple students and our program), there really aren’t many good excuses that sound acceptable. The ―I didn’t have time‖ or ―My schedule didn’t allow it‖ just don’t cut it… Tell us about some of the current events Just a question to make sure you don’t live in a bubble. What was the last book you read? But please have read the book, cause if it’s some unknown title, someone may ask you what it’s about and it’s kinda strange to say ―I’ve just started it so I don’t know yet.‖ Tell us a joke  Keep it clean!  Brett’s joke: o Sherlock Holmes & Doc Watson were camping. They went to sleep and were sleeping soundly until Sherlock woke up Watson. Sherlock said ―Watson, look up. What do you see?‖ Watson looked up at the sky and saw millions and millions of stars and the moon. Realizing that The Sherlock Holmes asked him the question, Watson wanted to give an impressive answer. Watson thought about it for a second and answered: ―From an astronomical point of view, I see the Milky Way and many different constellations to the North. ―From a holographic point of view, I see the clouds are coming from the East and we may have a chance of rain tomorrow. ―From a theological point of view, it shows how vast and powerful God is and how insignificant we are when compared to God. ―From an astrological point of view, I see that the moon is in Jupiter and if you are a Scorpio, you are going to have a good day tomorrow.‖ CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

209

Watson then asked, ―Why, what do you see Sherlock?‖ 

Sherlock took a drag on his pipe and replied, ―Someone stole our tent.‖ Hubert & Sandi say: Good luck remembering a long joke like that, but only tell a joke if you can tell the whole thing and remember the punch line. Please!

What do you do in your free time?  Usually the program isn’t looking for a geeky answer like ―I read podiatry articles.‖  Mention a hobby or activity you like to do on the weekend (like back in undergrad, when you had a life…and no, going to frat parties is not an acceptable answer). Be prepared to answer a question about one of your lower grades (if you have any) Especially if you have to re-test or re-take a class to pass. Who was your favorite resident? Who is your least favorite resident? Proceed to think of an answer with mucho cuidado (much caution)! What is your favorite color? Wouldn’t advise you to say black or white, cause technically those aren’t colors and it’s totally lame if you do say them. If you can be any animal, what would it be and why? Who is your favorite clinician in school and why? Who is your mentor? Please don’t say someone in your class! Who is our director? Please don’t ever mess this one up!

210

CROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION

A Surgery Review Booklet

(& a few other important items for externships) OCPM’s ACFAS Officers of 2005 Re-typed, Edited, Updated by the JPMSA in 2009 1

All pictures came from class notes / handouts. Most of the pictures were referenced from Dr. Hetherington’s book. 2

Table of Contents: Topic Charting

Page #

Surgical Consult Pre-Op Note Post-Op Order Admission Order & Note Post-Op Note Post-Op Visit

6 6 6 6 7 7

Layers of the Foot Key Lab Values Hospitalization Indications Post-Op Fever Etiologies Sutures

8 8 9 9

Types Selection Technique

10 11 11

Classification Systems Stewart, Salter-Harris Gustillo-Anderson, WatsonJones, Freiberg Berndt-Hardy, Hawkin Sneppen, Watson & Dobas, Kuwada Rowe, Sander’s Hardcastle, Dias, Danis-Weber Lauge-Hansen

MRI Anesthesia Anesthetics Dosing Onset/Duration Increasing Comfort Ankle Block Hemostasis = Tourniquet Pressures 3

12 13 14 15 16 17 18

19 20 20 20 21 21 21

Table of Contents (Continued): Topic Corticosteroid Injections Types Side Effects Cocktails Radiographic Data Joint Deformities Osteotomies Proximal Shaft Distal Internal Fixation Principles Rule of 2’s K-Wires Steinmann Pins Monofilament Wire Tension Band Wiring Staples Screws Anatomy Types Fixation Technique Selection Soft Tissue Anchors Plates

Page # 22 22 22 23 24 25-27 29-30 31-33 34 34 34 34 35 36 37 38-39 40-41 42-43 44 45 45-46

4

Table of Contents (Continued): Topic External Fixation Principles Complications Types Dynamics Care & Management Forefoot Pathologies / Surgical Procedures Hallux Limitus/Rigidus Hammertoes Etiologies for Contracted Digits th 5 Digit Arthroplasty Rearfoot Surgery Plantar Fasciotomy Haglund’s Deformity Keck & Kelly Osteotomies Tendon Transfers & Indications Adductor Hallucis Abductor Hallucis Extensor Hallucis Longus Jones Suspension Hibbs Tibialis Anterior STATT Cobb Tibialis Posterior Peroneus Longus Bunions based on Angles Other things to know…

5

Page # 47 48 48-49 50 50 51-52 53-56 57 58 59 59 60 60 60 60 60 61 61 61 62 62 63 67

CHARTING SURGICAL CONSULT 1. Chief Complaint 2. HPI (NLDOCAT) 3. Allergies 4. Medications 5. Social History 6. Medications 7. Family History

8. Primary Care Dr 9. Hospitalizations 10. RoS  Vitals / Vascular / Neuro / Derm / Musculoskeletal 11. Ancillary (x-rays, labs, ect…)

PRE-OP NOTE Surgeon Medications Pre-Op Dx Allergies Planned Procedure Diagnostic Data – Labs, x-rays, EKG, ect… Consent Form: Describe Procedure & Care / Complications / Alleviations / Expected Outcomes / Arrange Pre-Op Testing “Consent form was reviewed with patient, signed and placed in chart.” “All risks, possible complication and alternative treatments have been discussed with the patient in detail. All patients’ questions have been answered to satisfaction. No guarantees to the outcome have been made.” POST-OPERATIVE ORDERS: VANDIMAX Date/Time/Signature Vitals Activities Nursing Diet Ins/Outs Meds Ancillary X-ray

ADMISSION ORDERS & NOTE: ADC – VAANDILMAX Date/Time/Signature Admit to Dx Condition -

6

Vitals Activities Allergies Nursing Diet Ins/Outs Labs Meds Ancillary X-ray

POST-OP NOTE: SAPPA HEMI FC2P2 Surgeon Hemostasis – type Findings Assistants Estimated Blood Loss Pathology Pre-Op Diagnosis Materials – sutures/hardware Prophylaxis Post-Op Diagnosis Injectables – any post-incision Complications Procedure Condition Anesthesia – type / how much “Patient tolerated procedure and anesthesia well. Patient transported to recovery by anesthesia with vitals stable and vascular status intact.” Also may include.. Pathology – bone, ST; Condition – stable, guarded, fair, poor; Prophylaxis

POST-OP VISIT: SOAP Subjective 1. POV # ______, PVD #_______ 2. Procedure 3. N,V,C,F,SOB 4. Activity status 5. Pain / How controlled 6. Other Complaints Objective 1. How patient presents – walking, wheelchair 2. Vascular, Neuro, Derm, Musculoskeletal Assessment 1. Status Post-Op 2. Compliance Plan 1. Treatment 2. Dr & Residents 7

LAYER OF THE FOOT 1st Layer 1. Abductor Hallucis M. 2. Abductor Digiti Minimi M. 3. Flexor Digitorum Brevis M. 2nd Layer 1. Quadratus Plantae M. 2. Lumbricales M. rd 3 Layer 1. Flexor Hallucis Brevis M. 2. Flexor Digiti Minimi M. 3. Adductor Hallucis M. th 4 Layer 1. Dorsal Interossei M. (4) 2. Plantar Interossei M. (3) KEY LAB VALUES Chem 7 (136-145mEq/L) (97-107mEq/L)

(5-20mg/dL)

Na

Cl

BUN

K

CO

Cr

(3.5-5mEq/L) (23-29mmol/L)

CBC WBC (4500 11,000/L)

Glucose (<110mh/dL)

(M: <1.2 W: <1.1mg/dL)

(M: 14.4-16.6g/dL) (W: 12.2-14.7g/dL)

HgB HCT

Platelets (150,000-450,000μL)

(M: 43-49%) (W: 37-43%)

8

INDICATIONS FOR HOSPITALIZATION POST-OP 1. Fever >101.6o 2. Ascending Cellulitis / Suspect Osteomyelitis 3. Lymphangitis / Lymphademopathy 4. Immunosuppressed 5. Virulent / Resistant Organisms 6. Need for I&D Procedure 7. Need for IV Antibiotics 8. Failed response to outpatient therapy 9. Need a consult POST-OP FEVER ETIOLOGY 1. Wind – Pulmonary a. Aspiration / Pneumonia b. Occurs 24-48h c. Get chest x-ray 2. Water – UTI a. Occurs in 2-6d 3. Wound a. Occurs in 3-5d 4. Walk – DVT / Pulmonary Embolism a. Within 1st week b. Virchow’s Triad i. Hypercoagulation ii. Venous Stasis iii. Endothelial Damage 5. Wonder – drugs / fever / benign / medicines 9

SUTURES Absorbable Sutures Chromic Gut Monocryl Maxon Vicryl

Filament Type

Monofilament Monofilament Monofilament or Braided Dexon Mono- or Multifilament Dexon Plus Mono- or Multifilament Dexon S Multifilament PDS Monofilament Non – Absorbable Sutures Filament Type Stainless Steel Mono- or Multifilament Ethilon Nylon Monofilament Prolene Monofilament Novafil Monofilament Silk Nurolon Nylon Mersilene Ticron Ethibond

Multifilament Multifilament Multifilament Braided Multifilament

10

Total Absorption 70d 90d 90-120d 56-70d 90-120d 90-120d 90-120d 180d Advantages High strength, low tissue Rxn Elasticity/Memory Minimal Tissue Rxn Elasticity/Tensile strength Good Handling Consistent Tension Minimal Tissue Rxn Good Handling

SUTURE SELECTION 1. Bone 5. Subcutaneous Fat a. Stainless Steel a. Vicryl 2. Tendon 6. Subcuticular a. Prolene a. Monocryl b. Ethibond b. Vicryl c. Nylon 7. Capsule d. Polyesters a. Vicryl 3. Muscle 8. Skin a. PDS a. Nylon b. Vicryl b. Silk c. Prolene 4. Fascia Deep Tissue  taper needle; 3-0 suture a. Prolene Subcutaneous Tissue  taper needle; 4-0 suture b. PDS Dermal Layer  precision needle; 5-0 suture Capsule  2-0 or 30 suture Subcutaneous  4-0 suture Subcuticular  5-0 clear suture Skin  4-0 clear suture SUTURE TECHNIQUES 1. Simple Interrupted Good for infected wounds Individual know for each throw 2. Horizontal Mattress Everts skin edges well 3. Vertical Mattress Everts tissue edges well 4. Continuous Running Good to save time Good for large wound areas 5. Subcuticular (Running Intradermal) Leaves the best scar 11

STEWART CLASSIFICATION OF 5TH MET FRACTURES Type I

Supra-articular @ metaphyseal-diaphyseal junction True Jones! Type II Intra-articular avulsion, 1 or 2 fracture lines Type III Extra-articular avulsion, PB tears small fragment from the styloid process Type IV Intra-articular, comminuted fracture, assoc. with crush injury Type V Extra-articular avulsion @ of physis in children (SH Type I) SALTER-HARRIS CLASSIFICATION OF EPIPHYSEAL INJURIES Type I Epiphysis is completely separated from metaphysic Type II Epiphysis, and the growth plate, is partially separated from the metaphysis, which is cracked Type III Fracture runs through the epiphysis, across the growth plate from the metaphysic Type IV Fracture runs through the epiphysis, across the growth plate, and into the metaphysic Type V The end of the bone is crushed and the growth plate is compressed Type VI (Rang’s Addition) Avulsion of peri-chondral ring Type VII (Ogden’s Addition) Avulsion fracture of the epiphysis without involvement of the physis

12

GUSTILLO & ANDERSON OPEN FRACTURE CLASSIFICATION SYSTEM Type I Fracture with open wound <1cm in length Clean, minimal soft tissue necrosis Usually traverse or short oblong Type II Fracture with open wound >1cm in length Clean, minimal soft tissue necrosis Usually traverse or short oblon Type III Fracture with open wound >5cm in length Contamination and/or necrosis of skin, muscle, NV, & ST Comminuted  Type IIIa  Adequate bone coverage  Type IIIb  Extensive soft tissue loss with periosteal stripping and bone exposure  Type IIIc  Arterial injury needing repair NAVICULAR FRACTURE – WATSON JONES Type I Navicular tuberosity fracture Type II Avulsion fracture of dorsal lip Type III A: Transverse body fracture – Nondisplaced B: Transverse body fracture – Displaced Type IV Stress fracture Type I Type II Type III Type IV

FREIBERG CLASSIFICATION – AVN OF 2ND MET No DJD Articular cartilage intact Peri-articular spurs Articular cartilage intact Severe DJD Loss of Articular Cartilage Epiphyseal dysplasia; multiple head involvement 13

BERNDT-HARDY CLASSIFICATION OF TALAR DOME LESIONS Stage I Compression lesion or non-visible lesion Stage II Fragment attached Stage III Non-displaced fragment without attachment Stage IV Displaced fragment TALAR NECK FRACTURE CLASSIFICATION – HAWKIN’S Type I Non-displaced talar neck Disrupts blood vessels entering dorsal talar neck and intra-osseous vessels 20% chance AVN Type II Displaced talar neck fracture with subluxed or dislocated STJ Disrupts dorsal neck arterial branches and branches entering from inferiorly from sinus tarsi & tarsal canal 40% chance AVN Type III Displaced talar neck fracture with dislocated STJ & ankle joint Disrupts all 3 major blood supplies 100% chance AVN Type IV Displaced talar neck fracture with complete dislocation of STJ Ankle joint + subluxation or dislocation of the talonavicular joint Disrupts all 3 major blood supplies 100% chance AVN 14

SNEPPEN CLASSIFICATION OF TALAR BODY LESIONS Group I Transchondral / Compression fracture of the talar dome Group II Coronal/Sagital/Horizontal shearing fracture of the entire body Type I Coronal or Sagital A: Non-displaced B: Displacement of trochlear articular surface C: Displacement of trochlear articular surface with associated STJ dislocation D: Total dislocation of the talar body Type II Horizontal A: Non-displaced B: Displacement Group III Fracture of posterior tubercle of talus Group IV Fracture of lateral process of talus Group V Crush fracture of the talar body WATSON & DOBAS CLASSIFICATION – POSTERIOR LATERAL TUBERCLE OF TALUS (SHEPARD’S FRACTURE) Stage I Stage II Stage III Stage IV

Normal Lateral talar process with no clinical significance Enlarged posterior lateral tubercle of the talus (Steida’s Process) Accessory bone / Os Trigonum that may be irritated by trauma Os Trigonum + cartilaginous/synchrondrotic union with talus KUWADA CLASSIFICATION OF ACHILLES RUPTURE

Type I Type II Type III Type IV

Partial rupture Complete rupture <3cm gap Complete rupture 3-6cm gap Complete rupture >6cm gap

15

ROWE CLASSIFICATION OF CALCANEAL FRACTURES Type

I

A B C

Medial Tuberosity fracture Sustentaculum Tali fracture Anterior Process fracture

Type

II

A B

Posterior break fracture without Achilles involved Posterior break fracture with Achilles involvement

Type

III

Extra-articular body fracture

Type

IV

Intra-articular body fracture without depression

Type

V

A B

Comminuted, Intra-articular fracture with depression Comminuted fracture with severe joint depression

SANDER’S CT CLASSIFICATION OF CALCANEAL FRACTURES * Fractures are classified according to the number of intra-articular fragments and location of fracture lines # of Fractures Type I Any non-displaced intra-articular fracture Type II 1 fracture through posterior facet creating 2 fragments Type III 2 fractures through the posterior facet creating 3 fragments Type IV 3+ intra-articular fracture lines Location of Fracture Lines:

16

LISFRANC’S FRACTURE CLASSIFICATION – HARDCASTLE Type A: Total or Homolateral – Disruption of the entire Lisfranc joint – Transverse or Sagital plane – Most common type Type B: Partial B1 – Medial incongruity with the first met forced medially – Involves 1st met OR mets 2,3,4 but NOT 5 B2 – Lateral incongruity with lesser mets forced laterally Type C: Divergent C1 – Partial divergence with the 1st met medial and 2nd met laterally displaced C2 – Total divergence with the 1st met displaced medially and lesser mets displaced laterally DIAS CLASSIFICATION OF LATERAL ANKLE LIGAMENT INJURY Grade I  Partial rupture of CFL Grade II  Complete rupture of ATFL Grade III  Complete rupture of ATFL, CFL, &/or PTFL Grade IV  Complete rupture of all 3: ATFL, CFL, & PTFL + Partial rupture of the Deltoid Lig DANIS-WEBER CLASSIFICATION OF FIBULAR FRACTURES INVOLVED IN ANKLE FRACTURES Type A Transverse avulsion fibular fracture BELOW… (SAD) Type B Spiral fracture AT… (SER or PAB) … the level of Type C Fibular Fracture ABOVE… the syndesmosis (PER) 17

LAUGE-HANSEN CLASSIFICATION OF ANKLE FRACTURES SUPINATION ADDUCTION (SAD) ¤ Stage I Transverse avulsion of fibula @/below AJ level Rupture of the Lateral Collateral Ligament ¤ Stage II Oblique to Vertical fracture of the Medial Malleolus PRONATION ABDUCTION (PAB) ¤ Stage I Transverse avulsion fracture of Medial Malleolus – or – Rupture of Deltoid Lig ¤ Stage II Rupture of AITFL & PITFL – or – Tillaux-Chaput / Wagstaffe fracture ¤ Stage III Short oblique fracture of the fibula @ lvl of syndesmosis SUPINATION EXTERNAL ROTATION (SER) *** Most Common! ¤ Stage I Rupture of AITFL – or – Tillaux-Chaput / Wagstaffe fracture ¤ Stage II Spiral/Oblique fracture of fibula @ lvl of syndesmosis ¤ Stage III Rupture of PITFL – or – Avulsion fracture of Posterior Malleolus (Volkmann’s Fracture) ¤ Stage IV Transverse fracture of Medial Malleolus – or – Rupture of Deltoid Lig PRONATION EXTERNAL ROTATION (PER) *** Longest healing time! ¤ Stage I Transverse fracture of Medial Malleolus – or – Rupture of Deltoid Lig ¤ Stage II Rupture of AITFL & Interosseous membrane – or – Tillaux-Chaput / Wagstaffe fracture ¤ Stage III High Spiral Oblique fracture (Maisonneuve Fracture) ¤ Stage IV Rupture of PITFL – or – Avulsion fracture of Posterior Malleolus 18

MRI T1-Weighted  good for showing anatomical detail + Short TE + TR + Tissue with short T1 are brighter + Fat T2-Weighted  good for highlighting areas of pathology + Long TE + TR + Tissue with long T2 are brighter + Water, Edema STIR  Short Tau Inversion Recovery + Fat suppression + Heavily water–weighted image + Very Sensitive for Bone Marrow abnormalities Gadolinium (best for infection) + Contrast–enhanced chemical agent + Shortens T1 relaxation times  Increases signal intensity on T1 weighted images + Usually used in conjunction with fat suppression + Good for identifying ST masses, inflammation processes, & for staging bone and ST infection

TE = Time to Echo TR = Time of Repetition

dec TE + dec TR = T1-Weighted inc TE + inc TR = T2-Weighted

19

ANESTHETICS Esters  Higher incidence of allergies  Metabolized in Blood (Cholinesterase in plasma)  Types ~ Cocaine ~ Procaine ~ Cholorprocaine ~ Tetracaine Amides  Metabolized by CYP450 system in Liver  Types ~ Lidociane / Xylocaine (0.5, 1, 1.5, or 2% solutions) ~ Bupivicaine / Marcaine (0.25, 0.5, or 0.75% solutions)  C/I <12y/o ~ Mepivicaine / Carbocaine (1, 1.5, 2, or 3% solutions) Dosing: 0.25% solution = 2.5 mg/cc drug 0.5% solution = 5 mg/cc drug 1% solution = 10 mg/cc drug

1cc = 1mL

Ex: 5cc of 1% Xylocaine (lidocaine) = 50mg of Xylocaine given Ex: 3cc of 0.5% Marcaine (bupivicaine) = 15mg of Marcaine given Toxic Doses: Lidocaine Plain = 300mg w/ Epi = 500mg

Onset & Duration: Onset: 5min Duration: 1-2h

Marcaine

Onset: Duration:

Plain = 175mg w/ Epi = 225mg

20

10-15min 6-8h

6 Ways to Increase Comfort of the Injection: 1. Quick Stick 2. Slow Injection 3. Small Gauge Needle (large # = small gauge) 4. Small Syringe (less pressure) 5. Cold Spray 6. Warm the Solution (to body temp)

Draw up with 18G Inject with 25 or 27G

Ankle Ring Block: Superficial = Saphenous N., Sural N., Superficial Peroneal N. (IDCN, MDCN) Deep = Posterior Tibial N., Deer Peroneal N. ** Fact: If you mix Lidocaine and Marcaine, you will only have partial anesthesia deep into surgery. Only mix to avoid toxic doses.

Deep Fibular N. Saphenous N.

Superficial Fibular N. Talar Trochlea

M M

** Fact: If you need to inject more volume, use a small percent of drug solution.

Post. Tibial N.

L M

Sural N.

Achilles Tendon

Ex: 30cc of 1% gives more anesthesia than 15cc of 2% Saphenous N Posterior Tibial N Sural N Deep Peroneal N Superficial N

.5-1cc 1-3cc .5-1cc .5-1cc .5-1cc

give the most here since this N is the largest between 2 Long Extensor Tendons plantarflex & invert

Hemostasis = Tourniquet Pressures: Ankle: +100 over systolic ~250mmHg Thigh: +200 over systolic ~ 350mmHg 21

CORTICOSTEROID INJECTIONS Corticosteroid injections are used to control local inflammatory reactions Phosphates: short-acting (clear) Acetates: long-acting (cloudy) All corticosteroids are collagenilytic and therefore should not be injected into the same area of soft tissue more than 3-4 times per year. Side Effects: ~ Soft tissue atrophy ~ Tendon rupture ~ Skin discoloration (lightening) Cocktails Commonly used in Podiatry: 1. Plantar Fasciitis a. 1cc Kenalog-10 (10mg/mL) b. 0.75cc 1% Lidocaine c. 0.75cc 0.5% Marcaine 2. Joint Injections a. 0.2cc Dexamethasone Phosphate b. 0.5cc 1% Lidocaine 3. Intermetatarsal Neuromas a. 0.3cc Dexamethasone Phosphate b. 0.5cc 1% Lidocaine

22

Always draw up the Lido/Marc 1st followed by Dex or Kenalog!

RADIOGRAPHIC DATA Angle: Hallux Abductus Angle Proximal Articular Set Angle (PASA) Distal Articular Set Angle (DASA) Intermetatarsal Angle 1-2 2-5 4-5 Hallux Interphalangeal Angle (HIA) Metatarsal Length Metatarsus Adductus Tibial Sesamoid Position 1 = Medial to midline of hallux 2 = Touching midline medially 3 = 2/3 medial + 1/3 lateral to midline 4 = 1/2 medial + 1/2 lateral to midline 5 = 1/3 medial + 2/3 lateral to midline 6 = touching midline laterally 7 = lateral to midline of hallux Calcaneal Inclination Angle Talar Declination Angle TaloCalcaneal Angle (Kite) Böhler’s Angle Angle of Gissane Calcaneal Fracture resulting in Joint Depression  Böhler’s Angle ↓ Angle of Gissane ↑

23

Normal: 0-15o 0-8o 0-7o 0-8o 16o + 4o 8o + 2o 0-10o + 2o + 2mm 0-8o Positions 1-3

18-22o 21o 17-21o 25-40o 125-140o

CLASSIFICATION OF JOINT DEFORMITIES Positional Deformities: PASA + DASA < HAA PASA and DASA within normal range (0-8o) Joint is Subluxed Structural Deformities: PASA + DASA = HAA PASA and DASA abnormal Joint is Congruous Combined Deformities: PASA + DASA < HAA PASA and DASA abnormal Joint is Dislocated

24

PROXIMAL OSTEOTOMIES IM between 15-22 , normal PASA NOT for a short metatarsal o

I.

Closing Base Wedge 1-1.5cm from met-cuneiform joint 4-6weeks NWB

Indications:  Structural Lg IMA  Splayfoot  Juvenile/Recurrent HAV  Met Primus Elevatus  HAV + MetAdductus  C/I in Elderly

II.

Juvara – Types A,B,C A: Oblique, distal lateral to proximal medial with an intact medial cortical hinge B: same as A but the medial hinge is sectioned after wedge resection C: Oblique, without wedge resection

25

PROXIMAL OSTEOTOMIES CONTINUED… III. Opening Base Wedge Good for a short metatarsal Use medial eminence for the graft

IV. Crescentic 1.5cm from met-cuneiform joint Easy traverse plane correction Good for short metatarsal

26

PROXIMAL OSTEOTOMIES CONTINUED… V.

Double Osteotomy IM and PASA correction

VI. Proximal V Good screw fixation Unlikely to get elevates

VII. Lapidus IM > 18o Fusion of the base of 1st met to the medial cuneiform Indications:  Pain with motion at met-cuneiform joint  Hypermobility of 1st met-cuneiform joint

27

28

MIDSHAFT OSTEOTOMIES ** Troughing is unique to midshaft osteotomies I.

Ludloff Osteotomies IM 1-2 angle: 13-20o Abnormal HAA Normal to short 1st metatarsal Elevatus is a risk

II.

Mau IM 1-2 angle: 13-20o Abnormal HAA Normal to short 1st metatarsal Due to cut, decreases elevates potential

29

MIDSHAFT OSTEOTOMIES CONTINUED… III. Scarf – “Z” Dorsal to Plantar – 50:50 or 66:33 cut Very Stable, technically difficult 2 screw fixation

IV. Off-Set “V” Modification of the Austin Cut angled <55o

30

DISTAL OSTEOTOMIES HAV angle – 35 IM angle -- 16 o Some PASA correction o

I.

Reverdin Some PF possible

II.

Hohmann Very unstable; Rigid Fixation necessary Shortening occurs with fragment removal

31

DISTAL OSTEOTOMIES CONTINUED… III. Mitchell – “Step-down Osteotomy” Used for long 1st metatarsal Good visualization of possible change

IV. Wilson Dramatic shortening possible

32

DISTAL OSTEOTOMIES CONTINUED… V.

Austin / Chevron / Distal “V” Transpositional – PASA, IM, DF/PF possible Joint preserving Possible of Juvenile HAV Displace capital fragment ¼ to ½ bone width

VI. Reverdin Green / Distal “L” Cut 2/3 way through bone, then plantar cut

33

INTERNAL FIXATION 4 Main Principles of Internal Fixation: 1. Anatomical Reduction 2. Rigid Internal Fixation 3. Atraumatic Technique 4. Early active RoM Rules of 2’s: Fracture / Osteotomy site should be 2x’s the diameter of the bone 2 points of fixation is better than 1 2 threads should purchase the distal cortex 2 finger tightness Kirschner Wires (K-wires): Steel wires used as permanent or temporary fixation Dependent on diameter Available in both smooth and threaded Threaded wires provide more stable purchase BUT are weaker & harder to remove Both are measured by outer diameter ONLY maintain compression Sizes: 0.028, 0.035, 0.045, 0.062 inches Steinmann Pins: Very similar to K-wires Larger diameter than K-wires Provide Inc Stability Measured in 64ths Sizes: 8/64 (1/8), 7/64, 6/64…

34

INTERNAL FIXATION CONTINUED… Monofilament Wire: Malleable Steel Provide interfragmentary compression Measured in Gauges (small gauge = large diameter) Techniques:  Cerclage fashion  circling around a bone  Interfrag fashion  placed in between 2 fragments  always pull on the proximal fragment  most stable

35

INTERNAL FIXATION CONTINUED… Monofilament Wire Continued…  Box Wire fashion  2 boxes at 90o to each other  One wire is placed medial to lateral  Other is placed dorsal to plantar

Tension Band Wiring: Combines K-wire with MF wire Requires that there is a soft tissue structural component Two K-wire’s placed the parallel fashion across fracture site with the MF wire in a figure 8 pattern around the K-wire on the site opposite to the tendon’s anatomical pull. Size of wire measured in gauges -- Lower gauge; thicker wire 26 & 28 are common in Podiatry

36

INTERNAL FIXATION CONTINUED… Staples: Primarily used for fractures, osteotomies & fusions Inserted manually or with pneumatic gun Provide compression, distraction or maintain compression Be careful about thickness of bone – DO NOT use if cortical bone is greater than 2-3mm, may cause cortical fractures or not seat in bone properly Pre-Drills:

Neutralization

Compression 

= Divergent Lines

Distraction 

= Convergent Lines

Richards Staple: Os Staple: Uniclip:

GOLD STANDARD for major fusion Heat activated Has an aperture Requires a tool to compress the legs after insertion

37

INTERNAL FIXATION CONTINUED… Screws:  These features can differ depending on the function of the screw. Head

Has various configurations; hexagonal, cruciate, slotted…

Land

The curve-contoured underside of the screw head Increases the surface contact between the screw and the bone Reduces the chance from stress-risers

Shaft/Shank Thread

Area of the screw that is void of the thread pattern

The means by which the screw purchases the bone

Thread Diameter The diameter across the thread width Measurement is the value used to describe the screw size Core Diameter Pitch

Diameter between the thread patterns

Distance between the adjacent threads

Run-Out Junction where the shaft meets the thread Weakest point on the screw Avoid placing the run-out near the fracture / osteotomy site Lead

Distance that the screw advances with each turn (360o)

Rake Angle

Thread to axis angle

Tip Angle

Tip to axis angle

Tip

Either rounded (needs pre-tapping) or fluted (self-tapping) 38

INTERNAL FIXATION CONTINUED… Screw Diagram:

39

INTERNAL FIXATION CONTINUED… Types of Screws: 1. Cortical Screws Threaded the entire length of the screw Have smaller pitch for greater number of contacts between the screw and the dense cortical bone 2. Cancellous Screws Partially threaded Larger pitch to provide greater distance of contact between the screw and the less dense, porous cancellous bone 3. Cannulated Screws Hollow center down the length of the screw to be used over a guide wire Offers easier placement and less complications May have decreased pullout strength 4. Herbert Screws Ho head and two set of threads proximally not distally Proximal threads have greater pitch than the distal threads Indicated for intra-articular fractures Compressive strength of Herbert screw are less than conventional screws 5. Interference Screws Fully threaded, headless screw Does not provide interfragmentary compression but resists axial displacement of one fragment on another Indicated for stabilization of tendon grafts to bone and tendon reattachment 40

INTERNAL FIXATION CONTINUED… Types of Screws Continued: 6. Absorbable Screws Available in natural / synthetic polymers Most common absorbable polymers used are based on alphahydroxy acids such as L-lactic acid, glycolic acid, & para-dioxanone Need to be able to last 6-8 weeks

Basic Properties for the Ideal Absorbable Implant: ~ Posses and initial strength to meet biomechanical demands ~ Degrades in a predictable manner over time ~ Undergoes complete absorption without harm to surrounding tissues

41

INTERNAL FIXATION CONTINUED… General Screw Fixation Technique: ~ Place one screw perpendicular to the fracture / osteotomy line for maximal compression. Place the 2nd screw perpendicular to the longitudinal axis of the bone this provides greatest resistance to the axial loading forces on the bone. ~ If only a single screw placement is allowed – place the screw in an angle that is halfway between the angle that is perpendicular to the fracture line and perpendicular to the long axis of the bone Diagram: A. 2 Screw Technique B. 1 Screw Technique

42

INTERNAL FIXATION CONTINUED… General Screw Fixation Technique Continued: Load Screw Technique This technique is commonly used in plate fixation. Involves placement of 2 screws in the plate that is closest to the fracture line to be drilled offset away from the fracture line. As the screws are advanced the bone segments between the two screws are further compressed. Lag Screw Technique Placement of the screw so that ONLY the thread engages the distal cortex of the bone. Thus further advancement of the screw results in approximation and subsequent interfragmentary compression. Most effective in fracture / osteotomy that is 2x’s the width of the bone or has a fracture angle that is less than 40o. Partially Threaded Screw Insertion Technique 1. Thread / Pilot Hole 2. Countersink (increases surface contact between screw head and the bone) 3. Depth gauge (measures distance between the proximal and distal cortex) 4. Tap 5. Insert Screw Fully Threaded Screw Insertion Technique 1. Thread / Pilot Hole 2. Countersink 3. Glide Hole 4. Depth gauge 5. Tap 6. Insert Screw 43

INTERNAL FIXATION CONTINUED… Screw Selection Chart: Thread Diameter Mini-Fragment 1.5 2.0 2.7 Small-Fragment 3.5 4.0 (partial/cancel) 4.0 (full/cancel) Large-Fragment 4.5 4.5 (mall) 6.5 (partial/cancel) 6.5 (full/cancel)

Thread Hole

Gliding Hole

Tap Diameter

1.1 1.5 2.0

1.5 2.0 2.7

1.5 2.0 2.7

2.5 2.5 2.5

3.5 NA NA

3.5 3.5 3.5

3.2 3.2 3.2 3.2

4.5 NA NA NA

4.5 4.5 6.5 6.5

44

INTERNAL FIXATION CONTINUED… Soft Tissue Anchors:  Used for reattachment of tendons or ligaments  2 basic types: Expandable / Screw type  Complications: Improper Placement / Failure of Suture / Pullout Plates:  Various size and shape – allow alignment of the bones and stability across the fracture / osteotomy site  Stability allows for early passive RoM  Adequate screw fixation is important for the plate to function properly  Plate designs include semitubular, 1/3 tubular, ¼ tubular, T – plate, L – plate, calcaneal plate… Types of Plates: 1. Neutralization Plate a. Prevents torsional / bending forces from acting on the lag screws b. The ridge extension of the plate on the bone proximal & distal to the fracture / osteotomy site helps neutralize any extra forces along the bone segment 2. Compression Plate a. Generate compressive forces along the fracture / osteotomy site by either placing the plate on the tension side of the bone, offset drilling (AKA load screw technique) or pre-bending the plate.

45

INTERNAL FIXATION CONTINUED… Plates Continued… 3. Dynamic Compression Plate (DCP) a. Employs the concepts of offset drilling with unique plate designs to optimize the compressive forces of the plate b. Disadvantage is it increases periosteal damage and decrease intramedullary blood supply to the area, decreasing the overall strength of the bone segment 4. Limited Contact Dynamic Compression Plate a. Has a series of recessed undercuts on the undersurface of the plate which allows limited contact between the bone and the plate b. Generates less disruption to the vascular supply 5. Buttress Plate a. Anchored to the main stable fragment b. Supports the load-bearing bone c. Indicated in impacted fracture that results in comminution (e.g. tibial plateau and the tibial pilon fractures) 6. Bridge Plate a. Useful in unstable comminuted fractures by spanning the length of the comminution b. Frequently used with bone grafts to fill the voids in the bone

46

EXTERNAL FIXATION External fixation implements the use of wires, pins, and rods to keep bone segments in alignment or compression. Furthermore they allow distraction of bone segments by the principle of tension-stress effect. Advantages:  Use in open fractures, acute, fractures, infected fractures and nonunions  Requires minimal tissue dissection  Allows compression, neutralization, or fixed distraction of bone segments  Length can be maintained in a comminuted fracture  Allows access to the wound site for care, monitoring and dressing changes  Full weight bearing is allowed immediately post-operatively Disadvantages:  Requires skin and pin tract care  Difficult frame construction  Bulky frame  Fracture through the bone is possible  Refracture possible after frame removal  Expensive Basic Principles of External Fixation: 1. Frame should avoid and respect all vital structures in the area 2. Allow access to the wound site 3. Frame must meet the mechanical demand of the patient and injury

47

EXTERNAL FIXATION CONTINUED… Complications:  Pin irritation – avoid pin placement in muscle  Pin tract infection – most common complication (30%)  Neurovasculature Impalement – Anterior Tibial A. & Deep Fibular N. and they are most commonly involved  Delayed Union / Non-Union – due to faulty frame construction  Compartment Syndrome – due to increase in the intracompartmental pressures (mmHg)  Refracture – once the frame has been removed due to tension shielding, a rare complication Types of External Fixators: 1. Unilateral Fixators  Produces compressive or distraction forces  Used to fixate fractures, fuse joints, and lengthen  Available in small or large, it is attached to the bone by multiple half-pins screwed into the bone and attached to the fixator with the clamp  Main disadvantage – not create any sagital plane stability & therefore should not weight bear immediately post-op

48

EXTERNAL FIXATION CONTINUED… Types of External Fixators Continued… 2. Circulator Fixators  Produces compressive and distraction forces  Used to fixate fractures, treat non-unions, limb-lengthening , soft tissue lengthening, and correction of congenital deformities.  Utilizes trans-osseous wires with half-pins to position the wires in different plane stability  Limited by the circular frame’s ability to fit the extremity and patient’s comfort of wearing the apparatus 3. Hybrid Fixators  Combination of unilateral and the circular fixator  Used to treat tibial plafond fractures and pilon fractures  Utilizes trans-osseous wires and half-pins and footplate to allow early weight bearing 4. Taylor Spatial Frame Fixators  Newest external fixation device  Allows for reduction and stabilization of fracture  Its unique feature allows for reduction of complex triplane deformities

49

EXTERNAL FIXATION CONTINUED… Dynamization: After removal of the plate, the bone may be prone to re-fracture during weight-bearing because of weakening of the bone from disuse osteopenia. To prevent this complication it is important to gradually release tension in the trans-osseous wires and loosen the pins to allow the bone to gradually strengthen as it bears weight.

Fixator Care & Management: Pin sites need to be kept clean with sterile solution and applied antibiotic cream in order to prevent infection and seal the opening around the pins. Avoid applying Betadine around the pins in order to avoid corrosion.

50

COMMON FOREFOOT PATHOLOGIES AND SURGERIES Hallux Limitus / Rigidus Decreased or absent RoM at the 1st MPJ Normal RoM = 90o (20-25o PF + 60-65o DF) Radiographic Appearance AP  Focal joint space narrowing  Joint mice  Spurring  Asymmetry  Squaring of metatarsal head

Lateral  Dorsal Flag Sign  Spurring  Sclerosis  Metatarsus Primus Elevatus

Etiologies = TIN-MAC Trauma Infection Neoplasm of bone or soft tissue Metabolic Anatomic Structural = short/long 1st ray, Met Primus Elevatus 1. Meary’s Angle deviation (b/s talus should b/s 1st met) 2. Parallelism between 1st & 2nd metatarsals 3. Metatarsal parabola / protrusion deviation Biomechanical = pronation, hypermobile 1st ray Congenital

51

COMMON FOREFOOT PATHOLOGIES AND SURGERIES CONTINUED… Hallux Limitus / Rigidus Continued… Joint Procedures: Joint Preserving 1. Cheilectomy = Valenti (V-cheliectomy) 2. Osteotomies  Proximal Phalanx = Bonny-Kessel (proximal DFWO)  1st Metatarsal Waterman = Distal DFWO Mitchell = step-down shortening procedure Youngswick = chevron double dorsal cut elevates Sagital Z = corrects for elevates Lambernudi = diaphyseal PFWO, for elevatus Joint Destructive 1. Keller = Proximal Phalanx arthroplasty / for elderly / less functional  Complications – transfer metatarsalgia, stress fracture of 2nd, proximal migration of sesamoids 2. Implant = Hemi or Total – must cover cortical surfaces 3. McKeever = 1st MPJ arthrodesis – positioned dorsiflexed and abducted with no rotation  DF = 10-15o off weight bearing – one finger under toe  5-10o of abduction  Toe will no longer bend so patient cannot squat down Joint Distraction with External Fixator: 1. Cheilectomy, mini rail 2. 7mm distraction intra-operatively, 2 weeks rest, then 1mm distraction qd for 7d = Total 14mm Distraction

52

COMMON FOREFOOT PATHOLOGIES AND SURGERIES CONTINUED… Hammertoes Function of Lesser Digits:  Decelerate the foot  Stabilize the forefoot  Aid in propulsion  Provide kinesthetic sensation Function of Musculature:  EDL / EDB = dorsiflex MPJ – passive flexion at PIPJ / DIPJ  FDL / FDB = actively plantarflex MPJ, PIPJ, DIPJ  Interossei = prevent buckling  Lumbricales = hold digits rectus (plantarflex MPJ, dorsiflex PIPJ / DIPJ) Types of Deformities: Hammertoe Claw Toe Mallet Toe

MPJ Extension Extension Rectus

PIPJ Flexion Flexion Rectus

DIPJ Extension Flexion Flexion

Etiologies for Contracted Digits: 1. Flexor Stabilization (Most Common)  Weakness of intrinsic Interossei Ms  Adv. of Quadratus Plantae  Pronated foot type – flexors fire longer and harder  Causes AdductoVarus deformity on 4th and 5th  Late stance phase biomechanical abnormality  Tx = Derotational Arthroplasty

53

COMMON FOREFOOT PATHOLOGIES AND SURGERIES CONTINUED… Hammertoes Etiologies Continued: 2. Flexor Substitution (Least Common)  Weakness of Triceps Surae – Flexors gain mechanical advantage over extensors  Supinated foot type – late stance phase abnormality  Tx = suture FDL to Achilles tendon to strengthen muscles  Must perform Arthrodesis 3. Extensor Substitution  Weak Tibialis Anterior – extensor gains mechanical advantage over Lumbricales  Begins flexible and becomes rigid  reduce early w/ weight bearing  Pes Cavus / Ankle Equinus / TA weakness / EDL spasticity and pain are frequent symptoms  Swing phase biomechanical abnormality  Tx = Arthrodesis if Rigid Hibb’s Tenosuspension if Flexible

54

COMMON FOREFOOT PATHOLOGIES AND SURGERIES CONTINUED… Hammertoes Surgical Procedures: SOFT TISSUE 1. Tenotomy = stab incision medial or lateral to tendon deformities only  PF digit with blade in place – flexible deformities only  Older population only – lose strength & stability 2. Capsulotomy 3. Tendon Transfer 4. Girdlestone  Transfer FDL & FDB to dorsal head of proximal phalanx to restore intrinsic function 5. Hibbs  Transfer EDL to base of proximal phalanx or met head 6. Kuwada & Dockery  Modification of Girdlestone – drill hole in base of proximal phalanx and bring tendons up through it 7. Lengthening 8. Z-Plasty at level of MPJ 9. Percutaneous stab incision and splint **Complications: Muscle spasm caused by overcorrection, tenosynovitis, scarring, adhesion, weakness, bowstringing, and nerve entrapment OSSEOUS 1. Arthroplasty  Post – resection of base of proximal phalanx  Gotch & Kreuz – resect base of proximal phalanx and syndactylize digits 2. Arthrodesis  Lambrinudi – fusion of PIPJs and DIPJs  Young-Thompson – Peg-in-Hole Fusion (Peg from Prox.Phalanx)  High amount of shortening 3. Taylor – PIPJ fusion using K-Wire 55

COMMON FOREFOOT PATHOLOGIES AND SURGERIES CONTINUED… Hammertoes Sequential Reduction: 1. Z-Plasty 2. Arthroplasty 3. Extensor Hood Release 4. MPJ Capsulotomy 5. Volar Plate Release 6. Tendon Transfer (Girdlestone, Kuwanda & Dockery, Hibbs) ** Kelikian Push-Up Test: Performed between each step to determine if sufficient correction has been established. If you get dorsiflexion when placing GFR on the met head then do the next step. Hallux Hammertoe: Etiology:  Muscle imbalance  Iatrogenic after sesamoid removal or detachment of FHB  IPJ sesamoid binding FHL tendon Treatment: Flexible – IPJ fusion with EHL lengthening Rigid – IPJ fusion with Jones Tendon Transfer ~ Cut EHL distally from insertion ~ Drill hole transversely through 1st med head ~ Insert tendon through drill hole and suture back on itself

56

5TH DIGIT ARTHROPLASTY 1. Lazy “S” Incision  Lateral condylectomy of distal and middle phalanges with resection of head of proximal phalanx 2. Derotational Arthroplasty  Distal Medial  Proximal Lateral Incision 3. Complications  Floppy Digit  Edema (sausage digit)  Floating Toe with Metatarsalgia  Regeneration of Proximal Phalanx  Infection  Decreased sensation  Blue toe

57

REARFOOT SURGERY Spurs are incidental findings only and are rarely the cause of pain. 1. May be painful if directed plantarly 2. Must be present to be approved for orthotics Conservative therapies should be used for the first 3-9 months Plantar Fasciotomy: 1. Plantar L shaped incision at the medial midfoot 2. Release of the medial band of the plantar fascia 3. NWB for 3 weeks 4. Sutures out after 3 weeks Endoscopic Plantar Fasciotomy: 1. Small incision in the medial rearfoot 3 fingers from the posterior heel and 2 fingers up from the plantar foot 2. Blunt dissection to the fascia 3. Insert spatula across plantar aspect of foot, dissecting fascia from plantar fat pad – remove spatula 4. Insert trochar into slotted tube and insert through dissected incision – remove trochar 5. Insert scope into tube laterally and blunt probe medially – separate medial and central bands of plantar fascia 6. Insert cutting tool into medial tube and cut medial band of plantar fascia while pulling instrument out of the tube 7. Visually observe abductor hallucis muscle belly before removing tube and irrigating incision site

58

REARFOOT SURGERY CONTINUED… Haglund’s Deformity: Angles: Philip-Fowler Angle = normal 44-69o, >75o pathological Total angle of Ruck = Philip-Fowler + Calcaneal Inclination Angle – Normal up to 90o, pathological if > 110o Parallel Pitch Lines – most objective method of determining a Haglund’s deformity Procedures: Longitudinal incision lateral to TA Dissection down to posterosuperior Calcaneus Aggressive removal of pathologic bone, but don’t chase the bump If you need to reflect the TA, reattach with a soft tissue anchor and remain NWB for 3 weeks Keck & Kelly Osteotomy: Indicated for increased CIA angle with no Haglund’s deformity Dorsal wedge osteotomy of the posterior Calcaneus Rotate posterior aspect of Calcaneus dorsally after wedge removal – MAINTAIN PLANTAR HINGE Secure with cancellous screws NWB for 6 weeks

59

TENDON TRANSFERS Tendon Transfer – detachment of the tendon from insertion then relocate to new position Tendon Transplantation / Translocation – rerouting the tendon without detachment from its insertion Types: 1. Adductor Hallucis  Resect at insertion, pass under the joint capsule and reattach at medial aspect of the capsule  Indicated in HAV to realign the sesamoid apparatus 2. Abductor Hallucis  Transected at insertion, rerouted inner 1st met head and fixated at lateral base of proximal hallux  Indicated in Hallux Varus with an osteotomy 3. Extensor Hallux Longus  Transected at origin, rerouted under DTIL, fixated to lateral base of proximal hallux  IPJ needs fused  Indicated when have sagital component with Hallux Varus 4. Jones Suspension  EHL excised from insertion, drill a hole transversely through 1st met head, rerouted through hole and sutured on itself  Indicated with cock-up deformity, flexible cavus, lesser metatarsalgia, chronic ulcers, weak TA, flexible plantarflexion of 1st met 5. Hibb's Tenosuspension  EDL detached from insertion, bundled together and placed through midfoot at the base of the 3rd met or lateral cuneiform  Indicated to release retrograde buckling at MPJs, met equines, flexible cavus, claw toes 60

TENDON TRANSFERS CONTINUED… Types Continued... 6. Tibialis Anterior Transfer  3 incisions at (1) proximal dorsal leg, (2) TA insertion at medial plantar cuneiform / tubercle 1st met, and (3) the new area of insertion in the midfoot  Release from insertion, reroute out the proximal incision, with tendon, with tendon passer brought to new insertion (usually 3rd cuneiform)  Indicated for recurrent clubfoot, flexible forefoot equines, dropfoot, tarsometatarsal amputation, Charcot Marie Tooth deformity 7.

Split Tibialis Anterior Tendon Transfer (STATT)  3 incisions at (1) base of 1st met, (2) anterior leg over TA just lateral to medial malleolus and (3) over peroneus tertius at base of 5th met  Split tendon through proximal insertion, lateral slip passed through peroneus tertius sheath and sutured to tendon fixated to cuboid  Indicated for spastic RF equines, spastic equinovarus, fixed equinovarus, FF equines, flexible cavovarus deformity, DF weakness, excessive supination in gait

8.

Cobb Procedure  STATT but reroute to TA to PA tendon  Indicated for PT dysfunction

61

TENDON TRANSFERS CONTINUED… Types Continued... 9. Tibialis Posterior Tendon Transfer  3 incision (1) insertion of the PT at navicular tuberosity, (2) anterior leg, middle 1/3 just lateral to tibial crest and (3) one at new insertion at dorsal midfoot  Tendon released from navicular Tuberosity, dissected free at the medial leg insertion to expose the IM and the PT pulled through this opening then brought to new insertion level (usually 3rd cuneiform)  Indicated for weak anterior muscles, equinovarus, spastic equinovarus, recurrent clubfoot, dropfoot, complications from Charcot Marie Tooth, peroneal nerve plaste, leprosy, Duchenne’s MS  Muscle goes from a stance to a swing muscle during gait 10. Peroneus Longus Tendon Transfer  3 incisions (1) lateral, lower leg, (2) lateral cuboid and (3) base of 3rd met/lateral cuneiform  Suture the Peroneus Longus to the Brevis , cut the longus at the level of the cuboid and the tendon is brought through the proximal incision and back through the medical incision to the 3rd cuneiform  Indicated for anterior muscle weakness, dropfoot

62

TShwer

BUNION PROCEDURES TO KNOW BASED ON ANGLES IM Angle

12-16o

DASA

>8o

Proximal Osteotomy

Proximal Akin -- cylindrical akin w/ long prox phalanx -- oblique -- transverse -- Bonnel-Kessel  DF wedge

>8o

Distal Osteotomy

Reverdin Reverdin Green PASA

Distal Osteotomy

Austin Hohman (Neck) -- Trapaziodal o Normal: 0-8 Mitchell (Neck) Wilson (Neck) Reverdin Laird (Distal L) Short Z Waterman Youngswick o >16 Proximal Base Wedge Osteotomy Lapidus (Met-Cuneiform Fusion)Hypermobile Cresentic Juavara Proximal V of Kotzengerb Comments: with a thin Met shaft  may need to use a proximal procedure Mitchell – shortens the length of met shaft  used in Long Met Length ( >2mm longer than 2nd met) Taylor’s Bunion = Symptomatic when IM4-5 >9o Splayfoot = IM1-2 + IM4-5 >20o

Normal: 0-8o

Comments:

PASA Normal: 0-8o Comments:

63

Abnormal IM:12-16o Distal + Abn P Osteotomy PASA + IM Angle

IM: >16o + Abn P

Biplane Austin Reverdin Laird (Distal L)  PASA + IM Reverdin Green Biplane Mitchell  Roux Hohmann Shaft Mau Osteotomy Ludloff Scarf / “Z” Klotzenberg Juvara Proximal Lapidus w/ Reverdin Osteotomy V Osteotomy Logroscino (Base Wedge Reverdin) Cresentic Juavara Proximal V of Kotzengerb

Comments:

HAA

> 16o

Silver McBride Adductor Hallucis Tenotomy Lateral Capulotomy

Normal: 0-16o Comments: ST or Osseous Abnormality ↑ HAA + IM1-2 13-20o = Lodloff + Mau (+ ↑ PASA) = Scarf Z HIA

> 10o

Distal Akin

Normal: 0-10o Comments:

64

Tibial Sesamoid Position

4-7

Fibular Sesamoidectomy Fibular Sesamoid Release

Normal: 0-3 Comments: Lateral Deviation Angle Normal: 2.5o + IM4-5 Normal: 0-8o

IM: 8-12o Normal 2 Slight Increase

Distal Osteotomy  exostectomy  dist. metaphyseal osteotomy

LDA: Inc IM: > 15/16o Proximal Marked Inc Osteotomy LDA: ↑ Severe Lat Bowing

Comments:

65

Reverse Austin Reverse Mitchell Reverse Hohmann Reverse Wilson Reverse Mercado Base Wedge

66

Other Important Things to Know for 3rd Year Rotations & Externships Dr. Bodman’s Drugs

p. 68

Dr. Caldwell’s Drugs

p. 74

Dr. Caldwell’s Wound Care

p. 84

Ankle Scopes

p. 90

67

68

69

70

71

72

73

74

TShwer

β – LACTAMASE’S SENSITIVE PENICILLIN’S Penicillin V (PO) Penicillin G, Aqueous (IV)

** Tx: Clostridium Tetani if allergic to Tetanus Toxoid

Penicillin G, Procaine (IM)

G+: Strep G–: Eikenella corrodensHuman Bites Nisseria gonorrheaSTD Septic Joint Anaerobes: Clostridium perfringens

** Tx: Treponema Palidum (Syphilis) Tx: Strep Throat & Otitis Media

Ampicillin

Amoxicillin

** Used in kids instead of Augmentin!

G+: Strep G–: Eikenella corrodens Nisseria gonorrhea HELPS2 Anaerobes:

HELPS2: Haemophilus E. coli Listeria Proteus mirabellus Shigella Salmonella

RESISTANT PENICILLIN’S (3RD GENERATIONS) Resist MONDay’s! M Methacillin (IV) ** Toxic, not used!

O

Oxacillin (Bactocil)(PO) β–Lactamase Resistant Staph Aureus

N

Nafcillin (Unipen)(PO)

D

Dicloxacillin (PO)

If resistant to this = MRSA!

EXTENDED SPECTRUM PENICILLIN’S (4TH GENERATIONS) Carboxypenicillins Carbenicillin High Na+ loads  avoid pts w/ HTN Beware of Hypokalemia!

Ureidopenicillins

Ticaricillin Mezlocillin

Broad SpectrumDo NOT cover β–Lactamase G+: Good Coverage G–: ↑ Coverage Anaerobes: ↑ Coverage

** Tx: Pseudomonas aeruginosa

Piperazine Penicillin

Piperacillin

DRUG INTERACTIONS: Warfarin, Oral Contraceptives, Probenecid, Aminoglycosides C/I with pts on Methotrexate Rheumatiologist 75 Docs tell pts they are C/I! Pt must take all 10d of meds or else get post-strep glomerulonephritis

β – LACTAMASE’S COMBINATION DRUGS Piperacillin / Tazobactam (Zosyn)(IV)

Tx: Pseudomonas aeruginosa & Proteus mirabilis  Needs 4.5g q6h for pseudomonas

Amoxicillin / Clavulanic Acid (Augmentin)(PO) **Staph aureus is susceptible to Augmentin ≤ 35% due to MRSA

Ticarcillin / Clavulanic Acid (Timentin)(IV) Ampicillin / Sulbactam (Unasyn)(IV) **Unreliable against G– infections!

DOSAGE BOX: Zosyn = 3.375g q6h Augmentin = 875mg q12h Timentin = 3.1g q6h Unasyn = 3.0g q6h

76

Broad Spectrum G+: Strep, Staph aureus G–: Neisseria gonorrhea… Anaerobes: 

CEPHALOSPORIN’S 1ST GENERATION Cephalexin (Keflex)(PO) Cephadroxil (Duricef)(PO) Cefazolin (Ancef)(Parenteral)

G+: Good Staph aureus Staph epidermidis Strep – G : Some PEcK An: Some not B.fragilis

< 80% susceptibility to Ancef

2ND GENERATION Cefuroxime (Ceftin)(PO) (Zinacef)(Parenteral) Cefoxitin (Mefoxin)(Parenteral)

HEN – PEcKS: Haemophilus influenza Enterobacter aerogens Neisseria species Proteus mirabilis E. coli Klebsiella pneumonia Serratia

G+: Almost as good as 1st G G–: Extended HEN – PEcKS An: 

3RD GENERATION Cefixime (Suprax)(PO) Cefpodime (Vantix) (PO) Ceftriaxone (Rocephin)(Parenteral) *Not good for Staph

Ceftazidime (Fortaz)(Parenteral) Cefdinir (Omnicef)

G+: Significantly ↓↓↓ G–: Superior Coverage (Fortaz  Pseudomonas) (Rocephin  Neisseria) An: 

*Covers Staph & Strep better than 1st G.  MIC levels are superior to Cephalexin 4x’s better for Staph // 7x’s better for Strep

DOSAGE BOX: Omnicef = 300mg q12h

4 GENERATION Cefipime (Maxipime) TH

G+: More active against Staph aureus than 3rd G G–: Good Coverage (+ Pseudomonas) An:  EXTENDED GENERATION Ceftobiprole

G+:  – Active against MRSA G–:  An: 

DRUG INTERACTIONS: Avoid Cephalosporins if pt allergic to Penicillin! Cefdinir(2ndG) & Cefuroxime(3rdG) are allowed for Penicillin allergy! 



Due to different structure.

77

CARBAPENAM’S Imipenam–Cilastin (Primaxin) *ID specialists ONLY!

Meropenam (Merrem) *Mostly ID specialists ↓ Seizure Risk!

G+: Staph & Strep only (Inferior to Imipenam) G–:  (Superior to Imipenam) An:  

Ertapenam (Invanz)(IV/IM) G+:  G–: Limited An:   Doripenam

Broad Spectrum G+:  – Most G–:  – Most (pseudomonas – resistant) (mycoplasma – resistant) An:  – Excellent

DOSAGE BOX: Invanz = 1g qd CrCl < 30ml/min = 500mg 6h pre-dialysis

Broad Spectrum G+:  G–:  (pseudomonas) An: 

DRUG INTERACTIONS: C/I in pts with Penicillin allergy C/I in pts with Seizure History Ertapenam interacts with Probenicid.

78

MONOBACTAM Aztreonam (Azactam)(IV/IM)

G+:  G–:  (?pseudomonas) An: 

*OK for Penicillin Allergy No major renal toxicities; only dose adjust for renal insufficiency or dialysis

AMINOGLYCOSIDES Gentamycin Tobramycin Amikacin

G+:  G–: 

* NOT use on Diabetics or MyGravis Peak (30min post dose) & Trough (30min before next dose) levels are recommended

MRSA Proteus mirabilis Pseudomonas Klebsiella E. coli Salmonella Shigella

ADVERSE DRUG REACTIONS: Ototoxicity (Irreversible) Nephrotoxicity (Reversible) HypoK+ ––– Gentamycin HypoMg+ –– Amikacin

An:  GLYCOPEPTIDES 1ST GENERATION Vancomycin (PO/IV)

Tx: Endocarditis Prophylaxis for pts allergic to β-lactams - Keep for reserve cases!

G+:  G–:  An: 

DOSAGE BOX: Vancomycin = 1g slow push IV (over 60min)

IVMRSA POClostridium

difficile

DOSAGE ADJUSTMENT BOX: 50kg: 750mg Normal Trough = 5-10mg/dL 50-74kg: 1000mg If trough range >15mg/dL  75-90kg: 1250mg double the dose time interval >90kg: 1500mg

2ND GENERATION G+:  -- MRSA, VRSA, Strep, C.difficile Dalbavancin(PO/IV) G–: ? ADVERSE DRUG REACTIONS: An: ? 3RD GENERATION Telavancin

G+:  -- MRSA, VRSA, Strep G–: ? An: ? 79

Ototoxicity (Reversible) Nephrotoxicity (Reversible) Red Man Syndrome Vestibular Imbalance Thrombophlebitis

TETRACYCLINE’S Doxycycline

G+: 

Minocyline

G–: 

* Some Anti-Inflammatory properties seen on OA

Staph aureus MRSA E. coli Klebsiella Enterobacter Vibrio vulnificansSalt Water Rickettsia Chlamydia

Methacycline Tetracycline HCL

Absorption is limited by: ~ Food ~ Milk ~ Antacids ~ Iron

An:  

ADVERSE DRUG REACTIONS: NonSpecific GI Issues ~ Don’t give Doxycylcine before bed  erosive esophagitis Photosensitivity Photo-Onycholysis (Doxycycline) ?Acute Pancreatitis CONTAINDICATIONS: No Pregnant / Kids ~ tooth discoloration in kids under 8y C/I for pts on Digoxin -- ↑ Toxicity C/I for pts on AccutaneAcne -- ↑ ICP, Pseudomotor Cerebri Risk

MACROLIDE’S

* Erythrasma  Coral Red Woods Lamp

Erythromycin G+:  Staph / Strep / Corynebacterium minitussimum* Rarely used -- poor G–:  ST penetration ADVERSE DRUG REACTIONS: An:   GI Upset Oral Dose = 2x Risk of Sudden Death Combined with Ca2+ Chanel Blockers = 5x Risk of Sudden Death (Verpamil, Diltiazam)

Prolonged Heart Depolarization ~ Torsades de Pointes DRUG INTERACTIONS: Potent Inhibitors of CYP 3A4 Cyclosprine / Sirolimus / Tacromilus C/I for pts on Carbazepine & Theophyline

Azithromycin + (Zithromax) G :  Staph / Strep G–:  Detox in Liver Excreted in Bile An:   DOSAGE BOX: Zithromax = 500mg 1st Day (z-pack) 250mg qd next 4 days

ADVERSE DRUG REACTIONS: GI Upset Prolonged Heart DRUG INTERACTIONS:Potent Inhibitors of CYP 3A4 ↑Digoxin // ↑Coumadin HMGcoA Reductase ↑ 80

LINCOSAMIDES Clindamycin (Cleocin)

G+: 

DOSAGE BOX: Cleocin = 600mg 1hr pre-op Given as prophylaxis for bacterial endocarditis

G–:  An: 

* Good Bone Penetration * Poor CNS Penetration

Fulminate Group A StrepNecrotizing Fasciitis Group B Strep ~ may show resistance MRSA ~ may show resistance Staph Aureus** *Staph Aureus resistant to B. fragilis

ADVERSE DRUG REACTIONS: Diarrhea Pseudomembranous Colitis

erythromycin on C&S can develop inducible resistance to Clindamycin *C&S of organism is sensitive to Clindamycin but resistant to erythromycin  do NOT give Clindamycin because it will develop resistance

DRUG-DRUG INTERACTION: ↑Respiratory Paralysis with m. relaxants (Baclofen / Diazepam)

CHLORAMPHENICOL G+:  G–:  An:  Serious Infections Last resort for VRE

ADVERSE DRUG REACTIONS: Gray Baby Syndrome Severe Bone Marrow Toxicity Aplastic Anemia

.

SULFONAMIDES Trimethoprim–Sulfamethoxazole (Bactrim / Septra)* Beware in pts over 50 year old G+:  G–:  An: 

Staph & Strep MRSA

ADVERSE DRUG REACTIONS: Acute pancreatitis



DRUG-DRUG INTERACTION: T–S + Methotrexate = ↑ Bone Marrow Suppression T–S + Coumadin/Digoxin = ↑ Toxicity of C/D T–S + Oral Sulfonylureas = Hypoglycemia

81

5-NITROIMIDAZOLE Metronidazole (Flagyl) * Tx Pseudomembranous Colitis

G+:  G–:  An:  B. fragilis

ADVERSE DRUG REACTIONS: Peripheral Neuropathies N/V with Alcohol Consumption Dark Brown Urine DRUG-DRUG INTERACTION: ↑ Anti-Coagulation effects of Warfarin

DOSAGE BOX: Flagyl = 15mg/kg loading dose 7.5mg/kg q6h IV -or- 500mg tid

FLUORINATED 4-QUINOLONES Ciprofloxacin (Cipro) DOSAGE BOX: Cipro = 750mg bid

G+:  G–:  most active against P. aeruginosa infection of bones & joints

An:  Levofloxacin (Levaquin) DOSAGE BOX: Levo = 500mg qd (po/IV) * Post antibiotic effects (G+)

Moxifloxacin (Avelox) * Good in ST * Good for diabetic foot infections with inoperable atherosclerosis * May work against TB

CONTRAINDICATIONS: Under age 18 Pregnant / Nursing

* Attacks joints *Can cause Tendonitis / Rupture



G+:  Strep G–:  N. gonorrhea An:  

ADVERSE DRUG REACTIONS: GI / Headache / Phlebitis all are rare!

Broad Spectrum G+:  Staphsome resistance Strepenhanced G–:  An:  B. fragilis

DRUG-DRUG INTERACTION: Not give within 2hr of: Multivitamins, Antacids, Sulcralfate MANY interactions! – Theophyline, Caffeine, Warfarin, NSAIDs, ddI (HIV) May see… Torsades de Pointes & Ventricular Fibrillation **May produce a false (+) on viral assay for opiates

82

RIFAMYCIN Rifampin

DOSAGE BOX: Broad Spectrum Not given alone  Give with Cipro / Bactrim G+:  Staph aureus Strep epidermidis MRSA – G :  N. gonorrhea Mycobacterium An:  

* Turns fluids Orange * CYP 450 system * Tx Leprosy * Tx Vanco Resistant MRSA

STREPTOGRAMINS Dalfopristin/Quinopristin (Cipro) G+:  VRE * Reserve this drug!!! MRSA MRSE G–:  An:  

ADVERSE DRUG REACTIONS: Arthralgia / Myalgia Nausea Thrombophlebitis ↑ LFT’s Injection Site Reaction

OXAZOLIDINONES Linezolid (Zyvox) * Good bone penetration * Check weekly CBC’s

G+:  VRE MRSA VRSA G–:  An:  

ADVERSE DRUG REACTIONS: Mylosuppresion N/V lactic acidosis Optic Neuropathy Tx >1mo

CYCLIC – LIPOPEPTIDE Daptomycin (Cubicin) * Check weekly CPK’s DOSAGE BOX: 4mg/kg qd

G+:  MRSA VRSA G–:  An:  

DRUG INTERACTIONS: Tobramycin Statins  Myopathy

GLYCYLCYCLINES Tigecycline (Tygacil) * Check weekly CPK’s DOSAGE BOX: IV: 100mg Loading Dose 50mg bid

Broad Spectrum G+:  MRSA VRSA – G :  An: 83 

ADVERSE DRUG REACTIONS: N/V Tooth Discoloration

ORAL ANTIBIOTICS Itraconazole (Sporanox) Onychomycosis Tinea pedis(off label)

Dermatophytes Candida Molds 



DOSAGE BOX: Pulse Dosing = 2x 100mg tabs in AM & PM with food Take for 1 week of the mo. for ___ months

Terbinafine (Lamisil) Onychomycosis Tinea pedis(off label)



Dermatophytes 

DOSAGE BOX: Pulse Dosing = 250mg qd 1 week/mo over 2mo Normal = 250mg qd 3mo

Fluconazole (Diflucan) Dermatophytes Candida DOSAGE BOX: Pulse = 300mg/week Molds 

Griseofulvin (Gris-PEG) Chronic Tinea pedis

Dermatophytes 

ADVERSE DRUG REACTIONS: GI upset / Rash / Headache Hepatotoxicity  LFT’s ALT & AST DRUG INTERACTIONS: Statins Ca2+ Channel Blockers Tikosyn Erythromycin CONTRAINDICATIONS: Patient with CHF! ADVERSE DRUG REACTIONS: Rare Headache / Abnormal Taste Green Vision DRUG INTERACTIONS: CYP450 2D6 Cimetidine Cyclosporine Rifampin Nortriptyline Caffeine

ADVERSE DRUG REACTIONS: Severe Skin Rash Alopecia Drug Interactions: CYP450 3A4

ADVERSE DRUG REACTIONS: Paresthesia / Rash / Headache DRUG INTERACTIONS: Oral Contraceptives Warfarin Barbituates

DOSAGE BOX: 250mg tid (x4-8 weeks)

ORAL ANTIPARASITIC Thiabendazole (Mintezol) * Cutaneous Larva Migrans

Ivermectin

DOSAGE BOX: Mintezol = 10% aqueous solution qid Ivermectin = 200μg/kg po x1dose for 1-2days

84

WOUND CARE & DRESSINGS ACTICOAT = Nanocrystalline Silver (antimicrobial effect up to 7days)  Reduces Exudates while maintaining a moist wound environment  Moisten with sterile water (NOT SALINE!!! Silver reacts with Saline)  Effective against VRE & MRSA IODOSORB GEL / IODOFLEX DRESSING = Absorbent Iodine Cadexomer  Slowly releases small amounts of a 0.9% elemental iodine ALLEVYN FOAM  Moderate to High Exudate  Never use the adhesive type! HYPAFIX  Adhesive, non-woven fabric  Hold post-op dressings / catheters / drainage tubes in place HYDROGEL SHEETS = ElastoGel, Nu-Gel, Vigilon, Amerigel  Low Exudate  Re-Epithelializing wounds  NonAdhesive  Gas permeable  (+) Provides Moisture  qd change for infected wounds  (+) No trauma upon removal  (–) Potential to macerate surrounding skin HYDRO-GEL = Duoderm Gel, Nu-Gel, Restore, Hypergel  Low Exudate  Partial  Full thickness wounds  Use once granulation tissue is present  (+) No trauma upon removal  (+) Provides Moisture  (–) Potential to macerate surrounding skin

85

TShwer

TRANSPARENT FILMS = Opsite, Tegederm, Bioclusive, Epivew  Adhesive, Polyurethane film  Low Exudate  May be used over absorptive wound filter or hydrogels  NOT for INFECTION!  Superficial Wounds (Blisters)  (+) Up to 7d wear time (semi-permeable)  (+) Allows visual assessment  (+) Provides Moisture  (–) Potential to macerate surrounding skin with excessive drainage  (–) NOT absorptive  (–) Adhesive may tear healthy skin HYDROCOLLOIDS = Duoderm, Duoderm CGFControl Gel Formula, Tegasorb, Restore  Adhesive, Occlusive  Low Exudate  Granulating & Epithelializing Partial Thickness Wounds  May be used over absorptive wound filter or hydrogels  NOT for INFECTION!  Cover @ least 1inch of surrounding skin  (+) Up to 3d wear time  (–) May tear healthy skin  (–) Potential to macerate surrounding skin with excessive drainage  Change dressing before it leaks  Odor/Drainage are Normal FOAM = Acticoat Moisture Control, Allevyn, Polymem, TeilleAdhesive Border  Polyurethane  Adhesive or NonAdhesive  Moderate to High Exudates  Varying Thickness  Infected wounds if changed daily  Venous Leg Ulcers  (+) Up to 7d wear time  (–) May tear healthy skin

86

ALGINATE = Sorbsan, Dermacea Alginate, Kaltostat, Curasorb  Seaweed Polymer  Gel formed when fibers interact with wound fluid  Pad or Rope Form  Partial/Full Thickness Granulating Wounds  Moderate to High Exudates  (+) Haemostatic effect  (+) Up to 7d wear time  (–) Requires 2o dressing  Infected wounds if changed daily  Tan mucoid appearance upon removal  ALGINATE WITH COLLAGEN = Fibracol  90% Collagen, 10% Alginate  ALGINATE IMPREGNATED WITH SILVER ABSORPTIVE WOUND FILTERS  Sheets, Rope, Paste, Granules, Powder made of Starch Polymers  Deep Wounds  Heavy Exudate COLLAGEN BASED PRODUCTS: Medifil Particles/Pads/Gels, SkinTempNylon Mesh over collagen membrane  Use Collagen Gels for Dry Wounds  Use Sheets for Low  Moderate Exudative Wounds  Use Powders, Particles, Pads for Moderate  Heavy Exudative Wounds  Actions: Absorbent, Hemostasis, Chemotaxis, Provisional Matrix in wounds for Granulation tissue formation  PRISMA  colonized or contaminated wounds  55% Collagen // 44% ORC Oxidized Regenerated Cellulose  1% Silver  PROMOGRAN  55% Collagen // 44% ORC  Only matrix proven to bind & reduce MMPs Matrix MetaloProtinase  ORC/Collagen combo binds more MMPs in the dressing the ORC or Collagen alone  PEGASUS = Unite Biomatrix  Enzyme resistant collagen scaffold -- Fenestrated

87

RECOMBINANT DNA TECHNOLOGY  REGRANEX = Becaplermin  Recombinant PDGF platelet-derived growth factor  Attracts monocytes & fibroblasts -- inflammatory phase  Stimulates granulation tissue  Refrigerate  Regranex Gel 0.01%  15g tube, apply qd, spread evenly and thin (1/16th inch)  Cover in moist saline gauze dressing  PROCURAN = Thrombin–Induced Platelet Releasate  GF from patients own blood  50-200cc of blood drawn from patient  Spin down, separate, activate the thrombin  1 blood draw = 3mo of daily application GRAFTS  APLIGRAFT = Bilayered Skin Equivalent  Epidermis & Dermis Dermis side down  Newborn foreskin  FedEx in 24hr in petri dish – use immediately  Place a compressive wrap over it  DERMAGRAFT = Human Dermal Replacement  Newborn foreskin  Cover with Allevyn & Hypofix tape  DO NOT use with any other topical agent  OASIS  Small Interstine Submucosa Pig/Porcine  SIS scaffold attracts patients cells  Store @ room temp up to 18mo  INTERGRA  Collagen–GlycosAminoGlycan Biodegradable Matrix Cow/Bovine  Porous Matrix of cross-linked bovine tendon collagen/GAGs  Semi-Permeable Polysilxane (Silicone) layer  Sterile Preperation

88

 GRAFT JACKET  Processed Human Dermal Membrane  3-D Bioactive Frame – supports granulation tissue  Deep Wounds  GAMMAGRAFT  Irradiated human skin allograft  Epidermis & Dermis  Store @ room temp  After 24hr in place -- remove secondary covering and allow area to airdry for 2-3hr  once dried in place there is no need to recover it  (+) Patients can do this at home TOPICAL ENZYMES:  SANTYL = Collagenase  Digests collagen in necrotic tissue  Collagen in healthy tissue or in newly formed granulation tissue is not attacked  May be used as an Antibiotic Powder  Stop use when granulation tissue is well established  Accuzyme, Gladase  Papain Proteolytic enzyme from papaya  Urea  Protein denaturing agent  May have a burning sensation in patients RARE  Cleanse with normal saline, NOT water  Panafil  Papain  Urea  Chlorophyllin Copper Complex Sodium  Inhibits hemagglutinating & inflammatory properties of protein degradation products in the wound  Elase = FibrinolysinDesoxyribonuclease RARE 2 Find TOPICAL AGENTS FOR LOCAL BLOOD FLOW  XENADERM OINTMENT  Balsum of Peru  Increased blood flow to wound site  Castor Oil  Creates a moist environment  Trypsin  Maintains moist wound bed  Aluminum Magnesium Hydroxide Stearate  Fluid Repellent 89

ANKLE SCOPES PORTALS:  Anterior o AnteroMedial  Medial to Tibialis Anterior  Visualize: medial gutter & medial transchondral margins  Caution: TA, Saphenous V & N o Accessory AnteroMedial o AnteroLateral  Lateral to EDL or Peronial Tertius  Visualize: lateral gutter  Caution: EDL, Peronial Tertius, Superficial Peroneal N o Accessory AnteroLateral o AnteroCentral  Lateral to EHL  Caution: AntTibial A, Deep Peroneal N, EHL & EDL tendons o Medial Midline Portal  Posterior o PosteroMedial  Medial to the Achilles Tendon  Caution: Sural N, Lesser Saphenous V o Accessory PosteroMedial o Modified PosteroMedial o PosteroLateral  Lateral to the Achilles Tendon  Visualize: the posterior process of the talus & posterior media talar dome  Caution: T-D-A-N-H o Accessory PosteroLateral o TransAchilles  6 Central Points o Coaxial Portals o Med / Central / Lat – TibioTalar Artic o Posterior Inferior TibioFibular Lig 21 POINT EXAM: o Transverse TibioFibular Lig  8 Anterior Points o Capsular Reflection of the FHL tend o Deltoid Lig  7 Posterior Points o AntMed Gutter o PostMed Gutter o Med / Central / Lat – Talar Dome o Med / Central / Lat – Talar Dome o Ant TibioFibular Articulation o Post TibioFibular Artic o AntLat Gutter o PostLat Gutter o Anterior Gutter 90 o Posterior Gutter

91

92

93

94

95

96

97

98

99

100

PODIATRIC RADIOLOGY INTERPRETATION OF PEDAL RADIOGRAPHS X-ray interpretation is a written notation of pathological findings made in objective terminology. Correlation of radiographic findings along with clinical and lab findings allows a physician to arrive at differential diagnoses. X-ray interpretation follows the 5-step approach: 1. Quality of Film • Too light or too dark (background/film density) • Proper projection • Proper positioning • Adequate contrast 2. Soft Tissue Assessment • Increased ST density (edema, obesity) • ST calcification (vascular, traumatic, chronic) • ST contour – thicker medially and proximally • Foreign bodies (r/o artifact w/ multiple views) 3. Bone Assessment • Number of osseous structures – start distally and work proximally • Integrity and morphology of osseous structures – are cortices intact? Are there structural changes? • Density of osseous structures – evaluate 2nd MT o Rule of 1/3s – in individuals <40 y/o, middle 1/3 should be medullary, outer 2/3 should be cortical o Rule of 1/2s – in individuals >40 y/o, half bone should be cortical, half medullary o 1/3 of bone is lost before apparent on X-ray o Cortical bone lost at a rate of 2%/year (>35 y/o) o Medullary bone lost at a rate or 1% per year 4. Joints and Joint Spaces • Is there narrowing? Is it symmetrical/asymmetrical? • Absence of joint = coalition/joint fusion • Increased space is due to joint effusion 5. Biomechanical Assessment • Measure of angular relationships for treatment goals • Determines surgical procedure and post-op correction • Performed in angle and base of gait • Serial radiographs to check progression of healing Conclusion – use systematic approach to avoid missing details. Review the entire film. Do not let your eyes be drawn to the obvious. Cite only differentials which make sense and are defensible to you. RADIOGRAPHIC VARIANTS Identification of variants requires knowledge of normal anatomy. Often normal variants are mistaken for pathology. The simplest error in this regard is structural overlap due to wrong projections ordered. Benign fibrocortical defect – small area of discontinuity usually in long bones. Eventually fades away over time. Nutrient foramen – may look like a fx, but discontinuity “stops” halfway through the cortex. Ward’s triangle – area of low trabecular density in the anterior inferior portion of the calcaneus. Epiphyseal plates can look similar to fractures, if the X-ray passes through the plane of the plate. Closed epiphyseal plates

also leave epiphyseal scars which may look like stress fxs. These occur in predictable anatomical areas. Epiphyseal plates tend to close from medial to lateral in teenagers. Talar beaking is a finding on lateral of the distal neck of the talus that occurs secondary to capsular pressure. Trabeculae in some circumstances may be accentuated, and look possibly like a fx. The calcaneal apophysis is located at the posterior aspect of the calcaneus, and has irregular margins. It is often mistaken for a fracture. It also may be normally bifid. Compact bony islands are normal and benign variants. A simulated fracture may occur in any bone w/ more than one ossification center. The silver dollar navicular is a normal (small) variant of navicular development – be sure to r/o Kohler’s dz. A pronated foot may cause the spaces between bones in the midfoot to be accentuated, causing a simulated lisfranc’s fx. A pseudo-epiphysis is a secondary ossification center. The gun-barrel effect is seen when a bone (usually phalanx) is perpendicular to the film plane. It may look like a cyst. Distal phalangeal condyles are normal variants. Cone-shaped epiphyses may be normal but are frequently syndromic as well. ACCESSORY OSSICLES AND SESAMOIDS Accessory ossicles and sesamoids are normal variants in anatomy that occur in predictable locations. Accessory ossicles usually arise earlier, are larger, and irregular compared to sesamoids (which are usually present in tendons.) Os Trigonum (2-8%) – occurs posterior to the lateral tubercle of the talus. When fused (~18 y/o) is called steida’s process. Os Tibiale Externum (3-12%) – secondary ossification center of the navicular tuberosity. The pre-hallux type is pyramidal in shape, while the accessory navicular is in the PT tendon. Os Intermetatarsium (1-10%) – occurs btw the 1st cuneiform and 1st and 2nd MT bases. May fuse. Os Supranaviculare (1%) – located on the dorsal aspect of the TN joint (may look like fx/osteophyte). Os Calcaneus Secundarius (1%) – located at the anterior process of the calcaneus – may be confused w/ rowe fx. Os Sustentaculi (<1%) – is located posterior to the sustentaculum tali, often fused. Is assoc w/ STJ coalition. Os Supratalare is located on the dorsum of the talar head. Os Vesalinum (<1%) – occurs at the proximal 5th MT base. Usually confused w/ apophysitis, or a stewart/jones fracture. Accessory ossicle of the Hallux occurs usually at the base of the distal phalanx at the medial or lateral aspect. Os Subtibiale/Subfibulare (4%) - occur distal to the medial and lateral malleoli. R/o trauma Hallux IPJ Sesamoids (50%) – located at the IPJ of the hallux, may remain cartilaginous. Assoc w/ plantar HPKs. Lesser IPJ Sesamoids occur in the joint capsule and short flexor tendons of the lesser digits. Does not occur in the 3rd. Os Peroneum (20%) - a sesamoid in the PL tendon near the cuboid. Often is not ossified. Constant Sesamoids occur in the MPJ of the hallux and ossify around 10-12 y/o. The tibial sesamoid is larger and is commonly bipartite. Partitions occur in cardinal body planes, and their combined size is greater than a single sesamoid. You must r/o fx when dxing a bipartite sesamoid.

THE 5 STEP APPROACH TO PLAIN FILM ANALYSIS STEP 2: SOFT TISSUE ANALYSIS The soft tissue analysis of plain film incorporates two main features: 1. Tissue Density 2. Tissue Contour First you want to determine what kind of view you are looking at. The most common is of course the DP view of the foot, which may be taken WB or NWB. To tell the difference, look at the joint spaces and see if they are clearly visible. If the MPJs are clearly visible the view is probably WB, which is taken at 15 degrees as opposed to NWB, which is shot at 0. You may also look to see the ankle position (90 in WB.) The view is important because WB views will show the soft tissue somewhat distorted due to pressure. On the DP this presents as extra thickness of the S.T. on the lateral column, and on the lateral it presents as flatness on the plantar surface. The first point, density evaluation, requires knowledge of different tissue densities to be of any use. The least dense material is of course gas or air, which is pathologic. The next higher density is fat, typically seen in kager’s/bohler’s/toygar’s triangle, as well as on the plantar surface. Next dense from fat is water, which is the primary composition of the soft tissues including muscle and tendon. Muscular compartments of the foot as well as the tendo Achilles will be of this density. Next dense is atrophied or devitalized tissue, which is somewhat dehydrated. Like gas, tissues of this density are pathologic and should be explained fully. Next dense is calcific density, which is the density of calcium deposits in the tissues. This is most often pathologic. Next dense is ossific density, which is the density of bone. Bones are only slightly denser than calcified structures – they are normally differentiated by their internal architecture. Finally, the densest structures radiologically are metallic or glass structures, which are almost completely radioopaque. Objects of this density are almost always foreign bodies, although in many cases they simply represent fixation or implants from prior surgery. Pathologic changes in soft tissue density may be either an increase or decrease in character. Edema causes generally an increased radiodensity which matches that of muscle or tendon, usually in areas where fat density is normal. This is important in the posterior triangle as well as on the plantar surface of the foot as extravasation of blood or fluid will show up as an obliteration of normal fat anatomy on film. Edema also causes an increase in soft tissue contour, which is the second point to evaluate in soft tissue analysis. Edema is normally classified by its cause. Obstructive edema is caused by obstruction of the lymphatic channels draining the affected area. This may be normal for the individual with congenital lymph blockage, as in lymphedema praecox, but with insidious onset of obstructive edema a previously undiagnosed pathology may be at work. D/Dx include tumor, trauma, radiation (repeated exposure to radiation damages

lymphatic channels), inflammation, surgery, burns, infection, or helminthic infestation. Inflammatory edema is associated with systemic disorders, particularly arthridites and metabolic disorders. D/Dx include A vitaminosis, RCPS, melorheotosis, collagen vascular diseases, dilantin use, reynaud’s disease, and thyroid dysfunction (thyroid acropachy – nodular myxedema.) Traumatic edema will be localized to the site of trauma and should be consistent with the history. Besides direct trauma, this type of edema is seen in stress fractures, infection, and in surgical sites post-op. Of particular clinical significance is edema in the posterior triangle (bordered by the posterior flexor hellucis longus, the anterior tendo Achilles, and the posterior-superior calcaneus.) Edema or hematoma from injury to the tendo Achilles will cause this triangle to disappear, which is a pathologic finding. Another pathologic finding is the teardrop sign of the ankle, which is visible as increased tissue density surrounding the ankle joint. This is caused by extravasation of fluid to the ankle joint subsequent to trauma. Ligamentous sprain is visible as diffuse edema surrounding the area of the affected ligament. Burns and frostbite cause areas of devitalized tissue to show up on radiographs as areas of increased density. Small localized areas of increased density are visible in the case of focal gigantism associated with acromegaly. Bony growth is also affected in this disorder and diagnosis should be easy to make if it has not been made already. Heel pad thickening is a finding associated with a number of pathologies, and as such measuring the heel pad is recommended in routine analysis of NWB views. Possible D/Dx include acromegaly, dilantin use, plantar edema, plantar infection, obesity, trauma, myxedema, and thyroid acropachy. The accepted limit for normal heel pad thickness is 25mm. Soft tissue emphysema is a decrease in radiodensity due to the presence of air or gas in the tissues. Always pathological and often the sign of an emergent situation, S.T. emphysema is a worthy finding. Gas is almost always produced by bacteria, especially clostridium perfringens, which may produce superficial emphysema (radiographic emphysema) or deep emphysema (deep intramuscular emphysema). The only non-emergent emphysema finding is of a gas abscess which is a localized ulceration containing gas which does not spread to other areas. Gas abscesses are typically found only in the distal part of the digits. It is important to distinguish emphysema from the decreased radiographic density caused by a sinus tract leading to an ulcer. A sinus tract will always track back to the surface of the skin, whereas emphysema is contained within the soft tissues. Some disorders which affect only soft tissue contour are worthy of note as well. Ainhum’s disease is a thickening of fascial bands about the base of the proximal phalanges of the digits, causing a constriction of the underlying tissues that is visible on x-ray. This constriction eventually leads to autoamputation, and although it is easy to diagnose from Xray, there is no known treatment for this disorder. The sullivan’s sign sometimes seen on radiograph is a splaying of digits which are abducted away from each other at the level of the MPJ. This is caused usually by a space-occupying lesion like a neuroma or interstitial fibrosis following surgery. Sometimes, however, the etiology is biomechanical, due to the

unequal pull of flexor tendons that can result from DM motor neuropathy, or simply from closely positioned metatarsal heads. Vascular calcification is seen in varicose veins, monckeberg’s sclerosis, ASO, thrombophlebitits, and DVT. They appear on X-ray as thin parallel or curvilinear lines. Phleboliths are small round or oval calcifications that appear within superficial veins. Dracunculosis is a rare finding that is seen in patients who have had a history of filiaria medinasis infection. These helminthes, which burrow into the dermis of the foot, remain after death as bits of foreign tissue that sometimes calcify. The dracunculosis is the radiographic finding of these calcified helminthes, which present as curvilinear lines of radiodensity that do not follow any vascular anatomy. Hemosiderin deposits may calcify in tissues following the trauma or disease state that caused them. This type of increased radiodensity is typically seen in periarticular tissue, arthritic joints, or the subcutaneous area of the ankle. General calcification of the soft tissues can be distinguished from ossification by the degree of organization seen in the radiodense area. Calcification is non-homogenous and disorganized, giving a “salt and pepper” appearance. Ossification, in contrast, is highly organized, often exhibiting a trabecular pattern, and may have a cortex. In general, soft tissue calcification is much more common that ossification. Calcification etiologies are organized into three broad categories: metastatic, dystrophic, and calcinosis. Metastatic calcification is systemic calcification of a metabolic derivative, such as hyperparathyroidism, hypervitaminosis D, renal osteodystrophy, sarcoidosis, or cancer. The calcifications are caused by an imbalance in calcium or phosphorus metabolism. The calcifications may appear vascular, but are typically more numerous and less organized than vascular calcifications. Advanced hyperparathyroidism causes chunky calcification, in which separate calcifications conglomerate into calcified patches that are prone to ulceration. Dystrophic calcification is calcification of devitalized tissues without metabolic imbalance. Theoretically calcium precipitates in devitalized tissue, giving rise to this type of presentation. Examples of possible etiologies include ehlers-danlos syndrome, pseudoxanthoma elasticum, fibromatosis, tumor, cyst, hematoma, focal necrosis, trauma of any kind, and vascular disease. One peculiar finding is that of hemarthrosis, which is calcification of blood exudate in a joint space. These calcifications may aggregate as “pebbles” within the capsule, visible on x-ray, that can limit ROM of the affected joint (common in the ankle.) Calcinosis is the term applied to califications that are idiopathic in nature. There are four syndromes associated mainly with calcinosis. Calcinosis interstitialis universalis presents as a calcification of subcutaneous structures, progressing deeper with time. It may affect any soft tissue, but calcifications are generally laid down in linear aggregations parallel to the long axis of the limb. This condition is very rare and is diagnosed in youth. Calcinosis circumscripta is a distal subcutaneous calcification that is normally associated with collagen-vascular diseases,

particularly CREST syndrome. Calcinosis circumscripta associated with frank scleroderma is termed thibergeweissenback syndrome. These distal calcifications predispose the digit to ulceration. Tumoral calcinosis is not associated with cancer as the name implies, but rather is a descriptive term referring to the presentation of the calcification. Seen in renally compromised patients (usually DM type II), these calcifications begin near joints as small nodules that eventually grow in size to possibly impinge neurovascular structures, limit ROM, and cause ulceration. The typical presentation is near the 5th MPJ. This type of growth is benign. The last form of calcinosis is calcified bursa secondary to irritation (usually posterior heel, medial 1st MPJ, lateral 5th MPJ.) Soft tissue ossification is distinguished from soft tissue calcification by the degree of organization within the ossified segment, typically with trabecular patterns. Additionally, ossifications that occur near bone characteristically do not cause periosteal reaction. Progressive myositis ossificans (aka fibrodysplasia ossificans progressive) is a rare childhood disorder in which there is extensive and unexplained muscular ossification which causes extraarticular ankylosis and disuse osteoporosis. Neurological myositis ossificans has a similar presentation but occurs in conjunction with a neurogenic lesion (stroke, spina bifida, encephalitis, syphilis, brain trauma, myelomeningocoele, spinal cord hemisection, tuberculosis, and poliomyelitis). The calcifications occur at levels below the neurogenic lesion. Finally, myositis post-traumatica (circumscripta) is an area of localized ossification secondary to acute trauma. Ossification begins soon after the traumatic incident, but cortical formation is only seen 6-8 weeks after the incident. Ectopic bone within the muscle may also be seen parallel to the muscle fibers. On X-ray the mass appears similar to an egg, with well-defined borders. Histologically it contains the same sections as an epiphyseal plate. Foreign body analysis in soft tissue is vital to localizing the foreign body for surgical removal. Analysis of the film typically calls for the ”tunnel technique” in which a piece of paper is rolled up into a tube, which is used to analyze small segments of the film at a time. Often needles are placed in three planes near the affected area so that when films are taken the exact location of the object can be triangulated. For some foreign bodies, particularly wood, advanced imaging modalities (ultrasound, CT, MRI, xerogram) should be employed.

THE 5 STEP APPROACH TO PLAIN FILM ANALYSIS STEP 3: BONE EVALUATION OSTEOLYTIC DISORDERS Osteoporosis is an absolute reduction in bone mass and density. Osteopenia is a generalized term to denote a relative loss in bone density regardless of any etiology. Osteoporosis is the most common skeletal pathology, common in smaller older individuals who are less active. Females are affected more commonly then males overall. (Age-related, or “senile” osteoporosis affects men and women equally.) Environmental factors that contribute to osteoporosis include smoking, alcohol intake, estrogen deficiency, and the use of certain medications. The most common presentation of osteoporosis is vertebral fracture, followed by hip fracture. Bone loss in osteoporosis is mostly cortical (80%), but 33-50% of bone must be lost before the disease is evident on x-ray. Peak bone mass is realized at age 35, with involutional bone loss due to age beginning at age 35-40. Cortical bone is lost at a rate of about 1% per year after this point. Bone has a gray appearance on x-ray w/ the primary trabeculae accentuated and the secondary trabeculae reduced. Primary osteoporosis is that which has no underlying disorder. Secondary osteoporosis is caused secondary to a pathology like steroid tx, myeloma, metastasis, gastric sx, anticonvulsants, hyperparathyroidism, heparin, DM, alcoholism, disuse, hypogonadism, amenorrhea, and anorexia. Generalized osteoporosis affects all bones, particularly of the axial skeleton, and may be post-menopausal or senile. Postmenopausal osteoporosis affects females aged 51-75, and is caused by the increased osteoclastic action present in states of estrogen deficiency. Mainly only medullary bone is lost, with coarsened trabeculae. It is particularly associated with vertebral, hip, and colle’s fx (wrist.) Lab values for this type of osteoporosis are normal except for a decrease in PTH. Senile osteoporosis has about an equal distribution btw males and females over 70 y/o. There is a proportionate loss of cortical and trabecular bone due to generalized loss of osteoblast activity. Lab values show increased PTH. The most common presenting symptom is extra-capsular hip fx. Regional osteoporosis occurs only in a particular segment, usually due to disuse atrophy. Localized osteoporosis affects one part of a bone, and is due to tumor, arthritis, or infection. Diagnosis of osteoporosis is preferred with a device called a DEXA scanner, or dual-energy x-ray absorbiometry. This measures the absolute density of bone via penetrance of x-rays. CT can also be used to diagnose this disease. Osteoporosis is graded using the calcaneal index: Grade V (normal) – all trabeculae are uniformly present Grade IV (normal) – posterior compressive trabeculae are divided into two separate columns Grade III (borderline) – posterior tensile trabeculae are lost Grade II (osteoporotic) – anterior tensile trabeculae lost Grade I (severe) – all tensile, most compression trabeculae are lost Regional Complex Pain Syndrome (RCPS) also known as the “great mimicker,” manifests on x-ray as an acute painful regional osteopenia following minor trauma. Males and females are equally affected, and patients are typically over age 50 and of type A personality. Presenting s/sx are

progressive onset of pain, stiffness, swelling, and atrophy distal to the site of injury over a 3-6 month period. The cause is hyperactivity of the sympathetic nervous system. In type I RCPS no specific nerve damage can be identified. In type II RCPS direct nerve injury has occurred. In 70% of pts, the disease can spread up the extremity, sometimes even to the opposite limb. RCPS can also be staged. Stage I describes localized edema, muscle pain, joint stiffness, and vasospasm with duration of about 3mos. Additionally, trigger points form where touch causes pain out of character to the stimulus (causalgia.) Osteopenia is noted on x-ray distal to the lesion. Stage 2 includes increased pain and area of involvement, brawny edema, hair loss, brittle nails, and spotty osteopenia. (Osteopenia w/ areas of normal bone.) Stage 3 trophic damage becomes irreversible at this stage, w/ intractable pain, muscle atrophy, joint weakness, flexor tendon contracture (producing deformity) and deossification. Tx for RCPS includes pain tx (NSAIDs, opiates), nerve blocks, physical therapy, and sx sympathectomy. Osteomalacia is a lack of calcium in osteoid matrix laid down by osteoblasts, resulting in improper bone mineralization. Symptoms include muscle weakness, bone pain on palpation, and bone deformity. X-ray shows osteoid seams, lines of unmineralized bone that appear as pseudofxs (aka increment fx, looser line, umbua zonen, milkman syndrome). The cortex is thin and blurs into the medullary bone (endosteal blurring.) Rickets is osteomalacia seen in children, usually due to vitamin D deficiency (but also due to renal dz.) It typically affects children 6-12 months old, and will be accompanied by muscle tetany, irritability, and weakness. Physical development is impaired, bone growth is impaired and deforms. Cartilage in the epiphyseal plates hypertrophies and is surrounded by edema. CXR shows a rachitic rosary about the costo-chondral junctions. Proximal calcification of the metaphyses is absent, and margins are frayed and cupped. Pseudofractures are also seen in rickets as well as tibial/femoral bowing. Scurvy is a disease caused by long-term deficiency of vit. C. It takes 4 months to be apparent on X-ray, and typically affects infants aged 4-8months. Scurvy is characterized by improper collagen formation, leading to spontaneous capillary hemorrhage, osteopenia, and poor cartilage. Radiographically, there is a dense zone of provisional calcification (line of frankel), ring epiphyses (wimberger’s sign), irregular metaphyseal margins (corner sign), metaphyseal protuberance (pelken’s spurs), scorbutic zones (trummerfield zones), and sub-periosteal hemorrhage. Hyperparathyroidism is ostepenia due to overactivity of the parathyroid gland. Primary hyperparathyroidism is caused by parathyroid adenoma/carcinoma/hyperplasia, or an ectopic PTH-secreting tumor. Secondary hyperparathyroidism is caused by renal disease. Typical presentation is female, 30-50 y/o, weakness, lethargy, polydipsia/uria, hypercalcemia and kidney stones. Serum calcium and phosphate are elevated. The radiographic hallmark is sub-periosteal bone resorbtion (1), followed by accentuated trabeculae and reduced medullary bone (2), and formation of brown tumors. (3) Bone resorbtion typically

occurs first in the phalanges, and soft tissue ossifications may also be seen. Brown tumors are “holes” in the bone that are filled with osteoclast-laden fibrous tissue, seen in both primary and secondary forms. OSTEOBLASTIC DISORDERS Melorheostosis of Leri – “flowing hyperostosis” that looks like candlewax dripping down the bone. Etiology unknown. No gender predilection. Joint effusion w/ decreased ROM and contracture, one limb (monomelic) affected, muscle wasting, lymphedema all are symptoms. X-ray shows wavy cortical thickening, narrowing of endosteal space. Osteopathia Striata – “Voorhoeve’s Disease” most commonly seen in the hip metaphysic. Seen as a linear band of bone density of unknown etiology, typically coexisting with sclerosing dysplasias. Osteopetrosis – “Albers-Schoenberg Disease” also known as “brittle bone disease.” Medulla is completely destroyed – all bone is cortical. Existing bone thus has no shock absorbing ability and is very brittle. It is a hereditary disorder in which the osteochondroid tissue of developing bone fails to mature into medullary and lamellar bone. There are 2 types: osteopetrosis tarda (benign, a dominant trait) and osteopetrosis congenital (malignant, recessive trait w/ neck LAD and HSM.) Lack of bone remodeling results in long bones having an Erlenmeyer flask deformity (flared metaphysis.) Variably, some persons present with a spotty osteopetrosis which appears like a “bone within a bone” or as striations of normal bone with osteopetrotic bone. Osteopoikilosis – “Osteopathia condensans disseminata” or “spotty bone disease” is a hereditary disorder that presents as multiple compact bone islands existing within normal bone. The disease is asymptomatic and is usually an incidental finding. Turnover is also very high, such that two radiographs taken in the same year may show completely different presentations. 25% of patients have a coexisting dermatological problem (dermatofibrosis, scleroderma, syndactyly), 20% have arthralgia. X-ray shows multiple compact bony islands in long bones with uniform density. Rarely, bone islands may have a radiolucent center. Compact Bone Islands are normal variants seen in regular radiographs. They appear as small areas of radiodensity, usually in flat or tubular bones. What may appear normally as a compact bone island can rarely be a osteoid osteoma. Osteoid Osteoma is a painful benign tumor that is typically <1cm, appearing as a compact bone island with a radiolucent center. They are usually located near the cortex. Symptoms include pain at night, relieved by ASA. Dx w/ bone scan. Heavy Metal Poisoning can be by lead (plumbism), phosphorus, or bismuth. Lead lines at the metaphyses are visible on radiographs one month after exposure. Lead deposition may also be seen at the distal ends of the digits. Lead line density is determined by the amount of lead ingested, the width is the single-time duration of exposure, and the number equals the number of exposures. What may appear as lead lines in a 4 y/o or younger is actually a normal finding. Lead foreign bodies do not cause plumbism (unless located within a joint space.) Hypervitaminiosis A presents with dermatitis, pruritis, alopecia and skin yellowing. X-rays show solid periosteal bone at the ulna and metacarpals.

Hypervitaminosis D presents with nausea, anorexia, polyuria and polydipsia. X-rays show extensive calcification of blood vessels, soft-tissue, kidney, and peri-articular spaces.

BONE AND FRACTURE HEALING Bone Characteristics: Bones support our frame as well as protect the vital organs, provide a source of calcium, a site of insertion for tendons and ligaments, and provide the rigidity needed for movement against gravity. Bones comprise 1/10th of our body weight. They resist axial stresses very well but are weak against rotational forces. Tubular bones are built for axial support and locomotion. Flat bones are built for protection of vital organs. Bone Healing: Consists mainly of spontaneous regeneration. Tubular bone forms by endochondral ossification, flat bones by intramembranous ossification. The periosteum surrounds and protects the bone, and is made up of an outer fibrous layer and an inner “cambium” layer which contains osteocytes. It is this inner layer of the periosteum as well as the endosteum that are most closely associated with bone healing. FRACTURE TERMINOLOGY Avulsion Fx – pulloff fx consisting of a fragment of bone pulled off by a muscle, tendon, or ligament. Butterfly Fx – triangular shaped cortical fragment that is part of a communuted fracture. Chip/Corner Fx – small fragment of bone from a joint margin. Distinguish from a joint mouse, which is a piece of osteophytic bone that breaks off into a joint space. Closed Fx – does not penetrate the skin. Comminuted Fx – consists of more than 2 pieces. Fleck Sign – avulsion fx by the lisfranc’s ligament of the base of the 2nd metatarsal. Impaction Fx – telescoping of bone segments (also called “bayoneting”) that results in shortening of a segment. Greenstick Fx – incomplete fx in which one cortex is affected and the fracture line follows down the axial line of the bone. Torus Fx – trabeculae are buckled inwards with a cortical bulge around the fracture site Insufficiency Fx – aka pathological fx, caused by normal physiological stresses through diseased bone. Oblique Fx – fx is 45 degrees from the long axis of the bone Occult Fx – see also stress fx; subtle and difficult to identify Open/Compound Fx – skin is penetrated Simple Fx – two bone fragments are involved Spiral Fx – fx is circumferential and longitudinal in bone Stress Fx – due to repetitive stresses, no fx line is apparent but bony callus forms 10-14d on X-ray. Must rely on clinical Sx. Transverse Fx – fx at 90 degrees to the long axis of bone. FRACTURE REPAIR Displacement/Distraction – requires reduction Closed Reduction – realign fragments through manipulation of ST, stabilize w/ cast Open Reduction – realign fragments surgically, using ORIF Inflammatory Phase – Periosteum, haversian system damaged, bleeds to form hematoma. Osteocytes die from ischemia, creating necrotic tissue that induces the inflammatory response of vasodilation, edema, and macrophage attraction.

Reparative Phase – governed by vascularity, the reparative phase involves the formation of a callus which is mainly fibrin from inflammation invaded w/ pluripotent cells for healing. A collar callus forms around the bone to stabilize, dictated by the periosteum, while the internal callus is dictated by the endosteum and dictates bridging and union between the two segments. Compression encourages bone rather than fibrous tissue formation. Necrotic tissue is simultaneously removed. Clinical Union – the goal of reduction, clinical union is the resolution of symptoms w/ palpable rigidity to the affected bone. Clinical union precedes radiographic union. Remodeling Phase – begins while the reparative phase is winding down, in the remodeling phase the callus is resorbed and the trabecular bone remodeled along lines of stress, resulting in a bone that is stronger than when it broke. Cancellous bone heals faster than cortical bone, and has a smaller callus. Cortical healing is limited by vascularity and the amount of movement permitted during the healing phase. COMPLICATIONS OF FRACTURE REPAIR Delayed Union – union is not achieved w/in the expected time (6 wks.) This is due to inadequate reduction, soft-tissue imposition in the fx, excess ST destruction, vascular disruption, inadequate immobilization, fragment distraction, or inadequate fixation. AO principles dictate that bone healing fails in tension and heals in compression. Non-Union – complete arrest of bony repair, replaced instead by fibrous, cartilaginous, or synovial compensation for the fx site. It is variably classified as being diagnosable 6-8 months post-fx. Others say non-union is dx if no radiographic healing changes are seen for 3 months. Classification of non-union is by Weber and Cech, and are divided into two major categories, hypertrophic and avascular (or hypotrophic.) Hypertrophic Non-Union may be of the elephant’s foot type, the horse’s hoof type, or the oligotrophic type. Elephant’s foot type is usually due to early WB and inadequate stabilization. Horse’s hoof is caused by inadequate internal fixation that has allowed a small amount of movement. Oliogotrophic non-union has poor callus, and is usually due to inadequate alignment of fx ends. Avascular Non-Union – consists of four types; torsion wedge, comminuted, defect, and atrophic. Torsion wedge is incomplete healing of a fx in which there are three or more pieces, in which some pieces fuse together but others do not because of inadequate vascularity. It is sometimes seen with plate fixation, usually in the tibia. Comminuted non-union is the presence of one or more fragments that become necrotic, the callus fails, and any involved fixation may break from stress. Defect non-union is the loss of a devitalized fragment of cortical bone that leaves a dead space within the bone which cannot be bridged. Atrophic non-union is a long-term result of insufficient vascularity that causes fx ends to become osteopenic and atrophic. Radiographic Findings of Nonunion Sclerosis of the fracture ends, failure of changes of healing, progressive bowing, increased bone atrophy above and below fx site, excessive callus formation, and absence of remodeling. Bone scans show up “hot” in non-union; increased uptake at the fracture ends may be indicative of pseudoarthrosis formation. Pseudoarthrosis

This is a variant of non-union characterized by scar tissue and false joint formation. Congenital pseudoarthrosis is present at birth and is assoc w/ neurofibromatosis. It typically occurs in the distal tibia/fibula. Acquired pseudoarthrosis causes pain, instability, and bowing, with sclerotic bone ends and lucency between fragments. It is most common in the distal tibia. Malunion Bone healing that occurs in non-reduced fx, in which bones are in improper position. It can spontaneously correct in peds.

THE 5 STEP APPROACH TO PLAIN FILM ANALYSIS STEP 4: EVALUATION OF JOINT SPACE PEDAL COALITIONS A coalition is a union of separate things into a single body or group; true coalitions are intra-articular fusions of bones, and bar/bridge coalitions are extra-articular fusions of bone. A complete coalition is osseous and limits all motion. An incomplete coalition is a union by fibrous or cartilaginous tissue. A rudimentary coalition is an osseous projection which limits motion but does not produce a union of parts. A synchondrosis is a cartilaginous union, a synostosis is a bony union, and a syndesmosis is a fibous union of two parts. Coalitions are caused by accessory ossicles (os trigonum, os sustentaculi proprium), failure of mesenchyme to segment in development, trauma, DJD (causing a fibrocartilaginous fusion), inflammatory rheumatoid conditions, and fxs. Tarsal coalitions occur in 1-2% of the population and consist of the talo-calcaneal coalition (most common), calcaneonavicular, and talonavicular (least common.) Ossification of coalitions in the tarsus occur at different times. The age of ossificiation determines when symptoms occur. Talonavicular coalitions 3-5 y/o Calcaneonavicular coalitions 8-12 y/o Talocalcaneal coalitions 12-16 y/o S/Sx of coalitions include stiffness, decreased ROM, pain, peroneal spasm, anterior/posterior tibial spasm, local POP, pronation, cavus deformity, and fixed RF valgus. Peroneal spastic flatfoot is characterized by restricted STJ motion, RF valgus (in OKC), FF abduction, bowstrung peroneal tendon, and extensor digitorum longus spasm. D/Dx of coalitions include RA, JRA, trauma, neoplasm, acromegaly, CCPV, casting (causing peroneal contracture), extra-articular arthrodesis, overcorrected flatfoot, osteochondral dystrophy, infection, and N/M disease. Plain film analysis of coalitions is cheap and able to identify most symptomatic coalitions. IPJ coalition can be viewed on AP projection. Synphalangism is a congenital fusion of the IPJs. Intermetatarsal coalition may be viewed on AP and oblique views. Diaphyseal fusions are typically the result of trauma. Metatarsal cuneiform coalition may be viewed with AP, med oblique (medial column), or lat oblique (lateral column.) Navicular cuneiform coalition may be viewed with the AP and medial oblique projections. Navicular cuboid coalition may be viwed w/ AP or oblique. Calcaneocuboid coalition may be viewed on lateral or lateral oblique views (typically it is osseous and easy to pick up.) Talonavicular coalition can be viewed on AP and medial oblique. AP shows a “putter sign” of the fusion.

Calcaneonavicular coalition can be viewed on lateral and lateral obliqe, and shows an “anteater sign” on lateral. These fusions are more commonly cartilaginous or fibrous in nature. STJ coalition is the most common tarsal fusion, and usually is the middle facet (the posterior facet is least common.) Fusions of the sustentaculum tali or posterior process are also possible (though not common.) Anterior facet coalitions can be seen on lateral oblique isherwood projections but are most commonly dx though lateral CT. Middle and posterior facets are viewed on harris and beath axial projections (30, 35, 40, and 45°) or broden views. The posterior and middle facets should be parallel to one another, and the posterior facet should be about 2/3 the width of the calcaneus. Posterior fusion may be secondary to trauma involving the os trigonum. (Achilles pain, end ROM plantarflexion, deep ankle pain.) Radiographic Features of STJ coalition (lateral projection) Talar beaking Posteior TC joint space narrowing Rounding of lateral process of the talus Obscured middle facet “Halo” effect Do not confuse talar beaking w/ dorsal hyperostosis, which is caused by pathomechanics. Talar beaking occurs at the distalmost aspect of the talar neck, near the TN joint. It is caused by stress on the talonavicular ligament and impingement of the navicular on DF. The halo sign is a subtle finding, which is a ring of trabeculae that form around the coalition secondary to altered compressive forces. Computerized Tomography is the modality of choice for evaluation of coalitions (b/c of cortical definition.) It allows planar analysis which may be used to determine the extent of coalition and change to surrounding osseous structures. Nuclear Imaging is not very useful for the diagnosis of coalition. Increased uptake is seen adjacent to areas fusing, and decreased uptake in already fused areas. MRI allows planar and oblique analysis to more fully explore the nature of a coalition. T2 weighted images are particularly useful to note presence or absence of synovial fluid in an area. Syndromes associated with coalitions may aid in the diagnosis of a bony union, and vice versa. Common coalitions typically are axial, i.e. distal to proximal fusions, whereas syndromic coalitions tend to be medial to lateral in position. Apert’s Syndrome results in massive tarsal synostoses, as well as cranial synostoses and midfacial hypoplasia (“mouse” facies). The distal phalanx of the hallux and pollux are broad. Feet tend to have valgus attitude. Footwear is a problem Nievergelt-Perlman Syndrome typically has synphalangism and carpal fusion, moreso in the hands than feet. This syndrome may also present with an atypical clubfoot and tarsal fusions, which causes a ball-and-socket type of ankle joint. Other findings include congenital dislocation of the radial head and conduction deafness due to ear ossicle fusion. Phocomelia is defective development of the arms or legs, resulting in “flipper” extremities. Hemimelia is underdevelopment of a specific extremity, usually a belowknee deformity. These conditions cause unusual fusions. Tx of coalition includes immobilization and supportive therapy, orthotics, NSAIDs for pain, and possible surgical intervention (resection or arthrodesis.)

Conclusion – correlate coalitions w/ pts age. Be suspicious of changes in plain films. Consider advanced imaging to investigate further. (Special views, CT, MRI.)

ARTHRIDITIES Inflammatory arthridities are RA, erosive arthritis, psoriatic arthritis, reiter’s disease, ankylosing spondylitis, and enteropathic arthritis. Non-Inflammatory arthritis is degenerative joint disease. (Wait a minute – doesn’t arthritis mean joint inflammation?) Metabolic arthritis is gout and CPPD disease. Neuropathic arthritis is neuropathic joint disease. Miscellaneous arthridities are DISH, PHO, and pigmented nodular synovitis. PSORIATIC ARTHRITIS Seen in 7-15% of pts w/ psoriasis (80% if pt has nail changes.) Typically affects 20-50 y/o, M:F equal. HLA-B27 frequently positive, particularly w/ SI involvement. Distribution is asymmetrical and is most common in the DIPJs. Often confused w/ RA (for some reason.) Classic radiographic features Joint margin erosions working in to the center (similar to RA) – eventually leads to “pencil in cup” appearance Increased synovial fluid w/ increased intracapsular pressure Apparent wide joint space (due to erosions) Acroosteolysis – resorbtion of the distal phalangeal tuft Sausage digits Abundant periosteal activity (resulting in “whiskering”) Ivory Phalanx – due to abundant endosteal activity Osteopenia secondary to reduced activity Main-en-lorngette (telescoping) – long standing disease process resulting in collapse of diaphyses on themselves. Posterior/Inferior calcaneus hyperostosis (not heel spurs.) REITER’S DISEASE Classic clinical triad – conjunctivitis, urethritis, arthritis. Also 4th – derm lesions (keratoderma blenorrhagicum) Usually preceded by diarrhea. Typically males, 18-40 y/o. HLA-B27 positive almost always. Asymmetric distribution, primarily lower extremity. Attributed to chlamydial infection (endemic) or dysentery (epidemic) which are the two main types of Reiter’s. Epidemic form may affect women and children as well. Arthritis long-term symptom; conjunctivitis/urethritis resolves in weeks. Arthritic changes may also become chronic. Acute Stage - weight-bearing joints are more commonly affected. In the acute stage there is peri-articular ST edema, deossification of opposing articular structures, Achilles

inflammation/widening, and periosteal reaction (metatarsal metaphyses, phalangeal diaphyses, inferior surface of the calcaneus.) Retrocalcaneal bursitis is also common. Infracalcaneal exostoses (poorly defined or “fluffy”) form bilaterally and cause heel pain. Chronic stage – periarticular deossification, small marginal erosions, symmetrical loss of joint space, ankylosis. Specific findings – heel spurs in young men, Achilles edema, small joint space periosteal reactions, primarily foot s/sx. ANKYLOSING SPONDYLITIS Affects pelvic and spinal joints, ligaments, and tendons. Affects 15-25 y/o, usually males. Almost always HLA-B27 positive. Characterized by lower back pain due to arthritis at the sacroiliac joint, bony proliferation at enthesiopathies, spinal osteophyte formation, and lateral syndesmophytes. ENTEROPATHIC ARTHROPATHY Joint changes secondary to GI disease. Seen in young adults, w/ malaise, anorexia, wt. loss and arthritis. Typically sacroiliac, bilateral periostitis. X-ray findings are nonspecific. GOUTY ARTHRITIS Gout is the result of an inborn error of purine metabolism. It typically affects men age 40-50 y/o, and is characterized by elevated serum uric acid and negatively birefringent crystals in the synovial fluid. The most commonly affected joint is the 1st MPJ due to relative avascularity and lower temperature. Women only get gout after menopause. Characteristic of gout is extreme paroxysmal pain in the middle of the night. Primary gout is hyperuricemia due to over-production of uric acid or under-excretion of it by the kidneys. Secondary gout is due to medications (particularly HCTZ) and hyperparathyroidism. Urate deposits in relatively avascular tissues like cartilage, synovial tissue, ligaments, bursae, and subQ tissue. Hyperuricemia may never become symptomatic, and in fact may be reduced during an acute phase attack. A 24 hour urine collection is needed to diagnose accurately. X-ray findings of gouty arthritis only occur after several attacks. Thus radiographs in an early attack function mainly to r/o other pathologies (septic arthritis.) There is periarticular swelling of the joint margins, erosions of the joint margins, punched-out lesions resembling RA, and complete lysis of bone in the acute stages. Large tophi may form at joint margins and produce “rat bite” erosions peri-articularly that leave overhanging shelves of bone called martel’s sign. This is not seen for 5-10 years after the attack and merely signifies that a pt has had gout in the past. Tophus formation can occur in the absence of an acute gout attack, and subsequent erosions can cause subQ calcification and pathological fxs. The joint space is preserved in gouty arthritis. DJD may accompany the process, and the joint may be somewhat narrowed due to subchondral cyst formation, but is otherwise unaffected. Metastatic tumors of bone are an important d/dx to r/o when considering asymptomatic gout. CHONDROCALCINOSIS Pseudogout, or calcium pyrophosphate dihydranate disease, is a symptom similar in presentation to gout that causes the radiographic finding known as chondrocalcinosis. CPPD

crystals are weakly positive birefringent and simulate gout attacks when precipitated in joint spaces. The typical pt is over 30 y/o (usually ~60) and there is no gender predilection. The problem is associated with hyperparathyroidism, pseudogout, acromegaly, DJD, and DM. The typically affected joint is the knee, where the menisci as well as the articular cartilage may calcify as a result. It also can be seen in the wrist, hand, ankle, symphysis pubis, and elbow. True chondrocalcification is sometimes seen after trauma or with hyperparathyroidism. DEGENERATIVE JOINT DISEASE Also called osteoarthritis, DJD is a local, mechanically caused degeneration of joint function that occurs in conjunction with age and trauma, resulting in degradation of the articular cartilage. Primary DJD is the most common form and is due to aging. Secondary DJD is early onset due to trauma or injury to the joint. Joint space narrowing is asymmetric in DJD, the subchondral bone exhibits eburnation (pathologic sclerosis), the articular surface becomes broad and flat, and osteophytes form at joint margins, often breaking off to become joint mice within the articular space. Osteophytes typically bend towards the joint space, which causes locking of the joint in areas where there are osteophytes on either side of the articulation. Pseudocysts may also form in the subchondral bone in areas where the cartilage is completely worn away. It is important to note that the disgnosis of hallux rigidus and limitus, which are seen in patients with DJD of the 1st MPJ, cannot be diagnosed radiographically and are purely clinical diagnoses. Additionally, the hands of patients with DJD clinically may present with enlarged IPJs which are called bouchard’s nodes (PIPJ) or heberden’s nodes (DIPJ) that are simply the result of extensive osteophytosis in long-standing disease. Erosive osteoarthritis is a variant of DJD which affects primarily females aged 40-50 y/o. Clinically an increased ESR may be seen because there is an inflammatory component to the erosive component. The presentation is symmetrical and bilateral, and most commonly affects the IPJs of the hands. Radiographically erosive osteoarthritis appears like DJD except that the erosions are symmetric and take on the characteristic gull wing appearance that is specific to EO. RHEUMATOID ARTHRITIS RA is an inflammatory seropositive joint disease affecting primarily females between the ages of 20-40 y/o, but affect men and women equally beyond the age of 40. 70% of pts w/ RA are seropositive for rheumatoid factor. The small joints of the hands and feet, and articulations of the spine are typically affected. Early presentation in the foot can easily be mistaken for gout – most commonly small, C-shaped erosions appear at the base of the proximal phalanges. Radiographic changes are seen in 65% of pts who have had some disease process for at least 3 months (85% for >6 mos.) However, no clinical s/sx may appear until the disease has been present for 3 years. Early radiographic findings in RA include periarticular edema that is fusiform in shape around the joint, typically in IPJs and MPJs. Inflammation of the synovium creates pannus which results in bone deossification periarticularly, which progressively extends proximally over time.

Secondary trabeculae are resorbed while primary trabeculae are enhanced. Fibular deviation of the digits occurs secondary to bony deossification that destroys the medial collateral ligaments of the MPJs (except on the 5th MPJ.) Early on the joint space becomes noticeably widened as effusion and pannus formation characterize the disease process, and often this is the only presenting sign in undiagnosed RA. Joint space changes are most easily seen in the ankle joint radiographically. Near the joint periosteum may become irritated and periosteal elevation in the epiphyseal/metaphyseal region is seen. This creates lamellations which enlarge the bone near the articulation. Entheses and bursae near the joint may also become inflamed and enlarge. Localized bony erosions occur near the joint due to herniation of the pannus through capsule, producing an area of radiolucency with poorly defined borders. Erosions seen en face may appear completely within the bone, while laterally they may have a dot-dash appearance. Medial-plantar erosions of metatarsal heads 1-4 are most common. Later symmetrical joint narrowing is seen, particularly in the IP and TN joints (but never the CC joint.) RA-induced subluxations of MPJs and IPJs following ligamentous involvement cause the characteristic swan-neck (like mallet-toe) and boutonneire (like HDS) deformities. These deformities are also seen in SLE and post-rheumatic fever (jacoud’s) arthritis. Other deformities seen in RA include main-en lorgnette deformity (“opera-glass hand”) that is also seen in psoriatic arthritis. Late radiographic findings in RA have obviously no diagnostic value, but are used to track the progression of the disease. Characteristic features include subluxation and dislocation of the joints, ulnar deviation of the digits, destruction of joint space, and finally bony fusion and ankylosis of the joints altogether. Pathological fxs secondary to osteopenia may be seen. Overall, the MPJs are most severely affected in RA, with the IPJs of the 1st and 5th digits a close second in frequency. NEUROPATHIC JOINT DISEASE More commonly known as charcot foot, neuropathic joint disease is a destructive disease that occurs secondary to loss of proprioception, seen in DM (5%) and syphilitics (20%.) Clinically there is no protective sensation; instability and crepitation are present in the joint, and neurologically the pt suffers from ataxia and loss of DTRs. Besides the more common pathology, neuropathic joint disease can occur iatrogenically secondary to administration of indocin or steroids over long periods of time (notable because of the tx protocols for RA and gout recommend this.) The hypertrophic form of the disease affects large, WB joints, while the hypotrophic (atrophic) form affects NWB joints. Clinically both undergo 3 stages; fragmentation, coalescence, and reconstruction. Radiographically the hypotrophic form is characterized by bone resorption, diabetic osteolysis, and a “licked candy stick” appearance. The hypertrophic form is characterized by the six D’s: joint distension, density increase, debris production, dislocation, disorganization, and destruction. DIFFUSE IDIOPATHIC SKELETAL HYPEROSTOSIS (DISH)

DISH is a disorder of ligamentous ossification and calcification that affects the spinal and extra-spinal articulations. Typically it affects males over 50 y/o. It is associatied (20%) w/ DM. 40% are HLA-B8 positive. All parts of the spine, particularly the SI joint, are affected. Radiographically flowing hyperostosis is seen over 4 consecutive vertebral bodies, usually in the area of the anterior longitudinal ligament. In any case, the disc is preserved, differentiating this process from syndesmoses seen in ankylosing spondylitis. Extra-spinal presentations may be at any enthesis, producing whiskering at the bony attachment and ossification of the tendon or ligament while preserving the joint space. PULMONARY HYPERTROPHIC OSTEOARTHROPATHY (PHO) PHO is a disease caused by bronchogenic carcinoma that is described by the triad of digital clubbing, symmetric arthritis, and linear periostitis. It typically affects males 4060 y/o. The arthritis in this process, like many seronegative diseases, is nondescript in its clinical and lab findings. The arthritis is specific to the extremities only. Periostitis in long bones occurs in the metaphseal/diaphyseal region, appearing as a “double strip sign” on bone scans (dual cortices.) PIGMENTED VILLONODULAR SYNOVITIS This disorder is a proliferative pathology of joints that does not produce arthritis, but rather a mass within a joint or tendon sheath which may affect the joints secondarily. Typically it affects young males. Joint involvement is asymmetric. Radiographically there is a soft-tissue mass evident with localized bony erosions that have well-defined sclerotic borders. Calcification is unusual. SYSTEMIC LUPUS ERYTHEMATOSUS SLE is a connective tissue disorder involving nearly every organ system in the body. It is most common in females 2040 y/o, and is characterized by elevated ESR and ANA titer levels. Radiographic features are most readily assessed in the hands, and are characterized by reversible subluxation, dislocation, and varied deformity. Calcification and atrophy can occur secondary to deformity. Most radiographic findings are non-specific and there is no articular degeneration. SCLERODERMA Scleroderma is a connective tissue disease that also involves many organ systems and affects females predominantly (30-60 y/o.) Radiographic changes in scleroderma are most readily appreciated in the CREST syndrome, in which soft tissue calcification and acro-osteolysis may be seen. (r/o psoriasis)

line drawn from distal inferior aspect of calcaneus to anteriormost weight-bearing point of calcaneus

THE 5 STEP APPROACH TO PLAIN FILM ANALYSIS STEP 5: BIOMECHANICAL EVALUATION The biomechanical evaluation of radiographs is used for preop planning and post-op assessment of correction as well as for the evaluation of orthopedic pathology. Biomechanical readings are most sensitive to positioning errors, and so great care must be taken to ensure proper positioning in patients needing a biomechanical evaluation. AXES Greater Tarsal Axis (GTA) Line drawn parallel to the distolateral border of the calcaneus, most easily identifiable on AP radiograph. Lesser Tarsal Axis (LTA) Point A is placed on the distomedial aspect of the medial cuneiform. Point B is placed at the medial proximal aspect of the navicular articular surface. Point C is placed at the proximal lateral aspect of the cuboid and point D at the distal lateral aspect of the cuboid. The midline between points A & B and C & D are found and a line drawn between them. The line perpendicular to this is the lesser tarsal axis. Metatarsal Axis (MTA) Line drawn through the midpoint of the shaft of the 2nd metatarsal. (Or another metatarsal if specified.) Digital Axis (DA) Line drawn down the midpoint of the shaft of the digit in question. Collum Tali Axis Line drawn down the bisection of the talar neck. Collum Calcanei Axis Line drawn down the bisection of the distal 1/3 of the calcaneus. Hallux Axis Line drawn down bisection of the shaft of the proximal phalanx of the hallux. Calcaneal Pitch Axis

AP ANGLES Lesser Tarsal Angle = GTA + LTA Metatarsus Angle = LTA + MTA Used to evaluate for metatarsus adductus Digitus Angle = DA + MTA of measured digit Forefoot Angle = GTA + MTA Used to evaluate metatarsus adductus in peds Talo-Calcaneal Angle = collum tali + collum calcanei axes Used to evaluate pronation/supination Cuneo-Metatarsal Angle = MTA(1-3) + long axis of proximal cuneiform Used to evaluate hypermobility, lisfranc’s injury Calcaneocuboid Angle = Collum calcanei axis + line CD of LTA Used to evaluate lateral column integrity Talometatarsal Angle = column tali axis + 1st MTA Called Simmons Angle on AP Used to evaluate pronation/supination Intermetatarsal (IM) Angle = 1st MTA + 2nd MTA Used to evaluate bunion deformity Hallux Abductus (HA) Angle = hallux axis + 1st MTA Used to evaluate bunion deformity Hallux Interphalangeus Angle = hallux axis + bisection of distal phalanx of the hallux Metatarsal Break Angle = line between center of 1st and 2nd metatarsal heads + line between center of 2nd and 5th metatarsal heads. Tibial Sesamoid Position 1 = Tibial sesamoid medially clear of 1st MTA 2 = Tibial sesamoid laterally abuts 1st MTA 3 = Tibial sesamoid laterally overlaps 1st MTA 4 = Tibial sesamoid bisected by 1st MTA 5 = Tibial sesamoid medially overlaps 1st MTA 6 = Tibial sesamoid medially abuts 1st MTA 7 = Tibial sesamoid medially clear of 1st MTA Proximal Articular Set Angle (PASA) = line btw medial and lateral borders of metatarsal head articulation + line perpendicular to MTA. Distal Articular Set Angle (DASA) = line btw medial and lateral borders of proximal phalanx MPJ articulation + line perpendicular to digital axis. LATERAL ANGLES Talar Declination Angle = collum tali axis + ground Calcaneal Inclination Angle = calcaneal pitch axis + ground Talocalcaneal Angle = collum tali + calcaneal pitch axes Talonavicular Angle = collum tali + bisection of navicular Used to evaluate for metatarsal breaks 1st Metatarsal Declination Angle = 1st MTA + ground Talometatarsal Angle = column tali axis + 1st MTA Called Meary’s Angle on lateral projection Hallux Dorsiflexion Angle = 1st MTA + hallux axis Cyma Line = position of the talonavicular joint with respect to the calcaneo-cuboid joint on lateral projection. Radiographic Evaluation of Supination Talar declination angle decreases

Calcaneal inclination angle increases Talocalcaneal angle decreases Cyma line posteriorly displaced Subtalar joint/sinus tarsi accentuated (bullet hole sinus tarsi) Radiographic Evaluation of Pronation Talar declination angle increases Calcaneal inclination angle decreases Talocalcaneal angle increases Cyma line anteriorly deviated Pseudo-sinus tarsi seen (posterior facet of STJ; real sinus tarsi is obscured.) Metatarsus Primus Elevatus (MPE) Defined radiographically as an elevation of the 1st metatarsal with respect to the 2nd metatarsal. Implied in the development of 1st MPJ OA, sub 2nd metatarsalgia. Total Adductory Angle (TAA) Sum of the IM angle + the metatarsus adductus angle, used in the evaluation of bunion deformities and in surgical planning. A TAA >30° should warrant consideration of a proximal osteotomy in surgical bunion correction. Pre-Op Biomechanical Assessment IM angle HA TAA PASA DASA Hallux Interphalangeus Metatarsus angle MPE Sesamoid position Joint status Bone density 1st MT protrusion

RADIOGRAPHIC INTERPRETATION OF INFECTION OSTEOMYELITIS Osteomyelitis is the infection of bone, most commonly by bacteria but also possibly by fungus, virus, or parasites. The anatomy of vascular structures is most important when considering osteo, and the vascular anatomy of bone changes with age. In infants (0-1 y/o), blood vessels pass through the epiphyseal plate in tubular bones. Because of this, it is more common to see infection in the epiphysis because vascular channels here are more prominent than at a later age. In children (1-16 y/o), metaphyseal vessels end at the epiphyseal plate, creating loops and blind-ended sacs in the metaphyseal vasculature. The tortuosity of these vessels means that metaphyseal infection is much more common in children. The adult pattern begins around age 16. As the physis closes, the metaphyseal vessels can begin to cross back into the epiphysis again and so infection may be located anywhere in the bone. Sequestrum is an infected area that is dead due to cortical and medullary infarcts. Small sequestra can be eventually resorbed by osteoclasts, while large sequestra are walled off by the body and then expelled gradually through a sinus tract. Involucrum is periosteal new bone formation that occurs in response to bone infection, and represents the body’s attempt to prevent the spread of bacteria. Both sequestrum and involucrum are most commonly seen in hematogenous osteomyelitis. Cloaca is a defect in the involucrum that allows for drainage products of the infection to be expelled from the infected area. The cloaca commonly receives small bits of sequestrum that may have been broken down in the disease process. Exudate from the cloaca with involucrum will feel like sand between the fingers when handled. The

extent of the cloaca and its sinus tract to the outside of the body can be appreciated through the use of a sonogram, which is simply radiographic contrast media injected into the sinus tract that can then be visualized radiographically. Marjolin’s ulcer is a malignant degeneration of soft tissue within the cloaca to a squamous cell carcinoma. This occurs secondary to acidic pus and exudate from the cloaca irritating the tissues of the sinus tract. The infection must be very chronic (up to 20-30 years) for a marjolin’s ulcer to form, and it is only seen in long-standing osteomyelitis. Nevertheless, it should be kept in mind when treating a patient with history of bone infection. Brodie’s abscess is a localized suppurative infection of bone which is successfully walled off and is sterile. A brodie’s abscess is usually an incidental finding and typically is seen in children after osteomyelitis has resolved. A similar finding is an abscess that still contains bacteria, which can serve as a reservoir for reinfection in the future (however, brodie’s abscesses are sterile only.) Routes of infection in osteomyelitis include hematogenous spread (most common in children), direct implantation/inoculation, direct extension, and post-op infection. The most common infecting organism in children is H. Influenzae, although it is now much less common than it once was. In adults staph aureus is by far the most common infecting organism for all types of osteo (except plantar puncture wounds.) Hematogenous osteomyelitis, being primarily a disorder of children, is most commonly seen in the metaphysis of long bones. Bone destruction begins internally, then weakens the cortex, causes periosteal reaction, and finally breaks through to soft tissue. Being confined within bone initially, the route of pus evacuation can be appreciated on X-ray. Initially pus fills the medullary space for some distance before pushing through the periosteum. The codman’s triangle is a triangular space of pus bounded on one side by infected cortex and on another by elevated periosteum which attempts to lie down new bone. Notation of this on X-ray is usually diagnostic for hematogenous osteomyleitis. Direct implantation osteomyelitis typically occurs as a result of puncture wounds, human or animal bites, or open fracture. Staph aureus is the most common infecting organism in all cases except those of plantar puncture wounds that pass through a shoe, in which case the infecting organism is pseudomonas. E.Coli is sometimes implicated in direct osteo as well. In direct implantation there is no particular order to the infectious process, as the traumatic injury has already disrupted the cortex. Direct extension osteomyelitis is spread of infection to bone from a nearby soft tissue infection or ulcer. Nail infections and infected ulcers are the most common causative factor in this type. The order of infection tends to follow the opposite order as hematogenous osteomyelitis. Post-op infections may be due to staph aureus (again most common) or pseudomonas. This type of osteo is most commonly seen in the hip or knee following arthroplasty, especially when hardware is installed. Loosening of fixation with obvious radiolucency about the device indicates infection of this type and surgical removal is indicated.

X-RAY FEATURES OF OSTEOMYELITIS Initially, there are no osseous findings present on X-ray – plain film findings lag clinical findings 7-10d. In vertebral bones there may be up to a 21d lag. 30% of bone must be lost before the changes can be appreciated on plain films. Initially the only evidence of infection will be soft tissue changes, including deep ST swelling in hematogenous osteo adjacent to the infected area. Fat planes will be elevated, displaced, or obliterated altogether. Lines of lucency between muscles will be obliterated. Infection tracks usually distal to proximal and only rarely travels from medial to lateral (and vice versa.) Breakthrough to a joint space will produce swelling of the capsule, which in the ankle produces the classic teardrop sign which is also seen in hemarthrosis. Periosteal response to infection occurs usually 7-10d after the initial process has begun. The pattern of reaction is lamellar and progresses to formation of an involucrum. Involucrum tends to be less dense than the established cortical bone, even infected. The most distal the infection is in the body, the most subtle the periosteal response will be. Resolution of the infection will leave the involucrum to be remodeled and resorbed, however it may sometimes persist after the healing process is finished. Bony destruction appears “moth eaten” as there is a focal loss of bone density in the medullary bone, with sequestrum seen 3-6 wks after the infectious process has begun. Kissing lesions are opposed lesions seen across articular surfaces when the joint has been involved. Often these changes are subtle and may not be noticed unless serial radiographs are taken and analyzed. In slow-growing, rarer cases like fungal infections, the bone may be able to mount a more effective response against the causative agent, and sclerosis due to endosteal proliferation may be seen. This type of infectioncaused sclerosis is called sclerosing osteitis of Garre. Radiographic Signs Overview Early Signs Latent Period (10d extremities, 21d spine) Soft Tissue – fat plane elevation/displacement/obliteration, increased ST density Bone – motheaten cortical/medullary destruction, periosteal new bone formation (involucrum, codman’s triangle) Late Signs Soft Tissue – draining sinus/cloaca, debris, marjolin’s ulcer Bone – cortical destruction, involucrum, sequestrum, sclerosis Joint – loss of joint space, ankylosis, kissing lesions. Salmonella Osteomyelitis is a peculiar type of osteo that is sometimes seen in patients with sickle cell anemia. If a sickle cell crisis occurs in the intestinal vasculature, small infarcts can allow salmonella bacteria to travel from the gut to the bloodstream where they can seed in bones across the body. The osteomyelitis associated with this bacterial seeding is unique in that it predilects the diaphysis of long bones. BONE SCANS FOR INFECTION Technetium-99m Phosphate is the prototypical bone scan, and is the most commonly used in clinical practice. It reacts with calcium hydroxyapatite to form insoluble salts which precipitate in areas of bony turnover. This makes the Tc-99 scan ideal for infectious and/or traumatic processes of bone.

Although classically infection and inflammation about a bone cause a bone scan to read positive in that area, an increase in vasculature to an area may increase uptake of the isotope, as well as the articular surfaces of an inflamed joint. Thus, findings which would otherwise be normal clinically may show up as positive on bone scan and must be separated from pathology. Distal bones seem to be more sensitive to Tc-99 uptake, and can more easily show up hot even if only sustaining minor trauma. Overall, Tc-99 exposes the patient to only a small radiation dose, and is renally excreted. For this reason, it is generally recommended that the patient be wellhydrated (this also aids in contrast), and care must be taken in individuals with renal disease, especially if they have DM. The half-life of Tc-99 is 6 hours. Normal areas of increased uptake are the lacrimal glands, breasts, SI joint, kidneys, bladder, and the injection site of the isotope. Gallium-67 Citrate is another isotope that resembles the ferric ion. It binds to iron-related plasma proteins as well as organelles of leukocytes. This makes Ga-67 useful for visualizing the peripheral tissues because it marks the areas where leukocytes have localized. Ga-67 is also excreted renally, and has a long (78 hour) half-life. Podiatric indications for bone scan Osteomyelitis Trauma Inflammatory Arthritis Stress Fracture (if >7 hours) Tumors Non-specific pain (to check for occult causes) Combined use of bone scan isotopes can be used to differentiate the infectious process. Soft tissue infection can be distinguished from osteomyelitis by decreased uptake in the third phase of the Tc-99 scan, and will be strongly positive in Ga-67, whereas osteomyelitis shows up hot in all three Tc99 phases and is cold in Ga-67 scanning. When performed together, the Tc-99 test is done first because of the shorter half-life. Gallium is typically used to clarify the issue of infection site, but is not as effective at determining the course of an infection. The practice of using a gallium scan to determine when the infectious process (and thus the treatment regimen) is finished has been thoroughly disproved. Indium-111 isotope is a rarer, more specialized bone scan that tags WBCs in drawn blood with the isotope and re-injects them into the bloodstream. I-111 is useful in distinguishing osteomyelitis from neurotrophic joint changes in the diabetic individual, which is normally a very difficult clinical diagnosis. A negative I-111 scan would tend to r/o osteo and provide for a positive diagnosis of charcot, while the reverse is also true. COMPUTERIZED TOMOGRAPHY FOR INFECTION CT allows planar analysis of anatomy to determine the extent of infection. Although sensitive for soft tissue infections, CT tends to overestimate their involvement, and is much more reliable at determining bony involvement. Very subtle cortical or periosteal changes may be appreciated on a CT scan. MAGNETIC RESONANCE IMAGING FOR INFECTION In contrast to CT, MRI is much better at evaluating soft tissue infection versus bone infection. MRI cannot distinguish

between infection in a joint space and effusion in a joint, however, and this is a major limitation if joint involvement is suspected. The infected area appears dull on a T1WI, and more typically has greater intensity on a T2WI. THOUGHT PROCESS BEHIND THE RADIOLOGY OF INFECTION From plain films the distinction must be made as to the location of an infection. If soft tissue is suspected, MRI is the best modality. If bone is suspected, CT is the best modality. If the symptomatology is diffuse, the Tc-99 and Ga-67 bone scans should be considered to determine involvement.

BONE TUMORS AND TUMOR-LIKE LESIONS Evaluation of plain films – plain film analysis offers the most diagnostic information for the analysis of bone lesions. Biopsies of bone alone do not give the pathologist enough information to make a definitive diagnosis; clinical and radiographic evidence is needed to support what is seen under the microscope. Some lesions also may become activated or react against an invasive biopsy technique. Basic approach to solitary bone lesions 1) History – age, sex, and symptoms. Age of the patient is important because many tumors predilect younger or older patients. Ewing’s sarcoma, chondrosarcoma, and unicameral bone cysts are almost exclusively tumors of children, while metastatic tumors and multiple myeloma are only seen in older individuals. Osteosarcoma tends to affect younger patients, chondrosarcoma the middle aged, and fibrosarcoma the elderly. The tumors paraosteal osteosarcoma, giant cell tumor, and aneurismal bone cyst are the only tumors seen more commonly in women than men. Pain is the most common symptom in sarcomas. The character, onset, frequency, and aggravating factors should be assessed. 2) Location should be described in relation to the position in long bones, cortical or medullary, and eccentric or centrally located. Epiphyseal lesions include chondroblastoma, intraosseous ganglion, and clear cell chondrosarcoma. Physeal lesions are only seen in giant cell tumors. Metaphyseal lesions include metastatic tumors, osteomyelitis, osteo/chondro/fibrosarcoma, malignant fibrous histiocytoma, non-ossifying fibroma, and unicameral bone cysts. Diaphyseal lesions include lymphoma, eosinophilic granuloma, metastasis, multiple myeloma, and ewing’s sarcoma. Peripheral/cortical lesions include osteochondroma and para or periosteal osteosarcoma. 3) Rate of growth is characterized by the borders of the lesion. Permeative lesions have a wide zone of transition and are typical of fast-growing lesions, typically malignant tumors and osteomyelitis. Moth-eaten lesions have intermediate zones of transition with irregular borders. They may be malignant or benign tumors. Geographic lesions have welldefined sclerotic borders with a short zone of transition. This finding is typical of benign tumors and cysts (although lowgrade malignancies may also sometimes look like this.) 4) Periosteal reaction appearance may give clues to the type of tumor. Single-layer periosteal reaction is typical of osteomyelitis, benign tumors, and lower-grade malignant tumors. Onion-skinning is typical of repetitive insults to the periosteum, seen in osteosarcoma and ewing’s. Perpendicular periosteal reaction has a spiulcated, sunburst

appearance that is almost always malignant. Codman’s triangle is similarly a sign of malignancy in tumors. 5) Tumor matrix description can help determine the tissue type involved. Osseous lesions appear cloud-like and amorphous with usually a “fluffy” appearance. Cartilaginous lesions appear punctuate w/ C-shaped lesions and numerous small calcifications in the center are typical. Fibroosseous lesions have a ground-glass character with no discernible trabeculae. No visible matrix is a pertinent negative and may be a giant cell tumor or cyst. CT imaging of tumors is used to evaluate tumor matrix more effectively and determine cortical vs medullary lesions. MRI of tumors in used to asses soft tissue and marrow involvement, but does not provide much for osseous tumors. Osteoid Osteoma (OO) is a fairly common tumor seen in 1030 y/o. It is characterized by a visible central nidus of less then 1cm that is seen in the tibia/fibula or spine (causing painful scoliosis.) The nidus may or may not have a central area of calcification. Pain is felt at night and is described as a dull pain which responds to ASA. It may take 6-24 months to make a Dx. If near a joint the OO can cause joint effusion and pain that can look clinically like JRA. The main D/dx is stress fx. MRI is frequently misleading in dx. Tx is sx or radiofrequency ablation (90° C.) Osteoblastoma (OB) is a very large osteoid osteoma that is also very rare. It is seen in the same populations and in the same locations but with milder symptoms (despite greater size.) The nidus may be greater than 1.5cm and can have multiple internal calcifications. It causes less reactive sclerosis than OO. Osteosarcoma (OS) has several variants. Paraosteal and medullary (low grade) have good prognoses. Pagetoid and radiation-induced OS has a poor prognosis. Telangectatic OS causes many complications, but often responds to chemotx. Classically, OS is a medullary tumor seen in the metaphysis of 10-25 y/o. Most are seen in the femur near the knee. Diagnosis is by pain, X-ray, and elevated levels of alk phos. Radiographically it appears cloud-like with sunburst periosteal reaction and codman’s triangle. Skip lesions or lung metastasis indicates a poor prognosis. Paraosteal osteosarcoma (PaOS) is seen 5-10 years later then medullary OS and is more common in females. It causes dull aching pain and carries a better prognosis than OS, unless it extends into the medulla. Periosteal osteosarcoma (PeOS) is a rarer lesion that has similar age, location, and s/sx as medullary, but is located in the diaphysis and carries a better prognosis. Paget’s Disease (P) is thought to have a viral cause, and is seen primarily in English-speaking countries. Affected bones have a thick cortex and accentuated trabeculae. Paget’s predisposes an individual to OS, CS, FS, GCT, and MFH. Enchondroma (E) is a benign, intramedullary, cartilaginous lesion. It occurs in any age and is characteristically painless. It is normally seen in hands and feet and may cause pathological fx. The lesions appear geographic with central calcifications, possibly with endosteal scalloping or expansion. Ollier’s disease is the condition of multiple enchondromatosis that may predispose to malignancy. It is more common in children and causes growth disturbances. Maffucci’s disease is hereditary multiple enchondromatosis

with soft tissue telangiectasias as well. Prognosis for Maffucci’s is very poor, with almost 100% malignancy. Juxtacotical Chondroma (JC) is a solitary cartilaginous tumor that causes erosion of surrounding bone. The average age is 22 y/o and is seen most commonly in long bones of the hands and feet. The tumor is symptomatic, causing pain and swelling in the area. In 50% of cases ST calcification may also be seen, with erosion and “saucerization” of the bone. Chondroblastoma (CB) is a benign cartilaginous tumor of the epiphysis. It is seen in individuals with open growth plates (teenaged) and is geographic in nature. Calcifications are seen in 50% of cases. Pain and joint effusion may cause CB to be mistaken for arthritis, much like OO. Chondromyxoid Fibroma (CF) is a very rare tumor that is metaphyseal, geographic, and multiloculated. It occurs in all ages and is seen in the LE. Pain is “vague.” It may extend all the way to the physis. Osteochondroma (OC) is a cartilage-capped exostosis of bone. It is common in the general population, and is usually discovered in adolescence as a painless, hard “lump.” The location is usually metaphyseal, and the exostoses characteristically point away from the joint. Malignant transformation may have occurred if painful, greater then 2cm, or growing after skeletal maturity. Multiple hereditary osteochondromatosis (MHO) is a multiple variant that is autosomal dominant. It frequently causes growth disturbances in children and carries a 20% chance of malignancy. Benign Perosteal Osteochondromatous Proliferation (BPOP) is a very rare finding seen in adults aged 20-30 y/o. Sometimes also called “nora’s lesion,” BPOP is benign, but has a very high rate of recurrence if removed. Chondrosarcoma (CS) occurs de novo or secondarily from conversion of a benign lesion. The average age is 40 y/o. Pain is the primary s/sx. Lesions are typically geographic and metaphyseal, with lucent centers filled with small calcifications. Tx is w/ sx. Variants of CS include clear cell chondrosarcoma (CCC) which is an epiphyseal lesion (looks like CB but in older patients) and dedifferentiated chondrosarcoma in which part of the lesion is low-grade and another part is high grade. Non-Ossifying Fibroma (NOF) and its relative the Benign Fibrocortical Defect (BFOD) differ only in their location; the NOF is medullary and the BFOD is cortical. It is most common in children, and is usually asymptomatic unless there is a pathological fx. X-ray shows a sclerotic border in the growth plate to the diaphysis. DO NOT BIOPSY NOFs. With age the lesion usually regresses. Jaffe-Campanacii syndrome is multiple NOFs with café au-lait spots. Fibrous Dysplasia (FD) is a benign fibroosseous lesion of bone that is usually unilateral (75%) and has a geographic appearance. The hallmark radiographic feature of FD is a ground glass matrix. Dense areas of calcification may also be seen. FD presents typically with deformity and sometimes pain, secondary to fx. Albright’s syndrome is polyostotic FD with café au-lait spots and endocrine abnormalities. As opposed to Jaffe-Campanacci syndrome, where the lesions have a smooth border, albright’s syndrome lesions have a rough border. Mazabraud’s syndrome is polyostotic FD with intramuscular myxomas. The shepherd’s crook deformity is also a hallmark of this type of lesion.

Osteofibrous Dysplasia is an intracortical FD of the tibia (usually) seen in childhood. It is very uncommon. It is usually painless and has the characteristic ground glass appearance. It is associated with adamantinomas. Fibrosarcoma (FS) occurs in the 3rd to 6th decades of life and present as an aggressive lytic lesion with no matrix and no periosteal reaction. Its location is generally metaphyseal. It may also arise secondary to other lesions as well (including infarcts.) Giant Cell Tumor (GCT) is a locally aggressive lesion that is usually benign but not always. It presents as a lytic lesion in the metaphysis extending into the epiphysis (and is the only one to occur in this area.) There is no matrix associated with GCT. The lesion may destroy the cortex and invade the ST as well. It most commonly occurs in the femur, radius, humerus, and sacrum. It is slightly more common in females. S/sx include pain. The Giant cell reparative granuloma is a cousin of GCT presenting with lucent lesions of the hands and feet seen in children. It typically does not break through the periosteum. It may mimic and be hard to distinguish from brown’s tumors, even on histology. It is also called a solid aneurismal bone cyst. Unicameral Bone Cyst (UBC) is a very common benign lesion often seen in the distal calcaneus. It is medullary and fluid-filled, and may be an incidental finding (although it can cause pathological fx.) It is geographic, with sclerotic borders. It typically arises at a growth plate, migrating later into the diaphysis with age. 90% are seen in the humerus and femur. The hallmark of the UBC is the fallen fragment sign (piece of cortex within the center of the lesion.) Tx is observation, steroid injection, of sx bone graft packing. Aneurysmal Bone Cyst (ABC) is a lytic expansile lesion noted for the blood-filled cavities it forms. It may arise de novo or post trauma, or may be associated with CB, GCT, NOF, OB, CMF, or FD. It presents with pain in the long bones and axial skeleton. It is usually seen in teenagers. Its hallmark are fluid-fluid levels of two layers seen on MRI representing old coagulated blood and new, unsettled blood. Fluid-fluid levels are also seen in telangectatic OS, MFH, and FD. Interosseous Lipoma (IL) is a benign asymptomatic lesion that is typically an incidental finding. It is usually seen in the calcaneus. It can have a central area of calcification, but is noted for its central area of fat on CT and MRI. It is seen in the same locations as UBCs. Intraosseous Ganglion (IG) is a benign lesion of the subcortical bone typically seen in the middle-aged. It can present with pain. It may resemble a subchondral cyst on xray (but in the absence of DJD). It is most commonly seen in the medial malleolus. It may also look like GCT but with a lobulated matrix. Ewing’s Sarcoma (ES) is a common primary bone tumor seen in children, presenting with pain, low-grade fever, wt loss, and an elevated sed rate. It is rare in AAs. It has the appearance of a small blue-cell tumor which it shares with primary lymphoma and multiple myeloma. It is most common in the lower extremities. The lesion is permeative and has no matrix. It produces an onion-skin type periosteal reaction. The location can be metaphyseal or metadiaphyseal, and produces a soft tissue mass surrounding the lesion. A variant

of Ewing’s is primitive neuroendothelial tumor (PNET) which has the same appearance, prognosis, and treatment, but is associated with a chromosome translocation. Primary lymphoma of Bone appears similar to ES but in a much older patient. Pain is usually the presenting symptom, but there are no systemic signs. Multiple Myeloma (MM) is the most common primary malignancy of bone, seen in older individuals. It presents with pain, weakness, or neurological symptoms. It sometimes presents with a solitary bone lesion called a plasmacytoma. On x-ray there are cookie-cutter lesions that appear osteopenic and without sclerosis. Bone scans and MRI are unreliable in dx. MM commonly has the POEMS syndrome – polyneuropathy, oganomegaly, endocrine abnormalities, M proteins, and skin lesions. Hemangioma is a common benign or congenital lesion most commonly seen in the skull and spine. It appears to have vertical striations in the spine and radial spokes in the skull. CT shows a polka-dot pattern. It is usually asymptomatic. Hemangioendothelioma is a rare lesion seen in the lower extremities. It presents as a cortical defect similar to hemangioma. It is typically seen in the middle-aged. Eosinophilic Granuloma (EG) is a non-infectious granuloma with histiocytes and eosinophils proliferating. Most are seen in the skull and vertebrae, but it may also occur in the lower extremity. Langerhans Histiocytosis is unifocal EG in one organ system. Hand-Schuller-Christian Disease is multifocal in one organ system. Letterer-Siwe Disease is multifocal and multisystem. The average age of EG is 15 y/o. There is little periosteal reaction, and there may be a sequestrum (especially in the skull.) The lesions may appear punched-out. The typical presentation is with a spontaneous compression fx. They are typically diaphyseal. Bone scans are unreliable in dx. Adamantinoma is a rare, locally aggressive lesion seen almost exclusively in the tibia. It appears in the 3rd to 5th decades as an eccentric, lobulated lesion. Periostitis is rare. Local pain and swelling are apparent on examination. Metastatic bone tumors are the most common type of bone malignancy, primarily from the breast, prostate, lung, and kidney. Periosteal reaction is rare. Location is based on the tissue type. Blow-out lesions are renal and thyroid based. Peripheral and cortical lesions are lung metastases.

RADIOLOGY OF SYSTEMIC DISORDERS Changes in the trabecular pattern in bone are indicative of reconstructive mechanisms and may suggest systemic disease. Osteoporosis, osteomalacia, and hyperparathyroidism all cause a generalized loss and coarsening of the trabeculae. In many cases, this can also happen with anemias, storage diseases, and neoplastic disorders as well. Etiologies of abnormal bone texture include generalized overactivity of cancellous bone resorption, infarction due to disruption of blood supply, and growth retardation due to localized hypoxia (in children.) ANEMIAS Anemias that affect bone density include sickle cell anemia, thalassemias, and iron deficiency anemia. Sickle Cell Anemia puts pts at risk for salmonella infections seeded hematogenously, with osteomyelitis occurring in the

diaphyseal region. Marked edema of the hands and feet may be seen secondary to this infection. Bone density is lost in the spine, flat bones, and long bones with a coarse trabecular pattern. The hallmark is fish vertebrae that appears as a biconcavity of the vertebral bodies on lateral x-ray (with disc space preserved.) Periostitis is also seen in the hands and feet. Bones of the hands and feet can also be infracted in children with sickle cell – the hand and foot syndrome causes localized infarction leading to early closure of growth plates in the affected bones. This causes periosteal new bone formation (appearing 1-2wks post injury) and may lead to AVN. Cortical infarcts are more common, and the femoral head is most affected. Infarcts within long bones may present on x-ray as calcified fat necrosis, which may look like a tumor (fibrous dysplasia.) The bone infarcts can also make the bone prone to infection and pathological fx. Infarct of the distal tibia can lead to premature closure of the epiphysis laterally, causing a characteristic tibiotalar slant with a valgus attitude. Thalassemias are gene deletions of primary hemoglobin subunits, causing a microcytic hypochromic anemia. Radiographically they present similarly to sickle-cell anemia, with the notable exception that infarcts are generally not seen. Trabeculae may take on a “honeycomb” pattern and long bones typically take on an Erlenmeyer flask morphology. Secondary centers of ossification may be delayed. Iron Deficiency Anemia characteristically causes osteoporosis of the hands (in severe cases) and transverse striping of the metaphyses. Radiographic changes are more readily apparent in the pediatric population. LIPID STORAGE DISEASES Gaucher’s Disease is a disorder characterized by the accumulation of cerebrosides in reticuloendothelial cells. The lower extremities are more commonly affected. The classic presentation is ischemic necrosis of the proximal femur with Erlenmeyer flask deformity. Niemann-Pick Disease is an inherited abnormality of sphingomyelin metabolism seen most commonly in persons of jewish descent. Radiographically a widening of the medullary cavity, coarse trabecular pattern, thinned cortex, failure of tabulation, and loss of bone density are seen. The Erlenmeyer flask deformity is also seen. Sarcoidosis is a systemic granulomatous disease involving the skin, lungs, lymph nodes, and viscera. 10% of patients have bone involvement. Children are rarely affected. Radiographically dx is made with CXR; in the extremities the middle and distal phalanges can show cyst-like punched out lesions in the cortex. Pancreatitis causes fat necrosis of the bone marrow (which is also seen in cancer of the head of the pancreas.) Radiographically bone infarction follows the fat necrosis stage, with calcification and ossification of the affected marrow. The long bones of the hands and feet are most affected. Dysbaric Osteonecrosis (Caisson disease) is a pressureinduced osteoarthopathy seen in deep-sea divers. It presents as small localized infarctions of bone due to the formation of nitrogen bubbles within the body. Hemophilia is a disorder of blood coagulation due to plasma clotting factor deficiency. Classic hemophilia (A) is due to factor VIII, Christmas disease (B) is due to factor IX. Both

are X-linked diseases. Radiographically bleeding is apparent sub-periostally, intraosseously, and intra-articularly. The chronic hemarthrosis due to joint bleeding causes destruction of the hyaline cartilage secondary to lysosomal enzyme release in the breakdown of blood products. Hemophilia can also cause premature closure of the epiphyseal plates, causing tibiotalar slant seen also in sickle cell anemia. Metaphyseal and Diaphyseal Infarcts are usually due to occlusive vascular disease, sickle-cell anemia, caisson disease, infiltrative/collagen diseases, infection and/or idiopathic. The increase in bone density seen in an infarct is due to crushing of the avascular debris, calcification of fat necrosis, hyperemic removal of viable bone surrounding, bony apposition, and periosteal involucrum formation. ENDOCRINE DISORDERS Acromegaly/Gigantism are both disorders characterized by excess in growth hormone. The result is joint space narrowing, bony sclerosis, cyst formation, and osteophytes similar to DJD. It usually affects the acral skeleton most. In the foot there is seen sausage digits, enlarged sesamoids/MPJs, prominent metatarsal heads, prominent tufts and bases of phalanges, enthesis development, and constriction of proximal phalangeal shafts. Fat pad thickening is a radiographic hallmark of acromegaly. Hypertrophy of the bases and tufts of the distal phalanges causes secondary bony fusion resulting in pseudoforamina formation unique to this disease. Hyperparathyroidism causes generalized bone resorption subperiosteally, intracortically, endosteally, and subligamentous. Bone sclerosis and chondrocalcinosis are also seen. Brown’s tumors are unique to hyperparathyroidism. Renal Osteodystrophy is a disease of chronic renal failure that causes hyperparathyroidism, rickets/osteomalacia, osteoporosis, soft tissue calcification, and vascular calcification. Osteomalacia and Rickets primarily are caused by Vitamin D disorders, and cause bowing of the tibia and periarticular calcification. Hypoparathyroidism may be primary (deficiency or destruction of the gland) or secondary (gland unresponsive.) It causes spinal calcifications that appear like osteophytes (of DISH). Pseudohypoparathyroidism is the most common secondary disease, causing a short stature, round face, brachydactyly, exostoses, cone epiphyses, and wide bones. Women are more affected than men. Hyperthyroidism is characterized by a general catabolic state of the body, resulting in loss of connective tissue as well as increased bone turnover. Osteoporosis is a common initial finding. Other findings include accelerated skeletal maturation and myopathy. Thyroid acropachy is a complication of hyperthyroidism that includes progressive exopthalmos, hand and foot swelling, digital clubbing, pretibial myxedema, and periosteal new bone formation (middiaphyseal), particularly of the 1st metatarsal. The edema has a nodular appearance. Hypothyroidism (Myxedema) is caused by a deficiency of TSH, thyroid hormone, or iodine. In infants the disorder is called cretinism. In adults the disorder causes edema, dry skin, coarse hair, lethargy, fatigue, paresthesia, and bradycardia. Tarsal tunnel syndrome is also a common finding.

Paget’s Disease (Osteitis Deformans) is a disease of unknown etiology. It, as well as fibrous dysplasia, are known as the great masqueraders of bone disease. (Outside of bone, gout and syphilis are also known as great masqueraders.) Paget’s is normally seen in the axial skeleton, but can affect any bone. The pelvis, femur, skull, and tibia are most common. Its incidence is 4-6% in individuals over 40 y/o. Deformities associated with Paget’s include femoral bowing (shepherd’s crook), tibial bowing (sabre shin), liontiasis (lion facies), and pathological fracture (banana fxs.) Pseudofractures, seen also in osteomalacia/rickets, are also known as umbua zonen and looser’s lines – they represent demineralized areas of bone that are not actually fxs, although they appear that way on xray. The stages of Paget’s disease are 1) Destructive phase – increased osteoclastic activity and osteoporosis circumscripta, both difficult to dx early. 2) Combined phase – bone destruction/turnover and fibrous bone replacement. 3) Sclerotic stage – uniformly thickened trabeculae, ivory appearance of bone (see also psoriasis), and bone expansion. 4) Malignant degeneration – metaplasia to osteosarcoma (rare) Lab findings for Paget’s show elevated alk phos (x20) and hypercalcemia. UA may show urinary hydroxyproline. Bone scan shows multiple hot spots (sometimes solitary). Course is slow and treatement is with calcitonin and supportive therapy. Massive Osteolysis (Disappearing bone disease) is a disorder causing sudden resorption of large areas of bone without malignancy. It is associated with lymphangioma or hemangioma and clinically presents with pain. X-ray findings show apparent disappearance of bone, (tapering off in long bones), with no periosteal reaction noted. Diabetic Osteolysis is a disorder characterized by marked resorption with neuropathic changes. It is seen in the absence of an infectious process, although that is usually a d/dx. It may be the result of a viral infection. Radiographically a decrease in ST density, local osteoporosis, distal resorption, licked candy stick appearance, and apparent bone “regeneration” are apparent on x-ray. Poliomyelitis radiographically presents with severe cavus deformity, severe osteoporosis, short metatarsals and phalanges, and a ground glass appearance of medullary bone. Neurofibromatosis is a hereditary disease of mesodermal origin causing café-au-lait spots, skin neurofibromas, bone deformity, and local gigantism. Bone deformities include kyphosis, bony erosion, local overgrowth, overtubulation of long bones, pseudoarthroses, and lytic areas of bone.

AVASCULAR NECROSIS AND OSTEOCHONDRITIS DESSICANS Avascular Necrosis (AVN, epiphyseal ischemic necrosis, osteonecrosis, osteochondrosis, epiphysitis, and aseptic necrosis) is a disruption of the vascular supply of bone leading to the death of an osseous structure. Primary causes are unknown. Secondary causes can be fracture, sickle cell anemia, long-term corticosteroid use, and alcoholism. Clinically, AVN is variable and relatively minor in symptomatology. Pain and disability progresses as it is untreated. AVN normally lasts about 9 mos, but in some cases (legg-calve-perthes) it can last up to 8 years. Spontaneous

AVN occurs in the distal femur, femoral head, and metatarsal heads. Trauma-induced AVN occurs in the talus. Alcoholism-induced AVN occurs in the femoral head. Surgery can also be a cause of AVN. The Avascular Phase of AVN is the actual loss of blood supply, leading to bone death, failure of epiphyseal growth, minimal bony deformity, reactive hyperemia, synovial thickening, and edema. On x-ray you see a small epiphysis, normal bone density, increased joint space, capsular swelling, metaphyseal osteopenia, and a widened growth plate. The Revascularization Phase sees infiltration of new blood vessels and fragmentation of the dead parts. On x-ray you see a sclerotic rim, new bone deposited on old bone (snow cap sign), fracture inferior to the articular cortex (crescent sign), clefts and fragmentation, flattening of articular surfaces, a widened metaphysis, and “head within a head” appearance. The Repair and Remodeling Phase includes new bone deposition replacing bone resorption. On x-ray you see reconstitution of the epiphysis and the disappearance of clefts. The Residual Deformity (stage 4) includes restitution of the epiphysis, with the amount of deformity dependent on compressive forces on the affected bone. On x-ray you see a deformed articular surface, usually flattened. Legg-Calve-Perthes Disease is a true AVN of the capital fragment of the femoral epiphysis in children. Males are more commonly affected than females. 3-12 y/o is the average age. Prognosis worsens with later ages. 1 in 10 are bilateral. Clincally the pt has limp and a vague pain in the groin that may extend to the knee. Pain is exacerbated with activity. There is often muscle atrophy in the thigh and a history of trauma in the affected individual. The etiology is unknown. Blount’s Disease is not a true AVN, seen in infants affecting the medial tibial epiphysis. The failure of the growth plate in this area contributes to the formation of a tibia/genu varum. Osgood-Schlatter Disease is not a true AVN either, affecting the tibial tuberosity. It is caused by a partial disruption of the tibial patellar ligament (w/ or w/o avulsion). Commonly ossific nodules are seen with this disease, forming a large, prominent tibial tuberosity. The course is self-limiting and affects mainly males 11-15 y/o. Sindig-Larsen-Johannson Disease is not an AVN, but is looks similar to Osgood-schlatter disease. It is a traction induced avulsion fragment of the lower patella. Diaz Disease is a true AVN of the talus. It is usually caused by trauma, graded by the Hawkin’s classification system. A positive Hawkin’s sign indicates revascularization. Sever’s Disease is a non-AVN of the calcaneus. It is calcaneal apophysitis caused by traction of the calcaneus. It presents with heel pain and irregular ossification on x-ray. All radiographic findings, however, may also be seen in normal children. Examples include a sawtooth metaphysis, decreased metaphyseal density, increased density of the apophysis, and fragmentation of the apophysis. Males and females are affected equally. The primary D/dx for sever’s disease is spring heel (hematogenous osteomyelitis of the calcaneus.) In spring heel, the plantar tubercles typically show signs of deossification, not seen in sever’s disease. Kohler’s Disease is a true AVN of the navicular seen in males around 5 y/o. It presents with localized pain, edema, tenderness, and decreased ROM. Some pts have a

congenitally small navicular – an incidental finding of a very small navicular on x-ray may not be kohler’s. The appearance should be patchy or uniform sclerosis, collapse (silver dollar sign), and fragmentation of the bone. The joint space is usually preserved. Iselen’s Disease is a non-AVN of the fifth metatarsal base. It is actually a tractional apophysitis and is self-limiting. Freiberg’s Disease is a true AVN of the metatarsal heads. The second metatarsal is most commonly affected, particularly in pts w/ a long 2nd metatarsal. There is tenderness and pain over the affected MPJ, and the pain is exacerbated with activity. Infarction of the epiphysis leaves necrotic bone that causes degenerative changes and cortical thickening. Adaptive changes occur on the juxta-articular surface (flattening and broadening of the joint space.) Theimann’s Disease is a non-AVN of the fingers and toes that is extremely rare. It occurs secondary to trauma and is attributed to multiple ossification centers in the phalanx. Sesamoid AVN is called Trevor’s (fibular) or Renandier’s (tibial) and occur secondary to trauma and fracture. Osteochondritis Dessicans (OCD) is a disease of unknown etiology affecting children and adolescents, typically male. A small segment of necrotic bone forms subchondrally, which may heal spontaneously or become a joint mouse. Joint mice in these cases are typically symptomatic because the major component is cartilage, which is not visible on x-ray. Symptoms are joint effusion, pain on ROM, crepitation and locking and localized tenderness (vague to the ankle). The disease may be hereditary. There are two types of OCD – Insitu and displaced according to the fragment. Radiographically they look similar to talar dome fractures.

ADULT FOOT DISORDERS Heel Pain – Plantar: R/O soft tissue involvement, fissuring, tumor, and nerve entrapment. Plantar fasciitis presents radiographically as increased ST density of the plantar fascia, and deossification of the calcaneus with accentuation of the tensile trabecular patterns (do not confuse w/ stress fx.) Heel spurs are sometimes seen in plantar fasciitis but also can be caused by the pull of the FDB, Abd hallucis, Abd digiti minimi, and the long plantar ligament. Heel spurs account for 15% of all adult foot complaints. They are typically directed forward from the medial tubercle. They are assoc w/ obesity, pes cavus & pes planus, and osteophytosis. It is important to note that the size of the spur has no effect on the symptoms, and oftentimes the contralateral (asymptomatic foot) will have a spur of equal or greater size. 90% do not require any type of sx intervention to tx. Fluffy heel spurs are associated with certain arthropathies, particularly Reiter’s, ankylosing spondylitis, psoriatic arthritis, RA, and Paget’s disease. Other causes of plantar heel pain include calcified bursae, atrophied fat pad (measuring 15-23mm), steroid-induced calcification, and nerve entrapment. Nerve entrapment can be differentiated from plantar fasciitis by its response to steroids (relief in plantar fasciitis, no change in nerve entrapment), and with nuclear scanning (+ in plantar fasciitis). Heel Pain – Posterior: Tendo-Achilles (partial tear or complete tear/AODM), retro-achillean bursa (caused by shoe irritation), or retro-calcaneal bursae/Haglund’s deformity (most common.)

Heel Pain – Medial: Tarsal Tunnel Syndrome is caused by chronic irritation of the posterior tibial nerve in the flexor retinaculum and inferior to the medial malleolus (seen w/ RA, AODM, trauma, fx, and dislocation.) Medial calcaneal nerve entrapment and posterior tibial tendon dysfunction are other causes of medial heel pain. (Radiographically represented by increased TC angle, anterior Cyma line, and sagging of the metatarsocuneiform joint. Heel Pain – Lateral: Lateral heel pain is the most rare presentation. It can be caused by sural nerve entrapment, calcaneo-fibular irregularities, peroneal tendon problems, tarsal coalition, and ankle/RF varus deformities. Midfoot to Rearfoot Relationship: Calcaneal pitch is normally between 10-20 degrees – greater than this is pes cavus and less is pes planus. A supinated foot will have an accentuated or bullet hole sinus tarsi, while the pronated foot will have a pseudo sinus tarsi which is in fact the posterior subtalar joint facet being brought into the plane of the film. Cavus Foot Structure: Typically caused by neurological or muscular imbalance. Forefoot cavus has an apex at the lisfranc’s joint. Midfoot cavus has its apex at the chopart’s joint. Rearfoot cavus is calcaneal in nature and has a calcaneal inclination angle of >30 degrees (and claw toes.) Foot Faults are sections of the foot where adjacent segments are improperly aligned. Hindfoot/Subtalar/Midtarsal Fault Syndrome is characterized by an anterior Cyma line, pseudo sinus tarsi, increased talar declination angle, decreased calcaneal inclination angle, everted cuboid, and less than 85% coverage of the talar head. The cuneiform-navicular fault occurs at the CN joint. The medial cuneiform is plantarly displaced, and the CC joint has decreased joint space dorsally (with increased space plantarly.) The foot appears longer. Pes Valgo-Planus: The acquired form has a calcaneal inclincation angle >10 degrees (normal) but the inferior surface of the calcaneus is concave. The congenital form (CCPV) has a low calcaneal inclincation angle with a convex inferior surface of the calcaneus. Diabetic Neuropathy occurs an average of 16 years after the diagnosis of Type 2 DM (AODM). 74% present with a foot ulcer, particularly if loss of proprioception is involved. The forefoot ulcerates twice as commonly as the rearfoot. Charcot neuroarthropathy has three stages of destruction, coalescence, and remodeling. Stress Fractures (aka march/fatigue fx) occurs most commonly in the metatarsals, esp the 2nd (38%), then the calcaneus (28%), and tibia (24%). Early X-rays appear normal, however it may appear radiographically over time and as symptoms persist. Hallux Abducto-Valgus (HAV): Is evaluated biomechanically by radiograph. Normals: IM 10-20 PASA 0-8 HA 0-15 DASA 0-5 MA 12-15 Other factors evaluated are tibial sesamoid position, total adductory angle, metatarsal break angle, and bone density. The joint status is described as congruous, deviated, or subluxed. Positional HAV is one where PASA+DASAHA. Combined HAV is if the PASA+DASA >>>HA.

Hallucial Sesamoids are located in the tendon of FHB and ossify between the ages of 8-12 (earlier in females than males.) Up to 1/3 are multipartite, esp the tibial. Osteonecrosis of the tibial is termed renandier’s, while that of the fibular sesamoid is trevor’s. An interphalangeal sesamoid is present in 43% of individuals (esp males), and is usually bilateral. It may contribute to IPJ HPK formation.

PEDIATRIC RADIOLOGY Ossification of bones in the foot occurs sequentially from birth to adolescence, and knowledge of this order is necessary for a physician to determine the correct skeletal age of a patient. The talus, calcaneus, metatarsals, and sometimes cuboid are ossified at birth. Then the order of ossification is medial cuneiform at 6 months, intermediate cuneiform at 1 year, medial cuneiform at 1.5 years, and finally the navicular at 2.55 years. The sesamoids ossify around 7-8 years of age. Common variations include an independent ossification center of the medial malleolus (20%) or of the distal phalanx of the hallux, irregular epiphyseal plates, absent epiphyseal ossification in the middle phalanges, 5th digit synphalangism, bilateral/symmetric cone-shaped epiphyses (which fuse earlier than normal epiphyses), and pseudoepiphyses, fissues, and exostoses that may appear similar to fracture. An accessory navicular is seen in 10% of children, posterior to the navicular tuberosity, which can cause pes planovalgus deformity that requires sx excision. The navicular itself ossifies by multiple ossification centers which are asymmetrical and may look like kohler’s disease. Similarly, the calcaneal apophysis has multiple ossification centers which may look like sever’s disease. The calcaneus may also have a pseudocyst called the ward’s or neutral triangle which appears as a radiolucent circle/triangle in the anterior calcaneus (10%). The calcaneus often has compact bone islands as well. The apophysis of the 5th metatarsal base runs parallel to the shaft, and should be distinguished from a fracture. RADIOGRAPHIC EVALUATION OF THE PEDIATRIC PATIENT The standard AP in infants must use a simulated WB position which is accomplished with the knees flexed and held together and an additional 15 degree angulation of the tube. Lateral views are positioned similarly, with the beam aimed at the ankle. CT scanning is used in peds to determine tarsal coalitions as well as growth plate abnormalities. MRI can be used to evaluate unossified structures. GROWTH VARIATIONS Macrodactyly is a localized gigantism of the digits caused by fat infiltration, long-standing hyperemia (leading to hypertrophy), or neurofibromatosis. Kippel-Trenaunay Syndrome is a localized gigantism of the hands or feet, usually in only one extremity. Varicose veins and port-wine hemangiomas are also present. Larsen’s Syndrome is characterized by a double ossification center of the calcaneus with a cleft palate, joint dislocation, equinovarus/valgus foot, broad thumbs, and vertebral abnormalities. Gorham’s Disease (vanishing bone disease) is massive osteolysis following episodes of trauma that can to opposing bones across joint spaces. Radiographically the bones will

appear tapered with an absence of periosteal reaction. The primary d/dx is charcot foot. Neurofibromatosis is characterized by multiple neurofibromas with café-au lait spots, lipomas, kyphoscoliosis, enlargement of the foot bones, multiple ST densities, congenital pseudoarthroses (mainly in fibula/tibia), marked cortical thickening, and a hypoplastic pelvis. Dwarfism is a plastic condition of localized bony undergrowth. It occurs when tumor, radiation, or primary developmental defects cause the epiphyseal plates to prematurely close. The tibia is typically shorter than the fibula, the distal femoral metaphysis is hypoplastic, and the tibial and fibular metaphyses are cupped. Kyphosis is the most common skeletal abnormality. Equinus is a common foot deformity. There are 3 types of short-limb dwarfism: Rhizomelic Dwarfism is a shortening of the proximal segment (humerus or femur) Mesomelic Dwarfism is a shortening of the intermediate segment (tibia/fibula or radius/ulna) Acromelic Dwarfism is a shortening of the distal segment (hand, foot) Hurler’s Syndrome is a syndrome characterized by dwarfism, mental retardation, kyphosis, hepatosplenomegaly, and coarse facial features. Radiographically you see shortened shafts of the long bones with tapered ends, particularly in the upper extremities. There is also a coax valga and genu varum. Aplasia/Hypoplasia (dysmelia) describes any reduction malformation. The cause is unknown. They are classified by extent and orientation. Phocomelia is loss of the intermediate segment of a limb. Meromelia is partial absence of a limb. Hemimelia is absence of a half (longitudinally) of a limb. They are a part of Fanconi’s anemia and thrombocytopeniaabsent radius synd. Proximal femoral focal deficiency (PFFD) is assoc w/ absence of the ipsilateral fibula as well. Polydactyly is the most common excess malformation. It can be isolated or occur w/ syndromes. There is no sex predilection and it is most common in the AA population. 50% of cases are bilateral. The tetamy & McKusick classification is preaxial (tibial side of 2nd digit) or postaxial (fibular side of 2nd digit – 80%). The venn-watson classification is that preaxial polydactyly has a short metatarsal w/ wide metatarsal head. Postaxial has a Y or T shaped metatarsal, or complete metatarsal duplication. Brachydactyly is shortening of the digits due to hypoplasia or syndactyly. It is seen in pseudo(pseudo)hypoparathryroidism, turner’s synd, sickle-cell, Down’s, and fetal dilantin synd. Fusion deformities are errors of segmentation. Syndactyly can be simple (only soft tissues fused) or complex (varying degrees of bony involvement). Apert’s syndrome (discussed earlier) is manifested radiographically by multiple bony coalitions all over the body, leading to limitation of motion that is progressive. Nievergelt-Perlman syndrome is characterized by clubfoot, synphalangism, conduction deafness, ball&socket ankle joint, flexion deformities, and phocomelia or hemimelia. Carpenter’s syndrome is polysyndactyly w/ premature synostosis of the skull. Poland’s syndrome is syndactyly and digital hypoplasia.

Amniotic band syndrome (streeter’s bands) is the formation of constriction rings around the limbs, present at birth, which leads to distal loss of the limb. The cause is unknown. BIOMECHANICAL ABNORMALITIES Kite’s (TC) angle is normally 25-50° in peds; however, this angle requires the use of estimated axes for involved bones. Another method is to compare the long axis of the talus and 1st MT – they should line up. Rearfoot Valgus is characterized by a high Kite’s and talar declination angles, and is seen in flatfoot deformities, congenital vertical talus, and neuromuscular disease. Rearfoot Equinus is a calcaneal inclincation angle >90°. It is seen in congenital equinovarus and congenital vertical talus. Rearfoot Varus is characterized by a low Kite’s angle and nearly parallel talar and calcaneal axes. It is seen in equinovarus and some neuromuscular diseases. Pes Planovalgus is the most common cause of RF valgus. The etiology is uncertain but thought to be related to ligamentous laxity. On X-ray there is abduction of the forefoot, laterally displaced navicular, PF calcaneus, DF metatarsals, and PF talus. If seen w/ equinus or a short Achilles, it is termed hypermobile flatfoot. HAV is also a common finding. Peroneal spasm may be seen if there is tarsal coalition. Most are asymptomatic and require no sx. Pes Cavus is most commonly seen w/ neuromuscular disease, particularly CMT. Typically there is high calcaneal inclination, PF metatarsals, and clawed digits. Talipes Equinovarus (Clubfoot) is most common in males, Caucasians & Polynesians, and is hereditary. There are 3 etiologies – intrauterine pressure (most flexible), abnormal tendon/ligament attachment (difficult to treat), and teratologic (assoc w/ arthrogryphosis and myeolodysplasia. Clincally you see FF adduction, RF varus, equinus, and TN subluxation. On X-ray there is low Kite’s angle, FF adduction, PF calcaneus, and stair-stepping of the metatarsals. The talonavicular relationship is estimated – Simon’s angle should be btw 0-20°, TC angle should be >15 and talometatarsal <15° for normal. Tx is initially casting, then sx w/ FF correction first (then RF.) Congenital Vertical Talus is assoc w/ arthrogryphosis, myelomeningocoele, and chromosomal abnormalities. It is more common in males and it 50% bilateral. On X-ray it is similar to pes planovalgus, but talus is markedly PF, and calcaneus may be in equinus. With DF metatarsals this makes for a rockerbottom foot.

BASIC CXR INTERPRETATION CXR positioning: Standard positioning is with the patient facing the cassette for PA, or with their back to the cassette for AP projections. The patient is instructed to inhale fully to standardize the view. AP projections make the heart appear magnified b/c it is farther from the cassette – the PA projection shows clear lung fields and a normal-sized heart. Lateral films are taken with the pathological side closer to the film. Normally the position of the patient is standing, w/ arms raised and chin up. However, depending on the condition of the patient, sitting or decubitus positioning may be necessary. The standard position decreases enlargement and distortion of the heart and vessels, allows the diaphragm to move down, and shows air-fluid levels better in the chest. When

positioning the film on a viewbox, it should be placed as though the patient is facing you (i.e. heart facing their left.) Osseous Structures to be evaluated in the chest include the sternum, clavicles, scapulae, ribs, and thoracic vertebrae. On lateral view there are two areas of radiolucency called the retrosternal airspace and the retrocardial airspace – this is normal. You should be able to visualize 10 ribs in a normal individual. Intercostal spaces are named by the rib superior. The Diaphragm is divided into two on the AP view by the vertebrae, making a left and right hemidiaphragm. The right side is normally higher due to the liver (and moreso in HSM.) The Pleura can only be appreciated with pathology (pleurisy.) The Lungs should be evaluated in more depth than the rest of the chest X-ray because of subtleties that can be easily missed. It is recommended to first do a “quick glance” of the lungs to determine if they are the normal shape and density. Then, divide each lung into thirds in both the transverse and sagittal planes. Then examine each third separately from each other with respect to the anatomy of each and densities seen therein. If pathology is suspected, determine if it is confined within lobar divisions – almost all lung pathology except tumors are lobar in nature. The costophrenic angles are also important to note, as blunting of these angles may be a sign of infection or left ventricular hypertrophy. Bronchi are not normally seen on X-ray unless they are thickened, which is the case in cystic fibrosis, CHF, or lymphatic obstruction secondary to tumor. Supporting structures of the lungs are similarly not seen normally on X-ray, but in pathological processes these lung septa, as well as lymphatic channels, can be seen and are referred to as Kerley lines. Kerley A lines are apically located, extending out from the hilum or upper margins. Kerley B lines are basilar in location, found in the lower lung periphery, about the diaphragm. Kerley C lines appear anywhere in the lung, but have a crosshatch appearance. Kerley lines are seen in interstitial edema/fibrosis, sarcoidosis, pneumonia, lymphatic obstruction, connective tissue disease, RA, and scleroderma. The Mediastinum is the last part of the CXR to examine. Primarily noted in the mediastinum are the heart and great blood vessels. An area of increased density is seen usually on the left side of the trachea and is called the aortic knob – this is where the aorta turns back on itself. The size of the heart is estimated using the cardiothoracic ratio which is normally 2:1 (the heart should be half the width of the lungs in total.) Cardiomegaly, also known as a “boot-shaped heart,” can be caused by sports conditioning (normal), CHF, mitral valve stenosis, chronic HTN, pericardial effusion, and left ventricular hypertrophy. Masses in the medastinum usually represent aortic aneurysms. The trachea, located superiorly in the mediastinum, is used to determine the midline of the body in the CXR. When compared with the aortic knob (which should be slightly to the left) and the right atrium (which should be slightly to the right), it can be determined if the patient was standing in the correct position for the AP/PA view. In peds it is sometimes necessary to visualize the thymus, however it is normally obscured by other mediastinal contents. Therefore, it is the only case in which you take expiratory CXR views, so that the thymus may be allowed to deviate away from the midline and be visualized before the lung fields. Lastly, the hilar lymph nodes are located on

either side of the medistinum and are readily appreciable on X-ray when adenopathy is present. LUNG PATHOLOGY Alveolar processes appear as triangular-shaped areas of increased readiodensity, depending on the extent of involvement. This presentation is seen in pneumonia, advanced CHF, ARDS, and PE. Occasionally there may be the addition of fluffy margins in the case of longer standing pathology, due to extension of fluid through adjacent acini through the pore of Kohn. The silhouette sign is the name given to alveolar pathology that exists in close proximity to the heart or great vessels – the water-density of the pathology makes the outline of the heart and vessels (also water dense) to be indistinct. CHF and pulmonary edema cause the hilar lymph nodes and vessels to become more distinct on X-ray. The fanning out of the lymphatic vessels bilaterally produces a “batwing” or “butterfly” appearance and is described so radiographically. Interstitial processes are those that cause an increase in radiodensity of the interstitium, meaning bronchi, septa, and lymphatics. This type of pathologic process is seen in interstitial pulmonary edema, fibrosis, TB, viral pneumonia, metastatic tumor, connective tissue disease, and interstitial pneumonitis. Miliary TB is seen as multiple tiny focal areas of increased radiodensity. Asbestosis appears as an interstitial process in the basilar lung fields. Emphysema is a loss of interstitial density due to loss of tissue in the interstitium. Besides a change in density, the diaphragm is pulled low (making the lung fields appear “tall”), and the heart is deviated medially. On a lateral view, the sternal angle may be increased. Primary lung lesions may be seen virtually anywhere in the lung fields. A general rule of thumb when assessing primary lung tumor is that dense masses tend to be benign, while fluffy and ill-defined masses are more likely malignant. Also, if a lesion is particularly dense (meaning possibly a calcified center), it is increasingly likely that the lesion is a granuloma. Another way to differentiate tumor from granuloma is by looking at blood flow to the area – tumors tend to be associated with blood vessels anatomically, whereas granulomas are not. Also important to keep in mind is that (for some reason) nipples are visible radiographically, and it is important to note where these are initially, so that they are not mistaken for a tumor later. If a lesion is metastatic, it may take on a localized metastasis pattern (one large tumor surrounded by many small ones), or if from another source may be scattered throughout the lung fields. Central cavitation in large tumors is indicative of rapid growth and carries a poor prognosis.

NUCLEAR IMAGING Nuclear imaging (scintigraphy) is used to analyze a number of organ systems in the body, most commonly bone. This is due to the fact that bone loss must reach 33-50% to be detected radiographically, whereas with nuclear imaging changes can be detected within hours. Nuclear imaging can also pick up pathology that is not clinically visible. Most common pathologies indicated are bone tumors, osteomyelitis, stress fracture, non-specific bone pain, and AVN. The primary disadvantage to nuclear imaging is poor resolution, which makes this imaging modality non-specific (despite high sensitivity.) Uptake of the nuclear tracer in a bone scan occurs in an area where the normal process of bony turnover is upset in any way. Areas where turnover is increased (typical in injury) show up “hot” or darker on the image, whereas areas where infarction or compromised blood supply have occurred show up “cold” or blank. There are a variety of imaging agents available for use in bone scanning, each with advantages and disadvantages. In addition to availability and half-life, imaging agents also vary according to the carrier molecule that they bind. Technetium is the most common, and may be bound to phosphate (Tc-99, for bone), pernechate (for brain/blood flow, joint imaging), or albumin (for lung perfusion/VQ scans). Also available are gallium (Ga-67, for inflammation) and indium (I-111, also for inflammation). A new agent, ceretec, uses Tc-labeled leukocytes and has a shorter t½ as well as increased specificity over I-111. For most agents, renal dysfunction is a contraindication for use. The most basic bone scan uses Tc-99, which incorporates as phosphate in areas of new bone formation. The t½ is 6h, and requires adequate blood supply. Post-injection, uptake will be greatest in the bladder, SI joint, ASIS, kidneys, nasopharynx, lacrimal glands, and epiphyseal plates. Scanning for Tc-99 occurs in 4 phases. First is the dynamic/blood flow phase which is taken immediately after injection. Little is seen in this phase normally. The second phase, blood pool, occurs 1-6 minutes post-injection, and shows vascularity to a particular region. The third phase, bone imaging, is taken 2-4h post injection and shows bony turnover (usually the most important.) The last phase, delayed, is taken 24h post injection, and measures clearance of the Tc-99 agent from the tissue. For osteomyeltits, Tc-99 can pick up changes w/in 24h (compared to 10d for X-ray.) Gallium 67-citrate is a different agent which is not sensitive to osteoblastic activity, and has a long (72h) t½. It is used to image ST inflammation through binding to iron binding proteins in WBCs. Normal uptake is seen in the liver, spleen, stomach, lacrimal glands, intestine, salivary glands,

and breast. Ga-67 is taken up in tumors and abscesses w/in 2h, but is ideally scanned at 36-72h. It is less dependent on vascular supply than Tc-99, but is only sensitive to infection. Post-surgical sites can stay hot to Ga-67 for up to 2wks. Chronic osteomyelitis is negative in Ga-67, + in acute. Tc-99 remains positive in both. Indium is an agent that is tagged to leukocytes in the patient’s blood and reintroduced via I.V. It is more specific than Ga-67 but more dependent on leukocyte chemotaxis. T½ is 28d. I-111 is used to evaluate osteomyelitis (acute), DM neuropathy, joint infections, bone marrow, and ST infection. It may show false positives in inflammatory arthritis. COMPUTERIZED TOMOGRAPHY (CT) CT is an imaging modality that uses highly focused X-rays to create detailed images with subtle changes in tissue density and accurate descriptions of lesion location and size. Computerization also allows 3D reconstruction. The primary disadvantages of CT are cost and increased radiation exposure. It is indicated for trauma, coaltions, ST masses, and infection. The X-ray tube rotates around the patient in a CT scan, while opposite the tube are detectors that are used to create an image. The image produced is divided into a grid, of which each 2D segment is a pixel, which when coupled with the 3D depth is called a voxel. The depth of the voxel is determined by slice thickness. Each voxel is then assigned a number based on the amount of radiation that passed through that segment. If the density of tissue is greater than water, the number is positive, whereas if the tissue is less dense than water it gets a negative number. (Bone is 1000-3000, air is 1000.) In an image, the lowest density is represented by black, while the highest is white, and everything inbetween is a gray scale, as in X-ray. However, in CT particular densities can be windowed, that is, anything below the density window is black and anything above is white. This means that great levels of contrast can be achieved if only the desired pathological tissue is windowed (others are ignored.) Larger windows, then, have lower contrast values. When ordering CT scans, the specific area of interest should be stated (possibly w/ bone scan), along w/ plain films. Any lesions should have a measurement request, and reconstructions and magnification are avalible if appropriate. CT scans include a scout film, which shows the location of specific slices as well as slice thickness. The scout film looks similar to a plain film x-ray. Image reconstruction in CT is used to view sagittal plane slices, which are out of phase with the CT scanner and thus must be calculated by the computer. These reconstructed images are also called secondary slices. Finally, there is a specialized CT you can order called a scanogram, which is an image of the entire lower extremity from the pelvis, used to measure LLD. A scanogram is basically a scout film with measurements to determine absolute length of bony segments. Overall, CT terminology and analysis is very similar to plain films. It is most effective at analyzing osseous pathology, and is often used in conjunction with bone scans. It is less expensive than MRI but inferior to MRI for analysis of soft tissues.

MAGNETIC RESONANCE IMAGING (MRI) MRI is an imaging modality that allows for the visualization of hydrogen protons in the human body. Hydrogen protons are present in nearly all materials and are electrically charged, within a magnetic field, and spins on its own axis. This makes it ideal for differentiating between different tissue types and analysis of hydrogen proton concentration gives clues to the chemical makeup of the tissues analyzed. The most important component of an MRI scanner is the magnet, which can be permanent (exerting 0.4T) or superconducting (1.5-2.5T) and initiates the process by which the hydrogen protons may be visualized. In the first step of the process, magnetic field, the magnet is activated around the patients body in the area to be visualized. The second step, radiofrequency pulse, is a pulsing of electromagnetic energy in accordance with the precession (spin) of the hydrogen atoms, which is a frequency called the larmor frequency. This pulsing at the larmor frequency causes all the hydrogen protons to spin in the direction of the magnetic field. Then, in the last step, relaxation, the magnetic field is turned off, and the hydrogen atoms slowly return to their normal spin axes. The time which it takes for this to happen is termed relaxation also, and each tissue type has different relaxation rates. Measurement of spin relaxation is the basic principle behind how the MRI produces an image, and the intensity with which tissues show up on the image relate to time values associated with relaxation. One of these values is T1, which is the time it takes for a particular tissue to regain 63% of its longitudinal spin. Another value, T2, is the time it takes for a proton to lose 63% of its transverse spin. (Note: T2 is always a longer value than T2.) Other values include TR (time to repeat – the duration of one imaging cycle), and TE (time to echo – time in which magnetization is converted to RF signal.) Weighted images are those that emphasize a particular time value, to focus on a particular tissue type. A type of image called proton density is a balance of a long TR and short TE interval, which does not emphasize any particular time value. A STIR image is a special form of inversion recovery in which the T1 time is very short – this is also called “fat suppression” because fat tends to show up black. In addition to weighting images, contrast can be added (gadolinium, gadolinium DTPA) to visualize vascular lesions. NORMAL ANATOMY ON MRI Bone Marrow is mostly composed of fat, which has a short relaxation time and thus shows up at high intensity for T1

images or low intensity on T2 images. It should be homogenous in appearance. Cortical Bone lacks free hydrogen, so it appears to have low signal intensity on all images. Tendons and Ligaments have low hydrogen content also, (though higher than bone) and has low intensity in all images. Tendons are contrasted best in T1 weighted images, however. Subcutaneous Fat and all other fatty areas have a high T1 signal intensity and low T2 signal intensity. Vascular Supply to an area shows up with low intensity in MRI due to movement, called a flow void. This is why contrast media are required to visualize blood vessels on MRI. Muscle is intermediate in hydrogen density, and thus shows up intermediate intensity in all images. SAFETY CONSIDERATIONS MRI cannot be used with electrically or magnetically activated implants like pacemakers, defibrillators, or cochlear implants. Metallic objects located within the body will not cause harm, but cause artifact on the MRI readout which may render it useless. If it is suspected that a patient may have a metallic foreign body in the vicinity of the eyes, an orbital X-ray is indicated. Lastly, it has not yet been proven that MRI is safe to use on gravid females; for women in their first trimester, it is advised that a risk/benefit analysis be done before making the decision to go ahead with MRI. PATHOLOGY ON MRI Osseous trauma, including stress fractures, will typically show up as a decrease in signal intensity on T1WI in the area of trauma, with diffuse increase in intensity on T2WI due to localized inflammation to the area. STIR images can be utilized to see marrow edema. Avascular necrosis will show a well-defined line of demarcation between viable bone and devascularized bone on T1WI. Osteochondritis dessicans will show up as a decreased area of signal intensity on a T1WI in the acute stage, but as the condition becomes chronic intensity increases. ST infection is best visualized as increased intensity on T2 or STIR images due to inflammation in the area. The degree of contrast seen can differentiate abscess from cellulitis. Osteomyelitis shows high intensity on T2WI for cortical bone as well as low signal intensity on T1WI for medullary bone. Charcot neuroarthropathy shows up as a decrease in signal intensity on T1 and T2WI for affected joints. Bone tumors typically have a low to intermediate signal on T1WI and higher intensity on T2WI, although they may be high on T1WI if fat or blood-filled. Calcification within a tumor will also show up as lower intensity on all images. Soft tissue tumors also show up with low T1WI signal intensity and high T2WI signal intensity, however, the composition of the tumor will affect this. Benign lesions tend to be well demarcated, homogenous, and have a less pronounced change in signal intensity. Ganglion cysts are easy to pick out on MRI because of their very low T1WI intensity and very high T2WI intensity. Enchondroma shows up as homogenous and loculated with a high T2WI and STIR intensity due to cartilage. Calcifications may show up as a heterogenous intensity.

Lipomas tend to be superficial homogenous lesions with the same signal intensity as surrounding fat, unless calcifications are present.

MISCELLANEOUS IMAGING MODALITIES Xeroradiography is a dry process that uses electrostatic forces to produce an image. Positive xeroradiographs are used to visualize bone and non-metallic foreign-bodies. Negative xeroradiographs visualize soft tissue and metallic foreign bodies. Digital Radiography is an X-ray method by which plain films are replaced with phosphor plates that transfer the image to a digital signal. This process may produce very detailed images and can zoom in or out to the tastes of the interpreter. Liquid Crystal Thermography produces an image dependent on skin surface temperature. This is useful in diabetic neuropathy to predict the location of future ulcers, as well as vascular and dermatologic pathologies. Digital thermography is a similar process that involves recording an image with a thermal camera. Ultrasonography produces an image converted from highenergy sound waves. Contrast is produced by variations in the way that different tissues reflect sound. It is most useful for distinguishing solid from fluid-filled masses, and in most pathologies tissue alteration is significant enough for ultrasound to detect. Sinography is an X-ray taken after injecting a sinus with radioopaque fluid. It is used to determine the size and extent of a sinus tract and the location of potential abscesses. Sinography cannot be used if the patient is allergic to iodine. Local tissue necrosis and infection are other side effects. Arthrography is radiographic imaging of a joint space using injected contrast media. A single contrast arthrogram uses a single contrast agent, and is used to determine the extent of acute injury or ligamentous damage. Double-contrast arthrograms utilize both positive and negative (air) contrast media, and is used for chronic processes (such as OCD.) Arthrograms may not be taken if the patient has cellulitis in the area, and joint sepsis is a potential side effect. A normal arthrogram of the ankle should show smooth synovial lining with redundant ankle capsule, medial and lateral recesses, smooth and uniform articular cartilage, and a syndesmotic recess ~2.0cm to the interosseous membrane. In 15% of pts, there is a communication btw the ankle and posterior STJ facet. In 15-20% there is a communication btw the ankle and FHL/FDL sheaths. Pathology seen in an arthrogram is typically due to lateral ankle injury, and must be imaged w/in 48h of the incident. Contrast leakage is usually indicative of ligamentous injury. Injury of the ATF ligament shows extravasation anterior and lateral to the fibula. The CF ligament is close to the peroneal tendons and thus with CFL injury extravasation into these tendon sheaths is seen. Chronic injury to the CFL will have a persistent communication between these two structures. The PTF ligament is rarely injured and is always seen with either an ATFL or CFL rupture as well. Medial ankle injuries are extremely uncommon. Syndesmotic tears are associated with medial ankle ligament injury, and shows extravasation superior to the syndesmotic recess.

Other uses for arthrography besides ligament injury may be to visualize joint mice, synovial hypertrophy, joint infection (which shows uptake of contrast to lymphatics), and capsulitis. Tenography is the use of contrast media injected into a tendon sheath to visualize the course of the tendon it encloses. It is useful for visualizing post-traumatic tendon injury. Venography is the use of contrast media to visualize the course of a vein. It is the gold-standard for visualizing DVTs but cannot be used in pts w/ an iodine allergy. Side effects include allergic rxn, induced DVT, and localized skin necrosis. Arteriography is the use of contrast media to evaluate vascular supply. Its use is contraindicated in trauma, athrosclerosis, AV malformations, emboli, or tumors. Angiography is visualization of the arterial supply using computerized digial subtraction to remove non-vascular structures from the picture. It is indicated in evaluation of atherosclerosis and AV malformation.

CLINICAL ANTIBIOSIS Infection: Pathologic presence of bacteria in a wound or tissue site, numbering 106. It is clinically signified by inflammation, erythema, pain, warmth, and loss of function. History: Local signs of infection are edema, erythema, pain, warmth, and loss of function. Systemic signs of infection include fever, chills, shaking, nausea, vomiting, loss of appetite, and shortness of breath. Get history of prior tx, PMH, allergies, social Hx, travel Hx, and any pets the patient may have. Staph Epi is most common in IV/catheter or implant infections. Staph aureus is the most common post-op infection and cause of osteomyelitis. D/Dx: Gout, DVT (r/o w/ venous Doppler/venogram), chronic venous insufficiency (bilateral pitting edema, hemosiderin deposition), acute charcot, acute trauma, fungal infection, normal wound healing, post-surgical healing. Labs: WBC>10, left shift, elevated ESR, CRP. Hospital Admission: Indicated for osteomyelitis, large draining wound, sustained fever (over 101F/38C), diabetes, immunocompromised state, gas present in tissues, failure of PO antibiosis, lab results suggestive of sepsis.

PENICILLINS Original Penicillins Not used often – usually for gonococcus, anaerobes PEN G: IV or IM – 5-6 million U q4h PEN VK: PO – 250-500mg QID, causes hypokalemia Aminopenicillins Good broad spectrum, but useless against staph. AMPICILLIN: IM, IV, PO – 250-500mg QID or 2g q4h AMOXICILLIN: PO only – 250-500mg QID Semisynthetic PCNnase resistant, good vs. staph, used in specific situations NAFCILLIN: IM or IV – 1-2g q4-6h, metabolized in liver DICLOXACILLIN: PO – 250-500mg QID Uriedopenicillins (Expanded Spectrum) Active against pseudomonas, resistance is common CARBENICILLIN: Limited use in lower extremity TICARCILLIN: IV – 3-4g q4h, high in sodium PIPERICILLIN: Limited use in lower extremity

IV: CEFOXITIN (MEROXIN), CEFUROXIME (ZINACEF), CEFOTETAN (CEFOTAN) PO: CEFACLOR (CECLOR) 250-500mg TID, CEFUROXIME (CEFTIN), CEFPROZIL (CEFZIL) Third-Generation Cephalosporins More gram -, less gram +, fortaz also anti pseudomonal IV: CEFTRIAXONE (ROCEPHIN) 1-2g QD (long half-life) Rocephin principal antibiotic in Lyme disease treatment CEFTAZIDIME (FORTAZ): some antipseudomonal coverage PO: CEFDINIR (OMNICEF) 300mg BID, better staph coverage CEFPODOXIME (VANTIN), CEFIXIME (SUPRAX) Fourth-Generation Cephalosporins Good gram + and gram -, antipseudomonal CEFEPIME (MAXIPIME) IV, 1-2g q12h

CARBAPENEMS PRIMAXIN (IMIPENEM + CILASTATIN): PO 500mg q6h Gram +, gram -, anaerobes – cilastatin added to protect kidneys. Expensive, save for life-threatening infections MEROPENEM (MERREM) some antipseudomonal coverage ERTAPENEM (INVANZ): IV, IM, 1g q24h Good against enterobacteria, but not pseudomonas AZTREONAM (AZACTAM): IV, 1-2g q8h Only good against gram – anaerobes; use in combination

AMINOGLYCOSIDES Staph, strep, gram -, but not anaerobes ADRs: reversible nephrotoxicity, irreversible ototoxicity, Neuromuscular blockade if infused too quickly GENTAMYCIN, TOBRAMYCIN, AMIKACIN Loading doses: Gentamycin/Tobramycin 2mg/kg Amikacin 7.5mg/kg Maintenance: Gent/Tobra 3-5mg/kg/day (1-3 for children) Amikacin 15mg/kg/day Peak/Trough: Gent&Tobra 10 peak, 2 trough µg/ml, Amikacin 20-30 peak, 10 trough µg/ml Trough level: Gent/Tobra 2µg/ml, Amikacin 10µg/ml (Peak = immediately after dosing, Trough = 20-30 minutes before dosing)

FLOUROQUINOLONES Beta-Lactamase Inhibitors First choice antibiotics w/ cephalosporins Staph, Strep, Anaerobes, Gram - coverage TIMENTIN (TICARCILLIN + 100MG CLAVULANATE) IV – 3.1g q6-8h Empiric for DM foot infections, bites AUGMENTIN (AMOXICILLIN + 125MG CLAVULANATE) PO – 250/500/875 BID Good for outpatient DM, bites UNASYN (1 PART AMPICILLIN + ½ PART SULBACTAM) IV – 3g loading dose, 1.5g following doses Better at gram + but worse for gram – than timentin ZOSYN (PIPERICILLIN + TAZOBACTAM) IV – 4.5g q8h Better against enterococci

CIPROFLOXACIN (CIPRO): PO 500/750mg, IV 400mg BID Good gram – coverage, antipseudomonal Not for peds, Sx prophylaxis, or weak/tenotomized tendons LEVOFLOXACIN (LEVAQUIN): PO or IV 500/750mg BID Good for staph and strep, not as strong antipseudomonal MOXIFLOXACIN (AVELOX): PO or IV 400mg QD Good staph, strep, and antipseudomonal GATIFLOXACIN (TEQUIN): Not for foot infections, lengthens QT TROVAFLOXACIN (TROVAN): Taken off market for hepatic failure

SULFONAMIDES BACTRIM/SEPTRA (TRIMETHOPRIM + SULFAMETHOXAZOLE): PO only - QD dosing, double-strength (DS) 160mg TMX, 800mg sulfamethoxazole Broadest possible spectrum, not antipseudomonal Allergies common

CEPHALOSPORINS First Generation Cephalosporins Good for gram +, most common pre-op prophylaxis CEFAZOLIN (ANCEF): IV or IM, 1g q8h CEFALEXIN (KEFLEX): PO, 250-500mg BID/QID CEFADROXIL (DURICEF): PO, 500mg q12h Second-Generation Cephalosporins Used mainly for ear infections, pneumonia – not podiatry

MACROLIDES ERYTHROMYCIN: PO 250-500mg QD, IV 1g QD Good against staph, gram + and gram – anaerobes AZITHROMYCIN (ZITHROMAX): PO 500mg QD day 1, 250mg QD days 2-4. Postbiotic effect for 10 days following dosing. Gram +, some Gram – organisms, usually for pts who are allergic to other antibiotics, or peds (Paronychia) CLARITHROMYCIN (BIAXIN): Not often used for foot infections

TETRACYCLINES TETRACYCLINE, DOXYCYLINE, MINOCYCLINE Limited use in podiatry – mainly used for acne, Lyme disease

CHLORAMPHENICOL Mainly a historical footnote; rarely used anymore ANTI-ANAEROBIC MISCELLANY METRONIDAZOLE (FLAGYL): PO or IV, 500mg TID Mainly gram – but some gram +, amebiasis, colorectal Sx Used also to treat pseudomembranous colitis (see below) CLINDAMYCIN (CLEOCIN): PO 150-300mg BID, IV or IM 600-900mg q8h. Good bone penetrance, good for anaerobes Can cause pseudomembranous colitis ANTI-GRAM + MISCELLANY VANCOMYCIN (VANCOCIN): PO 125mg QD (only for c. difficile), IV 1g q12h – infuse slowly Good for all gram + except VRSA and VRE. Peak – 20-500µg/ml, Trough - 10µg/ml, like aminoglycosides (Trough is more important to determine efficacy of treatment) ADRs: nephrotoxicity, ototoxicity, red man syndrome (rash) Can be used for prophylaxis if PCN, clindamycin allergic SYNERCID (QUINUPRISTIN + DALFOPRISTIN): IV 7.5mg/kg q12h Used for VRE LINEZOLID (ZYVOX): PO, IV 600mg BID Used for MRSA, all gram +. Can cause thrombocytopenia RIFAMPIN: PO 300mg BID Good for resistant staph and strep Causes rash, orange discoloration of all body fluids. ADVERSE REACTIONS -Pseudomembranous Colitis – Clindamycin, cephalosporins, uriedopenicillins: Tx w/ metronidazole, oral vancomycin -Tendon rupture, cartilage degeneration – Ciprofloxacin -Ototoxicity (irreversible), nephrotoxicity (reversible), neuromuscular blockade – Gentamycin, Tobramycin, Amikacin -Ototoxicity, nephrotoxicity, red man synd. – Vancomycin -Hypokalemia – Pen G, Pen VK: Tx w/ K-exelate -Thrombocytopenia, bone marrow suppression – Linezolid -Rash, orange discoloration of body fluid – Rifampin -QT interval lengthening – Tequin ANTI-PSEUDOMONAL DRUGS Penicillins: Ticarcillin (weak), Timentin (weak) Cephalosporins: Fortaz (weak), Maxipime (strong) Carbapenems: Meropenem (weak) Quinolones: Cipro (strong), Levaquin (weak), Avelox (strong) Aminoglycosides: Tobramycin (strong) EMPIRIC TREATMENT OPTIONS Cellulitis: Unasyn, Zosyn, Timentin, Maxipime, Invanz, Avelox, Cipro, Levaquin, Bactrim. Open fractures: Gustillo & Anderson Type I or II – Ancef Gustillo & Anderson type III (any) – add Gentamycin If farm injury/wound contaminated with dirt, add Pen G SURGICAL PROPHYLAXIS Indications: Prolonged surgery, immunocompromise, trauma, implant surgery. Most Common: Ancef, Rocephin, Vancomycin, Clindamycin Never Used: Quinolones Administration: IV, ½h prior to surgery (usually done in OR) ANTIBIOTIC TIMELINE Soft tissue infection only: 10 days – 2 weeks Osteomyelitis: 4-6 weeks

LOWER EXTREMITY MICOBIOLOGY REVIEW GRAM + COCCI Staph Aureus – Coagulase + Incidence: Normal flora, common infection, high resistance ABx: 1st Cephalosporins, PCNase resistant PCN, Cleocin, Bactrim, Erythromycin, Vanco (resistant), Cipro (resistant) Staph Epidermidis/Saprophyticus – Coagulase – Incidence: Normal flora – Epi seen in implant sx, sap in UTI ABx: Same as S. Aureus Strep Pyogenes – Group A, Strep Agalactiae – Group B Incidence: Pyogenes usually superficial, Agalactiae seen in DM ABx: PCNs, 1st gen Cephalosporins, Cleocin, Vanco Strep Faecalis/Faecium – Group D/Enterococci Incidence: GI flora, highly resistant, ST infection component ABx: Gentamycin + PCN/Ampicillin/Amoxicillin or Vanco Peptostreptococcus/Peptococcus – Anaerobic Incidence: DM foot infections ABx: PCN, 1st gen Cephalosporins, Cleocin, Erythromycin GRAM + BACILLI Clostridium Tetani – Anaerobic, Spore-forming Incidence: Ubiquitous in environment, puncture wounds ABx: PCNs (mainly useless b/c of neurotoxin production) Clostridium Perfringens – Anaerobic Incidence: Fast growing, gas gangrene (necrotizing fasciitis) ABx: Sx debridement indicated – PCN, Clinda, Imipenem Corynebacterium – diptheroid Incidence: Nosocomial, Immunocompromised infections ABx: Clinda, Erythromycin, Vanco GRAM – COCCI Neisseria Gonorrhoeae Incidence: Major cause of septic arthritis is LE, resistant ABx: Rocephin, Cipro (resistant) GRAM – RODS (ENTERIC) Bacteroides Incidence: Most common in DM infection, resistant ABx: Flagyl, primaxin, clinda, 3rd or 4th gen cephalosporins Enterobacter/Citrobacter/Morganella/Serratia Incidence: Nosocomial infections, elderly ABx: 3rd gen cephalosporins, cipro, bactrim, aminoglycosides Escherichia Coli Incidence: Common in LE infections ABx: Any cephalosporin, ampicillin, cipro, bactrim Proteus/Providencia Incidence: Normal flora, common in interdigital infections ABx: Cephalosporins, Ampicillin, Cipro, Bactrim OTHER GRAM – RODS Aeromonas Hydrophilia Incidence: Injuries sustained under water (fresh water) ABx: Cipro, Bactrim, Primaxin, Aminoglycosides Haemophilus Influenzae Incidence: Most common in children, nosocomial infections ABx: 3rd/4th gen cephalosporins, bactrim, ampicillin Pseudomonas Aeruginosa Incidence: Ubiquitous; puncture wounds, underwater injuries most common. ABx: See left Eikenella Corrodens Incidence: Found in human bite wounds ABx: PCN, Ampicillin, Macrolides, Imipenems Pasturella Multicida Incidence: Cat and other animal bite wounds ABx: PCN, Ampicillin, β-lactamase inhibitors, bactrim.

LABS CHEMISTRY PANEL/BASIC METABOLIC PROFILE Na+

Cl-

BUN Glu

K

+

HCO3

-

Creat

GLUCOSE (Glu) Normal Range = 60-110 mg/dL Glucose is closely regulated so as to provide energy to all cells in the body without allowing any spillover into the urine. The excess of glucose seen in DM is the underlying cause for all complications of that disease. Increased in: DM, cushing’s syndrome, chronic pancreatitis, corticosteroids, phenytoin, estrogens, thiazides. Decreased in: Insulinoma, adrenocortical insufficiency, hypopituitarism, liver disease, malignancy, insulin, ethanol, propanolol, solfonylureas, tolbutamide.

BMP SODIUM (Na+) Normal Range = 135-145 mEq/L Sodium is the predominant extracellular cation. Levels of sodium generally reflect the hydration state of the patient. Increased in: Dehydration, polyuria, hyperaldosteronism, steroids, oral contraceptives, inadequate water intake. Decreased in: CHF, vomiting, diarrhea, sweating, nephropathy, adrenal insufficiency, thiazides, diuretics, ACE inhibitors, antidepressants, antipsychotics.

CALCIUM (Ca2+) Normal Range = 8.5-10.5 mg/dL Calcium is important in bone mineralization as well as a clotting cofactor. It is regulated by calcitonin and parathyroid hormone, and binds to albumin in serum. Increased in: Hyperparathyroidism, vitamin D excess, multiple myeloma, paget’s disease, sarcoidosis, vitamin A intoxification, addison’s disease, antacids, thiazides, lithium Decreased in: Hypoparathyroidism, vitamin D deficiency, renal insufficiency, magnesium/phosphorus deficiency, massive transfusion, hypoalbuminemia.

POTASSIUM (K+) Normal Range = 3.5-5.0 mEq/L Potassium is the primary intracellular cation and is the electrical balance to sodium. Potassium imbalance causes disruption in the function of neurons and muscles, and the symptoms of DKA are a result of the hypokalemia it produces. Potassium movement also accompanies glucose, and in the kidneys potassium is excreted at the expense of sodium. Potassium levels in the blood are affected chiefly by pH; acidosis is accompanied by hyperkalemia, and alkalosis causes hypokalemia. The action of catecholamines on beta receptors has a secondary effect of reducing blood potassium. Increased in: Hemolysis, tissue damage, acidosis, renal failure, addison’s disease, exercise, potassium-sparing diuretics, NSAIDs, β-blockers, ACE inhibitors, and TMX. Decreased in: Prolonged vomiting/diarrhea, hyperaldosteronism, cushing’s syndrome, osmotic diuresis, trauma, subarachnoid hemorrhage, adrenergic drugs, diuretics.

ANION GAP Normal Range = (Na+K) - (Cl+HCO3)<16, or Na - (Cl+HCO3)<12 Anion gap is an equation used to measure metabolic acidosis. Anions and cations in the body sum to zero; anion gap is a measure of the sum of all minor anions in the body. Increased anion gap indicates acidosis, whose etiology is characterized by the acronym SLUMPED; Salicylates, Lactic acid, Uremia, Methanol, Paraldehyde, Ethanol, and Diabetic ketoacidosis.

CHLORIDE (Cl-) Normal Range = 98-107 mEq/L Chloride is a secondary player in the maintenance of acid/base balance and is a placeholder in the anion gap. Retention causes acidosis, loss alkalosis. Increased in: Massive diarrhea, nephrotic syndrome, renal failure, diabetes insipidus, hyperparathyroidism, acetazolamide, androgens, salicylates. Decreased in: Vomiting, diarrhea, GI suction, DKA, respiratory acidosis, excessive sweating, acute intermittent porphyria, adrenal insufficiency, laxative use, corticosteroids, diuretics. BICARBONATE (HCO3-) Normal Range = 22-28 mEq/L Bicarbonate is the main component of the body’s buffer system and is the central player in regulation of blood pH. Bicarbonate levels are regulated by the kidneys. Increased in: metabolic alkalosis, compensated respiratory acidosis, volume contraction, mineralocorticoid excess, diuretics. Decreased in: Metabolic acidosis, compensated respiratory alkalosis, fanconi’s synd, volume overload, acetazolamide. BLOOD UREA NITROGEN (BUN) Normal Range = 8-20 mg/dL BUN is the end product of protein metabolism, and is directly related to the amount of protein ingested. It is a relative indicator of kidney function. Increased in: Renal failure, urinary tract obstruction, degydration, shock, burns, CHF, GI bleed, nephrotoxic drugs. Decreased in: Hepatic failure, nephritic syndrome, cachexia. CREATININE (Creat) Normal Range = 0.6-1.2 mg/dL Creatinine is a normal product of the breakdown of muscle tissue, and is produced at a constant rate. As such, it is an absolute indicator of kidney function, and the ratio of BUN to Creat in the blood can give clues to the etiology of a kidney problem. Increase in BUN and Creat is termed azotemia. 10:1 ratio is pre-renal azotemia, caused by insufficient renal blood flow. A less than 10:1 ratio is renal azotemia, which is indicative of renal failure. Increased in: Renal failure, urinary tract obstruction, nephrotoxic drugs, hypothyroidism. Decreased in: Reduced muscle mass.

PHOSPHORUS (P+) Normal Range = 2.5-4.5 mg/dL Phosphorus is the other mineral component to bone, and its levels in the blood are regulated chiefly by the parathyroid gland and vitamin D. Increased in: Renal failure, massive blood transfusion, hypoparathyroidism, sarcoidosis, neoplasms, adrenal insufficiency, acromegaly, hypervitaminosis D, leukemia, DKA, cirrhosis, respiratory acidosis, anabolic steroids, furosemide, clonidine, verapamil, HCTZ. Decreased in: Hyperparathyroidism, hypovitaminosis D, steatorrhea, malnutrition, bone marrow transplantation, alcoholism, diarrhea, vomiting, gout, osteoblastic disorders, respiratory alkalosis, pregnancy, hypothyroidism, dialysis, anticonvulsants, β-agonists, catecholamines, estrogens, insulin, ASA. ALBUMIN Normal Range = 3.4-4.7 g/dL Albumin is the principal carrier protein in the blood and is a measure of nutrition. Many hormones depend on albumin for transport in the blood. Increased in: Dehydration, shock. Decreased in: Liver disease, malnutrition, malabsorbtion, malignancy, nephrotic syndrome, hemorrhage, fistulas, estrogens. BILIRUBIN (Bili) Normal Range = 0.1-0.4 (direct), 0.2-0.7 (indirect) mg/dL Bilirubin is the product of heme metabolism, and is conjugated (direct bili) in the liver for biliary excretion. Direct vs. indirect values predict etiology. Increased in: Hemolysis (indirect), liver failure (indirect), hemorrhage (indirect), biliary obstruction (direct), cirrhosis/hepatitis (both), CHF (both) ALKALINE PHOSPHATASE (Alk Phos) Normal Range = 41-133 IU/L Alk phos is produced by osteoblasts and is an indication of skeletal turnover. Increased in: Biliary obstruction, paget’s disease, bone tumor, hyperparathyroidism, rickets, pregnancy, GI disease, hepatotoxic drugs. TOTAL PROTEIN Normal Range = 6.0-8.0 g/dL A group that includes albumin, total protein is an indicator of nutrition and is the principal determinant in blood oncotic pressure. Increased in: Gammopathies, dehydration, anabolic steroids, corticosteroids, epinephrine, androgens. Decreased in: Burns, nephrotic syndrome, malnutrition, chronic liver disease. ALANINE AMINOTRANSFERASE (ALT, SGPT) Normal Range = 0-40 U/L ASPARTATE AMINOTRANSFERASE (AST, SGOT) Normal Range = 0-35 U/L These liver function enzymes are an indicator of liver damage or pathology. Increased in: Hepatitis, cirrhosis, liver abscess, biliary obstruction, right-sided heart failure, ischemia/hypoxia, abdominal trauma, hepatotoxic drugs. Decreased in: Vitamin B6 deficiency

COMPLETE BLOOD COUNT

Hb

WHITE BLOOD CELLS (WBC) WBC Plt Normal Range = 5,000-10,000/µL Increases in the white count are normally attributed to infection, however many factors may affect it. Hct Increased in: Infection, inflammation, leukemia, lymphoma, corticosteroids. Decreased in: Aplastic anemia, B12/folate deficiency, sepsis, phenothiazines, chloramphenicol, aminopyrine. NEUTROPHILS (Segs) Normal Percentage = 40-60% Increased in: Infection, stress, inflammation, leukemia, DKA. Decreased in: Same as WBC count. MYELOCYTES (Bands) Normal Percentage = 0-5% Increased in: Acute infection, toxemia, hemorrhage, pernicious anemia. >20% is called “left shift” and usually signals acute infection, even if the WBC count is normal. LYMPHOCYTES (Lymph) Normal Percentage = 20-40% Increased in: Viral infection, thyrotoxicosis, adrenal insufficiency, ALL, CLL, chronic infection, allergic rxn, autoimmune dz, epinephrine. Decreased in: HIV, SLE. MONOCYTES (Mono) Normal Percentage = 4-8% Increased in: Chronic bacterial infection, inflammation, malignancy, TB, multiple myeloma. EOSINOPHILS (Eos) Normal Percentage = 1-3% Increased in: Allergic rxn, drug sensitivity, skin disorders, parasite infection, hodgkin’s dz, pulmonary infiltrative dz, menstruation. Decreased in: Inflammation, stress, corticosteroids. BASOPHILS (Baso) Normal Percentage = 0-1% Increased in: Allergic rxn, multiple myeloma, colitis, myxedema. HEMOGLOBIN (Hb) Normal Range = 14-18 (♂), 12-16 (♀) g/dl (Hb = 1/3 Hct) Central component to O2 transport in blood, required for adequate healing. Increased in: Dehydration, polycythemia, exercise conditioning, high altitude. Decreased in: Macrocytic anemia, Normocytic anemia, Microcytic anemia. HEMATOCRIT (Hct) Normal Percentage = 40-50% (♂), 35-45% (♀) (Hct = RBC x MCV) Is a measure of the percentage of whole blood made up of erythrocytes. Increased in: Dehydration, polycythemia, exercise conditioning, high altitude. Decreased in: Macrocytic, normocytic, microcytic anemias. PLATELETS (Plt) Normal Range = 150,000-450,000/µL Platelets are required for the cellular component of blood clotting. Increased in: Myeloproliferative disorders, bleeding, splenectomy, iron deficiency, malignancy, alkalosis. Decreased in: Bone marrow suppression, ethanol, splenomegaly, DIC, purpura, quinidine, cephalosporins, clopidogrel, heparin. RED BLOOD CELLS (RBC) Normal Range = 4.8-6.0 (♂), 4.1-5.5 (♀) x106/µL Increased in: Polycythemia. Decreased in: Anemia. MEAN CORPUSCULAR VOLUME (MCV) Normal Range = 80-100 fL Increased in: Liver dz, alcoholism, hemochromatosis, megaloblastic anemia, reticulocytosis, methotrexate, phenytoin, zidovudine. Decreased in: Iron deficiency, thalassemias, chronic dz anemia.

PROTHROMBIN TIME (PT) Normal Range = 11-15 sec PT is the monitor for the extrinsic clotting cascade. Increased in: Coumadin, liver dz, vit K deficiency, DIC, massive transfusion. PARTIAL THROMBOPLASTIN TIME (PTT) Normal Range = 25-35 sec PTT is the monitor for the intrinsic clotting cascade. Increased in: Heparin, coumadin, clotting factor deficiency (except XIII & VII), von willebrand dz, DIC, hemophilia. LACTATE DEHYDROGENASE (LDH)/CREATINE PHOSPHOKINASE (CPK) Normal Range = 88-230 U/L Normal Range = 32-267 U/L LDH is an important enzyme used in carbohydrate metabolism. It is used to detect MI – it rises 3-6h post MI and remains high for approximately 1 week. CPK is a muscle enzyme and is released in muscle turnover or muscle damage. It is also used as a marker to detect MI – levels rise immediately after MI and remain high for 2-3 days. URIC ACID Normal Range = 2.4-7.4 (♂), 1.4-5.8 (♀) mg/dL Uric acid is the end product of purine metabolism. Excess results in gout. Increased in: Gout, renal failure, leukemia, multiple myeloma, lesch-nyhan synd, lead poisoning, pregnancy, menopause, diuretics, ethanol, salicylates. Decreased in: Xanthine oxidase deficiency, fanconi synd, neoplasms, liver disease, high-dose salicylates, allopurinol.

Urinalysis SPECIFIC GRAVITY Normal Range = 1.001-1.035 Increased in: DM, dehydration, sweating, vomiting, diarrhea Decreased in: ↑ fluids, ↓ Na diet, nephritis, diabetes insipidus, aldosteronism PH Normal Range = 5-9 Acidic: Acetones, DM, gout, nephritis, leukemia, scurvy, saccharin, aspirin Alkaline: Blood transfusion, vomiting

GLUCOSE Normal Range = <300 mg/day Increased in: DM, Aspirin, hyperpituitarism, hyperthyroidism, chronic liver failure, pregnancy KETONES Normal Range = 10-20 (♂), 5-15 (♀) mg/day Increased in: DKA, PKA, starvation PROTEIN Normal Range = 10-200 mg/day Increased in: Multiple myeloma (bence-jones protein), UTI, hemorrhage, prostatic secretions, DM, lupus, nephrotic syndrome. -BILIRUBIN Presence indicates hepatitis (unconjugated) or biliary tract obstruction (conj.) -UROBILINOGEN Presence indicates intravascular hemolysis -BLOOD (Hematuria), NITRATES, LEUKOCYTE ESTERASE Suggestive of UTI -CASTS Hyaline casts may be normal. RBC/WBC casts suggest pyelonephritis.

Other Tests

MEAN CORPUSCULAR HEMOGLOBIN (MCH) Normal Range = 26-34 pg Increased in: Macrocytosis, hemochromatosis. Decreased in: Iron deficiency, thalassemia, lead poisoning, chronic dz anemia

HEMOGLOBIN A1C (HbA1c) Normal Range = 4-7% of total hemoglobin Increased in DM. The equation (33.3 x HbA1c – 27) estimates daily FBS over the last month.

MEAN CORPUSCULAR HEMOGLOBIN CONCENTRATION (MCHC) Normal Range = 31-36 g/dL (MCHC = Hb/(MCV x RBC)) Increased in: Spherocytosis, hemolysis, lipemia, cellular dehydration. Decreased in: Hypochromic anemias, sideroblastic anemia, chronic dz anemia

HUMAN CHORIONIC GONADOTROPIN (HCG/β-HCG) Presence indicates pregnancy or trophoblastic tumor. (Female only)

ERYTHROCYTE SEDIMENTATION RATE (ESR) Normal Range = <10 (♂), <15 (♀) mm/h Increased in: Infection (esp. osteomyelitis), inflammatory dz, malignancy, anemia, pregnancy, chronic renal failure, GI dz, endocarditis. Decreased in: Polycythemia, sickle-cell anemia, spherocytosis, CHF, hypogammaglobulinemia, high-dose corticosteroids.

RAPID PLASMA REAGIN (RPR) Presence usually indicates syphilis, but sometimes seen in leprosy, malaria, IV drug use, the elderly, mono, HIV, autoimmune disease, and pregnancy. SICKLE DEX Positive result indicates sickle cell anemia or trait; f/u w/ electrophoresis.

PAIN MANAGEMENT Pain Classification: Nociceptive – normal pain response seen in post-traumatic or post-surgical patients. Neuropathic – pathologic pain resulting from nerve lesions, neuropathy, entrapment, CRPS, or phantom pain. Acute pain is managed with analgesics and NSAIDs. Chronic pain is managed with NSAIDs and steroid injections. Nerve Fiber Types: Aδ fibers – slow, unmyelinated fibers, respond to mechanical injury, intense burns/freezing. C fibers – slow, thinly myelinated, respond to chemical, thermal, deep mechanical, “itch” type injuries. Spinal Tracts: Spinothalamic tracts to substantia gelatinosa (releasing substance P, enkephalins, etc.), dorsal column/medial lemniscus pathway, anterolateral tracts (spinoreticular, spinotectal.) Clinical Pain Types: Throbbing, dull ache = musculoskeletal pain (esp. w/ activity.) Stabbing, soreness = fracture Burning, tingling, numbness (paresthesia) = neuropathic pain -Tinel’s sign: Pain radiates proximally w/ percussion -Valleix sign: Pain radiates prox & dist w/ percussion Itching, superficial burning = skin/epidermal pain Burning, cramping, tearing = ischemic pain/claudication

* - Indicates avalibility of pediatric dosing 1 – Indicates better soft tissue penetration NARCOTIC ANALGESICS MORPHINE2 – 1-3mg IM q10minutes (or w/ PCA) HYDROMORPHONE (Dilaudid) 2 – 0.1-0.5µg IM q10minutes MEPERIDINE (Demerol) 2 – 10-30mg IM q1-4h PENTAZOCINE (Talwin) 4 – 30mg IV/IM q4h OXYCODONE (Oxycontin) 2 – 5mg PO q6h, 10-40mg PO q12h OXYCODONE w/ Acetaminophen (Percoset)2 – 2.5/325, 5/325, 7.5/500, 10/500mg PO q4-6h OXYCODONE w/ Aspirin (Percodan) 2 – 2.5/325, 5/325mg PO CODEINE w/ Acetaminophen (Tylenol #1-5)3 – 7.5/300, 15/300, 30/300, 60/300, 120/300mg PO q4-6h HYDROCODONE w/ Acetaminophen (Vicodin, Lortab, Zydone) 3 – 5/500, 7.5/750, 10/660mg PO q4-6h HYDROCODONE w/ Ibuprofen (Vicoprofen) 3 – 7.5/200mg PO q4-6h PROPOXYPHENE w/ Acetaminophen (Darvocet)4 – 50/325, 100/500, 100/650mg PO q4-6h PENTAZOCINE w/ Acetaminophen (Talacen) 4 – 25/650mg PO q4h (mixed opioid agonist/antagonist)

NSAIDS Use carefully w/ bleeding disorders, asthma, pregnancy, peds Salicylates ASPIRIN (ASA, Bayer, Ecotrin) – 325-1000mg PO q6h *DIFLUNISAL (Dolobid) – 250, 500mg PO q12h

NON-NARCOTIC ANALGESICS ACETAMINOPHEN (Tylenol) – 325-1000mg PO q4-6h Analgesic and antipyretic only- watch for hepatotoxicity TRAMADOL (Ultram) – 50, 100mg PO q4-6h TRAMADOL w/ Acetaminophen (Ultracet) – 37.5/325mg PO q4-6h LIDOCAINE (Lidoderm) – 5% patch (transdermal), 1-3 q12h

Propionic Acids *IBUPROFEN (Motrin, Advil, Nuprin) – 200, 400mg PO bid/tid KETOPROFEN (Oruvail, Orudis) – 25, 50, 75mg PO bid/tid FLURBIPROFEN (Ansaid) – 50, 100mg PO bid/tid *NAPROXEN (Naprosyn, Aleve) 1 – 250, 375, 500mg PO bid Do not use w/ H2 blockers, Propanolol NAPROXEN SODIUM (Anaprox) – 275, 550mg PO bid Longer t½ than regular naproxen

INJECTABLE CORTICOSTEROIDS Contraindications: Infection, joint instability, AVN, osteonecrosis, neurotrophic pathology, fungal infection. Short-Acting (t½ = 8-12h) HYDROCORTISONE (Solu-Cortef) Potency: 1† Dose: 20mg HYDROCORTISONE VALERATE (West Cort) same as above CORTISONE (Cortone) Potency: 0.8 Dose: 25mg PREDNISONE (Delta-Cortef) Potency: 4 Dose: 5mg

Indoles *INDOMETHACIN (Indocin) – 25, 50mg PO bid/tid Often used for management of gout SULINDAC (Clinoril)1 – 150, 200mg PO bid KETOROLAC (Toradol) – 15, 30mg IM/IV, 10mg PO q4-6h For acute pain only; do not use for >5 days, to max of 60mg ETODOLAC (Lodine) 1 – 200, 400mg PO bid/tid, -ER (extended release) 400-1200mg PO qid PIROXICAM (Feldene) 1 – 10, 20mg PO bid

Intermediate-Acting (t½ = 12-36h) TRIAMCINOLONE ACETONIDE (Aristospan, Kenalog) Potency: 4 Dose: 5mg TRIAMCINOLONE DIACETATE (Aristocort) Same as above PREDNISOLONE ACETATE Potency: 4 Dose: 4mg METHYLPREDNISOLONE (Solu-Medrol) Potency: 5 Dose: 4mg

Phenylacetic Acid DICLOFENAC (Voltaren) – 25, 50, 75mg PO bid, -ER 100mg PO qid COX2 Inhibitors CELEBREX (Celecoxib) – 100, 200, 400mg PO bid Cross-reactive w/ sulfonamide hypersensitivity VALDECOXIB (Bextra) – 10, 20mg PO bid MIROXICAM (Mobic) – 7.5, 15mg PO qid

Long-Acting (t½ = 36-54h) DEXAMETHASONE (Decadron) Potency: 25 Dose: 0.75mg BETAMETHASONE SODIUM PHOSPHATE (Solu-Span) Potency: 25 Dose: 0.6mg BETAMETHASONE ACETATE (Celestone) Same as above Pedal Injection Doses Location Corticosteroid PIPJ/lesser MPJ 0.25-0.5cc 1st MPJ/STJ 0.5cc Neuroma/Heel 0.5-1.5cc Achilles Bursa 0.5-1cc

Anesthetic 0.25cc 0.5cc 0.5-1.5cc 0.5-1cc

Total 0.5cc 1cc 1-3cc 1-2cc

2

– Indicates schedule II narcotic (high chance of abuse) – Indicates schedule III narcotic (low chance of abuse) 4 – Indicates schedule IV narcotic (minimal chance of abuse) † - Corticosteroid potency is calculated in comparison to hydrocortisone 3

Resect condyles from phalangeal head, cartilage from joint space Open intramedullary canal distally and shape peg proximally K-wire/polymeric absorbable pins Anatomy- NV bundle Post-Op- SxS 6 wks, K-wire out after 3 wks

SURGICAL DISSECTION 1.

ARTHROPLASTY- formation of moveable joint (for HDS) Def- resection of p.p. (Keller-removal of base; Mayoresection of 1/3 of MT head for implant; Stone is resection of 2/3 of MT head) Indications-HDS where deforming force has been removed, DJD, loss o joint cartilage Contra- deforming force is still present (arthroplasty will leave a flexible joint that will eventually deform) ProcedureIncision (elliptical located dorsally over PIPJ/DIPJ) Excise as much corn as possible Free EDL and retract Incise joint Free collaterals Head osteotomy at Sx neck Place K-wire Tuck and suture EDL Anatomy- NV bundle on either side of digit Post-Op- WB SxS 2-3 wks, k-wire 2-3 wks Complications: 1. Sausage toe- from increased swelling + fibrosis. (tx w/ acetate steroid inj (≤ .1 cc), coban wrap) 2. Flail toe- from increased head resection or base resection. (tx w/ syndactyly, implant, graft) 3. White Toe; check dressing, dangle leg, bend k-wire, reflex heat, local anesthetic block, nitro patch 4. Recurrence 5. Metatarsalgia 6. Floating toe 7. Hourglass appearance 8. Brachymetatarsia 9. Hallux Malleus

2.

HELOMA MOLLE (soft corn) commonly assoc w/ under lapping fifth toe or w/ ADDuctus deformity of 5th MPJ Def- 4th interspace HPK Ind- Interspace HPK due to bony prominence Contra- dermatologic conditions at incision site ProcedureLinear incision dorsolateral to EDL Lateral condylectomy of 4th p.p. base (hemiphalangectomy) Incision lateral elliptical to expose head of 5th proximal phalanx Arthroplasty of 5th p.p. Anatomy- dorsal common digital n. of intermediate dorsal cutaneous n. Post-Op- WB SxS for 2-3 wks Complications- Flail toe 5th, Destabilization of 4th MPJ, Inadequate bone resection (recurrence)

5.

DIGITI QUINTI VARUS Procedure- Elliptical incision perpendicular to axis of deformity (derotational skin plasty), arthroplasty of 5th Post-Op- WB SxS 2-3 wks Complications- under correction, flail toe, recurrence

6.

PEG-IN-HOLE ARTHRODESIS Def- snug fit can be used w/o fixation Ind- HDS long MT for maximum stability, suspected non-union pre-op, Inability to use K-wire Contra- short toe pre-op ProcedureLinear incision Free EDL and retract Incise joint Free collaterals

HALLUX IPJ FUSION Indications- DJD, Hallux HDS, assoc w/ hallux varus repair, jones tenosuspension ProcedureTransverse elliptical incision on dorsal IPJ, release capsule and supporting lig. Resect articular surface of hallux IPJ (w/ rongeur) Use 4.0 partially threaded cancellous screw Post-Op- BK NWB cast w/ toe plate for 6-8 wks, k-wire 6-8 wks or until X-ray healing Contra- poor bone stock or medical problems Complications- infection, fixation failure, malposition

END-TO-END ARTHRODESIS (OR “V”) Def- fusion of joint (fusion of 1st MPJ is McKeever) Ind- HDS where intrinsic muscle function has been compromised & digital/MPJ stability is lacking, provides stable lever arm on which the long and short flexors can function to assist MPJ stability Contra- rigid 5th toe does not tolerate shoe pressure ProcedureLong lenticular incision Free EDL and retract Incise joint Free collaterals Resect 1 mm cartilage from proximal and middle phalanx K-wire down axis of digit Suture EDL Anatomy- NV bundle Post –Op- SxS, K-wire 6-8 wks, WB to tolerance Comp- same ones as arthroplasty + “long” toe, immobile joint

3.

4.

7.

VALENTI ARTHROPLASTY Indications- Hallux limitus stage II/III, 1st MPJ DJD Contra- PF 1st ray ProcedureIncision dorsomedial 1st MPJ Capsulotomy + cheilectomy 45º osteotomy of 1st MT head, dorsal proximal to plantar distal 45º osteotomy of p.p, ┴ to 1st Free sesamoids, close Post-Op- SxS 3-6 wks, immediate ROM exercises Comp- metatarsalgia, sesamoiditis, loss of stability

8.

AKIN OSTEOTOMY Distal akin- for high HI (normal ≤ 10˚) Proximal akin- for high DASA (normal ≤ 8˚) Oblique akin-facilitates screw fixation, will correct some of HI & DASA Cylindrical- for long phalanx Contra- poor bone stock, medical conditions Post- Op- WB or NWB SxS 3-6 wks, K-wire 3-6 wks or loose Comp- hallux ADDuctus, hinge Fx, fixation failure, FHL/ FHB severed, tendonitis, IPJ/ MPJ stiffness

HALLUX ABDUCTO-VALGUS

HEAD PROCEDURES

-progressive, triplanar deformity w/ frontal plane hallux rotation, lateral deviation, & dorsal or plantar deviation -Goals 1. Pain free ROM of 1st MPJ 2. Restore normal osseous angles (PASA + IM) 3. 1st MPJ should be congruent 4. TSP ≤ 3 (4 or greater = crista erosion) 5. Cosmesis (bump should be gone) 6. PF & shorten 1st ray (decompress 1st MPJ to increase ROM) -Skin incision Curvilinear following deformity, located dorsomedial between bump and EHL tendon -Capsular incision Inverted L, lenticular -Bumpectomy Angled more medially at proximal aspect to avoid sagittal sulcus (see below) -Indications Evaluate total adductory angle; IM + MT< (see metatarsus ADDuctus) -Procedure All procedures include capsule tendon balance procedures (Silver/McBride) -Post- Op ROM exercises for all procedures

12. REVERDIN (1881)

CAPSULE TENDON BALANCE PROCEDURES 9.

Def- medial based incomplete wedge resection of MT head Ind- abnormal PASA w/ flexible 1st ray Procedure Two convergent cuts in metaphyseal portion of 1st MT head Distal cut is orientated parallel to the articular cartilage, proximal cut is perpendicular to long axis of MT Hinge is left intact for added stability Fixation- K-wire, absorbable pins, or screws (1 point normally, 2 if hinge is broken) Comp- sesamoiditis, DJD Post-Op- WB/NWB SxS 3-6 wks

13. REVERDIN-GREEN Def- Reverdin w/ transverse plantar “shelf” to avoid disruption of articular surface of 1st MT and sesamoids

14. REVERDIN-LAIRD Def- Reverdin-Green cut thru & thru for lateral transposition; corrects PASA and IM

SILVER BUNIONECTOMY (1923) resection of medial eminence, + Lateral release Latva lateral capsulotomy ADD hallucis release or transfer Fibular sesamoid release or “ectomy” EHB tenotomy JFK Deep Transverse MT ligament ADD hallucis release Lateral capsulotomy Fibular sesamoid EHB tenotomy Indications- pain w/ shoes / bump pain, no abnormal changes, no DJD, positional HAV, osseous <’s WNL Post-Op- WB SxS for approximately 3 wks, ROM exercises Complications- STAKING THE HEAD, hallux varus, stiff toe, under correction

Procedure

Def- Reverdin-Laird, depress capital fragment to PF 1st ray as well as correct IM and PASA

16. AUSTIN (CHEVRON) Def- corrects IM <, MT head is shifted laterally Ind- mild/moderate HAV, minimal tracking, painless ROM Contra- DJD of 1st MPJ Procedure V osteotomy w/ apex located at the midpoint of a vertical line connecting the ends of articular cartilage of the head. V cuts angled at 60° w/ apex distal Fixation- cancellous screw or K-wire through dorsal proximal shaft into capital fragment, aiming at crista Post- Op- SxS 4-6 wks WB Comp- AVN, dislocation, intra-articular Fx, incorrect <, overcorrection, undercorrection, stress riser

17. YOUNGSWICK (MODIFIED AUSTIN)

Sagittal Sulcus

Proper

15. REVERDIN-LAIRD-TODD

Staking the Head

Def- will PF & shorten as well as correct IM < Ind- good for hallux limitus Procedure- Austin, plus; resection of an additional rectangle of bone from the dorsal wing cut Fixation- same as Austin

10. MCBRIDE (1928) Silver bunionectomy, plus: 1. fibular sesamoidectomy 2. ADD hallucis & lateral head of FHB transfer to dorsolateral aspect of 1st MT Modified McBride- Silver w/ fibular tendon release Hiss procedure- ABD hallucis transfer dorsal and medial on p.p. Procedure-

11. KELLER ARTHROPLASTY (1877)

Def- Resection of base of 1st proximal phalanx at MPJ Ind- 1st MPJ HAV/DJD/hallux limitus, w/ osteopenia Contra- lesser metatarsalgia, unstable hallux Procedure Silver bunionectomy, plus: Removal of 1/3 base of proximal phalanx Reattach FHB tendon and capsule to p.p. Post-Op- SxS 3-6 wks WB Comp- Floating toe, flail toe, metatarsalgia

18. KALISH (MODIFIED AUSTIN) Def- long dorsal arm Austin (V = 55˚); reduces higher IM < Fixate- 2x2.7 cortical from dorsal distal to plantar proximal

19. GERBERT MASSAD (BI-CORRECTIONAL AUSTIN) Def- corrects PASA & IM (bi-correctional), 2nd cut is performed w/ a wide base medially and a wedge removed from D-M aspect of MT(wedge can also be taken from both wings) Use axis guides to PF/DF metatarsal head (see below)

(SCARF CONTINUED) Procedure

Axis is perpendicular no length

Longitudinal incision 1st Transverse cut is 2/3 the width of MT (1 cm both head & base) Frontal plane cuts at either end; dorsal cut is distal and plantar cut is proximal Angles- 45, 60, 70°; can use axis guide for multiplanar corrections Modifications- make a shorter arm (angled 70-90°) Fixation- two 2.7/2.4 osteomed, two threaded .062 k-wires Post-Op- WB or NWB 3-6 wks, ROM exercises Complications- troughing, stress riser, dorsal cortical Fx of proximal apex, overcorrection Inverted Scarf

Axis directed proximally
shorten

Axis directed distally
lengthen

The inverted Scarf provides greater resistance to disruption from weight-bearing forces (decreased

occurrence of stress risers)

SHAFT PROCEDURES 20. HOHMANN (1920) Def- trapezoidal shape osteotomy (cut wider medially to reduce PASA) performed at anatomical neck Ind- stage 3 bunion, pain free ROM of 1st MPJ, IM < 18 Negatives 1. shortens too much 2. sometimes ends too proximal in shaft 3. unstable; requires NWB + 2 pts of fixation Positives (same as Reverdin-Laird-Todd) 1. decrease IM < 2. decrease abnormal PASA 3. PF capital fragment Procedure Distal cut parallel to abnormal PASA Proximal cut perpendicular to long axis of MT shaft Capital fragment transposed laterally and plantarflexed Two points of fixation necessary Post- Op- NWB w/ slipper/BK cast 4-6 wks, ROM exercises Comp- elevation of capital fragment, dislocation of MT head, PASA overcorrection, hallux varus Others Mitchell- shortens MT DRATO- (Derotational Abductory Transverse Osteotomy) can have rotation of capital fragment in frontal plane

21. MEYER-SCARF “Z” Def- Z-shaped sliding shaft osteotomy Ind- painful bunion deformity, hallux abuts 2nd toe, negative MT <, IM < 14-17 Contra- narrow MT<

22. VOGLER OFFSET V Def- MT shaft osteotomy w/ long dorsal wing & short plantar wing Indications- bunion w/ ABDucted hallux, IM < 14-17, PASA 8-35 Procedure- Apex of osteotomy at meta/diaph jxn (can use axis guide) Dorsal cut 1st to exit at basal epicondyle (angle is 40˚) Distal fragment is transposed laterally to reduce IM < & swiveled to reduce PASA Fixate- two 2.7, 3.5, .062, or 5/64 K-wires Post-Op- slipper cast 4-6 wks, SxS 6-8 wks Comp- AVN

23. MAU Def- sliding MT shaft osteotomy from plantar proximal to dorsal distal (capital frag is more stable) Post-Op- NWB 3-6 wks Comp- AVN, troughing, dorsal displacement Fixation- 3.5 screw or Steinmann pin

24. LUDLOFF Def- sliding MT shaft osteotomy dorsal proximal to plantar distal Post-Op- NWB 3-6 wks Comp- AVN, troughing, dorsal displacement Fixation- 3.5 screw or Steinmann pin

BASE PROCEDURES 25. LOISON BALACESCU

Def- transverse base wedge of 1st MT base w/ medial hinge Ind- stage 3 bunion, IM>15 rectus, IM>12 MTA Contra- open epiphysis Procedure- Osteotomy 1-1.5 cm distal to 1st MTcuneiform articulation & parallel to MT base

Lateral base closing osteotomy perpendicular to WB surface to prevent dorsiflexion, using axis guides Fixation- no screws 1. .062 longitudinally through MT shaft & 1st cuneiform 2. 5/64 medial-distal to lateral-proximal through cut and into 3rd cuneiform Post-Op- NWB B/K cast 6 wks (NO EXCEPTIONS) Comp- 1st MT head elevatus (always), shortening, under/correction, hinge failure, nonunion w/ fixation failure Other: Trethowan - medial base opening w/ Reverdin

26. JUVARA

Def- proximal, oblique 1st MT base osteotomy Ind- stage 3 bunion, IM>15 rectus, IM>12 MTA Contra- open epiphysis, narrow MT Procedure Oblique osteotomy 1 cm distal to 1st MTcuneiform articulation, apex medially Osteotomy perpendicular to the WB surface to prevent dorsiflexion using axis guides Osteotomy oriented from proximal/medial to distal/lateral at an angle of 45˚-65˚ to the MT Distance of cut should be 2X the width of the bone Fixation1. Proximal Anchor Screw (2.7)- goes in 1st , medial to lateral perpendicular to shaft 2. Distal Compression Screw (2.7)- perpendicular to cut or split the perpendicular Post-Op- NWB BK cast for 6wks Complicationselevatus, shortening, under / over correction, hinge failure, nonunion, fixation Fx

Juvara A- hinge type Juvara B1-through & through, wedge -correct TP & SP Juvara B2- through & through, wedge - correct TP & SP, lengthen Juvara C1- through & through, no wedge - SP Juvara C2- through & through, no wedge - SP & lengthen

27. LAPIDUS

Def- 1st MT-medial cuneiform arthrodesis (stabilizes medial column to restore fulcrum for better function of PL) Ind- painful ROM at 1st MT-cuneiform articulation, hypermobile 1st ray, IM correction (angulated), FF splaying Procedure Dorsal incision ID & retract nerves, arteries, periosteum and tendons Incise joint, distract laterally Release tarsometatarsal ligament Resect cartilage minimally from both sides of articulation Bone graft prn to increase fusion rate & prevent shortening (DON’T jam 1st MPJ) Fixation- two 4.0 cannulated PT screw, side by side or crossed; two 5/64 pins crossed; 1/3 or ¼ tubular plate medially & one 4.0 PT cannulated screw from dorsaproximal to plantar-distal Post-Op- NWB, BK cast up to 12 wks or until X-ray healing Comp- malposition, bone graft failure, open epiphyseal plate, sesamoiditis due to excessive plantarflexion, shortening of 1st MT, metatarsalagia, transfer lesions, decreased hallux purchase, non-union, under correction

Other CRESCENTIC (Mann) prevents shortening 28. LAMBRINUDI Def- plantar based closing wedge osteotomy, to correct MPE Ind- MPE (resulting in painful hallux limitus) Contra- DJD of 1st MPJ, hypermobile 1st ray, PF 1st ray ProcedureIncision dorsomedial to 1st Met-Cun joint Osteotomy w/ base plantar, apex ~1cm from 1st cuneiform. Cut is 45° from plantar. Fixation: 3.5/4.0 screw Post-op- NWB 4-6wks in BK cast Comp- PF 1st ray, shortened MT, sesamoiditis, non/malunion

29. WATERMANN Def- dorsal based closing wedge osteotomy of 1st MT head Ind- hallux limitus Contra- MPE, short 1st MT ProcedureIncision dorsomedial to 1st MPJ Oblique osteotomy dorsal to plantar at margins of articular cartilage Vertical osteotomy from dorsal straight down to sesamoid apparatus Fixation: crossed K-wires Post-op- SxS 4-6wks, immediate ROM exercises Comp- stiff toe, non/malunion, sesamoiditis Others Modified Watermann- watermann + cheilectomy. Plantar hinge is left intact (to protect sesamoids.) Watermann-Green- Austin Youngswick procedure with a V angle of 120-140°. Corrects HAV and hallux limitus.

LESSER MT (DORSIFLEXORY)

30. JACOBY (DORSIFLEXORY “V”) Def- distal V osteotomy of lesser MT made from dorsal to plantar
allows MT to elevate Ind- propulsive plantar lesions Contra- structural plantar lesions Procedure V-shaped central MT head osteotomy w/ dorsal transposition of frag Bone cut MUST be proximal to plantar condyles and IPK Fixation- percutaneous .045 K-wire Post-Op- WB SxS 4-6 wks Comp- nonunion, malposition, unresolved callus, MPJ stiffness, transfer lesion, post-op DJD, floating toe, excessive bone callus, AVN, MT coalitions

4th IM Lateral deviation

6.47 2.64

8.71 8.05

31. TILT-UP Def- vertical wedge w/ cortical hinge located plantarly Fixation- 2.0 or 2.7 K-wire dorsal to plantar

32. JIMENEZ Def- oblique wedge w/ cortical hinge located plantar proximal Fixation- 2.0 or 2.7 K-wire

36. TAILOR’S BUNION EXOSTECOMY 33. STRAIGHT VERTICAL Def- through & through vertical cut to slide head up Fixation- .045 K-wire proximal dorsal to distal plantar

34. GIANNESTRAS Def- step down “Z” to shorten Ind- splay foot (?)

35. HELAL / WEIL Def- MT shortening procedure Ind- predislocation syndrome (usually presents with metatarsalgia of 2nd MT) Procedure- long proximal dorsal to distal plantar osteotomy Comp- displacement of capital fragment

Def- exostecomy of tailor’s bunion at 5th MT head Ind- F&B type I tailor’s bunion, stable 5th ray, little angular deviation, isolated hypertrophy of MT head, Pt. who can’t have an osteotomy, used in conjunction w/ MT osteotomy Contra- poor bone stock Post- Op- WB SxS 3-6 wks Comp- inadequate bone resection, MTJ subluxation, unstable 5th toe, hinge fx, non/malunion 37. REVERSE WILSON (HOHMANN) SLIDE Procedure Oblique cut lateral distal to medial proximal Slide capital frag over Fixation- .062 K-wire from proximal shaft into head

38. CHEVRON (REVERSE AUSTIN) Fixation- orthosorb pin

39. Z OSTEOTOMY (MINI “Z”) Fixation- 2.0 or 2.7 screw dorsal to plantar

TAILOR’S BUNION General- Incision lateral to EDL Closing wedges at the base will decrease blood supply Utilize Fallat & Bucholtz to assess angles Fallat & Bucholtz (F&B) Fallat and Buckholz (1980) claim to have devised a more accurate way of measuring the 4/5 intermetatarsal angle which has been adopted by several subsequent authors; it involves using the medial border of the shaft as opposed to a bisection of the shaft due to significant variations found between the widths of different fifth metatarsal shafts: Points are marked on the medial surface at the center and at the base of the metatarsal, and a line is drawn through these points, establishing the longitudinal direction of the proximal bone. The fourth metatarsal was bisected in the standard manner, since it is subject to less anatomical variation. Normal

Pathologic

40. WEDGE (REVERSE REVERDIN) Fixation- 2.0 or 2.7 screw

41. NEUROMA Dx- Muldur’s sign, X-ray, MRI D/Dx- Fx, RA, AVN (Freiburgs), neuropathy, bursitis/capsulitis Incision Dorsal, longitudinal, interMT that runs up onto either toe Plantar, longitudinal or transverse in the sulcus Post-Op- WB SxS 2-3 wks (plantar approach is NWB) Comp- stump neuroma, white toe, hematoma, HDS possibly

PLANTAR FASCIITIS

42. HEEL PLANTAR FASCIOTOMY Dx- find exact location of pain using: nerve conduction & EMG, bone scan, lab tests Ind- heel pain; initially 3 months of conservative care should be attempted (but is not always practical) NSAID Heel cup Pre-fabricated orthotic Ice Stretching P.O. steroids Steroid injection Acupuncture P.T. (ultrasound) Taping Procedure DuVries medial incision (oblique at posterior calcaneus) 3-5 cm Release fascia only Post-Op- WB SxS Comp- stress Fx, continued heel pain, increased fibrosis at fascial origin, severe lateral plantar n., sever nerve to ADDuctor Digiti Minimi, misdiagnosis DuVries- removal of heel spur along w/ plantar fascia release Snook & Chrisman- removal of portion of medial Calcaneal tubercle (Manoli found that Fx occurred) Gormley & Kuwada- heel spur resection, fascial release, partial fasciectomy

43. ENDOSCOPIC PLANTAR FASCIOTOMY (EPF) (+)- less post-op pain, less soft tissue damage (-)- more technically demanding Ind- at least 6-9 months of conservative tx w/o relief Contra- pt w/ atypical heel pain, abnormal EMG of foot, dysvascular foot Procedure Arthroscope inserted through lateral portal w/ probe through medial portal (to determine length of plantar fascia) Dorsiflex ankle & toes to put tension on plantar fascia & bulge FDB Incise lateral border of pre-measured cut, releasing plantar fascia lateral to medial Release of portion of deep abductor fascia

45. KECK-N-KELLY Def- dorsiflexory wedge osteotomy w/ a plantar hinge Procedure Incision lateral, inferior, and parallel to peroneal tendons Resect bump DF Calcaneal wedge osteotomy Fixate- 2 X staples or orthosorb pins Post-Op- NWB cast 6wks Comp- tendonitis, hinge breaks, posterior bone fragment

RETROCALCANEAL SPURRING 46. RETROCALCANEAL EXOSTECTOMY Etiology- equinus, variant arthritides, trauma Non- Sx Tx- ¼ “heel lift, NSAID, SLC, steroid injection Try conservative treatment for at least 3 months Procedure Incision: split TA or Zadek, lateral to Achilles Remove spur w/ osteotome (ALWAYS plantar to dorsal) or w/ rongeur Rasp until smooth Post-Op- repair TA w/ Mitek anchor p.r.n., BK (some AK) cast NWB 4-6 wks Comp- stress Fx, inadequate resection, tendonitis, tendon rupture, anchor failure

METATARSUS ADDUCTUS

CALCANEAL HYPEROSTOSES Def- “pump bump” at posterior/superior/lateral calcaneus Etiology- pathobiomechanics in rearfoot + constant, chronic irritation Dx Philip-Fowler angle- pathologic if > 75˚ Pavlov’s Parallel Pitch Lines- anything above the superior line is pathological Total angle= FF angle +Calcaneal inclination anglepathologic if > 90˚ Non Sx Tx- ¼ “heel lift, NSAID, SLC, orthoses, steroid injection

44. HAGLUND’S RESECTION Def- resection of dorsal hyperostosis Procedure Zadek incision on side w/ bump Osteotome plantar to dorsal Smooth w/ rasp Post-op- splint or cast 6-8 wks, Mitek anchor p.r.n. Comp- “chasing the bump”, Fx, tendonitis, rupture

47. HEYMAN, HERNDON &STRONG (HH&S) Def- mobilization of Lisfranc’s joint by capsular release Indications- pain, appearance (social concerns of child), difficult fitting in shoes, age- 3-7 y/o Procedure Incision: 1. 3 incision approach: medial to EHL, 2nd interspace, 4th interspace 2. 5 incision: difficult to close Accurately ID tarsoMT joint spaces Release all soft tissue & ligamentous structures at level of Lisfranc’s joint except 1/3 of the plantar-lateral aspects of the bases of MT 1-4 5th MT cuboid joint is left intact for stability Harris modification- 2nd MT osteotomy Post-Op- NWB, AK cast for 3 months (amount of time required for remodeling of MT) Note: NOT used much b/c of bad Sx results (painful scars)

Post-Op- NWB, BK cast for 6 wks Comp- under correction, mal-union, non-union Other Peabody & Muro- excision of the bases of three central MT, osteotomy of the 5th, mobilization & reduction of luxation of 1st metcuneiform joint & correction of any Lepird abnormal insertion of tibialis anterior tendon McCormick & Blount- arthrodesis of the 1st metatarsocuneiform joint along w/ an osteotomy of bases of central MT bases, in neglected cases wedge resection of cuboid Steytler & Van der Walt- oblique V-shaped osteotomies at bases of each MT w/ apex of V angled towards the RF FLATFOOT PROCEDURES - MEDIAL COLUMN STABILIZERS Soft Tissue

50. KIDNER

48. BERMAN GARTLAND Age- 7- adult Def- Crescentic osteotomies of all 5 MT bases Procedure Incision: 3 or 5 incision approach Crescentic osteotomies of all MT bases 1cm distal to articular cartilage Fixation- originally only fixated 1st and 5th Post-Op- NWB, BK cast for 6 wks Comp- under correction, mal-union, non-union

Def-soft tissue procedure/medial column stabilizer Ind- adjunct to osseous procedures for pes valgo planus deformity, os tibiale externum, hypertrophic navicular Contra- rigid adult pes valgus, PTTD, normal pes planus Procedure Medial curvilinear incision over navicular Resection of hypertrophic navicular Removal of OTE TP advancement (reattach plantar-distal) Spring ligament reefing Post-op- SLC for 4-6 wks, depends on other procedures Comp- PTT rupture, scoring of talar head, prominent talar head as a result of excessive navicular resection

51. YOUNG

49. LEPIRD Age- 7-adult Procedure Incision: 3 or 5 dorsal incision approach 1st & 5th MT
closing base wedge w/ base lateral w/ medial hinge left intact 2nd, 3rd, 4th MT
osteotomy from dorsaldistal to proximal-lateral keeping cortex intact, angled 45˚ to the perpendicular of shaft (proximal portion of osteotomy no closer than1cm from base) 2-4 MT
one screw is driven into osteotomy w/o tightening; lateral cortex is broken & MT are moved lat Screws are tightened Fixation- 2.0, 2.4, or 2.7 K-wire

Def- soft tissue procedure/medial column stabilizer Ind- adjunct, operative Tx of pes valgo planus, for pt greater than 10 y/o Contra- normal pes planus Procedure Incision: from 1st MT-cuneiform to medial malleolus Tendo achilles lengthening Tib anterior rerouted through key hole in navicular TP reefing (reattach plantarly) Modification- Split TA & pass only half through keyhole Post-Op- BK cast 6 wks, f/u w/ shoe wedging and PT Comp- navicular Fx, tendon problems, subluxation Osseous General Age- late teen – adult Ind- long standing flatfoot, faults & DJD on X-ray, RF in rigid valgus, PTTD symptoms, tendonitis, & sinus tarsitis Procedure- usually combined w/ TAL & desmoplasty, bone graft used prn to prevent shortening Fixate- 6.5, 7.0, 7.3 screws or stables Post-Op- NWB, BK cast for up to 12 wks or until bone healing on X-ray Comp- mal-union, bone graft failure

52. LOWMAN - TN fusion, reroute TA under navicular and suture to spring ligament.

56. SILVER Def-varus producing posterior calcaneal osteotomy w/ lateral opening wedge Ind- Sx correction of pes valgo planus deformity (frontal plane dominant), stable MTJ Procedure Lateral approach w/ L-shaped incision Opening wedge osteotomy w/ base lateral Comp- dehiscence

53. HOKE

Def- navicular, 1st, 2nd cuneiform fusion Indications- adult and adolescent pes valgo planus
stabilizes the medial column to lengthen the lever arm of the muscles affecting the longitudinal arch (used almost exclusively as an adjunct procedure in combination w/ ankle equinus correction and calcaneal osteotomy)

57. DWYER Def- varus producing posterior calcaneal medial closing wedge osteotomy Ind- Sx correction of pes valgo planus deformity (frontal plane dominance) Procedure Medial approach w/ L incision Closing wedge osteotomy w/ base medial Post-Op- BK NWB cast 6-12 wks Comp- difficulty in approach, nerve entrapment

54. MILLER - navicular, 1st cuneiform, & 1st MT base fusion Other Modified Hoke/Miller- arthrodesis of the NC joint, opening wedge osteotomy of the first cuneiform and distal advancement of an osteoperiosteal flap to include the plantar CN ligament

58. KOUTSUGIANNIS Def- arcuate through and through posterior osteotomy w/ medial transposition

FLATFOOT PROCEDURES - CALCANEAL OSTEOTOMIES 55. EVANS Def- anterior calcaneal osteotomy w/ wedge insertion
lengthens lateral column Ind- pathologic pes valgo planus (transverse plane dominant) Contra- flatfoot caused by neurologic disorders, < 6 y/o, supra-torsional abnormalities Procedure Determine compensated MTA prior to Sx Incision: oblique proximal to calcaneocuboid joint (avoiding sural n.) Retract peroneal tendons inferiorly Retract EDB superiorly Osteotomy 1-1.5 cm proximal to calc-cuboid joint (through and through) Insert trapezoidal graft (ideally from iliac crest) Perform medial arch tendosuspension & TAL as adjuncts

ATHROEREISIS Def- “joint lifting” to prevent abnormal joint motion (valgus at STJ), used in conjunction w/ either Kidner or Young procedure Goal

to prevent lateral talar process from dropping into the calcaneal sulcus stabilize STJ
decrease heel valgus
stabilize MTJ
increase efficiency of peroneus longus
PF 1st ray
stabilize medial column + increase arch height

Ind

pain w/ activity, causing pt to refrain from activity (+) family history orthoses ineffective FF deformities >50˚ TNJ disarticulation clumsy night cramps everted CSP Kite’s angle > 30˚ FF varus > 8-10˚ ↑ talar declination < ↓ calcaneal inclination < Hx of anterior cyma line Midtarsal break

Contra rigid (A) ankle valgus (A) skewfoot (B) < 3 y/o Comp Post-Op- NWB, BK cast 8-12 wks Comp- under/ over correction, shift of anterior fragment, delayed/non-union, cutting into one of facets, bone graft failure (10-12 wks), jamming of medial & lateral columns, DJD, peroneal tendonitis, damage sural nerve

infection sinus tarsitis implant breaks fx lateral talar process over/under correction

significant DJD (A) prior infection (A) equinus (B) structural FF varus implant malposition peroneal tendonitis Fx calcaneus talar beaking iatrogenic coalition

Note: ↑ Trephine- tool used to cut out a hole in calcaneus for implant

59. SELF-LOCKING WEDGE (PERMANENT) Def- to hold talus and calcaneus apart, screws into sinus tarsi & elevates STJ axis Ind- any age Types: MBA (titanium), Valenti (polypropylene), Viladot umbrella, Custom-carved plug Procedure Incision- long lateral over opening of sinus tarsi (3-4cm Grice) Cut out deep sinus tarsi plug (Hoke tonsil), leave attached anteriorly Square off posterior wall & floor of anterior calc. process Place K-wire through sinus MBA: Screw in correctly sized device 1 cm from lateral wall of calcaneus Check for proper placement and motion of calcaneus Post-Op- WB BK cast 2 wks (MBA)

60. AXIS-ALTERING (REMOVABLE) Def- holds bones apart and raises STJ axis back to normal (lateral process glides on top), drilled into calcaneus Types: Smith Sta-peg (straight top), Lundeen (concave top) Ind- younger pt; 3-13 y/o Procedure Incision: long lateral (medial to lateral) over opening of sinus tarsi (Grice) Cut out deep sinus tarsi plug (Hoke tonsil), leave attached anteriorly Square off posterior wall & floor of anterior calc. process Locate distal-lateral aspect of posterior facet of calcaneus Use osteotome to create two vertical & one longitudinal base cuts Drill hole in calcaneus w/ trephine Place device in hole Check for motion of calcaneus Post-Op- early ROM & WB in SxS
gradual increase in ambulation
3-4 wks return to normal

61. DIRECT IMPACT (PERMANENT) Types: Sgarlato mushroom Ind- any age

CAVUS FOOT PROCEDURES Ruch Classification of Cavus Foot Deformity Ruch 1- Flexible cavus Tx- Rigid fusion, MPJ release, Hibbs, Jones, Orthoses Ruch 2- Cavus becoming rigid- PFFR and RF varus Ruch 3- Rigid (Global) cavus 67% due to neuromuscular (CMT-most common)

62. STEINDLER STRIPPING Def- Soft tissue release/plantar fasciotomy Ind- peds pt. w/ significant contracture of both plantar fascia and musculature, flexible cavus deformity, pt w/ neurologic disease Procedure Incision- (DuVries medially) longitudinal along medial side of calcaneus Release plantar fascia Strip abductor hallucis, FDB, abductor digiti minimi from calcaneal periosteum Release long plantar ligament (along w/ it goes Quadratus plantae)

Note- if pt is young
can do a Dwyer and just cut plantar fascia Post-Op- Primary- 3 wks NWB BK cast w/ FF dorsiflexed Adjunctive- procedure dependent Comp- excessive fibrosis, nerve entrapment, myositis, fasciculitis, neuritis, damage vessels, HDS

63. DWYER Age- usually 10-12 y/o (beware of apophysitis) Ind- Ruch 2 Procedure Incision: parallel & inferior to peroneal tendons Straight or oblique wedge w/ base lateral (Osteotomy decreases supinatory force of the TA on calcaneus) Close by dorsiflexing FF Note-final position: approximately 0.5˚ valgus -closer the osteotomy is to STJ
the greater the amount of correction of TA on calc -can be modified for frontal or transverse plane deformities Fixation- two staples (most common), Steinman pin, screw Post-Op- NWB, BK or AK cast for 6 wks Comp- non-union, tendonitis, STJ DJD, hinge Fx, wound dehiscence, nerve entrapment, under correction

64. JONES TENOSUSPENSION Ind- Ruch 1, hallux hammertoe, hallux varus, double sesamoidectomy Procedure Cut & tag EHL at insertion Drill hole through MT head & feed EHL through hole Reattach tendon to itself w/ 2.0 or 3.0 non-absorbable Fuse hallux IPJ Post-op- NWB BK cast for 6 wks Comp- rigid PFFR, tendon dislocation, not enough tension on EHL, MT head Fx,

65. PERONEAL STOP

Def- takes out effect of PL on 1st ray, puts that force through the PB
ABDuct & evert foot Ind- Ruch 1 or 2 Procedure 1. PL is sutured to the PB w/ 3.0 nonabsorbable while foot is ABDucted and everted, OR 2. PL is cut (stab incision) along the length of PB & PL is weaved through 2 Suture stab ends so they won’t tear Post-Op- NWB BK cast for 4-6 wks Comp- peroneus brevis splits longitudinally, tendon problems, rigid PFFR

66. SPLIT TIBIALIS ANTERIOR TENDON TRANSPOSITION-(STATT)

Ind- Ruch 2, swing phase supinatus, invertors overpowering dorsiflexers, equinovarus deformity Procedure Incision: 1. linear over cuboid, 5th MT base 2. linear over 1st MT/cuneiform 3. linear or transverse over dorsum of tibia (5-7 cm proximal to AJ) Make stab incision & divide TA into medial & lateral halves over tibia Pass instrument (uterine packing forceps) from medial incision to tibia (under skin) Place umbilical tape through incision in TA

Use forceps to grab tape, pull out through medial incision, and split tendon in process Detach lateral half of tendon from its insertion & pass it up & out of tibial incision Pass instrument through the lateral incision to the tibia, grabbing medial TA Pull back through lateral incision Attach medial TA to cuboid or peroneus tertius (if present) Post-op- NWB BK cast for 6wks Comp- rigid cavus foot, tendon dislocation, tendon splits Other Hibbs- EDL is used for tenodesis of midfoot (3rd cuneiform) Combined Hibbs & Jones tendosuspension

67. COLE Def- dorsiflexory wedge through midfoot Ind- Ruch 3, severe anterior cavus, severe NM disease Procedure Incision- same incision as HH&S Dorsiflexory wedge of midtarsus w/ through & through cut extending from cuboid through cuneiform-navicular joints Fixation- staples Post-Op- NWB BK cast for at least 6 wks Comp- DJD, deformed foot, neuroma, tendon problems, non-union, fixation failure

REARFOOT ARTHRODESIS General Ind- instability, DJD, pain, trauma, failed implant, end stage flatfoot or cavus, RA, S/P infection,

Post-Op 1. Drain for 24-48 hrs 2. Posterior splint for up to 2 wks 3. NWB BK cast for 6 wks 4. WB BK cast for 6 wks Comp- non-union, mal-union, varus, fuse wrong joint (do diagnostic injection)

69. STJ ARTHRODESIS Incision- Ollier or lateral linear (reflect EHB Resect cartilage from talus & calcaneus using osteotome, power or curette Pack w/ bone chips to increase healing and to maintain height Position at 5˚ valgus Fixation- 6.5, 7.0, or 7.3 from dorsal to plantar thru posterior facet (can also use staples) Procedure

70. AJ ARTHRODESIS Incision- Kocher, or from fibula to 4th MT base Remove at least 2 cm of fibula & retain Remove top of talus & tibial plafond Resect ~1cm medial malleolus (prn) Pack all voids w/ bone chips Position TP: 5-10˚ ext, or matched to opposite limb FP: 5-10˚ of valgus SP: 0˚ Talus- 10mm posterior to tibia (will ↑ lever arm & ↓ stress distally) Fixation- 6.5, 7.0, or 7.3 cannulated, crossed angled down or put both in from talus on lateral side & up into tibia

Procedure

68. JAPAS Ind- Ruch 3, severe NM disease Procedure Incision: 1. 1st cuneiform-navicular 2. 2nd & 3rd cuneiform-navicular 3. 4th & 5th MT base-cuboid Thru & thru “V” cut w/ apex in navicular Medial arm through 1st cuneiform Lateral arm through cuboid Slide FF inferior and dorsiflex Fixation- 2 Steinman pins or 7/64 pins Post-Op- NWB BK cast for at least 6 wks Comp- DJD, deforms foot, neuroma, tendon problems, non-union, fixation failure

71. TRIPLE ARTHRODESIS Incision- Kocher or 2 Incision approach: curvilinear for STJ & CCJ; dorsomedial for TNJ (order varies) Fusion order: CCJ>STJ>TNJ Fixation- 6.5, 7.0, or 7.3 (or can use stables) 1. Ryerson (top of page) 2. Hoke- Head & neck of talus are used as a bone graft 3. Lambrinudi- Good procedure for drop foot Procedure

72. LATERAL STABILIZATION Single Ligament Replacement- peroneus brevis is used as an autogenous graft for recreating the CFL or ATFL 1.WATSON-JONES Procedure Graft is inserted through a drill hole in fibula (post
ant) approximately 2 cm from distal tip of malleolus Pass tendon through hole drilled in talar neck (dorsal
plantar) Return tendon through fibula (ant
post)

2. EVANS Procedure 4. Brewster countersink-

5. Triple w/ Dunn modifications-

3. LEE Procedure

Drill hole through fibula Tendon fed through hole & secured posteriorly at proximal portion of superior peroneal retinaculum

Entire PB graft is passed through from posterior to anterior through fibula Graft is anchored distally by performing a peroneal anastomosis A periosteal flap from the distal most anterior aspect of fibula reinforces new lig

6. Seiffert (beak)4. NILSONNE Procedure

Detach PB at level of musculotendinous junction Proximally, PB is sutured to PL While distal tendon is placed in a subperiosteal groove through fibula (posterosuperior to anteroinferior)

Double Ligament Replacement - designed to address chronic injury of both ATF & CF ligaments 1. CHRISTMAN & SNOOK Procedure Split PB tendon graft is harvested from proximal aspect of tendon Graft is routed through talar neck & then through distal fibula at it’s widest (anterior
posterior) Graft is then sutured to a periosteal flap created at the level of CF lig Last suture the distal end of graft onto itself

2. ELMSLIE Procedure

3. HAMBLY Procedure

4. WINFIELD Procedure

5. KELIKIAN Procedure

6. SEEBURGER Procedure

12 cm incision over PB tendon (5cm proximal to tip of lateral malleolus ending between base of 5th MT & malleolar tip Retract peroneals inferiorly Insert graft of tensor fascia lata in osseous canal through talar neck (sup to inf) Lace through canal in fibula from superoanterior
posteroinferior Then through a canal in calcaneus posterosuperior
anteroinferior Ends are sutured on themselves

7. SPLIT PERONEUS LONGUS Procedure Tendon identified & severed from muscle belly at proximal aspect
free up distally Periosteal channel is created in talar neck End of tendon is passed through Then through a trephine hole in fibula (ant
post) Bone plug is replaced in fibula Then passed through trephine hole in calcaneus Plug replaced
recreates CF lig

TENDO ACHILLES LENGTHENING Ind- gastroc or gastro-soleal equinus Post- Op- NWB BK cast for 3-4 wks followed by P.T. Comp- tendon rupture, sural neuropathy, shoe irritation, under/over correction Types: 1. White- slide lengthening

Split PL & suture it to lateral talar neck Then passed tendon from anterior
posterior through fibula Graft is then fixated to calcaneofibular ligament insertion

same as Hambly, but use PB instead of PL

Plantaris tendon is used to recreate lateral ligaments

2. Cummins

3. Hoke- triple hemisection slide

4. Conrad & Frost

Hemisection of PL as free graft to reconstruct ATF & CF lig 5. Baker- distal tongue-in-groove 5.Z- frontal (or sagittal) plane slide

THE ELECTROCARDIOGRAM Leads: Leads record the electrical activity of the heart occurring between two electrodes. Placement of leads on the body allows view of the heart in two planes – frontal and transverse. The 12-lead EKG views the heart from 12 different angles – 6 frontal and 6 transverse. There are three types of leads – standard limb leads (bipolar), augmented leads (unipolar), and chest leads (precordial.) Each lead has a positive electrode which “sees” the magnitude and direction of electrical forces in a specific part of the heart. If electrical activity moves towards the positive electrode, the EKG shows an upward waveform – if the electrical activity is away, it is a downward waveform. No electrical activity is represented by a straight line (isoelectric.) No leads view the posterior surface of the heart. Frontal Plane: Has 3 standard leads and 3 augmented leads. Standard leads: Lead I (Rt. Shoulder) – views lateral lt. ventricle, QRS is + Lead II (Lt. Shoulder) – views inferior lt. ventricle, QRS is + Lead III (Lt. Foot) – views inferior lt. ventricle, QRS is +, P ]may be +, -, or both Augmented leads: AVR (Rt. Shoulder) – view of the base of the heart, QRS is – AVL (Lt. Shoulder) – view of lateral lt. ventricle, QRS is 0 AVF (Lt. Foot) – view of inferior lt. ventricle, QRS is + Transverse Plane: Has 6 precordial (chest) leads. V1 (4th intercostal space rt.) – P +, -, or 0, QRS is – V2 (4th intercostal space lt.) – same as V1 V3 (midway btw V2 and V4) – Same as V1, V2 V4 (5th intercostal space, lt. midclavicular line) – P + V5 (5th intercostal space, lt. ant. axillary line) – P +, QRS + V6 (5th intercostal space, lt. midaxillary line) – P +, QRS + EKG stip paper: X axis = Time (sec), Y Axis = Voltage (mV). Speed = 25mm/sec. 1 box = 1mm = 0.04 sec. One large box = 5mm = 0.2 sec P Wave: Smooth and round, no more than 2.5mm tall. No more than 0.11 sec duration. + in I, II, AVF, V2-V6. PR Segment: Line btw P wave end and QRS beginning. PR Interval: P wave + PR segment. Represents depolarization of the atria and propagation through the AV node, bundles of His and Purkinje fibers. Normal = 0.12-0.2 sec. Long PR interval = delayed impulse (heart block), digitalis toxicity Short PR interval = impulses originating from ectopic focus QRS Complex: Q – downward, depolarization of IV septum R,S – Simultaneous depolarization of ventricles (mainly lt.) Overall positive, may be missing one component (variable) Normal = 0.06 – 0.10 sec Long QRS complex = ectopic purkinje/myocardial pacemaker ST Segment: Line btw QRS complex and T wave. Represents early ventricular repolarization. Displacement up or down from the isoelectric line is termed ST “elevation” or “depression.” ST depression (>1mm) = myocardial ischemia, digitalis tox. ST elevation (>1mm limb, >2mm chest) = myocardial injury T Wave: Represents ventricular repolarization, should be in the same direction as the QRS complex. Inverted T waves = myocardial ischemia Tall, pointed T waves = Hyperkalemia Rate: Pulse rate measured from the EKG, in 1 of 2 ways: 1) Count # of QRS complexes in 6 sec, multiply by 10 2) Count # of large boxes btw QRS complexes, divide into 300 Rhythm: Regular amount of time btw QRS complexes. Normal Sinus Rhythm = 60-100 beats/sec, uniform P waves, PRI 0.12-0.2 sec, QRS <0.11 Sinus Bradycardia = Regular rhythm, <60 beats/min Sinus Tachycardia = Regular rhythm, 100-180 beats/min Arrhythmia = Irregular rhythm (P waves, QRS uniform)

ATRIAL DYSRHYTHMIAS: Atrial dysrhythmias reflect abnormal electrical formation and conduction in the atria. The two mechanisms whereby electrical impulses are altered are changes in automaticity and triggered activity. Factors that cause a change in automaticity include ischemia, drug toxicity, hypocalcemia, and electrolyte imbalance. Factors that cause triggered activity are hypoxia, catecholamines, hypomagnesia, myocardial ischemia/infarct, and any medication that increases the repolarization time. (Triggered activity occurs in runs.) Most atrial dysrhythmias are non-life threatening, unless they affect the ventricular rate.

PRE-ATRIAL CONTRACTIONS (PACS): Appear early, before an expected beat. They are identified by their site of origin – either atrial, junctional, or ventricular. They occur when an irritable focus discharges out of sync with the SA node pacemakers – thus the rhythm and rate are unchanged, but there are premature atrial beats coexisting in the EKG. These P waves on the EKG may not be followed by QRS complexes. The PR interval may be normal or prolonged. PACs are common findings and may not signify pathology – emotional stress, fatigue, and CHF are all causes of PACs. They do not require intervention unless there is risk of progression to atrial flutter, in which case you should use beta-

blockers, calcium channel blockers, or anti-anxiety meds to reduce the risk. SUPRA-VENTRICULAR TACHYCARDIA (SVT): SVT is a tachyarrythmia originating in the heart above the level of the bundles of His. Sudden onset SVT is described as paroxysmal or PSVT. Characteristically, SVTs have a rate of 150-250 bpm, with regular rhythm and “different” looking P waves. SVTs are treated with synchronized cardioversion (fibrillation.)

wave.

ATRIAL FLUTTER: is a rapid atrial rate due to an ectopic pacemaker – usually an irritable focus that is firing regularly. Pulse rate is >300 bpm. It lasts for seconds to hours, brought on by PE, thyroid toxicosis, chronic ventilatory failure, ethanol abuse, CAD, hypoxia, and digitalis/quinidine toxicity. It is precipitated by PACs and is also assoc. w/ mitral/tricuspid valve dz. 5-10% of post-MI pts develop atrial flutter. It is treated with meds if cardiac function is normal. If not, digitalis or cardioversion is indicated.

ATRIAL FIBRILLATION: can be spontaneous and last an hour to days. Pulse rate is 400-600 bpm, which results in a decrease in output due to total dysfunction of the atria. The rate is variable, the rhythm is irregularly regular, P waves are indistinguishable, and the PR interval immeasurable. It is seen in pts. w/ rheumatic heart dz, CAD, PE, HTN, ethanol abuse, carbon monoxide poisoning, electrolyte imbalances, hyperthyroidism. Classic presentation is from overimbibing of alcohol at holidays, resulting in “holiday heart syndrome.” Tx is same as for atrial flutter, except pt also needs to be put on anticoagulants to prevent blood clot formation in the atria.

PRE-VENTRICULAR CONTRACTIONS (PVCS): form from an irritable focus in the ventricles. The normal rate of ventricular contraction originating from the VA node when the SA node is malfunctioning is only 20-40 bpm. The distinguishing feature on EKG is that PVCs show an elongated QRS complex (>0.12 sec) with a compensatory pause. Like PAC, PVC is a single beat, so rate and rhythm are not affected. It is also a normal finding that can be brought on by exercise, hypoxia, stress, and excess catecholamines. Tx depends on the S/Sx; usually no tx is required.

VENTRICULAR TACHYCARDIA: is distinguished by a rate of 150-250 bpm. P waves are often absent, and the PR interval is elongated when they are seen. The QRS is >0.12 sec and is difficult to distinguish from the T

VENTRICULAR FIBRILLATION: is distinguished by the lack of organized contraction of the ventricles. 80% of pts post-MI develop V-Fib if not tx in a hospital. Rate and rhythm are incalculable. Tx w/ CPR and cardioversion.

1ST DEGREE AV BLOCK: Distinguished by a PR interval >0.2 seconds that is the same for every beat. This situation can be normal if no Hx of heart dz, ischemia, injury, meds, etc.

2ND DEGREE AV BLOCK (TYPE I): Here the conduction delay occurs in the AV node. It is characterized by progressively lengthening PR intervals that result eventually in entirely missed beats. It usually is a sign of ischemia, typically in the area of distribution of the rt. coronary artery, or of medication.

2ND DEGREE AV BLOCK (TYPE II): Here the conduction delay occurs somewhere below the AV node, usually the bundle branches. The bundle branches are supplied by the left coronary artery and are injured in anterior wall infarcts. The EKG shows variably displaced or absent P waves and QRS complexes. This condition may progress suddenly to a complete AV block. Tx is by pacemaker; otherwise the prognosis is very bad.

Drugs To Know – Really… 1kg = 2.2lbs ANTIBIOTICS: Broad Spectrum: PCN ---- ZOSYN (Pipercillin / Tazobactam): • Staph, Strep, Entero, G -, Anaerobes/Aerobes, Pseudo… NO MRSA • 3.375 g IV q6h • 4.5 g IV q8h
Suspected Pseudo o + Gentamycin if Pseudo / G- / Systemic infxn PCN ---- AUGMENTIN: 500mg po q8h or 875mg po q12h – ST infxn INVANZ (Ertapenem) Carbapanem • Kills EVERYTHING except Pseudo • 1g IV / IM qd TYGACIL (Tigecycline) glycylcycline, static, 30S ribosome • G +, G -, Anaerob, MRSA, NO
pseudo, proteus • Slow infusion (30-60min) • SE = derivative of tetracycline (bone, teeth, peds) • 100mg dose, then 50mg q12h after • Liver pts lower dose, renal pt ok, no peds yet, no po MRSA: VANCOCIN (Vancomycin) • ALL G +, MRSA, NO G – • Follow Renal Funcion (Peaks/Trouphs) • Infuse over at least 45-60min to avoid red man o If get red man, Tx = Benadryl 10-50mg tid until symptoms go away • 1g IV q12h (max dose = 2g/day) • 125mg PO qid for C.dif, better than metro, but $$$ • Peak/Trough = 20-50ug/ml & 5 - 10ug/ml o Draw 1hr before dose(trough), and 1hr after administration (peak) • SE = oto and nephro, long term tx is worse • with aminoglycoside can
nephrotoxic ZYVOX (Linezolid) Oxazolidinone • ALL G + (including Entero, staph, VRE, MRSA) • 600 mg IV / PO bid • $$$ - don’t use if can use Vanc, or Bactrim + Rifampin • Better Bone Penetration than Vanc BACTRIM (TMP/SMX) (160mg/800mg) Sulfonamide • Good Staph, MRSA, some strep, NO Pseudo • SULFA • 1 tab PO bid, tid for severe infxn • + Rifampin beneficial o Good staph/strep, mycobac, some Go Used in combo b/c of quick resistance to it o 300mg PO bid o No adjustment for renal pt o combo with vanc, bacrim, minocycline for MRSA Anti-PSEUDOMONAL: PCN ---- ZOSYN (Pipercillin / Tazobactam): • Staph, Strep, Entero, G -, Anaerobes/Aerobes, Pseudo… NO MRSA • 3.375 g IV q6h • 4.5 g IV q8h
Suspected Pseudo

CIPRO (Ciproflxacin) • ALL G -, Pseudo, not good staph/strep, NO PEDS o Levaquin better for staph/strep, less pseudo, same G – o 500mg PO / IV qd (mild-mod) o 750mg PO / IV qd (complicated skin infxn) • SE = tendon ruptures, epiphyseal cartilage damage • 500mg PO bid, 400mg IV bid (mild-mod infxn) only use IV if pt has to be NPO… • 750mg PO bid (severe infxn, osteo) • Decrease to once daily for renal pts… • Proven Good bone penetration Other ANAEROBES: CLEOCIN (Clindamycin) Macrolide • Most G +, Anaerob, NO
MRSA, Clostridia • 600 – 900mg IV/IM q8h • 150-300mg PO bid or tid for outpatient • OK for renal pt, good bone penetration Metronidazole: 1g bolus, 500mg IV q6h over 1hr PCN --- UNASYN (Ampicillin/Sulbactam) B-Lactamase combo • G +, some G -, great Anaerob, Entero, NO MRSA • Emperic Rx for bite wounds • 1.5-3g IV / IM q6h • dec dose if CrCl drops below 30-50ml/min Gram + general: • Ancef: 1g IV/IM q8h 1 hour prior to sx • Keflex: 500mg po qid • Dicloxicillin: 500mg po qid • Clindamycin: 600mg IV q8h (PCN all) 300mg po qid • Vancomycin: 1g IV q12h over 1hr (PCN all) Gram – general: • Levaquin: 500mg po/IV qd Bug - Drug of Choice / Alternative / 3rd Line MRSA - Linezolid, Vanc / Rifampin / TMP – SMX S. Aureus - Keflex, Nafcillin / Vanc, Unasyn, Zosyn… Strep. Pyogenes - Ampicillin, Pen G/V, Amoxicillin / Unasyn, Zosyn, Ceph(1-3), Macrolide (Erythro), Vanc P. Aeruginosa - Zosyn, Aminoglycoside, Cipro, Cefepime / Levofloxacin E. Coli - Keflex, Ancef, Toby, Gent / Unasyn, Zosyn, Augmentin / TMP-SMX Clostridium Perfringens - Pen G +/- Clinda / Zosyn, Unasyn, Cefriaxone, Linezolid / Erythromycin Bacteriodes Fragilis – Metro, Unasyn, Zosyn, Primaxin IM(Imipenem + Cilastin) / Augmentin, Timentin, Clinda Gas Causing Bacteria: BECKS Bacteriodes, Enterococcus, Clostridia (4), Kleibsiella, Staph/Strep Clostridium (Anaerobic) Perfringes – gas gangrene, liquefaction necrosis, and hemolysis from α-toxins Difficile – pseudomem colitis – exotoxin kills enterocytes, need 3 neg toxin screens to clear Botulinum – food poison – flaccid paralysis – heat-labile toxin inhibits Ach release (antiSLUDGE) Tetanus – CNS – exotoxin blocks glycine release from Renshaw cells in spinal cord – titanic paralysis BacteriCIDAL ABx: Pen, Ceph, Vanc, Aminoglycosides, Fluoroquinolones, Metronidazole

Cephalosporin kills: 1st gen (Ancef, Keflex, Duricef) – PEcK 2nd gen (cefoxitin, cefaclor, cefuroxime) – HEN PEcKS Haemophilis influenza Enterobacter Neisseria Proteus E. coli Klebsiella pneumonia Serratia GRAM Stain steps: (water rinse after each step) 1) Gentian Violet 2) Alcohol 3) Grams Iodine 4) Safranin (140 – age) x weight(kg) -----------------------------------------Serum Cr x 72 (for women x 0.85) *Normal renal function = CrCl around 100 ml/min (it can be much higher) *The “loading dose” of aminoglycoside Tx is the same regardless of pts renal function. The only thing that changes is the maintenance dose. *There is a linear relationship between clearance and percentage of renal function. *if the CrCl is 50 ml/min, 50% renal function is assumed; therefore 50% of maintenance dose is calculated. If full dose = 5mg/kg/day, then 2.5mg/kg/day bid or tid should be administered. Creatinine Clearance =

Bacteria Growth Curve: Lag – metabolic activity without growth Log – rapid cell division Stationary – nutrient depletion slows growth Death – nutrient depletion and waste buildup
death Tetanus Prophylaxis: (0.5 cc Toxoid) (250 units TIG) Clean, Minor Wound Major or Dirty wound Toxoid Immunogl Toxoid Immunogl Unknown or YES NO YES YES 250U <3 doses 3 + doses
NO, unless NO NO, unless NO >10y since >5y since last dose last dose *Cannot put toxoid and TIG in same site. Must use other arm Aminoglycosides: Gent, Toby, and Amika Loading dose: Gent/Toby
2 mg/kg Amika
7.5 mg/kg Usual Maintenance: Gent/Toby
5-7 mg/kg/d q8-12h Amika
15 mg/kg/d usually q12h *CrCl must be calculated before maintenance dose given Usage limited to Life/Limb threatening Aerobic G – infxn Toby is the most effective against P aeruginosa Gent is best for Serratia Amika is RESERVED for organisms resistant to gent and toby They are active against staph/strep, but there are less toxic Rx NOT active against ANY Anaerobes! Amino’s require O2 to cross cell membrane Great for impregnating in beads because they are heat stable, low reactivity, water soluble. (ratio is 5:1)

Toxicities: Nephro
reversible starts several days after initial tx, see significant increase in serum Cr. + vanc
worse Oto
Irreversible, generally not seen for a few days.. Auditory
tinnitus, loss of hi freq, test by audiometric testing… Vestibular
dizzy, vomit, loss of balance in dark, nystagmus… Neuromuscular Blockade: drug accumulates at NM junction, inhibiting Ach release from n. The only way u get this is with Bolus administration
therefore infuse over 30 minutes Peaks And Troughs: (management and timing) Peaks are drawn immediately following administration of dose Troughs drawn 20-30 min before administration of next dose Levels should be ordered initially after 3rd dose… If WNL, do not need to order again unless there is a rise in serum Creatinine level. (Cr should be monitored about 3x/week) *Gent and Tobra: peak = 6-10, trough = less than 2 ug/ml *Amikacin: peak = 20-30, trough = less than 10 ug/ml Techniques for changing doses: {change amt or interval} Peak is Hi, trough is normal
Dec. amt Peak is Lo, trough is normal
Inc. amt Trough is Hi, peak is normal
Inc. interval Peak and Trough are HI
Dec dose & interval PAIN MANAGEMENT & CONCIOUS SEDATION --------------------------------------------------------*Remember – the duration of onset of reversal agents and analgesics or sedatives may be different… the reversal agent may wear off before the agent, leaving the agent to overcome the pt… VALIUM (Diazepam) – Benzodiazepine • onset = 1-5 minutes, half life = 30 hrs • sedative dose = 10-12mg • lasts 2-3 hrs VERSED (Midazolam) – Short acting Benzodiazepine • 4 X more potent than Valium • Amnesia • Watch for hypotension, mental and motor defects • onset = 3-5 min, half life = 1.2-12.3 hrs • sedative dose = 2.5-7.5mg • lasts 30-40 min FLUMAZENIL (Romazicon) – BZD Antagonist / competitive at GABA receptor – Versed reverse • Lasts 30-60 min • Onset = 1-2 min • Initial Dose = 0.2mg. May repeat at 1 min intervals to dose of 1mg MORPHINE SULPHATE – Opioid Narcotic • Dose = 1-5mg IV over 1 min, titrated every 6-10 min until analgesia is reached. (max = 12mg/hr) • Lasts approx 4 hrs • Watch O2 sats… respiratory depression DEMEROL (Meperidine) – weaker Narcotic • Onset = 3-5min, half life = 30-45 min • Avg Dose = 20-50mg

NALOXONE (Narcan) – Narcotic Antagonist – Morphine reverse • Lasts 20-30 min • Initial dose = 0.4 mg. May repeat every 2-3 min @ doses of 0.4-2 mg PERCOCET: (Oxycodone/Tylenol) class 2 • 2.5/325, 5/325, 7.5/500, 10/650 – 1 tab po q4-6h VICODIN: (Hydrocodone/Tylenol) class 3 • 5/500 1-2 tabs po q4-6h • ES (7.5/750) 1 tab po q4-6h • HP (10/660) 1 tab po q4-6h Thanks Mikey!: Remember that all narcotic brand names that end with "-cet" have Tylenol in them, while ending with "dan" is ASA. Ex - Percocet has Tylenol, Percodan has ASA NON-Codeine
STUUD STADOL (butorphanol) (opioid agonist-antagonist) 0.5-2mg IV or 1-4mg IM q3-4h prn pain TORADOL (ketorolac/NSAID) *30mg IV bolus or 60mg IM over at least 15sec 15-30 mg IV/IM q6h or 10mg PO q4-6h prn moderately severe acute pain… do not exceed 5 days
renal toxic starts in 30min-1h, duration = 4-6h 10mg PO q4-6h prn pain max daily dose = 120mg *ULTRAM (tramadol) 50-100mg PO q4-6h prn mod-sev pain. Max = 400 mg/d ULTRACET (tramadol 37.5mg + tylenol 325mg) 2 tabs PO q4-6h prn acute pain. Max = 8 tabs/day X 5d *DARVOCET (propoxyphene + tylenol) 50/325 (N50) 1-2 tabs PO q4h prn pain 100/500 (N100) 1 tab PO q4h prn pain DEMEROL (meperidine) 1-1.8 mg/kg up to 150mg IM/SC/PO or slow IV q3-4h 75mg IV/IM/SC = 300mg PO Random: ETOMIDATE – good to knock out pt for 5-10 min… you cant push this… ER doc has to… 10mg is good… (sedative like Propofol) NSAIDS: COX 1 groups: Salicylic Acid: ASA, diflunisal Proprionic Acid: ibuprofen, naproxen Acetic Acids: ketorolac(toradol), indomethacin, sulindac TORDADOL – Strong, IM / IV / PO 15-30mg q6h Do not exceed 5 days in a row
Renal Fenamates: meclofenamate Oximcam: meloxicam

3 things you will get called for if not in orders: Sleep: Ambien PO qhs prn sleep Pain: * Morphine IV 2-4mg q2-4h prn severe pain * Percocet PO 5/325mg q4-6h prn moderate pain N/V: Phenergan IM 12.5mg q4-6h prn N/V Local Anesthetic Max single Doses (avg 70kg male/60kg fem) Drug Class Max w/Epi Max NO epi Procaine ester 1000mg 750mg Lidocaine amide 500mg 300-350mg Marcaine amide 225mg 175mg 1% soln contains 10mg/ml 0.5% soln contains 5mg/ml 0.25% soln contains 2.5mg/ml Adjustments to Local Anesthetic Doses
Peds Child - Clarks rule: (weight in lbs / 150) x adult dose Infant - Fried’s rule: (age in months / 15) x adult dose EMERGENCY MEDICINES --------------------------------------ESMOLOL – Anti-HTN / B-blocker • Initial dose = 0.25-1.0 mg/kg over 30 sec. EPHEDRINE – Tx hypotension – sympathomimetic • Initial dose = 5-10 mg ATROPINE – Tx Bradycardia / Asystole – Anti-Cholinergic • Initial dose = 0.25 – 1.0 mg o Repeat every 3-5 min, max = 0.03 mg/kg EPINEPHRINE – tx anaphylaxis • 0.3-0.5 ml subQ of 1:1,000 solution, + antihistamine

Systolic Diastolic Rate spO2

Alarm Limits LOW HIGH 85 150 50 100 50 110 92 100

BLOOD CLOTTING --------------------------------------------------DVT: fat forty female smoker Risk factors: IAMCLOTTTTED Immobilization / Iatrogenic / Inflammatory bowel disorder / Inherited / Venous Insufficiency, Arrhythmia, MI / Malignancy / Mother(pregnant), Coagulopathy / CHF, Long term Immobility, Obesity / Old age, Trauma / surgery, Tourniquet, Tobacco, previous Thromboembolic event, Estrogen use, Diabetes Virchows Triad: Endothelial Damage, Hypercoaguable state, Hemostasis Diagnosis: venogram is gold standard, Doppler is non-invasive, Homan’s and Pratt’s sign, apply tourniquet above suspected thrombosis
pain at level of clot in 30-45 sec. PE Dx: gold standard = V/Q scan (ventilation / perfusion), spiral CT is very common 1st line, ST segment depression, dec pO2, pCO2, pH.

Prophylaxis: TED stockings, elevation of legs with knees flexed, early mobilization Heparin 5000 units SQ bid or beginning 1 hour pre-op, then 5000 units SQ q12h until pt ambulates Lovenox 30mg SQ bid Labs: (deficiencies in certain factors will INC. values) PTT – factors 1,2,5,8-12 (all but 7) Intrinsic [norm = 30-45 s] Prolonged in Heparin therapy, Normal in Von Willenbrand dz (7), initiated by factor 12 PT – factors 1,2,5,7,10 (Vit K) Extrinsic [norm = 11-16 sec] Prolonged in liver dz, vit K disorder, Coumadin Bleeding time – inc. in Von Willebrand dz [norm = 1-4 min] Prolonged in all platelet abnorm, norm in coag disorders D-Dimer – nonspecific marker in blood for clotting good to rule out, not in… 0-300 = norm, over 300 is positive * All are produced in Liver except factor 8 (Intrinsic) Platelet Count – norm = 250,000/uL of blood (50,000 = minor bleeding) Treatment: Assess PT/PTT to get baseline, Then IV Heparin 5,000-10,000 units, then 800-1,500 units per hr, maintaining PTT @ 2-2.5 times baseline daily. pt maintained at bedrest with LE elevated above hrt. *It takes approx 1 week for thrombi to become firmly adherent to endothelium and diminish risk of PE. Coumadin is started when long term therapy is planned. Tx 4-6w for calf DVT, and 3-6 months for proximal DVT. Coumadin dose: extrinsic – 2,7,9,10 liver = all but 8 takes 16-48h to cause measurable changes in PT, therefore begin tx 2 days before D/Cing heparin. Don’t start Coumadin until about day 3 of Heparin therapy… D/C heparin when PT is therapeutic. Keep INR 2 x normal Loading dose 10mg qd until PT increases, then smaller dose (5-7.5mg) to maintain PT in therapeutic range. No adjustments for renal failure Lovenox prophylaxis: 30mg SQ bid Lovenox DVT Tx: 1 mg/kg bid Heparin Reversal: Protamine Sulfate 1mg per 100 units of heparin Coumadin Reversal: FFP + Vit K FFP has all coagulation factors in it… **Peri-Op: Heparin – hold 8 hours prior to Sx (monitor PTT) DVT prophylax – give 5,000 u SQ 1hr pre-op, then bid until ambulatory Coumadin – hold 3-4 days prior to Sx (monitor PT/INR) STUFF-----------------------------------------------------------------------------------------------------------------------ASA: 1. Healthy 2. Mild systemic Dz 3. Severe systemic Dz 4. Severe systemic Dz + constant threat to life 5. Morbid, will not survive w/o Sx 6. Brain Dead (organ donor) Mallampati: 1. Entire uvula and tonsilar pillars visible 2. Tip of uvula and pillars hidden by tongue 3. Only soft palate visible 4. Only hard palate visible

History reminders: CC, HPI – onset, duration, type, trauma, radiating, exacerbates, relieves, pain 10/10, previous episodes, severity, previous tx… PMH, Meds, Allergies, Hospitalizations, Illness SurgHx SocHx – smoke, drink, drugs FamHx – DM, HTN, cancer… ROS – gen, skin, nodes, EENT, Breast, resp, cv, gi, gu, heme, endocrine, m/s, psych, neuron Residency Interview System of Thought: remember, they would rather you ask too many questions in the history than not ask enough… they will stop you… don’t ask for stuff you don’t need, cuz then your just guessing… they will let you dig your own hole, but will not lead you astray… On the phone with ER
ask
stable?, fever?, N/V intact?, get x-rays, CBC w/diff, CMP, blood cultures if appropriate (f/n/v, taken from 2 diff spots 20 min apart)… go ahead and get the ball rolling before u get there… 23h admit, IV Abx… start thinking empiric… 1. NLDOCAT – how long ago, where, pain, cause, did you walk on it, NPO status!, tried to treat it yet, something makes it worse, better? Infxn – had an ulcer before?, past Tx for it? Failed oral Abx?... 2. PMH, PSH, All, Med, SocHx, NPO if you forgot 3. Hx of MRSA
Vanc and Zosyn… MRE
Linezolid(Invanz) or Zyvox… 1st time infxn
Unasyn 4. PE: vitals, vasc, neuro, derm, ortho… a. if no pulse
Doppler, if not
TcPO2 b. open wound?, edema, eccymosis, erythema, digits cyanotic c. Probe to Bone? (89% +), undermine, fibrotic, granular, proximal streaking d. odor? (fruity - pseudo, pungeont – gas gangrene), e. drainage – purulent, serosanguinous, serous, dirty dishwater
clostridium f. ortho – dislocated, gross deformity, pain out of proportion, ROM, POP i. piano key test – DF/PF digits
pain = compartment syndrome g. Imaging – XR (most everything), MRI (infxn), CT (calc fx, pilon) h. Labs – CBC w diff, CMP i. Closed Reduction: i. Charnley’s 4 steps – increase deformity, distract, decrease deformity, cast/splint ii. Put on hrt monitor, pulse Ox, O2 (nasal cannula) iii. What was given to pt in ER?? iv. Push 2 & 2 or 3 & 3 mg Morphine and Versed or have ER doc give them Etomodate 5. Be prepared to reverse both of these meds
Naloxone (Initial dose = 0.4 mg. May repeat every 2-3 min @ doses of 0.4-2 mg) and Flumazenil (Initial Dose = 0.2mg. May repeat at 1 min intervals to dose of 1mg) 6. IV Abx, Pain Meds… 7. Schedule for Sx
I & D, Amputation, ORIF… PIMP LIST -------------------------------------------------------------------------------------------------------------1. Indirect dx of exercise induced compartment syndrome? Put sphygmomanometers on each calf and pump up until pt feels pain… affected side will feel pain at ½ of the pressure of the unaffected side 2. Volkman’s contracture? Compartment syndrome
ischemic necrosis
contracture of muscles
can cause HDS if QP is killed by compartment syndrome in Calcaneal compartment… can get renal failure due to myoglobinuria. 3. Arterial supply to talus? In order of significance? PTa, ATa, Perforating Peroneal a. 4. Principles of AO: Anatomic Reduction, Stable int. fixation, Atraumatic Technique, Early and pain free ROM (prevent cast dz) 5. Galvanic Corrosion? Rxn b/t titanium and stainless steel

6. Albumin – rising = anabolic, dropping = catabolic(bad). Renal failure
dec albumin, inc BUN/Creat, dec. urine. 7. TcpO2 – 30 + is ok, ABI over 0.45 is ok, good toe pressure = 30mm Hg 8. RIFLE classification of Acute Renal Failure: Risk – inc in serum creat X 1.5 or dec in GFR by 25% or Urinary Output <0.5mL/kg/h for 6 hours Injury – 2.0, 50%, 12 hours Failure – 3.0, 75%, 24 hours or anuria for 12 hours Loss – persistent ARF – no kidney function > 4wks ESRD – loss of kidney function > 3 months 9. Eponym for nerve medial to 1st mpj? Joplin’s n 10. Phalen’s sign? Compress n X 30 sec
re-create symptoms 11. How much force is required to break the lateral ankle ligaments? According to Attarian et al, the maximum load to failure for the CFL was 2 to 3.5 times greater than that for the ATFL (345.7 versus 139 newtons). 12. Angle between ATF and CF? 105 deg. 13. Post-op course for Brostrom? 3-4w NWB, 3-4w CAM walker, PT @ 6w 14. CFL is extracapsular 15. Brostrom Gould… who came up with what? Brostrom is primary repair of lig’s, Gould is imbrication (overlapping) & suturing of inferior Extensor retinaculum to reinforce… Vest over Pants stitch 16. Rix modification? Anchovie procedure… Keller with interpositional tendon or capsule pulled down into jt. 17. Moberg procedure? Closing base wedge with base dorsal of proximal phalanx of hallux. 18. Difference between community and hospital acquired MRSA? CA - generally susceptible to a wider range of antibiotics (usually susceptible to fluoroquinolones and TMP/SMX. Unlike HA-MRSA, CA-MRSA often arises in children and adults without any obvious risk factors. HA - 52% of S. aureus isolates recovered from patients in ICUs and 42% of S. aureus recovered from non-ICU patients are MRSA. Most are resistant to macrolides, fluoroquinolones, clindamycin, and TMP/SMX. CA-MRSA can be differentiated from HA-MRSA if the person meets all of the following criteria: diagnosis of MRSA was made in the outpatient setting or by a culture positive for MRSA within 48 hours after hospital admission; no past medical history of MRSA infection or colonization; no hospitalizations, admission to a nursing home, skilled nursing facility, or hospice, dialysis, or history of surgery in the past year; and no permanent indwelling catheters or medical devices that pass through the skin into the body. 19. Causes for Peroneal Subluxation? Shallow groove, muscle belly extending into groove, trauma… 20. Peroneus Longus ruptures more often in what foot type? Cavus 21. Will it damage the mechanics of the foot if you repair PB rupture by tenodesis to PB? No 22. Most common location for PL rupture? @ bend under cuboid 23. H & H cutoff for doing surgery? 30 & 10 for elective cases 24. % Muscle strength lost per grade? 50% lost in each grade 25. Ok to use self tapping screws in osteoporotic bone? NO 26. “worm gearing” in internal fixation? Crossing 2 screws and having them purchase eachother
better stability in osteoporotic bone. (to imagine it, hold out your index finger and cross them like swords… that’s how it would look like inside the bone) 27. Talar position in calc fx? Dorsiflexed 28. Deforming force in varus in calc fx caused by? Achilles & possibly sustentaculum tali. 29. 6 P’s of Compartment Syndrome? Pain, Paresthesia (30 min), Paralysis (late), Pressure (over 30mm Hg), Pink (good CFT unless severe case), Pulses (present unless arterial dz) 30. Precipitating factors to DKA? Infxn, omission of insulin, new onset DM 31. Drugs that may induce diabetes? Thiazides, Diuretics, Steroids, Phenytoin 32. What should blood glucose be for DM pt the am of Sx? 100-200 33. Mechanisms leading to HDS? Flexor Stabilization – pronated foot
hypermobility of FF
flexors fire early in gait to stabilize FF
overpower interosseous muscles leading to hammering of digits… Most common etiology Extensor Substitution - EDL overpowers lumbricles
a strait dorsal contracture of MPJ’s

Flexor Substitution – Supinated foot
weak triceps surae
deep muscles try to substitute (TP, FHL, FDL) fire earlier and longer
contracture of lesser digits… Least common etiology 34. AO screw size and order? Over, under, counter, measure, tap, screw… Mini frag – 1.5/1.1 2.0/1.5 2.7/2.0 Small frag 3.5/2.5 4.0/2.5 Standard 4.5/3.2 6.5/3.2 35. Bone Healing Stages Inflammation (2d-1w) – pain = protective, edema = splint Soft Callus (days-2m) – fibrous cartilage forms at each end Hard Callus (3-4m) – begins to ossify if ends are <1cm apart Remodeling (yrs) – callus resorbed, wolff’s law
bone will grow to meet the load placed on it… 35. 2 types of Bone Healing? 1o membranous – haversion remodeling – simultaneous remodeling and formation of bone, little/no motion or callus, good apposition
desirable 2o enchondral – cartilage/fibrous intermediates replaced by bone, involves callus/irritation, motion
NOT desirable 36. Types of Non-Unions? (Weber & Cech) Hypertrophic/Vascular – elephant foot, horse hoof, oligotrophic Tx = stable fixation alone Atrophic/Avascular – torsion wedge, comminuted, defect, atrophic Tx = decortication, bone graft, bone stimulator 37. Bunion Sx to correct high IM and PASA? Bicorrectional Austin, reverdin laird and todd, hohmann, logroscino, Peabody 38. What is Locroscino procedure? Reverdin + Loison-Balacescu. Take wedge from the reverdin and instet into an opening ABductory wedge at the base 39. Significance of Talar neck Fx (Hawkins)? AVN STJ arthritis I – nondisplaced 10% rare II – STJ 30% 60-75% III – STJ/AJ 90% 100% IV – STJ/AJ/TNJ 100% 100% 40. Vascularity to Talus: specific? PTa
a of tarsal canal (most of body)
posterior tubercle vessels DP/ATa
superior neck/head vessels Perf Per a
a of tarsal sinus (plantar neck/head) 41. Fill in the blanks? Dale Austin, DPM & Edward Leventen, MD published in 1981 42. Other classification system of AJ Fx? Ashurst and Bromer 43. Where are the following sweat glands found? Eccrine – palms, soles, axillae Apocrine – axillae, genitals, scent gland, puberty activates Sebaceous – all except palms, soles 44. Primary blood supply to long bones? Endosteal 45. IM nail for fibula? Ruch rod 46. Test for Morton’s neuroma other than Mulder’s? Gauthier’s test – side to side compression with DF/PF toes
pain = + 47. Tx for nail/digit trauma? Subungual hematoma
up to 25% = trephination (drill), over 25% = avulse nail, vicryl close Buddy tape 4-6w with fracture 47. Most common closed digit fx? 5th – bedpost fx 48. Most common complication with crush injury to digit? N entrapment/ lasting pain

49. Gissane’s Critical & Bohler’s Angles? * Gissane’s Angle formed by lateral process of talus and lateral surface of calcaneus. Norm = 120-140. Angle INCREASES in calc Fx

* Bohler’s Angle formed by tent like angulation which the sup/post aspect of the calcaneus makes with sup/ant aspect. Norm = 25-40. Angle DECREASES in calc Fx.

50. At what stage of intrauterine development do the lower limb buds first appear? 5th Week 51. Where is the tubercle of Tillaux-Chaput? Tibial side of the distal tibio-fibular joint. 52. Ligaments making up the Deltoid? Tibio-Navicular Ant. Talo-Tib Calcaneo-Tibial Superficial Deep
Post. Talo-Tib Posterior Talo-Tibial 53. Pneumonic for Diagnosis Options in most cases? TICAN Trauma, Infxn, Congenital, Acquired, Neoplasm 54. Why can’t you give NSAID’s to Asthma pts? COX inhibition converts Arachidonic Acid Pathway to produce more Leukotrienes, which are BronchoCONSTRICTORS! 55. Pyoderma Gangrenosum? Nodule or pustule that breaks down
raised, inflammatory border, boggy, necrotic base, pearly, rolls in, punched out, purulent drainage with hemorrhagic exudate, dusky red/PURPLE border. Associated with inflammatory disorders (Crohns, IBS, UC, RA). Histo – see mostly neutrophils. Tx – oral steroids, sulfa drugs, cyclosporine. PAPA syndrome –Pyogenic Arthritis, Pyoderma, cystic Acne 56. Where can these ligaments be found? Spring – from sust. Tali
navicular tuberosity Short Plantar – from ant. Tubercle of plantar calc.
proximal aspect of peroneal ridge on cuboid Long Plantar – from dist. Posterior aspect of medial calcaneal tuberosity
peroneal ridge (cuboid) and radiating to base of 2-5 MT’s 57. Nutrient a’s to these bones come from what a? Tibia – Post. Tibial a Fibula – Peroneal a Femur – Perforating branch of profunda femoral a. 58. Major pronator of foot? Peroneus Brevis 59. How does insulin work? Stimulates glycolysis & inhibits gluconeogenesis 60. Clinical findings of Osteogenesis Imperfecta? Multiple fx’s and blue sclerae 61. Syphilis caused by? Treponema Pallidum 62. 3o syphilis characterized by? Neuro-syphilis (tabes dorsalis), gummas, argyl-robertson pupil 63. Boney lesions presenting “codman’s triangle”? osteosarcoma and chondrosarcoma 64. Characteristic radiographic findings of: giant cell tumor
“soappy bubble appearance” with lytic borders UBC
fallen fragment sign OsteoChondroma
pointing away from adjacent joint 65. Dosage for: Amoxicillin – 250-500 mg pot id Pen G – 12-24 million u / day divided by q4-6h Timentin – 3.1 gram IV q4-6h Zosyn – 3.375 gm IV q4-6h or 4.5 gm IV q8h Unasyn – 1.5-3.0 gm IV q6h Augmentin – 875 mg po bid Erythromycin – 250-500 mg po qid Vanc – 1g IV q12h (or 125 mg po qid for c. diff only)

Clinda – 600 mg IV q8h or 300 mg PO bid-tid 66. Drugs active against Pseudomonas? Fortaz, Aminoglycosides, Ticarcillin(Timentin), Clindamycin, Imipenem (Primaxin), Aztreonam 67. Peak/Troughs? (ug/ml) Vanc - 25-40 / 10 Gent - 4-10 / 2 68. Which agents would you use for a pt with lime dz? Tetracycine’s 69. According to Ruedi & Allgower, what 4 principle steps must be followed in ORIF of comminuted Fxs of distal tibia? 1. Reconstruction of Fibula 2. Reconstruction of Lower articular surface of Tibia 3. Packing in of cancellous bone 4. Stabilization of medial aspect of tibia 70. Tx for Abx induced Diarrhea? D/C Abx, no anti-diarrheal agents, fluid/electrolyte support, Metro 500 mg po q8h or Vanc 125 mg po q6h 71. Local Anesthetics
Type and metabolism? Ester (met by plasma esterases): Procaine, Cocaine, Chlorprocaine, Tetracaine AmIde (met by liver enzymes) {2 I’s}: Lidocaine, Mepivacaine, Pilocaine, Bupivicaine, Etidocaine, Ropicacaine 72. Maximum Dose of Lidocaine and Marcaine? Lidocaine
4.5 mg/kg………7.0 w epi Marcaine
2.5 mg/kg……….3.2 w epi 73. Abx for MRSA? Vanc, Minocycline, Cipro/Rifampin, Bactrim/Rifampin, Linizolid, Cynercid 74. Dosage for: Ambien – 5-10 mg po qhs prn insomnia (non-BZD hypnotic) Benadryl – adult = 25-50mg po tid prn pruritis Peds = 12.5-25mg pot id prn pruritis Compazine – 50-100mg po q4-6h or 50mg IM q4-6h prn N/V Percocet – 1-2 po q4-6h prn pain 75. Analgesic for Codeine/Morphine Allergic pt? Darvon: 65mg po q4h Darvon-N: 100mg po q4h 76. Thurston-Holland sign? Spike of metaphyseal bone attached to the fractured epiphysis seen in salter harris 2 fractures. 77. Johnson & Strom Classification System? PTTD Stage 1: tendon normal, peritendonitis, mild weakness on single heel raise test, normal hindfoot alignment. Tx = break cycle of inflammation with 3-6 months of rest, NSAID’s, orthoses, synovectomy, tendon debridement, BK cast 3w. Stage 2: tendon elongated, mobile valgus RF, more POP to tendon, FF abduction (TMT sign), marked weakness on single heel raise test, XR signs of pronation, MRI
discontinuity, balling up of tendon. Tx = FDL transfer to nav, BK cast 6w + PT, Kidner, Young, STJ arthroeresis, Evans, Dwyer, Medial slide. Stage 3: elongated tendon, stiff valgus RF, more TMT sign. XR
stage 2 + DJD. Tx = STJ arthroeresis Stage 4: (added by Myerson) AJ involvement
valgus. Tx = pantalar or tibio-talo-calcaneal fusion. 78. What is Basset’s Lesion? Lesion on ant dorsal lateral aspect of articular cartilage of talus caused by rubbing from hypertrophic anterior inferior tib-fib ligament. 79. Brodies Abscess? Foci of bone destruction caused by OM filled with pus or connective tissue. 80. Charcot’s Triad? Symptoms of Multiple Sclerosis consisting of nystagmus, intention tremor, scanning speech 81. Coleman Block Test? Determines if associated varus deformity of the RF is flexible or rigid. Place pts foot on wooden block one inch thick (placing heel and lateral foot on block and medial MT heads off block) if RF corrects, it’s a FLEXIBLE condition. 82. What is a Crescent Sign? Early sign of AVN which represents a subchondral Fx through insertion of the individual trabeculae. 83. Crowe’s Sign? Axillary freckling, pathognomonic for Von Recklinghausen’s dz.

84. LE pathology occurring with Ehlers-Danlos Syndrome? Ligamentous laxity resulting in flat feet, genu valgum, congenital hip dislocation, scoliosis. 85. Possible causes for foot drop? CVA, Trauma, CMT, Polio, Freidrichs Ataxia, Infxn, Guillian-Barre Syndrome, Dejerine-Sottas Syndrome, Spinal Tumor/lesion. 86. What is the Hubscher Maneuver? DF the hallux in WB, the arch will rise due to windlass mechanism if no osseous restrictions are present. 87. What is the Kelikian Test? Tests whether or not the MPJ is reducible. Push up on plantar surface of MT head and see if toe straitens out. 88. Another name for the Intermediate Dorsal Cutaneous N? Lemont’s nerve 89. What is Marjolin’s Ulcer? A SCC that arises in chronic sinus due to OM. Must be long standing tract. 90. What is MosaicPlasty? OATS, Transplantation of cartilage and bone by way of a plug to fill a defect caused by OCD. 91. Name the material utilized to make Abx impregnated beads? Polymethylmethacrylate (PMMA) 92. Requirements for Abx to be used in Abx impregnated beads? Broad spectrum, low allergenic, heat stable, ability to leach from cement. 93. Floor and Roof of Porta Pedis? ABductor Hallucis
floor, Quadratus Plantae
roof 94. Somogyi Effect? Rebound phenomenon occurring in diabetics who take too much insulin in the evening resulting in hyperglycemia in the morning. When blood glucose levels drop too low, the body sometimes reacts by releasing counterregulatory hormones such as glucagon and epinephrine. These hormones spur the liver to convert its stores of glycogen into glucose, raising blood glucose levels. This can cause a period of high blood sugar following an episode of hypoglycemia. 95. Turk’s Test? Test whether n is entrapped due to varicosities beneath retinaculum. + if symptoms increase once tourniquet is inflated above venous pressure but below arterial pressure proximal to site of suspected entrapment. 96. Virchow’s Triad? Stasis, blood vessel injury, hypercoag 97. Valleix’s & Tinel’s sign? V – Proximal. T – Distal 98. Normal WBC count? 5,000 – 10,000 cells/ul 99. Normal Hemoglobin & Hematocrit Values? Male
14-18 g/dl & 40-54% Female
12-16 g/dl & 37-47% 100. What tests are in a CBC w/diff? WBC, RBC, Hgb, Hct, MCH, MCHC, MCV, Platelets, Segmented Neutrophils, Eosinophils, Basophils, Lymphocytes, Monocytes 101. Normal PT and PTT values? PT = 10.1-13.1 sec PTT = 23.5-34.3 sec 102. Tx for Malignant hyperthermia? Stop Anesthetic, Hyperventilate with 100% O2, Cool the pt, Dantrolene sodium. 103. Dosing regimen for Dantrolene Sodium? Intra-Op Crisis: 1mg/kg continuous Rapid IV Push until symptoms subside or max dose of 10mg/kg reached Post-Op Crisis: 4-8mg/kg/day po in 4 divided doses X 1-3 days Pre-Op Prophylaxis: 4-8mg/kg/day po in 4 divided doses for 1-2 days prior to Sx with last dose 3-4 hrs before scheduled Sx. Or 2.5mg/kg IV approx 1hr before anticipated anesthesia. 104. Causes of Post-Op Fever? (5 W’s) Wind (12-24h) – atelectasis, post-op hyperthermia Walk (24h) – Thrombophlebitis, PE Water (2d) – UTI Wound (3d) – Infxn Wonder Drug (anytime) – Drug Fever (PCN…) 105. 4 Reasons for severe intractable pain post-op? Sutures too tight, constrictive dressings, hematoma, ischemia 106. Tx for White Toe after surgery? D/C ice and elevation, place foot in dependent position, loosen bandage, warm compress proximal to N/V bundle, piston/rotate toe on k-wire, local nerve block proximal to area, vascular consult. 107. Differentiate between blue toe due to venous vs arterial insufficiency? Venous
warm & may blanch with pressure. Arterial
cold and does not blanch with pressure. 108. How many grams of carbohydrate are found in one liter of D5W? 50gm

109. Indications for AJ fusion? Arthrosis, severe angular deformity, irreparable acute trauma, bone tumor, chronic OM, failed AJ prosthesis, Paralytic deformities, salvage of avn of talar body. 110. Other name for clubfoot? TEV 111. Primary defect in clubfoot? Talar head and neck 112. Adduction of talar head/neck in transverse plane on body? Norm = 15-20 deg. TEV = 80-90 deg. 113. Types of Clubfoot? Congenital
Intrinsic(rigid) & Extrinsic(supple) Acquired 114. Classic Components of Clubfoot? FF ADDuction, RF Varus, RF or Ankle Equinus 115. AP TC angle, norm and Clubfoot? Norm = 20-40 deg. TEV = 0 deg 116. Factors Delaying Surgical Wound Healing? Local: incisions improperly placed within RSTL’s, Tissue Trauma to Wound lobes, improper irrigation (FB in wound), inadequate hemostasis, desiccation of tissues during surgery, infxn, prolonged dependency, local corticosteroids Systemic: uncontrolled DM, EtOH, malnutrition/malabsorption, steroids, anemia, platelet inhibiting drugs, obesity, age, hepatic dz 117. Goals of AO? Anatomic Reduction, Atraumatic Technique, Stable internal fixation, early active mobilization 118. Ideal fixation for physeal fx’s? smooth K-wire 119. Composition of Orthosorb pin? Poly-O-Dioxanone 120. How are bioabsorbable materials discarded by the body? Degraded by hydrolysis – eventually entering into KREB’s cycle and excreted into urine, feces, or expired CO2. 121. Advantages of biodegradable fixation? Avoids stress shielding or stress protection osteopenia Eliminates burden of secondary procedure Does not lead to image artifacts when using MRI or CT post implantation May be left in sites of infection as implants are bacteriostatic! 122. How long will suture maintain its strength? ~60d 123. Secondary causes of DM? Pancreatic dz, hormonal (cushings, acromegaly, pheochromocytoma), drug induced, genetic syndromes. 124. Diagnostic tests for DM? Hemoglobin A1C, oral glucose tolerance test, fasting BS > 140 mg/dl on more than 1 occasion 125. What is Whipples Triad? Whipple's triad or Whipple's criteria refers to three conditions that are considered by physicians necessary for proving hypoglycemia as the cause of a person's symptoms. 1. 2. 3. 126. 127. 128. 129.

Symptoms known or likely to be caused by hypoglycemia A low glucose (40 or less) at the time of the symptoms Relief of symptoms when the glucose is raised to normal

At what point in BS is pt Hypoglycemic? <50 Dosing for Metformin? 500mg po bid Dx test for DVT? Homan’s, Pratt’s, Doppler, Venograph Dx test for PE? Blood Gas (PaO2 < 80% mmHg with PaCO2 < or = norm EKG
Tachycardia (acutely) V/Q scan
area of ventilation but no perfusion 130. Reversal Agent for Heparin overdose? Protamine Sulfate (1mg / 100u heparin) 131. Peak onset of Coumadin? 3-5d (started once heparin is therapeutic) 132. Best Hematologic index of renal function? Creatinine (CrCl) 133. Dx of Septic Arthritis? Gram Stain, + synovial fluid culture, Juxta-Articular osteopenia after onset (7-10 days)

134. Phases of Technetium-99 Bone Scan? 1. Angiogram (just after injection) 2. Blood Pool (2-5 min) 3. Delayed (2-4 hrs) 4. Fourth (5-24 hrs) 135. Most common organism causing necrotizing fasciitis? Strep Pyogenes 136. Other name for Necrotizing Fasciitis? Hemolytic strep gangrene 137. Nikolsky’s sign? Shearing of normal epidermis in response to lateral pressure in staphylococcal scalded skin syndrome. 138. Organisms causing T. Pedis? T. mentagrophytes, T. Rubrum, E. Floccosum 139. Koebner’s Phenomenon? Replication of skin in pressure areas with Psoriasis 140. Abx for Sx Prophylaxis in PCN allergic pt? Cleocin 600mg IV or Vancomycin 1g IV 141. Dosing for Lamisil? 250 mg/d X 12w (90 days) 142. Sequential Release of hammertoe deformity following ineffective release of contracture demonstrated by Kelikian Test? 1. Arthroplasty at PIPJ 2. Extensor hood resection 3. Extensor tendon lengthening 4. Dorsal Capsulotomy 5. Plantar Capsule release 6. Arthrodesis / flexor transfer to extensor 143. Which cortex is left intact in a peg-in-hole fusion? Dorsal 144. How should administration of colchicine be altered in pt with renal/hepatic dysfunction as well as the elderly? Reduce by 50% 145. Xanthine Oxidase inhibitor? MOA? Allopurinol (for overproducers) Block the final step in urate synthesis 146. Uricosuric? MOA? Probenicid Increase renal excretion of uric acid 147. Dosing for Allopurinol? 300 mg/d 148. Muscles in Layers of Plantar Muscles? 1st – ABDuctor H, FDB, ABDuctor DM 2nd – Quadratus Plantae, Lumbricles All attach in some way to FDL 3rd – FHB, ADDuctor H, FDM 4th – Plantar and Dorsal Interossei th 149. 4 IM angle numbers? Buckholtz and Fallot IM: Norm = 6.47 Pathologic = 8.71 (over 9
symptoms) LatDev: N = 2.64 Path = 8.05 150. Rate of lengthening with Callus Distraction? 0.5 mm/d to 1 mm/d…. 4 x ½ turns per day 151. Normal Angle in Bunion Management? MAA = 15, HI = 0-10, HAA = 10-15, IM = 8-12, PASA/DASA = 7.5, IMA with MT adductus = 8-10 152. Procedure to correct a high HI angle
distal akin 153. The 5 main processes in bone graft healing? 1. Vascular ingrowth (1-2w) 2. Osteoblast proliferation (new bone formation) 3. Osteoinduction (BMP=inducer)(nonosseous tissue produce bone) 4. Osteoconduction (creeping substitution) (bone graft = scaffold) 5. Graft Remodeling (reformation of graft via wolff’s law)

154. Fowler and Philip Angle? Norm = 44-69

>75 = haglunds

Ruch said
if the F/P angle(44-69) + Calc Incl angle (20-52) If the sum is greater than 90
Pathology Pavlov’s Parallel Pitch Lines: Line 1 is the Calc Inclination angle line. Line 2 is Parallel to Line 1 and is at the level of the most superior point of the posterior facet of the calcaneus. If any part of the posteriorsuperior aspect of the calcaneus is ABOVE Line 2, that indicates pathology. 155. Procedures for Haglunds? Keck and Kelly – wedge from post/sup calcaneus Duvries – Transverse bumpectomy via lat. incision Fowler & Philip – transverse skin incision through posterior heel Dickenson 156. Foot type in pseudo-equinus? Cavus 157. Hoke TAL? Triple hemi-section with 1st and last section medially, and the central cut laterally 158. Flatfoot procedures to correct planar abnormalities? Transverse: Evans, CCJ distraction fusion, Kidner - resect accessory navicular/tuberosity, transposition of TP insertion from more lateral navicular attachment to a more plantar navicular attachment Sagittal: Lowman - TA inserts into spring lig, TaloNav fusion, Tal), Hoke - plantar base wedge/fusion of Nav-Cun(1&2) + TAL Miller – Nav-1stCun-1stMT + PT and spring lig advancement using osteoperiosteal flap Cotton – Opening Dorsal wedge in 1st Cun Lapidus – 1st MT-Cun fusion Young – Re-route TA through keyhole in Navicular TAL/Gastroc 159. Compartments and associated muscles? Full length of foot: Medial – ABd H, FHB Superficial – FDB, FDL tendons, Lumbricles Lateral – FDM, ABd DM FF Only: Adductor – Adductor H. 4 Interosseous – 4 Dorsal and 3 Plantar Interossei RF Only: Calcaneal - Quadratus Plantae, PT vessels and n. Communicates with Deep post. Comp in leg 160. Jones Tenosuspension? EHL transferred to neck of 1st MT + Hallux IP fusion. For cavus foot, PF 1st Ray 161. Cole procedure? DF wedge osteotomy Nav Cun jts + cuboid 162. DuVries osteotomy? DF fusion through MTJ for cavus foot 163. Japas osteotomy? Displacement “V” osteotomy through the cuboid, nav, and medial cuneiform

164. Most common jt to go into non-union in triple fusion? TNJ 165. HIBBS tenosuspension procedure? EDL transferred into midfoot. Indicated for functional equinus, prevents hammertoe formation 166. Surgical Procedures replacing ATF in lateral ankle instability? Utilizing PB – Watson Jones, Mini Watson Jones, McLaughlin, Lee Pouzet – PL, Weber – plantaris, Sefton – plantaris and long extensors, Haig – reinserts ATF 167. Surgical Procedures replacing ATF & CFL? Elmslie, Christman-Snook, Winfield, Storen 2, Split PB lateral ankle stabilization 168. Dosing of Ciprofloxacin? What type of drug? 200-400 mg IV q12h 250-750 mg po q12h 2nd gen quinolone 169. A good drug to give a diabetic pt with foot infxn in ER? Zosyn 170. Classification systems for OM? Cierny-Mader, Waldvogel 171. Tx for Necrotizing Fasciitis? 1.2 million U /day of Pen G 172. 7 Rules for Callus Distraction? 1. Maximum preservation of marrow and periosseous blood supply 2. Stable external skeletal fixation 3. A latency before commencing distraction 4. Distraction rate of 1mm/day 5. Distraction in small, frequent steps 6. A period of neutral fixation after distraction 7. Normal physiology use of the elongated limb 173. How many cortices of screw purchase on each side of the fracture are required when fixating the tibia with a plate? 6 (osteoporosis requires an inc in #) 174. Clinical signs of ischemic wound according to UT SanAntonio? Claudication, Rest pain, Absent pulses, Skin atrophy, absence of pedal hair, dependent rubor (or pallor on elevation), non-invasive study criteria: Transutaneous Oxygen < 40 mm Hg ABI < 0.80 Absolute Toe Systolic Pressure < 45 mm Hg 175. Which group of Abx has Achilles tendon rupture as one of its possible side effects? Flouroquinolones (cipro) 176. Physical signs following Achilles tendon rupture? Palpable complete defect of substance of Achilles tendon Enlargement of gap on passive DF Loss of spontaneous PF position of foot Loss of PF power + Thompson test 177. 4 Most common Anaerobic organisms to infect DM wounds? 1. Clostridium 2. Peptococcus 3. Peptostreptococcus 4. Bacteriodes Fragilis 178. Blounts Dz? Osteochondrosis of medial portion of proximal epiphyseal ossification center in tibia causing bowing of leg or legs. Limping and lateral bowing of legs… Infantile (under 6 yo) – caused by early walking and obesity True AVN Adolescent (8-15) – caused by trauma or infxn. No AVN 179. What is INVANZ and what is its dosing? New PCN derivative 1g IV/IM qd 180. Pain meds for pts allergic to narcotics? STUD Stadol 0.5-2mg IV or 1-4 mg IM q3-4h Toradol 10mg po q4-6h Ultram 50-100mg po q4-6h Darvocet 50/325 2 tabs po q4h or 100/650 1 tab po q4h

181. Vassal’s Principle? Mitigated by surrounding ST. When multiple fxs involved, after reduction of initial fx, other segments will relocate into a more favorable position. Accordingly, additional fractures may be fixed with less rigid or invasive methods or they ma not require fixation. (volkmans fx under 30%) 182. Pre-Dislocation Syndrome? Used to describe the acute, subacute, or chronic inflammatory condition of a lesser MPJ that is believed is a precursor to a lesser MPJ dislocation. 183. Who described pre-dislocation syndrome? Gerard Yu and Judge 184. What is the ideal position to fuse the AJ? 0-5 DF, 5-10 external rotation, 0-5 valgus, posterior displacement of talus under tibia
smoother stance phase of gait 185. Ilizarov’s law of tension stress? States that living tissue, when subject to slow steady distraction, can become metabolically activated in both the biosynthetic and proliferative pathways. 186. Latency period recommended for callus distraction? 4-5 days
2 weeks, depending on secondary factors 187. Time required for ex fix to stay in place once length has been achieved via callus distraction? 1:1 ratio (should equal the amt of time it took to achieve length) osseous consolidation should be confirmed radiographically. 188. T or F: Initiation of distraction can be initiated earlier when osteotomy is performed in metaphyseal bone vs diaphyseal bone? T (metaphyseal
7-10 days) (diap
full 2 weeks) 189. T or F: If radiographically visible callus is not noted on radiographic evaluation a few weeks after distraction has begun, the physician should d/c the distraction? F Lengthening process should be continued until desired length is obtained. (once desired length obtained, distraction ceases and immobilization of foot continues until mineralization is complete) 190. Name the Lateral Ankle Ligaments? ExtraCapsular – CFL IntraCapsular – ATF, PTF, Lateral TaloCalcaneal 191. Angle between CFL and ATF? 105 degrees 192. Function of CFL and its orientation in relation to Fibula? Stabilizes talus during ADDuction. Allows for normal supination of STJ. Oriented 20-45 deg from vertical bisection of fibula 193. Differentiating single, double, and triple lateral ankle ligament “tears” utilizing radiographic ant drawer test? Single
5-8mm anterior talar displacement Double
10-15mm Triple
>15mm 194. What is the Tension-Stress Effect? The governing principle that permits the gradual distraction of osseous and ST to achieve lengthening of the skeletal system It is directly affected by rate or frequency of distraction, stability of device you use to assist in distraction, position, and type of osteotomy. 195. Tx and Abx for Rat bites? Clense wounds, Fortaz (Ceftazidine), Oxacillin, Sodium, Flagyl (metronidazole) 196. Dosing for Fortaz? 1g IM/IV or 2g IV q8-12h 197. Specific sequence of release to be performed in the 1st IM space during a lateral release for HAV? ADDuctor H. tendon release, fibular ses. Release, tenotomy of lateral head of FHB, excision of fibular sesamoid 198. Fluid Resuscitation for pts with 3rd degree burn wounds? Quantity of fluid required is proportional to size (kg) and extent of burn as a measure of total body surface area (TBSA) 4 ml per 1% TBSA 1st 24hrs
plain lactated ringers with dextrose 199. Tetanus Prophylaxis in GSW? Previous immunization
0.5ml toxoid No previous
250 units Ig + 0.5ml toxoid

200. Torg Classification of 5th MT fractures: Type 1 – acute fx with absence of intramedullary sclerosis Tx = NWB BK cast Type 2 – Fx with delayed union & evidence of intramedullary sclerosis and widened fx margins Tx = immobilization or medullary curettage plus autogenous inlay bone graft for athletes to expediate healing Type 3 – Fx with non-union and complete obliteration of medullary canal by sclerotic bone Tx = bone graft 201. Treatment for Watson-Jones Fractures of Navicular? I. tuberosity fx
immobilization 4 weeks II. dorsal lip
immobilization 4w, 6w if CCJ injury or MTJ subluxation III. body
closed reduction, ORIF 202. How long before Hawkin’s sign presents on XR? 6-8w 203. What is the name of the lateral hockey stick incision? Palmer 204. Rowe Classification system? I A – Tuberosity B – Sustentaculum Tali C – Anterior superior process fx II A – Beak fx of posterior superior tuberosity B – TendoAchilles avulsion fx of post-sup tuberosity III Extra-Articular calcaneal body fx IV Fx involving STJ without jt depression V Comminuted fx with central or severe depression 205. Essex Lopresti Classification? Type 1
Tongue type 2o fx line extends posteriorly from 1o line to posterior Calcaneal cortex producing tongue type (Vertical force) Type 2
Joint Depression 2o fx line extends posteriorly from 1o line and exits on superior aspect of the calcaneus causing it to impact into body of the calcaneus 206. When are scout foot XR’s required according to Ottowa Ankle rules? If there is pain in the Midfoot and: 1) instability to bear weight both immediately and in ED (4 steps) 2) Bone tenderness at navicular or base of 5th MT 207. What are 3 mechanisms under Lauge-Hansen that can lead to Wagstaffe or Tillaux-Chaput fx? SER - I PAB – II PER – II 208. What are the 2 mechanisms under Lauge-Hansen that can lead to Volkmann’s Fx? SER – III PER – IV 209. Classification system for ankle diastasis without Fx? Edwards and Delee 210. What is the Pankovich classification system for? Maisonneuve fx’s 211. Application of syndesmotic screws? *2 screws to correct diastasis should engage a minimum of 3 cortices in non-lag fashion (3 point technique) *1 screw that engages 4 cortices can be used (4 point) 212. What type of Salter-Harris type injury is the most common acute physeal injury? Type 2 213. What is the Conti Classification used for? MRI – PTTD 214. Eckert & Davis Classification System? (peroneal sublux) Grade I – superior peroneal retinaculum ruptured from fibrocartilaginous ridge. Most Common Grade II – Fibrocartilaginous ridge goes with the retinaculum Grade III – Small amt of bone goes with retinaculum *Skiing is most common method of injury

215. Surgical Procedures for dislocating peroneals? Duvries – shelf cut out of fibula and slid back like a peg Kelly – fibula cut saggitally and rotated to deepen groove Jones – part of Achilles split and attached to fib. thru tunnel Zoellner & Clancy – deepening of the groove 216. What is the key diagnostic feature to distinguish RA from OA? Subchondral osteopenia noted in RA 217. Surgical Procedures for RA? Hoffman – MT heads 2-5 resected Clayton – MT heads and PP bases 2-5 resected Keller – PP of hallux base resection Gocht – PP bases 2-5 resected without MT heads 218. When should NSAID’s be stopped prior to sx? At least 1w 219. Describe one regimen for corticosteroid supplementation for pre-op RA pts? Methylprednisolone 40 mg IM night before Sx 40 mg IV during Sx 40 mg IM night of Sx 20 mg IM am & pm POD #1 20 mg IM pm POD #2 Continue Pre-op routine 220. What is a normal ABI value? 1.0 – 0.9 221. What is an acceptable ABI for a wound to heal post-op? >0.6 222. What is an adequate toe pressure to allow for healing? > 30 mmHg 223. What is an adequate toe pressure to allow elective Sx? Over 40-45 mmHg (norm = 60-80 mmHg) 224. Drug utilized to counteract Versed? Flumazenil 0.2 mg IV over 15 sec, then 0.2 mg q/min prn up to 1mg total dose 225. Phases of Skin Graft Healing? 1) Plasmatic Stage (24-48h) – fibrin layer formed between graft and host which serves to anchor and allow diffuson of nutrients to graft 2) Inosculation Stage (begins @ 48h) – revascularization of graft tissue. Graft will have a PINK HUE 3) Reorganization (continues for months) 4) Reinnervation (can take 1-2 yrs) * 3 and 4 start at the same time… 226. Diaz Classification? Lateral Ankle Ligament injury I – ATF II – CF III – ATF & CF IV – All 3 227. Degan Classification? For anterior process fx of calcaneus I – non-displaced involving only anterior process II – displaced extra-articular fx III – Large displaced intra-articular fx into CCJ 228. 2 tests that should be ordered with calc fx in ER? Lumbar spine and Pelvic XR Urinary Analysis (with fx pelvis, may have severed urethra) Medical emergency 229. Kuwada Classification? Achilles tendon tears on MRI I – Partially torn tendon (50%) II – Less than 3 cm tear in tendon
tx by sew end to end III – 3-6 cm gapping
graft IV – over 6 cm gapping
graft 230. 3 types of stitch for Achilles tear? Kessel, Bonnel, Krakow

231. 4 types of Gastroc Recession? Strayer, Vulpiun, Baker, McGlammry 232. Islan’s Dz? Osteochondritis of 5th MT base 233. Bushke Dz? Osteochondritis of cuneiforms 234. Goal of reduction in talar neck fx? < 2mm of displacement 235. Gold Standard for Tx of Hawkings Fx? ORIF w lag screws 236. 3 Elements influencing spontaneous (indirect) healing of bone? 1) Callus precursor – Granulation tissue forms first around the fragment and later between the fragments 2) Resorption – Fracture gap widens due to surface resorption of fragment ends 3) Filling of gap with new bone – bone formation progresses through a series of different steps from granulation tissue to cortical bone (indirect bone formation) Achieved through a process of internal remodeling of haversian systems. 237. What is the only process resulting in solid union in primary bone healing? The process of internal remodeling of the haversian system, uniting the fragment ends… 238. Causes of Hypertrophic and Atrophic Non-unions w Tx? Cause Tx Options Mechanical condition correct internal Hypertrophic of strain stability w splint or ORIF Atrophic/ Non-reactive

Impaired capacity for Biological Rxn

Apply bone graft + mechanical Stability

239. Phases of Wound Healing? Inflammatory Phase (1-7d) Influx of platelets & leukocytes
coagulation Release of cytokines and mediators Proliferative Phase (5-20d) {Re-epithelialization} Collagen fibers are produced
wound strength Angiogenesis, Fibroplasia, Wound Contraction Remodeling Phase (3w – 2y) Deposition of matrix materials, collagen deposition/remodel As long as scar is erythematous, remodeling is occuring 240. Which screws should be applied 1st in a pre-bent plate? The 2 inner screws (closest to the fx line) 241. When applying a buttress plate, where do you begin screwing? From middle outward 242. How many compartments in the foot? 9, according to Manoli and Weber 243. A devastating Degenerative dz of UMN’s and LMN’s? Amyotrophic Lateral Sclerosis (ALS) (Lou Gehrig’s dz) 244. Ages and Frequency of Tarsal Coalitions? #1 STJ(middle) 12 - 16 yo #2 CN bar 8 – 12 yo #3 TN 3 – 5 yo 245. Rigid Flatfoot Triad? Peroneal spasm, Stiffness, Pain
all can indicate tarsal coal. 246. Best radiographic view for CN bar? Med Oblq 247. At what age would sx intervention for a persistently painful CN bar be performed? Before age 14 248. Pre-Axial vs Post-Axial Polydactyly and most common? Pre – duplication of hallux or medial aspect of 2nd Post – Duplication of lat aspect of 2nd or anything lateral… Occurs in 80% of cases * Sx should be postponed until over 1 yo

249. Difference between UMN and LMN lesions? UMN LMN Voluntary control lost lost Tone spastic flaccid Reflex arc present absent Pathologic reflex present absent Atrophy little or none significant 250. What percentage of cavus foot pathology is linked to neurological problems? 75% 251. Neurological dz leading to “onion bulb” formation of the peripheral nerves leading to distal weakness and sensory loss? Dejerine – Sottas dz (hypertrophic interstitial polyneuropathy) Nerve enlargement is frequently palpable Nerve biopsy reveals concentric proliferation of Schwann cells around area of demyelinization. 252. Effects of oral corticosteroids on WBC count? Acute/Short term – Increases WBC count
rule out other causes
UTI, Pneumonia, Cdiff… *Once taper down is complete from dose of steroid, WBC will stay increased, but taper down as well for another 2 weeks. WHY!?!?!
NOBODY FRIGGIN KNOWS!!! Chronic use – Decreases WBC count along with immune system… 253. Neurological dz with weakness of LE anterior and lateral compartments, later upper extremity weakness primarily ulnar nerve distribution, beginning in late childhood/early adolescence and rapidly disabling? FREIDRICH’S ATAXIA 254. Neurological dz compares to CMT with addition of resting “tremor of the hands” and clinical finding of areflexia, intrinsic-pedal muscle atrophy, pes cavus, clumbsy gait, and poor equilibrium? ROUSSY – LEVY SYNDROME 255. Neurological dz resulting in abnormal lipid metabolism wherein phytanic acid accumulates in serum with associated findings of ichthyosis, night blindness, and preceeding febrile illness with peripheral muscle paresis, areflexia, dropfoot, pes cavus, and claw toes? REFSUM’s DISEASE 256. The 5 different types of spinal dysraphism (myelodysplasia)? Spina Bifida Spina Bifida Occulta Spina Bifida Cystica Meningoradiculocele Meningomyelocele 257. Neurological dz characterized by progressive disorder and cytoplasmic eosinophilic inclusions in neurons of substantia nigra? Parkinsons Dz
characterized by rigidity, resting tremor, bradykinesia, loss of postural reflexes, and festinating gait 258. Dz affecting anterior horn cells (LMN) of spinal cord, resulting in LE flaccid paralysis (areflexia, hypotonia, and weakness)? POLIOMYELITIS
central nervous system defect is non-progressive, however leaps to contracture that changes over time… 259. Neurological dz characterized by inflammatory demyelinating plaques in white matter of CNS and course relapsingi and remitting with ataxia, scanning dysarthria, and intention tremor? MULTIPLE SCLEROSIS 260. Dz with Ach receptor antibodies destroying the receptor site on postsynaptic membranes with hallmark of exercise induced fatigue? MYESTENIA GRAVIS 260. Radiographic angles of clubfoot? Kite’s(TC)
0-15 (norm = 20-40) Calc Inc A
~17 (norm = 20-25) Talar neck relative to body: Adduction
80-90 (norm = 10-20) Plantarflexion
45-65 (norm = 25-30)

261. Muscles innervated by medial plantar nerve? Lat. Plant N? Medial Plantar Nerve Lateral Plantar Nerve ABductor Hallucis ABd. DQ brevis FDB Quadratus Plantae 1st Lumbricle 2nd - 4th Lumbricles FHB ADDuctor Hallucis Flexor DQ brevis Plantar interossei 3rd & 4th Dorsal interossei 262. Coxa Valga? Angle of femoral inclincation > 128 deg Most commonly secondary to dysplasia of femoral head & usually bilateral Occurs concomitantly with Genu varum 263. Coxa Vara? Angle of femoral inclination < 120 deg Can occur secondary to trauma or abnormal development of femoral head and neck Common etiology of this condition is “slipped femoral epiphysis” May occur with Genu Valgum (knock knees) 264. Normal angle of femoral antetorsion (declinatation)? Birth
30-35 Adult
10-12 265. Femoral retrotorsion (external femoral torsion)? Femoral declination angle < 10 deg Knee jt deviated externally 266. Normal malleolar position and tibial torsion? 13-18
malleolar 18-23
tibial torsion ** tibial torsion is 5 degrees more than malleolar position 267. DOC for Clostridium? Pen G 268. DOC for E. Coli? Ampicillin + Gent 269. DOC for Klebsiella? Cefazolin 270. DOC for Salmonella, Shigella? Ampicillin 271. DOC for Staph. Aureus? Nafcillin 272. DOC for Staph. Epidermitis? Vanc 273. DOC for Strep (non-group D) Pen G 274. Carcinoma developing over chronic, non-healing wounds or ulcers? SCC 275. Most common skin cancer, with 4 types including__ and appearing as shiny nodule with surface telangiectasia? BCC Superficial, Pigmented, Nodular, Morpheaform 276. DOC for animal bites? Augmentin 277. What will decrease specific gravity? Diabetes Insipidus 278. _____ Protein is specific for Multiple Myeloma? Bence-Jones 279. WBC counts and difference between Leukopenia/-cytosis? LeukoPENIA (<4000) LeukoCYTOSIS (>10,000) Overwhelming infxn Bacterial infxn Viral infxn Inflammatory process Hypersplenism Tissue Necrosis Bone Marrow Depression Physical Stress 280. WBC INCREASE in Viral Infxns? MONOcytes & LYMPHOcytes 281. WBC INCREASE in Allergic Rxn? Eosinophils & Basophils 282. Hct DECREASES in? (% vol. of RBC’s in sample of anticoagulated blood) Anemia & Blood Loss

283. PT INCREASES in? Vit K Deficiency Biliary Obstruction Deficiency of Extrinsic or Common pathway factor Liver Dz Coumadin tx 284. PTT INCREASES in? Hemophilia A & B Von Willebrand’s Dz DIC Deficiency of Intrinsic or Common Pathway Factors Liver Dz Heparin tx 285. INCREASE in ALK PHOS? Liver & Bone dz Healing Fx / Bone growth HyperPTHism Obstructive Biliary Dz 286. Serum Creatinine INCREASES in? Renal Dz & Nephritis 283. Lactate Dehydrogenase is a reliable test for ____ when viewed with other tests? MI (elevated 12-24 hrs after MI) Pulmonary Infarction 284. What will Increase specific gravity? Dehydration, Fever, Vomitting, Diarrhea
ALL VOL. DEPLETION 285. Lowman? What plane Corrects? TNJ fusion, TAL, Transfer of TA under Navicular & sutures into Spring Ligament
SAGITTAL PLANE 286. Cotton? Which Plane Corrects? Opening dorsal wedge in 1st Cuneiform
Sagittal 287. Miller? What plane? Nav-1st Cun-1st MT fusion PT and Spring Lig advancement with osteoperiosteal flap
Sagittal 288. Which plane does a Lapidus Correct? Sagittal 289. Orientation of 2 semi-elliptical incisions in 5th digit derotation arthroplasty? Proximal-Lateral to Distal-Medial 290. Which bone scan is best for subacute and Chronic Bone infxn? GALLIUM 291. Why does cigarette smoking affect bone healing? Nicotine
vasoconstriction
less blood gets there
also inhibits osteoblasts CO
binds hemoglobin molecule irreversibly and stronger than O2
less oxygen in blood 292. Why cant aminoglycosides work on anaerobes? They require oxygen to cross cell memrane 293. Seeing Glass in the foot? Fragments as small as 0.5 mm seen if not obscured by bone No fragment larger than 2mm is completely obscured 294. Localization of FB? Place 3-4 different sized needles 90 deg from each other and take intraop XRs. Hemostasis is key 295. Most frequently encountered FB in foot? Needle 296. Best for seeing wood? CT is 100x more sensitive than XR 297. Plantar Fibromatosis resection? 5mm on all sides at least 298. Normal Compartment pressure in foot? Less than 6 mmHg 299. % of Calc Fx that induce compartment syndrome? Up to 10

300. Pressure Dx for Compartment syndrome? 30 mmHg or 10-30 mmHg BELOW Diastolic BP *HypOtensive pts can get compartment syndromes @ sub-normal pressures, so always check diastolic! 301. Intra-Op tx to prevent superficial infxn after trauma? 5% Acetic Acit (vinegar) to kill Pseudomonas 302. Surgical Technique for compartment syndrome? 3 incisions 2 dorsal incisions over 2nd and 4th MT down to bone Get med, lat, and interosseous compartments 1 medial incision (6cm long) center of incision should be 2cm distal to med mal. Get med, adductor, superficial, and calcaneal 303. Post op care of Foot Compartment Syndrome? Leave open 3-7d, delayed primary closure or split thickness skin graft(20% of time) 304. Watershed area of TA? 2-6cm proximal to insertion (72% of ruptures) 305. Dx of TA rupture? Palpable dell, Thompson/Simmons test, obliteration of Kagers triangle, Toygar’s Angle less than 150o
the angle of the posterior skin crease of the TA). Arnar’s sign
TA is angled Away from calc in Insertional zone, and is angled Toward the Talus in the Supracalcaneal zone 306. Re-Rupture rates with and w/o Sx? Whats better? W/Sx = 5.4% W/O Sx = 12.7% DO SURGERY 307. Post-Op Care? Early Mobilization
decreases adhesions and makes tendons stronger
More mature collagen, orient collagen fibers parallel to tendons longitudinal axis, which inhibits adhesions around tendon, increases tendon strength, vascularity, and number of collagen fibers. DO NOT CAST! 308. Crisman-Snook? PB is cut proximally and left attached at insertion. Then is threaded thru fibula from anterior to posterior, down thru calcaneus from posterior to anterior and then re-attached back to itself as it courses into the fibula anteriorly. Re-constructs ATFL and CFL. 309. Brachymetatarsia? Most common is 4th, associated with (Pseudo and PseudoPseudo HypoPTH, polio, downs…), 25x more common in Females. 310. According to Ilizarov’s data, can distraction osteogenesis increase the blood supply to an entire limb? Yes, by as much as 330%. 311. Why should cortiotomies be performed metaphyseally? The bone is wide, and mainly cancellous, therefore new bone will have a wider cross-sectional area. Also, the nutrient artery has already branched and is thus easier to preserve. Also, muscles with origins and insertions at metaphyseal regions are already adapted for extremity growth under the influence of epiphyseal growth zones. 312. Do an oblique or transverse cut for corticotomy? Oblique, because the surface area of growth will be much more, therefore increasing the regenerative process. 313. Talo-Crural Angle? {8-15o} *Used to determine normal Lateral malleolus alignment and length. 1 line is drawn along tibial plafond, the other is drawn connecting the distal aspects of the malleoli. Alternate method: line 1 is drawn perpendicular to tibial plafond, and the other is the intramalleolar line. {83 +/- 4o} *Angle should be within 2-5 degrees of the opposite side by either 314. Talar Tilt on stress AP? 6-8 deg difference = rupture 315. Evaluate for Medial ankle sprain? Medial clear space on Mortise should be less than 4mm 316. Test for Diastasis intra-op? Cotton test, bone hook around fibula and pull
if lateral shift of talus over 3-4mm, then fix 317. Stress XR for chronic lat ankle instability? 5 deg difference in inversion values = pathological If over 18 deg, then double ligamentous injury Anterior drawer subluxation if greater than 4mm 318. % of calcaneal fx associated with spinal fractures? 10-20%, most commonly L1 Always get lumbar spine, hip, and knee views as well as UA for possible bladder trauma. 319. Name of the fragment of calc fx attached to TA? Tuber

320. Triple or Wedge procedure for severe Cavus? If tibioplantar angle is Greater than 120o, then do Triple Tibioplantar angle is between long axis of tibia and plantar surface of foot. 321. Burn Classification? 1st Degree: sunburn/down to papillary dermis, no bullae 2nd : Deeper dermis, Bullae, painful, red/moist skin If over 15% of TBSA
admit 3rd: SubQ fat, destroy dermal structures, painless, chared If over 2-5% of TBSA
admit 4th: Exposed bone/tendon *any plantar 2nd/3rd deg burn
admit *any burn on pt under 2 or over 60
admit *any electrical burn
admit 322. TBSA (Total Body Surface Area) Rule of 9’s Trunk = 18%, Leg, arm, head = 9% each 323. Tx for Burns: 1. Fluid Replacement: LR’s for 1st 24 hrs, calculate volume with Baxter’s formula: 4 x (%TBSA) x weight(kg) = mL 1st/2nd 4h period
give ¼ of total each 3rd/4th ¼ of total are given at 8 hour intervals after 2nd dose *after 24h, give albumin + D5W @ ½ Original volume 2. stabilize fx, tetanus toxoid, Abx 3. get labs (electrolytes, Hct, BUN/Cr) 4. EKG if electrical burn 5. Sx – escharotomy, fascial release for Compartment synd 6. CFT checked q1-2h, dressing changes qd/bid, pain meds, elevation/splinting, PT for ROM 324. 3 most common bugs on burns? Pseudomonas, STREP, Clostridium 325. Normal Angles for Flatfoot Evaluation? Lateral: Pronation TaloCalc: 38-42 Inc Talar Dec: 21 Inc Calc Incl: 18-21 DEC Cyma line Ant displaced DP: TaloCalc: 17-22 Inc TaloCub: 17-25 Inc FF aDD: 12-15 DEC Less Tarsal: 5 aBD Inc Talo1st: 5-10 Inc 326. Order of Reduction in the treatment of Cavus? 1. ST release (Steindler strip) 2. RF fusion and osteotomies (dwyer, triple) 3. Midfoot fusions and osteotomies (Cole wedge = dorsal closing wedge, Japas V – cut midfoot in half with chevron) 4. MT/Digital sx (DFWO, digit fusions) 5. Tendon transfers (jones, hibbs, heyman, STATT, TPTT)
FF sx is NOT indicated until RF is fixed first! 327. Ruch Classification of Cavus? I: MT, MPJ’s, Digital cavus Tx = digit fusions, MPJ release, tenotomies, flexor transfers II: Rigid PF 1st ray + RF varus Tx = DFWO, Dwyer (closing pronatory), STATT (half of TA is relocated to lateral foot), Peroneal Stop (suture PL to PB) III: Severe Global RF and FF
N/M origins normally Tx = osteotomies, triple, tendon transfers

328. Tendon Transfers for Cavus? Jones – EHL sectioned and fused to 1st MTh c HIPJ fusion Hibbs – section EDL, attach to 3rd Cun + digit fusions Heyman – EDL relocated to MT bases + digit fusions STATT – lat ½ of TA relocated to lat side of foot TPTT – thru interosseous membrane to 3rd Cun (out of phase) Peroneal Stop – PL sectioned & fused to PB 329. Structures cut in Steindler Stripping? Plantar fascia, 1st layer of plantar muscles, long plantar lig. 330. Types of Plating Technique? Neutralization – protects an already reduced fx that has an interfrag screw already in place. It protects the reduced and stabilized fracture from shear, flexure, and torsion. All screw holes are drilled Concentrically. Axial Compression Plate – must be “pre-bent” away from the bone cortex. The fx must be relatively transverse as oblique fractures will shorten and displace. 1/3 tubular plate must be eccentrically drilled (load screw principle). When the screw head “seats”, it will bring the near cortex closer to the fx line, thus giving compression. Dynamic Compression Plate – thick plate. Holes are designed in oval shape that slope to allow creation of axial compression as the screws seat. The only holes that must be eccentrically drilled are the 2 closest to the fx. Once those are drilled and screws are seated, the rest can be concentrically drilled. Must be well-molded to bone. 1/3 tubular plates work best. Buttress Plating – used for unstable fx to maintain alignment of fragments despite lack of stability within injured bone. Gap healing may occur. Essentially serves as a bridge between larger fragments with intervening small fragments leaning against the plate. Devitalized bone should be replaced by cancellous graft under protection of the buttress. Tension Band Wire – Combines splintage of 2 smooth k-wires with stainless steel wire tension, to effect dynamic interfragmental compression. Dynamic interfragmentary compression is created with an eccentrically positioned tension wire used in conjunction with a load beam that converts the tension in the wire to compression across the fracture, usually requiring joint positioning that effects wire tension. Good spots for this are base of 5th, malleolar, and patellar fx’s. Can be done with plate as well if placed on convex side of bending bone. Used in a relatively neutral mechanical environment. This principle resists forces and uses them to enhance stability to the fixation site. Necessary external load will keep the fracture site together. Device is applied to tension side of bone to resist force on compressions side. 331. 1 unit of blood will raise the Hct how much? 3 percentage points 332. How much fluid does the avg full bladder contain? 400mL 333. Minimum water requirements for most pts? 2000 mL/day 334. Calculate Input of fluid per DAY? 1st 10 kg x 100 mL = 1000 mL + 2nd 10 kg x 50 mL = 500 mL + Remaining kg x 20 mL = ____ = per day • eg 70 kg man: o 1000 + 500 + (50 x 20 = 1000) = 2500 mL/d 335. Calculate Input of fluid per HOUR? 4 2 1 Rule: 4cc x 1st 10 kg = 40 + 2cc x 2nd 10 kg = 20 + 1cc x remaining kg = ___ = per hr eg 70 kg man: 40 + 20 + (1 x 50 = 50) = 110 cc/hr Typical rate is 100 cc/h
consult cardio/nephro if dialysis or CHF pt

336. Why does Lidocaine work faster but last less time than Marcaine? Lidocaine is closer to the body’s natural pH (7.4), therefore it acts more quickly, but it is also metabolized faster for the same reason. Marcaine is more basic, and thus takes longer to convert to a more natural pH so the body can absorb it… 337. What Diabetic Drug is contraindicated when administering IV iodinated contrast to a pt? Metformin (Glucophage) – may cause kidney damage if combined with contrast. Should hold metformin 48 hours before and after, with after being more important to withhold. The reason so if the pt goes into renal failure from contrast, the pts kidneys will not be further harmed by more metformin to deal with. If metformin DOES build up in the kidneys, can cause fatal lactic acidosis. 338. Tests to perform in office if u suspect LisFranc injury? FF Abduction stress views (under fluoroscopy if u got it) with ankle block. Look for Fleck sign. 339. How does pH affect K+ levels in blood? Acidosis
K+ shifts out of cells
Inc [K+] & vice versa Potassium Exolate gets rid of K+ 340. Perioperative Diabetic Medication Management? IDDM: if on Long acting insulin
take ½ dose in am If no Short acting insulin
hold day of Sx NIDDM: Well controlled
d/c orals am of Sx If on Chlorpropamide or Metformin
d/c 24-48h pre o Risk of lactic acidosis if patient develops renal problem perioperatively Not well controlled
insulin + glucose infusion IV fluids intra-op: D5W/0.45 NS to prevent hypoglycemia 341. DM pt morning of Sx? Check K+ levels
Insulin dec. serum K+ Diet controlled Diabetic < 200 mg/dl
no meds needed Diet controlled Diabetic > 200 mg/dl
consider regular insulin Type 2 Diabetic < 150 mg/dl
stop meds morning of surgery Type 2 Diabetic 150-250 mg/dl
take AM dose of oral agent Type 2 Diabetic >250 mg/dl
start regular insulin 342. Post-Op management of DM pt? Check post-op BS levels – 150 - 199 mg/dl
give 2 units regular insulin – 200 – 249 mg/dl
4 units – 250 – 299 mg/dl
6 units – 300 – 349 mg/dl
8 units – 350 – 399 mg/dl
10 units – > 400 mg/dl
12 units Regular oral and insulin therapy may be started again when the patient begins eating 343. HypoLipidemic Agent Peri-Op Management? 3 types: HMG-CoA reductase inhibitors (“Statins”), Bile acid resins, Fibrates * Discontinue 1 day before surgery and re-start the day after surgery, UNLESS IT”S A STATIN. Recent studies have shown that “statins” benefit patients during surgery by preventing vascular events through other mechanisms (plaque stabilization, decreased inflammation, decreased thrombogenesis) Continue Statins 344. Hypertensive Medication Peri-Op management? β-Blockers (Lopressor, Corgard, Tenormin), α-2 agonists, Ca ++ antagonists (Procardia), and ACE inhibitors (Capoten) can all be given the am of Sx, unless pt is taking ACE and is hypOtensive or taking the med for heart failure. *Sustained arterial HTN damages blood vessels in the kidneys, heart, and brain
increased incidence of renal failure, coronary disease, cardiac failure and stroke.

345. Post-op HTN episodes caused by? Pain, Reaction to endotrachial tube, Volume overload, Emergence excitement – Treated by eliminating cause and if necessary, giving sub-lingual Procardia, IV diuretics, nitropatch, sublingual nitroglycerine, or nitroprusside. 346. Dosing Regimens of Steroids? 1) Alternate Daily Dosing: Less side effects, though less effective 2) Daily Low Dose: <15 mg prednisone daily – Used for inflammatory arthritic processes – Most common dosing schedule 3) Daily High Dose – >15 mg prednisone daily – Used for life threatening autoimmune diseases 4) Pulse Methylprednisone: Used as “last resort” therapy – 1 gram IV over 45 minutes 347. Who Needs Perioperative Steroid Tx and Why? * Any pt taking at least 5mg/day of prednisone (or equivalent) for at least 5 days within the past 2 weeks or at least 1 month of sustained cortocosteroid therapy within past year considered at risk for acute post-op adrenal insufficiency * Without dose, pt may not be able to respond to surgical stress, resulting in consequences such as hypotension or death * Plasma ACTH and cortisol, urinary free Cortisol, and urinary metabolites of cortisol INCREASE in response to surgery, trauma, and other forms of critical illness in the otherwise healthy pt. 348. Perioperative Steroid Tx Regimen? NEW RECOMMENDATIONS Minor Sx Moderate Sx Stress Major Sx Stress Stress 50-75 mg 100-150 mg Daily Total 25 mg hydrocortisone hydrocortisone hydrocortisone equivalent/day equivalent/day x 1-2 equivalent/day x 2-3 days days Normal PO prednisone Pre-op dose or 10mg IV/20-25 25 mg IV/50 mg PO 50 mg IV hydrocortisone mg PO hydrocortisone hydrocortisone for non-dependent pts Case-Dependent Case-Dependent Intra-op None (Usually 25-50 mg ) (Usually 25-50 mg ) *If complicated, 25 mg *POD 1:12.5-25 mg *POD 1: 50 mg IV Post-op post-op IV /25-50 mg PO hydrocortisone q 6-8 h for *If uncomplicated, next hydrocortisone q 6-8 h 24-36 hours post-op day return to normal *Taper to prior *Taper to prior regimen dose. regimen over 1-2 days over 2-3 days 349. PeriOperative Anti-Rheumatic Drug Therapy? Most metabolized through kidneys, so check those pre-op. If kidneys ok, no need to change. If diminished, hold 1-2 weeks pre-op. 350. Peri-Op Warfarin/Coumadin? (UFH = unfractionated hepar.) 1) D/C oral Warfarin 4-6 days prior to surgery and monitor INR 2) If difficulty getting INR < 2.0, reverse oral anticoagulation with Vit.K (24-48 hours pre-op) or Fresh Frozen Plasma (immediate reversal) 3) Bridge with UFH / LMWH until 6-12 hours pre-operatively 4) Resume UFH / LMWH after 12 hours post-op along with warfarin 5) D/C UFH / LMWH when warfarin reaches therapeutic levels

351. Anti-Platelet Medication Peri-Op management? *Recommended to D/C aspirin, clipidogrel, or ticlopidine at least 5-7 days pre-operatively. – Reinstitute them when bleeding risk has diminished (adequate clotting has occurred) – Irreversibly inhibit platelet aggregation by inhibiting certain components of the clotting cascade (COX, TXA2, ADP-binding sites) – These effects last for the lifetime of the platelet (10 days) and takes at least 7 days for platelet function to return to 70% of normal (3 days for most NSAIDS). *Short acting NSAIDS (ex. Ibuprofen) should be stopped at least 1 day before surgery, while longer acting agents (ex. Naproxen) should be D/C at least 2-3 days pre-op. – Even though platelets lack COX-2, specific COX inhibitors such as Celebrex should still be stopped 2-3 days pre-op because of its effects on renal function. 352. Nerve Injury Classification? Neuropraxia: inject into n, recovery = 2-3 months Axonotmesis: axon cut, wallerian degeneration, rec is 2-3m if it happens Neurotmesis: Complete severance of n, irreversible 353. AO stands for? Arbietgemeinshaft fur Osteosynthesisfragen. In 1958, 15 swiss doctors agreed on this. 354. Osseous Stabilization laws? Wolf’s Law – bone produced under compression and resorbed under tension Piezoelectric effect – Compression leads to electro – and tension leads to electro + charges. - = bone formation Pauwel’s principle – Eccentric loading of bone causes one side under tension and the other under compression Vassal’s principle – Reduction of major fracture components leads to reduction of smaller components by ST. Hook’s Law – Amt of strain on bone is directly related to stress applied to bone. This is why we put pt in Sx shoe 355. Fx Stability Classification? Intrinsic: Charnley’s Classes I: transverse fx (most inherently stable) II: LONG oblq, spiral, or comminuted Fx are Unstable III: Potentially stable fx (SHORT oblq) when orientation is less than 45% from transverse axis of bone 356. Rule for screw vs bone size? Never use a screw greater than 40% of the diameter of bone 357. How much skin can you remove and still be able to close? 3:1 RULE
Length:Width • If less than 3:1, incision will have too much tension and will not close! 358. Probe to bone test %’s 66% sensitive, 85% specific, 89% predictive value 359. ESR for Dx of OM? ESR of 70 mm/h, 89.5% sensitive, 100% specific & positive predictive value. 360. Drago, Oloff, and Jacobs Classification of HL? Grade I: Functional, no DJD, passive ROM ok, loaded will be diminished ROM Grade II: Joint Adaptation, flattening of head, OCD, pain on EROM, passive ROM limited, dorsal exostosis, eburnation, lipping Grade III: Jt Deterioration, grade 2 but worse +, non-uniform narrowing of jt, CREPITUS, subchondral cysts, pain on FROM Grade IV: Ankylosis, Hallux Rigidus (<10 deg), deformity 361. Etiologies of HL? Long 1st, MPE, Hypermobile 1st, Gout, short 1st, trauma, septic, charcot, iatrogenic (mis, shortened MT, keep immobilized too long, avn) 362. 1st MPJ normal ROM and diff b/t func and structural HL? Unloaded = 65, Loaded = 20 Functional = only loaded is diminished, structural = both

363. Sx for HL? Cheilectomy Kessel & Bonney – for long pp or PFed Hallux – closing base wedge with base dorsal from base of pp of hallux Waterman – CBWO c base dorsal in 1st MTh Waterman/Hohmann – cut plantar cortex and realign head Regnauld(Enclavement) – cut out base of pp, reshape it, shorten pp, and replace base. Decompresses jt Youngswick Lambrinudi – CBWO c base plantar in 1st MTb (tx MPE) Keller Velenti – Mayo/Keller Fusion – 10-15o ABD, 15-25o DF, parallel to 2nd digit Implants – total, hemi, swanson 364. Stages of HAV? 1) Lat displacement of pp relative 1st MTh, sagittal groove/sulcus forms 2) Hallux ABductus, PASA inc, HDS of 2nd, EHL/FHL are bowing out into interspace, Abductor H slips plantarly
tibial sesamoid position #4
no cristae 3) INC IM angle, cuneiform split 4: Subluxed or Dislocated hallux, RA, 2nd toe lost buttressing power. 365. Reverdin? Green – shelf, corrects PASA Laird – shelf, IM and PASA
moves head Todd – shelf, IM, PASA, MPE
PF’s 1st MTh 366. Shaft osteotomies? IMA of 15-17 Scarf, Vogler Mau – proximal plantar to distal dorsal strait line Ludloff – opposite of Mau (would make an X thru bone if both were done) 367. Base Osteotomies? IMA of 18+ Loison Balacescu – CBWO c base lateral, intact med cortex Juvara – CBWO c base lateral, but oblique (A,B1,B2,C1,C2) 368. Bunionectomy Screw? 4.0 cancellous c 5.0mm head, partially threaded and total length, 16mm-52mm Normal 4.0 cancellous c 6.0mm head, 10mm-100mm 369. TRUE IM angle? = IM(measured) + (MAA – 15) 370. Synovial Sarcoma? Most common primary malignant tumor arising in foot 20-40 yo, grows slowly with metastases Tx = wide resection or amputation Survival rate = 5 years 371. Types of Autografts? Split Thickness – epi and part of dermis – most common Thin: less than 15 thousandths of an inch thick Revascularize quicker, contracts more Less elastic, mesh to allow drainage Thick: 0.016-0.020” thick – hard to vascularize Full thickness – epi and dermis, but no subQ Contracts less, harder to revascularize Better for WB or flexure points Skin Flap – transplanted neurovascular structures Composite Graft – skin and other tissue (bone, tendon, cart)

372. Skin Graft Healing Stages? I: Plasmatic Stage – (24-48h) Anchors graft with fibrin, granulation then replaces fibr II: Inosculation/Revascularization – (48-72h) Vasc proliferation, Anastomoses from bed, not edges PINKING UP Lymph drainage by day 4 Circulation by day 7 III: Reorganization/Epidermal Proliferation – (1w-months) ST reorganizes, regulation of vascular in/outflow IV: Reinnervation – (2-4w) can be up to 2y + 373. AMPLE history? Allergies Medications Past Illnesses/Injuries Last Food/Drink
6-8 h window Events preceding injury
self medication Effect of Prehospital tx 374. WBC w diff? INC DEC Neutrophils (PMN) Acute bacterial draining wound Bands(Myelocytes) Acute infxn Eosinophils Allergic rxn Lymphs Viral or syphilis HIV, Lupus, leukemia Monocytes Chronic bacterial SHIFT TO THE LEFT: Bands (myelocytes) OVER 20% PMN’s (neutrophil) OVER 70% *indicates infxn, toxemia, hemorrhage 375. Anemias? Microcytic: DEC MCV & MCH Fe deficiency or lead intoxication Macrocytic: (Megaloblastic) INC MCV & MCH Vit B12 def(pernicious) Secondary to malfunction of intrinsic factor or following gastrectomy Folic acid def (EtOH, malabsorb, pregnancy) Drugs – sulfa, methotrexate Normocytic: Acute hemorrhage, hemolytic, chronic dz 376. BMP Profile? K+: INC
acute renal failure, if over 7
cancel Sx! DEC
weakness, cramps, cause = diarrhea Ca++: Factor 4 in coagulation INC
bone demineralization – multiple myeloma DEC
low serum protein Phos: essential for metabolism of carbs and lipids INC
renal failure, healing fractures, pagets, mm DEC
hyperPTH, DM BUN: end product of protein metabolism produced in liver INC
kidney dz, DM, chronic gout, CHF DEC
Liver failure Creatinine: INC
kidney dz Uric Acid: 10mg/dL Total Protein (at least 7): INC
dehydration Albumin (3.6-5.1gm/100mL) INC
dehydration DEC
Liver dz (chronic), malnutrition

Total Bilirubin: byproduct of Hb from destroyed RBC’s. Indirect INC
liver failure, internal hemorrhage Direct INC
billiard duct obstruction Total INC
cirrhosis, acute viral hepatitis, CHF ALK PHOS: produced by osteoblasts INC
bone ca, child bone, fx, pagets, Lactate Dehydrogenase: functions in carb metabolism INC
kidney damage, acute MI (isoenzyme 1 is elevated 10-14 days post-infarction SGOT: enzyme acts as catalyst in amino acid metabolism through glycolysis INC
LIVER dz, MI 377. UA? Acetone: not normally found in urine
ketoacidosis Blood: kidney injury RBC = Glomerulonephritis WBC = Pyelonephritis Glucose: DM, excess IVF glucose, chronic liver dz Acidity: Acidic
acetone (ketoacidosis), DM Alkaline
blood transfusion, vomiting Proteins: Albuminuria
UTI, hemorrhage Bence Jones
Multiple Myeloma Specific Gravity: INC
DM, dehydration, sweating, vomit DEC
large fluid intake, dec salt intake 378. Pre-Op Orders? Admitting Labs: CBC, BMP, PT/PTT, FBS, UA, HcG if female, RPR, Sickle dex Diet: NPO after midnight MD or cardiology clearance CXR for all smokers and pt over 40 EKG: all pt c hx of cad and over 40 XR: foot 3 views, MRI, CT, Bone scan… Sedative: versed Anesthesia to see pt Betadine scrub of foot x 10 min 379. Post-Op Orders? Admit pt to floor Dx Conditon: stable, unstable guarded, critical Vitals: q 15min until stable then q routine Activity: ambulatory as tolerated, PWB with sx shoe, NWB c crutches, CBR, BRP Nursing: elevate foot, ice, check NVS, incentive spirometry to pt with instructions (if general anesth) Diet: ice chips to liquids to light snacks previous diet as tolerated Ins/Outs: D/C IVF when po intake tolerated Labs: CBC, H&H Meds: analgesics, symptomatic meds, Abx Ancillary: reece shoe to pt, PT to crutch train Xrays: post op 380. Elective major procedure DM bunion periop management? NPO after midnight Insulin controlled
FBS pre-op, start D5W IVF, hold regular,can give NPH Oral controlled
Same + hold oral med, if glucose>300
NPH SQ Diet controlled
Same + IVF dependant on pts needs Anesthesia will monitor BS if u ask

Post-Op
post-op glucose stat, may give 2nd ½ of NPH depending on glucose level, continue IVF until pt eats 381. Hx of gout, peri-op prophylaxis? If uric acid is >7, r/o kidney damage (BUN/Cr) Colchicine 0.5mg IV ½ hr pre-op 0.6mg po qd x 3d Dilute in sterile water, NOT D5W
it will precipitate 382. 5 signs of infxn? Rubor, Tumor, Dolor, Calor, Functio Laesa Bacteria
capillaries dilate
inc fluid in extravascular space
swelling
compression of nerves 383. Bone Scans? Tech 99: Sensitive, not specific, t½=6h, kidney metabol. Phase 1 – angiogram Phase 2 – blood pool Phase 3 – (3-4h) regional bone metabolism Phase 4 - (24h) Osteo BEST seen in late phase 4 Gallium 67: detects acute inflamm or infxn, t½=78h Binds leukocytes, bacteria, plasma proteins + trauma, inflammation, active infxn *if gallium shows more than tech
no osteo Indium 111: take blood from pt and label leukocytes Scan 19-24h later Hi sensitive, mod specific for acute ST infxn + OM - in noninfectious, inactive, chronic OM + in active OM HMPAO: Ceretic labeled leukocytes c tech 99 90% sensitive, 86% specific Best WBC scan for OM Acute OM
all + (gallium focal) Chronic OM
+ tech, - indium, - gallium Acute cellulitis
+ tech, + gall (diffuse), + indium Infected implant
+ tech, + gall Charcot
+ tech, - gall, - indium 384. What are the 2 types of etiologies of metatarsalgia? Structural (static): Long, short MT, PFed MT, Enlarged lat condyle of MTh, Trauma, Iatrogenic, Accessory sesamoid Tx = condylectomy, arthroplasty, implant Functional (dynamic): Pronation/hypermobility, Equinus, LLD, Compensation for Cavus, Hammertoe, High heeled shoes, Extensor/Flexor Substitution Tx = digital or MPJ sx, orthoses, heel lift, shoe mods 385. What are some D/Dx for metatarsalgia? Neuroma, ST mass, Friedberg, Fx (stress), verrucae, Tendonitis, gout, arthridities, plantar plate rupture/capsulitis, Pre-dislocation syndrome (do modified lochman test – dorsal drawer of mpj) 386. What are the following numbers? Success rates for distal and proximal osteotomies for MTalgia? 61% & 46% respectively Rate of transfer calluses? 40% What is the proper amt of elevation that you should try to achieve with an elevating MT osteotomy? 3.5mm – 5mm Less than 3.5
reoccurance, over 4-5
transfer 387. Name and explain some distal procedures for MTalgia? Condylectomy, arthroplasty, implant Jacoby V
v made dorsal to plantar with apex distal Vertical Tilt up
dorsal CBWO c apex prox/plantar

388. Why is it not a good idea to do shaft procedures for MTalgia? The nutrient artery to the lesser MT’s is approx 3cm proximal to the head… right where you cut! ** one procedure is the Giannestra’s step down Z – sagittal z – can elongate, PF, DF, Shorten… versatile, but hi AVN rate 389. Proximal procedures for MTalgia? DFWO vertical or oblique, proximal V 390. Post-Op care for these procedures? Head and shaft procedures
WB or NWB + Sx shoe x 3-6w (unless grafting) Base procedures
B/K NWB cast x 4-6w 391. How can you tell if a Tailor’s Bunion was induced by a PF or a DF 5th MT without touching the foot? Dorsal MTh hypertrophy
DF 5th, c or s path. Pronation Lateral MTh hypertrophy
PF 5th, subluxes c pronation 392. Explain what the landmarks are for axes of 5th MT IM & LDA measurement, and what are the norms/pathological according to Fallat and Buckholtz? IM: 6.47 / 8.71 – angle between bisection of 4th MT shaft and a line drawn along the Proximal ½ of the Medial surface of the 5th MT shaft. LDA: 2.64 / 8.05 – angle between the second line for the IMa and a line bisecting the head, neck, and articular surface of the 5th MT. 393. What is a pathological value for plantar declination angle for the 5th MT? over 10 degrees may be pathological (FAI 1990) 394. What is the 5th MTh Prominence value? What is the avg? Who came up with it? The distance between two parallel lines drawn along the lateral cortex of the 5th MT and the lateral most projection of the 5th MTh. The avg value is 4mm. Steinke and Boll 395. What is the classification system for tailors bunions? Fallat and Buckholtz
4 types i) enlarged lat. 5th MTh due to enlarged condyle, round head, true hypertrophy, exostosis tx = lat condylectomy ii) lateral bowing of 5th MT (IM = norm, no hypertrophy) tx = distal osteotomy iii) Increased IMa (LDA = norm) tx = Z osteotomy iv) Combo c at least one structural component (ii & iii) required tx = lat condylectomy & osteotomy for most proximal deformity 396. What is the rule for MT osteotomies as related to width? Limit transposition to 1/3rd of the MT width @ osteotomy 397. What are some Distal procedures for tailors bunions? Duvries lat. condylectomy – destabilize jt + recurrent (good for DM ulcers) Chevron – leave k-wire in for 3w Hohmann slide – unstable Wilson slide – oblq osteotomy from dist/lat to prox/med\ Yu CBWO – base medial
good to dec. LDA 398. What are some Shaft procedures for Tailors bunions? Yancey CBWO – intact lat hinge – distal, middle, or proximal placement (a,b,and c) Z osteotomy – transverse – very stable 399. What are some Base procedures for tailors bunion? Gerbert CBWO – base medially Estersohn OBWO – base laterally *reserved for extremely hi IMA 400. What are some complications for each procedure? Distal: Over medial translation/dislocation, hinge fx, MPJ dislocation, unstable 5th toe Shaft: Troughing, hinge fx, dislocation Base: non-union, hinge fx, elevatus c transfer callus 401. What forms a Heloma Molle? The head of the proximal phalanx of the 5th rubbing with the Lateral condyle of the proximal phalanx of the 4th toe.

402. What are the zones of toenail injuries? (nail bed injuries with ST loss) Zone 1 (distal aspect of nail) Cleanse & debride wound
try to cover, may let granulate, if over 1cm
skin graft may be used Zone 2 (middle of nail) Exposure of distal phalanx, reduce predominant bone, possible V-Y advancement flap or partial distal symes Zone 3 (proximal aspect of nail) Minimal survival of nail bed, debridement in OR, exise nail plate and groove to prevent nail spicule from regrowing, many go to distal syme’s amp 403. Good fluid management for HTN pt? Don’t use fluids with NaCl, NS, 0.5NS, LR
use D5W @ 5cc/hr 404. Tx for hypoglycemic? 50cc D50W + 1mg glucagon (if unconscious) 10-12g carbs (if conscious) 405. What is CRP? (C-Reactive Protein) A plasma protein, acute phase reactant produced by liver and adipocytes. Good to get a base reading to track effectiveness of treatment and disease progress. Viral infxn gives a lower value than bacterial. Low risk <1mg/L, High risk > 3mg/L. 406. What approaches does Myerson propose for fasciotomy of compartment syndrome in the foot? Dorsal: 2 longitudinal incisions over 2nd and 4th MT’s. The interosseous and central compartments are accessed through each webs space and the medial/lateral compartments using curved clamps. Medial: 1 incision between the aBductor Hallucis muscle and the inferior base of the 1st MT. The central compartment is decompressed with a curved clamp. 407. How common is pain on passive DF of the toes when trying to diagnose compartment syndrome of the foot? In Myerson’s article, it was the most reliable finding next to pain out of proportion (86%). Pain was difficult to distinguish from pain from injury. Other findings in this study: DP pulse absent in 12/14 pts, but dopplerable in 13/14. Light touch loss = 54%, Numbness = 46%, 2 point discrimination = 64%, pin prick = 15%. 408. Lets Talk Bunion Biomechanics? HI angle: (0-10)
Distal Akin DASA: (0-8)
Proximal Akin PASA: (0-8)
Reverdin if trackbound(wedge from 1st MTh) Green – lat cortex intact c shelf (PASA only) Laird – cut lat cortex and slide c shelf (PASA & IM) Todd – Laird + PF head as well (PASA, IM, MPE) HA angle: (10-15)
ST problem if PASA not involved HA angle alone
McBride or Silver Both
capsule tendon balance + head procedure) IM agle: (8-12 in rectus) (8-10 in adducted foot) 13-14
head (Austin, Reverdin Laird/Todd) 15-17
shaft (Scarf) 18+
Base (Lapidus, CBWO, OBWO, Juvara) *exception
can Kalish up to 17 deg MT ADDuctus angle: (<15) True IM angle = IM measured + (MAA – 15){amt of MT adductus over norm) *as MT adductus angle inc
more proximal MT protrusion angle: (+/-2mm)
+ = longer 1st MT Congruous
lines Parallel Deviated
lines intersect Outside jt Subluxed
lines intersect Inside jt Sesamoid Position: (1-3)
by 4, cristae is eroded

Types of 1st MPJ Deformities: Bne PASA,DASA, ST or both Positional ST angles normal Structural Bne NOT norm Combined both NOT norm

HA angle NOT norm Norm NOT norm

PASA +DASA
Cong or not NOT Cong NOT

409. Most common AVN site in Navicular? Middle 1/3 410. What NSAID is contraindicated in sulfa allergic pts? Celebrex 411. The age old question… What are the effects of NSAID’s on Bone healing? Short answer
nobody knows for sure Long answer
COX activity is essential for normal prostaglandin production and is believed to be the rate limiting enzyme in PG synthesis. All inflammatory responses are primarily mediated by PG’s (especially PGE2). PGE2 has been shown to increase blood flow to bone, callus formation, mineralization, trabeculae, osteoid formation, and accelerated remodeling. PGE2 and its receptors appear to be the main contributors to bone metabolism. Bone healing begins with the onset of inflammatory PG formation mediated by COX-2. PG’s are also synthesized by osteoblasts and are known to stimulate both bone formation and resorption. COX-2 is important in early or activated stages of healing, but likely exhibits little effect on the long-term healing process. COX-1 is mainly expressed in normal bone, while COX-2 expression is up-regulated during initial stages of bone repair process or under conditions of inflammation or neoplastic bone conditions. COX-2 inhibition is thought to affect bone healing through these pathways. In the animal models, both non and selective NSAID’s have been found to decrease bone healing. Indomethacin, rofecoxib, and COX-2 deficient were the three main drugs/gene therapies tested while rabbits and rats were the animals. Some studies blamed it all on COX-2’s, while others related the change to COX-1. Still others showed NO significant differences in fracture healing between non, selective, and control groups. On top of that, the COX-2 inhibitory concentrations in these animals are not known. As far as humans go, more of the same is true. Many studies were done on spinal fusion pts with toradol and ibuprofen showing both increased rates of non-union (up to 5x) and normal rates in another study. A study on fx healing in post-menopausal women with piroxicam tx did not decrease the rate of fx healing and actually reduced the osteopenia caused by ex-fix. Still other studies (2) on AJ and STJ fusion rates showed an insignificant INCREASE in union rate when treated with COX-2 inhibitors. These studies showed that their use in the short term does not negatively affect bone healing. Other studies (Brown et al.) showed that initial delays in bone healing recovered with time and no significant difference existed between control groups and tx groups at long term follow-up (12w). Other studies have shown the same. One explanation offered by Hill et al. for the absence of increased nonunion rates with COX-2 inhibition may be that a fusion model may not depend on inflammatory phase of bone healing or the pathway affected by COX-2 enzyme. Genetically, COX-2 deficient mice develop normal skeletons but have difficulty with fx repair in secondary bone healing models, suggesting that COX-2 is really only necessary in posttraumatic states. COX-2 may not be necessary for all types of bone healing. The general consensus of the literature is this: Both animal and human data suggest that there is no negative effect on bone healing when used in a short term manner (d/c after 6-12w post op). Therefore, pts can benefit from the decreased risk of narcotic use and have no increased risk of a nonunion following arthrodesis procedure. As far as fractures go, results do suggest that non-selective and selective inhibitors may have some effect on bone fx healing that is apparent at earlier stages of healing process, but it bears no significant impact on over-all long-term healing of the fx. Good read’s
“Review: Effects of cyclooxygenase inhibition on bone, tendon, and ligament healing” Radi et al. Iflamm. Res. 54 (2005) 358-366 “The role of cyclooxygenase-2 inhibition in foot and ankle arthrodesis” Hill et al. Foot and Ankle Clin N Am. 10 (2005) 729-242

412. How much Blood could a lap sponge sponge if a lap sponge could sponge Blood? (sorry… im getting bored) A standard dry 18-in. x 18-in. laparotomy sponge containing 25 mL, 50 mL, 75 mL, and 100 mL of blood will appear 50% saturated, 75% saturated, 100% saturated, and 100% saturated with excess blood dripping, respectively. A dry 12-ply 4-in. x 4-in. surgical sponge containing 5 mL of blood will appear completely saturated. A dry 3-in. x 11-in. extra-large perineum pad containing 25 mL of blood will appear 50% saturated, and a completely saturated perineum pad will hold approximately 80 mL of blood. 413. Describe the Trauma/Retention stitch. Far, then across to Near, then back to Near, then across again to Far, then tie over the entire length like a big simple. 414. What is the Glasgow Coma Scale? A neurological scale which aims to give a reliable, objective way of recording the conscious state of a person 6

5

4

3

2

1

Eyes

N/A

N/A

Opens eyes spontaneously

Opens eyes in response to voice

Opens eyes in response to painful stimuli

Does not open eyes

Verbal

N/A

Oriented, converses normally

Confused, disoriented

Utters inappropriate words

Incomprehensible sounds

Makes no sounds

Motor

Obeys Commands

Localizes painful stimuli

Flexion / Withdrawal to painful stimuli

Abnormal Extension to painful flexion to stimuli painful stimuli

Makes no movements

Highest Score = 15 (fully awake) Lowest = 3 (deep coma/death) Generally, Comas are Classified as: Severe, with GCS ≤ 8 Moderate, with GCS = 9-12 Mild, with GCS ≥ 13 415. At what point do you fixate a posterior malleolar fx? When it involves 25-30% of the surface. If any less is involved, Vassal’s Principal will take over when you correct the lateral malleolus. 416. How many times your normal body weight is placed on your Ankle jt when walking? 5x 417. How much does 1 unit of blood raise the H & H? 1&3 418. What is a condition that a pt can get from receiving too much normal saline? Hyperchloremic Acidosis

419. Lets talk about Disulfiram-like effects? Disulfiram (Antabuse) is a drug used to support the treatment of chronic alcoholism by producing an acute sensitivity to alcohol. Under normal metabolism, alcohol is broken down in the liver by the enzyme alcohol dehydrogenase to acetaldehyde, which is then converted by the enzyme acetaldehyde dehydrogenase to the harmless acetic acid. Disulfiram blocks this reaction at the intermediate stage by blocking the enzyme acetaldehyde dehydrogenase. After alcohol intake under the influence of disulfiram, the concentration of acetaldehyde in the blood may be 5 to 10 times higher than that found during metabolism of the same amount of alcohol alone. As acetaldehyde is one of the major causes of the symptoms of a "hangover" this produces immediate and severe negative reaction to alcohol intake. Some 510 minutes after alcohol intake, the patient may experience the effects of a severe hangover for a period of 30 minutes up to several hours. Symptoms include flushing of the skin, accelerated heart rate, hypotension (unless its Flagyl, then HTN), SOB/N/V, abdominal spasms, headache, confusion, flushing, decreased O2 sats, sweating. Drugs Associated with Disulfiram-like RXN to EtOH: Metronidazole (well documented, but some question it now), Griseofulvin, Ketoconazole, chloramphenicol, glyburide, glipizide, several thirdgeneration cephalosporins (including cefotetan and cefoperazone), chlorpropamide, Sulfonamides (Furosemide). Remember
many OTC syrups contain over 5% EtOH Treatment: Obvious
stop EtOH & offending agent. Give anti-emesis agents to stop vomiting.

2010 2010 - 2011 2011 EXTERNSHIP MANUAL PODIATRIC SURGICAL RESIDENCY PROGRAM SAINT FRANCIS HOSPITAL & MEDICAL CENTER PROGRESS NOTES You will write progress notes on both clinic and in-house patients on a daily basis. All notes must be co-signed by a resident. All notes will be in the S.O.A.P. format. This is also the way in which you will present patients to attendings and residents when and if the situation arises. While visiting, we expect the student to be preparing to become a resident which includes working up and presenting cases including differentials, offering treatment options and requesting ancillary testing when appropriate.

POST-OP NOTES The format is easily remembered by the mnemonic SAPPPPAHEMIC: S: Surgeon A: Assistants P: Pre-operative diagnosis P: Post-operative diagnosis P: Procedure(s) P: Pathology specimens sent (bone, C&S, aerobic, anaerobic cx) A: Anesthesia (general, local w/IV sedation) H: Hemostasis (tourniquet - location and duration) E: Estimated blood loss M: Materials (sutures, wires, pins, implants, drains, etc) 1

I: Injectables (local anesthesia, steroids) C: Complications (none) Then, briefly describe the patient’s condition post-op: “The pt. tolerated the procedure(s) and anesthesia well and was transported from the O.R. to the R.R. (recovery room) with VSS (vital signs stable) and VSI (vasc. status intact) to all digits of the______ foot.” ADMISSION/POST-OP ORDERS Admissions orders are done primarily through the CARE computer system and will be done by the resident. As an aid in writing orders, remember the mnemonic ADC VAANDILMAX: A: Admit to the service of Dr. ________/Podiatry D: Diagnosis C: Condition V: Vital signs (per routine, q4h) A: Allergies A: Activity level (CBR, commode to bedside, NWB L foot, BRP) N: Nursing orders (elevate leg on pillows, dsg changes, foot cradle) D: Diet (ADA, regular, low Na) I: IV’s/Ins and Outs (Hep lock) L: Labs (includes CBC, lytes, cultures, U/A, etc) M: Medications (regular meds, antibiotics, prn meds) A: Ancillary consults (Medicine, I.D., Vascular, P.T., etc) X: Radiological studies (Plain X-rays, nuclear studies, CXR, EKG, PVRs) REMEMBER TO DATE AND TIME ALL ORDERS!

PRE-OP NOTE This is a checklist to ensure and document all the necessary preparations have been made. Surgeon: Pre-op diagnosis: _____________________ Procedure: _______________________ Consent: (give status--signed & on chart or pending) CXR: (give results) EKG: (give results) Labs: (give all values: chem 7, cbc, PT, PTT, INR) Abx Pneumatic stockings Sub Q heparin Consult reports: (if necessary) “Pt. clear for O.R. in AM/this afternoon/etc.” “All risks, benefits, and complications have been explained to the patient, and no guarantees have been made.” ADMISSION NOTE 2

The admission note is the most involved of all the charting requirements. It closely resembles the detailed H & P’s you perform on new clinic patients at school. This note must be written within 24 hours of admission, as it provides a guide to the treatment plan. You will help the resident perform H & P’s, and you will have the opportunity to write admit notes. The components of an admit note are: Chief Complaint History of Present Illness Past Medical History Past Surgical History Medications with dosages Allergies

Family and Social History Review of Systems Physical Exam (including detailed lower extremity exam) Assessment and Plan

OPERATIVE NOTE Following each procedure, the surgeon must dictate a detailed narrative of the proceedings of the surgery. The standard format is: Patient’s name and Medical Record Number Date of Surgery, Surgeon, Assistant(s) Pre-op Diagnosis, Post-op Diagnosis, Procedure(s) Anesthesia, Hemostasis Detailed description of procedures (includes induction of sedation or general anesthesia, local anesthetic techniques, preparation and draping, and the procedure)

LABWORK SKELETONS Na / Cl / K / CO2 /

BUN / Glucose Cr /

WBC / Hgb/ Platelets / Hct/

Any other lab results or values are merely listed. Do not write that a lab is “WNL” and do not leave empty skeletons on a note. FINAL WORD ON HOSPITAL CHARTING The last few pages have been more than enough to swallow at one sitting. We do not expect you to be proficient at charting prior to your arrival - that is one of the things you are coming here to learn. POST-OP NOTE S: Surgeon A: Assistants P: Pre-operative diagnosis 3

P: Post-operative diagnosis P: Procedure(s) P: Pathology specimens sent A: Anesthesia H: Hemostasis E: Estimated Blood Loss M: Materials I: Injectables C: Complications The patient tolerated the procedure(s) and anesthesia well and was transported from the O.R. to the R.R. with VSS and VSI to all digits of the ___ foot. ADMISSION ORDERS A: Admit to service of Dr. __/Podiatry D: Diagnosis C: Condition V: Vital signs A: Allergies A: Activity level N: Nursing orders D: Diet I: IV’s/Ins and Outs L: Labs M: Medications A: Ancillary consults X: Radiological studies The following pages contain information that will be helpful in making your rotation, not only with St. Francis but all your rotations, go more smoothly. It, by no means, is meant to supplant the information you can receive by reading texts or journal articles. It is merely meant to provide you with a good background for what you will be dealing with most frequently while on rotations and working with patients. Having a good grasp of this information will make your transition from student to resident a much easier one. Reading an X-ray Unfortunately, many students find this to be one of the most difficult concepts to grasp while in school and on rotations. However, like most educational opportunities in life, if you can learn to organize your thoughts while staring at a radiograph, reading it becomes much easier. There are 5 basic steps to reading an x-ray and this includes the way in which it should be presented. 1. Overall quality- type of view (DP, Lat, Oblique), which foot, weight bearing, if there is adequate penetration, labeled correctly, etc. 2. Soft tissue- increased contour in a certain area, increased density, tissue emphysema, foreign body, tissue planes, etc. 4

3. Bone- are all cortices intact, periosteal reaction, density, etc. 4. Joint spaces- increase/decrease in joint space, changes in contour, etc. 5. Biomechanical exam- abnormal angles, cavus foot, pes planus, etc. The important thing is to have a picture in your head of what “normal” is and work slowly (to begin with) through each of the steps. Remember not to let your eyes be drawn to the obvious. Keep in mind the clinical exam and have an idea of what to expect to see prior to looking at the radiograph. Following those steps gives you an organized way to not only inspect each radiograph but to organize your thoughts when presenting it. Dermatology In your objective examination of a patient, it is necessary to be able to put into words what you see. Remember that some words such as ulcer, onychomycosis, xerosis, etc. are considered assessments, not objective statements. For example, it is not appropriate for you to write the patient has an “ulcer” in the objective. It is more appropriate to write the patient has a “desquamation of the skin” or something of that nature. The following are some common words/phrases to objectively discuss lesions of the skin. Macular- circumscribed, flat lesion Papular/nodular- circumscribed, solid elevation Vesicular/bullous- fluid-filled, elevated lesion Cystic- non-infected, deep-set collection surrounded by a wall of tissue Scales- thin flakes of dead epidermis Excoriations- scratch marks Erosions- essentially thick scratches that do not breach the dermis Ulcer- deep dermal defect that breaches the dermis or deeper Fissures- linear, deep epidermal cracks in the skin Pustule- elevated lesion containing pus, arising from infections of papule or bulla Abscess- deep collection of pus Ulcers Arterial Ulcers These occur distal to impaired arterial supply most commonly on the lateral aspect of the leg, when presenting on the lower extremity. However, they can occur anywhere that is susceptible to trauma such as the IPJ’s of the toes. Wound margins are even, sharply demarcated and punched out. These have minimum exudate and are very painful. Venous Ulcers The medial ankle is the most common location. They are mostly superficial. Moderate to heavy exudate. The ulcers tend to be large with irregular margins. Often surrounded by and associated with dermatitis and hyperpigmentation. Wagner Classification of staging diabetic ulcers: Grade 0: No ulcer (normal skin flora present) Grade 1: Superficial skin ulcer (predominantly gram + organisms present when infected and lesser numbers of gram – aerobes and anaerobes. 5

Grade 2: Deep ulcer through dermis possibly exposing tendon, ligament or joint capsule Grade 3: Deep ulcer with abscess, osteomyelitis or joint sepsis (polymicrobial infections with increased number of gram – and anaerobic species) Grade 4: Localized gangrene (forefoot or heel) Grade 5: Gangrene of the foot NPUAP pressure ulcer staging system: Stage 1: Non-blanchable erythema of intact skin. A defined area of persistent redness, blue or purple hews. Also known as a deep tissue injury. Stage 2: Partial thickness skin loss involving epidermis, dermis or both. An abrasion, blister or shallow crater. Stage 3: Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend to underlying fascia. Stage 4: Full thickness skin loss with extensive destruction, tissue necrosis or damage to muscle, bone or supporting structures. Vascular Evaluating a patient’s vascular status is essential to preventing a wide array of complications and morbidities. This includes both arterial and venous insufficiency to the foot. As a podiatric surgeon, one should be able to determine whether there is sufficient blood flow to a foot in order for it to heal. The following is a list of some of the most common ways in which vascular status is evaluated in a patient. A thorough and adequate history of the patient’s symptoms should be taken. This will include symptoms, location, characterization of the symptoms, effect of treatment, amount of disability, progression of symptoms, associated symptoms and complaints, any previous studies done. Ischemic pain associated with a wound is indicative of arterial disease. This type of pain may include numbness, coldness, burning, and pallor more severe with exercise. Intermittent claudication is associated with chronic arterial insufficiency. It is experienced as transient, exercised induced ischemic myalgia. It is most often seen in the calf muscles. With arterial blockage, this most often one joint or level above the muscle group in which the symptoms manifest. Rest pain usually develops as ischemic changes progress. This reflects severe ischemia. Blood is shunted from the periphery to a more central location when the person is sleeping. Metabolites build up in the muscle and cause pain. The patient will usually relate being awakened at night with pain and having to get up or dangle feet. There are several other symptoms and pieces of information that are related to vascular disease: 1. 2. 3. 4. 5. 6. 7.

Edema History of emboli Color and temperature changes- pallor, cyanosis, petechiae, telangiectasias Trophic changes and hair growth Past medical history- obesity, tobacco use, HTN, DM, age, etc. Ulcerations Gangrene- impairment of circulation 6

8. Palpation of pulses including femoral, popliteal, posterior tibial, dorsalis pedis (graded according to rhythm, symmetry and amplitude) Non-invasive Examination of Vascular Status Ankle/Brachial Index (ABI) Measurement obtained by dividing the ankle systolic pressure by the arm systolic pressure. Some clinical findings associated with the ankle/brachial index: A/B Index > .96 .71 - .95 .31 - .70 .00 - .30

Clinical Finding Normal Mild obstruction (intermittent claudication) Moderate obstruction (possible rest pain) Severe obstruction (rest pain/impending gangrene)

Monckeberg’s sclerosis can falsely elevate ABI readings.

Segmental Pressures These are taken at upper thigh, lower thigh, upper calf and ankle. Criteria based on the 110-20-30 Rule, we can predict potential obstructions. * An ABI of less than 1 may indicate obstruction. * The upper thigh pressure should be greater than 10mmHg greater than brachial pressure * Pressure differences of more than 20 mmHg for adjacent cuff sites on the same leg * Pressure differences of more than 30 mmHg over the entire leg. Doppler Signal These reflect flow velocity. The normal arterial pattern is triphasic. A monophasic signal indicates pathology. Digital Blood Pressure Attained by placing a cuff around the digit, staying away from the joint. Normal digital pressure is between 70-110 mmHg. Pulse Volume Recording (PVR) Reflects the volume of blood that pulses under a cuff. This is obtained by placing cuffs filled to 60 mmHg pressure around parts to be measured. Closely corresponds to direct intra-arterial recordings at the level being tested. The waveforms look like high teepees with a dicrotic notch. Changes in waveforms between segments reflect severe stenosis or occlusions. Neurology Presenting Problems: Can include pain, numbness, tingling, weakness, unsteadiness, and involuntary movements. Physical examination should begin with a good history of the problem at hand. After a good history is obtained, much information can be obtained simply by observation of the 7

muscles of the lower extremity. Observation can demonstrate muscle atrophy or even hypertrophy. The examiner can also visualize spasticity or even fasciculations. Muscle strength can be measured and graded: 0 = no movement 1 = trace movement 2 = movement with the aid of resistance 3 = movement against gravity 4 = movement against resistance supplied by the examiner 5 = normal strength Observing the patient’s gait can also give clues as to where the problem may originate. Also to be examined are a patient’s deep tendon reflexes (DTR). The symptoms often present in a dermatomal fashion, which can give certain clues about possible lesions that may occur at levels along the CNS. Certain methods of examination for nerve deficits can be done using equipment such as a tuning fork to test vibratory sense or a Semmes-Weinstein monofilament (10 g/ 5.07) to test light touch. Hoffman-Tinel's sign: A tingling in region of the distribution of the involved nerve with light percussion, results in paresthesias distal to the site of percussion. Due to nerve entrapment. Valleix Phenomena: A nerve trunk tenderness above and below the point of compression, with paresthesias proximal and distal to the point of percussion. Electromyography (EMG): When weakness is clinically difficult to attribute to nerve, muscle, or neuromuscular junction, electrical studies can establish topographically which nerves and muscles are affected. In EMG, the recording of electrical properties of muscle is displayed on an oscilloscope during needle insertion. Denervated muscle is recognized by fibrillations and fasciculations on the screen. Nerve Conduction Velocities (NCV): In nerve conduction studies the time for an impulse to travel along the nerve is termed the conduction velocity. If there is an increase in this conduction velocity, there is damage to the particular nerve involved.

Types of Neuropathy D - diabetic A - alcohol N - nutritional G - Guillan-Barre T - toxic H - hereditary R - recurrent A - amyloidosis P - porphyria 8

I - infectious S - systemic T - tumor

Reflex Sympathetic Dystrophy This syndrome is characterized by disproportionate pain in intensity, duration, and location, often from minor or unapparent trauma to an extremity. Clinical diagnosis is difficult due to the vague subjective data and subtle objective signs and symptoms. Early diagnosis is important because early treatment gives the best results. The sympathetic nervous system is always involved and is overactive. Symptoms occur distal to the trauma site. Manifestations of RSD include pain, first and foremost. The pain is usually excruciating and can be described as burning, aching or throbbing. The pain can be localized at first and then begin to spread. It is distal to the site of trauma to begin with but can spread proximally in later stages. RSD can also manifest itself with varied vascular related symptoms. Vasodilation can exhibit warm skin, dry skin, and hypohidrosis. Vasoconstriction can exhibit cyanosis, cool skin, edema of the part, and hyperhidrosis. Trophic changes involving the skin, muscles, bone and joints can occur in later stages. The examiner may see thin, atrophic skin, absent of hair and witness osteoporotic changes on x-ray. Treatment, when suspected, should include a pain management/ neurology consult, first and foremost. Other professionals to get involved with the case could be psychiatry, anesthesiology and physical therapy. Local anesthetic blocks have been shown to give some relief and may help in putting a stop to the pain cycle. Seddon's classification of nerve injuries: Neuropraxia: (first degree injuries) a conduction disturbance with complete recovery Axonotmesis: (second and third degree injuries) an incomplete division of supportive tissues of the nerve Neurotmesis: (fourth and fifth degree injuries) a complete division of a nerve Sunderland's classification of nerve injuries: First degree: only local changes to the myelin Second degree: injury to the axons that is incomplete Third degree: leads to more severe axonal injury with fibrosis Fourth degree: severe neuronal injury with the axons in complete disarray (no complete neuronal separation) Fifth degree: complete transection of the nerve (dismal prognosis) Neuromas (a misnomer) of the forefoot: Joplin’s - medial to the first metatarsal 9

Hauser’s - the first intermetatarsal space Heuter’s - the second intermetatarsal space Morton’s - the third intermetatarsal space Islen’s - the fourth intermetatarsal space Anesthesiology The American Society of Anesthesiologists (ASA) Physical Status Measure Class 1: Normal and Healthy - no known diseases Class 2: Mild Systemic Disease i.e. presence of essential hypertension or mild type II diabetes Class 3: Severe systemic disease that is not incapacitating i.e. severe diabetes, type I with vascular complications Class 4: Incapacitating systemic disease that is a threat to life i.e. advanced cardiac, renal, pulmonary, hepatic or endocrine insufficiency Class 5: Moribund patient who is not expected to live with or without surgery EMERGENCY OPERATION: any patient in one of the above classes who is operated on as an emergency (Letter E is placed next to the classification) Stages of Anesthesia Stage 1: Analgesia (characterized by variable degrees of analgesia and amnesia) Plane 1- Pre-analgesia (normal memory and sensation) Plane 2- Partial analgesia and amnesia Plane 3-Total analgesia and amnesia Stage 2: Delirium (extends from the loss of consciousness until the beginning of surgical anesthesia) (excitement and voluntary activity marked) Unconsciousness, irregular breathing, pupils dilated Stage 3: Surgical anesthesia (4 planes) Plane 1 (sleep)-Rhythmical breathing, eyeball centrally fixed, faint lid reflex Plane 2 (sensory loss)-Pupils slightly dilated, pulse and blood pressure normal Plane 3 (muscle tone loss)-Intercostal paralysis begins, increased pulse rate & decreased BP Plane 4 (intercostal paralysis)-Provides cessation of all respiratory effort and requires artificial ventilation for life support Stage 4: Medullary paralysis Plane 1- reversible respiratory failure Plane 2- irreversible cardiovascular collapse Local Anesthetics Function in such a way as to prevent sodium migration through the nerve membranes, which, therefore prevents depolarization of the nerve with inhibition of nerve conduction. These are divided into 2 classes of drugs: Esters and amides. Esters: Procaine (Novocaine): most toxic, and is considered the standard in comparing the potency and toxicity of other local anesthetics used for injections. 10

Esters are hydrolyzed by pseudocholinesterase in the plasma. Have a high potential for allergenicity associated with PABA. Amides: Lidocaine (Xylocaine): shortest duration & fastest action Bupivicaine (Marcaine): longest duration, least placental transfer, and greatest cardiac toxicity if given IV Amides are hydrolyzed in the liver. There is no cross sensitivity between amides and esters- can be substituted in case of allergy. Should use ½ dose in elderly, debilitated patients, and patients with hepatic disease. Pain and temperature lost first following nerve block, with loss of touch & motor function later. Injection into an acidic area (infection) converts the anesthetic chemically and does not allow for penetration into the cell membrane, and lessens its effectiveness. Maximum Allowable Single Dose in Normal Adults: Novocaine (1-2%): 750mg plain; 1000mg w/epinephrine Xylocaine (1-2%): 300mg plain; 500mg w/epinephrine Marcaine (0.25-0.75%): 175mg plain; 225mg w/epinephrine (.25% Marcaine= 2.5mg/cc, 0.5%= 5mg/ cc 1 % Xylocaine= 10mg/cc, 2%= 20mg/cc) Malignant hyperthermia Thought to be due to reduction in the reuptake of Ca by the sarcoplasmic reticulum necessary for the termination of muscle contraction Clinical features: Unexplained tachycardia, hypercarbia or tachypnea, acidosis, muscle rigidity even in the presence of neuromuscular blockade, hypoxemia, ventricular arrhythmias, hyperkalemia, fever is a late sign Treatment: 1. Discontinue all anesthetics 2. Dantrolene 2.5 mg/kg IV initially 3. NaHCO3 4. Hyperkalemia corrected with insulin and glucose (no calcium) 5. Arrhythmias treated with procainamide 6. Hyperthermia treated with refrigerated IV fluids, gastric, rectal and bladder lavage with cold saline, surface cooling with ice 7. Maintain urine output

Analgesics This is just a short list of some of the most commonly used pain medications for postoperative and inpatient pain management. Also included are some NSAID’s commonly used. Morphine sulfate: 2.5-10 mg SC/IM/IV q2-6h prn 11

Dilaudid: 1-4 mg SC/IM/IV q4-6h ; 2-8 mg PO q3-4h Percocet: (5/325, 7.5/325, 7.5/500, 10/325, 10/650): 1 tab PO q4-6h prn Oxycontin: (10, 15, 20, 30, 40) 1 tab PO q12h Darvon: 65 mg PO q4h prn Darvocet 50 (N-100, A-500): 1 tab PO q4h prn Demerol: 50-150 mg PO/SC/IM/IV q3-4h (decrease dose if given IV and dilute) Ketorolac (Toradol): 30-60 mg IM/IV x 1 dose only (do not exceed 5 days duration) Vicodin (500/5), Vicodin ES (750/7.5), Vicodin HP (660/10): 1-2 tab PO q4-6h Tylenol #3 (300/30): 1-2 tab PO q4-6h Ultram (tramadol): 50-100 mg PO q4-6h prn Motrin (ibuprofen): 400-600 mg PO q6h Naprosyn (naproxen): 250-500 mg PO q12h Mobic (meloxicam): 7.5-15 mg PO qd Celebrex: 200 mg PO q12-24h Trauma When describing any fracture, there are 6 characteristics that should be used. This is very useful when asked to describe a fracture to an attending while on the phone, such as in the ED at 2 a.m. Just like with an x-ray, organizing your thoughts will allow you to discuss the fracture in a more decisive manner. 1. 2. 3. 4. 5. 6.

Open vs. closed Shape Location Intra-articular vs. extra-articular Complete vs. incomplete Displaced vs. non-displaced

Example: A closed, transverse, through and through, extra-articular fracture of the 5th metatarsal base that is non-displaced. Example: A closed, spiral oblique, intra-articular, through and through, displaced fracture of the distal fibula. Open Fractures Classification (Gustillo and Anderson): Type 1: - Wound less than 1 cm long and clean - Minor soft tissue damage - Minimal comminution Type 2: - Wound more than 1 cm long without extensive tissue damage, flaps or avulsions - Slight crush injury with moderate comminution - Moderate contamination 12

Type 3: Extensive soft tissue damage, including muscles, skin, and neurovascular structures with a high degree of contamination Type 3A: Open fractures with adequate soft tissue coverage of bone despite extensive soft tissue laceration Type 3B: Open fractures having extensive soft tissue loss with periosteal stripping and bone exposure. Severe contamination. Severe comminution. Type 3C: Open fractures associated with arterial damage requiring vascular repair, regardless of soft tissue coverage General Principles of Treatment of Open Fractures 1. 2. 3. 4. 5. 6. 7.

Tetanus history Thorough H&P with complete neurological, vascular and musculoskeletal exam Complete x-rays Antibiosis admitted in the ED with cultures Immediate debridement and irrigation All foreign bodies should be removed All marginal and macerated tissue should be debrided and re-debrided as necessary after 48-72 hours. 8. Types 1, 2 and 3A get delayed primary closure within 5-7 days 9. Types 3B and 3C usually require skin flaps due to such a loss of tissue 10. External fixation for all type 3 and unstable type 2 fractures 11. Internal fixation should be used for articular and metaphyseal open fractures, preferably within 8 hours. Tetanus Prophylaxis (for adults) Clean and minor wounds: Toxoid given only if last dose was given > 10 years ago. TIG not given All other wounds: Toxoid given if last dose given > 5 years ago TIG not given TIG is only given in patients (any age) when they have never received a tetanus shot (usually pediatric patients) Compartment Syndrome This diagnosis should always be considered in a patient experiencing pain and swelling post trauma. This should be considered a clinical diagnosis (it can be measured, however) and is also considered a surgical emergency. Defined as increased compartmental pressure resulting in decreased perfusion and ultimate ischemic changes to the tissues. At rest, intramuscular pressure is approximately 5 mmHg. During a muscle contraction, the compartmental pressure can increase to 150 mmHg. At relaxation, the compartment 13

pressure rapidly drops, and within 5-10 minutes after relaxation, has returned to baseline. Intracompartmental pressures can be measured with a wicks catheter. During a compartment syndrome, pressures are over 30 mmHg. Any injury that causes an increase in compartmental pressure over this amount should undergo an immediate fasciotomy. Clinical findings include: 1. Pain out of proportion to clinical findings 2. Parasthesias 3. Pulselessness 4. None of the above. Perioperative Management of Patients In a healthy patient, there are 3 main areas to concentrate on in order to minimize the risks associated with any surgery: coagulation disorders, drug history and previous anesthetic complications. Certain labs and tests should be ordered for all cases. For local anesthesia: CBC-Diff, Chem-7, PT/PTT/INR, and EKG. For general anesthesia cases: CBC-Diff, Chem-7, PT/PTT/INR, EKG, Chest X-ray if smoker or older than 40 (according to some sources). Diabetic Patient 1. Early morning surgical preference 2. If surgery is delayed, start IV with D5W to avoid hypoglycemia (better sweet than sour) from remaining insulin or hypoglycemics from the day before. 3. Regular insulin should be used during the perioperative period. 4. Check pre-op potassium levels. Insulin reduces these levels. 5. Autonomic neuropathy can cause increased risks of gastroparesis and aspiration, resting tachycardia and orthostatic hypotension. 6. Pre-op blood sugar levels: a. Hypoglycemia in a pre-op patient, consider postponing the case b. Pre-op BS < 200 in diet controlled patient no meds are needed c. Pre-op BS 200-300 in diet controlled patient consider regular insulin d. Pre-op BS in patient taking oral hypoglycemics <150, do not take the drug on the morning of the surgery e. Pre-op BS in patient taking oral hypoglycemics 150-250, take morning dose of oral agent. f. Pre-op BS in patient taking oral hypoglycemics >250, start regular insulin 7. Avoid post-op hyperglycemia 8. For minor procedures in Type 2 DM patients undergoing minor procedures, discontinue the oral hypoglycemic one day before surgery and resume taking the medication when regular diet is resumed. Patient should not get any glucose IV. 9. For long, major procedures, it is safer to utilize IV insulin during surgery. 10. Administering insulin to Type 1 DM patients undergoing surgery: a. ½ the usual morning dose and start D5W IV and cover with insulin during case OR…. b. Start 500 ml D5W for the first hour, followed by 125 ml/hr of D5W with 1-2 Units of regular insulin 11. Begin a sliding insulin scale post-op

14

Patient on steroid therapy Steroids are used to treat many conditions including asthma, COPD, rheumatoid arthritis, and malignancy. They have an effect on three main areas of importance in the perioperative patient. Suppression of the hypothalamus/pituitary adrenal axis. Poor wound healing. Predisposition to infection. If a patient has taken more than 7.5 mg/ day of prednisone, then exogenous steroids must be supplied during the perioperative period. Otherwise there could be a resulting hypotension and cardiovascular collapse. For procedures, the regimen of exogenous steroids is: Hydrocortisone IV 100 mg pre-op and 100 mg post-op. Tapering of steroids is only necessary if coverage lasts longer than 3 days. Patients on anticoagulant therapy Heparin Therapy- inhibits intrinsic clotting pathway The half-life of heparin is 1.5 hours. When a patient is undergoing heparin therapy, the treatment regimen should be stopped the day before surgery. Effects are reversed with protamine sulfate. Dosage is regulated according to PTT when treating, not when prophylaxing. To prophylax for DVT, short term, give 5000 Units SC 2 hours prior to surgery and 5000 Units q12h until patient is ambulatory. Coumadin Therapy- inhibits extrinsic clotting pathway Half-life is 20-60 hours and is extremely variable according to rate of clotting factor catabolism. When a patient is on coumadin therapy, treatment should be stopped 5-7 days prior to surgery. If the surgery is necessary, heparin therapy can begin at that time and last until 2-4 hours before surgery. Effects are reversed by Vitamin K (delayed) or Fresh Frozen Plasma (immediate). Dosage is regulated according to PT/INR. Patient with clotting abnormalities Be sure to ask patient about previous bleeding problems, bruising, nose bleeds. Certain drugs can alter platelet function: aspirin, NSAID’s, steroids, antihistamines, IV penicillin and drugs listed above. Test to determine clotting issues: platelet count, PT, PTT, INR Cardiac patient Elective surgery should be postponed until 6 months post myocardial infarct and in patients with uncompensated congenital heart failure. All risk factors such as unstable angina and cardiac failure should be stabilized preoperatively. Pre-op studies should include the studies for the normal patient undergoing general anesthesia, plus EKG and chest x-ray. Nitrates and beta-blockers should be continued during the peri-operative period. EKG should be considered in any patient with a murmur. Gout patient Should receive colchicine 0.5 mg 3 times daily for 2-3 days prior to the operation and 4-5 15

days post-operatievly. Low risk patients do not need to be treated. Postoperative Care and Complications Fever (most common post-op problem) Temp > 101.6 PO. A simple pneumonic for remembering causes of fever in a post-op patient: Wind (1 day post-op)- atelectasis, aspiration Water (2 days post-op)- UTI, IV site phlebitis Wound (3 days post-op)- infection Walk (4 days post-op)- DVT Wonder (> 4 days)- drug reaction Of course, these are not set in stone and any can happen at any time. Clinical correlation should be made with all fevers. Chest Pain Possible causes include: MI, pulmonary embolus, pneumonia, anxiety, atelectasis, aspiration, CHF Treatment: EKG, chest x-ray, ABG’s. May also do ventilation perfusion radionucleotide lung scan, pulmonary angiography (most specific and sensitive for PE). Post-operative Infection Usually occurs 3-7 days post-operatively. Can occur sooner (Strep Group A). Signs/Symptoms: Pain, swelling, drainage, dehiscence, cellulitis, erythema, fever Treatment: Patient should be admitted to the hospital if they are experiencing systemic symptoms (nausea, vomiting, chills, sweats) or if they are immunocompromised or need surgical debridement. Perform local wound care including removing sutures and incision and drainage. Obtain a culture and sensitivity test. Obtain necessary lab studies. Begin empiric therapy with antibiotics and adjust per result of the C&S. Continue antibiotics for 10-14 days. Pain Management Pain medications were covered previously, but this information is in regards to pain as a complication to surgery. Injecting a long acting local anesthetic (bupivicaine) immediately postoperative will delay pain past the initial phases. A short acting steroid (dexamethasone) will help diminish postoperative swelling and inflammation. NSAID’s can be given to help reduce inflammation. Opiates Sedatives can reduce the anxiety associated with surgery, therefore reducing the pain. Nausea Antiemetics – Compazine, Phenergan, Reglan, Zofran

Constipation 16

First, if possible, get the patient moving. Walking can sometimes induce bowel movements in postoperative patients. Drugs- senna, lactulose, Colace, Dulcolax DVT Symptoms: red, hot, swollen calf with fever Diagnostic: venous duplex, venogram Treatment: Heparin IV 5,000-10,000 Units followed by a constant infusion of 1,0001,500 Units/hr. PTT is to be kept at 2 times the baseline and the PT is kept at 1.5 times the baseline. Coumadin should be started on admission (it takes 3-5 days to begin working). The patient should eventually be discharged home on coumadin. Internal Fixation Objectives of fixation devices 1. Eliminate motion at the fracture or osteotomy site. 2. Restore the normal anatomical alignment of the fractured site or the desired position of an osteotomized segment. 3. Assist in the physiological mechanism of bone healing. 4. Permit early mobilization of the area affected by the fracture or osteotomy. Cortical screws- function as either a positional screw (plate fixation) or a lag screw (exerts compression). Compression is only achieved when the threads of the screw do not engage the cortex of the near osteotomy or fracture fragment, accomplished by overdrilling. When screws are used alone for fragment fixation, two smaller screws provide increased resistance to shear and torsional stresses. When screws are used for interfragmentary compression, they should be inserted so that their direction bisects the perpendiculars to the fracture line and the long axis of the bone involved. Sufficient screw fixation can usually be obtained with oblique and spiral fracture patterns only when the fracture line is twice as long as the bone’s diameter. Short oblique or transverse fractures therefore need an interfragmentary lag screw and a neutralization plate. Cancellous Screws- fully or partially threaded. The cancellous screw thread height is greater than that of cortical. This allows for greater purchase in the softer metaphyseal and epiphyseal bone for which they were designed. If the threads are left crossing the interface between two fragments, no compression will be achieved as the lag effect will be negated. It then acts as a cortical screw. Herbert Screw- absence of a screw head. Characterized by the presence of threads with different pitches and leads on both its proximal and distal ends. The distal threads feature a tighter pitch and smaller lead and are separated from the proximal ones by an intervening smooth shank. This allows for interfragmentary compression.

17

Plate Fixation Static compression plates: tension is applied to the implant and compression is achieved at the fracture interface. Dynamic compression plates: beyond the compression of the fracture achieved through static compression, the implant is subjected to a physiological load, which generates additional compression at the fracture plane. Neutralization plates: initially a shaft fracture is fixated by interfragmental compression with a lag screw. A plate is then applied to neutralize or absorb any disruptive forcestorsional, shear or bending to which the bone and osteosynthesis may be subjected. Anti-glide plates: used as neutralization plates but placed on the posterior aspect of the fibula. Buttress plates: generally used to resist the tendency of metaphyseal fracture fragments to displace when subjected to compressive forces (tibial plafond or calcaneal plates). Pre-stressing (bending) the plates results in static interfragmentary compression. Contour the plate so that the center sits away from the bone to which it is applied. The screws securing the plate ends are inserted and tightened first (pre-stressing the plate in tension) so that as sequential screws are applied (progressively closer to the center) axial compression is developed along the underlying bone. AO Objectives 1. Atraumatic operative technique 2. Accurate anatomical reduction 3. Rigid internal compression 4. Avoidance of soft tissue damage 5. Early range of motion Techniques of stable fixation Single lag screw: A cortical screw with a glide hole or a cancellous screw with all the threads on the distal side of the fracture fragment. The screw should be placed so that the angle of the screw bisects the perpendicular of the fracture/osteotomy and the perpendicular of the longitudinal axis of the bone. Multiple lag screws: This technique is used in a long/oblique or spiral fracture, where the length of the fracture is at least twice the diameter of the diaphyseal bone involved. The first screw should be placed perpendicular to both cortices and be centrally placed. The second and third screws are placed perpendicular to the plane of the fracture. This prevents shearing. AO Technique of Screw Placement 1. Underdrill 2. Overdrill 3. Countersink 4. Measure 5. Tap 6. Screw insertion 18

Other Techniques of Fixation Circlage wire: The weakest form of internal fixation. Provides apposition of the osteotomy surfaces, but little stability. Most secure is two loops at 90 degree orientation to each other. K-wire: Crossed k-wires provide more rigidity than just one. Distraction of the fracture fragments can occur. This does not provide interfragmental compression. Threaded kwires are mechanically unsound and are rarely used. Tension banding: Monofilament wire threaded in a figure 8 pattern, used in combination with two k-wires to give interfragmental compression. This is good with Jones fractures and some ankle fractures. The plane of insertion of the 2 k-wires must be parallel to the plane of the drill hole for passage of the monofilament wire.

Infection and Antibiotics (Infectious Disease Society of America suggestions) Mild Infections 2 of the following characteristics: purulence, erythema, warmth, pain, tenderness, induration PO antibiotics: Dicloxacillin, Clindamycin, Cephalexin, TMP-SMZ, Amoxacillin/Clavulanate, Levofloxacin Moderate Infections Characteristics: cellulitis > 2 cm from wound, lymphangitic streaking, abscess, gangrene PO vs. IV antibiotics: TMP-SMZ, Augmentin, Levofloxacin, Cefoxitin, Ceftriaxone, Timentin, Ciprofloxacin + Clindamycin, Unasyn, Linezolid, Daptomycin, Ertapenem, Cefuroxime, Zosyn Severe Infections Characteristics: fever, chills, confusion, acidosis, hyperglycemia, tachycardia, hypotension, vomiting, leukocytosis, azotemia IV antibiotics: Zosyn, Levofloxacin, Ciprofloxacin + Clindamycin, Primaxin, Vancomycin + Ceftazidime Life Threatening Empirically cover S. aureus, Streptococcus, Enterobacteriaceae, Bacteroides fragilis IV antibiotics: Unasyn, Zosyn, Primaxin, Ertapenem, Fluorquinolone + 3rd generation cephalosporin, Clindamycin + Ciprofloxacin or Levofloxacin Ensure empiric Gram (-) coverage for diabetic foot ulcers: - Beta-lactamase inhibitors - 2nd and 3rd generation cephalosporins 19

-

fluoroquinolones clindamycin

Pseudomonas when suspected - Ciprofloxacin - Zosyn Cellulitis without an open wound - cover for beta-hemolytic Streptococcus and S. aureus Infected ulcer not previously treated with antibiotics - beta-hemolytic Streptococcus and S. aureus Chronic infected ulcer or previously treated with antibiotics - S. aureus, beta-hemolytic Streptococcus, Enterobacteriaceae Macerated ulcer secondary to soaking - Pseudomonas (often with another organism) Chronic wounds, prolonged treatment, broad antibiotic therapy - MRSA, VRE, extended spectrum beta-lactamase gram (-) rods - Also Dipthiroids, Enterobacteriacea, Pseudomonas, gram (-) rods Necrosis, gangrenous, stinky foot - Enterococci, Enterobacteriacea, non-fermentive gram (-) rods, obligate anaerobes Community-acquired MRSA - Clindamycin, Doxycycline, TMP-SMZ Patient with PAD - think anaerobe; Bacteroides; Metronidazole

20

21

Hershey Board Certification Review Outline Study Guide

by

Jonathan M. Singer, D.P.M. Diplomate, American Board of Podiatric Surgery Fellow, American College of Foot and Ankle Surgeons Diplomate, American Board of Podiatric Orthopedics & Primary Podiatric Medicine Fellow, American College of Foot & Ankle Orthopedics & Medicine

Edited by

Larry R. Goss, D.P.M. Diplomate, American Board of Podiatric Surgery Fellow, American College of Foot and Ankle Surgeons Fellow, American College of Foot & Ankle Orthopedics & Medicine Fellow, American Professional Wound Care Association Residency Director, Parkview/Roxborough/MCP Hospitals Clinical Instructor, Temple University School of Podiatric Medicine

Jason Miller, D.P.M. Other Contributors Christopher E. Attinger, M.D., Steven J. Berlin, D.P.M., Libby Cone, M.D., Douglas Glod, D.P.M., Larry R. Goss, D.P.M., Arthur E. Helfand, D.P.M., Edwin J. Juda, D.P.M., Peter F. Kelly, D.P.M., Steven Kravitz, D.P.M., Guido LaPorta, D.P.M., M.S., James Lawton, D.P.M., Jason Miller, D.P.M., Gene K. Potter, D.P.M., Ph.D., William H. Simon, D.P.M., John Walter, D.P.M., M.S., Fredrick E. Youngblood, M.D. © 2003 Pennsylvania Podiatric Medical Association

Acknowledgements William Goldfarb D.P.M. and Nancy Sullivan, for supporting me and believing this book could be done Larry R. Goss, D.P.M. and Jason Miller, D.P.M. for their academic contributions and updating this new addition James Lawton D.P.M. and Gene Potter, D.P.M. for their invaluable contributions in the general editing these review notes in the previous addition Jordon Fersel, M.D., for editing the chapters on Anesthesia and Emergency Medicine Deborah Wozniak, M.D., for editing the chapters on Perioperative Management, Fluid Management, and Postoperative Complications Warren Joseph, D.P.M., and Steven Maffei, D.P.M. for editing the chapter on Infectious Diseases Steven Kravitz, D.P.M., for editing the chapter on Biomechanics George Vito, D.P.M. for editing the chapter on Internal Fixation Peter F. Kelly, D.P.M. for writing the chapter on Lasers and Laser Physics Gene K. Potter, D.P.M., Ph.D. and Steven Berlin, D.P.M. for editing the chapters on Dermatology, Bone Tumors, and Soft Tissue Tumors Guido LaPorta, D.P.M., M.S. for writing the chapter on Ankle Arthroscopy Tracey Vlahovic, D.P.M. for editing the chapter on Dermatology

The Hershey Board Certification Review Outline Study Guide is prepared for distribution by the Hershey Surgical Seminars Committee Pennsylvania Podiatric Medical Association Guido La Porta, D.P.M., General Chairman

Author: Jonathan M. Singer, D.P.M. General Editors: Larry R. Goss, D.P.M. and Jason Miller, D.P.M. Copy/Content Editors: Larry R. Goss, D.P.M. and Jason Miller, D.P.M. Cover Design: Larry R. Goss, D.P.M. Coordinator: Nancy Sullivan Published by the Pennsylvania Podiatric Medical Association ISBN # 0-9639030-04 Copyright © 2003

Pennsylvania Podiatric Medical Association 757 Poplar Church Road Camp Hill, Pennsylvania 17011 (800)-841-3668 All rights reserved This book is protected by copyright. No part of this book may be reproduced in any form or by any means, including photocopying, or utilized by any information storage or retrieval system without written permission from the copyright owner. Accurate indications, adverse reactions, and dose schedules for drugs are provided in this book, but It is possible that they may change. The reader is urged to review the package information data of the manufacturers of the medications mentioned. The author has made every effort to ensure the accuracy of the information herein. However, appropriate information sources should be consulted, especially for new or unfamiliar procedures. It is the responsibility of every practitioner to evaluate the appropriateness of a particular opinion in the context of actual clinical situations and with consideration to new developments. The author, editors, and publisher cannot be held responsible for any typographical or other errors found In this book. Printed in the United States of America.

Table of Contents Chapter 1: Emergency Medicine Cardiopulmonary Resuscitation: page 2-3 Advanced Life Support: page 3-4 Office Emergencies: page 5-7 Medical Emergencies (Cardiac Dysrhythmias): page 7-9 Summary of CPR: page 9 Other Medical Emergencies: page 9-12 Shock: page 12-13 Blood and Blood Products for Emergency Use: page 13-17 Chapter 2: Anesthesia Anesthesia Classifications: page 20 General Anesthesia: page 20-23 Intravenous Anesthesia: page 23 Local Anesthesia: page 23-26 Special Cases for Lowering the Maximum Allowable Dose: page 26 Pediatric Anesthesia: page 26-27 Lumbar Epidural and Caudal Anesthesia: page 27-28 Complications of Endotracheal Intubation: page 31 Nerve Injury During Anesthesia: page 31-32 Other Medical Compliccations From Anesthesia: page 32-34 Chapter 3: Perioperative Management The Healthy Patient: page 36 The Diabetic Patient: page 36-38 The Hypertensive Patient: page 38-39 The Patient on Steroid Therapy: page 39-40 The Asthmatic Patient: page 40-41 The Alcoholic Patient: page 41 The Patient on Anticoagulant Therapy: page 41-42 The Patient With Clotting Abnormalities: page 42 The Rheumatoid Patient: page 43 The Sickle Cell Patient: page 43-44 The Cardiac Patient: page 44-45 The Pulmonary Disease Patient: page 45 Perioperative Management of the Infant and Child: page 45-47 Mitral Valve Prolapse patient: page 47-48 The Gouty Arthritis Patient: page 48

Water and Electrolyte Imbalance: page 6566 Oliguria: page 66 Chest Pain: page 67 Postoperative Hypertension: page 67 Postoperative Infection: page 67-68 Anxiety and Pain Management: page 68-69 Nausea: page 69 Constipation: page 69 Shivering: page 69 DVT: page 69-70 Compartment Syndrome: page 70-73 Hemorrhage: page 72-73 Septic Syndrome: page 73 Thyroid Storm: page 73-74 Chapter 6: Infectious Diseases Specific Diseases: page 76-81 Principles of Antiinfective Therapy: page 8184 Antibiotics: page 84-90 Drug Fever: page 90-91 Specific Antimicrobial Therapy: page 91-92 Surgical Considerations: page 92-93 Necrotizing Infections: page 93-94 Osteomyelitis: page 94-102 Septic Arthritis: page 102 Mycology: page 102-103 Viral Diseases: page 104 Rickettsial Diseases: page 104 Protozoan and Metazoan Infections: page 104-105 Chapter 7: Wound Healing Repair of Skin: page 108-111 Factors That Interfere With Wound Healing: page 111-113 Growth Factors in Wound Repair: page 113 Surgical Approaches: page 113-114 Wound Dressings: page 114 Suture Materials and Needles: page 115116 Tourniquets: page 116-118

Chapter 4: Preoperative Evaluation Screening Procedures: page 50-61 Summary of Perioperative Lab testing: page 61-62

Chapter 8: Plastic Surgery Skin Grafting: page 120-122 Local Cutaneous Flaps: page 122-124 Local Muscle and Cutaneous Flaps: Page 124 Fasciocutaneous Flaps: page 124-125 Microsurgery and Free Flaps: page 125-126 Diagrams of Skin Flaps: page 126-130

Chapter 5: Postoperative Care & Complications Fever: page 64-65 Altered Mental States: page 65

Chapter 9: Bone Healing Primary Bone Healing: page 132 Complications of Bone Healing: page 133135

Treatment of Nonunions: page 135 Fusion: page 135 Bone Grafting: page 135-137 Aseptic Necrosis Following 1st Metatarsal Osteotomy: page 138-139 Electrical Bone Stimulation: page 40 Cartilage Healing: page 140 Chapter 10: Burns and Frostbite Assessment and Treatment of Burns: page 142-145 Burn Deformities: page 145-146 Other Types of Burns: page 146 Frostbite: page 146-147 Chapter 11: Fluid Management and Replacement in the Surgical Patient Fluid Management: page 150-152 Complications of Total Parenteral Nutrition: page 152 Replacement Therapy: page 152-153 Blood Products and Indications for Use: page 153-156 Composition of IV Fluids: page156-157 Chapter 12: Bone Tumors Introduction: page 160 Staging Techniques: page 160-161 Surgical Staging System: page 161 Radiology of Bone Tumors: page 161-162 Bone Tumors: Page 163-168 Cystic Lesions of Bone: page 168-169 Other Tumors and Cancers: page 169-170 Bone Tumors: A Quick Reference Chart: page 170-171 Phases in Cancer Development: page 171 Benign vs. Malignant: page 172 Chapter 13: Dermatology The Skin: page 174 Dermatological Lesions: page 175-182 Chapter 14: The Arthropathies Causes of Joint Pain: A Summary: page 184 The Arthropathies: page 184-195 Lab Testing for the Arthropathies: page 195 Articular Disorders Affecting the Heel: page 195-196 Synovial Fluid Analysis: page 197 Charcot Foot: page 198-199 Chapter 15: Peripheral Vascular Disease Patient Evaluation: page 202-212 The Vascular Diseases: page 212-215 Chapter 16: Internal & External Fixation Objectives of Fixation Devices: page 218 Requirements of Implant Materials: page

218 Principles Affecting Internal Fixation: page 218 Internal Fixation Devices: page 219-229 AO Objectives: page 229 AO Principles: page 229-230 AO Technique: page 230-235 Jumping Screws: page 235-236 Other Techniques: page 236-238 Complications of Fixation Devices: page 238 External Fixation: page 239 Large Bone Fixation: page 239-252 Small Bone External Fixation: page 253254 Chapter 17: Nail Disorders & Surgery Nail Entities: page 256-260 Nail Anatomy: page 260 Surgical Nail Procedures: page 262-263 Chapter 18: Neurology Neurological Pathways: page 266 Presenting Features: page 266-270 Assessment of Clinical Problems: page 270278 Innervation of the Lower Extremity: page 278-281 Tarsal Tunnel Syndrome: page 282-284 Classification of Nerve Injuries: page 284285 Neuromuscular Causes of Cavus Foot: page 285 Types of Nerve Surgery: page 285-288 Chapter 19: Pediatrics Evaluation of the Pediatric Patient: page 290-293 Pedicatric Biomechanics-Normal Values: Newborn to Adult: page 293 Congential Deformities: page 293-302 Pediatric Radiology: page 302-304 Pediatric Gait Patterns: page 304-305 Intoe Gait: page 306-307 Pediatric Fractures: page 307-318 The Limp in Childhood: page 318-319 Juvenile Hallux Valgus: page 319-320 Biomechanical Examination of the Child: page 320-323 Corrective Casting Techniques in Infants: page 323-324 The Toe-Walking Child: page 324-326 Chapter 20: Drugs and Drug Interactions Introduction to Drug Interactions: page 328 Antibiotic Drug Interactions: page 328-329 Anticoagulant Drug Interactions: page 330 Antihypertensive Drug Interactions: page 330-331

Antipsychotic Drug Interactions: page 331 Cardiac Drug Interactions: page 331-332 Diuretic Drug Interactions: page 332 Non Steroidal Anti-Inflammatory Drug Interactions: page 332-333 Oral Contraceptive Drug Interactions: page 333 Mechanisms of Drug Interactions: page 333-335 Specific Drugs: page 335-344 Chapter 21: Surgery of the Congenital Foot Flatfoot Surgery (flexible): page 346-355 Subtalar Joint Blocking Procedures: (Arhroereises and Arthrodesis): page 355356 Flatfoot Surgery (rigid): Convex Pes Plano Valgus: page 356-358 Metatarsus Adductus Surgery: page 358362 Cavus Foot Surgery: page 362-367 Clubfoot Surgery: page 368-373 Chapter 22: Generalized Disease Conditions of Bone Soft Tissue Overgrowth: page 376 Abnormalities of Alignment: page 376-377 General Increased Bone Density: page 377 Osteopenia: page 377-378 Marrow Abnormalities: page 378379 The Dysplasias: page 379-380 Chapter 23: Radiology Standard Radiographic Techniques of the Foot and Ankle: page 382383 Specific Radiographic Studies: page 383-391 Anatomic Angles: page 391-396 Common Structural Measurements (Diagrams): page 396-402 Pediatric Radiology: page 402-406 The Osteochondritities: page 406-407 The Accessory Bones of the Foot: page 407 Chapter 24: Hallux Valgus & Related Disorders Goals of HAV Surgery: page 410 Anatomical Facts of the 1st MPJ: page 410-411 Predisposing Factors: page 412 Biomechanics: page 412-414 Etiology of HAV: page 414-415 Deformity Types: page 416-417 Radiological Measurements for HAV: page 417-418

Physical Examination: page 418-419 Preoperative Considerations: page 419 Arthroplasty Procedures: page 419 420 Capsule-Tendon Balancing Procedures: page 421-422 Implant Arthroplasty Procedures: page 422-426 Arthrodesing Procedures: page 426 429 Proximal Phalangeal Osteotomies: page 429-431 Distal Metatarsal Osteotomies: page 432-436 Proximal Metatarsal Osteotomies: page 436-438 Shaft Osteotomies: page 438-439 Combination Procedures: page 439 Other Procedures: page 439-440 Hallux Rigidus and Limitus: page 440-445 Hallux Varus: page 445-446 Hallux Hammertoe: page 446 Diff. Diagnosis of Pain In the Sesamoid Area: page 446 Complications of HAV Surgery: page 447 HAV Procedure Chart and Their Indications: page 448 Chapter 25: Trauma Medical Management and General Assessment of the Trauma Patient: page 450-451 Assessment of Lower Extremity Injury: page 451 General Evaluation and Treatment of Fractures: page 451-452 Calcaneal Fractures: page 452-460 Talar Fractures: page 460-463 Osteochondral Fractures: page 463 465 Navicular Fractures: page 466-470 Cuboid Fractures: page 470-472 Cuneiform Fractures: page 472 Fifth Metatarsal Base Fractures: page 472-474 Metatarsal Fractures: page 474-480 Ankle Fractures: page 480-493 Midtarsal Joint Dislocations: page 494 Tarsometatarsal Joint Dislocations/Fractures: page 494-498 Ankle Inversion Sprain: page 498 505 Deltoid Ligament Ruptures: page 506-507 Compartment Syndrome: page 507

508 Open Fracture Classification System and Tx: page 508-510 Soft Tissue Injuries: page 510-511 Crush, Gunshot, and Lawnmower Injuries: page 511-512 Puncture Wounds: page 512 Epiphyseal Plate Injuries: page 512-514 Digital Fractures and Dislocations: page 514-515 1st MPJ Trauma: page 516-517 Nail Bed Trauma: page 517-518 Toe Tip Injuries With Tissue Loss: page 518-519 Dog and Cat Bites: page 519 Chapter 26: Digital Deformities and Surgery Hammertoe Syndrome: page 522528 Mallet Toe Syndrome: page 528-529 Claw Toe Deformity: page 529 Overlapping 5th Toe: page 529-532 Hallux Hammertoe: page 532-533 Lesser Digital Arthrodesis: page 533 Hallux Interphalangeal Arthrodesis: page 533 Lesser Digital Arthrodesis: page 533534 Overlapping 2nd Toe: page 534 Syndactylization: page 534-535 Digital Implants: page 535-537 Floating Toe Syndrome: page 537 Blue Toe Syndrome: page 538-539 Polydactylism: page 539-541 Chapter 27: Muscle and Tendon Pathology Muscle Physiology: page 544-548 Principles of Tendon Repair: page 548-552 Tendon Lengthening and Tenotomy: page 552-554 Tendon Transfers: page 554-556 Tendon Grafts: page 556-557 Posterior Tibial Tendon Rupture: page 557-559 Posterior Tibial Tendon Dysfunction (Acquired Adult Flatfoot Syndrome): page 559-560 Peroneal Tendon Pathology: page 560-562 Achilles Tendon Rupture: page 562566 Lateral Ankle Stabilization Procedures: page 566-571 Postoperative Care and Training Following Tendon Transfer: page

571-572 Tenosynovitis: page 572 Chapter 28: Lesser Metatarsal Surgery Anatomy (Metatarsals 2-3-4): page 574-575 Differential Diagnosis of Metatarsalgia: page 575 Surgical Treatment of the IPK: page 575-578 Lesser Metatarsal Joint Replacement: page 578-579 Panmetatarsal Head Resection: page 579-581 Metatarsus Adductus: page 581-585 Freiberg's Disease: page 585-587 Tailor's Bunion: page 587-589 Splayfoot: page 589 Brachymetatarsia (Brachymetetopody): page 589-591 Skewfoot: page 591-592 Chapter 29: Ankle Conditions Differential Diagnosis of Chronic Ankle Pain: page 594 Tarsal Tunnel Syndrome: page 594597 Sinus Tarsi Syndrome: page 597599 Peroneal Subluxation: page 599600 Ankle Arthrodesis: page 600-602 Lateral Ankle Instability: page 603 Chronic Lateral Ankle Instability: page 604-607 Chronic Medial Ankle Instability: page 607 Ankle Equinus: page 607-611 Malunion and Nonunion of the Malleolei: page 611-614 Chapter 30: Heel Conditions Anatomy of the Heel: page 616-617 Radiological Evaluation of the Calcaneus: page 617-618 The Heel in Systemic Disease: page 618-621 Seronegative Arthritis and Heel Pain: page 621-622 Heel Spurs and Heel Spur Syndrome: page 622-623 Tumors of the Heel: page 623-626 Tarsal Coalitions: page 626-629 Sever's Disease: page 629-630 Causes of Heel Pain (a summary): page 630-631 Haglund's Deformity: page 631-632

Chapter 31: Amputations General Surgical Technique: page 634 Digital Amputations: page 634-635 MPJ Amputations: page 635 Transmetatarsal Amputations: page 635-636 Tarsometatarsal Amputations (Lisfranc's): page 637 Midfoot Amputations (Chopart's): page 638 Amputation of the Ankle (Syme's, Boyd, Pirogoff): page 638-639 Below Knee Amputation: page 639640 Chapter 32: Biomechanics Normal Values: page 641 Criteria of Normalcy in the Lower Extremity: page 642-643 Adult Biomechanical Examination: page 643-645 Common Structural Variations: page 646-648 Planes of Motion: page 648-649 Axes of Joint Motion: page 649-653 Angular and Axial Deformities in Children: page 654-656 Anatomy of Gait: Activity of Muscles: page 656-663 Observation of Gait: page 663-664 Subtalar Joint Measurements: page 664-666 Subtalar Joint Function: page 666667 Midtarsal Joint Function: page 667668 Chapter 33: Anatomy Neuroanatomy: page 670-676 Angiology: page 676-680 Myology: page 680-695 Arthrology: page 695-704 Chapter 34: Soft Tissue Tumors Soft Tissue Tumors: page 706-715 Chapter 35: Physical Medicine and Rehabilitation Physical Modalities and Diseases: page 718-720 Therapeutic Modalities and Procedures: page 720-730 Chapter 36: Arthroscopy Ankle Arthroscopy: page 731-740

Chapter 37: Laser Applications in Podiatric Surgery Laser and Laser Physics: page 741-751 Clinical Applications in Podiatric Surgery: page 751-775 Chapter 38: Specific Radiological Pathology MRI Pathology: page 777-800

Chapter 1: Emergency Medicine Cardiopulmonary Resuscitation Advanced Life Support Office Emergencies Medical Emergencies (Cardiac Dysrhythmias) Summary of CPR Other Medical Emergencies Shock Blood and Blood Components for Emergency Use

EMERGENCY MEDICINE Cardiopulmonary Resuscitation 1. Rescue breathing: Adult victim a. Check responsiveness: shake or tap gently and ask "ARE YOU OK ?" b. If unresponsive yell for help c. Open the airway: head tilt/chin-lift to open airway, and check for obstruction. Remove if present d. Check for breathing: if no breathing then give 4 quick breaths (Observe chest rise) e. Check for pulse (Carotid) for 5-10 seconds: if .pulse is present but there is no breathing then f. Start rescue breathing: inflate @1 breath every 5 seconds. Continue for 1 minute g. Reassessment: check pulse and breathing, if breathing then stop CPR. If no breathing but pulse present, then just continue ventilations. If no breathing and no pulse, then begin CPR h. Start chest compressions over sternum: using heel of hand with fingertips off sternum and with elbows straight; compress 181 /2 to 2 inches @ 80 to 100/ minute i. Provide proper ventilations: give 2 breaths after 15 compressions if working alone or 1 breath to every 5 compressions when two rescuers are present Note* Do not perform a precordial thump in an unwitnessed event 2. Rescue Breathing: Infant victim a. Check responsiveness b. If unresponsive call for help c. Open airway: if obstructed then clear d. Check for breathing: if no breathing then cover victim's mouth and nose with rescuer's mouth and give 4 puffs of air (Observe chest rise) e. Check for pulse (Brachial): if pulse present but no breathing f. Start rescue breathing: inflate @ 1 breath every 3 seconds, continue for 1 minute g. Reassessment: check pulse and breathing if victim is breathing then stop CPR- if victim is not breathing and pulse present then continue ventilationsif victim is not breathing and has no pulse then start chest compressions i. Infant chest compressions should incorporate 2-3 fingers on the sternum centered on an imaginary line between the nipples, compressing vertically 1/2 to 1 inch at a rate of 100/minute ventilations occurring after every 5 compressions Note* Do not perform a precordial thump in an unwitnessed event

3. Rescue breathing: Child victim a. All of the above holds true except that the rescuer feels for the carotid pulse compressions occurring one finger width above the substernal notch using the heel of the hand at a compression rate of 80-100/ minutemaintain cycles of 5 compressions to every 1 ventilation NOTE* Do not perform a precordial thump Advanced Life Support 1. Advanced cardiac life support: includes the use of drugs, defibrillation, intubation and military antishock trousers (MAST)- the basic protocol is as follows: a. Begin basic CPR (Airway-Breathing-Circulation) b. Determine circumstances (Past history-current medications) c. Begin IV and intubate d. Determine cardiac rhythms e. Determine blood gases f. Begin appropriate drug therapy. These drugs include:






i. Atropine: decreases vagal tone to increase heart rate used in sinus bradycardia/high degree AV block dosage- .5mg IV Q 15 minutes up to 2mg.






ii. Bretylium: used in V-fibrillation and V-tach when lidocaine and countershock fails dosage v-fib: 5-10gm/kg bolus Q 15 min to max 30mg/kg dosage v-tach: 5-10 mg/kg IV over 10 minutes, then 1 to 2 mg/min IV drip













iii. Calcium: should only be used to treat acute hyperkalemia, hypocalcemia, and calcium channel blocker toxicity (there is no data showing its effectiveness during CPR) increases cardiac contractility and excitability used in asystole dosage: calcium chloride 2-4 mg/kg Q 10 minutes (Approx 500 mg) used in pump failure dosage: 2.5-1 Omicrograms/kg/min iv. Dopamine: alpha, beta, and delta agonist used to support cardiac output, BP and renal perfusion in shock states dosage: start at 2-5 micrograms/kg/min, titrate to effect 20 micrograms/kg/min large dose has mostly alpha effect






v. Epinephrine: alpha and beta agonist, increases heart rate and contractility used in asystole, V-fibrillation, and cardiac arrest dosage: .5 to 1.0mg (5-10 ml of 1-10,000) IV Q 5 min



•

vi. Furosemide (Lasix): loop diuretic and vasodilator used for pulmonary edema and congestive heart failure dosage: starting dose is 0.5, mg/kg IV and total dose not to exceed 2.0 mg/kg IV















vii. Isoproterenol (Isuprel): pure beta agonist increases heart rate, contractility and consequently cardiac output used in asystole, symptomatic heart block and bradycardia dosage: 1 mg in 500 cc D5W to give a starting dose of 2 mcg/min, titrate to effect (to achieve a heartrate of 60 beats/minute) viii. Lidocaine (Xylocaine): decreases automaticity and raises v-fib threshold used to suppress PVC's, v-tach and v-fib gm/kg 50-100gm bolus, then 2-4mg/min IV drip ix. Procainamide (Pronestyl): decreases cardiac excitability, decreases automaticity of ectopic pacemakers, and slows conduction used to suppress ventricular ectopics when lidocaine fails dosage: 100mg IV with a rate of 20mg/min until dysrhythmia disappears or hypotension ensues, QRS complex is widened by 50%, or total of 1 gm of drug is injected






x. Propranolol (Inderal): beta blocker (to be used with caution in patients with COPD, diabetes and heart failure used to control recurrent ventricular and atrial tachydysrhythmia dosage: 1 mg IV Q 5 minutes to 5 mg total (total dose not to exceed 0.1 mg/kg) must administer slowly





xi. Sodium Bicarbonate: used to counteract metabolic acidosis dosage is based on blood pH or empirically, 1 mEq/kg IV (50-100 mEq or 1-2 amps)




g. Cardioversion as necessary (Defibrillation) for ventricular fibrillation Procedure as follows: 1. Use paste or pads on skin ii. Charge defibrillator with SYNCHRONIZATION switch off iii. Place paddles as directed on the handles: one on the right upper sternum and the other on the left anterior axillary line

iv. Apply paddles with firm pressure (turn off oxygen) v. Shout," clear", make sure no one is touching the victim vi. Press both paddle switches simultaneously to fire the unit vii. Repeat as necessary : Start at 200-300 joules- maximum output 400 joules Office Emergencies 1. Syncope- Vasovagal reflex (Primary shock; fainting) a. Defined as transient loss of consciousness due to sudden release of the arterial vasomotor tone and temporary insufficiency of cerebral circulation b. Causes are sudden extreme fear or pain or the effect of severe injury c. Differential diagnosis: epilepsy, hyperventilation, hysteria , carotid sinus syndrome, cardiac arrhythmia, drugs and orthostatic hypotension d. Signs and symptoms: pallor, sweating, slow pulse, yawning and marked transient hypotension e. Treatment is supportive: recumbent position, take B.P., pulse, spirits of ammonia, O2 and drugs (Atropine/Ephedrine) only if previous treatment fails 2. Local Anesthetic Toxicity a. Causes are too much volume or too concentrated solution; extreme rapid absorption b. Reactions- rapid and delayed; with cerebral stimulation and/or depression; respiratory stimulation; cardiac depression; hypotension; shock c. Signs and Symptoms: apprehension , nausea, BP elevation, convulsions, perioral tingling, or most seriously, post-ictal depression, respiratory depression, hypotension respiratory and cardiac arrest d. Treatment- mental changes/watch patient, respiratory depression/O2, hypotension/ vasopressors i.e. Ephedrine 20 mg IM convulsions/Valium 5 mg IV, and CPR if necessary Note* Ephedrine raises BP and causes tachycardia while Vasoxyl raises BP without tachycardia (due to the alpha effect) 3. Anaphylactic Reactions a. These are toxic reactions that occur in persons who are allergic by heredity or who have become sensitized to a given drug or therapeutic agent after previous administration. Respiratory obstruction is the cause of death b. Reactions- anaphylactic shock, angioneurotic edema (swelling of soft tissues of throat), asthma with acute bronchospasm, urticaria and pruritus c. Signs and symptoms of anaphylactic shock - skin wheals, itching, angioedema, laryngeal edema, bronchospasm (wheezing) dyspnea, cyanosis, apnea, vomiting, hypotension, cardiorespiratory collapse and death d. Treatment of anaphylactic shock (must be immediate)- .5cc epinephrine IV or IM (children 0.01 mg/kg), tourniquet and .25cc epinephrine at injection site, O2 & airway, Solu-cortef 200 mg IV and CPR if necessary

4. Allergic Reactions: a. End organ response of the skin b. Symptoms are hives, (urticaria), bronchial asthma, and G.I. upset c. Treatment: 25-50 mg IM Benadryl- if severe then treat as if anaphylactic reaction- if tongue swelling use epinephrine 5. Acute asthmatic attack: a. This is an intermittent airway obstruction, which is reversible- can be acute and severe leading to respiratory failure b. Causes- allergies, irritants, infections, extreme cold, drugs and emotion c. Signs and symptoms- recurrent attacks of wheezing dyspnea and cough d. Treatment- reassurance, rest, O2, drug therapy (epinephrine .5cc 1:1000 subQ every 20 min up to 3 doses - if no relief then aminophylline 5-6 mg/kg over 20 minutes, hydrocortisone 100mg) 6. Seizures (major convulsions): a. Defined as convulsive disorders characterized by abrupt transient symptoms of motor sensory, psychic, or autonomic nature, frequently associated with change in consciousness. Changes thought to be secondary to sudden transient alterations in brain function associated with excessive rapid electrical discharge in the gray matter. b. Causes: idiopathic, pathological states (brain tumor, CVA, head trauma), local anesthetic toxicity, and intoxications c. Signs and symptoms in grand mal (major epilepsy)- aura, severe generalized clonic, convulsive body movements followed by a period of flaccid coma, then a period of sleep (post-ictal depression)- with status epilepticus: recurrent and severe seizures with short or no intervals between seizures

d. Treatment- except in status epilepticus no specific treatment is necessary except to protect patients from hurting themselves- in status epilepticus start with Valium, then Dilantin, then phenobarbital prn 7. Hypertension: a. Defined as persistent elevated BP above normal for the patient (borderline hypertension BP>140/90) b. Signs and symptoms- headache, convulsions, visual changes, with acute rise in BP c. Treatment- start supportive therapy and reduce BP with sublingual nifedipine 10mg (Procardia) then send for medical evaluation 8. Insulin Shock (hypoglycemia): a. Defined as low blood sugar that occurs when a diabetic who has taken insulin, fails to ingest food or engages in too strenuous exercise b. Treatment- if conscious and able to swallow then give orange juice- if unconscious then give IV glucose 20 to 50 ml. of 50% solution NOTE* If the diabetic patient is seen when unconscious, and if the diagnosis of coma or insulin reaction is in doubt, give 50% glucose IV- this will overcome insulin reaction but will not generally harm patient in diabetic acidosis Medical Emergencies (Cardiac Dysrhythmias) 1. Myocardial Infarct (uncomplicated): Characterized on EKG by big Q waves a. Monitor EKG b.100% O2 with nasal cannula c. Start IV lines with D5W d. Sublingual nitroglycerin can help e. Relieve pain with morphine sulfate f. Do blood gases/pH/electrolytes g. Consider use of prophylactic lidocaine 2. Asystole: Characterized by a flat line on the EKG a. Use basic CPR, begin IV, intubate b. Give epinephrine and bicarbonate c. If ineffective give calcium chloride d. If ineffective give atropine e. If ineffective give isoproterenol' f. If ineffective repeat steps b-e and as a last resort can give epinephrine intracardially or using a transvenous or external pacemaker 3. Ventricular Fibrillation: The gravest of all arrhythmias characterized by irregular and uncoordinated movements of the ventricles a. Use basic CPR, begin IV's, intubate (if unconscious) b. Use precordial thump only if witnessed arrest then defibrillate with 200-300 joules- repeat prn

c. If unwitnessed event do not use countershock: first start with epinephrine and bicarbonate d. If no response give epinephrine and bicarbonate e. Defibrillate at 400 joules f. Use lidocaine or procainamide g. If no response use bretylium h. After successful conversion use lidocaine drip

4. Ventricular Tachycardia: a. Begin lidocaine b. Use CPR if no pulse/O2/ IV's (and unconscious) c. Use precordial thump if witnessed event d. Consider cardioversion and procainamide or bretylium if lidocaine ineffective

5. Third degree AV heart block: a. Use atropine .5mg IV followed by isoproterenol prn b. Pacemaker 6. Premature ventricular contractions (PVC's): (frequent) May lead to V-ib (if untreated) a. Lidocaine 100mg IV bolus followed by lidocaine IV drip

Wolff-Parkinson-White syndrome: a. Characterized by a short P-R interval and prolonged QRS time. There is a 40% incidence of episodes of paroxysmal tachycardia, atrial fibrillation and atrial flutter, as well as the possibility of sudden death. Can occur in healthy individuals b. Treatment: Digitalis, quinidine, propranolol, artrial pacing Summary of Cardiopulmonary Resuscitation 1. Establish the diagnosis: Apnea, no pulse, absence of heart sounds, absence of responsiveness, ashen gray color 2. Summon help: Time is critical; you only have 4-6 minutes to reestablish ventilation 3. Do not thump the patient's chest (not part of CPR any more) 4. Check for absence of breathing first. Displace the mandible forward, and clear the airway manually, then give 2 rapid respirations 5. Place support under patient's back and start mouth-to-mouth breathing and external cardiac compression (5:1 with two rescuer sequence or 15:2 solo). Depress the sternum 4-5 cm (1.5-2 inches) 6. Insert ET tube to ventilate with 100% oxygen (only by experienced personnel) 7. Start IV infusion by needle or cutdown. Administer epinephrine and sodium bicarbonate and repeat bicarbonate injections until arterial blood gases and pH results are known 8. Monitor EKG a. If V-fib: Closed chest compression, epinephrine, sodium bicarbonate, defibrillate (if not effective repeat countershock) 9. Inject epinephrine, and if defibrillation not successful, repeat 10. Following restoration of heart function inject lidocaine for excessive ventricular irritability 11. If asystole is present, heart function may resume following myocardial oxygenation by ventilation and external cardiac compression 12. If asystole persists inject epinephrine and sodium bicarbonate., calcium chloride and isoproterenol prn 13. If electromechanical dissociation is present take therapeutic steps as with asystole

14. Corticosteroids may be used to decrease cerebral edema 15. Postcardiac arrest therapy includes corticosteroids, diuretics, hypothermia, and hyperventilation. Monitor arterial blood gases, BP, EKG, CVP (central venous pressure), urine, electrolytes, and chest x-ray Other Medical Emergencies 1. Narcotics Overdose: a. Give Naloxone (0.2-0.4 mg IV or IM/ in children .01 mg/kg: repeat Q 5 min) 2. Acetaminophen Overdose (APAP): a. The major toxic effect is centrilobular necrosis of the liver with toxicity likely to occur after a minimum acute ingestion of about 10g (or 30 acetaminophen tablets) b. Perform plasma APAP levels- treatment based accordingly c. Emesis with ipecac or gastric lavage d. Administer ACETYLCYSTEINE if elevated APAP plasma level 3. Salicylate Overdose: (the most common cause of fatal drug ingestion in the pediatric age group) (Reyes syndrome) a. There is a relationship of signs and symptoms to the amount of ASA ingested i. Mild: >100mg/kg: hyperventilation, lethargy, tinnitus ii. Moderate: 200-300mg/kg: hyperventilation, vomiting, sweating, vertigo, hallucinations iii. Severe: 300-400mg/kg: hyperventilation, seizures, coma, shock b. Treatment begins with emesis with ipecac then gastric lavage c. Alkalinize the plasma ( helps promote secretion of salicylates) with push doses of bicarbonate d. If shock present start IV with Ringer's lactate e. Start dialysis if renal failure 4. Poisoning: a. Each type of poisoning is treated differently a. Begin basic CPR if necessary b. Determine ingested substance and give antidote if available NOTE* It is better to call hotline first for specific directions in the treatment of specific ingested agents c. If unconscious- protect airway with ET tube, lavage with 28 French NG tube, use 300m1 normal saline for adults (activated charcoal can be added) d. If conscious- use syrup of ipecac to induce vomiting, ambulate patient, and give large quantities of water 5. Pulmonary Embolism: Complete or partial blockage of the pulmonary vessels from an intravascular clot originating elsewhere in the body, usually the deep veins of the lower extremity a. Signs and symptoms can include chest pain, dyspnea, cough, sweats,

syncope, respirations >16/min, pulse >100/min, temp>37.8 degrees C, phlebitis and edema b. EKG can show ST-T wave changes c. Presumptive diagnosis made by lung scan- definitive diagnosis made by pulmonary angiogram d. Treat with bedrest, then Heparin 5000 units as loading dose followed by continuous infusion (25,000 units added to 500 ml D5W administered via IVAC) e. Prior to Heparinization do PTT- during treatment adjust to keep PTT 2X normal f. If thrombophlebitis present treat with elevation and moist heat (may need antibiotics) 6. Hypertensive Emergencies:
Hypertensive encephalopathy
Malignant Hypertension
Accelerated Hypertension
Hypertensive Crisis a. Diagnosis of Hypertensive encephalopathy or accelerated malignant hypertension is a clinical one and demands immediate aggressive therapy to lower BP b. Treatment initially should be Diazoxide (Hyperstat) 300mg by rapid IV bolus or can give hydralazine (should give Furosemide simultaneously- prevents fluid retention) 7. Malignant Hyperthermia (also see Chapter Anesthesia, Section: Other Medical Complications of Anesthesia): Defined as a catastrophic reaction to general anesthesia An inherited trait Incidence of 1 in 20,000 a. With exposure to inhaled anesthetic agent the patient exhibits fasciculations and increased muscle tone, with jaw clenching during the induction of anesthesia a typical early sign and body muscles becoming rigid and excessive body heat produced b. Anesthesia must be discontinued c. Patient must be cooled d. INTRAVENOUS DANTROLENE SODIUM HAS A THERAPEUTIC EFFECT e. If suspicious of malignant hyperthermia pre-op do CPK LEVEL- THIS LEVEL IS ELEVATED IN 79% OF THE PATIENTS WITH MALIGNANT HYPERTHERMIA f. Early signs: i. Tachycardia ii. Tachypnea iii. Unstable BP iv. Arrhythmias

v. Dark blood in the surgical field vi. Cyanotic mottling of the skin vii. Profuse sweating viii. Fever ix. Fasciculations g. Suggested treatment regimen: i. Stop anesthesia ii. Hyperventilate with 100% oxygen (8-10 liters/minute) iii. Start Dantrolene sodium IV as soon as possible (starting dose 1 mg/kg up to a maximum cumulative dose of 10 mg/kg by rapid infusion) iv. Start Procainamide IV if required for arrhythmias v. Initiate cooling -IV iced saline (not Ringer's)
surface cooling with ice and hypothermia blanket
Lavage of stomach, bladder and rectum vi. Correct acidosis and hyperkalemia with sodium bicarbonate vii. Monitor EKG, temp, urinary output, electrolytes, arterial pressure and blood gases, pH, and electrolytes viii. Maintain urine output of at least 2 ml/kg/hr: administer Mannitol and Furosemide (if necessary) ix. If necessary administer Insulin to provide energy to the cells and normalize the pH x. Administer oral Dantrolene for 1-3 days after the crisis NOTE* Avoid amide local anesthetics if a patient has a history of malignant hyperthermia reaction NOTE* Malignant hyperthermia is most frequently seen when halothane and succinylcholine are used together Shock The mechanism of shock is poorly understood, however, this phenomenon results in inadequate tissue perfusion with accompanying cellular injury and metabolic disturbances. Shock cannot be defined but it can be classified by etiologic means 1. General clinical presentation: a. Tachycardia b. Hypotension c. Low tension pulse (thready pulse) d. Collapsed superficial peripheral veins e. Oliguria f. Hypothermia g. Metabolic acidosis 2. Etiology: a. Hypovolemic: Caused by a reduction in circulating blood as a result of traumatic injury, GI bleed, crush injuries, burns, massive diarrhea, and peritonitis b. Septic: Caused by infections that produce an endotoxic or exotoxic

reaction. Most common gram (-)'s are E. coli, Proteus group, Pseudomonas, Klebsiella and meningococci. Less often involved are gram (+)'s such as staphylococci, streptococci, and clostridia c. Neurogenic: Severe injury to the spinal cord or brain can cause a loss in vasomotor tone resulting in vasodilation and hypotension from the loss of peripheral vascular resistance. Also psychogenic factors such as the sight of blood or surgery can produce shock d. Cardiogenic: Produced by hypotension arising from inadequate cardiac output as a result of serious arrhythmias, tamponade, Ml, CHF, and pulmonary embolism e. Metabolic: Caused by alterations in the fluid electrolyte balance as a result of systemic diseases such as diabetic acidosis, renal failure, or chronic respiratory diseases f. Anaphylactic: Occurs following the injection of heterologous sera, penicillin and other medications 3. Treatment of shock: a. Assess the physical status of the patient b. Lie the patient down and keep him/her warm c. Maintain airway administering oxygen at 8-10 liters/minute. If patient unable to breath on their own use Ambu bag (use- CPR if necessary) d. IV fluid replacement to avoid dehydration. Do not use lactate solutions NOTE* Expanding the intravascular volume is the primary goal in the initial treatment of hypovolemic shock e. Vasopressor drugs can be used providing there is sufficient blood volume to be effective (the mechanism and etiology of shock dictates the specific drug) f. Lab studies should be instituted such as pH, pO2, pCO2, serum electrolytes, BUN, lactic and pyruvic acids, and hematocrit g. Measure the urine volume (normally it should be above 30 ml/hour persistent oliguria below 25 ml/hr for more than 2 hours may cause renal cell necrosis) g. If infection is suspected cultures should be performed, and appropriate antibiotics initiated h. For allergic/anaphylactic reactions treatment as mentioned above should be instituted

NOTE* Patients with a history or suspicion of penicillin allergy may be tested as follows: Dilute penicillin G to a concentration of 1,000 units per ml and place 1 drop on a skin scratch on the forearm. If the test is positive a wheal will be seen within 15-20 minutes. If the test is negative, inject a small amount of this solution intradermally to double check. This indicates the decreased probability of anaphylactic response but does not totally rule out an allergic state. Keep a "shock kit" immediately available because even a test can initiate anaphylactic shock. Also the risk of testing is that patients may become iatrogenically sensitized to future doses Blood and Blood Components for Emergency Use (also see Ch. 11 Fluid Management) 1. Red Blood Cells a. Description: i. Available as "packed RBCs" of 250 cc, split units of 125 cc, or quad packs for newborns ii. Anticoagulants are used to prevent clotting and a small residual amount of plasma is present iii. Units can be prepared and combined with special filters to prevent febrile reactions (leukocyte poor) iv. Unit can be washed to prevent allergic reactions (washed RBC's) v. One unit can raise the hematocrit by 3% or Hb by 1 gm. b. Compatibility: i. The unit must be ABO compatible, but Rh compatibility not required but preferred ii. Rh positive blood can be given to patients especially those over 50 years of age, who are expected to use multiple units (10% will develop Rh antibodies 34 months later, and by this time the transfused Rh+ cells have been cleared) iii. When Rh- units are in short supply they should be saved for women of child bearing age c. Alternatives: i. Autologous transfusions: patients can donate up to 3 units of blood prior to surgery and have these units available if subsequent bleeding occurs during the procedure (the safest) ii. Directed transfusions: Patients can elect to have friends and relatives donate blood for upcoming surgery iii. Perioperative cell salvage: Patients may elect in certain operative procedures to have blood lost during surgery, recollected, filtered and transfused (sterile orthopedic procedures and abdominal aortic aneurysms) c. Indications for RBC's: i. Hypovolemia due to acute blood loss and associated with one or more of the following:
Acute bleeding with an actual or anticipated blood loss of 750 ml or more
Systolic blood pressure <90 mm
Tachycardia (pulse > 100)
Hct < 30% and documentation of a fall of 5% or more within 24 hours or

10% or more within one week
Central venous pressure < 3 cm/H20 ii. Chronic anemia:
Uncomplicated: Hct < 24 or Hgb < 8 mg (and not due to acute blood loss) with anemia syndrome
Complicated: Hct < 30% or Hgb < 10% with complications affecting oxygenation (cardiac or respiratory insufficiency)
Anesthesia pre-op: Hct < 30% or Hgb < 10mg iii. Hemodialysis NOTE* RBC's must be used within 4 hours after removal from the refrigerator and must return within 20 minutes to the Blood Bank if not used. Warming can result in bacterial proliferation if allowed to warm to room temperature before returning to refrigeration d. Adverse reactions: i. Infectious reactions:
AIDS: Risk is 1:20,000 to 1:40,000 for each unit transfused
Hepatitis (B C): less than 1
MV ii. Noninfectious reactions
Febrile: fever reaction most common. This reaction involving circulating antibodies in the recipient which react to HLA antigens in infused granulocytes
Allergic: associated with circulating serum antibodies within the recipient to infused immunoglobulins within the small amount of residual plasma of the red cell unit (hives, serum sickness, anaphylaxis)
Hemolytic: is a result of circulating naturally occurring antibodies in the recipient to antigens on the RBC's causing cell lysis
Graft vs. host disease: engraftment and multiplication of donor blood cells in an immunosuppressed recipient are possible, and here, immunocompetent lymphocytes become engrafted and cannot be rejected 2. Platelets: a. Description: Are a concentrate separated from a single donor by plasmapheresis from whole blood containing 5.5 x 1011 platelets in 200 300 cc of plasma and anticoagulant, and can be expected to raise the adult platelets count by 60-80,000 unless platelet antibodies are present b. Compatibility: ABO compatibility is preferred, but in emergencies or short supply any ABO group can be used (Rh is not a factor). c. Alternatives: Random donor platelets are obtained from a single unit of whole blood and contain 1 /10 the number of platelets in 30-50 cc, and 6-10 units are standard suggested therapy d. Indications: L Prophylaxis:
Platelet count < 20,000/mm3 or anticipated drop below 20,000 in the





next 24 hours Platelet count < 80,000 with surgery anticipated or in the acute post-op period
A platelet function defect with surgery anticipated or in the acute post-op period i. Bleeding:
latelet count < 20,000/mm3
latelet function defect (known or suspected) e. Adverse reactions: Same risks as RBC's

3. Cryoprecipitate: a. Description: Prepared by thawing fresh frozen plasma at 4°C and recovering the cold precipitate. Each bag of 'Cryo' contains 90 or more Factor VIII units and at least 150 mg of fibrinogen in less than 15 ml of plasma b. Compatibility: ABO compatibility is preferred but not required in emergency situations c. Alternatives: Fresh frozen plasma can be used if there are associated deficiencies of individual coagulation factors, massive blood transfusion, or when cryoprecipitate is in short supply d. Indications: i. Von Willebrand's Disease ii. Hypofibrinogenemia associated with bleeding or surgery (perioperative) iii. Dysfibrinogenemia associated with bleeding or surgery iv. Uremia associated with bleeding v. Factor XIII deficiency e. Adverse reactions: Same as with RBC's 4. Fresh Frozen Plasma: a. Description: Is the anticoagulated clear liquid portion of blood that is separated and frozen within a few hours of Whole Blood Collection. A unit of FFP contains about 200 units of Factor VIII as well as other coagulation factors. Volume is 250 cc. b. Compatibility: ABO compatibility required c. Alternatives: i. Specific coagulation factors (cryoprecipitate for low fibrinogen or von Willebrand's disease) ii. Crystalloid or albumin is the preferred product for volume expansion d. Indications: 1. Replacement of isolated deficiencies (Factor II, V, VII, IX, XI) ii. Reversal of Warfarin effect iii. Massive blood transfusion (greater than 1 blood volume within several hours) iv. Antithrombin III Deficiency v. Thrombotic thrombocytopenia purpura e. Adverse reactions: Same as with RBC's

NOTE* Allergic reaction, dermal and anaphylaxis can be severe. Treatment includes Benadryl 50 mg 1M STAT repeated Q 10-20 minutes prn. Steroids and fluids may be necessary in severe reactions 5. Albumin a. Description: A solution containing the albumin component of human blood, which can effect immediate and prolonged restoration of circulating blood volume by causing a shift of fluid from the interstitial spaces into the circulation and slightly increasing the concentration. of plasma proteins b. Action: 25% albumin will draw approximately 3.5 times its volume of additional fluid into the circulation within 15 minutes, and provides a means of replacing human plasma proteins c. Indications: i. Plasma or blood volume deficit secondary to surgery, hemorrhage, burns, or trauma: to support BP by expanding the plasma volume ii. Hemolytic disease in the newborn iii. Hypovolemic shock: to restore blood volume in increase CO iv. Hemodialysis: for the treatment of shock or hypotension when the patient is fluid overloaded v. Acute or chronic liver disease d. Contraindications: History of hypersensitivity or severe anemia or CHF e. Precautions: Solutions containing 5% albumin are usually indicated for hypovolemic patients, 25% solutions should be used when fluid and Na+ intake must be minimized (cerebral edema and pediatric patients) f. Adverse reactions: Rare

Chapter 2: Anesthesia Anesthesia Classifications General Anesthesia Intravenous Anesthesia Local Anesthesia Special Cases for Lowering the Maximum Allowable Dose Pediatric Anesthesia Lumbar Epidural and Caudal Anesthesia General Complications of Anesthesia Complications of Endotrachial Intubation Nerve Injury During Anesthesia Other Medical Complications From Anesthesia

ANESTHESIA Anesthesia Classifications The American Society of Anesthesiologists Physical Status Measure ( A classification system for patients undergoing surgery) Class 1 Normal and Healthy - no known diseases Class 2 Mild Systemic Disease i.e. presence of essential hypertension or mild type II diabetes Class 3 Severe Systemic Disease That Is Not Incapacitating i.e. severe diabetes, type I with vascular complications Class 4 Incapacitating Systemic Disease That Is A Threat To Life i.e. advanced cardiac, renal, pulmonary, hepatic or endocrine insufficiency Class 5 Moribund Patient Who Is Not Expected To Live With Or Without Surgery EMERGENCY OPERATION- any patient in one of the above classses who is operated on as an emergency (Letter E is placed next to the classification) General Anesthesia A reversible state of unconsciousness produced by anesthetic agents, with loss of sensation of pain over the whole body. The order of descending depression of the CNS during anesthesia is: cortical and psychic centers, basal ganglia and cerebellum, medullary centers, and spinal cord 1. Inhalation agents: a. Volatile liquids: i. Chloroform (no longer in use)
Advantages: Rapid induction and recovery, nonflammable, good muscle relaxation
Disadvantages: Myocardial depressant, hepatotoxic ii. Diethyl ether (no longer in use)
Advantages: Reliable signs of anesthesia depth, respiration stimulated, bronchodilator, circulation not depressed, good muscle relaxation, relatively safe and nontoxic (has lowest death rate following its use)
Disadvantages: Prolonged induction and recovery, irritating to mucous membranes of upper airway, dangerous in patients with full stomachs (emetic), flammable, and explosive iii. Halothane (Fuothane®)
Advantages: Rapid smooth induction and recovery, pleasant smell, nonirritating (no secretions), bronchodilator, nonemetic, nonflammable
Disadvantages: Myocardial depressant, may trigger malignant hyperthermia reaction, arrhythmia-producing drug, sensitizes the myocardium to the action of catecholamines, possibly toxic to the liver, postoperative shivering iv. Methoxyflurane (Penthrane(r): It is the most potent and least volatile anesthetic (no longer in use)
Advantages: Great margin of safety, good muscle relaxant, not sensitive to catecholamines, nonflammable
Disadvantages: Prolonged induction of anesthesia and prolonged recovery, nephrotoxic v. Enflurane (Ethraner)
Advantages: Pleasant smell, rapid induction and recovery, nonirritating (no




secretions), bronchodilator, maintains stability of the cardiovascular system, nonemetic, compatible with epinephrine Disadvantages: Myocardial depressant, smooth muscle relaxant, increase hypertension with increase depth of anesthesia, CNS irritant, possible hepatotoxicity

vi. Isoflurane (Forane®): Newest inhalation agent
Advantages: Rapid induction and recovery, nonirritating, bronchodilator, excellent muscle relaxation, maintains stable cardiac rhythm, compatible with epinephrine, nonemetic, nonflammable
Disadvantages: Depresses the cardiovascular system, shivering postoperatively, possible acute or delayed liver injury (less likely than with Ethrane or Halothane) b. Gasseous anesthetic agents i. Nitrous oxide: The least potent of the anesthetic gases, and the most frequently used inhaled anesthetic. In the absence of hypoxia, there is little effect on the heart rate, myocardial contractility, respiration, blood pressure, liver, kidney or metabolism. Oxygen 100% must be given at the termination of the surgery to prevent diffusion hypoxia
Advantages: Rapid induction of anesthesia and emergence, does not sensitize the myocardium to epinephrine, nonirritating, intense analgesia, nonemetic
Disadvantages: No muscular relaxation, possible bone marrow depression and fatal agranulocytosis from prolonged administration or exposure, and increased risk of spontaneous abortion with prolonged use ii. Cyclopropane (no longer in use) 2. Preanesthetic or suplementary agents a. Sedatives i. Pentobarbital (Nembutal®) and secobarbital (Seconal®): Used before surgery to relieve anxiety and tension (cerebral cortex depression). Have a short hypnotic effect and pronounced sedative action. Are used as an inducing agent and have no analgesic component ii. Phenobarbital iii. Chloral hydrate: One of the oldest and best hypnotics, and a very good alternative to barbiturates in children and the elderly (adult dose is .5-1 gm PO). Excreted by the lung. iv. Diazepam (Valium®): Produces a satisfactory sedative and amnesic effect. It is indicated to prevent and treat convulsions v. Hydroxazine (Vistaril®): Has sedative antihistaminic, antiemetic, and bronchodilating properties, but used primarily for its sedative properties.. Excellent premedication in patients with a history of bronchial asthma vi. Droperidol-fentanyl (Innovar(r): A 50-1 mixture of droperidol and fentanyl. Produces effects that are a combination of both drugs vii. Droperidol (Inapsine®): The main effect is tranquility and peripheral vasodilation, can cause dysphoria, good antiemetic, and when infused IV produces sleepiness and mental detachment b. Narcotic analgesics: 1. Fentanyl (Sublimaze®): Produces depression of ventilation which is short in

duration. Reversed by narcotic antagonist (Naloxone®). Can also produce muscle rigidity in large doses ii. Morphine: The standard analgesic narcotic drug for relief of severe pain. It depresses the CNS, reduces GI motility, constricts the bronchi (due to histamine release), and lowers the metabolic rate. It has strong sedative and analgesic properties iii. Meperedine (Demerol®): Has analgesic, sedative, and spasmolytic properties, and in conjunction with barbiturates induces amnesia. It can cause tachycardia and is contraindicated in patients with atrial flutter (and anything that causes increased intracranial pressure just as with any other narcotic) NOTE* The adverse side effects from the narcotic analgesics include respiratory depression, emesis, physical dependence. Asthmatics react poorly to morphine only due to histamine release (smooth muscle constriction) c. Tranquilizers: i. Phenothiazines: Are used for a preanesthetic medication because of their sedative, antiemetic, antihistaminic, and temperature regulating effects. May produce postoperative hypertension and lethargy. When given with narcotic analgesics, increases respiratory depression
horazine® (15-25 mg)
ompazine® (5-10 mg)
henergan® (25-50 mg) d. Belladonna compounds: i. Atropine: Decreases secretions and is the drug of choice to reduce bronchial and cardiac effects of parasympathetic origin. It increases the heart rate by blocking the vagus nerve, and stimulates the cerebral cortex. Atropine is superior to scopolamine as a vagolytic agent, therefore, can prevent severe bradycardia and asystole in the presence of vagotonic agents (halothane). Atropine and scopolamine are potent bronchodilators. Patients allergic to atropine can be given scopolamine + benadryl ii. Scopolamine: An effective drug for psychic sedation and amnesia. The drying effect is better than atropine iii. Glycopyrrolate (Robinol) NOTE* Diprivan is a new sedative/hypnotic (used with Versed and Fentanyl for balanced anesthesia) 3. Stages of Anesthesia a. Stage 1: Analgesia (characterized by variable degrees of analgesia and amnesia) i. Plane 1- Preanalgesia (normal memory and sensation) ii. Plane 2- Partial analgesia and amnesia iii. Plane 3-Total analgesia and amnesia b. Stage 2: Delirium (extends from the loss of consciousness until the beginning of surgical anesthesia) (excitement and voluntary activity marked) i. Unconsciousness, irregular breathing pupils dilated c. Stage 3: Surgical anesthesia (4 planes)

i. Plane 1 (sleep)-Rhythmical breathing, eyeball centrally fixed, faint lid reflex ii. Plane 2 (sensory loss)-Pupils slightly dilated, pulse and blood pressure normal iii. Plane 3 (muscle tone loss)-lntercostal paralysis begins, increased pulse rate & decreased BP iv. Plane 4 (intercostal paralysis)-Provides cessation of all respiratory effort and requires artificial ventilation for life support d. Stage 4: Medullary paralysis i. Plane 1: reversible respiratory failure ii. Plane 2: irreversible cardiovascular collapse

Intravenous Anesthesia 1. Ultrashort-acting barbiturates: In sufficient amounts these can provide all the anesthetic stages (may produce serious cardiovascular depression) for short minor procedures that do not require muscle relaxation b. Neuroleptoanalgesia: A neuroleptic drug (tranquilizer) plus a narcotic analgesic, when administered together produce the following psychophysiologic state: somnolence without total unconsciousness, psychological indifference to the environment, no voluntary movements, analgesia, and satisfactory amnesia c. Neuroleptoanesthesia: Combination of nitrous oxide, droperidol, fentanyl and muscle relaxants (a good choice for patients with little cardiac reserve) d. Dissociative anesthesia (Ketamine®): Produces a state where the patient becomes mentally dissociated from the environment

Local Anesthetics Function in such a way as to prevent sodium migration through the nerve membrane which, therefore prevents depolarization of the nerve with inhibition of nerve conduction 1. Chemical Classifications a. Esters of para-aminobenzoic acids i.. Procaine (Novocaine): most toxic, and is considered the standard in comparing the potency and toxicity of other local anesthetics used for injections ii. Chlorprocaine (Nesacaine®): least toxic, and rapid plasma hydrolysis by pseudocholinesterase b. Esters of Benzoic Acid i. Hexylcaine (Cyclaine®) ii. Tetracaine (Pontocaine): longest duration NOTE* Esters are hydrolized by pseudocholinesterase in the plasma Have a high potential for allergenicity due to PABA moiety c. Amides i. Lidocaine (Xylocaine®): shortest duration & fastest action ii. Mepivicaine (Carbocaine®): do not use in presence of renal disease iii. Bupivicaine (Marcaine®): longest duration, least placental transfer, should not be used in children under the age of 12 years old (package insert), and greatest cardiac toxicity if given IV iv. Etidocaine (Duranest®): four time more potent than lidocaine, but only twice as

toxic NOTE* Amides are hydrolized in the liver. There is no cross sensitivity between amides and esters- can be substituted in case of allergy. Should use 1 /2 dose in elderly, debilitated patients, and patients with hepatic disease. Pain 8 temperature lost first following nerve block, with loss of touch & motor function later. Injection into an acidic area (infection) converts the anesthetic chemically and does not allow for penetration into the cell membrane, and lessens its effectiveness 2. Vasoconstrictors (Epinephrine) a. Advantages i. Reduces the vascularity locally at the site of the injection (due to vasoconstriction) ii. Reduces the absorption rate of the local anesthetic iii. Permits a higher allowable single dose dose of local anesthetic to be used iv. Increases duration of action of the block b. Disadvantages i. Use cautiously in patients with hyperparathyroidism, arteriosclerotic cardiovascular disease, hypertension, and peripheral vascular disease ii. Creates vasospasm in the end arterioles which could lead to tissue necrosis, so should be diluted in the digits to 1:200,000-1:400,000 or not used iii. Can create reactive hyperthermic reaction iv. Should be avoided in patients receiving Halothane (since Halothane sensitizes the myocardium in the presence of exogenously administered catecholamines) 3. Hyaluronidase (Wydase) a. Permits more rapid spread of solutions into the tissues, to facilitate regional block anesthesia. b. There is increased incidence of toxic reactions caused by local anesthetic drugs when hyaluronidase is used c. Reduces the duration of action when used with local anesthetics for nerve blocks 4. Regional Nerve Blocks a. Advantages i. Causes minimal interference with such preexisting diseases as diabetes, renal failure, or heart conditions ii. Eliminates the risk of pulmonary aspiration during induction of general anesthesia iii. Requires little postoperative nursing b. Ankle Block i. Saphenous nerve: the only nerve at the ankle that comes from the femoral nerve, lies medial to the greater saphenous vein at the ankle ii. Posterior Tibia] nerve: branch of sciatic nerve, lies in 3rd compartment of lacinate lig. iii. Sural nerve: made up from branches of the tibial and common peroneal nerves iv. Superficial Peroneal nerve: becomes superficial 7-8cm above the ant-lat ankle v. Deep Peroneal nerve: lies between the EHL and the anterior tibial

5. Maximum Allowable Single Dose in Normal Adults: a. Novocaine® (1-2%): 750mg plain 1000mg w/epinephrine b. Pontocaine® (0.1-0.25%): 75mg plain 100mg w/epi c. Xylocaine® (1-2%): 300mg plain 500mg w/epi d. Carbocaine® (1-2%): 500mg plain e. Marcaine® (0.25-0.75%): 175mg plain 225mg w/epi NOTE* There is no advantage in using a higher % solution- there is no stronger or longer anesthesia, therefore, with a lower % solution you can inject more volume. One must know how to convert % solutions to mg/cc (.25% Marcaine= 2.5mg/cc, 0.5%= 5mg/ cc 1 % Xylocaine= 10mg/cc, 2%= 20mg/cc) 6. Complications due to local anesthetics: See Chapter, Medical Emergencies a. Systemic reactions are associated with high blood levels which ordinarily result from overdoses, rapid systemic absorption, or inadvertent I.V. administration. The adverse reactions mainly effect the heart, circulation, respiration, and CNS i. Effects on the heart and vessels: Direct myocardial depressant , hypertension, bradycardia, thready pulse, pallor, clammy skin, sweating, cardiac arrhythmias possibly leading to cardiac arrest ii. Effects on medullary centers: depressed respiration, apnea, vascular collapse iii. Effects on the CNS: Nausea, emesis, talkativeness, euphoria, perioral tingling, restlessness, dizziness, anxiety, excitement, and disorientation. This can be followed by muscle twitching, convulsions, coma, respiratory failure and heart failure b. Vasovagal Reflex (Syncope) c. Anaphylactic Reaction d. Allergic Reaction (mostly due to esters due to PABA moiety) e. Reactions. due to epinephrine f. Local reactions : Skin slough, swelling, abcess, ulceration NOTE* Therapy for these reactions includes: a. For convulsions: Valium®, ultrashort-acting barbiturates and artificial ventilation b. For respiratory depression: Oxygen and artificial ventilation and control of airway c. For cardiovascular collapse: Vasopressors, IV fluids, and CPR

NOTE* When an allergy is suspected (but unknown) then an amide (frequently lidocaine) should be chosen. If the patient has a history to paraben sensitivity, preparations without araben should be tested (single dose vials). Preparations without epinephrine should be used because it may mask a positive skin test Special Cases For Lowering Maximum allowable Dose 1. Debilitated geriatric patient: 1 /2 or less of the adult dose 2. Pediatric Patient: i.. Clark's Rule: used for children older than 1 year Weight of child in pounds X The adult dose= ADJUSTED DOSE 150 ii. Fried's Rule: used for infants Age in months X The adult dose= ADJUSTED DOSE 15 iii. Cowling's Rule: Age (next birthday) = Percent Adult Dose 24 Pediatric Anesthesia 1. Preoperative medications: Given up to 1 hour prior to surgery, to decrease anxiety and to calm the child as well as dry secretions and decrease vagal stimulation. a. Sedative/hypnotics: Barbiturates, Chloral hydrate b. Anticholinergic agents: Scopolamine, atropine c. Narcotics: Meperidine, morphine 2. Anesthesia: a. Create a warm environment during anesthesia as children have poor autothermoregulation mechanisms (inability to shiver) NOTE* The infant and child lose much of their ability to maintain normal body temperature during and after anesthesia and their temperature fluctuates with that of the environment. In most cases, unless vigorous attempts are made to conserve body heat, the child may become cold and even cyanotic, especially after 2 hours of surgery. Hypothermia leads to depressed respiration and hypoxia follows. This predisposes the child to arrhythmias and V-fibrillation, and is the most common cause of cardiac arrest and shock in the very young b. Inhalation agents: Halothane and nitrous oxide with .neuromuscular blockade remain the principle agents (Enflurane® and lsoflurane® are now being used frequently). The margin of safety of volatile agents is very low, and deep levels of inhalation anesthesia for intubation of the infant can be quite hazardous c. Fetanyl in conjunction with halothane-nitrous oxide induction is good for short surgical procedures. This regimen reduces inhalation requirements, intraoperative

movement, coughing, and laryngospasm while' producing postoperative analgesia and shortened discharge times. The halothane dosage is then gradually reduced as the narcotic effects are noted NOTE Fetanyl is given 1 microgram per kg IV 20 minutes prior to the end of the surgery (must be administered cautiously to premature infants) d. Succinylcholine: A muscle relaxant used to quickly establish an airway especially when regurgitation and aspiration pneumonitis is a real risk. Its downside is: masseter spasm when used in conjunction with halothane (difficult to differentiate from malignant hyperthermia), rhabdomyolysis, and cardiac dysrhythmias Lumbar Epidural and Caudal Anesthesia Lumbar epidural anesthesia is accomplished by injecting the local anesthetic solution into the epidural space of the lumbar area of the vertebral canal. Entrance to the epidural space is usually made at or below the level of the second lumbar vertebrae 1. Indications: a. Lower extremity surgery when a general anesthetic may be risky for the patient due to a preexisting medical -problem (i.e. asthma, rheumatoid arthritis affecting the cervical spine, bronchitis, or emphysema, etc.) b. Patients who are not suitable candidates for muscle relaxants (myasthenia gravis) 2. Contraindications: a. Severe hemorrhage or shock b. Local infection at the proposed puncture site c. Septicemia d. Preexisting neurologic disease e. Extremes of age f. Chronic backache or preoperative headache g. Hypotension or marked hypertension 3. Advantages of epidural anesthesia over spinal anesthesia: a. Allows segmental anesthesia b. Postoperative headache does not occur c. Hypotension is less likely d. Can be maintained 1-2 days into the postoperative period as a useful method for relief of pain e. Do not have to remain In bed as long as with spinal anesthesia, therefore, can be used in outpatient surgery 4. Advantages of spinal anesthesia over epidural anesthesia: a. Less local anesthetic drug is needed than with epidural b. Less time is needed to achieve an adequate block than with epidural c. The level of anesthesia is more predictable d. Easier to perform 5. Anatomy of the epidural space:

a. The spinal cord is located within the spinal canal and is enveloped by the meninges, the dura being the outermost. The spinal cord seldom extends below the L1 vertebrae but occasionally extends to the upper level of L2 b. The dura is attached to the margins of the foramen magnum; this prevents the passage of drugs from the peridural space into the cranial cavity. The dura sac ends at the lower border of S2 c. The epidural space is located between the spinal dura centrally, and the ligamentum flavum and the periosteal lining the spinal canal peripherally. It extends from the base of the skull (foramen magnum), where the periosteum of the skull and the dura fuse, to the coccyx d. The epidural space contains areolar connective tissue and fat, arterial and venous networks, Iymphatics, and the spinal nerve roots

Anatomy of the epidural space: The spinal cord ends at L2. The subarachnoid space ends at S2 General Complications of Anesthesia 1. Awareness under anesthesia: Frequency of occurrence is greatest in obstetric procedures, and patients having emergency surgery for trauma have a higher incidence a. Periods at risk: Induction, intraoperatively (light anesthesia), postop (muscle relaxants used without sufficient sedation) b. Monitoring: EEG, pulse volume plethysmography, clinical signs (decreased chest compliance, bronchospasm, lacrimation, hypertension, pupil size, eye movement) 2. Hypoxemia: a. Definition: Deficient oxygenation of the blood (hypoxia: is reduction of oxygen

supply to a tissue below physiologic levels despite adequate perfusions of tissue by blood) b. Control of ventilation: i. PaCO2 is the most important regulator of ventilation ii. The respiratory response to hypoxemia is located solely in the peripheral chemoreceptors, most importantly the carotid bodies c. Causes of hypoxemia: i. Hypoventilation: Drugs, medullary disease (encephalitis), anterior horn cell disease (polio), disease of nerves to the respiratory muscles (Guillain Barre', diptheria), disease of the neuromuscular junction (myasthenia gravis) respiratory muscle disease (muscular dystrophy), and sleep apnea ii. Absolute shunt: perfusion without ventilation iii. Relative shunt: ventilation perfusion inequality iv. Diffusion block: impaired diffusion of 02 from alveolus into the pulmonary capillary blood d. Biochemical changes of hypoxia: The main effect is cessation of oxidative phosphorylation at the mitochondria) level, causing conversion to anaerobic metabolism, reduced energy production and increased production of H+ and lactate i. Cerebral effects (loss of autoregulation, loss of electrical activity) ii. Cardiovascular effects (increased heart rate) iii. Pulmonary effects (pulmonary vasoconstriction) iv. Renal effects (acute renal failure) v. Hepatic effects (decreased portal circulation) e. Compensatory mechanisms: i. Hyperventilation ii. Pulmonary redistribution iii. Increased cardiac output iv. Increased hemoglobin concentration v. Changes in oxygen hemoglobin dissociation curve 3. Hyponatremia: Serum sodium less than 136 mEq/L a. Symptoms: The severity of symptoms depends upon the the rate of decrease of serum sodium as well as the actual decrease in the serum sodium i. Symptoms occur when serum sodium falls below 120 to 125 mEq/L ii. Symptoms include confusion, anorexia, lethargy, nausea, vomiting, coma, and seizures b. Treatment: i. Correct underlying disorder (give insulin if due to hyperglycemia) ii. If hypovolemic-hypotonic: treat with isotonic saline iii. If hypervolemic-hypotonic: treat with restriction of water and consider diuretics iv. Symptomatic hyponatremia: treat with hypertonic saline 4. Hypokalemia: Serum potassium less than 3.5 mEq/L a. Signs and symptoms: Results in disorders of muscle physiology i. Respiratory arrest may occur with potassium concentration less than 2 mEq/L ii. Depressed myocardial contractility iii. Cardiac arrhythmias iv. Renal effects (decreased glomerular filtration rate, increased ammonium

production) v. Endocrine effects (decreased aldosterone and insulin release) b. Causes of potassium loss: i. GI ii. Diuretics iii. Renal tubular acidosis iv. Cushing syndrome 5. Hyperkalemia: a. Etiology: i. Decreased excretion (renal failure, hypoaldosteronism) ii. Extracellular shift (acidosis, ischemia, rhabdomyolysis, drugs such as succinylcholine) iii. Administration of blood, potassium penicillins, salt substitutes iv. Hemolysis b. Signs and symptoms: i. Muscle weakness ii. Paresthesias iii. Cardiac conduction abnormalities (become dangerous as K+ levels reach 7 mEq/L) c. EKG: i. Peaked T waves ii. ST segment depression iii. Prolonged P-R intervals iv. Loss of P wave v. QRS widening vi. Prolonged Q-T interval d. Treatment: i. EKG changes treated with CaCl2 ii. NaHCO2 iii. Glucose and insulin iv. Kayexalate v. Dialysis 6. Hypothermia: a. Effects: i. Decreases 02 consumption and CO2 production by 7-9%/°C in all tissues ii. Effects blood gas transport: shifts the oxygen dissociation curve to the left, hemoglobin's affinity for oxygen increases 6%/°C decrease in temperature (may put oxygen delivery at risk) iii. Respiration: hypoxic ventilatory drive may be depressed or absent in presence of hypothermia iv. Cardiovascular function in the anesthetized patient:
Heart rate and cardiac output decrease as temperature falls
EKG changes (sinus bradycardia, prolonged PR interval, widened QRS complex, prolonged QT interval, dysrhythmias at 28°C, ventricular fibrillation or asystole below 28°C)
Blood viscosity increases 2-3%/°C decrease in temperature v. Renal and Hepatic:




Kidneys have largest proportionate reduction in blood flow with glomerular filtration rate decreased by 60%
Hepatic blood flow is decreased vi. Central nervous system
Function is altered (sedation, cold narcosis, progressive slowing of EEG, or EEG becoming flat) b. Treatment: Warming of patient Complications of Endotracheal Intubation 1. Airway reflexes 2. Laceration or bruising 3. Dental trauma 4. Retropharyngeal dissection 5. Aspiration 6. Esophageal intubation 7. Endobronchial intubation 8. Dislocation of the mandible or arytenoid cartilages 9. Increased airway resistance 10. ET tube obstruction 11. ET tube cuff rupture 12. Laryngeal/tracheal/pulmonary Infection 13. Laryneal or vocal cord ulceration 14. Chronic hoarseness/vocal cord paralysis Nerve Injuries During Anesthesia 1. Factors predisposing to nerve injury: a. Tourniquets b. Hypotension c. Pre-existing ischemic disease (diabetes) d. Use of muscle relaxants allowing overstretching of limbs e. Positioning of the patient which results in stretching or prolonged pressure on a nerve 2. Postoperative upper extremity complications: a. Brachial plexus injuries are the most common 3. Postoperative lower extremity injuries: a. Sciatic nerve injury occurs with external rotation of thighs and legs, or if the knees are extended b. Femoral nerve due to excessive angulation of the thigh c. Common peroneal nerve is most frequently damaged (compressed in a brace of lithotomy equipment) d. Saphenous nerve is damaged by compression against the medial tibia] condyle e. Obdurator nerve is compressed by undue flexion of the thigh to the groin

Other Medical Complications from Anesthesia 1. Pulmonary embolism: a: Etiology and risk factors: 1. 95% of PE arise from deep venous thrombosis in the lower extremities

ii. PE is responsible for 20% of postoperative deaths. iii. Older patients undergoing more extensive surgery are at high risk iv. Highest risk patients have a history of thrombophlebitis, hip or pelvic fractures, and major lower extremity orthopedic procedures v. Other risk factors include acute M1, prolonged immobilization major trauma, oral contraceptive use, CHF, pregnancy b. Diagnosis: Remains problematic i. Signs and symptoms:
Dyspnea, pleuritic chest pain. hemoptysis, tachypnea, cough, wheezing and fever ii. Major emboli may cause syncope and cardiovascular collapse iii. Lab studies: 2. Postoperative nausea and vomiting: The vomiting center of the brain is located in the reticular formation of the medulla. Impulses transmitted by fibers of sympathetic and parasympathetic nervous system initiate the process of vomiting. Motor impulses that initiate vomiting are carried in Cranial nerves V, VII, X, and XII to the upper GI tract and through cervical and thoracic nerves to the diaphragm and abdominal muscles a. Predisposing factors: i. Females more prone (probably estrogen related) ii. Obesity iii. Certain anesthetics (opioids, nitrous oxide, volatile anesthetics, barbiturates) iv. Pain, hypotension, or hypoglycemia in postop period v. Type of surgery (middle ear, ophthalmic, peritoneal irritation, surgery that results in blood in the stomach) b. Effects: i. Autonomic:
Tachycardia or bradycardia
Hypotension or hypertension ii. Disruption of suture lines iii. Aspiration iv. Prolonged hospitalization c. Prevention: i. Metroclopramide 10-20 mg IV ii. Droperidol 0.63-1.25 mg IV iii. Cimetidine 300 mg IV or po iv. Ranitidine 150 mg po or 50 mg IV v. Scopolamine 1.5 mg transdermally (patch) d. Treatment: i. Keep patient supine ii. Antiemetics 3. Malignant hyperthermia: Thought to be due to reduction in the reuptake of Ca by the sarcoplasmic reticulum necessary for the termination of muscle contraction a. Clinical features: i. Unexplained tachycardia ii. Hypercarbia or tachypnea

iii. Acidosis iv. Muscle rigidity even in the presence of neuromuscular blockade v. Hypoxemia vii. Ventricular arrythmias viii. Hyperkalemia ix. Fever is a late sign b. Treatment: i. Discontinue all anesthetics ii. Dantrolene 2.5 mg/kg IV initially iii. NaHCO3 iv. Hyperkalemia corrected with insulin and glucose (no calcium) v. Arrhythmias treated with procainamide vi. Hyperthermia treated with refrigerated IV fluids, gastric, rectal and bladder lavage with cold saline, surface cooling with ice vii. Maintain urine output c. Anesthesia for MI-L suseptible patients i. Possible pretreatment with Dantrolene ii. Local or regional anesthesia should be considered or iii. General anesthesia with non-triggering agents such as:
Barbiturates
Propofol
Benzodiazepines -Narcotics
Nitrous oxide d. Associated syndromes: An increased risk of MH reported in association with a number of disorders, and therefore, these patients should be treated as suseptible to MH: • Duchenne muscular dystrophy • King-Denborough syndrome (dwarfism, mental retardation, and musculoskeletal abnormalities) • Central core disease 4. Pulmonary aspiration: a. Pathophysiology: Due to passive regurgitation and seen more commonly in unconcious, obese, pregnant, and patients with full stomachs b. Types of pulmonary aspirate: i. Particulate matter ii. Liquid gastric contents iii. Blood c. Incidence: About 10-20% perioperatively and intraoperatively (5% mortality) d. Diagnosis: Difficult to differentiate from other causes of pulmonary insufficiency. Signs and symptoms are tachypnea, tachycardia, cyanosis and respiratory acidosis e. Treatment: i. O2 ii. Tracheal intubation iii. May need intravascular fluid replacement iv. Antibiotics if bacterial infection develops

v. Bronchoscopy may be necessary to relieve airway obstruction

Chapter 3: Perioperative Management The Healthy Patient The Diabetic Patient The Hypertensive Patient The Patient on Steroid Therapy The Asthmatic Patient The Alcoholic Patient The Patient on Anticoagulant Therapy The Patient With Clotting Abnormalities The Rheumatoid Patient The Sickle-Cell Patient The Cardiac Patient The Pulmonary Disease Patient Perioperative Management of the Infant and Child Mitral Valve Prolapse Patient The Gouty Arthritis Patient

PERIOPERATIVE MANAGEMENT Healthy Patient The operative mortality for a healthy patient (ASA Class1) undergoing elective surgery is approx. 1 in 10,000. The risk is minimized by paying attention to 3 areas of the history: COAGULATION DISORDERS, DRUG HISTORY AND PREVIOUS ANESTHETIC COMPLICATIONS - For local anesthesia order: CBC/Diff, UA and PT/PTT. For general anesthesia order: CBC/diff, UA, PT/PTT, SMA 6, pregnancy test, chest x-ray (if over 40 years old or if HX of smoking)

The Diabetic Patient 1. Given early morning surgical preference. 2. If surgery is delayed start IV with D5W to avoid hypoglycemia from remaining insulin or oral hypoglycemics from the day before. Check BS q2-3h. NOTE* Remember the phrase," BETTER SWEET THAN SOUR". 3. Consult family physician for Insulin requirements. 4. Chlorpropamide has a half-life of 60 hours and thus should be stopped more than 24 hours prior to surgery (best stopped 2-3 days before). 5. Diabetics with a propensity towards ketoacidosis require IV glucose and insulin. 6. It is recommended that regular insulin be used during the perioperative period. 7. Check pre-op potassium levels (the administration of Insulin reduces the serum potassium levels. Therefore potassium replacement is needed when insulin is to be administered in patients with hypokalemia. 8. Patients with severe diabetic autonomic neuropathy have an increased incidence of gastroparesis and aspiration (increased chances for sudden death). Autonomic neuropathy can result in a resting tachycardia and orthostatic hypotension (BP drops 20mm Hg from a lying to a sitting position) 9. Preop blood sugar levels (mg/dl): a. If hypoglycemia is present pre-op consider postponing the case b. If pre-op BS in diet-controlled diabetic is below 200: no meds needed c. If pre-op BS in diet-controlled diabetic is about 200 (some say 300): consider regular insulin d. If BS in Type II diabetic is < 150: stop the drug on the morning of the surgery e. If BS in Type II diabetic is between 150-250: take AM dose of oral agent f. If BS in Type II diabetic is > 250: start regular insulin

10. Monitor long term glucose levels by measuring glycosylated hemoglobin (HbA1C): should be between 3 and 6% (realistically between 7-10). 11. Avoid post-op hyperglycemia: A BS greater than 250 inhibits phagocytosis, leading to an increase in post-op infections, esp. gram negative. 12. For minor procedures in NIDDM (TYPE II) patients well controlled on oral agents (other than chlorpropamide) d/c the drug one day before surgery and follow a NO INSULIN-NO GLUCOSE protocol during surgery and reinstitute the regular oral therapy when the patient begins eating 13. Well controlled IDDM patients undergoing short, minor procedures may also be managed on a NO INSULIN-NO GLUCOSE protocol 14. For long, major procedures it is safer to utilize intravenous insulin therapy during surgery 15. For IDDM (TYPE I) patients undergoing surgery, the regular insulin administration can be done a couple of ways: a. Administer 1 /3 to 1 /2 the patients usual AM dose and start D5W IV and cover with insulin as per fingerstick BS or b. Start 500ml D5W for the first hour, followed by 125 ml/hr of D5W with 1-2 units of regular insulin (1 unit is used in patients taking < 20 units pre-op). c. Give usual dose of insulin plus 50 gm of carbohydrate for each missed meal d. SubQ. insulin 6-10 units Q6h 16. Post-op BS levels can be managed as follows: a. 150-199 2 units b. 200 -249 4 units c. 250-299 6 units d. 300-349 8 units e. 350-399 10 units f. >400 12 units

The Hypertensive Patient 1. Two types: a. Essential hypertension (most common) b. Secondary hypertension: due to renal disease, endocrine disease, oral contraceptives, pregnancy and coarctation of the aorta. 2. Evaluate by taking BP 3 different times to eliminate other factors such as stress. Note * Take the initial reading in each arm. A significant difference shows certain diseases. 3. Check the heart: there may be left ventricular hypertrophy with systolic aortic ejection murmur. NOTE* An S4 gallop is the most common finding in hypertension 4. Check the optic fundi: they may show retinopathy (indicator of the severity of the disease). 5. Primarily treated by step-care approach: a. Step 1- Start with a diuretic (or start with a calcium channel blocker) b. Step 2- Add a beta blocker c. Step. 3- Add a vasodilator d. Step 4- Add a combination drug 6. Types: a. Diuretics: Thiazides: Dyazide, Maxide, Hydrodiuril b. Beta-Adrenergic Blocker: Tenormin, Lopressor, Corgard, and Inderal c. Loop Diuretics: Lasix d. Potassium Retaining: Aldactone, Triamterene, Amiloride e. Calcium-Entry Blocker: Cardizem, Procardia f. Combination- Dyazide, Maxide g. Central Sympatholytics: Clonidine (Catapres) h. Angiotensin Converting Enzyme Inhibitor: Capoten, Vasotec i. Arteriolar dilators: Hydralazine, Minoxidil

j. Alpha andrenergic blockers: Minipress, Hytrin NOTE* Diuretics are first line drugs used to treat hypertension, CHF and lymphedema. There is concern regarding diuretics because of the hypercholesterolemic effect of thiazides linked to ASHD 9 ischemic heart disease. Thiazides can cause hyperglycemia, hyperuricemia and hypokalemia (pre-op patients taking thiazides should have potassium checked). Therefore these drugs are going out of favor as a first line drug for hypertension, replaced by calcium channel blockers and ACE inhibitors. Loop diuretics (Lasix) are used in hypertensive patients with fluid retention refractory to thiazides and in patients with impaired renal function. Beta blockers are effective in treating hypertension because they decrease the heart rate, cardiac output and decrease renin release. These drugs prevent angina. Beta blockers can precipitate bronchial asthma, Raynaud's phenomenon and aggravate existing peripheral vascular disease. ACE inhibitors are often used as a first line drug in treating hypertension. They work by inhibiting the renin-angiotensin-aldosterone system. They are effective vasodilators for the treatment of CHF. Clonidine is a second line drug in treating hypertension. A severe rebound in blood pressure may occur if the drug is abruptly discontinued, therefore, should be continued perioperatively (4-6 hr pre-op) 7. Secondary hypertension is treated with elimination of the etiological factor, where possible 8. For severely hypertensive patients (BP of 160/90 or higher), elective surgery should be postponed until adequate control achieved 9. All antihypertensive medications should not be discontinued preoperatively EXCEPT GUANETHIDINE and should be taken at 6 AM (FOR AM SURGERY) if medication is normally taken in the morning 10. Acute elevations of BP are usually seen postoperatively which can be due to: PAIN, REACTION TO ENDOTRACHIAL TUBE, VOLUME OVERLOAD, AND EMERGENCE EXCITEMENT 11. Post-op hypertensive episodes are treated by eliminating the cause and if necessary giving the following: sub-lingual Procardia or can give diuretics IV or nitropatch, sublingual nitroglycerin, or nitroprusside NOTE* Procardia given sublingually reduces blood pressure quickly, but does not drop it below normal 12. These patients are very sensitive to vasopressors: DON'T USE EPINEPHRINE!!!! 13. Potassium levels in all patients taking diuretics must be measured pre-op

and adequately replaced prior to surgery to prevent hypokalemia associated cardiac arrhythmias

The Patient on Steroid Therapy 1. Steroids are utilized for the following: asthma, COPD (chronic obstructive pulmonary disease), autoimmune diseases (RA) and malignancy. They have an effect on three major areas of importance in the perioperative setting: a. Suppression of the hypothalamus/pituitary adrenal axis (HPA) b. Poor wound healing c. Predisposition to infection

NOTE* There will be suppression of the HPA axis if any patient has taken more than 7.5mg/day of prednisone for longer than one week prior to surgery 2. Therefore, if a patient has taken more than 7.5mg/day of prednisone, then exogenous steroids must be supplied during the perioperative period. Otherwise there could be a resulting HYPOTENSION AND CARDIOVASCULAR COLLAPSE 3. For minor procedures the regimen of exogenous steroids is: Hydrocortisone IV or IM @ 100 mg the evening before surgery, 100 mg prior to the start of the procedure, and 100 mg Q 8h for 24 hours (there have been modifications of this utilizing 100mg hydrocortisone pre-op and 100mg post-op) NOTE* For minor procedures done under local sedation the following can be done: 15 mg prednisone PO 6AM before the surgery, 15 mg prednisone PO that same afternoon, and 15 mg prednisone the next afternoon following the surgery 4. For major procedures the dosing is the same as above except the doses Q8h should continue until the stress of the postoperative period has passed. 5. Tapering of steroids is only necessary if coverage lasts longer than 3 days

6. Special care must be taken with patients who have Addison's disease.

The Asthmatic Patient 1. Consider local or spinal anesthesia 2. Continue asthma medication up until 1 & 1 /2 hours before surgery (take with a sip of water) 3. Inhalant medications are used as prescribed by the M.D. and can be used up to 1 & 1 /2 hours prior to surgery 4. Aminophylline via continuous infusion of 800 mg In 500 cc D5W at 20cc per hour (5cc per hour for children). You can adjust the rate according to the theophylline level

The Alcoholic Patient 1. Should have 3-4 days of rehydration (to prevent DT's), vitamins, proper diet, and no alcohol intake prior to coming to surgery 2. Nutritional status should be evaluated. This is done via measurement of serum albumin and total lymphocytes a. Serum albumin (<2.3 gm/dl): A measurement of nutritional status for the previous week. Not a good indicator of nutritional status for the day of surgery b. Total lymphocytes (<900): A good indicator of nutritional status for the day of surgery. This measures the response to stress

Patients on Anticoagulant Therapy 1. Indications for anticoagulants: a. PERIOPERATIVE PROPHYLAXIS FOR PREVENTION OF DVT's b. ISCHEMIC HEART DISEASE, c. ATRIAL FIBRILLATION d. MITRAL STENOSIS e. TIA's (transient ischemic attacks) f. Prosthetic heart valves 2. Heparin type: a. Inhibits intrinsic clotting pathway b. Used as short term therapy for prophylaxis against DVT's 5,000u subQ 2h before surgery & 5,000u subcQ Q 12 h until pt ambulatory c. DOSAGE REGULATED ACCORDING TO PTT (that's when you are treating, and not prophylaxing) d. EFFECTS REVERSED WITH PROTAMINE SULFATE 3. Coumadin type: a. Inhibits extrinsic clotting pathway b. Used as long term therapy c. DOSAGE REGULATED ACCORDING TO PT d. EFFECTS CAN BE REVERSED BY VIT. K (delayed) OR FFP (immediate)

4. For patients undergoing surgery, stop anticoagulants 3-6 days prior to surgery and reinstate therapy postoperatively 24 hours after the procedure. If you are worried about your patient not being on anticoagulants, you can stop coumadin 3 days prior to surgery and start a heparin drip and stop that 2-4 hours preoperatively

The Patient With Clotting Abnormalities 1. History is essential. Ask about: previous surgical bleeding problems, bruising easily, frequent nose bleeds 2. Drugs that alter platelet function: ASPIRIN, NONSTEROIDALS, STEROIDS, ANTIHISTAMINES, HIGH DOSES OF IV PENICILLIN (ESPECIALLY CARBENICILLIN), and HEPARIN 3. Tests to determine bleeding diathesis: PLATELET COUNT, BLEEDING TIME (Lee-White), PT, AND PTT NOTE* Bleeding time is especially useful if the patient is on aspirin, as aspirin stops platelet aggregation (must stop aspirin 1 week prior to surgery) 4. Bleeding diseases: a. Von Willebrand's Disease i. Abnormal factor VIII, PROLONGED PTT & BLEEDING TIME ii. Treat with fresh frozen plasma b. Hemophilia i. Type a: factor VIII deficiency ii. Type b: factor IX deficiency iii. Type c: factor XI deficiency iv. ALL 3 TYPES HAVE NORMAL BLEEDING TIME AND PROLONGED PTT v. Treat with: Factor replacement, fresh frozen plasma, whole blood, cryoprecipitate (4-6 units preoperatively and postoperatively), lyophilized concentrate c. Vitamin K Deficiency i. Vit K effects both intrinsic and extrinsic clotting pathway ii. PTT & PT are prolonged iii. Treat with 10 mg of vit K subQ: normalizes pt in 8 hrs. NOTE The hemophiliac patient must achieve a level of 70-100% prior to surgery, with a minimum of 40% being attained for 10 days NOTE* Due to the increased incidence of Hepatitis C and HIV with these patients, use caution

The Rheumatoid Patient 1. Order CERVICAL SPINE X-RAYS PRE-OP (predisposition for atlas/axis dislocation) 2. If patient is on steroids, you must supplement as per the previous recommendations (see The Patient on Steroid Therapy) 3. If patient is on nonsteroidals, discontinue perioperatively as it will alter bleeding times 4. If the patient is on antimalarials (chloroquine) for RA therapy, since a frequent complication is eye problems the patient should consider a preoperative consultation with an ophthalmologist. 5. If the patient is receiving gold salts for RA therapy, their potential toxic side effects should be looked for (urticaria, skin eruptions, mouth ulcers, eosinophilia, albuminuria, and leukopenia), especially in the urinalysis which can document substantial protein loss. If the drugs are not withdrawn after the onset of the side effects, patients can experience life threatening exfoliative dermatitis, nephritis, and thrombocytopenia 6. If the patient is on penicillamine for RA therapy, one can possibly expect potential decreased or slowed wound healing as this drug affects collagen synthesis. Vitamin C supplementation is useful in these patients. 7. If the RA patient is on immunosuppressive drugs (methotrexate, captopurine, azothioprine, and cyclophosphamide), the patient is more prone to infections due to the side effects of these drugs (increased bleeding time, bone marrow suppression leukopenia, thrombocytopenia). You should consider preoperative antibiotics in these patients. Note* These patients have been therapeutically immunosuppressed to decrease the severity of their autoimmnune response, and are therefore, prone to infections

The Sickle Cell Patient 1. LOCAL ANESTHETICS A PRIORITY 2. Avoid respiratory depression with narcotics and sedatives- avoid hypoxia with general anesthesia 3. Avoid using a tourniquet in patients with sickle-cell disease 4. Avoid hypoxia, dehydration, and acidosis intraoperatively and postoperatively 5. Complications of surgery can include: delayed healing, increased incidence of

wound dehiscence, leg ulcerations, bone infection (osteomyelitis is usually caused by Salmonella), and aseptic necrosis. NOTE* In the preoperative evaluation of the patient suspected of having sickle cell disease or trait the following tests are indicated: a. Sickle-cell prep b. Hemoglobin electrophoresis (for those with uncertain hemoglobinopathies)

NOTE* There is no specific therapy presently available for this disease. Treatment consists of symptomatic relief along with adequate hydration and analgesics. Oxygen therapy, alkalizing measures, and vasodilators have been used in attempts to shorten the crisis

The Cardiac Patient 1. The cardiac patient is at a higher risk during the perioperative period, and the factors which give the most post-op cardiac complications are: a. S3 GALLOP WITH JUGULAR VEIN DISTENTION b. M.I. WITHIN 6 MONTHS c. RHYTHM OTHER THAN SINUS ON PRE-OP ECG d. GREATER THAN 5 PVC's PER MINUTE BEFORE SX. e. AGE GREATER THAN 70 YEARS OLD f. PREMATURE ATRIAL CONTRACTIONS g. SIGNIFICANT AORTIC STENOSIS 2. Elective surgery should be postponed until 6 MONTHS postmyocardial infarct and in patients with uncompensated congenital heart failure 3. All risk factors such as unstable angina and cardiac failure should be stabilized preoperatively 4. Pre-op studies should include the studies for the normal patient undergoing general anesthesia, plus EKG, chest x-ray 5. Nitrates and Beta blockers should be continued during the perioperative period 6. Echocardiography should be considered in any patient with a pathological heart murmur 7. Endocarditis prophylaxis (indications): a. Prosthetic heart valve b. Prior hx of infective endocarditis c. Cyanotic congenital heart defect d. Surgically constructed systemic or pulmonary conduit e. Hypertrophic cardiomyopathy

f. Mitral valve prolapse with regurgitation, valve thickening, or both Not recommended for the following: a. Atrial septal defect b. Surgically repaired ventricular septal defect c. Patent ductus arteriosus d. Isolated Mitral valve prolapse e. Mild tricuspid regurgitation f. Previous rheumatic fever or Kawasaki disease without valvular dysfunction g. Cardiac pacemaker h. Implantable defibrillator Antibiotic Regimen: Amoxicillin 2gm IV 30 min pre-op followed by 1gm q8h post-op IF PENICILLIN ALLERGY: Vancomycin 1gm IV or Clindamycin 300mg PO pre-op and 150mg post-op. NOTE* Probably the best prophylaxis (when indicated) should be IV penicillin or 1st generation cephalosporin NOTE* DRUG ADDICTS ARE PRONE TO SUBACUTE BACTERIAL ENDOCARDITIS WITH TRICUSPID VALVE INFECTION SO ADMINISTER AN ANTISTAPH/STREP ANTIBIOTIC PRE-OP (DICLOXICILLIN)

The Pulmonary Disease Patient: 1. The major post-op complications are atelectasis and infection 2. Smoking and obesity increase pulmonary risk 3. Use incentive spirometry post-op to prevent problems (start preop) 4. D/C smoking at least 1 week prior to surgery 5. Treat all respiratory infections prior to surgery 6. Administer Heparin 5,000u subQ in selected cases for prophylaxis for venous thromboembolic disease. These patients are the ones with previous history of a. IDIOPATHIC THROMBOPHLEBITIS b. CHF c. OTHER DISEASES WHERE VENOUS STASIS MAY OCCUR 7. Consider the use of preoperative incentive spirometry (prevents atelectesis which can lead to pneumonia) 8. Consider arterial blood gas in patient with pulmonary history a. If pCO2>45 mmHg and P02<55 mmHg then the patient will require pulmonary function studies and possible use of bronchodilators (theophylline)

9.Consider the use of sequential compression devices in the pulmonary patient (stockings) preop, postop, and intraoperatively

Perioperative Management of the Infant and Child 1. Preoperative evaluation: a. Laboratory evaluation: i. CBC ii. ESR iii. PT/PTT iv. FBS v. Sickle-cell test (in young blacks) vi. Urinalysis

2. History and physical: a. Examination via the pediatrician b. Vital signs should be recorded. Temperature should be taken rectally in children under 3. Rectal temps may run 1 ° higher than oral temps. Pulse rates and respiration rates may be higher in children, and corresponding systolic blood pressure readings may be much lower than for adults

3. Preoperative medications: Drug administration in the hospital must be individualized for the child's level of growth and development, the form of the drug, and the reason for medication

a. Proper dosage can be calculated via Young's Rule, Cowling's Rule, or Clark's Rule i. Young: Divide the child's age by the age plus 12= The child's dose ii. Cowling: Divide the age at the next birthday by 24 iii. Clark: Divide the weight (in lbs) by 150 to give the appropriate fraction.of the adult dose b. Sedatives: Used as a preanesthetic agent to decrease apprehension and provide ease of induction i. Barbiturates: secobarbital, pentobarbital, and amobarbital. The sedative dose of barbiturates is 2 mg per kg orally TO

NOTE* Barbiturates are not generally recommended in infants as they can cause paradoxic restlessness and excitement ii. Chloral hydrate: A nonbarbiturate sedative-hypnotic, safe for infants and children. Can be administered in juice or soft drinks to decrease the unpleasant taste and minimize gastric irritation. The dosage ranges from 250 mg to 500 mg orally, up to three times daily. It may be given at 50 mg per kg at bedtime, up to 1 gm per dose 4. Fluids: Intraoperative fluid replacement is especially important in infants and children because their reserve available to compensate for fluid loss is small (have a large surface area for their mass). You must assess the fluid loss carefully. The estimated fluid loss can be satisfactorily replaced with Ringer's lactate 5. NPO: The routine order of NPO should be avoided a. No solid food or milk should be given for 12 hours prior to surgery, but fluid intake should have a minimal interruption b. Infants younger than 6 months are not placed on NPO status until 4 hours prior to induction and those from 6 months to 3 years are placed on NPO status 6 hours prior to surgery. For children over 3 years, NPO status should be 8 hours prior to induction 6. Postoperative pain: Avoid injections if at all possible (fear) a. Pentobarbital suppository: Dosage is 30 mg for children 1-5 years, 60 mg for those 6-10 years, and 90 mg for those 11-14 years b. Codeine (3 mg per kg) for mild pain c. Meperidine (1-1.5 mg per kg) for moderate pain 7. Antinauseants: Should be used sparingly, and doses should be adjusted a. Promethazine: Dosage 12.5-25 mg rectally or orally b. Vistaril®: Dosage 50 mg daily in divided doses for those under 6, and 50-100 mg daily in divided doses for those over 6 c. Emetrol®: OTC antinauseant, free of toxicity and side effects, and works immediately to control vomiting (1-2 tsp for infants and young children at 15 minute intervals until vomiting ceases)

Mitral Valve Prolapse Patient The majority of these patients are asymptomatic, so when is there the necessity of preoperative antibiotic prophylaxis to prevent bacterial endocarditis? Those individuals with evidence of mitral valve regurgitation (seen on echocardiogram) are at risk for life threatening complications and are given antibiotic prophylaxis. Asymptomatic patients are not usually given antibiotic prophylaxis unless it is for a high risk procedure producing a bacteremia (dental procedures, tonsillectomy and adenoidectomy, bronchoscopies, I & D of infected tissues, and GI and GU procedures). Podiatric procedures on low risk patients, are not usually prophylaxed unless there is infected tissue. 1. Clinical Symptoms: a. Chest pain b. Palpitations c. Syncope d. Dyspnea e. Arrhythmias (tachycardia) f. High levels of anxiety 2. Cardiogenic findings: a. Late or holosystolic murmur with or without a midsystolic click b. ST wave changes c. T wave inversions d. Q-T elongation 3. Antibiotics: a. Amoxicillin or clindamycin PO b. First generation cephalosporin (Ancef), Unasyn, or Vancomycin IV

Gouty Arthritis Patient The trauma of a surgical procedure can precipitate an acute attack of gouty arthritis, but the perioperative management of patients with gout has not been standardized. High-risk patients may include those with attacks in the past year, marked relief after a test course of colchicine, and a documented need for antihyperuricemic medication. Moderate-risk patients are those with past episodes of acute monarthritis resembling gout clinically and hyperuricemia during the acute episode (no joint aspiration for documentation). Low-risk patients are those with asymptomatic primary hyperuricemia, asymptomatic hyperuricemia associated with drugs, or some primary medical state (leukemia or other myeloproliferative disorders or solid tumors) 1. Treatment: a. High-risk patients: Should receive colchicine in a dose of 0.5 mg 3 times daily for 2-3 days prior to the operation and 4-5 days postoperatively (colchicine or indomethacin should be used when antihyperuricemic therapy is instituted) NOTE* Allopurinol rather than uricosuric drugs is indicated for patients excreting more than 600 mg of uric acid in 24 hours b. Moderate-risk patients: Given colchicine prophylactically as in high risk patients

c. Low-risk patients: Need not be treated NOTE* Postoperative attacks of gout are managed as in any patient with acute gouty arthritis

Chapter 4: Preoperative Evaluation Screening Procedures Summary of Perioperative Laboratory Testing

THE PREOPERATIVE EVALUATION An adequate pre-op preparation of the surgical patient is of the utmost importance. The quality of pre-anesthetic care largely determines the outcome, especially in patients with significant medical problems. What will constitute proper pre-anesthetic screening will vary from patient to patient according to their physical status and chronological age. The anesthetic technique applicable to healthy patients for simple procedures will differ from a more complex technique for major procedures.

Screening Procedures 1. The History: A medical history obtaining relevant information: a. DOES THE PATIENT HAVE AN M.D. AND IS HE/SHE PRESENTLY TREATING THIS PATIENT b. PRESENT or PAST MEDICAL PROBLEMS c. PREVIOUS HOSPITALIZATIONS/SURGERY & PROBLEMS WITH ANESTHESIA OR CLOTTING OR SCAR FORMATION d. TAKING ANY MEDICATIONS FOR ANYTHING (RX OR OTC'S) e. ANY KNOWN ALLERGIES f. FAMILY HISTORY ( SICKLE CELL, DIABETES, HYPERTENSION, REACTION TO ANESTHESIA, ETC.) g. SOCIAL HISTORY (SMOKING, DRINKING, DRUGS ETC.) h. REVIEW OF SYSTEMS 2. The Physical Examination: a. Vital Signs: B.P., TEMP, PULSE, AND RESPIRATIONS b. Review of systems: HEAD AND NECK, LUNGS AND HEART (AUSCULTATION), ABDOMINAL, GI, GU, EXTREMITIES, NEUROLOGICAL, DERMATOLOGICAL, VASCULAR, AND ORTHOPEDIC/BIOMECHANICAL NOTE* ONCE THIS INFORMATION IS KNOWN THE PATIENT'S PHYSICAL CONDITION CAN BE CATEGORIZED ACCORDING TO THE CLASSIFICATION OF PHYSICAL STATUS ADOPTED BY THE AMERICAN SOCIETY OF ANESTHESIOLOGISTS (ASA PHYSICAL STATUS)- See section Anesthesia 3. Laboratory Testing: BLOOD WORK, URINALYSIS, EKG AND CHEST XRAY (CXR) a. Complete Blood Count (Normal adult values): i. WBC- 4,800-10,800/mm3

NOTE* A WBC GREATER THAN 11, 000= LEUKOCYTOSIS Leukocytosis due to: a. AN ACUTE BACTERIAL INFECTION (Viral infection usually has normal WBC's) b. INTOXICATIONS (GOUT, HEAVY METAL POISONING, VACCINES) c. HEMOLYSIS d. HEMORRHAGE e. MYELOPROLIFERATIVE DISORDERS f. NORMAL VARIANT g. STRESS h. DEHYDRATION/ HEMOCONCENTRATION

NOTE* A WBC LESS THAN 4, 400= LEUKOPENIA Leukopenia can be due to: a. SEVERE INFECTION OR SEPTICEMIA b. HEPATITIS c. DRUGS (SULFA, ANALGESICS, BUTAZOLIDIN, THORAZINE) d. TRAUMA AND AIDS e. MYELOPROLIFERATIVE DISORDERS (MOST COMMON)

ii. WBC differential: allows for identification of the proportions of each type of WBC for a more specific diagnosis of a disease entity Divided into 2 groups: Granulocytes (neutrophils, eosinophils, basophils) and Nongranulocytes (lymphocytes, monocytes) NON-GRANULOCYTES: Lymphocytes (20-40%): involved in antibody production, function in cellmediated immunity, delayed hypersensitivity, graft rejection, defense against intracellular organisms such as tubercle bacillus, brucella, and neoplasms. An Increase can indicate VIRUSES (MOST COMMON), GERMAN MEASLES, BRUCELLOSIS, CONGENITAL SYPHILIS, THYROTOXICOSIS, PERTUSSIS, AND MONONUCLEOSIS. A decrease can indicate HODGKIN'S DISEASE, DRUGS. OR IRRADIATION, AND IMMUNOLOGICAL DEFICIENCY DISORDERS. Monocytes (4-8%): transform into macrophages which destroy/ingest bacteria etc. An Increase can indicate RECOVERY FROM ACUTE INFECTIONS, SUBACUTE BACTERIAL ENDOCARDITIS, MYCOTIC/RICKETTSIAL/PROTOZOAL & VIRAL INFECTIONS, HEMATOLOGIC DISEASE, LEUKEMIA, AND HODGKIN'S DISEASE. GRANULOCYTES: Neutrophils (45-65%): same as PMN's (either SEGS 40-60% or Bands 05%). The first specific line of defense for the body, an increase being called a SHIFT LEFT (of immature neutrophils, called bands) usually indicating an acute bacterial infection. A decrease in neutrophils, NEUTROPENIA, may indicate an

OVERWHELMING BACTERIAL INFECTION, SEVERE FUNGAL OR VIRAL INFECTION, BONE MARROW DEPRESSION, AUTOANTIBODIES, BONE MARROW REPLACEMENT, HYPERSPLENISM, AND MATURATION DEFECTS (VITAMIN DEFECTS) An Increase in neutrophils, NEUTROPHILIA, can indicate: INFECTION Neutropenia may be the earliest clue to marrow failure (TYPHOID), TOXIC AGENTS, PHYSICAL OR EMOTIONAL STIMULI, TISSUE NECROSIS, HEMORRHAGE, HEMOLYSIS, AND HEMOLYTIC DISORDERS, OR RECENT STRAINED DEFECATION (VALSALVA MANEUVER). NOTE* Usually with a shift left there is a characteristic relative fall in lymphocytes with neutrophil leukocytosis and increase in young forms. When the infection subsides and the fever drops, the total number of leukocytes decreases Eosinophils (1 -3%): contain histamine and transport alkaline phosphatase, an increase indicating INTESTINAL PARASITES, ALLERGIC REACTIONS, URTICARIAL SKIN ERUPTIONS, LEUKEMIA, GI DISTURBANCES OR SCARLET FEVER. A decrease can indicate SEVERE INFECTIONS, CUSHING'S SYNDROME, ELECTRIC SHOCK THERAPY, AFTER INJECTION WITH ACTH OR EPINEPHRINE. Basophils (0-1 %): contain heparin and transport alk phos and histamine, an increase is associated with POLYCYTHEMIA, LEUKEMIA, CHICKEN POX, SMALL POX. A decrease can be due to ACUTE INFECTIONS AND ACTH OR CORTICOSTEROIDS iii. PLATELET COUNT (150,000-400,000): Platelet disorders should be suspected in patients exhibiting PETECHIAE in the skin or mucosa. THROMBOCYTOPENIA: Decreased platelet count, is seen with THROMBOCYTOPENIA PURPURA, APLASTIC ANEMIA, OR SEPTICEMIA. NOTE* The most common cause of thrombocytopenia is chemotherapy

Decreased platelet count increases the risk for hemorrhage. If the platelet count is less than 60,000 give platelets (1 unit will raise the count 5,000/cu mm. For any elective surgery the thrombocytopenic patient should be postponed • THROMBOCYTOSIS: Increased platelet count seen with splenectomy, malignancy, and patient is prone to form clots with this condition iv. RBC's: (Male, 4,700,000-6,100,000mm3) (Female, 4,200,0005,400,000/mm3)

An increase may be due to POLYCYTHEMIA, METASTATIC CARCINOMA AFFECTING THE MARROW, THALASSEMIA, INCREASED ALTITUDE, EXERCISE OR EMOTIONAL STRAIN v. RETICULOCYTE COUNT (.5-1.5% OF THE TOTAL RED COUNT): • It is the best indicator to assess marrow activity • Increases found with IRON DEFICIENCY AND MEGALOBLASTIC ANEMIA (recent bleeding/hemorrhage is the #1 cause) • Decreases found with MACROCYTIC AND APLASTIC ANEMIAS vi. HEMATOCRIT (Males 43-53% Gm/dl) (Females 35-47% Gm/dl): NOTE* THE HCT IS USUALLY 3 TIMES THE Hb • • •

That portion of the total blood volume occupied by red cells versus plasma Increased with POLYCYTHEMIA, DEHYDRATION OR ADDISON'S DISEASE Decreased with anemias and hemorrhage

vii. • • •

HEMOGLOBIN (Males 12-17) (Females 11-16): Gives red cells their oxygen carrying capacity Increased with POLYCYTHEMIA, HEMOLYTIC ANEMIA, AND PORPHYRIAS Decreased with other anemias, HEMOGLOBINOPATHY and hemorrhage

viii. MCV=HCT/RBC: Reflects the size of the red cell Decreased MCV Iron deficiencies Thalessemia Lead poisoning Sideroblastic anemia Hypernatremia

Increased MCV Pernicious anemia (B12 and Folate deficiency) Liver disease Hypothyroidism Leukemia

ix. MCH=Hb/RBC: Is an estimate of Hb in the average cell x. MCHC=Hb/HCT: An estimate of Hb In an average cell

Anemias: Anemia may result from inadequate production of RBC's due to deficiency states of bone marrow failure or to excessive loss or destruction of erythrocytes. Precise diagnosis is needed for treatment with 4 basic tests used: a. Hematocrit and hemoglobin b. Reticulocyte count: low= marrow is the site of pathology normal or high count= good RBC production but cellular destruction peripherally c. Peripheral smear (with bone marrow biopsy) to examine the shape and color of the RBC. d. Platelet count Also can do COOMBS test (DIRECT): do when the HCT is falling, elevated bilirubin, don't have obvious bleeding, and have hemolysis on the peripheral smear Macrocytic: either megaloblastic (B 12 or folic acid deficiency) or chronic liver disease (OH'ism), hypothyroidism Normocytic: due to sudden loss of blood, hemolytic anemias, anemias caused principally by impaired production, and anemia of chronic disease (DM or RA) Hypochromic -microcytic: seen with iron deficiency (most common cause), thalassemia, and sideroblastosis Normochromic-microcytic: seen with bone marrow suppression, hemolysis, chronic infections, and inflammatory diseases

Note* Pernicious anemia, in which B, 2 is not absorbed when gastric mucosa is unable to produce intrinsic factor, resulting in a liver depletion of B12 and subsequently a disturbance of DNA. Diagnosis is via SCHILLING TEST. Pernicious is part of an autoimmune complex

NOTE* Sickle-Cell Anemia is seen in 1:600 American blacks. Variants of sicklecell disease are types of hemolytic anemias caused by the substitution of valine for glutamic acid in the B-globin chains of HbA, the normal adult hemoglobin. Three principle variants exist: a. Homozygous state (SS) or true sickle-cell anemia b. Heterozygous state (AS) or sickle-cell trait c. Double heterozygous state (SC) consists of two abnormal hemoglobin chains Patients with SS or SC hemoglobinopathies are usually aware of their disorders because of previous crises, while the AS patient is usually asymptomatic. Three major factors contribute to red blood cell sickling: a. The Hgb-S concentration b. The partial pressure of oxygen c. The pH

b. Tests for Hemostasis: i.. Platelet count: for quantification purposes ii. Prothrombin time: measurement of extrinsic blood coagulation pathway (normal 11-13 seconds) PT will be long with deficiencies of prothrombin, Factor V, Factor Il, or Factor X • Affected by coumadin type anticoagulants iii. Partial thromboplastin time: measurement of intrinsic blood coagulation pathway (24-26 seconds is normal) and should be within 5 seconds of the control (control is up to 45 seconds in some labs). iv. Bleeding time (Lee-White): a standard in vivo assay that measures the effectiveness of platelet plug formation. This test is performed in patients who are suspected of having a qualitative platelet disorder, such as patients having recently taken ASA or who have von Willebrand's disease NOTE* The mechanism for blood clotting may be divided into 3 stages: Stage 1: The production of plasma (extrinsic) or tissue (intrinsic) thromboplastin to form prothrombin activator. Stage 2: The conversion of fibrinogen to fibrin by the proteolytic action of thrombin. Stage 3: The conversion of fibrinogen to fibrin by the proteolytic action of thrombin. Calcium is required for all stages.

NOTE* Coumadin prevents the conversion of vitamin K to its active form, thereby impairing the formation of vitamin K-dependent clotting factors. It is an anticoagulant indicated for the prophylaxis or treatment of venous thrombosis, pulmonary embolism, atrial fibrillation with embolization, and as a prophylaxis of embolism after myocardial infarction. Coumadin therapy should be monitored by monthly international normalized ratio (INR) testing. The test represents a standardized or corrected prothrombin time since results for prothrombin time may vary by institution. The INR should be obtained preoperatively for any patient on coumadin (Warfarin) and should range from 2 to 3. The dosing of the coumadin should be adjusted preoperatively so that the INR is maintained at the low end of of the therapeutic range. Holding the dose of coumadin for 2-3 days prior to elective surgery will provide protection against intraoperative bleeding without compromising prophylaxis of the patient. If necessary, the coumadin effects on the INR may be reversed by the administration of vitamin K1 or fresh frozen plasma c. Sequential Multiple Analyzer (SMA) SMA 12 has the following tests: ALBUMIN, ALKALINE PHOSPHATASE, BILIRUBIN, BLOOD UREA NITROGEN, CALCIUM, CHOLESTEROL, LACTATE DEHYDROGENASE, SGOT, GLUCOSE, PHOSPHATE, TOTAL PROTEIN, AND URIC ACID SMA 16 adds the following four electrolytes: NA, K, CL, AND C02

1. Albumin (3.6-5.2 Gm/dl): A blood protein from the liver-a good indicator of hepatic health
Reduced levels are a problem and can result in EDEMA
Increased levels can cause dehydration
Reduction due to: LIVER DISEASE, MALIGNANCY, MALNUTRITION, KIDNEY PATHOLOGY AND LARGE SKIN WOUNDS WITH SERUM LOSS SUCH AS BURNS ii. Alkaline Phosphatase (35-137 U/dl):
Found in the liver, bone, placenta and lung as tissue-specific forms Anything that stimulates osteoblastic activity increases the Alk Phosphatase: METASTATIC BONE CANCER, GROWING CHILD, OSTEOGENIC SARCOMA, PAGET'S DISEASE OF BONE, MONONUCLEOSIS, PREGNANCY, GROWTH AFTER FRACTURE NOTE* The most common cause of elevated liver alkaline phosphatase is common duct obstruction, and the second most common cause is bed rest in the hospitalized patient iii. Bilirubin (less than 1.2 mg/dl):
It is a pigment of bile from RBC breakdown in liver, spleen and marrow.
Problems develop from abnormal production and decreased excretion Total bilirubin divided into direct and indirect fractions (direct increased due to direct hepatic obstruction- indirect due to liver disease. Bilirubin increased with: CIRRHOSIS, ACUTE VIRAL HEPATITIS, CHF, HEMOLYSIS AND SEPTICEMIA iv. Blood Urea Nitrogen (5-25 mg/dl): Is an end product of protein metabolism and produced only in the liver and excreted by the kidney.
BUN increased with: DIABETES AND PROTEIN BREAKDOWN, KIDNEY PATHOLOGY, FEVER AND PROTEIN BREAKDOWN, CHF, RBC BREAKDOWN AND STARVATION (dehydration is #1 cause)
BUN decreased with: HYDRATION, LIVER PATHOLOGY AND DECREASED PRODUCTION v. Calcium (4.5-5.5 mg/dl): Serum calcium increased with any disease of bony demineralization such as: MULTIPLE MYELOMA, CANCER OF BONE, EXCESSIVE CALCIUM INTAKE, HYPERPARATHYROIDISM AND HYPERVITAMINOSIS D. Serum calcium decreased with: RENAL FAILURE (#1), POOR ABSORPTION, MALNUTRITION, HYPOPARATHYROIDISM, PSEUDOHYPOPARATHYROIDISM AND DIARRHEA vi. Chlorides (98-110 meq/L):
Usually lost from the urine or GI fluid which carry the chloride ion
Chlorides decreased with: DEHYDRATION (#1), VOMITING, DIARRHEA,




ULCER AND FLUID LOSS, EDEMA, DIURESIS, GI OBSTRUCTION AND INFECTION. Rare to have elevated chloride, if so, can indicate CYSTIC FIBROSIS

vii. Cholesterol (150-220 mg/dl):
Produced from food and endogenous production (mostly in the liver)
Used for membranes, STEROID hormones and bile acids.
Increases: IDIOPATHIC, HYPOTHYROIDISM, DIABETES MELLITUS, PANCREATITIS
Decreases: MALABSORPTION, LIVER DAMAGE AND POOR PRODUCTION viii. Creatinine (under 1.2 mg%):
Produced from creatine in muscle tissue and excreted by the kidneys -Not elevated in the blood until 50% of renal function obliterated
Any major reduction in creatinine clearance of urine indicates kidney impairment ix. Glucose (70-110 mg/dl):
The liver produces glucose from protein (gluconeogenesis).
Blood glucose is filtered through the kidney glomeruli and reabsorbed in the proximal tubule, and if renal threshold is exceeded glucose is spilled into the urine.
Elevated with: DIABETES MELLITUS, CUSHING'S SYNDROME, ACROMEGALY, STRESS, BURNS, SHOCK, ACUTE PANCREATITIS, OBESITY, ACTH ADMINISTRATION AND AGE
Decreased with: INSULIN SHOCK, ISLET CELL TUMOR, NUTRITION, GLUCAGON DEFICIENCY, ADDISON'S DISEASE AND HYPOTHYROIDISM (Hypoglycemia may be precursor to DM) x. Lactate Dehydrogenase (208-378U/L):
This is a glycolytic enzyme that functions in carbohydrate metabolism which is found in the kidney, liver, heart, RBC's.
Increased with any tissue damage, therefore it is NOT SPECIFIC xi. Total Protein (6.4-8.3 g/dI):
Contains albumin and globulins and rarely is total protein increased since most disease states lower body reserves
Increased with: DEHYDRATION caused by vomiting and diarrhea
Albumin:Globulin Ratio= 1.5:1-2.5:1 xii. Phosphate (8-12 mg/dl):
it is absorbed in the intestine, stored in bone, and excreted by the kidneys
Elevated with: RENAL FAILURE, HYPOPARATHYROIDISM, INCREASE VIT D INTAKE, BONE DISEASE, FRACTURES, PAGET'S DISEASE OF BONE, MULTIPLE MYELOMA
Decreased with: HYPOVITAMINOSIS D, DIABETES, HYPERPARATHYROIDISM (MOST COMMON IS POOR NUTRITION)

xiii. Potassium (3.5-5.1 mEq/l): Very important element in the pre-op evaluation
Decreased K produces muscle cramps and arrhythmias while increased K produces arrhythmias and cardiac pathology
increased with: USE OF MINERALCORTICOIDS, RENAL FAILURE, ACIDOSIS, DIABETIC KETOACIDOSIS.
Decreased with: ALKALOSIS, DIARRHEA, DIURETICS, INSULIN, MALABSORPTION AND STARVATION (#1 cause is with excess IV's) Symptoms don't start until serum levels fall below 2.5 mEq/L -Cardiac standstill can occur when levels exceed 7.5-8.0 mEq/L xiv. SGOT (AST 1-45 IU/L):
The enzyme used in glycolysis and energy production and found mostly in the liver, heart, and also in the muscle, kidney, and pancreas.
Sudden increase seen with MI, also with liver and lung pathology NOTE* Elevated SCOT (AST) seen in pulmonary embolism postoperatively


Elevated in: CARDIAC DAMAGE, LIVER DAMAGE, SKELETAL PATHOLOGY, PANCREATIC PATHOLOGY. The SGOT parallels the SGPT AL , whose normal values = 1-60 IU/L, except the SGOT shows higher values with MI and the SGPT has higher values with LIVER PATHOLOGY

xv. Uric Acid (2.8-8.0 mg/dl):
Manufactured from purine metabolism
The pH of urine must be close to 7.4, as uric acid is poorly soluble as the pH decreases with crystals forming depositing in tissues across the cell membrane. Therefore alkalinization of the urine increases uricosuric activity. NOTE* WHEN TREATING GOUT CHECK THE pH OF THE URINE xvi. Serum Amylase: NOT USUALLY DONE PREOPERATIVELY
Enzymes produced in the pancreas and used for the digestion of starch
Elevation due to cellular destruction of amylase in the pancreas or poor renal excretion, due to: PANCREATITIS, PERFORATED ULCER, PANCREATIC DUCT OBSTRUCTION, AND RENAL FAILURE.
Decreased due to CHRONIC PANCREATIC OBSTRUCTION. xvi. Acetone: Detected by dipstick urine test- should be negative
ketone body from fat metabolism
Elevated with: STARVATION, STRESS, DIABETES, LOW CARBOHYDRATE DIET NOTE*AS KETONES INCREASE pH DECREASES

xvii. Acid phosphatase: NOT USUALLY DONE PREOPERATIVELY
Found in the male prostate, the male urine, RBC's and platelets (female).
High levels consistent with METASTATIC CARCINOMA OF THE PROSTATE
Can also be elevated with MULTIPLE MYELOMA AND PAGET'S DISEASE OF BONE NOTE*: SERUM PROFILE LIVER- BILIRUBIN, CHOLESTEROL, SGOT, SGPT, ALKALINE PHOSPHATASE, ALBUMIN KIDNEY- CHLORIDE, CREATININE, BUN, PHOSPHOROUS, PROTEIN, TOTAL PROTEIN, LDH, Na, K, C1, Co 2 CARDIAC- LDH, CPK, SGOT, ELECTROLYTES, BUN ARTHRITIC- LATEX FIX, ESR, VDRL, ANA, ASO TITER, URIC ACID, LE PREP (RARELY DONE- ANA MORE ACCURATE)

4. URINE ANALYSIS: a. A multitest dipstick is used on the urine to get rough readings on glucose, acetone, bile, urobilinogen, protein and blood. The urine is then centrifuged and the solid matter goes to the bottom and is then examined microscopically for red/white/epithelial cells, crystals and casts. b. Also checked is the color, clarity, pH and specific gravity c. The specific gravity range is 1.020-1.032. (when concentrated in the AM) A measure of the kidney's ability to concentrate and the SG is elevated by extra glucose (diabetes) and protein due to increased concentration in the fluid. d. All glucose in the urine is competely reabsorbed by the proximal tubules, therefore the appearance of glucose in the urine when the blood glucose levels is below 180 (250 IN SOME TEXTS) may signify proximal tubule damage. e. Small amounts of protein are found in the urine (albumin and globulins), however, large amounts in excess of 4gms daily indicate glomerular disease (mostly albumin) f. Ketone bodies accumulate due to altered lipid metabolism, most frequently as a consequence of diabetes mellitus or low carbohydrate diet g. OCCULT hematuria occurs from: EXCERCISE (#1), CYSTITIS, HEMORRHAGE, MENSTRUATION, GLOMERULONEPHRITIS, HYPERTENSION, POLYCYSTIC DISEASE AND RENAL THROMBOSIS i. Microscopic hematuria seen with acute infection, sickle cell anemia, excercise, menses and SBE. h. GROSS hematuria associated with stones, tumors, TB, and acute glomerulonephritis. i. Normal urine is slightly acidic, pH usually below 5.3, is-altered by diet or medications i. An alkaline urine in the presence of metabolic acidosis suggests Renal Tubular Acidosis. NOTE* An alkaline urine is most commonly seen in a proteus UTI

j. Normal findings in the urinary sediment includes up to : 1 RBC, 5 WBC'S, AND AN OCCASIONAL CAST. k. Abnormal findings in the sediment include: RBC'S, WBC CASTS, YEAST, CRYSTALS OR EPITHELIAL CELLS. l. Casts are protein conglomerations in the shape of the renal tubule. Two types of casts: i. CELLULAR- RBC, WBC, EPITHELIAL CELLS, OR ANY COMBINATION IN A PROTEIN MATRIX NOTE* With WBC casts, the cells become emulsified in the protein matrix and may be found in pyelonephritis, acute glomerulonephritis, or SLE. The cells in RBC cell casts are emulsified in protein matrix and are indicative of glomerulitis. Casts containing fat droplets are called fatty casts and are associated with nephrotic syndrome

ii. PROTEIN- are composed entirely of protein m. Crystals in the urine may indicate stones or certain metabolic diseases n. Bile present indicates hepatic obstruction or constipation o. Urobilinogen can be present due to HEPATITIS p. Catecholamines: elevation in the urine is indicative of pheochromocytoma or extramedullary chromaffin tumors, malignant hypertension, progressive ms. dystrophy, myasthenia gravis, and drugs. (this is not usually done preoperatively) 5. Pregnancy testing: Should be performed on all women within childbearing years 6. Chest x-ray: This compliments the H & P as a starting point for the diagnosis and evaluation of suspected pulmonary disorders. Abnormalities seen on the x-ray are: CHF, pulmonary masses, pleural effusions, pneumonia. Remember that the chest xray alone is not a good indicator for operative risk 7. Electrocardiogram: Recommended that all patients over the age of 40 have this test done, however, a poor predictor of ischemic heart disease and perioperative cardiac morbidity and mortality. Electrocardiography is a graphic representation of the electrical currents associated with the contraction of the heart muscle. The basic function of the electrocardiographic monitor is to amplify the small voltage formed by the depolarization of the heart so that it can be presented on the screen for visual monitoring or so that a graphic record can be made. a. Conduction mechanism of the heart

i. Sinoatrial node (SA): The electrical impulse is formed in the SA node, which is the physiologic pacemaker of the heart, located at the junction of the right atrium and superior vena cava ii. Atrioventricular node (AV): After the SA node the impulse speeds to the AV node, at the junction of the atria and ventricles

iii. Bundle of His: After the AV node fires, the impulse travels to the bundle of His, then the right and left bundle branches, Purkinje's fibers, and the ventricles b. The normal electrocardiogram: i. P wave: Indicates the results of the electrical activity during atrial depolarization that initiates atrial contractions
P-R interval: Represents the time it takes the impulse to spread from the SA node to the ventricles (normal time 0.12-0.20 sec)

Normal EKG Tracing

i. QRS complex: Is due to the depolarization of the ventricles, which triggers their contraction. It indicates the time it takes for ventricular depolarization (normal time 0.06-0.10 sec) ii. T wave: Occurs at the end of ventricular systole b. The recording paper has horizontal and vertical lines: i. Horizontal lines: Indicate voltage and are 1 mm apart (1 mm represents 1 mV) ii. Vertical lines: Indicate time and are separated by an interval of 0.04 sec. The heavy vertical lines represent 0.2 sec intervals, and the five large squares represent 1 sec iii. Heart rate per minute: Is determined by counting the number of QRS

complexes that occur in 3 seconds (15 large squares) and multiplying by 20 c. EKG (ECG) leads: i. Standard lead (I, II, Ill): Are bipolar indirect leads, that record the difference between two points on the body, in electrical events formed by the cardiac action. The electrodes are attached to the left arm, right arm, and left leg. The right leg is used for a ground. The terminals are placed as follows: • Lead l: right arm, left arm • Lead II: right arm, left leg • Lead III: left arm, left leg ii. Unipolar extrmity leads: Indicate the electrical potentials at one point. The electrodes of the three limbs are attached together to form one electrode, called the central terminal lead. The differences of the electrical potentials are recorded between the central terminal and each of the three extremities • Lead aVr: is positioned at the right arm • Lead aVL: is positioned at the left arm • Lead aVf: is positioned at the left foot iii. Precordial leads: Are unipolar leads that indicate the variation of electrical potentials at a given cardiac anatomic site. The central terminal lead is used, and the exploring electrode is positioned in the chest and in six different locations, V1 to V6

Summary of Perioperative Laboratory Testing 1. Blood studies: a. CBC: Hgb, Hct, RBC, WBC, platelets, red cell indices (MCV MCH etc.), WBC differential (segs, lymphs, bands, etc.) b. Serum electrolytes: Sodium, potassium, chloride, calcium, magnesium c. Liver studies: i. Hepatocellular enzymes: SGOT/ALT ii. Studies of obstruction: Alkaline phosphatase, glutamyltransferase (GGT), and 5' Nucleotidase iii. Evaluation of jaundice: Bilirubin (conjugated or unconjugated) iv. Other liver studies: Albumin, prothrombin time (PT) d. Renal studies: Blood Urea Nitrogen, creatinine, serum electrolytes (mediated by kidney), creatine e. Cardiac enzymes: Lactic dehydrogenase (LDH), SCOT (AST), creatine phosphokinase (CPK) f. Clotting: Partial thromboplastin, prothrombin, bleeding time, INR 2. Urinalysis: a. Dipstick: Protein, blood, glucose, ketones, pH b. Microscopic exam: RBC's, WBC's, cellular casts, bacteria, crystals 3. Pulmonary function tests: a. Static lung volumes: Total lung capacity, functional residual capacity, residual volume, vital capacity b. Dynamic volume measurement: Forced vital capacity (FVC), forced vital capacity in 1 second (FEV1), and FEV1 /FVC

4. Arterial blood gas: Oxygenation, carbon dioxide, 02 saturation, pH 5. Chest x-rays: Cardiac size, calcifications, lung masses, pleural effusions, infiltrates, interstitial patterns 6. EKG: a. Rate b. Rhythm c. Intracardiac conduction times (PR interval, QRS interval, QT interval) d. Chamber enlargement (hypertrophy of myocardium) e. Myocardial infarction patterns (pathologic Q waves) f. ST segments of ischemia

Chapter 5: Postoperative Care & Complications Fever Altered Mental States Water and Electrolyte Imbalance Oliguria Chest Pain Postoperative Hypertension Postoperative Infection Anxiety and Pain Management Nausea Constipation Shivering DVT Compartment Syndrome Hemorrhage Septic Syndrome Thyroid Storm

POSTOPERATIVE COMPLICATIONS The number of potential post-operative problems is large, with some occurring more frequently. Those are FEVER, ALTERED MENTAL STATUS, WATER & ELECTROLYTE DISTURBANCES, RENAL FAILURE, CHEST PAIN, SHORTNESS OF BREATH AND HYPERTENSION (A hospitalized patient developing cough, fever and an abnormal chest x-ray after prolonged general anesthesia and a patient with the same fin dins following a procedure done under local anesthesia must be viewed differently)

Fever Temperature> 101.6 orally: Fever is the most common post-op problem. The time of occurrence is an important clinical guide in determining the etiology. Fever can also occur without any associated pathological conditions. WIND (PULMONARY EMBOLISM, ATELECTASIS AND PNEUMONIA) WATER (URINARY TRACT INFECTION) WALKING (THROMBOPHLEBITIS- between 3-10 days postop; positive Homan's sign) WONDER DRUGS (DRUG FEVER- the patient is less ill than the fever would suggest) WOUND (SEPSIS) WOW (BREASTS: MASTITIS) -Usually ObGyn WOMB (ENDOMETRITIS)-Usually ObGyn 1. Fever within 24 hours (THE MOST COMMON) can be due to: a. ATELECTASIS FROM HYPOVENTILATION b. ASPIRATION OF ORAL OR GASTRIC CONTENTS c. DRUG REACTIONS (IF PATIENT RECEIVED BLOOD THEN ADD TRANSFUSION REACTIONS) 2. Fever after 24 hours following surgery can be due to: a. ATELECTASIS & ASPIRATION b. WOUND INFECTIONS c. IV SITE PHLEBITIS d. UTI e. DVT f. HEPATITIS

NOTE* IF A FEVER DEVELOPS WITHIN THE FIRST 6-8 HOURS FOLLOWING SURGERY, THE MOST LIKELY CAUSE IS AN ENDOCRINE IMBALANCE WHICH MAY LEAD TO A TEMPORARY THYROID CRISIS OR ADRENOCORTICOID INSUFFICIENCY. SHOULD FEVER DEVELOP 8-10 HOURS AFTER SURGERY, A PULMONARY MALFUNCTION SHOULD BE ENTERTAINED AS THE LIKELY CAUSE. URINARY TRACT INFECTIONS ARE THE MOST LIKELY CAUSE OF FEVERS AT THE SECOND OR THIRD POSTOP DAY (URGENCY, FREQUENCY, PAIN, AND BACTERIA). BACTERIAL INFECTIONS OCCUR 3-7 DAYS POST-OP: WITH THE EXCEPTION OF GROUP A STREP, WHICH CAN OCCUR EARLIER. A SPIKING TEMPERATURE IS INDICATIVE OF AN INFECTION, ALONG WITH TACHYCARDIA, CHILLS, MALAISE, LETHARGY, AND LOSS OF APPETITE ALL IV LINES AND HEPARIN LOCKS SHOULD BE CHANGED EVERY 2-3 DAYS TO PREVENT INFECTION. DIABETIC FEMALES AND ELDERLY MALES ARE AT HIGHEST RISK FOR UTI'S.

3. DO NOT TREAT THE FEVER WITH ANTIPYRETICS UNTIL THE CAUSE IS DETERMINED (There are exceptions to this rule: patient discomfort, delirium or convulsions and the precipitation of heart failure 4. Risk factors: a. Surgery over 2 hours in time b. Transfusion c. Pre-existing infection d. In place prosthesis or shunt

Altered Mental States

1. Can develop In: ELDERLY PATIENTS, METABOLIC DISORDERS, HYPONATREMIA, HYPOGLYCEMIA, HYPERGLYCEMIA (MOSTLY HYPO), ACIDOSIS (SEPSIS, SHOCK AND DIABETIC KETOACIDOSIS), Ml, ARRYTHMIAS, CVA'S & DRUG PROBLEMS (TOXICITY AND DRUG INTERACTIONS)

Water and Electrolyte Disturbances 1. Can develop as a result of: IMPROPER FLUID REPLACEMENT, INCREASED BODY LOSS (Vomiting and fever), MEDICATIONS AND STRESS 2. FLUID ADMINISTRATION OF 2000-3000 MIDDAY IS NEEDED TO MAINTAIN A DESIRED URINE OUTPUT OF 1000-1500 ML/DAY 3. FEVER INCREASES WATER LOSS (FOR EACH DEGREE ABOVE NORMAL WATER LOSS IS INCREASED BY 100-150 ML/DAY 4. Sodium disorders (Na): a. HYPONATREMIA (Na<125 meq/L): Can occur post-op. Symptoms are lethargy, confusion, coma, muscle twitch, nausea, vomiting and cardiac problems. Treated by restricting fluids to 1000-1500 ml fluid/day. Can occur from i. HYPONATREMIA WITH VOLUME EXCESS ii. HYPONATREMIA WITH VOLUME DEPLETION iii. HYPONATREMIA WITH NORMOVOLEMIA b. HYPERNATREMIA (Na>145 meq/L): Symptoms are confusion, stupor, coma, muscle tremors, seizures, pulmonary and peripheral edema. Treated with D5W slowly over 24 hours 5. Potassium disorders (HYPO OR HYPERKALEMIA): can occur post-op, and can be life threatening a. HYPOKALEMIA (K<2.5) occurs in the following: i. PATIENTS GETTING DIURETICS ii. VOMITING iii. DIARRHEA iv. BRITTLE DIABETES v. ANTI-PSEUDOMONAL ANTIBIOTICS vi. HIGH DOSES OF STEROIDS (See section Pre-op Evaluation- SMA) b. HYPERKALEMIA (K>4.5) is seen less frequently but is far more lethal than HYPOKALEMIA and can manifest itself with weakness, hyperactive reflexes, and cardiac manifestations/standstill c. Treatment of hyperkalemia must be immediate: Give Calcium Chloride, then Sodium Bicarb or even D50 with insulin (and KAYEXELATE if necessary)

Oliguria 1. Due to: a. BLADDER OBSTRUCTION b. THE COMBINATION OF BEDREST/PROSTATIC HYPERTROPHY/ANALGESICS (DEMEROL***)

c. ISCHEMIC INSULTS d. NEPHROTOXIC DRUGS 2. To approach a patient with acute renal failure you must do the following: a. Measure urine volumes and medication use b. Assess hydration and cardiovascular status c. Bladder catheterization a possibility d. Fresh urine analysis- with examination of the sediment e. Labs: serum and urine sodium, creatinine, osmolality and BUN f. Special tests: RENAL FAILURE INDEX AND FRACTIONAL EXCRETION OF SODIUM MEASUREMENT

Chest Pain 1. Etiology: a. MI b. PULMONARY EMBOLUS c. PNEUMONIA d. ANXIETY e. ATELECTASIS f. ASPIRATION g. CHF 2. Treatment: a. Must perform EKG, chest x-ray, arterial blood gases (establishes probability of a diagnosis) b. May do VENTILATION PERFUSION RADIONUCLEOTIDE LUNG SCAN (A negative study R/O P.E.) c. If doubt remains, can do: PULMONARY ANGIOGRAPHY (Most specific and sensitive test for P.E.) d. A distinction should be made between ASPIRATION PNEUMONIA AND ASPIRATION PNEUMONITIS. NOTE* The former is caused from aspiration of sterile/acidic gastric contents and results in a chemical pneumonitis. The latter occurs when polymicrobial oral secretions are introduced into the pulmonary system.

Post-op Hypertension 1. Etiology: a. Noxious stimuli (most common): Pain, excitement (emergence from general anesthesia), shivering, and mild hypothermia b. Drug induced: Withdrawal from beta blockers c. Metabolic abnormalities: Pheochromocytoma, Cushing's syndrome d. Miscellaneous: Fluid overload, distended bladder, tight cast 2. Treatment: Try to establish the etiology

a. Treat pain and anxiety first, and warming of the patient b. If the hypertension persists, it can be treated with sublingual Procardia 20 mg, IV Furosemide (if volume overload, distended bladder), or ideally a drug which is fast acting, titratable, rapidly reversible, efficacious, and with no side effects that can offset the cause of the hypertension NOTE* Sudden decreases in blood pressure accompanying treatment of hypertension can have catastrophic results: seizures, CVA's, acute Ml, renal failure, and death

Postoperative Infection 1. Can occur 3-7 days postoperatively 2. Group A Strep can occur earlier 3. Symptoms a. Increased throbbing pain b. Swelling 4. Signs a. Wound drainage b. Wound dehiscence c. Erythema d. Fever 5. Treatment: Decide on hospital or outpatient therapy NOTE* Admit to hospital with systemic manifestations (fever/shakes/chills, lymphangitis, lymphadenopathy), debilitated host ( Diabetic, PVD, alcoholic, immunosuppressive therapy, burn patients), need for IV antibiotics, resistant organism, risk of deep space infection, deep space necrosis or wet gangrene, suspicion of osteomyelitis, need for extensive surgical debridement, and failure of outpatient. therapy a. Consider ID consult/ internal medicine consult/ vascular consult prn b. Perform local wound care/release and remove sutures/ incision and drainage as necessary c. Perform gram stain and aerobic/anaerobic/fungal/acid fast cultures (as necessary) from wound site and blood cultures if indicated d. Obtain necessary lab studies (CBC,Hb, urinalysis, chemistries) e. Begin antibiotics as per gram stain a clinical evaluation and judgement/ reevaluate as per C & S f. Continue appropriate antibiotic at least 10 days (especially when treating strep, to prevent post strep glomerulonephritis. May consider IV antibiotics)

Anxiety and Pain Management 1. Pain complaints reflect not only tissue injury, but many psychological dimensions of suffering as well. a. A long acting local anesthetic injected at the end of the surgery will delay postoperative pain past the initial phases.

b. The injection of a short-acting soluble steroid will help diminish painful swelling and inflammation associated with the lag phase of healing. c. NSAID's can many times be the sole postoperative medication because inflammation is the hallmark of the initial and most painful postoperative phase. d. Opiates or opiate-like drugs can be used in combination with ASA or acetaminophen. These drugs should be considered if NSAIDs have failed to alleviate the pain. e. Excessive anxiety will greatly reduce the pain threshold, therefore sedatives can greatly help these patients. f. Toradol® IM/IV has been found to be very effective immediately postoperatively in eliminating pain (non-narcotic) Note* The side effects of narcotics are: hypotension, respiratory depression, urinary retention, nausea, and reduced peristalsis.

Nausea 1. Prolonged vomiting can lead to dehydration therefore must be prevented or controlled. 2. Postoperative nausea responds well to: a. Phenothiazine antiemetics (Compazine, Phenergan, Trilafon). b. Other treatment can include the use of antihistamines (Benadryl, Atarax) c. Tigan 100mg IM, can be of benefit d. In children you can use Emetrol (5-10ml Q 15 minutes) NOTE* Can prevent postoperative nausea by using a Scopolamine patch behind the ear. This is applied preoperatively and worn perioperatively and postoperatively. The only adverse effect is blurred vision postoperatively

Constipation 1. Can be a problem especially with elderly patients a. Begin treatment 1st with the mildest treatment, a laxative cathartic, milk of magnesia (watch the electrolytes) b. If unsuccessful then try Colace 50-250mg c. If unsuccessful then use a contact cathartic, Dulcolax Note* All laxatives and cathartics are contraindicated in patients with cramps, colic, nausea, vomiting and any undiagnosed abdominal pain.

Shivering 1. Can occur postoperatively and is not associated with fever or infection, but as a reaction to general anesthesia (22-50% of cases). The incidence seems to be increased in prolonged cases and in those involving large amounts of blood loss, fluid administration, or both. Shivering may also be seen after

epidural anesthesia. Shivering is associated with several undesirable physiologic effects. Oxygen consumption, carbon dioxide production, and metabolic rate may increase as much as 500% above baseline levels a. Treatment is IM injection of 12.5-25mg of Demerol b. Bear hugger forced air warmer

DVT 1. Lower extremity surgery plus the use of pneumatic tourniquets for hemostatic control, immobilization, obesity, bedrest, and oral contraceptives are all predisposing factors a. Symptoms: Fever (101 °F) after 24 hours, calf tenderness b. Signs: Swelling of the calf in the later stages c. Diagnostic tests: Duplex scan, venogram NOTE* A painful swollen leg and a positive duplex scan are criteria to initiate treatment for a DVT. However, a swollen/painful leg plus a questionable scan requires a venogram for adequate criteria to initiate treatment

NOTE* Fever may be the only initial warning but also occurs with other postoperative problems, therefore, must work up the patient completely prior to initiating treatment d. Treatment: After drawing blood for a coagulation profile, treat with Heparin IV 5000-10,OOOU followed by a constant infusion of 1000-1500U/HR. The PTT is kept at 2 times the baseline and the PT is kept at 1 and 1/2 the baseline. Coumadin is also utilized (to help prevent pulmonary emboli) and should be started upon admission, to the hospital as it takes 3-5 days to start working. The patient can eventually be discharged on p.o. Coumadin

Compartment Syndrome Two criteria must be fulfilled for this diagnosis to be made: a. a space that is limited by fascia, skin, or bone must be present b. increased compartment pressure caused by a decrease in compartment size or an increase in the size of the contents within that compartment must be present Usually diagnosed in the arm and leg, also occurs in the foot, and can follow several types of injuries, most commonly multiple fractures or crushing injuries. This entity should be considered in the differential diagnosis in patients presenting with a painful swollen foot post trauma 1. Definition: Increased compartmental pressure resulting in decreased perfusion and ultimate ischemic changes to the tissues on the compartment. This can eventually result in contractures and poorly functioning limbs. a. Physiology: At rest the intramuscular pressure is approximately 5 mm Hg.

During a muscular contracture the pressure can increase up to 150 mm Hg or more. At relaxation, the compartment pressure rapidly drops, and within 5-10 minutes, has returned to baseline. With a compartment syndrome, there is no drop of pressure 2. Types of compartment syndrome: a. Acute: Occurs when the resting pressure in the compartment exceeds the available perfusion pressure. This is usually the result of trauma with hemorrhage or gross muscular edema causing the increased compartmental pressure. If untreated tissue necrosis is inevitable b. Chronic: Occurs when the resting pressure is higher than the normal resting pressure but not so high as to cause hyperprofusion. Following excercise, the time for pressure to return to baseline is protracted. This results in a relative prolongation of the ischemic time resulting in symptoms during or following exercise. Actual muscle necrosis is unusual 3. Diagnosis: Measurement of an increased intramuscular pressure in the compartment via a wicks catheter (usually greater than 30mmHg) NOTE * Heppenstal demonstrated that the key element of an alteration in aerobic metabolism was the difference between the Mean Arterial Pressure (MAP) and the Intramuscular Pressure (P). He determined this difference as "p. The lowest "p to maintain normal metabolism was 30mm Hg in normal and 40 mm Hg is traumatized muscle. The formula used to determine ^p is as follows: MAP = Diastolic + 1/3 pulse pressure P = Compartment pressure

MAP -P ^P Case 1: A 30 year old female suffered a crushing injury to her foot. Her blood pressure was 140/80. The patient was essentially stable, but had a painful and swollen foot. X-ray examination was normal. With these findings a compartment syndrome is suspected. A Wicks catheter measured pressure in the central compartment at 50 mmHg. Therefore, does a compartment syndrome exist? According to the above Heppenstal's formula a compartment syndrome does not exist in this case. Using the above formula, the ^p in this case= 45. This value is greater than 40 and therefore the patient does not have a compartment syndrome. Therefore, the most accurate way of determining the presence of a compartment syndrome would be to measure the compartment pressure and then use Heppenstal's formula.

4. Clinical Findings:

a. Pain out of proportion to the clinical findings b. Paresthesias c. Pulselessness d. Or none of the above Note* The patient might present with a pulse because the vascular collapse occurs first at the arteriolar level 5. Associated complications: a. Comminuted fractures b. Severe soft tissue injuries c. Post-ischemia swelling d. Intramuscular hematomas associated with bleeding diathesis e. Crush injuries 6. Compartments of the foot: 4 a. Medial compartment: Its borders are the medial and lateral intermuscular septum, the medial portion of the plantar aponeurosis, the tarsus (proximally) and shaft of the first metatarsal (distally). It contains the abductor hallucis flexor hallucis brevis, and the FDL tendon b. Central compartment: Its borders are the medial and lateral intermuscular septum, the central portion of the plantar aponeurosis, the tarsus (proximally) and interosseous fascia (distally). It contains the flexor digitorum brevis, FDL tendon with lumbricals, quadratus plantae, adductor hallucis, PT and peroneal tendons c. Lateral compartment: Its borders are the lateral intermuscular septum, lateral portion of the plantar aponeurosis, and the associated osseous components. It contains the abductor digiti minimi, flexor digiti minimi, and opponens digiti d. Interosseous compartment: Its borders are the metatarsals and the interossei fascia. It contains the interossei 7. Treatment: a. Fasciotomy 1. Double dorsal technique NOTE* Midfoot and forefoot: 2 dorsal longitudinal incisions, one over the 2nd metatarsal and the other over the 4th (deepened down to the metatarsal shaft) where a hemostat is passed into each adjacent interosseous space, where the interosseous muscle is stripped from its corresponding metatarsal. The wound is closed secondarily in 5 days. If closure cannot be completed, then skin grafting is employed ii. Extensile medial incision iii. Combined approach

Hemorrhage

The incidence of major hemorrhage is low considering the total number of surgeries done in the U.S. The use of blood products is an important decision that any surgeon must make considering the impact of AIDS seen in transfusion medicine today. 1. Physiology of anemia: a. Sufficient amounts of Hb and cardiac output must be present to supply tissue demands b. A 20-30% volume loss leads to hypotension and shock, the end result is tissue hypoxia c. As the hemoglobin decreases the cardiac output increases (cardiac output is increased as stroke volume increases) d. The hematocrit level requiring transfusion is still under debate. However, it is considered advisable to consider transfusion when the Hb is 7 Gm/dl or less. Some will transfuse if Hb is under 10 Gm/dl, which is an HCT of 30% 2. Types of transfusion (see chapter, Fluid Replacement) a. Autologous blood: i. Preoperative donation: must be done 1 week prior to surgery ii. Euvolemic hemodilution: removal of the RBC mass at the time of surgery and replacement with either colloid or crystalloid to maintain intravascular volume iii. Cell salvage: blood is collected by automated cell washing devices ( it is contraindicated in cases where infection is present and where cancer cells may be encountered). The automatic cell washers contain clear plasma and platelets, and there is no clotting function transfused with the product b. Homologous blood: Blood bank blood 3. Complications: a. WBC-mediated allergic type reaction, or immune reaction to minor group factors b. Human error causing major cell lysis, mistyping, and hemolytic transfusion reactions c. Disease transmission i. Hepatitis B and C are greatest risks ii. AIDS (1-50,000 transfusions reported) NOTE* See chapter 11 Fluid Management, section Blood Bank

Septic Syndrome In patients who have had recent major surgery, prompt and accurate diagnosis of sepsis often is difficult. Many of the features commonly attributed to sepsis (fever, leukocytosis) are normal phenomena in the postoperative period 1. Criteria: The most important criteria is evidence of an infection based upon a high index of clinical suspicion using the following a. Fever > 101 °F or hypothermia < 96°F b. Heart rate > 90 beats per minute c. Respiratory rate > 20 breaths per minute

d. Evidence of organ dysfunction e. A PaO2 < 75 mmHg f. Elevated plasma lactic acid levels g. Altered mentation NOTE* Among the most devastating complications seen in bacteremic shock is the development of adult respiratory distress syndrome (ARDS) 2. Treatment: a. Empiric broad spectrum antibiotics in maximum doses

Thyroid Storm This represents the extreme state of decompensated thyrotoxicosis. Thyrotoxic patients inadequately prepared are at great risk for developing thyroid storm from the stress of surgery 1. Signs and symptoms: a. Tachycardia b. Fever c. Arrhythmias d. Agitation, psychosis, coma (CNS always affected) e. GI symptoms (abdominal pain, jaundice vomiting f. Dyspnea 2. Treatment: a. Propranolol 1-2 mg IV with continuous cardiac monitoring. Repeat every 5 minutes until the pulse rate drops to 90-110 b. PTU 300 mg PO q6h (antithyroid drug: propylthiouracil) c. Saturated solution of potassium iodide 10 drops PO q8h d. Hydrocortisone 200 mg IV q8h e. General supportive therapy with acetaminophen, IV's and peripheral cooling 3. Prevention: a. Good history b. Appropriate lab tests (T3, T4, TSH, serum cholesterol) c. Endocrinology consult to determine if thyroid disease is primary or secondary and to monitor treatment

Chapter 6: Infectious Diseases Specific Diseases Principles of Antiinfective Therapy Antibiotics Drug Fever Specific Antimicrobial Therapy Surgical Considerations Necrotizing Infections Osteomyelitis Septic Arthritis Mycology Viral Diseases Rickettsial Diseases Protozoan and Metazoan Infections

INFECTIOUS DISEASE Specific Diseases 1. VIRAL HEPATITIS: types A, B, non-A, non-B, C, E, and delta a. Hepatitis B, non-A and non-B cause chronic liver disease that can lead to cirrhosis NOTE* ALL HEALTH CARE WORKERS SHOULD BE INOCULATED AGAINST THE HBV- IT IS NOW AVAILABLE AS A 3 PART INOCULATION, FOLLOWING A SIMPLE BLOOD TEST CHECKING FOR HEPATITIS B ANTIBODIES

b. Hepatitis A (Infectious hepatitis) is common and occurs by oral fecal contamination or ingestion of contaminated food c. Hepatitis A is usually diagnosed by finding IgG anti-HAV within 2-3 weeks of illness, and the lgG anti-HAV thereafter d. Hepatitis B may be associated with a chronic carrier state and chronic liver disease, with IV drug abuse and homosexuality being common risk factors ( 10% of these patients are asymptomatic and become carriers, they can transmit the virus to others who can get liver disease) e. Hepatitis non-A and non-B account for 90% of transfusion related hepatitis f. Drug induced hepatitis by the following: ACETAMINOPHEN, HALOTHANE, ALPHAMETHYLDOPA, ISONIAZID, DIPHENYLHYDANTOIN AND PHENOTHIAZINE IT IS TREATED BY THE WITHDRAWAL OF THE DRUG g. ACETAMINOPHEN is widely used and can cause irreversible liver damage when more than 10 grams is ingested (can cause more damage in the alcoholic or malnourished patient) h. N-ACETYLCYSTEINE given p.o. within 24 hours of ingestion of ACETAMINOPHEN enhances the liver's ability to clear the metabolites and prevent toxicity 2. AIDS: HIV a. HIV is one of a number of RNA retroviruses possessing a unique enzyme, REVERSE TRANSCRIPTASE, which allows the virus to synthesize DNA from RNA or synthesize DNA backwards; as RNA viruses they can make DNA that may interfere or incorporate into the DNA of the host cell b. TARGET-THE IMMUNE SYSTEM: i. HIV infection follows viral recognition of certain molecular receptors (CD-4) on the surface of human cells, both the T4 lymphocyte and on the macrophages and monocytes (This is the key cell surface glycoprotein which the AIDS virus recognizes and renders those cells carrying this marker susceptible to infection). As a consequence the HIV infection can lead to immunodeficiency ii. With depression of the circulation of the T-helper lymphocyte population, host response is impaired to a variety of potential pathogens: bacteria, mycobacteria, viruses, fungi and helminths iii. It is known that 40-50% of individuals infected with HIV and having less

than 400/mm circulating T-helper cells will develop the manifestations of AIDS within 2 years, 80-85% will develop manifestations of AIDS if their T-helper lymphocyte count is less than 200/mm iv. Also associated with depression of the T-helper lymphocytes, the naturalkiller (NK) lymphocytes' function are also disrupted (these NK cells are involved in immune surveillance against neoplasms and virusinfected cells) v. Also associated with depression of the T-helper lymphocytes is depression of immunoglobulin (antibody) producing B-lymphocyte, which ultimately leads to the body's decreased responsiveness to vaccines c. TARGET -THE CNS: HIV also targets the central nervous system leading to a subacute encephalitis (AIDS encephalitis) d. CLINICAL MANIFESTATIONS: A classification for the clinical spectrum of HIV for adults has been proposed by the C.D.C.: thinking of the potential consequences of the virus infection on a time line i. GROUP I- Includes people manifesting acute HIV, transient and selflimited, characterized by fever, rash, malaise, lymphadenopathy. Incubation period 4-6 weeks after exposure (can be longer). The illness is characterized by serologic conversion to HIV (+ anti-HIV antibody test) ii. Group II- Asymptomatic infection with a positive serology and virus culture, a positive serology but no manifestations of CNS disease (called a Latent state) iii. Group III- Persistent generalized lymphadenopathy, palpably enlarged lymph nodes (> 1 cm) at 2 or more extra-inguinal sites persisting for more than three months in the absence of any other cause: May have other manifestations of the disease iv. GROUP IV- Other diseases; individuals in this group have one or more significant immunodeficiency or CNS disease, divided into 5 .subgroups according to manifestations:
Subgroup A: Constitutional disease (fever, weight loss)
Subgroup B: Neurologic disease (progressive dementia, peripheral neuropathy and myelopathy)
Subgroup C: Infectious diseases (pneumonia, histoplasmosis, herpes simplex, cryptococcosis, et. al.)
Subgroup D: Secondary cancers ( Kaposi's sarcoma, non-Hodgkins lymphoma)
Subgroup E: Other diseases (chronic lymphoid interstitial pneumonitis) e. CLINICAL MANIFESTATIONS BY ORGAN SYSTEMS: i. General- fatigue, weight loss, fever and sweats ii. Dermatologic- rashes (particularly fungal), seborrheic dermatitis, psoriasis, nail changes and pigmented lesions iii. Pulmonary- unexplained cough and shortness of breath iv. Head/ENT- persistent sinus congestion, sore throat, discoloration of the oral mucosa and tongue v. Gl- diarrhea vi. Neurological- headaches difficulty comprehending, behavioral changes, numbness or tingling f. TESTING: Seroconversion to a positive HIV antibody test may occur from 4-8 weeks following the acute illness (fever, fatigue, diarrhea, weight loss, night sweats, and generalized lymphadenopathy).

i. The ELISA (enzyme-linked Immunosorbant Assay) is the primary screening test to detect the antibody to HIV-1 ii. The Western Blot (Immunoblot) test is used to confirm the validity of the ELISA test. iii. A new detection test called the Polymerase Chain Reaction (PCR) demonstrates amplified proviral DNA in lymphocytes, months to years before antibody can be detected by ELISA or Western Blot technologies 3. SYPHILIS: a contagious systemic disease caused by the spirochete Treponema pallidum, characterized by sequential stages and by years of symptomless latency a. Primary syphilis: the primary lesion or CHANCRE appears within 4 weeks of infection and can be seen on the penis, anus, rectum, the vulva and cervix in women, and also on the lips, tongue and buccal mucosa b. Secondary syphilis: cutaneous rashes ( of the palms and soles-macules, papules or pustules- ranging in color from pink to pale red) appear within 6-12 weeks after infection and most are florid after 3-4 months. Some patients exhibit lymph node enlargement. There are constitutional symptoms of malaise, headache, anorexia, joint pain and nausea. At this stage some develop syphilitic meningitis c. Tertiary syphilis: can be divided into benign tertiary syphilis of the skin bone and viscera, cardiovascular syphilis and neurosyphilis. The typical lesion is a GUMMA (a chronic granulomatous reaction that leads to necrosis and fibrosis), appearing most commonly just below the knee, the upper trunk, the face and the scalp, but can occur anywhere in the body d. Tests: i. VDRL: (a flocculation test where a reagin antibody in the patient's serum reacts visibly with CARDIOLIPIN, the antigen). Reported as REACTIVE, WEAKLY REACTIVE, BORDERLINE OR NON-REACTIVE ii. FTA-ABS: fluorescent treponemal antibody absorption, MORE SPECIFIC THAN THE VDRL iii. Darkfield Microscopy: demonstration of the spirochete taken from exudates iv. Other tests: For secondary and tertiary syphilis can include, biopsy of lesions, echocardiography and radiology, EKG and CSF e. Treatment: Penicillin (for all stages) with a serum level of .03 IU/mL for 6-8 days for infectious syphilis. NOTE* Treat as follows: Benzathine penicillin 1.2 million units IM in each buttock (primary) with two additional injections Q 2 weeks of above (secondary). Benzathine penicillin 2.4 million units IM Q 1 week X 3 weeks (benign tertiary) 4. GONORRHEA: Caused by Gram (-) diplococcus, Neisseria gonorrhea. Has arthritic and dermatological manifestations (hemorrhagic bullae). a. Diagnosis: You must use a special collection kit for a C & S that generates carbon dioxide, called a Jembec plate. Otherwise you must take your specimen and plate it immediately on chocolate agar, since the organism is so fastidious.

Treatment of uncomplicated urethral gonorrhea is via Ceftriaxone, 250 mg IM X 1 plus Vibramycin 100 mg BID X 7 days (there are also other alternatives 5. MENINGITIS: Most bacteria cause an ACUTE SEPTIC MENINGITIS, but TB and syphilis cause SUBACUTE MENINGITIS. Viral infections cause ACUTE ASEPTIC MENINGITIS, while fungal infections and malignancies cause SUBACUTE ASEPTIC MENINGITIS a. Acute Septic (Bacterial) Meningitis: 3 bacteria account for 80% of all cases, NEISSERIA MENINGITIDIS, H. INFLUENZA AND STREP PNEUMOCOCCUS (H. flu occurs in most children > 1 yr and S. pneumo most common cause in adults) b. Signs and symptoms: A sore throat can precede fever, headache, stiff neck and vomiting which characterize ACUTE MENINGITIS. Adults and children become desperately ill within 24 hours c. Diagnosis: Since acute bacterial meningitis, especially meningococcal, can be lethal in hours, accurate diagnosis and treatment are urgent, therefore any unexplained fever in infants between age 3 months and 2 years of age warrants close monitoring and, if necessary, lumbar puncture. When bacterial meningitis is suspected, antibiotics should not await the results of diagnostic tests. NOTE* A petechial or purpuric rash can occur in generalized septicemia. Check blood cultures, CT scan, lumbar puncture or any secretion or serologic test looking for the bacteria or bacterial antigen

d. Treatment: Antibiotics as per culture and sensitivity, to continue 1 week after fever subsides e. Differential diagnosis: Subacute bacterial endocarditis (microbial infection of the heart valves) 6. SUBACUTE BACTERIAL ENDOCARDITIS: A previous episode of infective endocarditis, a history of rheumatic valvular disease, patients with congenital heart lesions (Mitral valve prolapse + murmur) and prosthetic valves are high risks for developing endocarditis infections. Therefore, should these patients should be prophylaxed with antibiotics for clean podiatric surgery? According to Warren Joseph, D.P.M., there are NO recommendations by A.H.A. for prophylaxing in clean orthopedic surgery a. Causative organism: Strep more common than Staph aureus b. Signs and symptoms: Sudden. onset of fever, chills, weakness and often times aching joints. Findings include petechiae of the oral mucosa and skin, especially the trunk and painful fingertips and erythematous lesions of the palms and soles (Janeway's lesions). The most common clinical finding is a heart murmur c. Diagnosis: Is by blood culture and echocardiogram (to see vegetations on the valves). Obtain 6 different blood culture specimens at different fever spikes 7. LYME DISEASE: This is a tick (Ixodes dammini) transmitted, spirochetal

(Borrelia burgdorferi) inflammatory disorder best recognized clinically by a skin lesion, erythema chronicum migrans (Stage 1), red macule or papule that expands often with a central clearing to as large as 50 cm. Accompanying the skin lesion, or preceding it are malaise, fever, chills, headache and stiff neck. Neurologic abnormalities (Stage 2) like Bell's palsy and arthritis (Stage 3), especially the knees, can develop in patients within weeks to months of the skin lesion. a. Differential diagnosis: In children juvenile RA and adults Reiter's syndrome and atypical RA b. Treatment: In adults, tetracycline 250mg QID for 10-20 days and for children and pregnant women, penicillin V 500 mg QID (early stage) 8. TETANUS: Tetanus is caused by an exotoxin (tetanospasmin) elaborated by Clostridium tetani, a gram positive, anaerobic, bacillus. The toxin enters the CNS along the peripheral motor nerves or may be blood borne to the nervous tissue, and binds to the ganglioside membranes of nerve synapses. Once fixed the toxin cannot be neutralized. a. Signs and symptoms: Stiffness of the jaw, difficulty in swallowing, restlessness, headache, fever, sore throat and later difficulty in opening jaws, spasm of facial muscles with elevated eyebrows b. Prognosis: Mortality is high in the young and old patient and drug abuser c. Prophylaxis: At the time of injury, 0.5 mL of toxoid elicits a protective antibody level in a previously immunized patient; this booster is not necessary if is it known beyond doubt that the patient has received a booster within the past 5 years. An inadequately immunized patient should be given tetanus immune globulin (human) 250-500 u. IM depending upon the wound potential. At the same time, the first of 3 0.5 mL doses of absorbed tetanus toxoid should be given sub-cutaneously at another site. The second and third doses are given at monthly intervals. Tetanus Immunization Guidelines* 1. If the patient never immunized and the patient has a dirty wound: a. TIG (tetanus immune globulin) 250 U IM and b. dT (diptheria tetanus toxoid) IM 2. If immunized and the patient presents with a dirty wound a. Give dT booster if the last booster was greater than 5 years in the past 3. Every adult should have dT boosters every 10 years *Center for Disease Control recommendations

9. RABIES: Is an acute infectious disease of mammals, especially carnivores, characterized by CNS irritation followed by paralysis and death. Rabid animals transmit the infection by biting animals or humans. Rabies can also be transmitted by exposure of a mucous membrane or fresh skin abrasion to infected saliva. a. Diagnosis: Examination of the infected animal's brain for Negri bodies, or if the animal is healthy and when practical, observation of the animal by a

veterinarian for 10 days. b. Prophylaxis: see guide to follow

POSTEXPOSURE ANTIRABIES GUIDE Animal and Its Condition SPECIES CONDITION AT TIME OF ATTACK Wild animal Regard as rabid unless (skunk/fox) proven negative Domestic dog/cat Healthy & available for observation Escaped (Unknown) Rabid or suspected rabid

TREATMENT OF EXPOSED HUMAN RIG followed by HDCV None Consult with public health officials RIG followed HDCV

NOTE* RIG= Human rabies immune globulin, gives passive immunization HDCV= Human diploid cell virus, gives active immunization (Series of 5 IM deltoid area injections @ day 1,3,7,14 and 28)

c. Wound Care: The wound should be cleansed immediately and thoroughly with a 20% solution of medicinal soft soap or 1 benzalklonium chloride. Deep puncture wounds should be flushed not scrubbed, using a catheter and soapy water (25 ga rubber angiocatheter needle on a large syringe). Do not cauterize or suture the wound. For large defects, pack open. (This treatment holds true for all bite wounds, except add Augmentin/tetracycline/Cipro to cover prophylactically against sepsis)

PRINCIPLES OF ANTIINFECTIVE THERAPY "The decision to institute antibacterial therapy requires a careful assessment of the probability of infection; the likely cause of infection; the probable susceptibilities of the infecting organism to the available antibiotic drugs; and host factors likely to influence the presentation, clinical course, and outcome of the infection. If infection is not currently present but the clinical circumstances in the host suggest that the risk of infection is high, PROPHYLACTIC antimicrobial therapy may be implemented. If infection is suspected but not proved, EMPIRIC therapy designed to treat the most likely pathogens is initiated, until an accurate diagnosis can be made. If the site and causative organism are known then DEFINITIVE therapy can be initiated".* *Zier BG, Essentials of Internal Medicine in Clinical Podiatry, Philadelphia, Saunders, 1990, pg 327

1. INFECTION: is contamination above 105 bacteria per gram of tissue in a healthy adult and as little as 102 in the presence of an artificial joint. A developing coagulum begins to surround bacteria after 3 hours, protecting it from antibiotic lavage and prophylactic antibiotic doses

NOTE* Infection is a clinical diagnosis. It is not defined by some artificial lab finding that most labs do not even do. Just because a contamination is above 105 doesn't mean you cannot close an open wound. It is a clinical evaluation, not a laboratory one. This numerical value (105) is only utilized here as it has appeared on numerous board examinations NOTE* There have been studies proving that 70% of all implants have slime forming bacteria present in large numbers, yet there is no infection. Therefore the value as mentioned 102 is only mentioned as a reference point for the board examinations

a. Diagnosis: Is made by a combination of factors to include signs and symptoms, prior therapy, medical history, allergies, social and travel history, physical examination (includes vital signs) and laboratory diagnosis i. Physical Findings: Warmth and erythema along the incision or wound with possible exudates NOTE* The 5 cardinal signs of infection are: RUBOR, TUMOR, DOLOR, CALOR, and FUNCTIO LASEA ii. Systemic signs consistent with fever > 100 degrees F or 37.7 C, with lymphadenopathy, lymphangitis, shakes, chills and malaise iii. Lab Studies- X-rays, Bilaterally (always serve as a base line for future reference) Gas in tissues indicates pathology (could also be H202 lavage, if utilized) Osteomyelitis takes at least 10-14 days to show on x-ray Bone scans/ Gallium scans/ Indium scans (IF OSTEO IS SUSPECTED) CBC & Diff/ SMA 18-24/ ESR/ Urinalysis Gram Stain (Blue/positive, Red/negative) Aerobic/ anaerobic/ fungal/ acid fast cultures) Blood cultures (when septicemia is suspected

Note* A left shift is an increase in the number of immature PMN'S or band cells. When the percentage of bands is greater than 20 or when the percentage of bands or segs together add up to 80, this is considered a shift to the left. Infection, toxemia, and hemorrhage will cause a shift left. Liver disease and megaloblastic and iron deficiency anemias will cause a shift to the right

NOTE* Anaerobic cultures should be obtained in the following circumstances: a. A putrid odor from the wound b. A deep abscess, pain without discharge c. Significant tissue necrosis (gangrened. Gas formation e. Failure to recover pathogens in the aerobic culture 8 Gram stain f. The failure of the infection to respond to antibiotics that are not active against anaerobes g. Infection secondary to animal or human bite h. Previous therapy with amino glycosides i. Black discoloration of blood containing exudates (may fluoresce red under UV) NOTE* Anaerobic bacteria are very difficult to culture even in the best of conditions. The 4 major anaerobes are: a. Peptostreptococcus (most common) b. Peptococcus c. Clostridium d. Bacteroides

NOTE* A gram stain can be performed within 10 minutes and provides gross identification of the pathogen to allow for proper selection of antibiotics. A culture is most accurate and also checks the resistance of pathogens to the antibiotics. However, a culture does not diagnose an infection, that is a clinical finding.

NOTE* For osteomyelitis, the most definitive diagnosis is by bone biopsy. With an ascending cellulitis and no area of drainage, there is a less than 10% chance of obtaining a pathogen by injecting .5cc sterile saline (without bacteriostatic agent) along the leading edge of the cellulitis and reaspirating the solution back into the syringe and sending it for culture. If septicemia is suspected, blood cultures should be ordered from 2 different sites at the start of a fever spike.

2. Indications for hospitalization: a. Systemic manifestations (fever/shakes/chills, lymphangitis, lymphadenopathy) b. Debilitated host ( Diabetic, p.v.d., alcoholic, immuno-suppressive therapy, burn patients) c. Need for IV antibiotics (Resistant organism, risk of deep space infection, deep space necrosis or wet gangrene) d. Osteomyelitis (most times) e. Need for extensive surgical debridement f. Failure of outpatient therapy

3. Indications for consultations: a. For medical management of systemic disease b. Utilizing a toxic antibiotic c. Gram negative septicemia d. Patient on immuno-suppressive therapy e. Patient with abnormal renal/hepatic function 4. Management of soft tissue post-op Infections: a. Decide on hospital or outpatient therapy b. Consider ID consult/ internal medicine consult/ vascular consult prn c. Perform local wound care/release and remove sutures/ incision and drainage as necessary d. Send specimen for gram stain and aerobic/anaerobic/fungal/acid fast cultures (as necessary) e. Obtain other necessary lab studies f. Begin antibiotics as per gram stain & clinical evaluation and judgement/ reevaluate as per C & S g. Continue appropriate antibiotic at least 10 days (especially when treating strep, to prevent post strep glomerulonephritis) 5. Preoperative antibiotics are indicated in the following circumstances: Valvular disease (when indicated), surgery in the presence of an artificial joint or the implantation of a new one, contamination, prolonged procedure or extensive dissection, debilitated host and patients with shunt a. Consider using: Ancef 1 gm IV preoperatively (can also use postoperatively, 1 gram Q8H in 2 additional doses prn) b. If penicillin allergic- then Vancomycin 500mg tot gm IV, or Clindamycin 300mg po pre-op c. Prophylactic antibiotics in the diabetic: Postop infections in diabetics are usually monomicrobial. Most common pathogens are Staph aureus, Staph epi, Strep pyogenes and Pseudomonas. Best drugs are 1st gen. cephalosporins, vancomycin or clindamycin in the penicillin allergic patient d. Antibiotics should be administered no less than 5 minutes before inflation of the tourniquet and no more than one hour before surgery. Note* The current literature states that there is no significant difference in postoperative infection rates between one dose, two dose, three dose or one week of prophylaxis 6. Identification of organisms by morphology (Gram stain):







Organism Staphylococcus Streptococcus Clostridium Corynebacterium Gram Negative: Neisseria Pseudomonas Haemophilus/Pasturella E. Coll/Shigella/Serratla/ Enterobacter/Bacteroldes Gram Positive:

Morphology Cocci in grape-like clusters Cocci In chains Bacilli (rods) with a "racquet shape" Rods In "Chinese characters" Diplococcus (usually Intracellular) Slightly curved rod Coccold rods Straight rods

Antibiotics The best antibiotic is the one that has the narrowest spectrum, the safest, the cheapest 1. The Penicillins a. Penicillin G: Parent compound introduced in the 1940's i. Good gram(+) and weak gram(-) coverage ii. Fallen out of favor since many resistant strains (Staph 100% Beta lactamase producing) iii. 1 mg PenG= 1667 units iv. Available as Aqueous (10-30 million u/day) and Procaine (600,000 u Q1 2h) b. Penicillin VK: i. Used in severe erysipelas and rheumatic fever prophylaxis c. Methicillin: i. For PCN-ase resistant organisms ii. IV form only iii. Can cause thrombophlebitis d. Oxacillin/Dicloxicillin/Cloxacillin/Nafcillin: (PRP's) i. PCN-ase resistant ii. Good gram(+) coverage iii. Oral form can cause diarrhea iv. Requires frequent dosing, Q4-6 hours e. Ampicillin: Increased gram(-)coverage i. Not PCN-ase resistant ii. Used with UTI, typhoid fever and salmonella infections iii. Used pre-op for endocarditis prophylaxis iv. Used in combination with aminoglycosides for gram(-) septicemia f. Carbenicillin: The original anti-pseudomonal penicillin i. Can be combined with aminoglycoside for pseudomonas infection ii. Not used much now since has high sodium content, hepatotoxic, neurotoxic and causes bleeding disorders iii. Oral form: Geopen (UTI's only) g. Ticarcillin: A 4th generation penicillin active against pseudomonas i. 2-4 times more potent than carbenicillin vs pseudomonas ii. Has increased anaerobic activity

h. Piperacillin: As above, gram(+) 9 (-) activity i. Azlocillin: As above but superior to ticarcillin/piperacillin vs pseudomonas aeruginosa i. Neurotoxic/Hepatotoxic j. Mezlocillin (Mezlin): A 4th generation penicillin with good gram(-) and anaerobic activity i. Can be used for Pseudomonas/B.fragilis NOTE* The adverse effects of the penicillins can manifest as hypersensitivity, hematologic, renal, hepatic, G.l., and C.N.S. reactions. a. Hypersensitivity (approaches 10%): Type 1: anaphylaxis, laryngeal edema, accelerated urticaria Type 2: Coombs positive hemolytic anemia Type 3: serum sickness; urticaria after 72 hours Type 4: contact dermatitis usually after accidental exposure b. Hematologic: Neutropenia: nafcillin/carbenicillin Platelet dysfunction: carbenicillin c. Renal: Interstitial nephritis/cystitis: methicillin Electrolyte imbalance: ticarcillin/carbenicillin/ penicillin G d. Hepatic SGOT elevation: oxacillin e. G.1. N.V.D.: amoxicillin/ampicillin f. C.N.S. Seizures (rare): penicillin G

2. The Clavulanates a. Amoxicillin/clavulanate (Augmentin): Adds clavulanic acid to ampicillin which inactivates the beta-lactamase enzymes: i. PCN-ase resistant ii. Spectrum of activity increased vs gram (-) to include E.Coli & Klebsiella, also good Staph and Bacteroides coverage iii. The oral drug of choice for cat, dog and human bites iv. Dosed at 250-500 Q 8h (for other than endocard prophylaxis) b. Ticarcillin/clavulanate (Timentin): Has greater gram(-) coverage than any 4th gen. penicillin i. Has good gram(+) coverage and covers anaerobes well (i.e. B. fragilis) ii. Good drug for initial therapy for moderate diabetic foot infections iii. Has high sodium load/use cautiously in hypertensive-renal pt's iv. Dosed at 3.1 Q 6-8h (3gm ticarcillin + 100mg clavulanate) 3. The Sulbactams a. Ampicillin/ sulbactam (Unasyn): i. Similar to Timentin but has much lower sodium load

ii. Adds sulbactam, a beta-lactam inhibitor iii. 99% coverage against B.fragilis/not good against pseudomonas and good against enterococcus iv. Dosed at 1.5-3g Q 4-6h. NOTE* Unasyn has better gram (+) coverage than Timentin, but weaker gram (-) coverage 4. The Tazobactams a. Piperacillin/Tazobactam (Zosyn) i. Similar to Timentin in coverage and spectrum ii. Adds Tazobactum a Beta lactamase inhibitor iii. Has greater activity than pipericillin iv. Dosed @ 3.375 gm Q 6 hrs 5. The Cephalosporins Semi-synthetic compounds derived from the mold, cephalosporum acremonium. There is a cross reactivity with penicillin allergic patients from 5-20% depending upon the source. As a whole, these antibiotics are well tolerated, non-toxic and broad spectrum. They are categorized in generations, which define their spectrum. As you go from first generation to third generation you INCREASE GRAM NEGATIVE COVERAGE AND DECREASE GRAM POSITIVE COVERAGE. a. 1st generation: i. Keflin (cephalothin), Keflex (cephalexin), Ancef (cefazolin), Cefadyl (cephapirin), Anspor & Velocef (cephradine), Duricef (cephadroxil) ii. ACTIVITY vs gram (+) cocci: S. aureus and epidermidis, Strep pyogenes and pneumonia iii. Activity vs gram (-): Proteus mirabilis, E. coil, Klebsiella pneumonia (PECK) b. 2nd generation: i. Mandol (cefamandole), Mefoxin (cefoxitin), Ceclor (cefaclor), Zinacef (cefuroxime), Ceftin (cefuroxime axetil), Monocid (cefonicid), Cefotan (cefotetan), Lorabid (loracarbef), Cefzil (cefprozil) ii. ACTIVITY vs gram (+): is variable to Staph , still OK to Strep NOTE* Zinacef® and Mandol® are better than 1st generation for Staph coverage iii. Activity vs gram (-): as with 1st generation (PECK) plus H. flu, Enterobacter & Neisseria (HENPECK) c. 3rd generation: i. Claforan (cefotaxime), Cefobid (cefperazone), Cefizox (cefizoxime), Rocephin (ceftriaxone), Fortaz (ceftazidime), Suprax (cefixime), Vantin (cefprodoxime proxetil)

ii. ACTIVITY vs gram (+): variable to both Staph and Strep iii. Activity vs gram (-): as with 2nd generation (HENPECK) plus Serratia, Morganella, Providencia, Citrobacter and Pseudomonas NOTE* ROCHEPHIN HAS THE LONGEST HALF LIFE OF ANY 3RD GENERATION CEPHALOSPORIN, THEREFORE CAN BE DOSED AT ONCE A DAY. FORTAZ and CEFOBID HAVE THE BEST ACTIVITY AGAINST PSEUDOMONAS. METHICILLIN RESISTANT STAPH AS WELL AS GROUP D STREP (ENTEROCOCCI) ARE RESISTANT TO ALL CEPHALOSPORINS NOTE* Probenecid 500 mg QID blocks tubular secretion doubling the antibiotic concentration of penicillin and cephalosporins NOTE* The top 8 questions and answers about cephalosporins: 1. Are the 1st generation cephalosporins more effective against grampositive organisms than 2nd or 3rd generation cephalosporins? The most commonly used 1st generation cephalosporin is cefazolin. This drug is excellent against group A streptococci, pneumococci but it less effective against these gram positive organisms than some of the 2nd and 3rd generation cephalosporins. 3rd generation cefotaxime, ceftizoxime, and ceftrriaxone, are more active against pneumococci and some hemolytic and non hemolytic streptococci than the first generation cephalosporins. These 3rd generation cephalosporins inhibit resistant streptococcus pneumoniae as compared to 1st and 2nd generation cephalosporins.

2. Why do cephalosporins not inhibit enterococci? Enterococci to not bind to cephalosporins adequately. Enterococci produce a f-lactamase which makes a cult wall to enter. Enterococcal superinfection is more common after cefriaxone or 2nd generation cefuroxime. 3. What is the best way to administer Rocephin? A 2g. dose exceeds the ability of the drug to bind to protein, therefore, more drug reaches the tissues during a single 2g. dose than 1g. dose given in two doses. 4. Which of the cephalosporins are effective against Pseudomonas aeruginosa? Ceftazidime has the highest activity of all the cephalosporins. Also cefoperazone has activity against many P. aeruginosa but must be given on a 6 hour interval. 5. Can cephalosporins be used in patients who are allergic to penicillin? Cephalosporins may be administered to patients who have hat only cutaneous reactions to penicillin. Anyone who has hat anaphylaxis to penicillin should be skin tested with the breakdown products of penicillin prior to any cephalosporin administration, ant if no wheal or flare it would be safe to administer. Most reactions occurred during the 1960's when penicillins ant cephalosporin were packaged in the same plant, which probably caused cross contamination. It is also possible to be allergic to cephalosporin ant not to penicillins. 6. Can children with osteomyelitis be treated with oral cephalexin? Cephalexin has excellent absorption ant may be used to treat Staphylococcus aureus osteomyelitis in children. Cephalexin produces very high blood levels ant is well tolerated by children, Studies show that 4-6 weeks of this therapy is as effective as parenteral therapy. 7. Which cephalosporins inhibit anaerobes? Clinical studies show that ceftizoxime ant ceftoxitin are both equally effective against anaerobes which cause human infections. Those cephalosporins totally ineffective against anaerobes are ceftriaxone ant ceftazidime. 8. What would be the 1st choice for meningitis at present? When dealing with Neisseria meningitis in the U.S., penicillin is still effective. If the meningitis is caused by H. influenza or by S. pneumoniae, the choice of therapy would be cefotaxime or ceftriaxone. In the newborn cefotaxime combined with an amino glycoside toes not cause the alteration in gut flora that ceftriaxone toes. For S. marrewscens ant Acinobacter, ceftizoxime is the 3rd generation cephalosporin of choice. Ceftazidime is useful in treating meningitis caused by P. aeruginosa.

6. Other Beta-Lactams: a. Imipenem/Cilastatin (Primaxin): Is an extremely potent antibiotic with the broadest spectrum of an available beta lactam including anaerobic coverage/ most expensive antibiotic on the market. Cilastatin is added to prevent renal hydrolysis (destruction of imipenem) i. May be the drug of choice in severe/limb threatening diabetic infections ( as initial therapy) other than clinda/genta/ampi ii. Major therapeutic use for Gram (+) cocci and aerobic gram (-) bacilli iii. A 3% cross sensitivity with penicillin allergic patients

Dosed at 0.5-1 gram Q 6h IV up to 4gm/day b. Azreonam (Azactam): Is ONLY effective against gram (-) aerobes, including P. aeruginosa i. Can be combined with clindamycin in penicillin allergic patients when gram(+)and anaerobes are suspected 7. Quinolones: a. Ciprofloxacin (Cipro): i. Its main benefit is it's p.o. gram (-) coverage ii. Can be used for methicillin resistant staph but should be combined with rifampin (300 mg BID) in the treatment of these infections iii. Contraindicated in its use with children as it can cause cartilage degeneration iv. Can be combined with clindamycin (Cleocin) or metronidazole (Flagyl) in the treatment of diabetic foot infections v. Oral therapy for osteomyelitis when caused by Pseudomonas vi. Rarely a first line antibiotic b. Ofloxacin (Floxin): i. As with the above, but with better gram (+) coverage ii. Dosed for soft-tissue infections at 400 mg Q 12 h 8. Aminoglycosides: a. Streptomycin: (used in treatment of TB) b. Kanamycin (used as an irrigant) c. Gentamycin: used with methylmethacrylacte beads (PMMA) for osteomyelitis and in triple antibiotic therapy for serious infections d. Potentially ototoxic in patients with renal problems NOTE* Gentamycin is a good drug for use with PMMA because of its good water solubility, heat stability, and broad antibacterial spectrum. Most studies have fabricated PMMA beads utilizing 1-2 g of antibiotic powder to 40-60 g of PMMA

d. Tobramycin (less ototoxic than gentamycin) e. Amikacin (reserved for serious infections against aminoglycoside resistant organisms) f. As a group these antibiotics have well documented toxicities (ototoxicity/hepatotoxicity). g. They are essentially anti-gram negative agents, but do have gram positive coverage. When using these antibiotics it is beneficial to, have an ID consult and you should perform peak/trough serum levels as well as creatinine clearance and BUN tests (if BUN elevated increase time span between doses or lower the dose)

NOTE* Aminoglycosides (gentamycin/tobramycin) must be monitored to keep the peak level just below 10 micrograms/ml and the trough level below 2 micrograms/ml and Amikacin peak at 20-30 µ/ml and trough less than 10 µ/ml. The peak should be drawn within 30 minutes after infusion of the drug and the trough level should be determined by drawing another blood sample 15 minutes prior to the next dose. The calculated dose of aminoglycosides should be given Q 12 or 24 h (never Q 8) NOTE* Two techniques can be used to change the dose of amnoglycosides when inappropriate levels are found: a. Raise or lower the amount of the dose b. Increase or decrease the time interval So…. if the peak is high and trough is normal: decrease the amount if the peak is low and the trough normal: increase the amount if the peak is normal and trough high: increase the time interval if the peak is high and trough high: decrease the dose/increase the time* Joseph WS Handbook of Lower Extremity Infections, Churchill Livingstone, N.Y., 1990, pg. 182

9. Other antibiotics: a. Vancomycin: i. Indicated in penicillin allergic patients or those patients needing coverage against gram (+) organisms, including methicillin resistant Staph ii. It is possibly nephrotoxic and should be monitored carefully iii. Red neck syndrome occurs if infused too quickly (not an allergy)/severe hypotension can result iv. Oral form is for pseudomembranous colitis only NOTE* Peaks and troughs for vancomycin can be done. The peak is 20-30, and the trough is <10 b. Clindamycin: i. It is used extensively for anaerobic infections and in the penicillin allergic patient for gram (+) coverage ii. Can cause pseudomembraneous colitis c. Tetracycline: i. A broad spectrum antibiotic used for rocky mountain spotted fever, Lyme disease, and H. pylori infection ii. To be avoided in children and pregnant/ nursing mothers (brown teeth) d: Metronidazole (Flagyl): i. An amebicidal drug also with excellent anaerobic coverage ii. Can be combined with Cipro for more complete coverage e. Erythromycin, clarithromycin (Biaxin), azithromycin (Zithromax)

Drug Fever

Fever is considered to be drug induced if no other infections or noninfectious cause is present on the basis of clinical or laboratory evidence, if there is no known underlying disease or condition, if the temperature elevation is temporarily associated with the administration of a "sensitizing" medication and if the fever disappears within 72 hours of discontinuation of the medication. The most reliable diagnostic clue is a relative bradycardia or PULSE/TEMPERATURE DISSOCIATION in patients with 102 degrees F or above. This pulse/temperature dissociation is unreliable in neonates, patients on cardiac medications and patients with systemic diseases accompanied by bradycardia. The treatment is to discontinue the causative agent and avoid antipyretics.

Specific Antimicrobial Therapy 1. Gram (+) cocci (Penicillinase resistant): When a gram stain report is received and initial therapy is to be started prior to receiving a C & S the following should be considered due to the increasing number of betalactamase organisms: Dicloxicillin 500 mg qid p.o., Nafcillin 1 gm IV Q6h, Ancef 1 gm IV Q8h, Duricef 500mg bid, Timentin 3.1 gm Q6h IV and Unasyn 1.5-3.0 gm Q6h IV 2. Gram (+) cocci + penicillin allergy: Vancomycin 500mg or 1 gm Q6 and Q1 2 H IV or Clindamycin 300 Q 6h po, Erythromycin 500 mg Q6h po 3. Methicillin (nafcillin/oxacillin) resistant gram (+) Staph: Vancomycin 500 mg Q 6h IV or 1 gm Q12h, Cipro 500 Q 12h po + Rifampin 300 mg Q1 2h po (Rifampin synergizes the anti-gram (+) effect of Cipro when in combination with it), Minocycline, Trimethoprim/sulfa 4. Gram (-): When a gram stain is received and initial therapy is to be started prior to a C & S the following should be considered: Cipro 750 mg Q1 2h, Azactam 1 gm Q8h IV, Gentamicin 3-5 mg/kg _IV following a loading dose, Timentin and Fortaz 1-2 gms Q8h IV, Zosyn (tazobactam/piperacillin) 3.375 gm Q6 IV 5. Anaerobic coverage: Flagyl 500 mg Q8h po, Clindamycin 600-800 mg Q8h IV or 300 mg bid-tid po, Primaxin, Timentin, and Unasyn 6. Antipseudomonal coverage: 4th generation penicillin (in combination with another antibiotic), Fortaz 1-2 gm Q 8h, Azactam 1 gm Q8h, Gentamycin 3-5 mg/kg IV following a loading dose, Cipro 750 mg Q 12h 7. Antifungal coverage: Diflucan 100 mg od, Amphotericin B (very severe side effects), Ketoconazole (Nizoral), Griseofulvin, and Sporanox 100mg 8. Antihelminthic Coverage: Thiabendazole (Mintezole) for cutaneous larva migrans and hook worms, and Gamma Benzene Hexachloride (Kwell) for parasitic skin infestations caused by scabies.

9. Pregnancy: Antibiotics that are probably safe to use are aztreonam, cephalosporins, erythromycins (not estolate), and penicillins. However, conversely, the antibiotics that are definitely not safe are the tetracyclines and metronidazole. Always check with a patient's physician before giving antibiotic to a pregnant women NOTE* When administering antibiotics to females on birth control pills, you must advise them that the activity of these medications are reduced and that they must utilize some other form of birth control during the time the antibiotics are utilized. P.S. Document that you said this in your chart

Note* MIC is measured in microgram per milliliter, the amount of antibiotic needed to inhibit a specific organism and each organism will have its own MIC to a given antibiotic Note* The dosage for children is calculated based on age and body weight according to Young's Rule, Clark's Rule and Cowling's Rule (see anesthesia section)

Note* Adjusting the dosage of antibiotics in patients with compromised renal function is based on a calculation called the Estimated clearance of Creatinine (ml/mm) is as follows: ECC (men)= (140-age) X weight (kg) Creatinine concentration (mg/dl) X 72 ECC (women)= ECC (men)x 0.9

Surgical Considerations Probably the single most important factor in the control of a postoperative infection is local care of the wound. Unless all areas of abscess formation and pus are drained and devitalized tissue excised the adjunctive therapy of moist dressings, antibiotics etc., will be of little value. The exception to this is a rapidly ascending cellulitis without areas of abscess formation in which surgical debridement would be of no value. 1. Outline of General Surgical Principles: try not to use tourniquets, try using regional anesthesia and not local anesthesia which can spread the infection: a. Sterile skin prep of foot b: If a post-op infection, release all skin sutures c. Explore the extent and depth of the infection, breaking up any loculations if present, not extending into uninvolved areas d. If the infection has gone below the subcutaneous layer explore and remove any deep sutures or necrotic tissue, opening the wound to the deepest portion of the infection

e. If the infection penetrated the joint capsule, the capsule must be opened, if an implant is used it must be removed, the bone and cartilage must be carefully inspected to determine the involvement f. If an infection extends proximal and distal to a joint both the proximal phalanx and metatarsal neck must be explored g. If osteotomies have been done external fixation devices should be removed h. Once the extent of the infection is determined all devitalized soft tissue and bone must be removed i. Samples of deeper tissue and bone, if excised, should be submitted to pathology for microscopic .examination as well as to microbiology for culture and sensitivity tests j. All implant material when removed should be sent to microbiology for culture and sensitivity tests in order to isolate organisms which may be firmly attached to the device and not found within the soft tissues k. The wound should then be copiously lavaged with large volumes of 1% Betadine solution followed by sterile saline or Ringer's lactate l. The wound should be packed open with 1/4 or 1/2 inch iodoform gauze for hemostasis and drainage and covered with gauze soaked in sterile saline or Ringers lactate. When this dries it acts as a mechanical debriding agent m. Immobilize and elevate the extremity n. Keep extremity warm (can use Microtemp heating unit at 102°F) o. Post surgically, the packing should be changed on a daily basis, and as the wound starts to granulate less and less packing is necessary p. When granulation tissue has completely filled the defect, closure of the wound is attempted, however, for small to moderate surface defects, delayed primary closure with skin adhesive strips to gradually bring the skin edges together is attempted within three days after surgical debridement q. If repeated cultures are negative and clinical appearance of the wound is clean and well granulated, then the patient can return to the operating room for irrigation and resuturing of the wound, which is attempted within 4-5 days. This type of delayed primary closure should be avoided if the defect is large and/or if the suture closure places excessive tension on the wound r. If the defect is large the patient may undergo skin grafting when conditions are right

Necrotizing Infections The classification of necrotizing infections is difficult. Prompt and oftentimes empirical medical and surgical therapy must be initiated to save life and limb. Even with early intervention the rate of amputation and mortality is high, with all of these patients having some underlying predisposition: trauma, surgery, burns, malignancy, diabetes mellitus, immunosuppression, human bite wounds, injection injuries, puncture wounds and PVD. 1. Necrotizing Fasciitis: Widespread necrosis of subcutaneous tissue YOU MUST TREAT THIS WITHIN 48 HRS a. Signs and Symptoms: i. Fever, tachycardia, anemia, shift left and > bilirubin ii. Hot/edematous/indurated/erythematous extremity iii. The skin is shiny and smooth with vescicles & bullae filled with a

reddish-brown fluid iv. Cutaneous anesthesia v. Later: Tissue slough with grey necrotic subcutaneous fat and fascia b. Causative organisms- Strep predominates c. Diagnosis: i. Extensive necrosis of the superficial fascia ii. Toxic reaction/altered mental states iii. Absence of muscle involvement iv. Absence of clostridium as the primary organism v. No major vascular occlusion is present d. Differential diagnosis- Lymphangiitis, Clostridial gas gangrene, synergistic (the aerobes help the anaerobes proliferate) necrotizing fasciitis/cellulitis and progressive bacterial synergistic gangrene e. Treatment: i. Stabilize the patient medically ii. Penicillin/Gentamycin/Clindamycin or Primaxin iii. Aggressive incision and drainage with multiple incisions iv. Daily irrigation and packing 2. Synergistic necrotizing cellulitis/fasciitis is closely related to necrotizing fasciitis, with a pathogenesis related to diabetes and obesity, however this condition involves the entire muscle compartment resulting in muscle necrosis. There are systemic manifestations with presence of the reddish-brown "dishwater" pus. The gram stain is mixed with gram(+) & (-) and there is a mixed aerobic & anaerobic infection (Bacteroides/ Peptococcus). The prognosis is poor with amputation a probability. 3. Clostridial Myonecrosis is also known as gas gangrene or clostridial myonecrosis. It can present itself after injury, bums or trauma. There is a tense swelling of the skin with a reddish-brown drainage containing gas bubbles. There is the appearance of gas on soft tissue x-ray. The muscles undergo necrosis and exhibit a color change to a reddish-purple. Clostridium perfringens is usually the causative organism. The diagnosis can be made by gram stain and Fluorescent Antibody Test. Prognosis and treatment as above, with massive I & D and IV antibiotics (Penicillin). 4. Nonclostridial Myonecrosis is similar to the aforementioned but slower to progress. The causative organisms can be anaerobic Strep (Peptostreptococcus) or a combination of aerobic and anaerobic organisms (synergistic). Treatment is similar to that of all necrotizing infections.

Osteomyelitis 1. Definitions: a. Osteomyelitis- infection of bone (chronic OM & acute OM, the distinction of which will determine treatment regime) b. Sequestrum- dead necrotic bone separated from the affected bone c. Involucrum- a chronic process where new bone is laid down around dead bone d. Cloaca- an opening in along the cortex from where the pus drains

e. Rarefaction- localized loss of bone density (earliest radiological finding when 30-50% of the osseous mineralization has been lost) f. Bone abscess ( Brodie's abscess)- localized focus of infection within bone usually found in the metaphyseal region of tubular bones, but can be occasionally found in the diaphysis (Chronic/subacute OM) f. Chronic Sclerosing Osteitis (Garre's)- a low grade infection causing sclerotic reaction without destruction or sequestration 2. Classifications: a. Hematogenous (AHO)- a form of OM caused by spread of bacteria via the bloodstream, originating within cancellous bone, which will result in radiographic findings that start inside the bone and eventually work out to the cortex and periosteum. Seen mostly in the metaphyseal region in children with open epiphyseal plates, occurring most commonly in the calcaneous and femur. In adults it is most commonly seen in the metatarsal heads b. Direct Extention- is secondary to trauma or surgery, will first effect the periosteum, then the cortex and finally the marrow. Proteolytic enzymes destroy Sharpey's fibers c. Contiguous- is the spread of infection from contiguous soft tissue to the underlying bone, also will first effect the cortex and finally the marrow d. Vascular insufficiency 3. Pathophysiology (Small Vessel Osseous Anatomy) I. From the last stages of intrauterine life up to the first six months, growth cartilage is established but not yet limited by bone on the epiphyseal side a. Vessels from the metaphysis penetrate the end of the anlage, perforating the pre-existing plate b. At their ends, those vessels expand forming large venous lakes resembling metaphyseal sinusoids, which are situated close to the surface of the epiphysis c. This explains the frequency of infection of the joint and of the epiphyseal side of the preliminary growth cartilage in the infant d. Any severe damage to the cells at the epiphyseal side of the growth plate is irreversible and consequently, joint damage and arrest or disorganized growth may result in the infant e. The isolation of the epiphysis from the metaphysis caused by the epiphyseal plates provides protection both for the epiphysis and the joint. This explains the rarity of joint infections and epiphysitis in children II. Physiological factors a. Intrinsic host defense: Acute hematogenous osteomyelitis (AHO) localizes in the metaphyseal region because of the phagocytic function in the area of bone. The normal individual displays abundant phagocytic activity in the medullary region of bone. AHO occurs in the medullary region of the diaphysis in sickle cell disease because of inpaired host defense b. The cortex of the child's bone is thick in the diaphyseal region but thin and porotic in the metaphyseal region, therefore, an infection usually spreads laterally through the metaphysis toward and through the thin porotic cortex. c. Pus usually spreads through the Haversian system to the subperiosteal

space, with the periosteum being stripped from the cortex: The blood supply to the cortex is eliminated either by rupturing as the periosteum is elevated or by bacterial emboli. The periosteum in the child displays 3 differences from the adult: it is thick, well, vascularized, and loosely attached to the bone. d. There are 3 commonly involved metaphyses whose adjacent joints are not safe from an early infection (child). The following are the joints whose metaphysis is intra-articular: hip joint, shoulder joint and ankle joint (distal lateral aspect of the tibial metaphysis is intra-articular). 4. Clinical Presentation and Diagnosis The clinical presentation is variable and may depend on the age of the patient, the virulence of the organism, the stage and type of disease process. NOTE* The tenets of treatment include identification of infecting organism, selection of appropriate antibiotic and surgical excision of dead bone a. Symptoms (AHO): i. Local warmth over the infected area ii. Pain and tenderness on ambulation and palpation iii. Pseudoparalysis (often the only complaint in kids) and possible subtle gait changes iv. Palpable swelling if the infection has ruptured the cortex into the periosteum v. Ulceration or soft tissue lesion(s) may produce contiguous OM vi. Concurrent infection: Measles/chicken pox may give strep AHO. Middle ear infections may give hemophilus/pneumococcus/staph AHO b. History & Physical: In pediatric AHO recent infections may be implicated as causative pathogens c. Laboratory Exams: i. Same basic studies as with management of inpatient infection ii. Leukocytosis or a shift left is not commonly seen in acute or chronic OM iii. Sed Rate is usually increased (a nonspecific exam useful to monitor the response to treatment) d. Radiographs: i. Always take bilateral x-rays for comparative purposes ii. The lytic process in bone is not visable on x-ray until at least 30%50% of the osseous mineralization of the area has been lost iii. The first bone changes occur 10-14 days following the onset of symptom iv. Baseline radiographs must be taken- (look at the soft tissue first, may find edema in the contiguous soft tissues, with swelling of one tissue layer as compared to another) v. Three stages of soft tissue changes have been discribed in children with AHO: small deep local. soft tissue in region of metaphysis, swelling of muscles and obliteration of lucent plane between them and superficial subcutaneous soft tissue edema which occurs 3 days after onset of symptoms (if aspirate bone during this phase, should be able to extract pus).

vi. Additional radiographic findings are: periosteal elevation, metaphyseal destruction (children), regional osteoporosis, sequestrum and involucrum. vii. Radiographic findings in chronic OM are: thickened/irregular/sclerotic bone, elevated periosteum, chronic draining sinus and sequestrum e. Aspiration (bone/joint biopsy): Confirms the diagnosis, identifies the organism and aids in determining the treatment plan. f. Blood Cultures: i. Are positive in 50% of cases of septic arthritis and osteomyelitis. ii. The joint fluid in septic arthritis is sterile in 30% of the cases- look at the blood cultures. g. Wound cultures: i. Sinus tract cultures frequently yield gram(-) organisms which are not responsible for the underlying bone infection. ii. If Staph aureus is cultured out, there is a 50% chance that this organism is producing the associated osteomyelitis. h. Bone cultures: i. Take specimens for gram stain, aerobic, anaerobic, fungal and acid fast cultures ii. Take a specimen for histology i. Bone Scans: i. In most patients with osteomyelitis, bone scintograms become positive within 48-72 hours after onset of clinical symptoms (precedes the x-ray changes by 10-14 days) ii. Predominant scintigraphic finding is a "hot spot" (increased tracer localization) iii. The exception to this are "cold spots" which is due to NO delivery of the tracer due to necrosis or a fulminating destructive osteomyelitis not accompanied -by significant reparative processes
99m Technetium MDP: is currently the most frequently used radionuclide It is renally excreted, has a half-life of 6 hours, deposits more in trabecular than cortical bone and provides more anatomic information with less time, exposure and expense than Gallium 67 imaging. 99m TC MDP may continue to show abnormal isotope accumulation after infection subsides as a result of continued bone repair.
Three Phase Bone Scan: is used to differentiate OM from cellulitis. Phase 1- at time of injection shows an immediate radionuclide angiogram or dynamic blood flow, OM and cellulitis both show increased uptake at this point. Phase 2: 5-10 minutes after injection looking for focal increases (blood pool image) cellulitis and OM are still positive at this point. Phase 3: 4 hours after injection (delayed static scan), cellulitis becomes quiescent at this point. j. Gallium 67: Almost all IV injected Gallium binds to transferrin, with 1/3 excreted by the G.I. tract and 1/3 by the kidneys. More tracer is localized in the metaphyseal area. Imaging is done 48 hours after tracer administration. Resolution of anatomical detail for bone lesions is considerably less with Gallium than with 99m TC MDP, with higher radiation exposure. This scan is

preferred to 99m TC MDP in evaluating the response to treatment and is not as dependant on blood flow. More specific in differentiating. bone tumors from osteomyelitis and more reliable in assessing subacute and chronic infections. k. Multiple Tracer Studies: When both types of study are needed the bone scan scan should precede the Gallium scan by 24 hours. The following lists some scenarios when multiple studies are used: (+) 99m Tc MDP & - Ga67= chronic osteomyelitis diabetic osteoarthropathy implant loosening/ectopic bone (-) 99m Tc MDP & (+) Ga67= cellulitis (+) 99m Tc MDP & (+) Ga67= acute osteomyelitis implant loosening (+) 99m Tc MDP & (+++) Ga67= infection in the presence of an implant

l. 111 Indium White Cell Scanning: This scan is much more specific for infection. With this scan, white blood cells are labeled with the tracer (Indium) and injected intravenously. This technique was developed to detect leukocyte accumulation at sites of inflammation and abscess formation. Scans are performed 24 hours after injection. A positive scan is defined as a focal accumulation of leukocytes that is higher than in the surrounding bone. This technique is reserved for complicated posttraumatic or post-surgical patients with equivocal conventional bone scans, in cases where 99m TC MOP scanning reveals false positive results because of rapid turnover. Therefore, it may be more accurate in detecting acute infections. NOTE* Limitations of Scans: Some patients show multiple hot spots at an early stage of S. aureus septicemia but do not progress to OM. You can have a negative scan with a confirmed OM due to impaired blood supply (falsenegative). You can have difficulty in differentiating OM from cellulitis. You can have difficulty in differentiating normal bone repair from bone infection (falsepositive). m. Computerized Tomography: An additional technique that can be used to evaluate OM, especially the articular surfaces and periarticular soft tissues. Also with OM, elevation of attenuated values in the marrow space is an early sign of an acute bone infection. The non-specific destruction of cortical bone and new bone formation can be seen in this way and the progression and/or recession of disease may be monitored. n. Magnetic Resonance Imaging: MRI distinguishes soft-tissue structures more readily than any other imaging modality. It can differentiate osteonecrosis and aseptic necrosis since most artifacts of bone occur in fatty tissue which is easily imaged by MRI. Can be used on OM by evaluating the marrow. This is because water has a high proton content and MRI measures water content of various body tissues (CT measures specific gravity). The more water the higher the

signal intensity. The following tissues are ranked on the relative Spin-Echo Grayscale from brightest (short T1 and/or long T2) to darkest (long T1 and/or short T2 and/or low proton density): fat, marrow, cancellous bone, brain, spinal cord, viscera, muscle, fluid filled cavities, ligaments, tendons, blood vessels, compact bone and air. (SEE SECTION ON RADIOLOGY) 5. Acute Hematogenous Osteomyelitis a. Is a result of blood stream dissemination of bacteria emanating from an identifiable focus of infection or developing during transient bacteremia unrelated to a discernable infection b. Blunt trauma to long bones precedes AHO 33% of the time, femur, tibia and humerus in that order. c. Infections usually begin in the metaphysis d. Large cortical involucrum formation is typical of AHO in the child e. Three common sites of damage based on age of the patient: epiphyseal anlage and joint in the infant, cortex of shaft in the child and joint and marrow in the adult f. AHO (infants): i. Causes severe and often permanent epiphyseal damage and joint infection ii. Only transient damage to shaft and metaphysis iii. Adjacent joint effusion 60-70% of the time iv. Group B Strep, S. aureus and E.coli are most frequent organisms v. Calcaneal AHO reported secondary to repeated venipunctures g. AHO (child): i. Extensive cortical damage with involucrum formation ii. Permanent damage to growth cartilage and to joints is rare iii. Chronic OM is a rare complication iv. S. aureus and epidermidis 60-90% cases v. Salmonella seen with sickle cell (in the diaphyseal area) vi. H. flu implicated in kids under 2 years h. AHO (adult): i. Relatively common in IV drug users with #1 pathogen being Pseudomonas ii. Usually affects axial skeleton and/or irregularly shaped bones (wrist/ankle) iii. The cortex is absorbed instead of sequestering iv. The whole bone is invaded and frequently results in chronic infection of the whole marrow 6. Contiguous Osteomyelitis: a. Most common form of OM seen in podiatry. b. Chronic ulcerations may frequently lead to contiguous OM. c. May develop when an infection arises in an area adjacent to bone in which a malignancy is present or bone has received radiotherapy. d. Staph aureus is the most frequent pathogen. 7. Osteomyeltis associated with peripheral vascular disease: a. Commonly found in patients with diabetes mellitus or with severe p.v.d. b. Usually a mixed aerobic and anaerobic infection.

8. Chronic Osteomyelitis: a. Long standing OM is associated with sequestration. b. Indolence of the infection is sometimes related to the suppressive effects of antibiotics in low doses. c. Staph aureus is the most common pathogen. d. The phalanges and metatarsal heads are the most common sites. e. The sed rate is elevated in 57% of these patients. f. Increased warmth over the infected area found in 94% patients. g. Pathogens residing in the "dead bone" if not removed along with the sequestra, can cause acute flare ups as late as 50 years after the initial episode. NOTE* Dead bone (sequestrum) acts as a foreign body The sequestrum must be surgically removed 15-30% of individuals with acute OM or those with chronic OM who have undergone surgical debridement, develop active flare ups h. Squamous cell carcinoma has been reported as a late sequel of chronic OM (foul smelling discharge, increased pain, increased drainage and enlarged mass), in local draining skin sinuses. 9. Osteomyelitis secondary to puncture wounds: a. Usually caused by a nail driven into the foot. b. Suspicion should arise with patients who present with persistent cellulitis despite soaks and antibiotics and when an I&D produces a foreign body. c. Pseudomonas is the most common organism. 10. Brodie's Abscess: a. A small metaphyseal lesion with well defined margins which is often tibial and which occurs in young males prior to epiphyseal closure. b. The complaint is recurrent pain, with relief from aspirin, therefore must r/o osteoid osteoma. c. S. aureus is the predominant organism. d. Treated with debridement and curettage and antibiotics e. Can act as site for local flareups and systemic infections 11. Treatment: Conceptually, It is easy to formulate and describe principles to follow in planning therapy for a patient with osteomyelitis. a. The principles that should be considered in the treatment of OM are: i. A definitive bacterial diagnosis is required ii. The choice of antibiotics depends on the susceptibility of the etiologic agent, and the least toxic, least expensive, bacteriocidal antibiotic should be administered iii. Surgical intervention must remove devitalized bone that is inaccessible to antibiotics and may provide a culture medium for continued bacterial growth.

NOTE* Despite the apparent clarity and simplicity of these statements, diffilculties can arise in their application. This standard set of principles is aimed at providing a clinical and bacteriological cure. However, in treating osteomyelitis, one must also consider the best functional result for the patient. The patient may decide that intermittent short course antibiotic therapy for control of chronic osteomyelitis is more acceptible for functional needs than amputation of the affected limb. It becomes imperative to involve the patient in these difficult decisions. b. A debate rages regarding the length of parenteral antibiotic therapy (36 weeks). c. Surgical debridement generally expedites the resolution of the infection and can decrease the duration of parenteral antibiotic therapy. d. The spectrum of pathogens causing OM secondary to a contiguous focus or PVD is usually broader than found in AHO. The selection of antimicrobials for contiguous focus OM must be based on C&S from the infected bone. e. OM secondary to PVD is commonly associated with a mixture of aerobic and anaerobic organisms. The isolation of anaerobes on C&S, presence of organisms on a gram's stain that fail to subsequently grow in vitro, and the existence of a foul odor should guide therapy towards anaerobic bacteria. Gram positive anaerobes such as Clostridium or peptostreptococci can be adequately treated with penicillin. However, anaerobic OM usually involves gram negative organisms such as Bacteroides fragilis which can be treated by clindamycin or metronidazole. Mixed aerobic/anaerobic infections can be treated with combined antimicrobial therapy. Third generation cephalosporins (except Claforan for B. frag) are resistant to 20% of the anaerobes so should not be used. f. In a study of oral therapy it was found that S. aureus OM was treated successfully with 1-2 weeks of IV antibiotics to stem the acute flare up followed by oral therapy (cloxacillin/dicloxicillin or clindamycin + probenecid) for as long as 6-12 months (J. Medicine 1976). g. Treatment for puncture wound OM involves a good history (including a tetanus history), x-rays, cleanse foot with Betadine, remove any foreign body making the entrance wound larger if necessary, take deep cultures, flush well and if gross contamination pack the wound open NOTE* Oral antibiotic therapy prescribed after the original puncture wound may contribute to a later OM infection h. Implantation of gentamycin/ methylmethacrylate beads has been shown to be helpful as adjunctive therapy for contiguous focus OM.

Septic Arthritis 1. Occurs most commonly in infants and children 2. Adults will generally have an underlying disease 3. Pathogens vary according to the age of the patients with S. aureus

predominating in all age groups a. H. influenza 2nd most common organism in patients under 2 b. N. gonorrhea 2nd most common organism in adolescents c. Enterobacter and pseudomonas 2nd most common organisms in patients older than 50 4. Diagnosis is made via sterile aspiration of pus with a positive gram stain and C&S. Radiographic diagnosis reveals loss of subchondral cortical bone with preservation of underlying supporting trabeculae 5. Treatment: a. Serial aspirations vs. surgical decompressions b. Suction irrigation c. Parenteral antibiotics d. Do not use intra-articular injections of antibiotics (can cause a superinfection or a post-infection synovitis)

Mycology Fungi are heterotrophic, eukaryotic, chlorophyll-free, thallophytic organisms. They reproduce by spores, which germinate into long filaments called hyphae. The hyphae grow and branch and develop into a mat of growth called the mycelium. Spores are produced from the mycelium. Fungi are divided into 4 groups
Phycomycetes
Blastomycetes
Ascomycetes
Fungi Imperfecti (most pathogenic fungi are in this group) Those fungi affecting humans can be divided into either superficial (dermatophytes) or deep fungi Diagnosis is based upon microscopic examination (KOH prep) and culturing the organism on Sabouraud's medium. Additionally, a Wood's light can be used for the diagnosis of some organisms, Calcoflour White stain is used with fluorescent microscopy, India ink smear for detecting cryptococci in the CSF, Gomori Methamine Silver and Neutral Counter stain for histopathology slides 1. Superficial Mycoses a. Tinea Versicolor b. Candidiasis c. Onychomycosis d. Tinea capitis e. Tinea corporis f. Tinea pedis g. Tinea cruris h. Trichomycosis axillaris

2. Deep Subcutaneous Fungal Infections a. Sporotrichosis: granulomatous infection of the skin and subcutaneous tissue, spread via lymph channels, skin lesions present as raised erythematous plaque-like lesions, a chancre will develop at site of entry and has rare systemic manifestations (Amphotericin B). Often occurs in those working with roses, whose thorns inoculate the organisms. b. Blastomycosis: begins as a papular lesion which ulcerates and spreads with a pustular border. Treatments include local excision of the early lesion or the drug 2-Hydroxystilbamidine. c. Mycetoma: is a chronic granulomatosis infection of the soft tissue and bone. It requires the triad of an indurated swollen lesion, draining sinus and unilateral presentation for a clinical diagnosis. It is seen in endemic proportions in some third world countries. "Sulfur granules' describes material that exudes from the sinus. It is a form of 'Madura Foot`. d. Madura foot: may either be fungal (Madurella mycetoma/Pertriellidum Boydii) or bacterial (Nocardia/Actinomyces/Streptomyces/Achnomadura). Diagnosis is via gram stain, KOH prep, and testing with Saubouraud's (fungal) or blood agar (bacterial). Longstanding infections will produce multiple osteolytic lesions in bone. Treatment involves sulfonamides, local wound care, and debridement or amputation in severe cases. Infectious disease specialist should be consulted NOTE* In addition to the above there are actinomycosis, candidiasis, chloromycosis, coccidioidomycosis, cryptococcosis, geotrichosis, histoplasmosis, nocardiosis, aspergillosis, and mucormycosis. These are more common in immunosuppressed patients, e.g. AIDS, uncontrolled Diabetes mellitus, malignancies (especially of hematopoietic and lymphoid tissues) NOTE* Antifungal therapy can consist of the following: 1. Imidazole and Triazoles: inhibit ergosterol synthesis in the fungal cell wall 2. Imidazoles: econazoles, ketoconazoles, sulconazoles, terconazole, clotrimazole, oxiconazole 3. Triazoles: itraconzole, fluconazole 4. Miscellaneous: allylamine, terbinafine (Lamisil), griseofluvin

Viral Diseases Viruses are the smallest and most simple biologic units that can manifest the essential aspects of a living substance. Some important facts about viruses are:
They are composed of an outer coat of protein and an inner core of nucleic acid
The viruses reproduce heritable characteristics in a predictable manner during multiplication and demonstrate genetic continuity
A virus infected cell is immune to reinfection by the virus and also immune to infection from other viruses usually related to the one which infected it
The virus infected cell can support the reproduction of the virus which entered it and may produce new virus particles in a relatively short time
The most common form of damage in cells supporting viral reproduction is a cytopathic effect which leads to deterioration and results in death and disintegration

Viruses are classified according to the target organ and similarity of action. They are: 1. The pox group (vaccinia and smallpox) 2. Neurotrophic viruses (poliomyelitis, rabies, and arthropod-transmitted encephalitis including Japanese, St. Louis encephalitis, equine encephalitis and aseptic meningitis) 3. Viseotrophic viruses (yellow fever, infectious hepatitis and homologous serum hepatitis) 4. The herpes group 5. Varicella and herpes zoster 6. The myxoviruses (mumps and influenza) 7. The lymphogranuloma psittacosis group 8. Miscellaneous viruses (measles, rubella, Coxsackie viruses, the common cold, warts, etc.) 9. Bacteriophage

Rickettsial Diseases Rickettsial diseases are caused by intracellular microorganisms which are classed between bacteria and viruses, and have characteristics of both. These pleomorphic, cocco-bacillary organisms can cause acute, febrile, self-limited symptoms usually accompanied by a skin rash. The group of diseases includes typhus, Rocky Mountain spotted fever, tsutsugamushi, and Q fever. Diagnosis is via serologic testing (the Weil-Felix test is useful)

Protozoan and Metazoan Infections These infections are common in the warmer climate countries. When a parasite invades a host, there are 4 possibilities:
The parasite may die at once
It may survive without causing symptoms


It may survive and cause disease
It may kill the host Protozoa are one-celled organisms and metazoa are invertebrates made up of many cells (such as worms) replicating directly within a human host 1. Protozoan infections a. Amoebic dysentery b. Malaria c. Trypanosomiasis d. Leishmaniasis e. Toxopiasmosis 2. Metazoan infections (parasitic) a. Nemathelminthes (roundworms) b. Platyheiminthes (flatworms) i. Trematoda (flukes) ii. Cestoda (tapeworms) c. Hirudinea (leeches) d. Arthropoda (insects and related species), as in scabies, fleas, tunga penetrans, maggots (myiasis) etc. NOTE* Stool examination for the egg larvae and the organisms themselves are diagnostic for some intestinal protozoa and metazoa. Blood smears using special staining techniques aid in the diagnosis of some protozoan infections. Some special stains can detect protozoa in tissue biopsies

Chapter 7: Wound Healing Repair of Skin Factors That Interfere With Wound Healing Growth Factors in Wound Repair Surgical Approaches Wound Dressings Suture Materials and Needles Tourniquets

WOUND HEALING Repair of Skin There are three basic phases of wound repair: Inflammatory, Fibroblastic and Maturation 1. Phase 1-Inflammatory Phase Substrate or Lag Phase : This stage lasts 3-4 days and has 3 parts, vascular, hemostatic and cellular. a. Hemostasis is obtained via active vasoconstriction of blood vessels damaged in the wound. Aggregation of platelets also leads to the formation of a hemostatic plug. b. Platelet adhesion is in part stimulated by exposure of the platelets to the proline and hyroxyproline matrix of mature collagen and other connective tissue components exposed by the injury. c. Once platelets are exposed to and adhere to the connective tissue matrix, the platelets are activated. This can only occur in the presence of von Willebrand components of factor VIII which is released from adjacent endothelial cells. Activation involves the release of ADP from the platelet. The ADP stimulates other platelets to stick to one anotherplatelet aggregation. d. Platelets store calcium and 5-hydroxytryptamine in intracytoplasmic granules as well as many other growth factors. These are released upon adhesion and promote further platelet aggregation and vasoconstriction. This process is termed "degranulation" e. Platelet stimulation results in activation of phospholipase and hydrolyzed membrane lipids and the liberation of arachidonic acid. Arachidonic acid is converted by platelet cyclo-oxygenase into thromboxane A2. Thromboxane A2 further stimulates platelet aggregation and is also a potent vasoconstrictor. f. Contractile protein in the platelet, thrombosthenin, promotes clot retraction. Clot retraction will not occur unless platelets are present. g. Coagulation occurs due to the activation of clotting factors. i. Intrinsic system ii. Extrinsic system The end result is the activation of factor X which then converts prothrombin to thrombin. Thrombin then converts fibrinogen to fibrin monomers, which polymerize to form a fibrin clot. Fibrin besides promoting hemostasis, provides a scaffolding for the ingrowth of cells at a later stage. h. Platelets release a number of other factors at this point which promote wound healing. These include: i. Proteolytic enzymes activate the complement system. Also released is 12-HPETE which in turn stimulates the release of leukotriene B4 an important chemotaxic agent. ii. Various platelet derived growth factors which promote various components of wound healing. (See below) h. Other substances in the plasma increase vascular permeability. Histamine is released by mast cells. Histamine increases vascular permeability by causing contraction of endothelial cells and uncovering

gaps between the cells. Histamine is also a powerful vasodilator. Serotonin released from the platelet and kinins made from plasma alpha globulins at the site of injury, also increase vascular permeability. i. Neutrophils, attracted by the chemotaxic factors arrive in the wound about 6 hours after the injury. They reach their highest numbers at 1-2 days post injury. If no infection is present, their numbers decline after this. Neutrophils are responsible for wound debridement through the release of collagenolytic and fibrinolytic enzymes. Additionally, neutrophils ingest bacteria. j. Lymphocytes reach their maximum number in the wound at day 6. The most important role of the lymphocyte is the synthesis of lymphokines. Two of the best known lymphokines are the migration inhibition factor (MIF) and macrophage activation factor (MAF). MIF attacts macrophages to the wound and MAF activates them. k. The macrophages attracted to and activated in the wound are actually derived from monocytes in the blood. They are the most important inflammatory cells involved in wound healing for the following reasons: i. They are the only cells able to tolerate the low oxygen tensions at the wound edge. ii. They appear in the wound during the first 5 days and have a long life span (7-10 days). iii. Wound healing is severely inhibited in the absence of monocytes. iv. They process and present antigens to the lymphocytes to initiate immune response. NOTE* Activated macrophages have a number of roles. a. Wound debridement- accomplished by the production and secretion of proteinases, such as collagensase, etc. b. Ingestion of bacteria and cell debris c. Capillary formation-neovascularization is a direct effect of macrophage stimulation through cytokines d. Antigen processing and presentation l. Migratory fibroblasts originate from mesenchymal cells near the wound edge. These cells become bound to the fibrin laid down in the wound and proliferate. They then produce glycoproteins. Collagen synthesis begins on the 5th day post injury and lasts 2-4 weeks. m. Eosinophil concentration reaches a peak in the injured area between days 7-14. They may be associated with collagen remodeling and synthesis occurring at the same time. There are very few and their role is unclear. n. Fibronectin is a glycoprotein produced by fibroblasts, endothelial cells and hepatocytes. Among the functions attributed to fibronectin are: i. Fibronectin coats macrophages, aiding in opsonization and phagocytosis. ii. Fibronectin is found on the surface of fibroblasts, where it may aid on the adhesion of these cells to the extracellular matrix. iii. Fibronectin cross-links with collagen and glycosaminoglycans. This results in increased adhesion of epidermal cells and endothelial cells to the dermis.

iv. The matrix formed by fibroblasts and fibronectin creates a framework over which epidermal cells may migrate. 2. Phase 2- The Proliferative Phase (Migratory/Lag Phase): This stage lasts from 520 days and has three parts: epidermal regeneration, neoangiogenesis, and collagen synthesis. a. Epidermal regeneration: i. The cells at the wound edges flatten out and develop pseudopods (extensions of their cytoplasm), then migrate across the wound, only migrating over viable tissue, at a rate directly proportional to the oxygen tension of the tissues which is highest under hyperbaric conditions. The aforementioned fibrinfibronectin network serves as a framework over which this migration occurs. ii. Intracellular contractile filaments (actin) develop at the periphery of the migrating cells. These filaments align themselves with the fibrinectin strands in the extracellular matrix. The interaction of these strands actually pulls the epithelial cells along. iii. Other changes occur- the basement membrane under the epidermal cells changes; the epidermal cells themselves elongate in the direction of the wound defect; mitotic activity of the epidermal cells dramatically increases, and the division and movement of epidermal cells may be under the direction of epidermal growth factor (EGF). b. Neoangiogenesis: The formation of new capillary buds from blood vessels near the wound occurs at the same time as the migration of the epidermis. The development of capillaries towards the center of the wound may be under the influence of growth factors released by macrophages. As oxygen tension increases with the opening of new vascular channels, these growth factors are inhibited and capillary growth slows and then stops. c. Collagen Synthesis: i. Within the injured dermis, fibroblasts (surgeon's cell) begin to appear at the end of the inflammatory process, and adhere to the dermal collagen and fibrin. As the capillary structure returns to the wound and oxygen tension increases, fibroblast replication slows. As oxygen tension further increases, fibroblasts begin synthesizing collagen. ii. There are at least 5 types of collagen. iii. Collagen production by the fibroblasts are under control of at least 5 growth factors. iv. Collagen at this point represents 50% of the scar. v. The amount of collagen in the healing wound reaches a maximum at two to three weeks post injury. Remodeling now begins. Note* The wound reaches 35% of its original strength around the 14th day. The tensile strength of the wound now equals the strength of the suture and sutures can be removed at this point.

Tension on the wound stimulates production of collagen which is initially beneficial. Therefore excessive tension should be avoided making skin incisions along the relaxed skin tension lines and using steri-strips when possible. NOTE* A number of factors influence epithelial repair: It has been shown that cortisone delays formation of granulation tissue and wound closure; causes thinning of the dermis and atrophy of collagen fibers; and causes a decrease in fibroblast and new blood vessel proliferation. This effect can be reduced by vitamin A. Data is conflicting and there are no dosage amounts or periods of time described as being a minimum for steroids to have their deleterious effect on wound healing. Therefore, injections of post-op steroids which is done routinely in podiatry to reduce post-op pain and edema should be studied more scientifically. 3. Phase 3-The Remodeling Phase (Maturation)- Can last up to a year At two weeks post injury, a wound has regained only 35% of its tensile strength. By one month this has increased to 40-50%. A number of processes occur during the remodeling phase: a. The entire remodeling process is really an equilibrium between enzymatic processes lysing and resorbing old collagen and forming new collagen. b. Wound contraction is part of this remodeing stage of healing. Contraction progresses at 0.6 to 0.7 mm/day independent of the wound size, but certain shapes heal faster. Round wounds do not contract as quickly as rectangular or stellate wounds. Skin grafting diminishes wound contraction. Note* Only after 6 months and preferably not before a year do you really know what a scar will look like, therefore, any attempt at scar revision should wait at least this long. Factors That Interfere With Wound Healing 1. Age: Growth rate and multiplication of fibroblasts decrease with age. 2. Inadequate Perfusion: Inadequate perfusion of skin, subcutaneous tissue, or bone results in a decrease in oxygen delivery to the wound, thereby impairing healing. 3. Infection: Infection leads to tissue destruction and edema, both of which interfere with the healing process. 4. Edema: Interferes with tissue perfusion and leads to tissue destruction. 5. Poor Nutrition: Protein depletion results in alterations in collagen synthesis and cross-linking. 6. Vitamin and Trace Element Deficiencies: a. Vitamin A deficiency can interfere with wound healing, and may reverse wound healing problems associated with steroids.

NOTE* Vitamin A taken p.o. to help reverse the effects of steroids can also reverse the effectiveness of steroids in the condition for which they were originally intended (kidney transplant; vitamin A can cause rejection). However, topically vitamin A can be very effective. Have the pharmacist mix 1000 units of vitamin A per gram of Bacitracin ointment for steroid patients to apply topically to a wound b. Vitamin C deficiencies lead to scurvy, a disease associated with the failure of collagen synthesis. 7. Steroid and Cytotoxic Medications: a. Steroids slow protein synthesis when given exogenously. Steroids interfere with capillary budding, slow fibroblast proliferation as well as the rate of epithelialization. b. Cytotoxic drugs commonly used in chemotherapy, inhibit cellular proliferation. In general, wound healing is slowed but not prevented. 8. Radiation: Microvascular changes occurring after tissue is exposed to radiation at therapeutic doses will lead to perfusion problems if that tissue is later injured. All cell types involved in healing may be adversely affected by radiation. Malignant change may also occur. 9. Diseases Which are Associated With or Predispose to Chronic Wounds: a. Diabetes Mellitus: i. Deposits in the arteries interfere with tissue perfusion. ii. Diabetic neuropathy leads to reduced sensation and gait abnormality iii. Metabolic problems lead to a reduction in nutrients available for wound healing. iv. Impaired phagocytosis seen as part of the disease spectrum on diabetics leads to an increase in bacterial infections and subsequent tissue destruction. b. Venous Stasis: Poor venous return leads to an increase in tissue pressure. The increase in tissue pressure results in underperfusion of the skin and wounds, as well as accumulation of inhibitory metabolites c. Collagen Vascular Disease: These diseases have an autoimmune basis and result in capillary damage leading to poor tissue perfusion and hypoxia, and immune response to other cells or cell constituents 10. Treatment of Non-healing Wounds: a. Debridement of necrotic tissue b. Control of infection c. Control of diabetes mellitus d. Nutritional support e. Avoidance of trauma f. Aggressive intermittent compression and elevation to eliminate limb edema g. Tapering of steroids (paradoxically, topical steroids applied to wound in patients with collagen vascular disease may control the vasculitis and actually

stimulate wound healing) h. Revascularization of an ischemic wound through angioplasty or reconstructive vascular surgery i. Use of hyperbaric oxygen j. Plastic reconstructive surgery k. Application of growth factors (still experimental)

Growth Factors in Wound Repair With the production of a platelet derived wound healing formula (PDWHF) known as PROCUREN, a mixture of 5 platelet-produced growth factors, angiogenesis and other aspects of wound healing are stimulated. The 5 growth factors are 1. Platelet derived growth factor (PDGF) 2. Platelet derived angiogenesis factor (PDAF) 3. Platelet derived epidermal growth factor (PDEGF) 4. Transforming growth factor (TGFB) 5. Platelet factor 4 (PF-4)

Surgical Approaches Skin incisions are planned according to established principles: a. Anatomical landmarks including vital structures should be identified and marked with a skin scribe prior to the initial incision (listen with a doppler for arterial flow) b. Tension on the healing incision must be avoided c. Easy access to all structures involved must be possible d. The incision should be long enough to avoid excess traction on the wound margins (remember that skin heals from side-to-side and not from end-to-end) e. Vital nerve and blood vessels should be identified and protected, with skin incisions made parallel to them f. Incisions should be parallel to relaxed skin tension lines (RSTL) whenever possible g. Excessive manipulation and damage to the deeper tissues must be avoided by following the lines of cleavage (RSTL) and planes of fascia h. Scars over bony protuberances or weight bearing surface points should be avoided i. Longitudinal incisions or incisions perpendicular to the RSTL should be located in areas of relatively little skin movement j. Longitudinal incisions that cross flexion or extension surfaces of joints should be avoided or at least made in a curvilinear fashion to allow for flexibility and scar contracture

NOTE* An incision perpendicular to the RSTL will gap widely whereas an incision made parallel to the RSTL will remain approximated. The RSTL are created by the directional pull of structures underlying the relaxed skin. The RSTL are important for the direction they convey. Optimal healing can be produced by ensuring that the collagen in the scar forms parallel to the adjacent dermal collagen. Skin expands and contracts along the of direction of muscle pull, so that if an incision is made parallel to this direction, then the body responds by depositing increased amounts of collagen to strengthen the scar. To find the RSTL one simply relaxes the skin in the area by passive manipulation or in areas where there is not much motion the RSTL can be found by pinching the skin over the area. This will form furrows. Pinching in line with the RSTL will form a regularly shaped furrow and pinching oblique to the RSTL will give rise to an S -shaped furrow

Wound Dressings Optimum wound dressings should remove excess exudate and toxic components, maintain a high humidity at wound/dressing interface, allow gasseous exchange, provide thermal insulation, afford protection from secondary infection, be free from particulate or toxic contaminants and allow removal without trauma at the dressing change. 1. Categories: a. Alginates: i. Sorbsan® ii. Kaltostat® b. Hydrogels: i. Carrington® ii. Core Care® iii. MPM® iv. Intrasite® v. Sososite® vi. Biolex® vii. Vigilon® c. Foams: i. Flexan® ii. Hydrosorb® iii. Mitraflex® iv. Polymem® v. Epilock® d. Hydrocolloids: i. Ultec® ii. Triad® e. Isotonic Saline: i. Dermagran® f. Zinc Saline: i. Dermagran®

g. Transparent dressings: i. Tegaderm® ii. Proclude® h. Hydrophilic dressings: i. Dermagran®

Suture Materials and Needles 1. Classification of surgical sutures: a. Absorbable: i. Natural filament (from animals):
Plain gut
Chromic gut ii. Synthetic multifilament:
Dexon-S® (polyglycolic acid)
Vicryl® (polyglactin 910) iii. Synthetic monofilament:
PDS® (polydioxanone)
Maxon® (polyglyconate) b. Nonabsorbable: i. Natural filament
Surgical silk
Dermal silk (Perma-hand)
Surgical linen ii. Metal iii. Synthetic monofilament:
Dermalon®, Ethilon® (nylon)
Surgilene® (polypropylene)
Novafil® (polybutester) iv. Synthetic multifilament
Neurolon®, Surgilon® (nylon)
Mersilene®, Dacron®, Tevdek®, Ethibond®, Ticron® (polyester) NOTE* Two principles should be kept in mind when choosing suture and the caliber of suture. The first one is that the less reactive the suture the less risk that it may potentiate infection (woven sutures tend to be more reactive than monofilamentous ones). The second one is that the less the amount and smaller the caliber of the suture used, the less foreign material is left inside the wound to potentiate infection. Among the absorbable stitches the monofilament polyglycolic PDS (looses strength in 60 days and is absorbed in 180 days) is the least reactive. The woven polyglycolic, Dexon/Vicryl (looses strength in 30 days and is absorbed in 7090 days) is minimally reactive. Among the permanent stitches, nylon is minimally reactive. Nonabsorbable woven silk, woven cotton, or absorbable plain/chromic gut should not be used (with specific exceptions) as they cause acute inflammatory reactions.

2. Biologic properties: All suture materials elicit a foreign body reaction within the tissues, which lasts for 5-7 days and is relatively the same for all suture materials. It has been reported that monofilament sutures and uncoated sutures produce far less reaction than multifilament and coated sutures. Also synthetic sutures cause less tissue reaction than sutures derived from natural materials. The best suture appears to be synthetic, monofilament and nonabsorbable 3. Needle characteristics: a. Design: I. Eye
Closed eye
French eye
Swaged (eyeless) (most commonly utilized) II. Body
Straight (Keith needle)
Half curved
Curved (either 1/4, 3/8, 1/2, or 5/8 circle) III.Point
Tapered Cutting
Reverse cutting
Paper cut or diamond point
Precision-point or hand-honed reverse cutting Tourniquets 1. Indications: To exert enough pressure on the arterial blood flow to a limb to produce a bloodless field. Single cuff tourniquets are generally used for operations lasting less than 90 minutes 2. Contraindications: The final decision whenever to use a tourniquet rests with the attending physician a. Open fractures of the leg b. Post-traumatic hand reconstruction c. Severe crushing injuries d. Elbow surgery (with excess swelling) e. Severe hypertension f. With skin grafts in which all bleeding points must be readily distinguished g. Compromised vascular circulation or in the presence of an arterial graft h. Diabetes mellitus i. Sickle cell disease (relative contraindication) as severe postoperative pain could result NOTE* Test the hemoglobin and type and level before using a tourniquet on patients with sickle cell disease or trait

3. Precautions:

a. Carefully exsanguinate the extremity (this prolongs the pain free tourniquet time) b. In the presence of malignant tumors, painful fractures, or infection elastic bandage (Esmarch) exsanguination must not be done, only elevating the limb for 3-5 minutes is acceptable c. Do not use an elastic bandage for exsanguination in cases where bacteria, exotoxin, or malignant cells could spread through the general circulation d. Inflation must be done rapidly to occlude arteries and veins simultaneously e. Frequent irrigation is recommended when working under tourniquet control to prevent tissue drying f. Prolonged tourniquet time can produce permanent or temporary tissue/nerve/blood vessel damage. It can also produce changes in the coagulability of blood with an increase in the clotting time g. If the blood does not return to the limb within 3-4 minutes after release of the tourniquet, the limb must be placed in a dependent position 4. Adverse Effects: a. A dull aching pain b. Stiffness, weariness, reactive hyperemia, skin discoloration c. Pathophysiological changes due to pressure, hypoxia, hypercarbia, and acidosis of the tissue can occur after one and one-half hours of tourniquet use. Symptoms of tourniquet paralysis are: i. Motor paralysis and loss of touch sensation ii. Loss of proprioceptive responses d. Intraoperative bleeding due to: i. An underpressurized cuff ii. Insufficient exsanguination iii. Insufficient cuff pressure iv. Blood entering through the nutrient vessels of the long bones v. Inadequate cuff size 5. Pressure Settings: For each patient, the tourniquet should be set to the minimum effective pressure, taking into account such factors as obesity preoperative systolic pressure, maximum anticipated rise in the patient's blood pressure during the surgery, and the presence of hypertension a. Published literature suggests an effective tourniquet setting be 75-100 mm Hg above preoperative systolic pressure above the upper limbs, and two times the preoperative systolic pressure for the lower limbs when using single bladder cuffs 6. Inflation Time: a. Depends upon the patient's anatomy, age, and absence of vascular disease b. For reasonably healthy adults, there is general agreement that 2 hours should not be exceeded without releasing the tourniquet for 15-20 minutes before reinflating, and during this time the limb should be elevated about 60° with steady pressure to the incision

7. Release of Tourniquets: a. When the tourniquet is released the wound should be protected from blood surging back by applying pressure dressings and if necessary elevating the limb b. If color is not back back within 3 minutes, lower the extremity c. It has been reported in the literature then upon the release of bilateral thigh tourniquets (at the same time) a patient developed asystole. Therefore, this article suggests that when utilizing bilateral thigh tourniquets, that there be a 5 minute delay between deflation of the cuffs

Chapter 8: Plastic Surgery Skin Grafting Local Cutaneous Flaps Local Muscle and Myocuteneous Flaps Fasciocutaneous Flaps Microsurgery and Free Flaps Diagrams of Skin Flaps

PLASTIC SURGERY When considering soft tissue reconstruction one always needs to go through a decision tree in evaluating options from the simplest to most complex reconstructive technique depending upon the patient's health, resultant changed biomechanics, and soft tissue defects location: 1. Allow the soft tissue defect to heal by secondary intention 2. Close the wound primarily 3. Apply a split thickness or full thickness skin graft 4. Use a local fascial, fasciocutaneous, muscle or musclocutaneous flap 5. Use a microvascular free flap transfer

Skin Grafting 1. Definitions: a. Consists of harvesting epidermis with a varying thickness of accompanying dermis and placing it on a recipient base., b. Split thickness: Includes epidermis and a portion of dermis (the more dermis included, the thicker the graft) c. Intermediate split thickness: contain more dermis d. Thick split thickness grafts: contains most dermis f. Full thickness grafts: contain all the epidermis and dermis, no fascia or fat but has the sweat and sebaceous glands g. Grafts can be autografts (same individual), allografts (same species), isografts (twins), and xenografts (different species) h. A free skin graft is completely detached from the body during its transfer from the donor site 2. Anatomy of skin: a. The epidermis represents 95% of the skin thickness and dermis 5% b. The dermis contains sebaceous glands, except in the palms and soles c. The dermis is principally made up of collagen and elastin d. The subcutaneous tissue contains the sweat glands and hair follicles (except in the palms and soles that lack hair) e. The blood supply arises out of a vascular network that lies on top of fascia and sends vertical branches up through the subcutaneous tissue and dermis. The vessels arborize along the way and terminate as capillary buds between the dermal papillae (the thinner the graft, the more vessels are transected) 3. Preparation of the recipient site: a. Must have no infection for a successful graft (a bacterial count of less than 100,000/gram of tissue) To sterilize a wound: i. Surgical debridement ii. Topical Sylvadine for 4-5 days plus IV antibiotics: or iii. Biological dressings (pig skin or amnionic membranes) plus IV antibiotics b. Must be well vascularized for a successful graft (pH at 7.4, Tcp 02> 40 mm Hg

and epithelialization at the border) c. If the wound is fresh then you can graft onto dermis, fat, fascia, paratenon, or periosteum d. You cannot graft onto cortical bone or tendon e. Granulation tissue contains bacteria and must be removed at the time of grafting f. Hemorrhage must be controlled g. Thorough irrigation 4. Split thickness skin graft: a. The thinner the graft the higher the chances of a successful take, due to in part to the higher number of transected blood vessels through which primary revascularization can be established b. The thinner graft will shrink more at it heals (about 50-70% of its size) because the decreased amount of dermis is less effective in inhibiting secondary contraction c. The thinner the graft the greater the chance for hyperpigmentation d. The thinner the graft, the more susceptible it is to trauma, because of the absence of rete pegs and the loss of lubricating sebaceous glands e. A thin skin graft is usually .012-.013 inches thick f. Donor site bleeding minimized with topical thrombin or dilute concentration of epinephrine and dressed with Xeroform or Scarlett Red, Opsite or Tegaderm, and/or Biobrane (semipermeable dressing) g. Recipient site bleeding must be controlled (topical thrombin or dilute epinephrine) and if not place the skin graft back onto the donor site and return to the OR in 24-48 hours h. Graft cut with a BrownAire or Zimmer air driven dermatome are reliable (can be cut by a Humby or Goulian knife by hand but is difficult). For power: i. Set desired width by using a width guard (either 5 cm, 8 cm, 10 cm) ii. Set thickness by turning knob (usually .012-.013") and introduce a #15 scapel blade between the cutting blade and base to check thickness NOTE* A # 15 scapel blade is the proper thickness of the graft, so by placing this blade into the dermatome, provides a double-check i. Meshing the donor graft allows for removal of hematomas or seromas and increases its size (do not mesh at a ratio greater than 1 1 /2 to 1) j. Inset the graft using a Stent tie-over dressing (or a bolster dressing). The bolster is built by first placing Xeroform® on the wound then normal saline soaked cotton in the center. The nylon suture used at the wound's periphery are then crossed over and tied to each other, forcing out the water in the cotton. This allows the graft to conform exactly to the recipient site h. The foot and leg should then be placed in a posterior splint to eliminate movement/shearing i. Dressing changed in 5-7 days if meshed, and if unmeshed at 48 hours to check for fluid accumulation (if accumulation occurs, it should be aspirated with a needle

j. The graft on the extremity should be kept elevated for 7-10 days, until venous circulation is fully established 5. Physiologic phases in skin graft take: a. Plasmatic imbibation phase during first 48 hours (graft is ischemic at this time) b. Inosculatory and capillary growth phase phase starts after 48 hours when capillary budding from the recipient bed makes contact with the graft. c. Circulation occurs between the 4th and 7th day 6. Full thickness skin graft: a. Best donor site for full thickness grafts are the flexor surfaces such as the groin, anticubital fossa, and popliteal fossa, and then closed primarily, leaving a linear scar. b. The length to width ratio of the donor graft should be at least 3-1 c. The donor graft is then sewn into the recipient site d. Perforations should be made into the donor graft to allow for seroma removal e. Revascularization is more tenuous with a full thickness graft than with a split thickness graft f. Full thickness graft usually takes primarily, there is no contraction of the wound, lubrication of the skin is normal, and there is no change in skin color or texture g. Neurotization occurs in the following order: pain, light touch, then temperature h. Sensory recovery starts at 4 weeks and can take up to 1-2 years 7. Reasons for graft failure: a. Lack of compression of the graft to the recipient site b. Movement/shearing c. Infection (second most common cause) d. Seroma e. Hematoma (most common cause) NOTE* It is important that the pressure on the graft does not exceed 30 mm Hg or else blood flow to the graft will be compromised

Local Cutaneous Flaps 1. Anatomic principles of skin flaps: a. It is not the length to width ratio but rather the presence of an artery at the base of a flap that determines its success. Therefore the preoperative use of a doppler enables one to determine whether the flow to a particular area of the foot is antegrade or retrograde (the flow can be redirected due to an occlusion of either the anterior tibial or posterior tibial artery) b. A defined area of skin receives blood from 3 sources i. Cutaneous artery: direct cutaneous arteries run in subcutaneous fat parallel to the skin, and are usually accompanied by two venae commitantes (veins

that drain the area supplied by the cutaneous artery) ii. Musculocutaneous artery iii. Fasciocutaneous arteries c. The flaps that have a direct blood supply (direct cutaneous artery flaps) have a larger length to width ratio, than traditional random flaps and can be used as: i. Axial pattern flaps (traditional name) and can be used as a pedicle flaps (a flap dissected free at its base, of most of the tissue surrounding the artery and veins thus giving the flap added mobility) ii. An island flap: where the vascular pedicle is dissected completely free for a certain length and the flap is transferred to a local site separate from the donor site while the pedicle is buried under intervening tissue iii. A free flap: where the pedicle is totally detached and then hooked up by microsurgery to recipient vessels anywhere in the body d. Musculocutaneous flaps consist of muscle, subcutaneous fat and skin, with the muscle receiving its blood supply according to one of 5 patterns NOTE* In the foot it is preferable to harvest the muscle without the overlying skin paddle as skin graft over the muscle, as the blood supply to the overlying skin has a very narrow range and can cause significant donor defects if harvested as a unit e. The fasciocutaneous system is the chief source of blood supply to the skin. It arises from a major regional artery as perforators that pass along the fascia between muscle bellies and then fan out at the level of the deep fascia (an example is along the long axis of the 3 arteries, posterior tibial, anterior tibial, and peroneal i. Example of a faciocutaneous flap of the foot is the medial plantar flap NOTE* A random flap with is obligate 1:1 length to width ratio in the foot is a flap based on unknown vascular anatomy. Axial pattern flaps have an identifiable blood flow at their base and have a length to width ratio that depends upon the angiotome which the artery serves. These flaps must be preplanned, and can be extended beyond their angigtomes using delay principles 2. Local flaps: a. Local flaps are adjacent to the defect and are either rotated on a pivot point or are advanced forward from their base to cover a defect. They include a minimum of the epidermis, dermis and subcutaneous tissue. The donor site is either closed primarily or skin grafted b. Flaps that rotate about a pivot point i. Rotation flap: is designed when a pie shaped triangle defect is created to remove a lesion or preexistent defect. The flap includes skin and subcutaneous tissue ii. Transposition flap: are rectangular in shape with rounded edges and can be

rotated 900 iii. Limberg flap: is a type of transposition flap that depends on the looseness of the adjacent tissue, and is used when the defect has a rhomboid shape (angles of 60° and 1200) iv. Z-plasty is a type of rotation flap that is used to lengthen an existing scar and to reorient them along lines of minimal tension. The Z-plasty consists of 3 limbs of equal length on the shape of a Z, and the angles between the limbs can vary from 30° to 90 0, and the wider the angle the more the theoretical gain in length NOTE* Clinically, 60° has been found to be the most useful and yields a theoretical 75% gain in length, however, the actual gain in length is anywhere from 28% to 45% less than calculated. The length of the center of the limb also determines the amount of length gained, and the longer it is, the larger the gain v. Interpolation flap: has a soft tissue pedicle with a distal skin island which is rotated into a defect that is close to but not adjacent to the donor site vi. Island flap: is a specialized interpolation flap where the only link between the cutaneous flap and its bed is the neurovascular bundle. This can be very useful in the foot, as the results are aesthetic, sensate, and very functional c. Advancement flaps: i. Advancement flaps: are moved directly forward to fill a defect without rotation or lateral movement. A rectangular incision of skin dissected out and advanced into the defect thereby creating a folding of tissue at both ends of its base (burrow's triangles), which are removed so that the skin can be sutured together ii. V-Y flap: is a V shaped flap whose sides are advanced creating a Y when the incisions are closed. Can also use a double V to Y flaps when a defect is to large for one (defects 3-4 cm wide) Local Muscle and Myocutaneous Flaps One can transfer simple muscle or muscle with overlying skin to cover a soft tissue defect. It is critical to know the anatomic blood supply of the muscle and skin 1. Abductor digiti minimi flap: Is a muscle flap used to fill defects of the lateral ankle joint or skin 2. Abductor hallucis brevis muscle flap: The medial counterpart of the abductor digiti minimi. If more bulk is needed it can be harvested with the medial half of the flexor hallucis brevis muscle 3. Flexor digitorum brevis muscle flap: can only be considered in the well vascularized non-diabetic foot, as its harvesting may lead to charcot changes by weaking the midfoot arch Fasciocutaneous Flaps

These flaps are thin, pliable, and reliable, however, are not as useful as muscle in treating osteomyelitis because the blood flow per centimeter2 i s 3-5 times less 1. Dorsalis pedis flap (direct cutaneous blood supply): Is a direct skin flap in the foot, can be used as a free flap, its advantage is that it is thin and can be used as a sensory flap if the superficial nerve is incorporated a. The potential flap territory overlies the artery b. It is mandatory to know when using this flap whether the arterial flow is antegrade or retrograde, which vascular system supplies the first dorsal metatarsal artery, and whether the anterior branch of the peroneal artery is dominant (if the distal portion of the flap is supplied by the vascular blood supply from the sole of the foot, then a delay of that portion of the flap should be done to avoid distal flap necrosis) c. Should be only used in well vascularized patients as a 2nd resort because of donor site morbidity 2. Filet of toe flap (direct cutaneous blood supply): Similar characteristics as that of the sole of the foot (it is filling and sensate), a toe has to be sacrificed. It can be rotated locally, or carried with its neurovascular bundle for more proximal placement 3. Lateral calcaneal artery fasciocutaneous flap (direct cutaneous blood supply): Derives its blood supply from the calcaneal branch of the peroneal artery. In order to dissect this flap, it is critical to doppler out the artery along its full length, and the artery should lie along the mid axis of the flap which allows for a 8x4cm vertical flap to be harvested. If the viability is questionable, dissection is stopped and the flap delayed for 5-7 days. It is best to start with a lateral incision down to the periosteum, and dissect up in a retrograde fashion 4. Plantar flaps: The blood supply to the sole of the foot is supplied by the medial and lateral branches of the tibialis posterior artery. a. Lateral plantar artery flap b. Medial plantar artery flap: better than the lateral artery flap because it is based on the less important medial plantar artery and is designed over a nonweight-bearing portion of the sole, and can include the abductor hallucis ms. to give the flap extra bulk Microsurgery and Free Flaps This has revolutionized the ability to cover soft tissue defects. Can include fasciocutaneous, musculocutaneous, osteocutaneous, and osteomusculocutaneous flaps 1. Donor site does not include the foot, and donor site morbidity is minimal 2. The free flap has to have adequate inflow through one of the three distal arteries (preferably the distal posterior tibial or dorsalis pedis). If adequate flow does not exist, then revascularization via in-situ by-pass graft is mandatory first

3. Free flap anastamosis, whenever possible, should always be done end to side so that the distal flow is not compromised 4. For the dorsum of the foot a fasciocutaneous free flap from either the parascapular area, the radial forearm, the lateral arm or the temporalis fascia with STSG (the advantage are that these flaps are thin, have minimum donor morbidity, and have reliable vascular pedicles 5. The muscle flap for the sole of the foot comes from either the serratus anterior or gracilis muscle 6. If metatarsals and skin need to be replaced then a osteocutaneous flap from the contralateral fibula is used, or parascapular osteocutaneous flap NOTE* The advantage of using vascularized bone is that the risk of infection is diminished and the bony union is more rapid Diagrams of Skin Flaps

Chapter 9: Bone Healing Primary Bone Healing Complications of Bone Healing Treatment of Nonunions Fusion Bone Grafting Aseptic Necrosis Following 1st Metatarsal Osteotomy Electrical Bone Stimulation Cartilage Healing

BONE HEALING Primary Bone Healing The two basic requirements for primary bone healing are an intact vascular supply to the bone and rigid stable fixation of the fracture fragments. Primary bone healing consists of simultaneous remodeling and formation of new bone at the fracture site. The intermediary phase of fibrocartilage formation as seen in callus bone healing is actually bypassed, as new bone is formed intentionally at the fracture margins. Primary bone healing is the direct reconstruction of the fragment edges by haversian remodeling. This is the same homeostatic mechanism that occurs in the living intact osseous skeleton on a daily basis. There are six phases of the reparative process: 1. Hematoma: will form between the fracture fragments immediately after the injury up until 1-3 days 2. Organization of the hematoma: slow shrinkage of the hematoma resorption of devitalized bone, periosteal and endosteal cells from osteoblasts at wound edges, from 3-10 days 3. Formation of fibrous/cartilaginous callus: this time of this phase will be directly proportional to the proper apposition of fracture fragments and immobilization of the affected body part, from 10-40 days 4. Primary bone callus: the bone callus becomes denser and fracture clefts fill in with bone matrix to bridge the fracture site, from 40-80 days 5. Absorption of the primary bone callus: transformation of this material to secondary bone callus, from 80-120 days 6. Remodeling of new bone: responding to the stresses placed upon it, after 120 days

NOTE* When compression and rigid fixation devices are utilized, bone will repair across the fracture gap by direct primary bone repair, with bone callus being minimal or nonexistent. Healing at points of contact along the fracture surface begins with the advance of a capillary bud from the haversian canal. This organized structure advances in a linear direction and crosses the fracture line depositing lamellar new bone along its path. The tip of the complex is a group of large multinucleated cells that function as osteoclasts. They cut their way through existing osteoid and cross the fracture line into the surface of the opposite fracture fragment (called the cutting cone). The osteoclasts are followed closely by a capillary loop as the cutting cone creates a tunnel in the existing bone substrate. The wall of this tunnel is lined by cells with osteoblastic activity. These cells produce a concentric pattern of new lamellar bone as the cutting cone passes and this is loosely deposited along the course of the haversian canal to exist as mature lamellar bone.

NOTE* Underlying diseases such as rickets, osteomalacia, Paget's Disease of Bone, hyperparathyroidism, osteoporosis and osteitis fibrosa cystica may all cause a delay in bone healing

Complications of Bone Healing Without an intact vascular supply to bone or rigid stable fixation problems occur: irritation callus or secondary bone healing, malunion, delayed union, non-union or pseudoarthrosis. 1. Secondary bone healing Involves the formation of fibrous tissue (Phase 3), primary bone healing does not. 2. Malunion is a misalignment of the fracture fragments along any of the three body planes including axial rotations, caused by inadequate reduction and inadequate immobilization. 3. Delayed union is the inability of the fracture to heal within an acceptable time period. a. Diagnosis is by radiographic evaluation b. Treatment is by rigid external or internal immobilation c. A good prognosticator for healing is the formation and evaluation of the bone callus d. Treatment involves stimulating bone callus formation and can be enhanced by bone drilling, onlay grafts, external electric current and magnetic field induction e. Bone scans are of little value in differentiating delayed from non- unions 4. Non-union can be an end stage of a delayed union, due to inaccurate reduction, interrupted or inadequate immobilization, severe local trauma to soft tissue and blood supply in the fracture site, impairment of bony circulation following open reduction, infection with secondary osteomyelitis of bony fragments, loss of bony substance and distraction of bony fragments, age, compromised host, anemia or anticoagulant therapy. a. Unless a non-union is aggressively treated, it will usually result in a pseudoarthrosis; the difference between them is that an atrophic nonunion does not have the fibrocartilaginous surface seen in a pseudoarthrosis b. Time frame for a non-union is usually 8 months following the initial fracture c. Diagnosis is by radiographic evaluation revealing gapping at the fracture site with no bone callus; in some cases the fracture ends will begin to round off (atrophic or non-reactive pseudoarthrosis); or will mushroom developing a flaring (hypertrophic or elephant foot type pseudoarthrosis) and form a joint space with synovial fluid filling the gap.

NOTE* Hypertrophic non-unions can be either Elephant type (maximum callus /hypertrophy-best chance for healing), Horsefoot type (moderate callus/hypertrophy) and Oligotrophic type (minimal callus/hypertrophy-least reactive) NOTE" Atrophic non-unions can be either Torsion wedge type (butterfly fragment with unilateral healing), Comminuted (gap+numerous pieces), Defect type (no osseous integrity) and Atrophic type (rounded edges) no osseous integrity. d. Pseudoarthrosis is classified as non-infected, previously infected or actively infected; non-infected are further subclassified according to their location, diaphyseal vs metaphyseal (most diaphyseal pseudoarthroses are atrophic) e. Radiological studies: i. Serial x-rays should be taken spanning time demonstrating a lack of progress. ii. Tomograms studies and CT scans can provide information of the bone callus and the healing process. iii. Bone scans are used to differentiate hypertrophic vs. atrophic nonunions/pseudoarthrosis whereby a (+) bone scan would indicate a hypertrophic/elephant foot type; a (-) bone scan would indicate an atrophic/nonreactive type since it is relatively avascular. f. Treatment of hypertrophic pseudoarthrosis: rigid immobilation and electrical bone stimulation (cathode is inserted in the operative site set at 20 microamps). Bone forms under electronegative conditions. NOTE* Bone stimulation is either implantable/invasive or non-invasive. Neither will work for a synovial pseudoarthrosis. Non-invasive devices will not work where the fracture gap is wider than 1 cm., and do not use during pregnancy or in the presence of a pacemaker. Invasive stimulators may be used with pacemakers and when the fracture gap is greater than 1 cm., also do not use during pregnancy. Types of stimulators: constant direct current (semi-invasive), pulsed direct current (invasive), inductive coupling electromagnetic stimulation (non-invasive), capacitive coupling electromagnetic stimulation.

Note* Implantable bone stimulators have no known contraindications or adverse effects, however, it is recommended that they not be used in the presence of active OM or pathologic fracture from malignant bone tumors. g. Treatment of atrophic non-union/ pseudoarthrosis: must resect the area involved and replace with new bone using rigid internal fixation for approx. 16 weeks minimum h. Metaphyseal pseudoarthrosis, because of its proximity to the joint space cannot be easily tension banded or fixated with a plate 5. Previously infected pseudoarthrosis/open infected pseudoarthrosis a. The infectious process within bone will respond much quicker to antibiotics only in the presence of a stable fracture fragment (stabilizing the

fracture fragment stabilizes the vascular bed), therefore, it is proper medical practice to maintain rigid internal fixation in the treatment of osteomyelitis b. The goals of treatment are to provide a wide surface contact between the fracture fragments under high compression, using whatever means is necessary c. Dead bone and non-viable soft tissue is removed d. When bone loss is identified, the defect is filled with decorticated bone or pure autogenous cancellous bone graft e. Metal implants and fixation devices should be left undisturbed as long as they afford rigid immobilization of the fragments. As soon as a sufficiently strong bony bridge develops both the fixation devices and the remaining sequestered bone are removed 6. Assessment of fracture healing a. Standard x-rays b. Stress fluoroscopy c. Tomography/CT scans d. Intraosseous venography: intramedullary injection of Renografin-76, with sequential x-rays taken at 30 second intervals to access the presence or absence of medullary flow across the fracture e. Signs and symptoms: pain, warmth and tenderness

Treatment of Nonunions The nonunion must be viewed as more than a fracture that has not healed. There is often edema, pain, joint stiffness and deformity in the bone, resulting in impaired function. Consequently, the first principle in the repair of nonunions is the restoration of function. Treatment of nonunions follows 4 basic concepts: I. Resection of useless tissue is required to allow healing II. The osteogenic capacity must be augmented by bone grafting III. The osteogenic capacity must be stimulated by electricity IV. The bone has the capacity to unite but has had inadequate immobilization, so the foot now should be adequately immobilized during healing. 1. Open nonunions vs. closed: When considering the above concepts one must first consider whether the nonunion is open (with extensive soft tissue damage) or closed. a. Open nonunions are less frequent and more difficult to manage b. Open nonunions frequently require multiple autogenous cancellous grafts (poor vascularity so cortical is a poor choice). c. Stabilization of an open nonunion is critical- can use external skeletal fixators (stability with minimal trauma to surrounding soft tissues) d. Following the above stages split/full thickness skin grafting can be applied next over a bed of granulation tissue. e. The type of treatment of a closed nonunion (most common) depends upon the type and etiology, which as previously discussed is based on vascularity

f. Proper evaluation of the nonunion is made via technetium scanning g. Approx. 20% of nonunions require bone grafting h. Electrical stimulation can be used but requires patient selection (satisfactory position of bone fragments, no interposed soft tissue, and positive bone scan) Fusion The basic concept of fusion is to eliminate motion where motion normally occurs through primary bone healing. This is accomplished by removing cartilagenous surfaces, obtaining anatomical apposition and utilizing some form of rigid fixation to obtain primary bone healing. Primary bone healing means membranous bone formation not endochondral bone formation, without evidence of fibrous tissue, cartilage and no evidence of callus formation. External callus is evidence of motion at the fusion site and endochondral bone formation. Fusion occurs quicker in cancellous bone where there are more osteons and. better blood supply available than in cortical bone.

Bone Grafting 1. There are essentially two types available: a. Autogenous (isograft): from the same person or twin b. Allograft: from the same species- two types available fresh and lyophilized 2. Indications for bone grafting are: osteogenesis, Immobilization, and replacement a. Treatment of delayed and nonunions, and pseudoarthroses. b. Augmentation of defects. c. Facilitation of arthrodesis d. Bone blocking procedures e. Reconstructive procedures (for opening wedge and bradymetatarsia procedures) f. Autogenous grafting to treat OM 3. Cortical vs. Cancellous

Cortical Cancellous a. Denser ....................................................................... Less dense b. Few viable cells .......................................................... Many viable cells c. Gives stability ............................................................ Fills defects d. Never revascularizes ................................................... There are vascular channels that unite at the graft-host junction immediately e. Does not facilitate osteogenesis ................................ Facilitates osteogenesis (by osteoconduction and osteoinduction f. Used with fixation devices ........................................ Not used with fixation devices (soft) g. Incorporation is slow ................................................. Incorporation is fast h. Incompletely repaired/incorporated ......................... Completely replaced by new bone i. Allows for creeping substitution ................................ Allows for creeping substitution j. Fenestration of graft helpful (drill holes) .... ............. Fenestration not done if made parallel to long axis of bone k. Radiolucency when healing (immediate).... .............. Radiodensity when healing because it quickly revascularizes l. Has haversion systems ............................................... No haversion systems Note* Corticocancellous grafts (from the iliac crest) gives the best combination. It looks like the first metatarsal head. Cortical graft looses 80% of its strength immediately. The weakest point in the cortical graft is at 8 weeks. 4. Autogenous bone a. is the material for most situations, the advantages are: viable cells and immunological compatibility b. the disadvantages are: donor site morbidity, insufficient quantity, increased OR time, additional risks arising from surgery at the donor site. c. Soaking in sterile saline prior to use is detrimental; proper short-term storage should be to place the graft in a closed container covered with a moistened saline sponge without immersion. d. Sources are: iliac crest (much bleeding and pain), fibula, and lateral calcaneus (small amounts). e. Procedure to remove graft from the calcaneus is as follows: A lateral incision is made over the calcaneus, posterior to the neutral triangle, avoiding the sural nerve and deepened by layers to bone. Drill holes are made outlining a cortical window which is then removed with a power saw. If cortical bone is not needed it is replaced on the lateral side, after packing the defect with lyophilized bone and covering the area with

periosteum. Must keep the calcaneus nonweight bearing until evidence of healing is present. 5. Lyophilized Allograft (bone bank bone) a. To reduce the antigenicity and increase immunological compatibility the dead bone is freeze dried; this reduces the moisture content to less than 5% NOTE* It is important that potential donors do not transmit disease so must be carefully screened by serological tests, autopsy, and blood and tissue bacteriological cultures, before and at implantation surgery

b. Lyophilized allografts vs. autogenous isografts Lyophilized Freeze dried/devoid of water Osteogenic precursor present Non-cellular bony matrix Osteoinductive property is lost present Requires good recipient bed Allows for healing by creeping substitution Unlimited amounts No morbidity of donor site Less OR time Try using autogenous first

Autogenous Fresh/water present Same Cellular bony matrix Osteoinductive property Not as critical Same Limited amounts Morbidity of donor site Increased OR time The preferred material for repair of nonunions, especially avascular nonunions

Note* Place lyophilized allografts in Ringer's lactate for 45 minutes prior to use

c. No difference in post-op infection rate of lyophized grafts vs. autogenous grafts 6. Healing of grafts is by creeping substitution, osteoconduction and osteoinduction a. Creeping substitution: the temporal and spatial repair activities whereby new viable bone replaces necrotic bone. b. Osteoconduction: the scaffolding effect of the bone graft that acts as a conduit for migration of viable cells (allows creeping substitution to take place). c. Osteoindudion : the presence of a bone morpheogenic protein (inductor substance) that causes nonosseous tissue to become osteogenic.

7. Grafting techniques Include: cortical onlay, peg, inlay, and peg-in-hole a. Papineau technique used to treat OM and infected nonunions: excision of necrotic bone, cancellous bone grafting and skin coverage 8. Healing is monitored with x-rays, Tc-99 scans, tomograms and CT. A gradual blurring of cortical margins occurs, with eventual crossing of the trabecular pattern across the graft-host junction. Impending disaster is signaled by sclerosis or dissolution of the graft. Aseptic Necrosis of the First Metatarsal Head Following Osteotomy Aseptic bone necrosis following metatarsal surgery can present itself. Stripping away too much periostium or allowing the bone to "heat up" by the bone saw are potential sources. A diagnosis can be made by bone scans and later xrays, after the onset of pain, swelling, and erythema. 1. Etiology of bone necrosis: a. Major trauma (osteotomy) b. Minor trauma (contusion) c. Steroid therapy d. Arteritis e. Occlusive PVD f. Antecedent phlebitis g. Post-irradiation h. S/P renal transplant i. Hyperuricemia/gout j. Collagen vascular diseases (RA) k. Sickle-cell disease l. Alcoholism/pancreatitis m. Hyperlipidemia n. Osteoporosis/osteomalacia 2. Bone Circulatory Networks: a. Nutrient artery b. Endosteal artery c. lntracortical systems d. Metaphyseal-epiphyseal e. Diaphyseal f. Marrow capillaries g. Periosteal h. Venous pathw 3. Arterial Circulation: Six groups of vessels a. Nutrient b. Periosteal c. Proximal metaphyseal d. Proximal epiphyseal e. Distal metaphyseal f. Distal epiphyseal

4. Radiological Classification of Bone Necrosis: a. Stage 1: Pre-radiologic (avascularity/precollapsed) i. The joint space/epiphyseal contour/trabeculae are WNL ii. Joint space may be stiff and painful b. Stage 2: Probable (revascularization phase with bone deposition and resorption/collapsed) i. Joint space/epiphyseal contour are WNL ii. Altered trabecular pattern (osteoporotic/sclerotic/sclero-cystic) c. Stage 3: Definite (bone healing phase/early and late degenerative arthritic changes) i. Joint space is WNL ii. Epiphyseal contour is disrupted and flattened iii. Trabecular collapse, arcuate sclerosis, cysts, and sequestrum d. Stage 4 (phase of deformity) i. Joint space narrowed (cartilage disruption) ii. Epiphyseal collapse iii. Trabecular destruction (sclerosis and cysts) iv. Epiphyseal collapse 5. Clinical Signs and Symptoms: a. Stage 1: Usually asymptomatic with minimal pain and/or stiffness b. Stage 2: Usually significant pain and stiffness, but can be asymptomatic c. Stage 3: Pain, stiffness, and limitation of motion, but can be asymptomatic 6. Clinical Lab Findings: a. Elevated ESR (nonspecific finding and not diagnostic) 7. Clinical Radiological Findings: a. Bone scan: Early (pre-collapse)- localized cold scan b. Bone Scan: Later- Hot 8. Differential Diagnosis: a. Arthrosis b. RSD c. Infection 9. Treatment of Aseptic Necrosis: a. Eliminate weight bearing b. Peripheral vasodilators c. Indomethacin d. Avoid steroids e. Core decompression, autogenous cancellous graft f. Pedicle muscle graft, decompression, bone graft g. Chilectomy, decompression or osteotomy, decompression h. Joint replacement (prosthesis) i. Arthrodesis

10. Recommendations/Precautions: a. Preserve capsular and periosteal attachments b. Accurate hemostasis, avoid tamponade c. Caution with modified Austin osteotomies (long-arm), Offset V osteotomy, and long Z osteotomies d. Caution with distal subchondral osteotomies, especially in the elderly e. Avoid hemi-implant in combination with distal osteotomy f. Use stable fixation, protective ambulation g. Use routine serial radiographs h. Consider bone scan early

Electrical Bone Stimulation The use of electrical energy in an effort to effect the healing of bone was initially described in 1812. A variety of therapeutic devices are currently available to provide electrical stimulation in the treatment of nonunions of bone. The discovery of stress related and steady-state electrical potentials, resulted in the hypothesis that Wolff’s law of bone was in effect mediated by electrical impulses. Therefore the application of exogenous electropositive currents to stimulate osteogenesis is the basis for bone stimulation. 1. A variety of methods have been employed to develop exogenous electrical potentials: a. Constant direct current: i. EBI:
Implantable
Contraindicated in osteomyelitis
Available in either 24 or 36 weeks life span b. Pulsed direct current: i. EBI:
Used for a 6 hour treatment/day ii. AME:
3 hour treatment/day
Has even distribution c. Capacitively coupled electrical field i. Bioelectron: d. Low intensity ultrasound i. Exogen®

Cartilage Healing 1. Normal Cartilage: a. Consists of chondrocytes in a glycoprotein hydrated matrix that may contain collagen and/or elastin i. Type Il collagen ii. Ground substance (glycosaminoglycans and water) b. Nutrition is through synovial fluid (there is no blood supply to the cartilage) 2. Healing phase: a. Necrosis

b. Inflammation c. Repair via metaplasia and replication 3. Types of injury: a. Partial thickness: Usually these injuries do not heal, using shaving and drilling of articular surface may lead to the development of fibrocartilage ingrowth b. Osteochondral heals via: i. Type II collagen: similar to hyaline cartilage ii. Type I collagen: fibrocartilage

Chapter 10: Burns and Frostbite Assessment and Treatment of Bums Bum Deformities Other Types of Burns Frostbite

BURNS AND FROSTBITE Assessment and Treatment of Burns A tissue injury caused by thermal, chemical, or electrical contact resulting in protein denaturation, wound edema, and loss of intravascular fluid volume due to increased vascular permeability. Systemic effects such as hypovolemic shock, infection, or respiratory tract injury pose a greater threat to life than do local effects. NOTE* R.J. Hinshaw has proven that the. bum progresses over a 48 hour period following the initial insult. D.M. Jackson has outlined the histopathology in the burn wound, showing 3 zones: the zone of hyperemia, zone of stasis, and the zone of coagulation. 1. The severity of the burn is judged by the quantity of tissue involved, which is represented by the percentage of the body surface area (% BSA) burned and by the depth of the burn. a. Critical burns: Hospitalization required i. Second degree bums exceeding 30% BSA ii. Third degree burns exceeding 10% BSA iii. Burns complicated by respiratory tract injury, major soft tissue injury, and fractures iv. Third degree burns involving critical areas (hands, face, feet) b. Moderate burns: Hospitalization recommended for observation i. Superficial second degree of > 15% BSA ii. Deep second degree burns of 15-30% BSA iii. Third degree burns of less than 10% BSA excluding the hands, feet, and face c. Minor burns: Outpatient management i. First degree burns ii. Second degree bums < 15% BSA iii. Third degree bums < 2% BSA 2. The depth of the burn is described as first, second, third degree, and recently fourth and fifth degree. Burn depth is difficult to determine in the early stages of the injury. a. First degree (epidermis only, does not blister, painful, heals in 5-10 days): Involves only a redness of the skin, very sensitive to touch, usually moist, no blisters, and the surface blanches to light pressure. This indicates mild inflammation. The most common 1st degree burn is sunburn. The rate and severity at which a person will burn is dependent upon the radiation, the absorptivity of the skin, and the length of exposure. First degree burns from fires may result from a much greater amount of radiation received during a shorter period of time. However, the two do not vary directly. The same total amount of heat received by radiation may be more damaging if received during a shorter period of time. Freezing of skin and body tissues

may produce similar effects to those of heat burns b. Second degree (epidermis and dermis, mostly hyperemic, moist, may blister, painful, can take a month to heal: More serious than 1st degree burns with the formation of blisters (usually), and in the more severe cases, fluid collects under the skin. The skin beneath the blisters is extremely sensitive, red in color, and exudes considerable amounts of fluid. Second degree burns are many times more painful than 1st degree burns, since nerve endings may be exposed (in 3rd degree bums the nerve endings are deadened by injury and edema). The broken blisters will expose the body to possible sources of infection c. Third degree (destruction of entire dermis and all deep epidermal elements, avascular, pale to black in color, dark red in children, either heals by secondary intention or needs skin grafting, painless): Generally do not have blisters, the surface may be white and pliable with pressure, or black and charred and leathery, the subdermal vessels do not blanch on pressure, and the area is usually anesthetic/hypoesthetic. The skin, subcutaneous tissue, red blood cells, capillaries, and sometimes muscle are destroyed. Burns may be white, light gray, brown or even charred black. Burns caused by direct contact between the skin and high temperature substances, may be hundreds-of-times more damaging than heat flow by radiation or convection of air because of tissue destruction, loss of plasma from the body, and disturbance of the body's fluid and chemical balance. All of these cause shock. Destruction of capillaries can cause gangrene. Pain may be present at more shallow wound edges. d. Fourth degree: Burning of muscle (electrical burns) e. Fifth degree: Burning of muscle (electric and radiation burns) NOTE* Laser Doppler flowmetry may have some advantage in predicting or delineating areas of burned skin that will heal spontaneously vs. those that will require skin grafting.

3. 85% of burns are small and may be treated on an outpatient basis, more extensive burn patients (>1 5% BSA in adults, >10% BSA in children) treated as inpatients. 4. Objectives of burn wound care: a. To prevent progression of the injury b. To prevent infection c. To provide an environment in which healing will proceed as rapidly as possible (remove dead tissue and protect viable tissue)

NOTE* According to Jackson's theory, three zones of injury exist: a. The zone of hyperemia: minimally injured tissue at the periphery of the bum wound b. The zone of stasis: less seriously injured tissue which may or may not necrose c. The zone of coagulation: the center of the bum consists of dead tissue which must be debrided 5. Early treatment: a. The wound should be cooled with cold wet compresses or by immersing it in ice water, especially if the patient has to wait for debridement. Continue this treatment as long as the patient does not get frostbite b. If the wound is not cooled, oxygen free radicals continue to be released by the drying cells causing arachidonic acid release 6. Treatment of severe burn patients: a. Inpatient: i. Stop the burning process: removing all clothing and smoldering material ii. Establishment of airway: intubate when breathing is rapid and shallow and patient is in apparent respiratory distress iii. Replacement of acute plasma loss: especially in 3rd degree burns, Ringer's lactate first, and plasma later iv. Manag3m3ociated life-threatening major trauma v. Diagnosis of metabolic abnormalities especially proteins, fluid, and electrolytes vi. Protection from bacterial contamination: Pen G 5 million units is given daily for 3 days as prophylaxis against streptococcal cellulitis. Topical therapy includes the use of one of the following: silver nitrate solution 0.5%, mefanide acetate 10%, and silver sulfadiazine 1 %. vii. Tetanus prophylaxis is mandatory viii. Control of pain ix. Operative management: excision of skin (escharotomy) results in burn wound bed that requires closure with skin graft material Technique of skin grafting is as follows: the wound is treated with topical antibiotics until the day, before surgery; saline wet dressings are then applied every 3-4 hours to reduce the debris and bacterial count of the wound. A wound C&S is taken 48 hours before surgery. The debridement is carried out surgically with a Goulian or Humby knife to tangentially excise the eschar until punctate bleeding is encountered. If this is not available or it is a large area a motor driven dermatome may be used to debride, the eschar. In small wounds a #20 blade is sufficient. Hemostasis can be provided with topical thrombin or a lidocaine with epinephrine soaked gauze. Absolute hemostasis and a bacterial count of less than 105 is essential. A skin graft is taken with a Pagget or Brown power dermatome, and is meshed via a meshing machine to permit expansion of the graft. It is rarely necessary to go beyond an expansion ratio of 1:3 (See section on plastic surgery). A graft with a larger expansion ratio will give a more disfiguring scar. Staples are used on the wound edges, and Xeroform® is used to cover the area. A plaster splint is applied to protect the area from shearing.

b. Outpatient: i. Remove the burning agent ii. Wound cleansing iii. Debridement of the blisters if present and debridement of all debris iv. Application of Silvadene® cream covered with sterile non-adherent dressing changed twice a day, thoroughly cleansing the wound with sterile saline prior to the next application of antibiotic cream. v. Elevation of the extremity vi. Penicillin p.o. or erythromycin or 1st generation cephalosporin vii. Prophylaxis against tetanus viii. Analgesics 7. Dressings: a. Avoid occlusive dressings as they can promote infection b. For partial thickness, clean superficial burn use a biosynthetic bilaminar membrane dressing (Biobrane®). Place tightly against the wound and wrap with compressive gauze (contraindicated in infected wounds) c. Nonadherent gauze (Xeroform®, Scarlet Red®) if the burn is too old or the biosynthetic dressing is not available d. Heterografts (EZ Derm®), a pigskin graft can be used in deep second or dirty third degree wounds NOTE* The deeper the bum the more frequently the dressing should be changed

8. Topical antibacterials: Effective for maintaining low subeschar bacterial counts a. Silver sulfadiazine (Silvadene): Poor penetration of eschar, good against pseudomonas, enterobacter, E. coli, Candida, Staph, avoid in sulpha anaphylactic allergy b. Mefenide (Sulfamylon®): Best penetration of eschar, good against pseudomonas and broad range of bacteria c. Gentamycin (Garamycin®): Can cause renal toxicity d. Nitrofurazone (Furacin): Can cause renal toxicity NOTE* These creams are contraindicated in clean partial thickness wounds such as donor sites where healing by epithelialization is desired. These medications may inhibit epithelialization 9. Complications: a. Adhesions and contractures b. Late developmental deformities c. Chronic burn ulceration d. Squamous cell/basal cell carcinoma, and melanoma e. Burn scar with nerve entrapment f. Burn dermatosis, pigmentary changes

g. Polyarthrosis of fingers and toes h. Traumatic neuralgias and neuropathies NOTE* Bacteremia is the major cause of death in patients hospitalized with bums. These infections may result in pulmonary infections, UTI's, and endocarditis Burn Deformities Forces must be exerted to prevent bum scar formation and eventual contracture. Prevention of deformities begins with the initial care. This includes consulting a physiatrist to help in the fabrication of splints, expeditious surgery, aggressive rehabilitation, orthoses, and Jobst® type pressure stockings. 1. The dorsal foot burn (most common) wound contracture results in dorsiflexion of the rear foot and hyperextension of the m.p.joints, with the toes being pulled toward the midaxial line. Plantar deformities consist of flexion of the foot and toes, and an equinus deformity. 2. Surgery for Late Deformities: a. This requires precise planning b. For most burn scar deformities, release of the contracture and split/full thickness grafting will usually be sufficient. Placing the incision across the area of maximum tension assures the greatest release. c. TAL lengthenings can be performed as necessary d. Extensor tenotomies may or may not be indicated Other Types of Burns 1. Electrical: Can be either low tension or high tension. The type of current, amperage, voltage, area of the body through which it passes, duration of the exposure, and the resistance of the body structures all influence the magnitude of the injury. a. Low Tension: When the voltage is less then 1000 V. Mostly seen in the hand while in the home. b. High Tension : Usually industrial in nature. The burn is the result when the electrical energy upon meeting resistance is converted to thermal energy. These injuries require immediate escharotomy and a decompression fasciotomy to salvage an extremity. 2. Chemical Burns: Factors which influence the severity of a chemical injury are the concentration or pH of the solution, the mode of action of the agent, the vehicle, the volume, and the duration of contact. Emergency treatment of a chemical injury requires knowing precisely what agent caused the injury and the immediate application of the proper antidote. In nearly all chemical injuries the most effective expedient is water (immediate and copious). Water washes away the chemical, reduces the rate of reaction, mitigates the hygroscopic action of the chemical, and restores the wound pH to normal. Frostbite 1. Classifications: a. By degree:

i. First degree: Freezing without blistering (peeling may be present) ii. Second degree: Freezing with clear blistering iii. Third degree: Freezing with skin death (ulcers, blisters, and subcutaneous involvement) iv. Fourth degree: Freezing with full hemorrhagic thickness involvement and ultimate loss or deformity of body part (frostbitten tissue appears white to blue white, and is firm or hard) b. Superficial vs deep i. Superficial frostbite: Chillblains
Mildest form of cold injury
Edema of the dermis, vasculitis of the deep and superficial vessels, blanching followed by white, waxy frozen appearance
Beneath the superficial skin, tissues are normal
Bullae may occur after warming
Rewarm in whirlpool 108°F 20-40 minutes with analgesic support ii. Deep frostbite:
Mostly involves the extremities
Tissues are icy hard without deep tissue resilience (resembles frozen meat) -No sensation
Rewarm rapidly in whirlpool as above but with narcotic analgesia c. Trench foot: Caused by exposure to wet, cold weather, with the temperature not necessarily below freezing i. Initially, the foot becomes edematous due to tissue hypoxia and vascular damage. The tissue becomes cold, white or cyanotic, pulses and sensation are decreased ii. The predominating pathology is vasospasm iii. Warming the extremity causes a cascade of events, which leads to the second phase, the hyperemic state. iv. The hyperemic state is one where the extremity is hot, dry, reddened, marked by bounding pulses and severe pain (this state is often identical to frostbite) v. Recovery from trench foot is characterized by decreasing edema and the return of normal pulses d. Hypothermia: The basis of hypothermia is dehydration. The difference between mild and severe hypothermia is the core temperature. Severe hypothermia (below 90°F) the heart and lungs begin to fail and metabolic problems appear 2. Rewarming procedure: a. Before thawing protect the injured part b. Do not rub or massage the area c. Take core temperature with hypothermia thermometer d. Rewarm extremities 100-108°F in a whirlpool with thermometer control e. Leave blisters and blebs intact f. Administer narcotics prn for pain g. Do not debride the injury h. Tetanus prophylaxis i. Antibiotics? j. After thawing, do not allow the area to refreeze

k. Protect the area from mechanical damage 3. Complications: a. Can result in burn-like injuries b. Sensitivity of the affected part c. Raynaud's-like phenomenon d. Muscle atrophy and fat tissue loss e. Skin texture affected with the epidermis generally dry with fissuring and depigmentation f. Punched out lytic lesions in the bone seen on x-ray g. Paresthesias h. Hyperhidrosis i. Pain may be secondary to permanent vasoconstriction, suggesting loss of autonomic vascular control and resulting in hypoxia to nerve endings and other local tissues.

Chapter 11: Bone Tumors Introduction Staging Techniques Surgical Staging System Radiology of Bone Tumors Bone Tumors Cystic Lesions of Bone Other Tumors & Cancers Bone Tumors: A Quick Reference Chart Phases in Cancer Development Benign vs. Malignant

TUMORS OF BONE, BONE MARROW AND CARTILAGE Introduction Diagnosis of bone tumors is not the singular effort of the clinician, but rather the work of a team consisting of attending surgeon, radiologist, and pathologist who will evaluate the history, provide a comprehensive examination, and order appropriate tests. Differential diagnosis on xray is an interesting academic excercise, but actual diagnosis is more important. Radiologic study has been compared to physical examination of the lesion in its context. Laboratory adjunctive testing will provide clues to some conditions. MRI and scans will help to delineate tumors. Radionuclide uptake procedures can help to locate occult metastatic or synchronous lesions. Occasionally, even angiography can be helpful. Bone tumors are either primary or metastatic. Primary bone tumors can be either benign or malignant. After a complete history and physical examination, and lab studies, the management of bone tumors can be divided into 3 phases: (1) radiographic staging, (2) diagnosis, and (3) treatment. The radiographic staging is designed to provide information concerning the diagnosis and the anatomic extent of the lesion. The definitive diagnosis always requires biopsy. Only after these first 2 phases are complete can a rational treatment plan be established and carried out. In formulating a treatment plan, the. histogenetic type of tumor, local extent, and possibility of distant disease must be considered. Clinical factors such as age, size, occupation, life-style, and expectations also play a key role in the treatment options available

Staging Techniques The purpose of radiographic staging of a bone tumor is two-fold. The first is to obtain information concerning a possible diagnosis, and the second is to define the anatomical extent of the lesion 1. Staging techniques: a. Plain radiograph demonstrates the bone involved, the region of the bone, the extent and type of destruction, and the amount of reactive bone formed. It also gives some information of benign vs malignant tumors (plain film x-rays are a must in the staging of bone tumors) b. Radioisotope scans (99m Tc MDP) can estimate the local intramedullary extent of the tumor and screen for other skeletal areas of involvement. It can give information about the biologic aggressiveness of the tumor via its uptake. This study is also important in post-treatment followup c. CT: Greatly aids in the diagnosis and anatomic location. Using contrast with CT aids in the identification of the major neurovascular structures as well as the enhancement of wellvascularized lesions. CT is the best study for evaluating cortical penetration and osseous detail, and valuable in the assessment of matrix calcification or ossification. CT is the best technique for detecting pulmonary metastasis, replacing whole lung tomography.

d. MRI: The best information is obtained when MRI and CT are interpreted together. MRI more accurately demonstrates the local intramedullary extent of tumors than with gallium67 citrate or any other method. MRI is the best technique for demarcating the soft tissue component of bone tumor and its relationship to neurovascular structures without utilization of contrast material e. Arteriography: Since the advent of CT anti MRI with contrast, this technique is not used much, except in a difficult anatomic location such as the shoulder girdle or pelvis f. Biopsy:, The purpose of biopsy is to obtain adequate tissue for accurate diagnosis and grading while avoiding potential detrimental effects to the patient or compromise of the definitive surgical procedure

Surgical Staging System The information generated by the history, physical examination, radiographic studies, and biopsy has been incorporated into a staging system for musculosketetal tumors. The surgical staging system reflects the biologic behavior of the lesion and its degree of aggressiveness. It is based on a combination of the histologic grade (G), anatomic site (T), and the presence of distant metastasis (M) 1. Staging system: a. Grade (G): Divided into benign (GO), low grade malignant (G1), and high grade malignant (G2). Grade is based upon a combination of histologic, radiographic, and cytologic characteristics and biologic characteristics b. Anatomic site (T): Is divided into intracapsular (TO), extracapsular /intracompartmentaI (T1), and extracapsular/ extracompartmentaI (T2) c. The stages of malignant lesions are designated by numerals 1, II, and III

Radiology of Bone Tumors 1. Making a diagnosis: When attempting to diagnosis bone tumors it is important to know: the age and sex of the patient, which bone is involved, is it well demarcated, its size and shape and location, type of periosteal reaction, any soft tissue involvement, any pain and what relieves the pain, pattern of bone destruction, appearance of the tumor matrix, appearance of trabeculation, cortical erosion penetration or expansion, and a good medical history. a. Pattern of destruction: geographic, motheaten or permeative i. Geographic- usually seen with benign tumors, least aggressive pattern of bone destruction, indicative of a slow growing lesion, has a smooth or irregular but well-defined margin which is easily separated from the surrounding normal bone by a short zone of transition. Some metastatics can look like this. ii. Motheaten- may be demonstrated by a malignant bone tumor, OM, or . hematopoietic tumors, indicative of rapidly growing lesion, less well-defined with a longer zone of transition from normal to abnormal bone iii. Permeative- demonstrated by certain malignant bone tumors and rarely OM, most aggressive pattern of bone destruction, rapid growth potential, poorly demarcated and not easily separated from the normal surrounding bone b. Size, shape and the margin of the tumor

1. Size- in general, malignant primary bone tumors are larger than benign ones and when first discovered primary malignant tumors may be greater than 6 cm in size (in some cases) ii. Shape- tumor with greatest diameter at least 1.5 times its least diameter may include Ewing's sarcoma, chondrosarcoma and large cell lymphoma (reticulum cell sarcoma) iii. Margin- sclerosis of the surrounding normal bone indicates a slow growing lesion, indicating pressure with periosteal or endosteal reaction c. Tumor matrix: calcification or ossification 1. Matrix calcification- cartilage tumor, may appear centrally located, ring-like, or fleck-like radiodensity, seen with chondromas, chondrosarcomas and chondroblastomas ii. Matrix ossification- bone tumor, seen with osteoid osteoma and osteogenic sarcoma d. Trabeculation: i. Giant cell- delicate and thin ii. Chondromyxoid fibroma- course and thick iii. Aneurysmal bone cyst- delicate and horizontal iv. Non-ossifying fibroma- loculated v. Hemangioma- striated and radiating e. Cortical Erosion: Penetration and Expansion The bone cortex serves as a barrier to the further lateral growth of "certain tumors such as nonaggressive medullary lesions which generally expand in the direction of least resistance within the medullary canal. Other lesions, however, may penetrate the cortex in variable lengths to those aggressive bone lesions which may penetrate the entire thickness of the cortex in one or more places f. Type of periosteal response: Buttressing, Codman's triangle, sunburst, onion skin and hair-onend i. Buttressing (thick periostitis)- indicative of a slow growing tumor whereby an expansile mass presses against the periosteum, which thickens the cortex with new layers of bone ii. Codman's triangle- a triangular elevation of the periostium seen in osteogenic sarcoma and other conditions (see Quick Reference Chart) iii. Sunburst pattern- delicate rays of periosteal bone formation separated by spaces containing blood vessels, seen with hemangioma, Ewing's sarcoma and osteogenic sarcoma iv. Onion skin pattern- production of multiple layers of new periosteal bone, exemplified by Ewing's sarcoma, eosinophilic granuloma, and lymphoma of bone v. Hair-On-End pattern- similar to sunburst pattern, indicating the most malignant type of tumor, where rays of periosteal bone project in a perpendicular direction to the underlying bone (Ewing's sarcoma) g. Part of the bone involved: Epiphyses, metaphyses or diaphysis i. Epiphyses- chondroblastoma, giant cell tumor, subchondral cyst, and hemangioma ii. Metaphyses- solitary bone cyst, osteogenic sarcoma, chondromyxoid fibroma, nonossifying fibroma, and chondrosarcoma iii. Diaphysis- solitary bone cyst, aneurysmal bone cyst, non-ossifying fibroma, Ewing's sarcoma, enchondroma, fibrous dysplasia, giant cell tumor, and eosinophilic granuloma

Bone Tumors 1. Osteoma (hyperostosis, periosteal osteoma): a. Is a benign, reactive, expansile tumor-like lesion that may be pedunculated b. It usually arises from intramembranous bones and may occur posttraumatically c. Some may represent osteochondromas whose cartilage cap has ossified d. May occur subungually e. These may be: i. Ivory: compact ii. Spongy: trabecular iii. Mixed f. Multiple osteomas may occur in Gardner's Syndrome g. Excision is curative 2. Enostosis: a. An uncommon, benign, intramedullary island of ossification b. It may be reminiscent of osteoblastic metastatic visceral cancers c. These are often asymptomatic, incidental radiologic findings d. They may occur with Multiple Enchondromatosis and with keloid formation 3. Osteoid Osteoma: a. Is a benign, osteoblastic, slow-growing lesion that may occur in cortical or medullary bone b. The soft tissue center is its NIDUS c. Some (but not all) patients experience nocturnal, intermittent pain that becomes a "boring" type of constant pain d. It many cases (but not all), pain is relieved by salicylates e. X-rays often show a sclerotic rim of bone around the radiolucent nidus f. Sometimes the nidus is sclerotic and not visable unless MRI or scans are done g. Pain may be referred to adjacent joints h. Lesions adjacent to joints may erode the cartilage i. Surgery consists of en-bloc resection to include the nidus, (x-rays should be done of the specimen removed to make sure the nidus was removed) j. Lesions usually are under 2 cm in diameter, affecting patients in the 1025 year age group (mostly males) 4. Osteoblastoma (osteogenic fibroma, spindle cell variant of giant cell tumor, giant osteoid osteoma): a. Is a benign, fast-growing tumor that usually affects males (ages 10-20) b. Pain is not relieved by salicylates in most cases c. Lesions are usually metaphyseal or diaphyseal d. It usually exceeds 2 cm in diameter, and lacks the sclerotic rim around the soft tissue center e. Older lesions may show a mottled pattern of thin calcifications

Chapter 12: Bone Tumors Introduction Staging Techniques Surgical Staging System Radiology of Bone Tumors Bone Tumors Cystic Lesions of Bone Other Tumors & Cancers Bone Tumors: A Quick Reference Chart Phases in Cancer Development Benign vs. Malignant

TUMORS OF BONE, BONE MARROW AND CARTILAGE Introduction Diagnosis of bone tumors is not the singular effort of the clinician, but rather the work of a team consisting of attending surgeon, radiologist, and pathologist who will evaluate the history, provide a comprehensive examination, and order appropriate tests. Differential diagnosis on x-ray is an interesting academic excercise, but actual diagnosis is more important. Radiologic study has been compared to physical examination of the lesion in its context. Laboratory adjunctive testing will provide clues to some conditions. MRI and scans will help to delineate tumors. Radionuclide uptake procedures can help to locate occult metastatic or synchronous lesions. Occasionally, even angiography can be helpful. Bone tumors are either primary or metastatic. Primary bone tumors can be either benign or malignant. After a complete history and physical examination, and lab studies, the management of bone tumors can be divided into 3 phases: (1) radiographic staging, (2) diagnosis, and (3) treatment. The radiographic staging is designed to provide information concerning the diagnosis and the anatomic extent of the lesion. The definitive diagnosis always requires biopsy. Only after these first 2 phases are complete can a rational treatment plan be established and carried out. In formulating a treatment plan, the. histogenetic type of tumor, local extent, and possibility of distant disease must be considered. Clinical factors such as age, size, occupation, life-style, and expectations also play a key role in the treatment options available Staging Techniques The purpose of radiographic staging of a bone tumor is two-fold. The first is to obtain information concerning a possible diagnosis, and the second is to define the anatomical extent of the lesion 1. Staging techniques: a. Plain radiograph demonstrates the bone involved, the region of the bone, the extent and type of destruction, and the amount of reactive bone formed. It also gives some information of benign vs malignant tumors (plain film x-rays are a must in the staging of bone tumors) b. Radioisotope scans (99m Tc MDP) can estimate the local intramedullary extent of the tumor and screen for other skeletal areas of involvement. It can give information about the biologic aggressiveness of the tumor via its uptake. This study is also important in post-treatment followup c. CT: Greatly aids in the diagnosis and anatomic location. Using contrast with CT aids in the identification of the major neurovascular structures as well as the enhancement of well-vascularized lesions. CT is the best study for evaluating cortical penetration and osseous detail, and valuable in the assessment of matrix calcification or ossification. CT is the best technique for detecting pulmonary metastasis, replacing whole lung tomography.

d. MRI: The best information is obtained when MRI and CT are Interpreted together. MRI more accurately demonstrates the local intramedullary extent of tumors than with gallium-67 citrate or any other method. MRI is the best technique for demarcating the soft tissue component of bone tumor and its relationship to neurovascular structures without utilization of contrast material e. Arteriography: Since the advent of CT anti MRI with contrast, this technique is not used much, except in a difficult anatomic location such as the shoulder girdle or pelvis f. Biopsy:, The purpose of biopsy is to obtain adequate tissue for accurate diagnosis and grading while avoiding potential detrimental effects to the patient or compromise of the definitive surgical procedure

Surgical Staging System The information generated by the history, physical examination, radiographic studies, and biopsy has been incorporated into a staging system for musculosketetal tumors. The surgical staging system reflects the biologic behavior of the lesion and its degree of aggressiveness. It is based on a combination of the histologic grade (G), anatomic site (T), and the presence of distant metastasis (M) 1. Staging system: a. Grade (G): Divided into benign (GO), low grade malignant (G1), and high grade malignant (G2). Grade is based upon a combination of histologic, radiographic, and cytologic characteristics and biologic characteristics b. Anatomic site (T): Is divided into intracapsular (To), extracapsular/intracompartmental (Ti), and extracapsular/ extracompartmental (T2) c. The stages of malignant lesions are designated by numerals I, II, and III

Radiology of Bone Tumors 1. Making a diagnosis: When attempting to diagnosis bone tumors it is important to know: the age and sex of the patient, which bone is involved, is it well demarcated, its size and shape and location, type of periosteal reaction, any soft tissue involvement, any pain and what relieves the pain, pattern of bone destruction, appearance of the tumor matrix, appearance of trabeculation, cortical erosion penetration or expansion, and a good medical history. a. Pattern of destruction: geographic, motheaten or permeative i. Geographic- usually seen with benign tumors, least aggressive pattern of bone destruction, indicative of a slow growing lesion, has a smooth or irregular but well-defined margin which is easily separated from the surrounding normal bone by a short zone of transition. Some metastatics can look like this. ii. Motheaten- may be demonstrated by a malignant bone tumor, OM, or hematopoietic tumors, indicative of rapidly growing lesion, less well-defined with a longer zone of transition from normal to abnormal bone iii. Permeative- demonstrated by certain malignant bone tumors and rarely OM, most aggressive pattern of bone destruction, rapid growth potential, poorly demarcated and not easily separated from the normal surrounding bone b.

Size, shape and the margin of the tumor i. Size- in general, malignant primary bone tumors are larger than benign ones and when first discovered primary malignant tumors may be greater than 6 cm in size (in some cases) ii. Shape- tumor with greatest diameter at least 1.5 times its least diameter may include Ewing's sarcoma, chondrosarcoma and large cell lymphoma (reticulum cell sarcoma) iii. Margin- sclerosis of the surrounding normal bone indicates a slow growing lesion, indicating pressure with periosteal or endosteal reaction c. Tumor matrix: calcification or ossification i. Matrix calcification- cartilage tumor, may appear centrally located, ring-like, or fleck-like radiodensity, seen with chondromas, chondrosarcomas and chondroblastomas ii. Matrix ossification- bone tumor, seen with osteoid osteoma and osteogenic sarcoma d. Trabeculation: i. Giant cell- delicate and thin ii. Chondromyxoid fibroma- course and thick iii. Aneurysmal bone cyst- delicate and horizontal iv. Non-ossifying fibroma- loculated v. Hemangioma- striated and radiating e. Cortical Erosion: Penetration and Expansion The bone cortex serves as a barrier to the further lateral growth of certain tumors such as non-aggressive medullary lesions which generally expand in the direction of least resistance within the medullary canal. Other lesions, however, may penetrate the cortex in variable lengths to those aggressive bone lesions which may penetrate the entire thickness of the cortex in one or more places f. Type of periosteal response: Buttressing, Codman's triangle, sunburst, onion skin and hair-on-end i. Buttressing (thick periostitis)- indicative of a slow growing tumor whereby an expansile mass presses against the periosteum, which thickens the cortex with new layers of bone ii. Codman's triangle- a triangular elevation of the periostium seen in osteogenic sarcoma and other conditions (see Quick Reference Chart) iii. Sunburst pattern- delicate rays of periosteal bone formation separated by spaces containing blood vessels, seen with hemangioma, Ewing's sarcoma and osteogenic sarcoma iv. Onion skin pattern- production of multiple layers of new periosteal bone, exemplified by Ewing's sarcoma, eosinophilic granuloma, and lymphoma of bone v. Hair-On-End pattern- similar to sunburst pattern, indicating the most malignant type of tumor, where rays of periosteal bone project in a perpendicular direction to the underlying bone (Ewing's sarcoma) g. Part of the bone involved: Epiphyses, metaphyses or diaphysis i. Epiphyses- chondroblastoma, giant cell tumor, subchondral cyst, and hemangioma ii. Metaphyses- solitary bone cyst, osteogenic sarcoma, chondromyxoid

fibroma, non-ossifying fibroma, and chondrosarcoma iii. Diaphysis- solitary bone cyst, aneurysmal bone cyst, non-ossifying fibroma, Ewing's sarcoma, enchondroma, fibrous dysplasia, giant cell tumor, and eosinophilic granuloma

Bone Tumors 1. Osteoma (hyperostosis, periosteal osteoma): a. Is a benign, reactive, expansile tumor-like lesion that may be pedunculated b. It usually arises from intramembranous bones and may occur posttraumatically c. Some may represent osteochondromas whose cartilage cap has ossified d. May occur subungually e. These may be: i. Ivory: compact ii. Spongy: trabecular iii. Mixed f. Multiple osteomas may occur in Gardner's Syndrome g. Excision is curative 2. Enostosis: a. An uncommon, benign, intramedullary island of ossification b. It may be reminiscent of osteoblastic metastatic visceral cancers c. These are often asymptomatic, incidental radiologic findings d. They may occur with Multiple Enchondromatosis and with keloid formation 3. Osteold Osteoma: a. Is a benign, osteoblastic, slow-growing lesion that may occur in cortical or medullary bone b. The soft tissue center is its NIDUS c. Some (but not all) patients experience nocturnal, intermittent pain that becomes a "boring" type of constant pain d. It many cases (but not all), pain is relieved by salicylates (asprin) e. X-rays often show a sclerotic rim of bone around the radiolucent nidus f. Sometimes the nidus is sclerotic and not visable unless MRI or scans are done g. Pain may be referred to adjacent joints h. Lesions adjacent to joints may erode the cartilage i. Surgery consists of en-bloc resection to include the nidus, (x-rays should be done of the specimen removed to make sure the nidus was removed) j. Lesions usually are under 2 cm in diameter, affecting patients in the 1025 year age group (mostly males) k. Associated pain relieved by apsrin 4. Osteoblastoma (osteogenic fibroma, spindle cell variant of giant cell tumor, giant osteoid osteoma): a. Is a benign, fast-growing tumor that usually affects males (ages 10-20)

b. Pain is not relieved by salicylates in most cases c. Lesions are usually metaphyseal or diaphyseal d. It usually exceeds 2 cm in diameter, and lacks the sclerotic rim around the soft tissue center e. Older lesions may show a mottled pattern of thin calcifications f. There is a debate as to whether these lesions can undergo malignant transformation 5. Osteogenic Sarcoma (osteosarcoma): a. Is the second most common primary malignant bone tumor of the body b. It is not common in the feet (occurs 2% of the time) c. The most common site is in the region of the knee d. Most lesions are solitary, a few are multiple, metachronous or synchronous e. Most patients are teenage males f. Cortical lesions seem to have a better prognosis than medullary lesions g. There are many subtypes and radiographic appearances vary h. Codman's triangle in x-rays represents a cuff of subperiosteal new bone at the borders of a lesion that rapidly elevates periosteum, forming a bone spicule NOTE* Codman's triangle is seen in osteogenic sarcoma, but is not diagnostic for it as it is also seen in other bone lesions, including chondrosarcoma, Ewing's sarcoma, giant cell tumor of bone, simple bone cyst and any sarcomas arising in the context of Paget's disease of bone

i. The "sunburst" appearance (on x-ray) of some early osteogenic sarcomas also is not diagnostic, since it can also be seen in Ewing's sarcoma and in hemangioma of bone j. The serum alkaline phosphatase is quite elevated in active osteogenic sarcoma and can be used as an index of recurrence or late metastasis (i.e. if it rises from normal levels after tumor resection) k. Secondary osteogenic sarcoma arises after age 40 from pre-existing conditions such as Paget's disease of bone, fibrous dysplasia of bone, nonossifying fibroma of bone, bone infarcts, solitary osteochondroma, and multiple enchondromatosis l. Radiographic diagnostic aids include angiography, MRI and Gallium scans NOTE* Extraosseous osteogenic sarcoma is a well recognized entity. The rare juxtacortical type may show a periosteal "string sign" on x-rays 6. Osteochondroma (osteocartilaginous exostosis): a. Is the most common benign bone tumor b. The most frequent form in the foot is the subungual (Dupuytren's) exostosis c. Multiple forms exist and are known as multiple cartilaginous exostoses, hereditary multiple exostosis, hereditary deforming dyschondroplasia, and diaphyseal aclasis

d. While the classic type has a hyaline cartilage cap, the subungual types have fibrocartilage caps e. Excision is curative if the overlying soft tissue which acts as perichondrium (and therefore is a source of recurrence) is removed with the lesion f. Malignant transformation is rare, but is recorded 7 . Chondromas: a. Are benign neoplasms b. Solitary enchondromas appear as intramedullary (central) lucencies derived from rests of epiphyseal cartilage c. They may become symptomatic after local trauma, usually in adults between 30 & 40 years of age d. Pain without history of local trauma suggests malignant transformation e. Multiple enchrondatosis (Ollier's disease) is a cartilage dysplasia that can be quite deforming, and carries a high risk for malignant transformation f. Multiple enchrondromatosis occur as part of Maffuci's (Kast-Maffuci) syndrome (angiochondromatosis). Persons with this syndrome may show areas of vitiligo, as well as pigmented lesions g. Metachondromatosis is a dominantly inherited mime of multiple enchondromatosis, but the lesions regress h. Periosteal (juxtacortical/eccentric) chondroma is a rare lesion and is also called ecchondroma i. The lesions are sharply circumscribed on x-ray j. Size and location determine surgical approach 8. Chondroblastoma (Codman tumor): a. Is a benign lesion of immature cartilage b. Most lesions are epiphyseal c. Most patients are males, ages 10-20 years d. Secondary changes may resemble aneurysmal bone cyst e. Lesions are painful and appear cystic on x-ray, with a thin overlying shell f. Fine trabeculations ("chickenwire calcifications") may present in older lesions g. Curettage followed by packing with bone chips may be curative NOTE* Some prefer curettage followed by freezing with liquid nitrogen and packing with bone chips h. Recurrences are more frequent when there is a concurrent aneurysmal bone cyst or arteriovenous malformation i. Radiation therapy may work, but presents a risk of radiation-induced sarcoma 9. Chondromyxoid Fibroma: a. In general, is a rare tumor, but does affect the feet b. Most frequently seen between the ages of 10 & 20 years

c. Foot lesions seem to be more frequent in the 30-40 age group d. These are painful lesions that are lucent on x-rays, and which may appear lobular or bubbly e. Some lesions are quite aggressive f. En-bloc resection or amputation may be necessary 10. Chondrosarcoma: a. Is a malignant, potentially metastatic cartilage tumor that may show myxoid and/or osseous elements b. It Is the third most common malignant bone tumor c. Most frequently seen between the ages of 40 & 60 d. Lesions may be primary or secondary, the latter arising in such preexisting lesions as Paget's disease of bone, osteochondroma (single or multiple), Maffuci's (Kast-Maffuci) syndrome, Ollier's multiple enchondromatosis, and bone cysts e. The types range from the well differentiated through the clear cell and mesenchymal (anaplastic) types f. Patients demonstrate a painful limp and a mass may be palpable g. On x-ray, the tumors may be lucent or. may demonstrate calcifications h. Angiograms, scans, and MRI are helpful adjuncts i. Amputation is the indicated treatment,- the level depending upon the location and size of the tumor 11. Desmoplastic Fibroma of Bone (endosteal fibroma): a. Is rare and occurs between the ages of 10 & 20 years of age (in most cases) b. The borders appear indistinct on x-ray, suggesting malignancy c. These may be aggressive (although benign) causing pathologic fractures and pain d. En-bloc resection with bone grafting seems the best approach to prevent recurrence e. Periosteal desmoids are related and are aggressive, and have to be differentiated from parosteal fasciitis 12. Fibrous Dysplasia of Bone: a. May be monostotic or polyostotic (the polyostotic form affects the feet the feet more often than the monostotic form, and may be part of the McCuneAlbright syndrome in some cases) b. There may be pain and swelling with pathologic fractures c. The lucent lesion has a sclerotic rim and may expand surrounding bone d. Polyostotic forms may give rise to osteogenic sarcoma, chondrosarcoma, or intraosseous fibrosarcoma e. Monostotic forms may be cured by en-bloc resection and packing with bone chips, or curettage depending upon size and location of the lesion 13. Nonossifying Fibroma: a. Is a benign process seen most frequently between the ages of 10 El 20 years b. Occurs in the metaphyseal areas of bone c. It is the active and proliferating form of fibrous cortical defect of infants

and young children ("metaphyseal fibrous defect") d. Symptoms may be absent, or with growth of the lesion, there may be pain, swelling, and pathologic fracture e. X-rays show a lucent, eccentric lesion that may be loculated within a sclerotic rim f. Treatment consists of curettage and packing with bone chips g. Fibrous cortical defect may be associated with osteochondritides of the tibia and femur 14. Paget's Disease of Bone: a. Is a benign, premalignant condition of bone that may be monostotic or polyostotic and which is rare in the feet b. Most cases occur after age 40 years of age c. There are well defined, sharply bordered areas of bone resorption and bone deposition, the latter in a haphazard structure ("woven bone") d. The osteoid and bone deposition is sufficient to thicken the affected bones, sometimes causing deformities e. Some suspect a viral infection of osteoclasts as the etiology f. In the active stages, levels of urinary hydroxyproline are significantly elevated g. The highest levels of serum alkaline phosphatase occur in this condition h. Development of pain may herald malignant transformation i. Paget's sarcoma refers to any sarcoma that develops in the setting of known Paget's disease of bone (these include osteogenic sarcoma, chondrosarcoma, fibrosarcoma, and malignant fibrous histiocytoma) 15. Eosinophilic Granuloma (Langerhans cell granulomatosis, Taratynov's disease): a. Is an uncommon bone lesion that may occur as solitary or multifocal lesions b. Involvement of foot bones is extremely rare c. Once considered malignant, this condition is now considered benign even though irradiation and chemotherapy are used in some cases of multifocal disease d. Diagnosis is confirmed by open biopsy, during which small defects may be curetted and packed with bone chips e. A "tempo phenomenon" is seen, such that osseous lesions come and go without treatment f. Large lesions may require en-bloc resection g. On x-ray, lesions may appear "punched out" or irregular and ragged h. Lesion edges may appear slanted or bevelled, suggesting depth to the lesion i. Overlapping lucent lesions suggest a "hole within a hole" 16. Soft Tissue Malignant Tumors: a. Occur as primary bone lesions and differ from their soft tissue counterparts only by location b. Examples include intraosseous fibrosarcoma, malignant fibrous histiocytoma, leiomyosarcoma, angiosarcoma, Kaposi's sarcoma, adamantinoma, and angioendothelioma

NOTE* Secondary malignant bone tumors are metastases from visceral carcinomas or other soft tissue sarcomas. These intraosseous malignancies cause pain and bone destruction, appearing irregular on x-ray 17. Soft Tissue Benign Tumors: a. May also arise as primary bone tumors b. These include hemangiomas (solitary or multiple), lymphangiomas, glomus tumors, and giant cell tumors of bone c. Tumor-like lesions affecting bone include penetrating epidermal inclusion cysts, pseudoepitheliomatous hyperplasia in fistulas leading from bone, hypertrophic pulmonary osteoarthropathy, and giant cell reparative granuloma of the digits (considered by some to be a variant of giant cell tumor of bone)

Cystic Lesions of Bone These have to be differentiated from bone tumors 1. Unicameral (Simple) Bone Cyst: a. Generally are asymptomatic lytic lesions, that are thought to be interosseous synovial cysts as a result of entrapment if synovium during bone development b. Classically, these have been treated by curettge and packing. Curettings are very sparse. Cryosurgery is risky due to possible damage to nearby epiphyses c. Recently, treatment success has been reported with one or more aspirations of fluid followed by introduction of a steroid d. Most cases arise in males over-20 years old e. Those in the calcaneus arise in Ravelli's triangle f. Pain may suggest a fracture of the wall, and a "fallen fragment sign" represents a fracture chip within the cyst 2. Intraosseous Ganglion: a. May give a similar x-ray appearance as a unicameral cyst b. May be painful c. A synovial cell lining is seen in the excised tissue (which is not seen in the curettings from a simple bone cyst) 3. Aneurysmal Bone Cyst: a. These are arteriovenous malformations grafted onto some other lesion, such as a chondroblastoma, chondromyxoid fibroma, giant cell tumor of bone, osteoblastoma, fibrous dysplasia and hemangioma of bone b. The cyst is filled with unclotted blood c. Curettage and packing yields a high recurrence rate d. Cryosurgery can be more successful if bleeding is stopped first, so that there are no warm areas where tissue can survive the treatment e. Irradiation is the last resort f. For long bones en-bloc resection followed by packing with bone chips may be warranted

g. Radiographic examination supplimented by MRI can aid in the diagnosis h. These cysts lack a sclerotic wall, and may demonstrate flecks of bone formation as well as septae i. These cysts show irregular borders and may cause bulging of the overlying cortex j. Sometimes a Codman's triangle is present k. It is a very rapidly growing lesion, hence, it shoes a "quick tempo phenomenon"

Other Tumors and Cancers 1. Ewing's Sarcoma: a. Is a very malignant, small-cell bone tumor whose histogenesis is unclear b. It is rare in the black population c. It is the fourth most common malignant bone tumor, and is seen most frequently under the age of 20 years d. Symptoms and signs are nonspecific, and pathologic fractures may occur e. On x-rays, nonspecific "onionskin" changes and lytic lesions may be present, and affected areas may be swollen, painful, and tender f. Primary treatment is amputation since irradiation may result in changes causing pain and impaired function g. The foot can (uncommonly) be the primary site, so that consultations are necessary to determine (and watch for) lesions elsewhere h. Chemotherapy is also used in treatment 2. Leukemias and Lymphomas: a. Rarely arise as primary intraosseous foot lesions but may appear there as secondary lesions b. Bones may show rarefactions and cortical thinning c. Affected bones may be painful and tender, and pathologic fractures may occur d. The patient may be anemic, debilitated and otherwise quite ill e. Lymph nodes and spleen may be enlarged f. The CBC, differential, bone marrow smear, biopsy and lymph node biopsy may establish the diagnosis 3. Plasma Cell Dyscrasias (multiple myeloma): a. This can manifest itself in the feet b. Multiple myeloma is the most common primary malignant bone tumor c. Most cases occur in males 40-70 years old d. Bone pain (worse on weightbearing) and tenderness are present e. Lytic "punched out" bone lesions may be seen in earlier stages, the lytic lesions being more diffuse later f. Pathological fractures may occur g. Serum protein electrophoresis reveals a monoclonal gammopathy h. Urine shows Bence-Jones protein i. Amyloid is produced and carpel tunnel syndrome may develop j. There is a progressive anemia, erythrocyte aggregation (Rouleaux formation), cryoglobulinemia, hypercalcemia, reversal of the A/G ratio, M

proteinemia (light chains) and an elevated erythrocyte sedimentation rate k. Skin manifestations may include plane normolipemic xanthoma and necrobiotic xanthogranuloma, the latter (when it does occur) often precedes the onset of the disease 4. Metastatic Cancers: a. Metastatic cancers from visceral organs may occur in the bones of the feet b. They may be osteolytic or osteogenic c. These are rapidly developing lesions that may cause pain and pathologic fractures d. There are no specific signs or symptoms, but a history of treatment for a malignant tumor (even years earlier) may provide a clue

NOTE* Of course, even with such a history, a suspect lesion may not be a metastasis, it may be an independent and entirely coincidental lesion

Bone Tumors: A Quick Reference Chart 1. Most Common Malignant Primary Bone Tumors: #1 multiple myeloma #2 osteogenic sarcoma #3 chondrosarcoma #4 Ewing's sarcoma NOTE* The most common bone tumor is metastatic tumors from other sites, but this group does not constitute primary malignancy in bone II. Most Common Benign Primary Bone Tumor: #1 osteochondroma (bone spur, subungual exostosis, and other variants) III. "Onionskin" Periosteal Reactivity Can Be Seen In: #1 osteomyelitis (especially Garre sclerosing type #2 eosinophilic granuloma #3 Ewing's sarcoma #4, lymphoma of bone IV. Codman's Triangle Is Seen In Some Cases Of: #1 osteogenic sarcoma #2 chondrosarcoma #3 Ewing's sarcoma #4 "Paget's" sarcoma #5 unicameral bone cysts #6 giant cell tumor of bone V. "Sunburst" Periosteal Reaction Can Be Seen In: #1 osteomyelitis

#2 Ewing's sarcoma #3 hemangioma of bone VI. "Paget's" sarcomas that arise in bone In the setting of Paget's disease of bone: #1 osteogenic sarcoma #2 chondrosarcoma #3 fibrosarcoma #4 malignant fibrous histiocytoma

NOTE* They may also arise in bone independent of Paget's disease of bone

VII. "Tempo Phenomenon" Is Associated With: #1 aneurysmal bone cyst: (rapid growth=quick tempo phenomenon) #2 eosinophilic (Langerhans cell) granuloma: (interosseous lesions may appear and disappear without treatment=tempo phenomenon) NOTE* Carcinoma vs. sarcoma A carcinoma is a malignant tumor demonstrating a sheet-like cellular arrangement, usually arising from epidermis and from visceral organs. A sarcoma is a malignant tumor arising from supportive tissues of the body, such as muscle, bone, cartilage, tendon, synovium, fat, endothelium, schwann cells, histiocytes, fibroblasts, blood cells, and other immuno cells

Phases in Cancer Development 1. Definitions: a. Preneoplastic: A long phase with no known identifiable cellular features to predict malignant transformation b. Incipient: May be a long phase. A proliferative process is seen that has to be judged as to whether it is benign or malignant, by histology and biological behavior. In some cases it is not clear, and the lesion must be watched. It is in this context that dysplasias are viewed with suspicion and followup (many carcinomas do not show such a phase) c. In-situ: A short phase, in which the malignant process has not passed through the basement zone of its tissue of origin to another tissue (carcinomas show this phase, sarcomas do no )t d. Local invasion: A short phase, in which malignant cells have passed to an adjacent tissue through the basement zone bordering the tissue of origin, while attached to the tumor source. At this time it is considered locally infiltrative e. Extention: A short phase during which the malignant tumor has largely replaced local tissues by infiltrating broadly in all directions, but remains contiguous with the original tumor mass f. Metastasis: A short phase, in which sites of malignant tumor (of the original type) appear in other parts of the body, but they are not contiguous with the original tumor site. Metastases may take many routes and appear in any one

or more sites Benign vs. Malignant Tumors 1. General Characteristics of Benign and Malignant Tumors: Benign Tumor Uniformity of cell nuclei Architectural nuclear and cellular order Restraint in growth Usually not recurrent Does not metastasize Very difficult to culture cells cells (3) Does not develop resistance to antineoplastics May kill patient if impinging on vital structures

Malignant Tumor Atypical Cell nuclei (1) Architectural disorder (loss of polarity) Growth often rapid (poorly restrained growth) Frequently recurrent Frequently metastasizes (2) Relatively easy to culture Resistance can develop to antineoplastics May kill the patient for many reasons (4)

KEY 1. Pleomorphism, hyperchromasia, abnormal mitoses, abnormal number of mitoses, multinucleation, bizarre forms 2. The single most definitive determinant of malignancy 3. Cells develop 'immortality' in culture, and may show changes in cytogenic patterns, medication resistance, cell morphology and behavior, and subclones may emerge 4. Impingement on vital structures, size, metastasis to multiple sites, bleeding, immunosuppression, unusual secretions that induce or inhibit other functions of nontumor cells, necrotic changes, other metabolic changes

Chapter 13: Dermatology The Skin Dermatological Lesions

DERMATOLOGY The Skin The skin is one of the largest organs of the body exhibiting a wide range of functions which include: mechanical protection, formation of a barrier to water transfer, immune responses, thermoregulation, perception of the environment, excretion, limitation of harmful radiation, and nutrition. The skin is composed of two layers the epidermis and the dermis. 1. Epidermis: a. This is composed of a stratified squamous epithelium containing cells that become specialized for the production of keratin. b. There are five strata in the thickness of the epidermis i. Stratum basale ii. Stratum spinosum iii. Stratum granulosum iv. Stratum lucidum v. Stratum corneum c. Specialized cells of the epidermis and their role: i. Melanocytes are specialized cells for the production of melanin pigment and are located in the basal cell layer. Melanin offers protection to UV-B radiation. There are two forms of melanin in the human skin: Eumelanin (brown or black) and Pheomelanin (red and yellow). ii. Langerhans cells residing in the epidermis play an important role in skin immunity. iii. Merkel cells demonstrate dense core neurosecretory granules and are thought to be part of the cutaneous sensory system. 2. The Dermas: a. The dermis is composed primarily of connective tissue and consists of two layers: a papillary layer and reticular layer i. The papillary layer lies between epidermal rete ridges and contains many nerve endings and capillaries ii. The reticular dermis lies below the papillary dermis and above the subcutaneous fat. It contains arterioles, venules, capillaries, larger nerves, and adnexal structures 3. Skin Adnexal Structures: a. Pilosebaceous structures: (hair, sebaceous glands, arrector pill muscle) are present on the dorsal aspect of the foot and toes. Hereditary factors and various acquired conditions contribute to the amounts b. Sweat glands: Are present throughout the foot. These are eccrine types c. Nails: Are present on the dorsal-distal aspects of all toes 4. Special Structures: a. Vater-Pacini Corpuscles: In the deep dermis are sensors for pressure b. Glomus bodies: In the toe tips function in blood shunting as an aid to temperature regulation. The shunt is a narrow branch of the arterioles that connect directly to a venule, bypassing capillaries. This shunt is the SuquetHoyer canal

Dermatological lesions 1. Primary lesions: a. Macules: Circumscribed flat lesions measuring up to 1 cm. in diameter b. Patch: Flat lesions measuring more than 1 cm. in diameter. They may form as a consequence of coalescence of macules c. Papules: Circumscribed, solid elevations measuring up to 1 cm. in diameter, and elevated due to an intradermal infiltrate d. Plaque: A circumscribed, solid elevation exceeding 1 cm. in diameter, but usually not over 2 cm. in diameter e. Nodules: Circumscribed, solid elevations exceeding 2 cm in diameter, but not usually exceeding 3 cm. in diameter f. Tumors: Circumscribed, solid elevations of larger size than nodules NOTE* The definitions may be somewhat artificial because of colloquial usage such as "tumor nodules", and some informal overlap occurs in the use of the terms "nodule" and "tumor".

g. Vesicles: Fluid-filled, elevated lesions, under 1 cm. in diameter (small blisters) h. Bullae: Fluid-filled, elevated lesions, exceeding 1 cm. in diameter (large blisters) i. Cysts: Non-infected, deep-set collection of material surrounded by a histologically definable wall (sebaceous cyst, mucous cyst, epidermal inclusion cyst, etc.) j. Burrow: An intraepidermal tunnel usually caused by insects (scabies, tunga penetrans/chigoe) 2. Secondary lesions: a. Scales: Products of imperfect and frequently rapid epidermal turnover, occurring in "papulosquamous" diseases, with a great deal of exfoliation. Examples include psoriasis, lichen planus, dermatophytosis b. Excoriations: Scratch marks, usually seen where there is pruritus. These show epidermal discontinuities. c. Erosions: These are deep excoriations in the epidermis, but the dermis is not breached. These leave no scars upon healing d. Ulcers: Deep epidermal defects in which the dermis or deeper tissues are exposed. These may leave scars when healed e. Crusts: These are "scabs", i.e. aggregations of dried serum or blood with other cellular debris f. Fissures: Linear, deep epidermal cracks in the skin, penetrating to the dermis and common in areas of dry skin g. Scar: Also called "cicatrix", and resulting from inflammatory or traumatic destruction of subepidermal connective tissue. Scarring is a normal reaction, and that final portion of dermal healing called " fibrosis" i. Hypertrophic scarring represents an abnormal response that will eventually

reduce itself ii. Keloids represent abnormal scarring responses that continue beyond the borders of the inciting injury, and progress to cause contractures andinterference with function. They also may cause cosmetic problems, and can be quite deforming. Treatment is a major problem. Before any elective surgery is undertaken, a careful history and examination should elicit the risk of keloid formation h. Pustule: An elevated, circumscribed lesion containing pus, and arising from infections of papules, vesicles or bullae. i. Abcess: is a deep circumscribed collection of pus ii. Furuncle (Boil): is an abcess originating in a hair follicle iii. Carbuncle: an abcess involving several adjacent hair follicles, with interconnecting sinuses NOTE* Sinus tracts connect cavities, abcesses, etc. under the skin; fistulas connect abcesses to the body surface

3. Vesiculobullous Disorders: a. Viral: Herpes simplex, herpes zoster (shingles), Kaposi's varicelliform eruption, varicella (chicken pox), variola (small pox), molluscum contagiosum, hand-foot mouth disease (coxsackie Al 6 virus) NOTE* Tzanck smear of fluid from vesicles or bullae for identification of multinecleated giant cells or other viral cytopathic effects b. Fungal: T. mentogrophytes, T. rubrum, T versicolor (etiological agent is Malassezia furfur), other fungi and yeasts c. Other: i. Benign familial pemphigus (Hailey-Hailey disease), pemphigus vulgaris and its variants (autioimmunity to intercellular epidermal glycoproteins), bullous pemphigoid (eosinophils in bullae), dematitis herpetiformis (neutrophils in bullae) often present with gluten enteropathy, Darier's keratosis follicularis, bullous impetigo NOTE* Nikolski Sign is present in pemphigus and in bullous impetigo. It consists of pressing an existing bulla vertically with the finger tip and seeing an adjacent bulla form as the fluid is gently forced peripherally to cleave the epidermis ii. Epidermolysis bullosa (all 16 types) represents a defect in skin development such that trauma results in blisters, some forms being fatal. The feet are affected by many types, such as the Weber-Cockayne and EB dystrophica dominant types 4. Dermatitis (Eczema):

a. Contact dermatitis: i. Primary irritant: acids caustic chemicals, etc. ii. Allergic: poison ivy, poison oak, shoe ingredients, sock dyes, etc. b. Atopic dermatitis: Affected individuals show atopy, asthma, hayfever, and other forms of allergic rhinitis, blood serum with >IgE. Three stages, infantile (2 months-2 yrs), childhood (4-10), and adult (12-25). It is usually symmetrical, and is diagnosed by the area of involvement, and the familial history of allergy not the rash itself (biopsy non-specific) c. Dermatophytid (ID) reaction: Allergic reaction incited by a fungal infection. There are other ID reactions as well, in other dermatoses d. Dyshidrosis: Pompholyx of palms and soles (difficult to treat) 5. Papulosquamous diseases: Represent a category of dermatitis that produces an inflammatory papule and scaling. This goup includes a. Psoriasis: Chronic disease characterized by epidermal hyperplasia and a greatly accelerated turnover rate of cells. Discrete papules may coalesce to form erythematous plaques. The lesions are covered by "micaceous" silver scales. Seen on the elbows and knees most frequently, lesions tend to favor extensor surfaces. The Koebner phenomenon is the occurrence of a lesion at an area of trauma, and also occurs in other skin diseases b. Pustular psoriasis: Sterile pustules on the soles. Very difficult to treat. Nails may be pitted c. Lichen Planus: Inflammatory and pruritic disease of the skin and mucous membranes. The lesions appear violaceous and may show a network of white lines (Wickham's striae). Oral lesions have white lace appearance. Nail changes may include pterygium. Lesions tend to favor the flexor surfaces. Bullous lichen planus on the soles of the feet may become squamous Ca. d. Pityriasis Rosea: Pruritic macules and papules, oval shaped, lesions appear with distinctive 'collarette' of scaling on a pink base. Onset of herald patch, a solitary lesion on the buttock or trunk that precedes the others and that follows the skin lines. The disease is self limiting e. Secondary Syphilis: Oval pink macules (non-pruritic) occur on the palms and soles, associated lymphadenopathy, malaise, sore throat and low grade fever. (+VDRL). Hyperkeratotic pitted papules may occur on the palms and soles f. Pityriasis Rubra Pilaris: Type I shows small follicular papules, distinct location dorsal portion of digits, 'nutmeg grater' appearance; lesions coalesce to form plaques. Palmoplantar hyperkeratoses arise. Most patients are clear of lesions within 3 years. There are 4 other disease subtypes. 6. Painful tumors of the skin (ANGEL): Pain frequently occurs but not in all cases a. Angiolipoma: Vascularized tumors of adipose tissue b. Neurilemoma: A benign tumor of Schwann cells (Schwannoma) c. Glomus tumor: Arises from glomus body in the nail bed d. Eccrine spiradenoma: An eccrine sweat duct tumor, paroxysmal spasms of pain e. Leiomyoma: A smooth muscle tumor (arrector pili muscle and vascular smooth muscle pilar leiomyoma and angioleiomyoma, the latter also called

vascular leiomyoma) 7. Non-malignant pigmented lesions: a. Epidermal melanocytes: Nevus spilus (present at birth), solar lentigo, and ephilides (freckles) b. Dermal melanocytic lesions: Blue nevus, junctional nevus (can become malignant melanoma), compound nevus, halo nevus (Sutton's nevus, leukoderma acquisitum centrifugum) and Spitz's nevus (benign juvenile melanoma, spindle and epitheloid cell nevus). About half the cases occur in adults 8. Pre-malignant lesions: a. Actinic keratoses: Solar keratoses, pre-malignant, can become squamous cell Ca, usually scaly and telangiectatic and confined to the epidermis. TX: 5 FU, surgical excision b. Xeroderma pigmentosum: Genetic disease with sensitivity to sun, basal/squamous carcinomas can develop, as well as melanomas c. Bloom's syndrome: Genetic defect involving skin with sun sensitivity, growth retardation and sometimes immunodeficiencies. A high risk for leukemia and lymphoma, as well as GI carcinomas d. Ataxia telangiectasia: Genetic defect involving skin and nervous system. Numerous ectasias appear, many affecting the lower extremities. Sinopulmonary infections are common. High risk of leukemia and lymphoma e. Porokeratosis of Mibelli: Papular lesion with central keratosis that expands to form a circinate lesion with a furrow containing keratin. Some may precede development of squamous carcinoma. Some are hereditary. 9. Malignant Lesions: a. Basal Cell Carcinoma: i. There are 5 clinical subtypes, the most common of which is the noduloulcerative or "rodent ulcer" type ii. These are essentially nonmetastastic (with the exception of a few situations) iii. The Basal Cell Nevus Syndrome (Nevoid Basal Cell Epithelioma Syndrome/Gorlin's Syndrome) demonstrates many abnormalities including "ham-colored pits" on the palms and soles that are basal cell carcinomas. In this syndrome, basal cell carcinomas are aggressive iv. Bazex Syndrome demonstrates hyperkeratoses of the palms and soles preceding and associated with visceral carcinomas (acrokeratosis neoplastica) and basal cell carcinomas resembling tricoepitheliomas v. Basal cell carcinomas also occur in the Linear Unilateral Basal Cell Nevus vi. In general lesions should be excised in toto, in full depth and with a border about 3 mm of clinically normal skin vii. Contributors to the development of basal cell carcinoma include old wounds, burns, ultraviolet irradiation, and x-irradiation b. Squamous cell carcinoma: i. The in-situ form is Bowen's disease which has not invaded the dermis, and which is confined to the epidermis ii. Marjolin's ulcer is a squamous cell carcinoma arising in a scar or in the

epithelium at the edge of a chronic ulceration iii. Bowen's disease may appear as a reddish, irregular, sharply bordered lesion with crusting or scaling. It may be present for many years. Invasive lesions may be solid, ulcerated, or verrucous (verrucous carcinoma, epithelioma cuniculatum). Some are more aggressive than others. Metastases may develop. Lesions should be excised in full depth and with a clinically normal boarder of 3-5 mm. Contributors to the development of squamous cell carcinoma include old wounds, burns, chronic ulcers or fistulas, x-irradiation, ultraviolet irradiation, certain arsenical and other organic compounds iv. Lesions that resemble squamous cell carcinoma: • Keratoacanthoma: A lesion thought to arise from hair follicles, in some cases it may occur as single or multiple lesions. Single lesions develop quickly, grow and ulcerate. They may be very difficult to differentiate clinically and or histologically from well differentiated squamous cell carcinoma. The central area usually contains a keratinous plug. Treatment is excision in full thickness. Use of retinoids is preferred by some for treatment. Some investigators consider keratoacanthoma to be a very low grade squamous cell carcinoma that is "self healing" if left alone. Some types heal with scarring if left alone • Pseudoepitheliomatous hyperplasia: A thickening of epidermis due to hyperplasia of keratinocytes. It is clinically and histologically benign, and occurs in chronic wounds such as the edges of ulcers or fistulas c. Sweat gland (eccrine) carcinoma: There are many types. These are uncommon, but can be slow-growing and aggressive. Metastases do occur in many cases. Many are asymptomatic small papules or nodules that have been present for many years and suddenly enlarge. Some ulcerate. Suspect lesions should be excised in full depth and with 3-5 mm borders of normal skin d. Sebaceous carcinoma: Extremely rare in the feet, these have no distinct presenting symptoms or signs. Metastasis is a risk. These lesions, if primary in the feet (not metastatic to the foot) will not be found in the plantar tissues which lack pilosebaceous structures. These should be excised in full depth with a 3-5 mm boarder of clinically normal skin e. Merkel cell carcinoma: Also called trabecular carcinoma, these cancers are quite uncommon, but have been reported in the foot. They are very aggressive and metastatic. There is no distinct presentation. These lesions should be excised in full depth and with a 3-5 mm boarder of clinically normal tissue. Also called Primary Neuroendocrine Carcinoma of Skin (PNCS) f. Melanoma: A highly malignant tumor of melanocytes showing strong association with ultraviolet irradiation of high intensity. Lighter skinned persons are more apt to develop melanomas in sun-exposed areas. The types are: i. Lentigo maligna melanoma: Almost never occurs in the foot and is most common on the face. They are the least aggressive (in-situ form=lentigo maligna) ii. Superficial spreading (pagetoid) melanoma: Most common type in all body areas. Moderately aggressive. Histologically can resemble Paget's disease of the breast (hence its name) iii. Nodular melanoma: Arises anywhere in the body. Most aggressive and

malignant iv. Acral melanoma: Occurs on the extremities and is the most common type seen in the feet of black and oriental patients. Aggressive type NOTE* Some consider the nodular type to represent a late phase of all the other types, i.e. the "vertical growth phase" as compared to the earlier "radial growth phase". Also, the true nodular type may represent a very aggressive form with a very short radial growth phase Clark's Classification (according to histologic level of invasion) Level 1: Intraepidermal (including adnexae) to dermoepidermal border Level 2. Intradermal and into the papillary dermis Level 3: Intraepidermal and down to border of papillary and reticular or dermal areas Level 4: Intraepidermal and down into the reticular dermis Level 5: Intraepidermal, through all dermal layers and into subcu. Tissue NOTE* Difficulties with Clark's classification as a method of prognosis is that the skin thickness varies in different areas. Tumors in the papillary dermis may push reticular dermis down, only giving the appearance of penetration so that level may be overestimated. Identification of levels, and therefore interpretation, is subjective. The border between papillary and reticular dermis is not always clear Breslow's Classification (according to the thickness of the melanoma) NOTE* This is determined by direct measurement of numerous tissue sections to obtain a figure. The criteria for measurement are not the same as depth of invasion so that Breslow's and Clark's classifications may not necessarily correspond Survival is in terms of 5 years disease free 1. Under 0.76 mm: Generally excellent survival (virtually 100%) 2. 0.76-1.5 mm: Moderate survival (possible lymph node invasion) 3. Over 1.5 mm: Poor survival and increasingly poor with greater thickness (probable lymph node and perhaps visceral invasion) g. Amelanotic melanoma: Not different from other melanomas except for the lack of visible pigment. Therefore, it is extremely dangerous because it is often misdiagnosed and therefore is deeply invasive and thick by the time of diagnosis, and probably has metastasized to the lymph nodes and viscera h. Subungual melanoma: This must be confirmed with biopsy. The clues to this lesion are i. Pigmented lesion of recent origin with no history of local trauma to cause a hematoma ii. Pigmented lesion that does not move distally as the nail grows iii. Sudden development of melonychia striata (pigmented stripe in the nail) iv. Chronic non-pigmented lesion that does not respond to treatments (based

on clinical impression) within a reasonable period v. Dusky, irregular pigmentation in eponychial tissue (Hutchinson's sign) h. Biopsy: i. Ideally, should be excisional including full depth to the subcutaneous fat ii. Incisional biopsy from one or more edges, including clinically normalappearing skin, and always in full depth iii. Incisional biopsy of nodular portion of lesion (if present) as well as edge(s), in full depth NOTE* For all malignant tumors: 1. Excise as indicated by the type and extent (surgical consultation) 2. Consult with oncologist for, chemotherapy, irradiation (if indicated) 3. Arrange to detect metastases to other areas/organs (consult with diagnostic radiologist, pathologist, and others as needed) 4. Follow-up care by those involved as attending team 10. Miscellaneous conditions: a. Discoid lupus: Exacerbated by sunlight, lesions are erythematous/scaling/telangiectic b. Drug induced SLE: SLE can be induced by hydralazine, procainamide, isoniazid, penicillamine, griseofulvin, phenylbutazone, methyldopa and oral contraceptives c. Dermatomyositis: Adult form may be associated with visceral malignancy d. Scleroderma: i. CREST syndrome represents one type- C (calcinosis cutis), R (Raynaud's), E (esophageal involvement), S (sclerodactyly) and T (telangectasias). May be associated with Sjogren's syndrome ii. Localized scleroderma= morphea iii. Generalized type= progressive systemic sclerosis e. Sarcoid: A chronic granulomatous Inflammatory disease affecting various organ systems with erythema nodosum of the legs (plaques on the extremities) Dx: chest x-ray, Kveim test and other immunologic tests f. Erythema nodosum: Acute inflammatory/immunologic disorder with panniculitis and painful nodules on the anterior shins. It may be associated with infections, drugs, sarcoidosis, ulcerative colitis g. Granuloma annulare: Self-limiting chronic inflammation of dermis with annular papules. The generalized papular form has been associated with diabetes mellitus h. Necrobiosis lipoidica: Very similar histologically to granuloma annulare and frequently associated with diabetes mellitus i. Pigmented purpuric diseases: There are many types that may be of the "palpable purpura" type, or it may be nonpalpable (Shamberg's dermatosis, Majocchi's purpura, Henoch Schonlein purpura) NOTE* Purpuric lesions can also be seen with thrombocytopenia, meningococcemia and gonococcemia

j. Diabetic dermopathy: May include Bullosus Diabeticorum, ulcers, necrobiosis lipoidica, cutaneous reaction to insulin, trophic changes (preulcer) related to circulation, etc. k. Petechial hemorrhages: May be seen in meningococcemia, gonococcemia, platelet deficiencies, leukemias, scurvy, salicylate poisoning, bacterial endocarditis (including subungual splinter hemorrhages), anticoagulant overdosage, other bacterial infections (systemic) etc. 12. Ulcers: The following table lists the more common causes of lower extremity ulcerations

Chapter 14: The Arthropathies Causes of Joint Pain The Arthropathies Lab Testing for the Arthropathies Articular Disorders Affecting the Heel Synovial Fluid Analysis Charcot Foot

THE ARTHROPATHIES Causes of Joint Pain: A Summary 1. Joint disease: the arthropathies 2. Bone disease: fractures, primary or secondary tumors, osteochondritis, osteomyelitis, etc. 3. Soft-tissue lesions: sprains and strains, tenosynovitis, overuse syndrome, direct trauma, bursitis, "soft tissue rheumatism" 4. Arthralgia: defined as joint pain in the absence of objective joint disease, seen with a. The Arthropathies- either preceding the development of local signs or in some conditions in which there may be no local signs. Important examples are polymyalgia rheumatica and temporal arteritis, SLE, and polyarteritis nodosa. b. Infections- particularly viral and rickettsial i. Viral: influenzia (25% cases), glandular fever, psittacosis, yellow fever, sandfly fever ii. Rickettsial: all types of typhus iii. Bacterial: septicemia, subacute bacterial endocarditis, thyphoid salmonella, gonorrhea iv. Spirochaetal infections: secondary syphilis, leptospirosis, relapsing fever v. Protozoan/metazoan: kala-azar and other tropical diseases c. Drugs- immunizations, serum sickness d. Protein abnormalities- e.g. mixed IgG IgM cryoglobulinemia 5. Referred pain: particularly common in the knee due to hip and prostate disease and in the shoulder due to some abdominal conditions, esophageal conditions, cardiac conditions, neurologic conditions neurological conditions and pulmonary conditions 6. Psychogenic: Joint pain may be a manifestation of psychological disturbance and "rheumatism" may become a source of complaint in the anxious or neurotic patients

The Arthropathies 1. Anklosing Spondylitis (Marie Strumpell Disease): a chronic condition of the spine (bamboo spine) and sacro-iliac joints in which early inflammatory changes are followed by progressive restriction of spinal movement, with radiological calcification of spinal ligaments (seronegative disorder). a. Signs: chest expansion reduced (< 5cm), limited spinal movements, tender bony points (heel) b. Symptoms: gradual onset of low backache and/or pain in buttocks c. X-ray: shows bamboo spine, and "whiskering" of ischial tuberosities d. Labs: ESR >, mild anemia, (-) latex fixation, synovial fluid shows inflammatory/neutrophils e. Tx: Exercises, NSAIDS

2. Arthrogryphosis Multiplex Congenita: a rare congenital disorder characterized by stiff, deformed joints and muscle wasting. a. Clinical features: painless deformities (equinovarus feet, flexion deformities of knees), stiff joints b. Tx: correction of deformities, surgical and nonsurgical 3. Avascular necrosis: a group of conditions in which bone infarction is not associated with sepsis but is usually due to interference with blood supply, either by abnormalities of the vessel wall such as arteritis, pressure on the vessels from outside, trauma, thrombosis, or embolism. Clinical disease results only when the surface of the joint is involved causing arthritis. The condition may be: a. Traumatic: following fractures b. Secondary to existing arthropathies: RA, severe OA, psoriatic arthropathy, neuropathic joint c. Secondary to systemic conditions: sickle cell disease (particularly sicklecell thalassemia and sickle-cell-hemoglobin C disease), high dose steroid therapy, pregnancy, extensive burns endocarditis, Caisson disease, and scleroderma d. Idiopathic: avascular necrosis may occur in middle aged men and is the cause of Perthes' disease in children e. Types: Legg- Calve'- Perthe's disease (femoral capital epiphyses), Blount's disease (proximal tibial epiphysis), Osgood Schlatter's disease (tibial tuberosity), Sever's disease (calcaneal apophysis), Freiberg's disease (2nd metatarsal head), Diaz/ Mauchet (talus), Islen's disease (base of 5th metatarsal), Thieman's disease (phalanges), Kohler's disease (navicular and patella), Treve's disease (medial sesamoid), Buchman's disease (medial cuneiform) f. X-rays: small areas of infarction which appear sclerotic or porotic, areas of joint surface collapse into underlying infarction producing flattening, necrotic osteochondral fragments may separate completely or partially g. Tx: immobilation, physical therapy, surgery 4. Drug Induced SLE (the Hydralazine Syndrome): a condition resembling SLE but induced by procainamide, hydralazine, isoniazid, oral contraceptives, penicillin, sulfonamides, tetracycline, griseofulvin, phenylbutazone, reserpine and methyldopa. It is suggested that patients with this condition have a heredity "lupus diathesis" which is made manifest only when the drug is given. Arthritis occurs in 50% of the cases and can occur synchronously or up to 4 weeks prior to the skin rash. a. X-rays: normal b. Labs: L.E. cells (90%), A.N.A. (100%) c. Tx: stop the drug, steroids for symptoms prn 5. Erthema Nodosum: an acute self-limiting condition characterized by the development of crops of tender nodules in the skin of the lower leg and arthritis occurring in 50% of the cases occurring with the nodules or preceding them by up to 4 weeks. The nodules are first bright red, later dark red, and then fade

like bruises. This condition occurs in sarcoidosis (common in Great Britain), various infections (particularly strep, measles, etc.), ulcerative colitis, malignant diseases, and drug sensitivities. a. Joints affected: knees and ankles most commonly b. Symptoms: sudden onset of pain without swelling c. Signs: variable (none to red swollen joints), fever common d. X-rays: normal e. Labs: >ESR, LA Fix occasionally (+), must do complete work up to find cause f. Tx: rest, MAIDS 6. Gaucher's Disease: a rare condition transmitted as an autosomal recessive trait characterized by the abnormal accumulation of glucocerebrosides in reticulo-endothelial cells. The characteristic feature is the Gaucher cell, a lipid filled macrophage that contributes to the arthritis and eventually avascular necrosis. Severity is variable and can occur at any age. a. Joints affected: hips are most common, 70% unilateral b. Symptoms: pain and stiffness c. Signs: hip held in flexion and adduction with limb shortening d. Course: untreated hip involvement will progress to complete destruction of the joint with secondary OA e. X-ray: areas of porosis/sclerosis, aseptic necrosis, Ehrlenmeyer flask appearance of lower end of femur f. Labs: anemia, sometimes leukopenia and thrombocytopenia, bone biopsy shows Gaucher cells (lipid-filled "bubbly' macrophages) g. Tx: rest, immobilization with no weight- bearing in early cases, surgery in advanced cases 7. Gonococcal arthritis: arthritis due to gonococcal infection of the joints, beginning 3-17 days after being infected. a. Joints affected: knee is the most common area, ankles(40%), asymetrical, polyarticular (75%), "Gonorrheal heel" b. Symptoms: sudden onset of severe pain and swelling, fever, rigors c. Signs: Warmth, erythema, tenderness, edema of joint and periarticular soft tissues d. Course: effective treatment produces complete cure in 1-4 weeks e. Associations: skin lesions (50% cases) maculopapular, hemorrhagic f. X-ray: normal in the acute stage g. Labs: mild leukocytosis, >ESR, gonococcal antibodies detectable (90%), organism may be recovered from the blood and genital tract h. Tx: Penicillin (procaine penicillin 1-2 megaunits + benzylpenicillin 1 megaunit daily for 5 days) or tetracycline 250mg. q.d.s. for 7 days. VDRL should be done before treatment, since antibiotics may mask early signs of concurrent Syphilis. 8. Gout: a disorder of purine metabolism, characterized by hyperuricemia and the deposition of urate crystals in joints, resulting in acute attacks of arthritis. In the later stage there is deposition of urate in the soft tissues and the kidney, with a chronic arthritis.

a. Joints affected: 1st m.p.joint (75%), monoarticular (90%) b. Symptoms: prodromal irritability with sudden onset of pain often 3-6 am, precipitated by surgery, trauma, starvation, alcoholic excess, and drugs (ASA, thiazides), usually males>females c. Signs: red/hot/swollen/tender joint, between attacks the joints are normal until tophaceous stage, must differentiate from septic arthritis d. Variants: Secondary gout (5%) cases due to myeloproliferative disorders (polycythemia rubra/vera) and during the treatment of malignant disease. Other variants are renal failure, Lesch-Nyhan syndrome and glycogen storage disease (von Gierke's disease) e. X-ray: normal in early stages, with the joint space preserved until late in the disease, periarticular swelling and punched out/radiolucent areas in the affected joints f. Labs: synovial fluid and tophaceous deposits contain needle-shaped crystals which are strongly negatively birefringent, uric acid greater than 6mg./100ml, >ESR (uric acid serum levels may not be elevated during acute attack) g. Tx: responds to indocin, phenylbutazone or colchicine (.6 mg./hr until relief or NVD), if no response then ACTH. Later uricosurics or allopurinol (used in tophaceous gout) 9. Hemophilia: a group of disorders of blood coagulation mechanisms due to deficiencies of various factors. The most common form is inherited by males, the females being unaffected carriers. It is inherited as an X-linked recessive trait. Attacks of arthritis are due to hemorrhage into joints and recurrent hemoarthrosis leads to a degenerative arthropathy which is characteristic of hemophilia. a. Joints affected: knee (70%), ankle (20%), monoarticular, asymmetrical b. Symptoms: sudden onset of very severe pain sometime after mild trauma c. Signs: joint is red, warm, swollen and very tender, after repeated attacks there is limited ROM and crepitus, eventually muscle wasting d. Course: complete recovery but later deformities and degenerative changes e. X-ray: normal with early attacks, later small superficial erosions and cysts appear with a loss of joint space and flattening of joint surfaces f. Labs: prolonged PTT time, confirmed by Factor VIII assay, blood stained synovial fluid g. Tx: complete immobilization while in the acute stage, give missing factor (cyroprecipitate or fresh plasma), analgesics, avoid aspiration, gentle physiotherapy 10. Hypothyroidism: deficiency of thyroid hormone may cause a variety of rheumatic manifestations: pain and stiffness in proximal muscles, polyarthritis, monoarthritis associated with osteolytic lesions usually in children, carpal tunnel syndrome, secondary gout, hypercholecterolemia. a. Joints affected: knees, wrists, ankles, usually bilateral and symmetrical b. Labs: confirm by > cholesterol, < thyroxin level, abnormal EKG c. Tx: thyroxin 11. Neuropathic Joint (Charcot): disorganization of a joint and destruction of

joint surfaces associated with diminished pain sensation which is most commonly due to: tabes dorsalis, diabetes mellitus, syringomyelia, CharcotMarie-Tooth disease, meningomyelocele, hemiplegia, and leprosy. a. Joints affected: monoarticular, depends on localization of pain loss b. Symptoms: 50% have acute onset of pain and swelling, pain is absent in the later stages c. Signs: acute stage, red/warm/tender/swollen joint; chronic stage, bony swelling and recurrent effusion/instability/crepitus/grotesque deformities d. Course: acute inflammatory stage lasts for up to 6 months, with subsequent slow progression for years until deformities occur e. X-ray: sclerosis of the bone ends, loss of the joint space, loose bodies, massive osteophytes, periarticular calcification, fractures f. Labs: essentially normal chemistries. Do immunologic tests (antibodies to listed bacterial infections) g. Tx: rest in the acute stage, MAIDS, stabilization with braces and splints, arthrodesis for instability 12. Conditions associated with neuropathic joints: a. Tabes Dorsalis: knee is most common site (70%), with ankle and feet (30%), Argyll Robinson pupil (80%), absent DTR's b. Syringomyelia: 50% have cervical spondylosis on x-ray, loss of pain and temperature in the upper extremities, equinus deformities c. Diabetes Mellitus: 1 % of diabetics and 5% with diabetic neuropathy have a neuropathic joint, foot is most common site (80%), absent ankle jerk, sensory loss 13. Osteoarthritis: a common degenerative condition of a joint surface associated with aging. OA may be primary or secondary to: obesity, unrecognized congenital hip dislocation, any condition causing irregularity of the joint surface including avascular necrosis, repeated trauma, septic or other arthritis. There is a wide spectrum of clinical manifestations: a. Secondary OA one joint definite cause

Primary OA one to six joints no definite cause Heberden's nodes (sometimes)

Primary generalized OA polyarticular Heberden's nodes usually

b. Joints involved: D.I.P. joints of the hands, lumbar spine, 1st M.P.J., P.I.P. or M.C.P. of hands NOTE* Heberden's nodes occur over the distal ipj's, and Bouchar’ s nodes occur over the proximal ipj's (Bouchard's nodes are associated with gastric dilatation) c. Symptoms: pain with or after movement/relieved by rest, worse towards evening, stiffness of affected joints after immobility, but not generalized morning stiffness (post static dyskinesia) d. Signs: bony swelling and tenderness, acute episodes may be accompanied by warmth/erythema/effusion e. Course: chronic with exacerbations, sometimes related to trauma

f. X-ray: degenerative changes with non-uniform loss of joint space/loss of subchondral bone (subchondral sclerosis)/subchondral cysts (do not break through the cortex)/osteophytes/later, irregularity of the joint surface/joint mice g. Labs: ESR normal, synovial fluid: see chart h.Tx: NSAIDS, physiotherapy, surgery if symptoms severe and persistent 14. Osteochondritis Dissecans: a condition characterized by the separation of avascular osteochondral fragments from the surface of the joints. If separation is complete, loose bodies are found within the joint. a. Joints affected: knee is most common (85%), monoarticular (75%), ankle frequently b. Symptoms: pain (mild) worse after exercise c. Signs: often none, effusion occasionally d. Course: acute a isode recovers after a few months with OA following after a few years (50%) e. X-ray: separation of a fragment or fragments of bone from the joint surface, sclerosis of the fragment and the crater from where it comes from, osteoarthritic changes later f. Labs: uneventful g. Tx: immobilization in non-weight bearing cast/ spontaneous healing in younger cases, with surgery for fixation of a fragment or removal of loose bodies 15. Paget's Disease of Bone (osteitis deformans): a disorder of unknown etiology affecting one or more bones particularly the skull, femur, and tibia. The condition is rare before the age of thirty. Approx. 80% of patients with radiological changes also have symptoms, usually bone pain and deformities.Areas of increased density and of decreased density. a. Symptoms: pain indistinguishable from OA, limp b. Course: chronic and slowly progressive leading to OA c. X-ray: 1st change is localized porosis (in skull called osteoporosis circumscripta), bone often expanded and thickened, with fractures of the long bones. Distinct border between normal and abnormal bone d. Labs: >Alk Phos, Ca normal (ALK PHOS reaches extremely high serum levels) e. Tx: analgesics, disodium etidronate (inhibits bone resorption and mineralization) 16. Palindromic Rheumatism: an uncommon condition, probably a variant of RA, characterized by recurrent/acute/self-limiting attacks of arthritis. a. Joints affected: hands, wrists, knees and feet, with each patient having 1-3 prominent sites b. Symptoms: sudden onset of severe pain and stiffness c. Signs: swollen/red/tender joint d. Course: attacks occur at irregular intervals, averaging 20 per year. There may be years of freedom between attacks or hundreds of attacks in one year. Attacks last a few hours/days, seldom more than 1 week, with complete recovery follows the attack

e. X-rays: normal f. Labs: >ESR, latex fix (+) 50% cases g. Tx: indomethacin, phenylbutazone or ASA for acute attacks, gold therapy may produce remission 17. Psoriatic Arthritis: a common skin disease (psoriasis) with associated arthritis in 10% of cases, with the skin manifestation preceeding the arthritis by many years. A seronegative disease. Sometimes joint symptoms precede skin lesions a. Joints affected: polyarticular, with small joints of the hands predominating (70%). There are three patterns (distal type- d.i.p.j.'s and p.i.p.j.'s, seronegative indistinguishable type- joint involvement indistinguishable from RA, deforming type- causes arthritis mutilans) b. Symptoms: pain is seldom prominant except in the deforming type c. Signs: acute stage- red/hot/swollen joint (sausage toe), chronic stageswollen joints d. X-rays: erosions within the joint, sclerosis of the joint margins, proliferation of bone, cysts, ankylosis, destruction of bone ends in the deforming type, mushrooming of the joint surfaces e. Labs: ESR normal except in the acute stage, (+) HLA-B27 (in many cases), latex fix (-) f. Associations: pitting of the nails (90%), hyperuricemia (30%) g.Tx: analgesic and NSAIDS, avoid systemic steroids, avoid antimalarials cause exfoliative dermatitis) 18. Pyrophosphate Arthropathy: a condition caused by the deposition of crystals of calcium pyrophosphate dihydrate (CPPD) into joints. This condition does not resemble gout and should not be called pseudogout. The term chondrocalcinosis articularis should be reserved for the radiological appearance of cartilage calcification. There are three clinical patterns of the disease: recurrent acute arthritis, chronic degenerative arthritis (resembles RA), and chronic arthritis with acute episodes. Typical onset is age 60. a. Joints affected: knee is most common site, can affect ankles/toes/fingers, usually monoarticular and symmetrical b. Symptoms: pain and stiffness, sudden onset c. Signs: acute red/ hot/ swollen joint d. Course: attacks last weeks/months e. Associations: diabetes mellitus present in up to 50% cases, hypercalcemia, hemochomatosis f. X-ray: affected joints eventually show calcification of cartilage and degenerative changes Labs: synovial fluid changes (see synovial fluid chart), >ESR, leukocytosis, crystals seen microscopically in fluid and biopsy-crystals polarize g. Tx: injection of joints with hydrocortisone, indomethacin 19. Reiter's Disease: a triad of arthritis/conjunctivitis/urethritis which usually follows non-specific (non-gonococcal) urethritis, occurs in males (20-1). A dermatitis may also be present. A seronegative disease.

a. Joints affected: knee (90%) and ankle (75%) most common, feet (40%), polyarticular/asymetrical b. Symptoms: acute onset of joint pain and swelling, dysuria, and penile discharge c. Signs: red/hot/swollen joints in the acute stage d. Course: 1st attack resolves within 6 months, rarely becomes chronic, 50% relapse, 20% have continued relapsing/chronic arthritis e. Associations: urethritis, conjunctivitis, circinate balanitis, keratoderma blenorrhagica, tenosynovitis (usually achilles), plantar fasciits, heel pain, back pain f. X-ray: periarticular osteoporosis with erosions, fluffy periosteal new bone formation (calcaneal spur) g. Labs: >ESR, (-) latex fixation, (+) HLA-B27 (in many cases), joint fluid is inflammatory, gonococcus found in GU tract in some cases. Other bacterial infections may be present. Reiters disease is also seen in AIDS h. Tx: rest, analgesics, MAIDS, antibiotics (if indicated) 20. Rheumatoid Arthritis: a chronic and widespread chronic deforming polyarthritis characterized by bilateral/symmetrical joint involvement, erosions on x-ray, positive latex fixation tests, and pathologically a chronic proliferative synovitis with villous hypertrophy, infiltration of lymphocytes and plasma cells, and lymphoid nodules. Occurs in 6% females and 2% males world-wide. An autoimmune disease a. Diagnostic criteria: • morning stiffness • pain on motion or tenderness in 1 joint • swelling in 1 joint, swelling in another joint • symmetrical joint swelling • subcutaneous nodules • x-ray changes typical of RA • poor mucin ppt. from synovial fluid • characteristic histologic changes in the synovial membrane • positive Rheumatoid factor • characteristic histologic changes showing palisading granulomas Definite rheumatoid arthritis= 5 of the above Probable rheumatoid arthritis= 3 of the above b. Joints affected: small joints of the hands and feet (75%) especially the m.p.j.'s, and the p.i.p.j's, usually bilateral and symmetrical. Also calcaneus affecting the posterior-superior surface near the achilles insertion (forms a posterior calcaneal recess) with non-well demarcated heel spur. Larger, proximal joints are frequently involved. c. Symptoms: insidious onset of joint pains and stiffness, generalized morning stiffness, accompanied by general ill health, fatigue and weight loss which can precede joint symptoms by a few months. d. Signs: swollen/tender joints with limited ROM due to effusion or synovial thickening, muscle wasting around the affected joints

e. Special features: ulnar deviation hands, boutonniere deformity of p.i.p.j., baker's cyst of knees, atlanto-axial subluxation of cervical spine, cricoarytenoid joint involvement causeshoarseness/dyspnea/dysphasia/bronchitis f. Course: either episodic or persistent, episodic has average patient having 3 attacks of arthritis once every 2 years each lasting 6 months; persistent has chronic arthritis with partial remissions and exacerbations, joints tend to become burnt out g. Non-articular manifestations: i. Periarticular soft tissues- nodules (Haygarth's nodes at affected joints), tenosynovitis, bursitis, synovial cysts, muscle wasting, ligamentous laxity ii. Skin- tight like scleroderma, leg ulcers iii. Eyes- Sjogren's syndrome iv. Heart- pericarditis, granulomatous lesions in myocardium v. Nerve- carpal tunnel syndrome/tarsal tunnel syndrome vi. Blood- anemia, Felty's syndrome (splenomegaly/leukopenia) h. X-ray: early changes include periarticular osteoporosis, joint space widening; later changes include uniform joint space narrowing thinning of the cortices synovial erosions, pseudocysts that erode through the cortex (OA cysts have a sclerotic boarder), subluxations and deviations joint fusions and widespread osteoporosis i. Labs: anemia, >ESR, latex fixation (+) 80%, ANA (+), RA (+), synovial fluid changes (see chart), blood protein (plasma fibrinogen and globin increased; decreased total protein) j. Tx: NSAIDS, rest modalities, intraarticular steroid injections, synovectomy, gold injections (Myocrisin) @ 10, 20, 30, 40 mg I.M. at weekly intervals then 50 mg. weekly up to 1 g., then a maintenance dose of 50 mg. monthly if results good (must check WBC's) 21. Septic Arthritis: Infection of a joint with pyogenic bacteria. Most common organism is Staph aureus (50%). Can occur in any age group but more frequent in kids and geriatrics (should be considered when examining any monarticular erythematous, hot, swollen joint) NOTE* The bacteriology in septic arthritis is most frequently as follows: Neonates: Streptococcus and gram negative organisms Children (6months to 5 yrs): H. influenza common Teenagers: Neisseria gonorrhea have higher incidence Adults: P. aeruginosa common after puncture wound Adults with sickle-cell: Salmonella common Compromised patients (burn victims, drug users): Serratia marcescens pyarthrosis a. Joints affected: knee most common, 90% monarticular b. Symptoms: rapid. onset of pain and swelling, can have elevated temperature, malaise, tachycardia, and confusion c. Signs: swelling with effusion/tenderness/warmth and painful limitation of motion, febrile

d. Course: untreated, leads to joint destruction (OM/ankylosis) e. X-rays: normal initially, osteoporosis after 2 weeks f. Labs: >WBC's, synovial fluid (see chart), blood culture and synovial fluid culture (+) NOTE* The joint aspirate should undergo the following studies: C&S, gram stain, examination for crystals, WBC count and differential

NOTE* The WBC's in joint aspirate in a septic joint is usually higher then 100,000, however, in gonococcal arthritis the WBC's is usually below 50,000 g. Tx: antibiotics, rest, aspirations (?? damage to the joint), open debridement (permits lysing of adhesions and debridement of necrotic bone or soft tissue present, arthrotomy performed in patients with advancing osteomyelitis 22. Sickle-Cell Disease: a condition inherited as an autosomal intermediate, in which hemoglobin A is replaced by hemoglobin S. Heterozygotes are not anemic and do not have arthritis. Homozygotes are severely anemic and have thrombotic crises which commonly cause arthritis as a result of local bone infarcts. Usually seen in blacks with the onset in the first 10 years of life. a. Joints affected: polyarticular, hands and feet common sites, often migratory b. Symptoms: sudden onset of severe joint pains or backache c. Signs: often none, occasionally affected joints are swollen/red/tender, fever common in a crises, painful ankle ulcers d. Course: joint pain subsides spontaneously within days, life span greatly reduced e. X-rays: areas of osteoporosis or sclerosis, periosteal proliferation affecting the shafts of the metatarsals f. Labs: in vitro sickling tests and hemoglobin electrophoresis confirm the diagnosis g. Tx: analgesics, IV bicarbonate may help, urea compounds, pentoxophylline, avoid hypoxia/hypotension/tourniquets 23. Still's Disease (Juvenile Rheumatoid Arthritis): a chronic polyarthritis resembling R.A. clinically and histologically, but beginning before the age of 16 (peak ages, 1-3 & 10-15). a. Joints affected: as with the adult + involvement of the cervical spine/TMJ's/d.i.p.s. (more) b. commonly affected, less symmetry than RA c. Symptoms: pain often mild d. Signs: joints warm/tender/red/swollen with effusion and synovial thickening, fever (50%) e. Course: better prognosis than in adults especially if earlier onset f. X-ray: erosions less common, periosteal reaction may occur in phalanges and mets g. Labs: >ESR, latex fixation (+) in 20% cases

h. Tx: ASA, rest, maintain full ROM, gold or immunosuppressive drugs only in severe progressive cases, short course A.C.T.H. useful for severe relapse 24. Systemic Lupus Erythematosis (S.L.E.): an autoimmune condition characterized by the presence of antinuclear factor and other autoantibodies. The diagnosis is often made on the basis of multi-system involvement. a. Joint pain occurs in 90% cases, and arthritis usually occurs at onset but may precede other systemic features by up to 20 years. b. Joints affected: Commonly seen in the p.i.p.j.'s, also in the wrists, knees, ankles and elbows, is polyarticular with a distribution resembling RA c. Symptoms: sudden onset of pain and stiffness which may be precipitated by exposure to sunlight or stress, morning stiffness (50%) d. Signs: 50% have none, but the characteristic finding is slight soft tissue swelling, fever common e. Course: 70% survive 5 years and 50% 10 years, prognosis is much worse with renal involvement f. Associations: rash of face (butterfly), renal disease, pericarditis, Raynaud's phenomenon, and liver disease g. X-ray: usually normal h. Labs: >ESR, ANA (+) 100%, LE cells present (80%), latex fixation (+) 30% i. Tx: prednisone 30-60 mg/day initially reducing slowly to a maintenance dose of about 15 mg.day NOTE* Some medications precipitate SLE (see earlier chapter) 25. Ulcerative Colitis: a condition in which severe ulcerative inflammation of the colon causes fever, anemia, and the passage of blood/mucus from the bowel. Arthritis is of 4 types, colic arthritis, ankylosing spondylitis, arthritis associated with erythema nodosum, and pseudohypertrophic osteoarthropathy. In ulcerative colitis 10% develop arthritis, in Crohn's disease 4% develop arthritis a. Joints affected: knees and ankles, usually 1-3 joints in each attack, usually asymetrical b. Symptoms: sudden onset of pain/swelling, often associated with relapse of colitis c. Signs: effusion, painful limitation of motion d. Associations: skin lesions (erythema nodosum/pyoderma gangrenosum) e. X-ray: joints normal f. Labs: >ESR, Synovial fluid shows WBC's up to 40,000 g. Tx: NSAIDS and analgesics, appropriate tx for colitis h. Younger patients may go on to develop GI adenocarcinomas after 10 or more years of disease.

Laboratory Testing for the Arthropathies 1. Synovial Fluid analysis: should be approached with caution so as to prevent hemoarthrosis or septic joint. When the joint is punctured an attempt should be made to extract all the fluid present. The analysis of the joint fluid is

of some importance in the diagnosis of certain diseases. (See chart) 2. Serologic tests: a. Erythrocyte Sedimentation Rate: nonspecific, reflects the presence of tissue injury and inflammation, as a screening test may be overrated b. C-reactive protein (CRP): nonspecific test for inflammation, a most sensitive indicator of rheumatic fever c. Rheumatoid factor: are a heterogenous group of antiglobulin antibodies primarily found in patients with rheumatoid arthritis. The antibodies react to specific antigenic determinants on the crystallizable fragment of human IgG. RF has been found among several classes of immunoglobulins, including IgM, IgA, IgG, and IgE d. Latex fixation: are also used to detect RF, with IgG used as the antigen e. Antinuclear antibodies (ANA): are a heterogenous group of antibodies detecting many nuclear constituents; including deoxyribonucleic acid (DNA), deoxynucleoprotein (DNP), histone, and ribonucleicacid (RNA). The ANA antibodies were 1st noted in the sera of patients with SLE. Only a test reactive for double- stranded DNA is diagnostic for SLE f. Histocompatibility antigens (HLA-B27): is associated with the seronegative diseases g. VDRL: screening test for syphilis (but not specific for it) h. ASO titer: done with CRP where Rheumatic fever is suspected i. LE prep: rarely done today because of the accuracy of the ANA 3. CBC and differential 4. Uric Acid: May be normal during acute gouty attacks 5. Test for Lyme disease (Lyme titer) 6. Test for AIDS: ELISA (and If reactive then do a Western Blot)

Articular Disorders Affecting the Heel Systemic inflammatory disorders such as RA, anklosing spondylitis, psoriatic arthritis, Reiter's syndrome, gout, and Behcet's syndrome have all been reported to cause heel pain. Signs and symptoms of these disorders include local soft tissue swelling and occasional erythema associated with diffuse aching type pain. Various symptom complexes highlight certain arthritides (like Reiter's). Radiographic erosive and proliferative bone changes in these patients include posterior and inferior calcaneal spurring, retrocaicaneal swelling, Achilles tendon thickening, and posterior and inferior calcaneal erosions. These changes occur in various combinations and each disease entity has its own usual but not exclusive calcaneal target site.

Calcaneal target sites A: Rheumatoid Arthritis B: Ankylosing spondylosis and psoriasis C: Reiter's syndrome McGlamry ED: Comprehensive Textbook of Foot Surgery, Williams & Wilkins, Baltimore, 1987, with permission

SYNOVIAL FLUID After aspiration note volume, clarity, turbidity, blood-staining, and viscosity. Divide as follows: 2 ml. in a tube containing EDTA for cell count and differential

At least 1 ml. in a sterile container for microscopy and culture. Ask for urgent Gram stain or special culture media if indicated

Remainder: examine a wet film for crystals under polarized light. Note presence or absence of clot formation after standing

RESULTS: The characteristics of synovial fluid depend upon the presence or absence of inflammation of synovium. Non-inflammatory fluid is clear, viscous, fails to clot on standing, and contains less than 1000 cells per c.mm., predominantly mononuclears. Inflammatory fluid is non-viscous, may clot, and contains an increased number of white blood-cells. These changes may be slight or gross, depending on the severity of the inflammatory process. Fluid with a high whitecell count is turbid and this does not necessarily mean that it is septic. The characteristics of inflammatory and non-inflammatory fluid are summarized in the following table. Synovial fluid characteristics in individual arthropathies are shown with other laboratory features of the conditions. NON-INFLAMMATORY E.g., Osteo-arthrosis or Traumatic -Arthritis

INFLAMMATORY Rheumatoid Arthritis,

Septic Arthritis

Gout or Pyrophosphate Arthropathy

Appearance

Clear

Often turbid

Colour

Yellow

Yellow/green Brown/green Yellow

Viscosity

High

Low

Low

Low

Clots ?

No

Yes

Yes

Yes

Approx. W.B.C. (per mm.3)

1,000

30,000

100,000

10,000

Predominant cell

Mononuclears

Neutrophils

Neutrophils

Neutrophils

Crystals

No

No

No

Yes

Culture

Sterile

Sterile

Positive

Sterile

Turbid

Clear with Bakes of fibrin

IDENTIFICATION OF CRYSTALS. Uric acid crystals are needle-shaped and strongly negatively birefringent (blue across the plane of the first-order red compensator); pyrophosphate crystals have square ends and are weakly positively birefringent (blue along the plane of the compensator). SPECIAL TESTS 1. Complement levels are low in rheumatoid arthritis and high in Reiter's disease. 2. Latex tests parallel serum titres in patients with rheumatoid arthritis; there is a high incidence of false positives in other conditions and the test has little diagnostic value.

Charcot Foot 1. Disorders producing a Charcot joint: Diabetes mellitus (most common cause), tabes dorsalis, leprosy, syringomyelia, spina bifida, meningomyelcoele, congenital insensitivity to pain, chronic alcoholism, spinal cord injury and compression (all have decrease in pain sensation in the presence of uninterrupted physical activity in common) 2. Mechanism of destruction: Precipitated by a single injury or by repetitive moderate stress applied to bones and joints. The results are fractures, effusions, and ligamentous laxity followed by erosion of articular cartilage, fragmentation, luxation, distintegration, and finally collapse of the foot. The consequence of trauma is a hyperemic response, which promotes additional resorption of bone and increases the susceptibility to further injury and progressive deterioration NOTE* Eichenholtz divided the disease process into 3 radiographically distinct stages: a. Development: The acute destructive period, which is distinguished by joint effusions, soft tissue edema, subluxation, formation of bone and cartilage debris (detritus), intra-articular fractures, and fragmentation of bone b. Coalescence: Noted by a lessening of edema, absorption of fine debris, and healing of fractures (reparative phase of healing has begun) c. Reconstruction: Further repair and remodeling of bone take place in an attempt to restore stability and homeostasis Neuropathic osteoarthropathy can be arrested during the Development stage if diagnosed before the disease has a chance to mature 3. Pathogenesis: a. Sensory-motor neuropathy: Loss of protective sensation, absent DTR's, diminished vibratory sense, muscle weakness, ankle equinus b. Autonomic neuropathy: Sympathetic denervation loss of vasomotor control, increased peripheral blood flow, increased artiovenous shunting, increased bone blood flow, hyperemia c. Minor trauma: Repetitive moderate stress, repetitive impulse loading, trabecular microfractures, inadequately protected fractures and sprains, surgery d. Other factors: Metabolic abnormalities which weaken bone, renal transplantation, immunosuppressive treatment, steroid-induced osteoporosis, decreased cartilage growth activity, glycosylation of collagen 4. Diagnosis: a. Medical history, clinical manifestation, and radiologic findings b. Technium and Gallium scans, MRI (low signal Intensity in T, and T2weighted images within the bone marrow space adjacent to the involved joint), and bone biopsy and cultures in equivocal cases

5. Treatment: Based on the acuteness of symptoms, the anatomic pattern of bone and joint destruction, the degree of involvement (deformity, fractures instability, etc.) and the presence of infection a. Immobilization: At least 3 months of non-weight-bearing cast immobilization prior to resumption of partial weight-bearing (always check the asymptmatic limb during this time) b. Orthoses and shoes: A patella tendonbearing brace with molded shoes to decrease the load on the foot c. Surgery: Ostectomy, arthrodesis i. Criteria for surgery: Instability, deformity, recurrent ulceration, refractory to conservative treatment, must be quiescent, circulation intact, no active infection, medically stable

Chapter 15: Peripheral Vascular Disease Patient Evaluation The Vascular Diseases

PERIPHERAL VASCULAR DISEASE The podiatric physician should be able to decide whether the patient is at risk for developing complications based on arterial and venous insufficiency to the tissues of the foot. The podiatrist should be able to evaluate whether there is sufficient blood flow entering the foot and leg to sustain its normal nutrition, to heal, and to sustain nutrition following surgery. The lower extremity is predisposed to the development of vascular disease. Some of the causes are: hypertension, hypercoagulability of blood, the natural aging of the blood vessel walls, diet, tobacco use, oral contraceptives, prostaglandins and even gravity. A misdiagnosis of vascular disease may result in significant morbidity.

Patient Evaluation 1. Vascular History: the chief complaint and history of the present illness often preclude the immediate diagnosis of vascular disease. Some clues to follow: a. Attempt to establish time relationships accurately (date of onset, etc.) b. Attempt to separate symptoms that appear to be superficially similar c. Try to identify the exact location of the symptom d. Characterize the symptom as to type and severity e. Delineate factors that aggravate or alleviate symptoms f. Determine the effect of self-treatment or treatment by other physicians g. Determine the progression/rate of symptoms h. Evaluate the amount of disability imposed by the symptoms i. Analyze any associated conditions or complaints j. Document any previous studies and their results NOTE* A study by Hershey et al (1984) revealed that majority of patients with PVD undergoing major vascular reconstruction will have concomitant problems: 60% had an abnormal EKG, 20% had a previous Ml, 7% had CHF, 4% had previous arrhythmia and 7% had a previous CVA. Thus, PVD occurs most frequently in the older population or as part of conditions that compromise vascular integrity (such as diabetes mellitus) 2. Pain: Arterial, venous, and even lymphatic diseases present with manifestations, however, painful extremities are not necessarily a manifestation of a disturbance in peripheral circulation. a. History: Mode of onset, characteristics, progression, location, duration, excerbating and alleviating factors, pain on walking flat surfaces/hills, distance walked b. Ischemic Pain: Severe persistent pain associated with ulcerated or gangrenous ischemic tissue is indicative of a more severe arterial disease. Ischemic complaints in order of frequency are pain, numbness, coldness, tenderness, burning, fullness, and pallor, more severe during excercise and localized in the muscles c. Intermittent Claudication: The classic pain associated with chronic arterial

insufficiency is that of intermittent claudication. This symptom is defined as a transient, exercise induced ischemic myalgia, characterized by aching, cramping, tiredness, or tightness of the affected muscle group. Most often seen in the calf muscles. The extent of claudication is determined by measuring the number of blocks walked, prior to the onset of symptoms (a treadmill can be substituted -set at 120 steps/minute and claudication time measured). Generally with arterial blockage, the lesion occurs one joint or level above the muscle group in which the symptoms manifest. The differential diagnosis of intermittent claudication is- musculoskeletal disorders, venous claudication, shin splints, tendonitis, Morton's neuralgia, vitamin B1 deficiency, metabolic disorders (McCardle's disease), and pseudoclaudication of spinal disease. Intermittent claudication generally is not an indication for reconstructive surgery unless the symptoms are debilitating. d. Rest Pain: As the disease and ischemic changes progress, rest pain develops, usually insidiously.
Rest pain reflects severe ischemia. Rest pain is produced by the body's shunting blood from the periphery to a more central circulation when the person is sleeping. A buildup of metabolites occurs in the muscles, resulting in pain. Usually the patient is awakened every night at the same time, and must get up or dangle the feet to alleviate the pain, sometimes these patients sleep in a recliner to avoid this pain; Note* No podiatric elective surgery should be done in patients with these symptoms. e. Ischemic neuropathy: Ischemia due to chronic/acute arterial occlusion will result in an hypoxic condition of the peripheral nerves. Pain is sharp, shooting, poorly localized, radiating throughout the entire extremity following no distinct nerve root. Pain described as tearing, pulling, or agonizing discomfort.

Areas of occurence of intermittent claudication Clinics in Podiatric Medicine and Surgery: Peripheral Vascular Disease, January 1992, Volume 9:1, Saunders, Philadelphia, with permission

3. Edema: Can be a manifestation of many diseases, so must be carefully evaluated as to whether it is bilateral from systemic disease or unilateral from a regional condition, is the edema pitting (can be graded) or nonpitting, and when/if does the edema disappear. The edema associated with systemic disease is generally pitting and bilateral, involving the entire lower leg/foot/toes

Common causes of Edema in the lower Extremity a. Systemic: CHF, nephritis, nephrosis, hypervolemia, hypoproteinemia, hypothyroid, hyperadrenalism, lymphedema b. Local: lymphangiectasis, lymphatic obstruction (filaria, tumors), pelvic or abdominal masses, varicose veins, venous stasis, thrombophlebitis, popliteal vein obstruction c. Drug induced: corticosteroids, estrogen, progesterone, androgens, phenylbutazone, MAO inhibitors, hydralazine, methyldopa d. Other causes: angioneurotic edema and pretibial myxedema, Milroy's disease 4. History of Emboli: Arterial emboli should be suspected whenever there is a sudden and marked decrease in circulation to an extremity, with sudden cyanosis of the foot or toes; a. The source of arterial embolus is the heart in over 90% cases. b. Conditions associated with emboli are: i. mitral stenosis ii. acute MI iii. bacterial endocarditis iv. prosthetic valves v. aneurysms vi. stroke 5. Color and Temperature Changes: The color of the skin is directly proportional to the degree of perfusion of arterial blood and oxygen saturation of hemoglobin in the subpapillary venous plexus. a. Pallor associated with sudden arterial occlusion, results from the absence of arterial perfusion b. Cyanosis occurs with decreased arterial perfusion of chronic arterial insufficiency c. Red/warm skin of erythromelalgia is the vasodilatory effect of the disease d. Petechiae or pinpoint areas of cutaneous bleeding indicate capillary fragility, which may arise in a number of conditions e. Purpura, bluish/black areas of subcutaneous bleeding is the result of clotting abnormalities or other diseases (see section Dermatology) f. Telangectasias are visible dilations of capillaries which can result from arterial or venous insufficiency g. A drop in skin temperature of 6-8 degrees may indicate ischemia 6. Trophic Changes and Hair Growth: The nutritional changes of the skin and appendages is directly affected by cutaneous circulation. Alterations in arterial- flow can cause thickening, brittleness, longitudinal ridging and slow growth of the nails. This can be confused with onychomycoses. The disappearance of hair on the foot can be indicative of reduced arterial flow. 7. Past Medical History: Ten risk factors have been associated with arteriosclerosis- chronic cigarette smoking, hypertension, diabetes mellitus, hypercholesterolemia, hyperlipidemia, obesity, stress, lack of exercise, age, and genetics. a. Family history: Of any of the above b. Medications/allergies

c. Medical care d. Social factors e. Past medical history: Important to assess the healing ability. Factors that reduce the healing potential are anemia, alcoholism, uncontrolled diabetes, neuropathy, rheumatoid arthritis, SLE, scleroderma, severe pulmonary disease, polycythemia, sickle cell disease, treatment with antineoplastic drugs, radiation therapy, high doses of prednisone, dialysis, and poor nutrition. Note* Adequate blood flow does assure adequate healing potential, but inadequate blood flow will contribute to poor healing 8. Ulcerations: Commonly, ulcerations of the lower extremity may be the first sign of PVD, however, they may occur secondary to hematologic, endocrinic, dermatologic or systemic disease. Vascular ulcerations can be due to ASO, venous stasis, thromboangiitis obliterans, acute arterial occlusion, Raynauds phenomenon, emboli, and systemic hypertension. (See Section Dermatology) 9. Gangrene: Due to impairment in circulation, can be either wet or dry. Remember, pedal gangrene is not a diagnosis, but it is a symptom.

An adequate workup is required to determine the causes a. Drugs- amphetamines, amobarbital, pentobarbital, meperidine HCL, hydroxyzine HCL, sodium thiopental, propoxyphene HCL and ergotamine (oral). When injected IV to the tissues these can produce extensive necrosis. b. Infectious Processes- meningococcic, staphylococcic or streptococcic bacteremia (SBE), cholera, typhus fever, typhoid fever, pneumonia, and trichinosis can produce gangrene of the digits. c. Spontaneous Acute Occlusive Arterial Disorders- arterial embolism (arteriosclerosis), spontaneous arterial thrombosis (thromboangiitis obliterans, CHF, cardiac arrthymias) d. Venous Thrombosis e. Trauma to blood vessels f. Compartment Syndrome g. Exposure to low temperatures- frostbite h. Mechanical, neurotrophic and metabolic factors i. Vasospastic disease j. Connective tissue diseases 10. Palpation of Peripheral Pulses: Peripheral pulses that are evaluated are the radial, femoral, popliteal, posterior tibial, anterior tibial (dorsalis pedis), and peroneal. These pulses should be graded according to rhythm, symmetry, and amplitude. a. Factors that reduce pulse amplitude: CHF, rapid atrial fibrillation, numerous premature contractions, paroxymal tachycardia, aortic stenosis,

shock, and myocarditis. Also included are: coarctation of the aorta, Leriche's syndrome, dissecting aneurysm of the aorta, tumors of the abdominal cavity compressing arteries, and edema overlying the artery. Also included are: Vasospasm (Raynaud's disease, acrocyanosis, livedo reticularis, later stages of frostbite, causalgia, post-traumatic vasomotor disorders, disuse atrophy), chronic occlusive arterial disorders affecting the large arteries, acute occlusion of large arteries, organic occlusion of small arteries, congenital/acquired A-V fistula, Monckeberg's sclerosis, and trauma to large arteries b. Factors that increase pulse amplitude: Hyperthyroidism, hypertension, aortic insufficiency, marked anemia, fever, physical exertion, and erythromelalgia. Also included are: lumbar sympathectomy, early stage of causalgia, Paget's disease of Bone. Also, Quincke's pulse is seen in the toenails in cases of aortic regurgitation, patent ductus arteriosis, very slow heart rate with increased central pressure, extreme increase in venous return and extreme dilatation of the small arteries and arterioles. In cases of coarctation of the aorta, Quincke's capillary pulsations are seen in the fingernails (dueto the increased pressure above the coartation) but not in the toenails (due to the decreased pressure below the coarctation) Note* Please refer to Chapter 33: Anatomy, for description of the complete circulation of the foot, however, some important arterial anatomic facts are presented here: 1. The posterior tibial is the largest of the three pedal arteries and bears major responsibility for perfusing all the plantar intrinsic muscles. 2. The dorsalis pedis is second in importance and is responsible for perfusing the dorsum of the foot. 3. Ten percent of the normal population does not have a dorsalis pedis artery, so the perforating peroneal can take its place. 4. Lack of pedal pulses may suggest anatomic variation rather than PVD, if no other suggestions of vascular insufficiency are present

Palpation of peripheral pulses and corresponding arteriograms (femoral and popliteal)

Palpation of peripheral pulses and corresponding arteriograms (anterior and posterior tibial)

Note* When the PT is absent the DP can function as primary artery of the foot. The entire foot can even be perfused by one pedal artery since they all interconnect (an important concept in vascular reconstruction). Each toe has 4 digital arteries, with the plantar arteries being larger than the dorsal ones. The lateral plantar digital artery of the hallux is larger than the medial plantar digital artery of the hallux. The medial plantar digital artery of the lesser toes is larger than their lateral plantar diqital artery.

Vascular anatomy to foot showing alternate circulation with absent DP artery Clinics in Podiatric Medicine and Surgery: Peripheral Vascular Disease, January 1992, Volume 9:1, Saunders, Philadelphia, with permission

11. Non-Invasive Measurements of Arterial Flow: The most important measurements of arterial inflow are easy to perform and consist of the following a. Ankle/Arm Pressure (Ankle/Brachial Index)- is the measurement obtained by dividing the ankle systolic pressure by the arm systolic pressure. Use a 8MHz Doppler Ankle/Arm Ratio A/A ratio= 0.96 or more A/A ratio= 0.71-0.95 A/A ratio= 0.31-0.70 A/A ratio= 0.00-0.30

Clinical Finding Normal Mild obstruction (intermittent claudication) Moderate obstruction (intermittent claudication/rest pain) Severe obstruction (rest pain/impending gangrene)

NOTE* Falsely elevated ankle pressures are seen with diabetes mellitus. This is due to either ASO or Monckeberg's medial calcific sclerosis. The ABI should not be the sole criteria for vascular assessment in these patients. Note* If there is doubt about whether the ABI is falsely elevated, the modified Carter exercise test can be used to differentiate. Additionally, listen to the sounds of the artery, it should be either bi or triphasic. Any abnormal swishing sound would indicate a proximal obstruction. b. Segmental Pressures- taken at the upper thigh, lower thigh, upper calf, and ankle. The ABI is noted. The criteria for this test are based on the 1-10-20-30 Rule of Thumb. Note* The ABI index if less than 1 may indicate an obstruction. The upper thigh pressure should be greater than 10mmHG greater than the brachial pressure, if less there may be an obstruction. Pressure differences between adjacent cuff sites on the same leg that exceed 20mmHg may indicate obstruction (some sources use a 30 mmHg drop between sites). Pressure differences of 30mmHg over the entire leg may indicate obstruction. c. Doppler Signal- Doppler recordings reflect flow velocity in a specific vessel, the frequency of the emitted beam is altered by any object moving faster than 6 cm/sec. If waveforms are being recorded, the faster the blood can flow, the steeper is the recorded waveform. The qualitative audible Doppler signal, when made into a tracing, shows that the normal arterial pattern is a triphasic picture. A monophasic sound indicates arterial pathology. d. Photoplethysmography- is a modality used to provide an indication of skin blood flow. The emitted beam of the PPG sensor is reflected by hemoglobin molecules located in the cutaneous microcirculation. A photoelectric detector measures this reflected beam and the signal is transformed to be displayed as a recorded waveform looking more like a narrow teepee. This waveform is representative of pulsatile flow in the subpapillary plexus of the skin. This test should be correlated with digital Doppler tests, noting discrepancies in the waveforms. e. Digital Blood Pressure- this is obtained by placing an appropriate-sized cuff around the digit, staying away from the joint. In normal digits without any pathology the pressure is generally between 70-110 mmHg, and have waveforms that look more like teepees than igloos. f. Pulse volume recording (PVR)- pulse volume recording, reflects the volume of blood that pulses under a sensor cuff, obtained by placing cuffs filled to 60 mmHg pressure around the parts to be measured. The PVR closely corresponds to direct intra-arterial recordings at the level being tested. The waveforms look like high teepees with a dicrotic notch. Changes in waveform morphology between segments reflect severe stenosis or occlusions. The waveforms should be analyzed for changes existing between segments and for differences between left and right.

g. Five-Minute Reactive Hyperemia Test- used to aid in the differentiation of vasospastic foot pathology from organic disease. In vasospastic disease, blood flow is limited by increased tone of smooth muscles surrounding the blood vessels; in organic disease by material clogging the lumen of the vessels. This test can also be used to predict the success of a contemplated sympathectomy. 12. Invasive Measurements of Assessing Arterial flow: a. Angiography for PVD is generally performed as a preoperative or screening evaluation of the arterial tree in patients with non-healing ulcers, rest pain, severe claudication, gangrene, and absence of pulses. Non-invasive examinations should precede angiography to select the appropriate candidates since this test is not without its potential complications. The compounds used are either ionic or nonionic, both with high iodide contents for its radiodensity. They cannot be done in anyone who has iodine allergy. History of use of similar compounds (such as an IVP for renal studies) and of thyroid disorders/medications is necessary, with appropriate consultations. Ionic Contrast vs. More painful on injection Use in patients < 60

Nonionic Contrast Less painful Patients > 60 Use with patients with previous contrast reaction, history of asthma, allergy to shellfish, cardiovascular disease, renal failure, a diabetes

Both are toxic and can cause renal failure, hypotension, direct myocardial depression, pulmonary edema, bronchospasm, convulsions and even stroke NOTE* Adequate preparation of the patient is essential with hydration to prevent renal complications. This involves infusing approx. 1000cc sterile fluids within 24 hours of the procedure. Also given is Mannitol (12.5 g) in patients with an elevated creatinine to effect an osmotic diuresis to minimize nephrotoxicity. Oblique and lateral views are taken. b. Digital substraction angiography (DSA) is a method of performing angiography that uses computerized techniques to enhance contrast visualization. The image before contrast injection is electronically subtracted from the contrast images, leaving only opacified vessels on the final image. A DSA image can only be obtained at one position per injection of contrast. DSA complements regular angiography. 13. MRI: This study is now being done to assess distal runoff in the foot when angiography is questionable or to double check angiography when attempting to save a limb.

The Vascular Diseases 1. Treatment of Chronic Arterial Occlusive Disease: Patients with chronic lower extremity ischemia should be divided into those with claudication and those with limb-threatening ischemia. a. Claudicators: Treatment can consist of conservative management including exercise, elimination of tobacco/caffeine etc., control of medical conditions. Pharmacological management includes Trental (pentoxifylline) which alters blood flow characteristics by "softening" the RBC. b. Limb Threatening Ischemia: Gangrene, rest pain, or tissue loss is an indication for revascularization. Options for revascularization include endarterectomy, balloon angioplasty, atherectomy, and bypass grafting (insitu autologous vein or prosthetic material-Gortex). NOTE* In diabetics the most common site of occlusion is just above the trifurcation in the leg. Femoral popliteal and popliteal-peroneal bypasses are most common procedures in these individuals.

The treatment goal is to bypass all hemodynamically significant disease down to the level of a continuous outflow artery to the foot.

2.. Venous Disease: The venous system is characterized by low pressure, distensibility and high capacity. It is driven by the effects of respiration on intraabdominal pressure, the calf muscle pump, and the venous valves. Veins are superficial or deep, connected, by perforators. a. Venous Thrombosis (DVT): Conditions predisposing a patient to DVT include prolonged immobilization, bedrest with a recent MI, women confined to bed during pregnancy or post Caesarean section, obesity, an underlying malignancy, use of a tourniquet, a history of ulcerative colitis and Behcet's syndrome, inherited hypercoagulative states and oral contraceptives. Patients can present with pain and swelling of the leg, but additionally DVT's can be silent. A patient with suspected DVT should undergo venography for a definitive diagnosis. Treatment is with heparin initially (full anticoagulation via IV administration), then coumadin to prevent pulmonary emboli, and to inhibit further DVT NOTE* Treatment with heparin is as follows: after drawing blood for a coagulation profile, 5000 to 10,000 U of intravenous heparin is given followed by a constant infusion of 1000 to 1500 U/hour. The activated thromboplastin time is kept at 2-2.5 times the baseline. DVT prophylaxis is with subcutaneous heparin Q 8-12 hours. A long term sequelae of DVT is postphlebitic syndrome characterized by failure of the calf muscle pump, increased ambulatory venous pressure, pain, edema, skin and soft tissue changes, and ulceration.

b. Pulmonary Embolism: A potentially lethal complication of DVT. Heparin coagulation is the treatment of choice. There are vena cava devices to prevent pulmonary embolism while the patient is being treated for DVT. c. Superficial Venous Insufficiency: Results in primary varicose veins. d. Deep Venous Insufficiency: Results in secondary varicose veins are related to incompetent perforator veins or deep venous system insufficiency. 3. Diabetes and PVD: Diabetes is the seventh leading cause of death in the United States. Vascular complications of diabetes are accelerated by hypertension, cigarette smoking, hypercholesteremia, hyperglycemia, the duration of diabetes, and the degree of blood sugar control. a. Pathogenesis: The three most important factors that influence the vascular complications of diabetes are- the duration of diabetes after puberty, elevated blood sugar levels, and blood pressure. Diabetic microangiopathy is a result of metabolic abnormalities caused by an absolute or relative insulin deficiency. The development of neuropathy is a critical factor in the rapid progression of peripheral arterial disease with the concurrent development of autonomic denervation. b. Pathophysiology: Microangiopathy is characterized by the thickening of the basement membrane and arteriovenous shunting. Hypercoagulability of blood components is recognized as a significant factor in diabetic angiopathy. Hypertension can cause a threefold increase in atherosclerosis in the diabetic. Note* The use of Beta blockers for the treatment of hypertension is contraindicated in the diabetic because of the unopposed alpha action. Calcium channel blockers or ACE inhibitors are the recommended drugs for diabetics. c. Signs end Symptoms: Pain is the most common symptom. The three signs are- blenching of the foot upon elevation, delayed venous filling time after elevation, end rubor on dependency. Other signs end symptoms ere pulseless feet, subcutaneous fat tissue atrophy, shiny skin, absent hair growth on the lower extremities, and thickened nails. d. Treatment: Exercise and diet, cholesterol control, cessation of cigarette smoking, daily aspirin (?) (suppress prostaglandin production in platelets/suppresses platelet aggregation), blood sugar control, blood pressure control, drugs (PV dilators). Note* Treatment for venous stasis ulceration is almost always conservative, 'with compression therapy with graduated elastic compression stockings (30-40 mm Hg), Unna Boot with DuoDERM hydroactive dressings etc., or the "Oregon Protocol".

4. Vasospastic Disorders: a. Raynaud's Vasospasticity: Divided into Raynauds phenomenon, syndrome and disease. Phenomenon is the clinical presentation of the discoloration

sequence of pallor, cyanosis, end rubor accompanied by paresthesias. Syndrome is the bilateral end symmetric recurrence of the phenomenon that persists for longer periods of time with each incident, and is associated with an underlying collagen or autoimmune disorder, or with organic arterial disease. Disease is the state of a consistent recurrence of discoloration with associated paresthesias upon exposure to cold or emotional crisis that has not been identified to coexist with any other disorder 2 to 3 years after the original presentation. All of these forms of vasospesticity ere precipitated by exposure to cold water, ice, cold ambient temperature, cold humid air, or a chilly wind. b. Acrocyanosis: A condition characterized by persistent uniform cyanosis of the feet and toes end associated plantar hyperhidrosis. Unlike Raynaud's, the vesospesticity extends proximally beyond the digits. c. Livedo Reticularis: A condition involving the arterioles of the skin presenting with livid discoloration in a reticular pattern (mottled or lacelike red-blue discoloration). Has an annular form, livedo annularis, and a grapelike form, livedo annularis racemosa d. Medications: The traditional vasodilators, isoxsuprine, pepavarine, niacin are used in Raynaud's cases. Nitroglycerine 2% ointment applied in a 0.75 inch strip on the dorsum of the foot Q 5 hours has been beneficial when oral vasodilators have failed. Calcium channel blockers (nifedipine end diltiezem) have recently been studied for these disorders. 5. Lymphatic Diseases: Can be either primary or secondary lymphedema a. Primary lymphedema: The classic indication of primary lymphedema is soft tissue swelling as a result of lymph accumulation. This swelling arises without cause and may not present bilaterally. It is associated with aplasia, hypoplasia, or hyperplasia of the lymphatic channels, trunks, or nodes. i. Milroy's Disease: Congenital/hereditary form of lymphedema, with the edema noted at birth to be firm but pitting, chronic, permanent, and confined to the lower extremity. ii. Congenital Lymphedema: Congenital although no family history is determinable, more prevalent than Milroy's disease, edema may be present in the lower or upper extremities. iii. Lymphedema Praecox: Hereditary, noncongenital manifesting itself in early life (ages 9-25), seen predominantly in girls, a rapid onset involving one foot and ankle, progresses to a nonpitting form. Treatment is with an intermittent compression pump and compression stockings. b. Secondary Lymphedema: Results from acute, repetitive or chronic lymphangitis secondary to a known cause. The inflammation may be due to direct trauma, foreign bodies, infection, or as a complication of venous insufficiency with associated venous hypertension. It also may result as an extention of acute cellulitis or deep thrombophlebitis. i. Traumatic Lymphedema: From direct impact or lacerating injury to the large pre- and post nodal collecting lymphatics, nodes, and major trunks. ii. Infectious Lymphedema: From bacterial or filarial infections iii. Neoplastic and Foreign Body Lymphedema iv. Postphlebitic Lymphedema v. Neuroplegic Lymphedema

c. Direct Lymphangiography: The gold standard of lymphatic system imaging

Chapter 16: Internal & External, Fixation Objectives of Fixation Devices Requirements of Implant Materials Principles Affecting Internal Fixation Internal Fixation Devices AO Objectives AO Principles AO Technique Jumping Screws Other Techniques Complications of Fixation Devices External Fixation Large Bone External Fixation (Ilizarov Technique) Small Bone External Fixation of the Foot

INTERNAL & EXTERNAL FIXATION Objectives of Fixation Devices 1. Eliminate motion at a fracture or osteotomy site. 2. Restore the normal anatomical alignment of the fractured site or the desired position of an osteotomized segment. 3. Assist in the physiological mechanism of bone healing. 4. Permit early mobilization of the area affected by the fracture or osteotomy.

Requirements of Implant Materials 1. Materials must be resistant to corrosive environment of the body, yet inert to any foreign body reaction. 2. Material must have strength and durability to endure the stress loads placed upon it during implantation, bone healing, and subsequent function of the involved part. 3. Material must be available in various sizes and shapes and practical, enabling fabrication into fixation devices suitable for implantation, without the need for complicated hardware or technique. 4. Metals must be compatible with the surrounding environment, thus reducing the pitting and crevice corrosion phenomena which would lead to fatigue fracture of the implant device. 5. Use of similar metals within the fixation device to prevent the anodecathode "battery affect", or the production of hydrogen ions from saline fluid within the body. Acidic environment leads to rapid corrosion and fatigue fracture of implant devices. 6. Should be relatively inexpensive.

Principles Affecting Internal Fixation 1. Alignment and stability across the fracture site must be developed and maintained during fracture healing to effect bone healing. 2. Tension Band Principle: Load-bearing through a bone creates one convex and concave surface subjected to compressive and tension forces. Accordingly, implant devices are applied to the convex surface of bone or to the side of tension, to prevent gapping from tensile forces. The gapping forces are counteracted with proper positioning and selection of the device. This causes counterreactive force of compression across the fracture site, enhancing proper fracture healing. 3. Neutralization Principle: Specific anatomic sites are exposed to multiple stresses, which include torsional and axial loads. These forces may change with dynamics of muscle and joint activity. The various load forces are neutralized at the fracture site with plating in combination with bone screws to minimize movement, especially with multifragmented fractures.

Internal Fixation Devices 1. Suture Material: a. Absorbable and non-absorbable sutures are used to re-approximate an

osteotomy site. This is done when the osteotomy can be closed without any tension. If a non-absorbable material is being used, this fixation device is then considered a permanent type. b. The only advantage of this material is that it is very easy to use. c. The disadvantages are that is provides poor compression and low tensile strength. 2. Stainless steel wire: 316 LVM surgical steel a. Monofilament is better than braided to achieve compression as it is twisted down on itself. b. Its advantages are: i. Its simplicity ii. Adequate compression when used properly iii. Minimal amount of foreign material left in the bone iv. Acceptable in various anatomic locations independent of surface irregularities and bone cuts. v. Easily retrieved, if necessary, postoperatively, and visable on x-ray c. Its disadvantages are: i. Difficulty in achieving equal compression along the fracture/osteotomy site ii. Possible trauma to bone as the wire is pulled through iii. Requires good -bone stock iv. Becomes a permanent fixation device. v. Fatigue fracture of wire with motion at the fracture site d. Size used is generally 28 gauge. e. Tension band wiring using monofilament and K-wires. This technique provides greater stability than that provided by either component used separately. The tension band principle applies to bones that are eccentrically loaded. The application of a tension band device on the tension side of a bone allows dynamic compression to be generated on the opposite cortex. f. MRI may be a problem if wire is present in the foot. 3. Kirschner Wire: 316 LVM surgical steel a. Designs: i. Come in different lengths and can also be cut to size ii. Come as single or double ended iii. Come as threaded or smooth iv. Tips are either trochar (slip the least along the cortical bony surface and have the greatest holding power), diamond, or cut tip (poorest holding power) b. Sizes include: .028", .035", .045", .062". c. The advantages are: i. Application to many sites requiring minimal dissection for fracture immobilization ii. Can be inserted percutaneously without the need for surgical exposure,

specifically for implantation iii. Can be easily removed following surgery once fracture healing is accomplished iv. Ability to fixate multiple small fragments v. Can prevent motion on all three body planes, including axial rotation by using multiple pins vi. Can immobilize joints by passing wire through a joint surface, thus preventing undesirable motion vii. Can be incorporated within the cast to protect fixation and maintain position viii. Is considered a temporary device d. Its disadvantages are: i. Creates a track from the external surface of the wound into the bone ii. Can be a potential source for introducing bacteria iii. Requires good patient compliance during the postoperative phase iv. Threaded wires are difficult to remove v. Threaded wires across a fracture site will maintain separation of fracture fragments after expected necrosis occurs at fracture. vi. Can break with the bone if exposed to excessive pressure vii. Can migrate or slip out of the bone 4. Stelnmann Pins: 316 LVM surgical steel a. Very similar to Kirschner wires except for their size. b. Size ranges from 5/32 to 1 /8 inches in diameter (1.9 mm to 4.7 mm). c. Their rigidity is proportional to the fourth power of their diameter (as with K-wires). d. Advantages are the same as with K-wires. e. Disadvantages are the same as with K-wires. f. The primary stabilization of subtalar arthrodesis has frequently been performed using these pins. g. Are well suited to providing provisional fixation of subtalar and ankle arthrodesis as well as calcaneal fractures. 5. Absorbable Pins (Polydioxanone/Polyglycolide): At the present time there are two types of pins available. They were originally designed for fixation of osteochondral fragments, which were previously treated via excision and abrasion or fixation with K-wires, screws, or adhesives, which would leave extensive osteochondral defects. a. Orthosorb (polydioxanone) (Johnson & Johnson): i. This pin is available in only one length (1.3 mm x 40 mm long) and is very flexible. ii. A tapered variety allows for better compression of osteotomies as they are inserted into the pilot hole iii. Has been used with success in digital fusions because of its flexibility iv. Can be cut with a bone cutting forceps v. Lose their strength in 4-8 weeks and are totally absorbed in 9-12 months

b. Biofix (self reinforced polyglycolide)(Acuflex): i. Various diameters from 1.5 mm to 4.5 mm ii. Various lengths from 10 mm to 70 mm and is very rigid iii. Lose their strength in 4-8 weeks and are totally absorbed in 6 months iv. Must be cut with a bone saw or it will shred 6. Staples: Various 2 prong and 4 prong staples are available and are supplied with templates to assure proper implantation. Available in surgical steel and titanium. a. Their application is limited and are best suited for bones with high cancellous/cortical ratios. b. When used primarily in diaphyseal bone there is a propensity for the cortical bone around the staple legs to become communited as the staple is inserted, resulting in compromised fixation. c. Advantages are: i. Easily removable ii. Can be a permanent implant iii. Provides fixation on one plane developing static compression across the fracture fragment site. d. Disadvantages are: i. Should not be used in incomplete fractures independently, unless secondary devices or complete non-weight bearing are utilized. ii. Staples can dislodge iii. Staples can fatigue fracture e. Have been used for calcaneal osteotomies, triple arthrodesis, tib-fib syndesmosis diathesis, medial and lateral malleolar fractures (with malleolar screw), and epiphyseal plate injuries. 7. Osteoclasps: 3/16 LVM stainless steel a. Available in five sizes, 8 mm, 10 mm, 12 mm, 14 mm, 16 mm. b. The device requires secondary instrumentation for template positioning of drill holes, and additionally, a tension stat to implant the osteoclasp under proper tension. c. Advantages: i. Can be used in various anatomic locations without the need for additional surgical exposure ii. Completely internal and can be considered a permanent implant iii. Creates fixation with dynamic compression across the fracture site d. Disadvantages: i. Limited to incomplete osteotomy where cortical hinge is intact on the opposite side of placement of the osteoclasp device ii. Technical difficulty with implantation iii. Implant may have to be remodeled which weakens its compression force and may result in spontaneous loosening

8. Bone Screws: Are used to reappose fracture fragments, their primary advantage over any other type of fixation device is that they can provide compression and thus more rigid fixation. Cortical bone screws require pretapping of drill holes and the thread is finer, whereas cancellous bone screws can be used for self-tapping locations to create a lag effect across a fracture site. Cancellous screw threads are much larger and grasp greater surface area of bone to achieve fixation. a. Four basic structural dimensions are employed to precisely characterize screws: i. Root or Core diameter is the minimal diameter of the screw not including the threads (Fig. 2). NOTE* The tensile strength of screws is proportional to the square of the root/core diameter, and the shear strength of screws is proportional to the cube of the root/core diameter. ii. Thread diameter is the maximal diameter including the screw threads (Fig. 1). iii. Screw pitch is the distance between two successive threads (fig. 3). iv. The lead is the distance a screw advances when turned one complete revolution. b. Other screw parts are: i. Screw head: either cruciform or hexagon ii. Screw land: the undersurface of the screw head iii. Screw tip: either round, pointed, or fluted

Al 4.0 mm Partially threaded cancellous screw 1.75 mm pitch

B2 4.0 mm Fully threaded cancellous screw 1.75 mm pitch (Formally 3.5 mm cortical screw C3 3.5 mm Fully threaded cortical screw 1.25 mm pitch D4 3.5 mm Fully threaded cancellous screw 1.75 mm pitch Reprinted from Ruch JA, Vito GR Corey SV (eds); Podiatry Institute Internal Fixation Workbook. 8th ed., Podiatry Institute Publishing, Tucker, Georgia, 1992, with permission

iv. Screw shank: the distance between the land and the start of the screw runout (Fig. 4) v. Screw runnout: the distance from the end of the shank to the first thread ( Fig. 5). vi. Screw thread: either assymmetric (buttress) or symmetric (Fig. 6) NOTE* Bone possesses a significantly lower modulus of elasticity than metal alloys. The buttress AO thread is designed to maximize the volume of bone between threads and increase the holding potential of the screw in the weaker bone matrix. c. Cortical Screws: (see figure 7) i. Function as either a positional screw (provide plate fixation) or a lag screw (exerts compression) ii. Compression is only achieved when the threads of the screw do not engage the cortex of the near osteotomy or fracture fragment, accomplished by overdrilling. iii. Cortical screws measuring 3.5 mm in diameter are used in lag fashion to provide interfragmentary compression in the distal fibula, rearfoot, and occasionally the metatarsals. iv. Screws measuring 2.7 mm, 2.0 mm, and 1.5 mm are also employed to stabilize metatarsal fractures or osteotomies. Screws measuring 1.5 mm are used in the proximal phalanx of the hallux for fracture fixation.

v. When screws are used alone for fragment fixation, two smaller screws provide increased resistance to shear and torsional stresses. vi. When screws are used for interfragmentary compression, they should be inserted so that their direction bisects the perpendiculars to the fracture line and the long axis of the bone involved. Note* If one screw is used for a base wedge osteotomy with an intact cortical hinge, the angle of insertion of the screw should bisect the perpendiculars of the long axis of the osteotomy and the long axis of the bone. If the screw is placed at an angle greater than this, the cortical hinge will disrupt.

vii. Sufficient screw fixation can usually be obtained with oblique and spiral fracture patterns only when the fracture line is at least twice as long as the bone's diameter. viii. Short oblique or transverse fractures, therefore need an interfragmentary lag screw and neutralization plate. d. Cancellous Screws: (see figure 7) i. Come either fully or partially threaded ii. Cancellous screw thread height is greater than that of cortical. This allows for greater purchase in the softer metaphyseal and epiphyseal bone for which they were designed. iii. Screw head fixation can be augmented in osteoporotic bone with a washer. iv. If the threads of a cancellous screw are left in a position crossing the interface between two fragments, no compression will be achieved, as the lag affect that is desired from this screw will be negated. It then acts as a cortical screw. v. Cancellous screws 6.5 mm in diameter are used in ankle and subtalar arthrodeses. vi. Lisfranc's injuries are amenable to 4.0 mm cancellous screws. vii. Fractures of the talus and calcaneus are frequently stabilized with cancellous screws (in these locations are generally augmented with washers or small plates).

e. Washers: i. Generally used in osteoporotic bone. ii. Used with cancellous screw for increasing the purchase power on the near fracture cortex. iii. Can be used with screws to provide increased surface area as well as barbs for the reattachment of ligaments or transferred tendon insertions. f. Malleolar Screws: i. Are self-tapping and possess a sharp pointed tip that was designed to allow insertion without predrilling. ii. Due to their large size, 4.0 cancellous screws have replaced them. g. Cannulated screws: The complications involving placement of screws in complicated fractures can be greatly minimized with this type of screw. i. This type of screw can be inserted over a guidewire through its entire length, after the guidewire is properly placed in the bone. This minimizes bony trauma. ii. When a cannulated screw is to be used, the K -wire (guidewire) serves a dual purpose of maintaining reduction and providing a guide for screw placement. h. Herbert Screw: i. Originally designed for osteochondral fractures (also used for scaphoid fractures of the hand), due to the absence of a screw head. ii. Characterized by the presence of threads with different pitches and leads on both its proximal and distal ends. The distal threads feature a tighter pitch and smaller lead and are separated from the proximal ones by an intervening smooth shank. This allows for interfragmentary compression. i. Reese Arthrodesis Screw: Right/lefthanded threaded screws which are used for digital fusions. Note* A screw can be used alone for internal fixation whenever the fracture or osteotomy is at least twice as long as the diameter of the bone at the level of the fracture or osteotomy. A screw inserted at right angles to the fracture or osteotomy plane gives the best interfragmental compression, but provides no stability under axial loading. A screw inserted at right angles to the long axis of the bone gives the best resistance to axial loading, but decreases the interfragmental compression. Based on the previous 3 principles, a cortical lag screw is inserted so that it bisects the angle formed by the perpendicular to the fracture plane and the perpendicular to the long axis of the bone 9. Intermedullary Fixation (Nails): These are long pieces of metal of various available diameters which are placed in the medullary canal of a fractured/osteotomized long bone to stabilize the site. a. They are: i. Rush pins ii. K-wires ii. Inyo nails (tapered V-shaped stainless device used for fractures of the distal fibula) b. Are wedged into the medullary canal after the canal is reamed to a diameter slightly smaller than the nail to be used, and then removed after healing is completed.

c. Of all the internal fixation devices used, this one delays bone healing the most by damaging the medullary blood vessels when it is inserted. d. The other major drawback it is limited control of the rotational forces of the fracture fragment. 10. Plate Fixation: Are temporary fixation devices which serve a particular function and then are removed. Plates can function in several fashions, depending upon how they are applied and the resulting bone-plate construct geometry. These functions include rigid fixation through interfragmentary compression, buttressing, and neutralization. Depending upon the mechanical circumstances, a plate may provide more than one of these functions. a. The following plates are utilized: i. Static Compression Plates: Tension is applied to the implant and compression is achieved at the fracture interface. ii. Dynamic Compression Plates: Beyond the compression of the fracture achieved through static compression, the implant is subjected to a physiologic load which generates additional compression at the fracture plane iii. Neutralization Plates: Initially a shaft fracture may be fixated by interfragmental compression with a lag screw. A plate is then applied to neutralize or absorb-any disruptive forces; torsional, shear, or bending to which the bone and osteosynthesis may be subjected iv. Anti-Glide Plates: Are used as neutralization plates but placed on the posterior aspect of the fibula. v. Buttress Plates: Are used to maintain separation of bone during bone grafting procedures to gain or maintain length. Are generally used to resist the tendency of metaphyseal fracture fragments to displace when subjected to compressive forces. Specifically designed plates by the AO group are spoon and cloverleaf plates for the distal tibia, and the malleable H or double-H plates for the calcaneus. b. Pre-stressing the plate results in static interfragmentary compression, and is performed by contouring the plate so that its center sits away from the bone to which it is applied. The screws securing the plate ends are inserted and tightened first (pre-stressing the plate in tension) so that as sequential screws are applied (progressively closer to the center) axial compression is developed along the underlying bone. In addition, eccentrically plated screws may be inserted (as a compression device) for interfragmentary compression. c. Plates also function to protect lag screw fixation. Oblique or spiral fracture of the metatarsals or the distal fibula can be stabilized with interfragmentary lag screws. The addition of a plate then serves to neutralize the bending, torsional, and shear forces that would otherwise jeopardize the fixation obtained by lag screws alone. d. The AO group has developed 1 /3 and 1 /4 tubular plates which are easily contoured. e. The advantages of plates are:

i. Allows for complete reduction of fracture fragments and proper anatomical alignment. ii. Can be implanted permanently or removed at a later date. iii. Creates rigid fixation with stabilization and/or dynamic compression across the fracture site. f. The disadvantages are: i. Significant amount of surgical dissection for implantation of plate and screws. ii. High degree of difficulty with irregular or multifragmented bone fractures. iii. Technical difficulty for implantation, potential fatigue fracture of bone plate with motion. iv. Should be applied to the tension side of the fracture to avoid breaking the bone plate. iv. Results in a degree of bone necrosis beneath the plate. 11. External Fixator Devices: These devices are available in a variety of sizes depending upon the location to be used. Their prime indication is severe trauma, especially associated with open fractures. Also can be used in the treatment of infected fractures, non-unions involving the ankle, arthrodesis of the subtalar joint or ankle joint, acute and chronic OM, and chronic septic arthritis. NOTE* Specific guidelines for their use have been outlined by Kenzora and Edwards and associates in The Foot and Ankle. They recommended the use of various configurations of Hoffman's external fixators in order to: a. Stabilize open fracture-dislocations b. Maintain length where bone is lost or extensively comminuted c. Prevent soft tissue contractures d. Control joint position for delayed ankle arthrodesis e. Provide easy access for bone and soft tissue reconstruction

a. Charnley compression clamp: Has been utilized in combination with Steinmann pin fixation. It is applied on each side of the extremity and attached to an exiting pin. Turn-buckle style adjustments are made on each side of the extremity forcing compression across the fracture site. b. Hoffman fixator devices: Were designed for the small bones of the hands and feet, and have greatly enhanced the use of external fixator techniques in fracture repair and bone grafting techniques. c. Advantages: i. Ability to be adjusted during the healing phase ii. It is only a temporary device iii. Its ability to provide rigid fixation while allowing ready access to surrounding soft tissues for debridements and dressing changes as necessary iv. Neighboring joint motion can be preserved d. Disadvantages:

i. Difficult to use and requires special instrumentation ii. Pin-tract loosening and infection iii. Requires good patient compliance iv. Creates a bulky external apparatus which will hinder the activity of the patient AO Objectives 1. Atraumatic operative technique 2. Accurate anatomical reduction 3. Rigid internal compression fixation 4. Avoidance of soft tissue damage 5. The AO tenet: "Life is movement, movement is life". AO Principles 1. Intrinsic Factors Affecting Stable Fracture Reduction: a. Stable fractures: i. Are transverse fractures b. Unstable fractures: i. Long oblique fractures ii. Comminuted fractures iii. Spiral fractures c. Potentially stable fractures: i. Short oblique 2. Extrinsic Factors Affecting Stable Fracture Reduction: a. The disruptive mechanical forces are bending, shear, and torsion. 3. Mechanical Basis for Stable Fixation: a. Types of interfragmental compression i. Static compression: a constant and uniform force across a fracture/osteotomy site, accomplished by lag screw technique, a preloaded plate, or external fixator. ii. Dynamic compression: is the combination of a statically loaded fixation device to a functionally loaded fracture configuration (the tension band concept). b. Splintage: A technique applied when interfragmental compression is not possible and is used in combination with interfragmental compression when it alone is not adaquate to provide stable fixation. c. Combinations: combination of techniques of interfragmental compression and splintage (i.e. a single lag screw plus reinforced by a plate). 4. Techniques of Stable Fixation: a. Single lag screw: A cortical screw with a glide hole or a cancellous screw with all the threads on the distal side of the fracture fragment. A single lag screw can provide adequate interfragmentary compression, however, is not able to withstand shearing and bending loads, so the fracture/osteotomy must be protected. i. Angle of screw insertion: Should be placed so that the angle of the screw bisects the perpendicular of the fracture/osteotomy and the perpendicular of

the longitudinal axis of the bone. If the angle of the screw deviates from the plane of the fracture, there is a shift of the near fragment in the direction of the course of the screw as the screw is tightened and compression is created. b. Multiple lag screws (two or more): Are used in a long/oblique or spiral fracture, where the length of the fracture is at least twice the diameter of the diaphyseal bone involved. i. Angle of screw insertion: when fixating a fracture/osteotomy with several screws, the first screw should be perpendicular to both cortices and be centrally placed. The second and third screws (placed on either side of the first screw) are placed perpendicular to the plane of the fracture. This prevents a frontal plane shift, called the shear effect, of the longitudinal relationship of the fracture fragments. These secondary screws can also be placed so that they bisect the angle between the perpendicular of the fracture and the perpendicular of the cortical surface. This reinforces interfragmentary compression.

AO Technique 1. Instrumentation: i. Thread hole drill bit: (1.1, 1.5, 2.0, 2.5, 3.2 mm) ii. Glide hole drill bit: (1.5, 2.0, 2.5, 2.7, 3.5, 4.5 mm) iii. Countersink: (Mini Fragment Set 1.1 and 2.0 mm tip) (Small Fragment Set 2.0 mm tip) (Large Fragment Set 3.2 and 4.5 mm tip) iv. Depth gauge: (Mini/Small/Large) v. Tap: (1.5, 2.0, 2.7, 3.5 mm @ 1.25 pitch) (3.5 mm @ 1.75 pitch) (4.5 and 6.5 mm) vi. Screw Driver: (Cruciform/Hexagon head) v. Drill and Tap Sleeve: (protection for the soft tissue/ reduces the need for excessive retraction when the drill bit Is aimed obliquely at the bone/the serrated end anchors well to cortical bone and prevents slippage of the drill bit)

2. Sequence For Screw Insertion: a. 1.5 mm Cortical Screw i. Pre-drill (0.035 K-wire= 0.9 mm) ii. Thread Hole (1.1 mm) iii. Countersink (Mini) iv. Overdrill near cortex (1.5 mm) v. Depth gauge (Mini) vi. Tap (1.5 mm) vii. Screw Placement b. 2.0 Cortical Screw i. Pre-drill (0.045 K-wire= 1.1 mm) ii. Thread Hole (1.5 mm) iii. Countersink (Mini) iv. Overdrill near cortex (2.0 mm) v. Depth gauge (Mini) vi. Tap (2.0 mm) vii. Screw Placement c. 2.7 Cortical Screw i. Pre-drill (0.062 K-wire= 1.6 mm) ii. Thread Hole (2.0 mm) iii. Countersink (Small) iv. Overdrill (2.7 mm) v. Depth Gauge (Small) vi. Tap (2.7 mm) vii. Screw Placement d. 3.5 Cortical Screw i. Pre-drill (0.062 K-wire= 1.6 mm) ii. Thread Hole (2.5 mm) iii. Countersink (Small) iv. Overdrill (3.5 mm) v. Depth Gauge (Small) vi. Tap (3.5 mm) vii. Screw Placement e. 3.5 mm Cancellous Screw i. As with 3.5 Cortical Screw but eliminate the 2.5 mm Thread Hole f. 4.0 Cancellous (partially threaded) i. Pre-drill (0.062 K-wire= 1.6 mm) ii. Thread Hole (2.0 mm) iii. Countersink (Small) iv. Overdrill (3.5 mm) v. Depth Gauge vi. Tap (3.5 mm) vii. Screw Placement g. 4.0 Fully Threaded Cancellous Screw i. Pre-drill (0.062 K-wire= 1.6 mm) ii. Thread Hole (2.0) iii. Countersink (Small) iv. Depth Gauge

v. Tap (3.5 mm) vi. Screw Placement h. 4.5 Cortical Screw i. Pre-drill (0.63 K-wire= 1.6 mm) ii. Thread Hole (3.2 mm) iii. Countersink (Large) iv. Overdrill (4.5 mm) v. Depth Gauge vi. Tap (4.5 mm) vii. Screw Placement i. 6.5 mm Cancellous Screw (partially threaded) i. Pre-drill (5/64 K-wire) ii. Thread Hole (3.2 mm) iii. Countersink (Large) iv. Depth Gauge v. Tap (6.5) vi. Screw Placement j. 3.5 mm Cortical Screw (using a T-Sleeve) i. 3.5 mm drill (proximal cortex only) ii. 3.5 mm x 2.0 mm drill sleeve iii. 2.0 mm thread hole of the far cortex iv. Countersink v. Depth Gauge vi. Tap (3.5 mm) vii. Screw Placement k. Exercise: Modified Austin With 2 x 2.7 mm Cortical Screw Placement i. Osteotomy performed with lateral shift of the capitol fragment ii. Temporary fixation (0.045 K-wire) iii. Temporary fixation: pilot hole for the proximal screw (0.062 K-wire) iv. Pilot hole for the distal screw (0.062 K-wire) v. 2.0 mm thread hole (distal screw) vi. Countersink (distal screw) vii. 2.7 mm over drill (distal screw) viii. Depth gauge (distal screw) ix. 2.7 mm tap (distal screw) x. Insert 2.7 mm distal screw xi. Remove proximal temporary fixation xii. Proximal screw insertion (as just described) xiii. Remove distal temporary fixation xiv. Tighten screws 3. Plating Procedures: a. Prestressed Plate: Because of the linear design of these plates, this technique is best used in long bone fractures. The axial load created by a prestressed plate is a form of static compression, and can be accomplished three ways:











1. Load Screw Technique: The most common plate technique in the foot and ankle. These plates are thin and are semi 1 /3 and 1 /4 round. They are to be used for tension only and do not provide rigidity against bending (provided by the thicker Dynamic Compression plate). Performed by using eccentrically drilled holes, (for the initial two holes) one just proximal and one distal to the fracture/osteotomy site. As the screws are tightened down they move the fracture fragments together. This can be done as a result of the ovoid design of the screw holes in the plate. These are the load screws. The other screws must be centrally placed or they will dislodge these load screws. To prevent the fracture surface from gapping on the opposite side of the tension surface, the plate can (and should) be prebent at its center. It now acts as a leaf spring and resists gapping of the opposite cortex. The use of this concept is limited to transverse metatarsal fractures and arthrodesis of first metatarsal-cuneiform arthrodesis.

ii. Dynamic Compression Plate: This incorporates the load screw technique with the added effect of geometrically designed slots within a plate.
These plates are thicker and stiffer than tension plates.
These geometrically designed slots have two features: they are oblong and longitudinally placed, and they have two different slopes (the first acute slope is the compression slope/the second slope is the gliding slope). Both of these features allow for linear motion.




All the screws can be used as load screws (because there is space for the first two screws to glide after the other screws are tightened down).
There are individual plates corresponding to the 2.7 mm/3.5 mm/4.5 mm cortical screws. iii. Tension Device: This can be done only with large bones. It is done by anchoring a tension device to one of the fragments and to a free end of a plate, then anchoring the plate to the other side of the fragment and then tightening the tension device. This causes interfragmental compression.

Jumping Screws In case of screw failure you must have a backup or alternative. This explains how to change screws properly 1. To go from a 1.5 to a 2.0 mm screw: Use a 1.5 mm thread hole, followed by a 2.0 overdrill 2. To go from a 2.0 to a 2.7 mm screw: Use a 2.0 thread hole followed by a 2.7 overdrill (may need to re-countersink) 3. To go from a 2.7 to a 3.5 mm cancellous screw: Use a 3.5 overdrill 4. To go from a 2.7 to a 3.5 mm cortical screw: Use a 2.5 thread hole followed by a 3.5 overdrill 5. To go from a 2.7 to a 4.0 mm cancellous screw (may be the best choice): Needs no instrumentation 6. To go from a 3.5 cancellous to a 3.5 mm cortical screw.: Use a 2.5 mm thread hole 7. To go from a 3.5 cortical to a 3.5 mm cancellous: Needs no

instrumentation 8. To go from a 4.0 cancellous to a 3.5 mm cortical screw: Use a 2.5 thread hole followed by a 3.5 overdrill NOTE* Never retap after the first screw fails

Other Techniques 1. Splintage: A technique used to splint or protect a reduced fracture. The primary uses of splintage are: when interfragmental compression cannot be used, epiphyseal fractures, and to protect a tenuous interfragmental compression. 2. Circlage Wiring: The classic application in podiatry is the dorsal loop technique for an abductory closing wedge osteotomy, even though is has proven to be the weakest form of internal fixation. It does provide apposition of the osteotomy surfaces, but provides little stability. The most secure fixation is two loops in a 90 degree orientation to each other 3. K-wires: A single K-wire rarely provides any rigidity, however, crossed Kwires are best. This is not without its shortcomings as distraction of fracture fragments can occur. K-wire fixation alone does not afford interfragmental compression. K-wires do offer stability when used in combination with intraosseous loop techniques. Threaded K-wires are rarely used as they are mechanically unsound. 4. Tension Banding: Monofilament wire threaded in a figure 8 fashion, used in combination with two K-wires to give interfragmental compression (Figure 11). Good with Jones fracture, and some ankle fractures. The plane of insertion of the 2 K-wires must be parallel to the plane of the drill hole for passage of the monofilament wire

Figure 11: Tension Band Wiring Techniques Reprinted from Ruch JA, Vito GR, corey SV (eds); Podiatry Institute Internal Fixation Workbook. 8th ed., Podiatry Institute Publishing, Tucker, Georgia, 1992, with permission

Note* The tension band principle is applied when an eccentric load is placed on a bone, and reduction is attempted. The eccentric load creates a concavity on one side (which is under tension), and a convexity on the other side which is under compression. The tension band absorbs the tensile force, and the bone (load beam) absorbs the compressive forces. The 2 areas that are easily accessible to this principle in podiatry are the 5th metatarsal and the two malleoli Principles: a. Neutralize the distracting force and convert to a compressive force b. Apply the tension band to the tension side only (convex side) c. K-wires eliminate the rotational instability

Complications of Fixation Devices 1. Infection: Despite long-standing efforts directed at eliminating this complication, there appears to be an irreducible minimal infection rate destined to plague both patient and physician. The potential exists for the growth of resistant bacterial strains or superinfections as a result of increased use of antibiotics. Studies involving the use of prophylactic antibiotics have shown a decrease in the incidence of postoperative infections when fixation devices are used (first-generation cephalosporins given preoperatively provide good coverage against Staph aureus and many gram(-) rods, and are most widely used). Implants frequently need to be removed in the presence of a deep infection, however, should be left in place in the absence of bony union even with the presence of an infection (infections are difficult to manage without stability, and so do better with stabilization). 2. Slippage of the Fixation Device: Screws, K-wires, as well as the rest of the fixators can lose purchase and slip out of place. When this happens, the device must be removed and replaced with an alternate. 3. Mechanical Failure: Has not been a frequent problem. 4. Inappropriate Use of Fixation Devices: This is a significant problem. Next to infection this is the most common cause of implant failure. 5. Stripping of a Screw Head/ Breakage of a Screw: When stripping occurs a vise grip is used. When a cancellous screw is removed after many months it can break. A cancellous screw is unable to cut bone when it is backed out, and if excessive torque is applied when bone has grown in around the smooth shank, the screw can break.

External Fixation An external fixator can be used in many different ways in the fixation of the osseous skeleton. However, the use of an external fixator is presently limited in foot an ankle surgery. With the understanding of the techniques and training now available, should become a more popular method in the surgeon's armamentarium. The techniques discussed will be divided into large bone and

small bone fixation

Large Bone Fixation 1. Ilizarov technique: This method of external fixation was developed in Kurgon, Russia and has been used successfully to treat surgical and traumatic fractures, osteomyelitis (without sequestrectomy or even antibiotics), non-unions, osteotomies, fusions, pseudoarthrosis, angular deformities, limb shortenings, and joint contractures using a surgical technique that respects osteogenic tissues and their vascular supply while preserving the weightbearing function of the limb. This is all due to the massive neovascularization coupled with mechanical control of the limb permitting not only histogenesis of bone, muscles, nerves, and skin, but also transformation of pathological states such as osteomyelitis, fibrous dysplasia and pseudoarthrosis into normal bone. This technique requires strict adherence to certain surgical, anatomic, and mechanical principles. Surgically, it is necessary to maintain the periosteum, endosteum, and bone marrow with its blood supply, via transection of only the bony cortices. It is important to understand that this technique is very difficult to master, has a long learning curve, and is technically demanding. Because of the complexity of the different methods of assembly, no surgical technique brochure could possibly explain all of the variations of usage. a. Components: The Ilizarov external fixator is a modular apparatus consisting of parts that can be assembled in an unlimited number of configurations. With one or more rings affixed to each bone fragment, the frame can be used to compress, distract, angulate, or rotate bone segments with respect to each other. In this manner, deformities can be overcome while at the same time the limb is made stable enough to permit weightbearing and functional use. i. Transfixation wires: The mainstay of the Ilizarov system, consisting of 1.5 and 1.8mm the latter utilized for lower extremity adult pathology/deformity. NOTE* After a transfixation wire is inserted, one end of the wire is secured to the frame, the other end of the wire is tensioned before final fixation ii. Olive wires: A Kirschner wire with a small bead on it used to abut against cortical bone to stabilize or pull bone segments. Can serve several functions: can act as a stabilizing element, can act as a fulcrum or rotation point around which a deformity correction occurs, or can act as a traction element to pull bone in a desired direction iii. Rings: Can be either half-rings, full rings, 5/8 circle rings and Omega rings (for the shoulder). The half-rings can be bolted together (sizes from 80-240 mm in diameter) and then the wires are secured to them. One ring can be bolted to another ring via threaded rods tightened by a nut on the end. iv. Arches: Arches are large, heavy, curved plates used most commonly for fixation of the upper femur, and come is three diameters, 90, 110, and 140mm v. Nuts and bolts: Among other things, these secure the half-rings together. The bolts come in 10, 16, and 30mm lengths and the head of the bolt fits a 10mm metric wrench

vi. Fixation bolts: Are used to secure wires to the rings and are either cannulated, grooved, or cannulated with a tapped head. A cannulated bolt is used when a wire passes across the center if a hole at the point of fixation, a grooved bolt is used whenever a wire is tangential to a fixation hole, and a cannulated bolt with a tapped head is used when wire fixation is needed in a crowded situation where a connecting rod, socket, plate, or other hardware must be attached to the same ring position as a wire. vii. Washers: There are plain washers, grooved washers, and paired spheric washers. A grooved washer can serve for wire fixation anywhere, and if a wire is far off a ring's plane for fixation, enough washers can be stacked on a long bolt to secure the wire. A pair of grooved washers surrounded by a pair of nuts on a threaded rod can also secure a wire. A pair of spheric washers are useful in compensating for angulation between a ring and a threaded rod and allow about 7.5° of anglation in a hole viii. Threaded rods: Are the basic connectors between the support rings and come in lengths from 30 to 400 mm ix. Telescopic Tubes: Are used to prevent frame deformity when there is a long distance between the support rings x. Ratchet telescopic rods: Incorporates a ratchet mechanism to simplify distraction, which the patient can rotate to extend the rod 0.25 mm, and is calibrated so that the surgeon can assess the elongation or shortening xi. Posts: Come with one, two, three, or four holes, can have many functions. Two being to act as a fixation point for wires off the plane of a ring, to act as a swivel for ring rotation as well as points for pushing or pulling a ring xii. Buckles: Were Ilizarov's original fixation device xiii. Plates: Can function as wire attachment points, as a stable supporting element in push configurations designed simultaneously to angulate and to translate ring clusters with respect to each other, or to simply enlarge the diameter of, a small ring
Straight plates
Paddles
Twisted Plates xiv. Sockets: They function not only as interconnectors between threaded rods, but also as spacers to raise a point of attachment off the plane of a ring or plate xv. Bushings: Due to its configuration, will slide along any rod in a fixation frame. The free movement of such an assembly is used to build a mechanism for counterrottation of rings or traction on threaded rods or as a slide assembly to move componants along threaded rods xvi. Wire tensioners: Are either spring-loaded or threaded. Are used to, apply tension to the transfixation wires b. Ring selection: Allow 2-3 cm of clearance between the inner edges of rings and the “skin” c. Wire and pin placement: The pins and wires must be placed in certain locations at specific anatomical levels. The following diagrams show proper pin placement at different levels

d. Wire tensioning: To achieve enough stiffness in the wires to maintain stability and overcome intrinsic tissue resistance, the wires must be stretched like a tightrope. The multiplanar fixation with tensioned wires provides an optimal environment for bone formation. The fixation resists bending and torsion, thus minimizing shear forces at the bone-healing interface. The use of a Richards dynamometric wire tensioner is preferred to accurately tension each wire. A calibration scale is noted on this instrument from 50 to 130 kg of force. A tension of 70-110 kg is utilized with a 1.5 mm diameter wire and 70-130 for a 1.8 mm wire e. Hinge placement: Complex deformities consist of more than one of the following deformities: length, rotation, angulation, and translation. The actual sequence of correction of complex deformities can vary, however, in general, length must be achieved prior to offset and translation, and rotation should be accomplished last. Once the plane of deformity and the maximum angulation and translation have been determined, determination of hinge placement is necessary. This is worked out by geometry (see Figs 1-5)

f. Ilizarov corticotomy: The method of limb lengthening or bone lengthening consists of external distraction of a surgically created osteotomy or corticotomy via a percutaneous, subperiosteal incision, perserving periosteum and endosteum. After a latency period after a corticotomy anywhere from 7-14 days, distraction of the bone can begin, anywhere from .5 to 1.0 mm per day. This is called distraction osteogenesis g. Techniques in fracture reduction: Several factors are taken into consideration when a frame is constructed: size and number of fracture fragments, plane of the fracture lines, condition of the soft tissues, and proximity of the fracture fragment of the joint and intra-articular involvement. As a general rule one should achieve 2 levels of fixation in each major fracture fragment (2 rings applied to any bone segment). The diatance from a fracture line to a ring is usually 3-4 cm, giving enough room for compression or distraction, or angulation and translation. The angle formed by 2 wires crossing a fracture fragment should approach 900 for maximum stability. Intra-articular fractures should be reduced prior to diaphyseal fractures h. Illustration of techniques for the foot and ankle:

Malleolar fractures

Standard assembly for a transsyndesmotic fibular fracture of the posterolateral rim with medial lesion or in presence of Volkmann fragment: a) Ilizarov technique (Malzev-Kirienko); b) Hybrid Advanced technique with internal osteosynthesis (1 = open reduction, 2 = centralization, 3 = fixation) (Catagni).

Catagni, M.A., Malzev, V., Kirienko, A., Advances In Ilizarov Apparatus Assembly, A. Bianchi Maiocchi (ED), Medicalplastic srl, Milan, 1994

The universal joint allows movement of the ankle during the postoperative period.

Standard assembly for a malleolar fracture (Malzev-Kirienko).

Lateral view of the assembly for reduction and compression of the medial malleolus.

Catagni, M.A., Malzev, V., Kirienko, A., Advances In IlIzarov Apparatus Assembly, A. Bianchi MaIocchi (ED), Medicalplastic srl, Milan, 1994

Distal articular (tibial plafond fractures)

Standard configuration for a typical comminuted fracture of the tibial plafond (Malzev-Kirienko).

Catagni, M.A., Malzev, V., Kirlenko, A., Advances In IlIzarov Apparatus Assembly, A. Bianchi MaIocchi (ED), Medicalplastic srl, Milan, 1994

CatagnI, M.A., Malzev, V., Kirlenko, A., Advances in Ilizarov Apparatus Assembly, A. Bianchi Maiocchi (ED), Medicalplastic srl, Milan, 1994

Equinus foot

Apparatus assembly after correction of the equinus foot;

a) Standard apparatus assembly for correction of an equinus foot deformity. b) Diagram of wire insertion at trascalcaneal and transmetatarsal sites. A fourth wire in the tarsus may be placed according to severity of the case (Malzev-Kirienko). Catagni, M.A., Malzev, V., KIrienko, A., Advances In IlIzarov Apparatus Assembly, A. Bianchi Maiocchi (ED), Medicalplastic srl, Milan, 1994

Small Bone External Fixation of the Foot 1. Orthofix modulsystem (Pennig minifixator): Allows for secure fragment fixation, with minimum of invasive surgery a. Can be applied under fluorscopy, using minimally invasive threaded rods b. Allows for 2 pairs of wires to be placed as little as 6 mm apart c. Fracture reduction is possible on all planes d. Allows for lengthening, treatment of non-unions, soft tissue correction, and any technique for compression or distraction

Indications for use:






Fractures Aseptic and infected non-unions Corrective osteotomies Lengthening Replantation

PROXIMAL FRACTURES OF THE FIRST METACARPAL ASEPTIC AND INFECTED NON-UNIONS CORRECTIVE OSTEOTOMIES LENGTHENING

Chapter 17: Nail Disorders & Surgery Nail Entities Nail Anatomy Surgical Nail Procedures

NAIL DISORDERS AND SURGERY Nails are excellent indicators of systemic disease and may provide invaluable diagnostic information. The nails are equally sensitive to environmental and physical stimuli and may provide vital clues that indicate toxic exposure and traumatic insult. Owing to the great cosmetic value of the nail, any physical derangement to the structure can bring the patient to your office. You should check for the following nail presentations: discoloration, anonychia, brittleness, hypertrophy, koilonychia, onycholysis, pitting, pterygium, onychomadesis, splitting, striations, nail thinning, ridging, change in nail consistency, change in nail configuration, and nail clubbing.

Nail Entities 1. Anonychia: Is the complete absence of one or usually more than one nail. This condition is a rare congenital anomaly. i. Caused by ischemia, frostbite, toxic and infectious states, Raynaud's disease, Darier's disease, lichen planus, subungual neoplasm, fungal infections, psoriasis, and injuries. 2. Paronychia: Is an infection usually accompanying onychocryptosis. Staphlococcus is most common organism. Candida is a common pathogen also. Cultures for bacteria and for fungi are indicated. 3. Beau's Lines: Transverse ridges in the nail plate, 0.1-0.5 mm wide by 0.1 mm deep appear in the lunula and progress forward. Beau's lines are a sudden arrest of function of the nail matrix. The width of the Beau's lines are directly related to the duration of the illness. i. Caused by typhus, diptheria, syphilis, malaria, leprosy, influenza, scarlet fever, vascular diseases, diabetes mellitus, hyperthyroidism, ACTH therapy, psroriasis, diffuse alopecia, and exfoliative dermatitis. 4. Clubbed Digits: A characteristic bulbous deformation of the terminal phalanges topped by marked convexity of nails, with the nail becoming hard, lustrous and thick. As the disease progresses, advanced clubbing and angulation of the nail results in Lovibond's angle (> 160 angulation of the nail). i. May be subclassified as hippocratic nails, pulmonary hypertrophic osteoarthropathy, pachydermoperiostosis, or other diseases ii. Can be caused by: congenital heart defects, cirrhosis of the liver, chronic diarrhea, SBE, neoplasms of the lung and emphysema. 80% of clubbing is seen in conjunction with respiratory ailments, but it may be seen in many nonpulmonary acquired and hereditary conditions. 5. Darier-White Disease: Similar to alopecia areata. This condition will cause changes such as red and white longitudinal streaks that run the length of the nail. 6. Eczematous Conditions: Many types of eczematous dermatitis such as atopic

and contact dermatitis frequently affect the nail folds causing damage to the nail matrix. As a result, many changes 'to the nail plate occur, such as Beau's lines, onychorrhexis, subungual hyperkeratosis, and onycholysis. Nail color may change to yellow, green, grey, or black. 7. Onychomycosis: Fungal infections are common, usually caused by dermatophytes. In the cases of monilia and yeast it is reported that onycholysis will develop without destruction of the nail plate. Other diseases mimic this condition, such as psoriasis. i. Distal and lateral onychomycosis: Most common type, caused by T. rubrum, T. mentogrophytes, and E. Floccosum. ii. Proximal subungual onychomycosis: caused by T. rubrum, T. megnini, T. schoenleinii, and T. tonsurans. iii. White superficial onychomycosis: usually T. mentagrophytes and mold fungi iv. Diagnosis by KOH prep and growth on Sabouraud's agar 8. Glomus Tumor: Neoplasia of the arteriovenous shunts (Suquet-Hoyer canals) in the nail beds that constitutes the glomus bodies leads to a purplish tumor that causes extensive pain. The nail bed will appear as a blue-red distortion and the nail plate can have variable distortions. The lesion may be tiny and colorless. 9. Green Nails: Usually caused by a local Pseudomonas infection or Candida albicans. Pseudomonas produces a green pigment called pyocyanin. 10. Keratoacanthoma: This may develop in the nail beds with serious consequences to the nail and subungual structures. The lesion appears suddenly, ulcerated, and both clinically and histologically resembles squamous carcinoma. Underlying bone may be involved. 11. Koilonychia: Means spoon shaped nails and describes a characteristic deformity in the form of a concave shape. i. Occurs with hypochromic anemia, Plummer-Vinson syndrome, thyrotoxicosis, Raynaud's disease, gastrointestinal disorders, nail bed tumors, and syphilis. 12. Leukonychia: A transverse spot or striation porcelain white in color of the nail plate. There are 5 types: i. Leukonychia punctuate (pinhead spot): associated with psoriasis, dyshidrosis, typhus, scarlet fever, measles, arsenic and lead poisoning and microtraumas. ii. Leukonychia striata (transverse): looks like Mee's lines and found with scleroderma. iii. Leukonychia totalis (entire nail): Seen in leprosy, hypochromic anemia, arsenical poisoning, cachexia, and Bart-Pumphrey Syndrome. iv. Partial Leukonychia (nail is all-white but has a distal pink band) As found in Hodgkin's disease, chilblains, metastatic Ca, and leprosy.

v. Longitudinal Leukonychia (longitudinal white stripes): Found in Darier's disease and arsenic poisoning. 13. Lichen Planus: Will result in atrophy of the nail plate and pterygium formation, which is considered pathognomonic for the disease. 14. Malignant Melanoma: Acral lentiginous melanoma is the most dreadful of malignancies found under or around the nails. When the melanotic whitlow is present, there is an elevation of the nail that can be mistaken for glomus tumor, subungual exostosis, or profuse granulation (see chapter 13, Dermatology: Malignant tumors) 15. Mee's Lines: Is an eponym for horizontal striations that appear in the nails as a consequence of arsenic and thallium poisoning. 16. Onychauxis: This is the thickened, elongated, raised irregular nail. The color can be changed from white to a mixture of green, yellow, brown, or black, all of which may obliterate the lunula. i. Can be caused by trauma, fungal infection, nutritional disturbances, circulatory disorders, acute rheumatic fever, secondary syphilis, TB, psoriasis, ichthyosis, eczema, hyperuricemia, RA, venous stasis, hyperglycemia, hyperthyroidism, leprosy, peripheral neuritis, tabes dorsalis, and scleroderma. 17. Onychogryphosis: Is an exaggeration of onychauctic condition. 18. Onychoheterotopia: Means ectopic or abnormal position of the nails. 19. Onychomalacia: Refers to softness of the nails and is synonymous with hapalonychia. 20. Onycholysis: Detachment of the nail bed from the overlying plate creates a space between nail plate and nail bed in which keratin forms. This occurs in numerous conditions: i. Due to trauma, contact dermatitis due to nail polish, cement and topical drugs, fungal infection, Pseudomonas infection, psoriasis, hyperthyroidism, pregnancy, iron deficiency anemia, lichen planus, and many others. 21. Onychomadesis: The shedding of nails from the proximal to the distal free edge. The pathology in this condition involves lesions to the matrix and the hyponychium. i. Due to epilepsy, peripheral neuritis, peripheral thrombosis, embolic occlusions, diabetes mellitus, syphilis, hemiplegia, syringomyelia, and many others. 22. Onychorrhexis: Means the breakage of nails, the nail becoming thin and fragile with exaggerated dermal epidermal subungual sulci. i. Due to hypochromic anemia, hypocalcemia, lichen planus, RA, radiation, arsenic and lead poisoning, leprosy, and syphilis.

23. Onychophagia: Means nail biting. 24. Onychoschizia: The nail becomes very fragile, and as a result, distal splitting of the nail occurs. There are two or more laminations overlying each other. The nail appears multilayered. i. Due to acromegaly, chronic eczema, metabolic acidosis, peripheral nerve lesions, trauma, infectious diseases, hyperthyroidism, and hypochromic anemia. 25. Pterygium Ungium: Overgrowth of the eponychium so that the lunula and much more of the nail plate is covered by a wing (pterygium) of soft tissue. i. Due to scleroderma, Raynaud's disease, vasospastic disorders, leprosy, dermatomyositis and peripheral neuritis. 26. Squamous Cell Carcinoma: This occurs under nail plates usually as a result of a progression from squamous cell Ca in situ (Bowen's disease). It must be differentiated from keratoacanthoma. (see Dermatology section) 27. Splinter Hemorrhages: These are caused by capillary fragility in the longitudinal vessels of the nail bed. i. Due to: scurvy, SBE, CHF, vasculitis, tetanus, hemophilia, and hypoparathyroidism 28. Periungual Fibroma: May be either acquired or congenital. Congenital fibromas are often associated with tuberous sclerosis, a disorder characterized by periungual fibromas, mental retardation, seizures, and adenoma sebaceum. (see Dermatology section) NOTE* Changes in nail color are markers for disease of blood, endocrine system, cardiovascular and peripheral vascular systems, and toxicity of drugs, chemicals or metals: a. Yellow nails: may suggest Addison's disease or diabetes mellitus b. Blue nails: may be a sign of cyanosis or heavy metal poisoning c Green nails: Pseudomonas infection d. Black-brown discoloration: may be normal pigmentation, Peutz Jaegher disease (also have brown macules on the palms and soles), Addison's disease, junctional nevus, or melanoma e. White nails: may be hereditary, a sign of anemia, fungal infection, BartPumphrey Syndrome f. White striae: arsenic poisoning or drug toxicity g. White spots: injury to the nail plate, psoriasis h. Alternating white lines with pink nail (Muercke's lines): may suggest anemia, chronic liver disease, nephrotic syndrome, or Darier- White disease i. Reddish nails (or combination of red/white/brown): may be signs of localized neoplastic disease

Nail Anatomy 1. The matrix is a stratified epithelium that produces hard keratin. Proximal matrix forms the superior nail and the distal matrix forms the lower nail. 2. Hyponychium is an epithelial layer of the nail bed and really does not produce much nail plate keratin. It does help, however, in subungual debris production. 3. Predominantly nail develops from the matrix, but the proximal nail fold, lateral grooves, bed, and hyponychium can all be onychogenic. 4. The nail plate can be separated into 3 zones with predominantly different beginnings. The uppermost layer is generated by the proximal nail fold, the plate by the matrix, and the deepest section of the nail plate is contributed to by the nail folds and bed. 5. The nail matrix is found on the proximal slope of the distal phalanx and extends medial and lateral to the phalanx. The germinal matrix extends laterally as far as the width of the nail plate just distal to the lunula and with the same curvature. Proximally it extends to 1 1 /2 to 2 1 /2 times the length of the visible lunula. 6. The lunula is a white semi-lunar area corresponding to the anterior matrix. 7. The nail bed consists of the hyponychium and corium over the matrix.

Surgical Nail Procedures Nail prob lems t h at dicta te sur gica l interve ntion are abscess , persiste nt pai n, regrowth or spicule development. Chronic nail infections may lead to OM due to the close proximity of the nail and the dorsum of the proximal phalanx. 1. Phenol and Alcohol Chemical Matrixectomy: i. Should always do preoperative CBC/Diff and FBS. ii. This procedure has been done in well controlled diabetics, but should be avoided in patients with PVD. iii. Phenol and lidocaine are teratogenic and should not be used in the pregnant patient. 2. Sodium Hydroxide Matrixectomy: i. Acetic acid used to neutralize ii. Apply 10% NaOH till capillary coagulation iii. Same criteria apply as for Phenol-Alcohol procedure NOTE* The following are cold steel procedures. The indications are: chronically recurring ingrown toenail, failed Phenol-Alcohol procedure, chronic hypertrophic ungual labia, subungual exostosis in combination with dystrophic, hypertrophic or mycotic nail, patient in whom chemical or thermal bum is contraindicated (diabetes?), excision and biopsy of nail/nail bed/matrix tissue, in conjunction with bunion procedures, patients who will not comply with postoperative regimen of Phenol-Alcohol procedures, cosmetic reconstruction of deformity, and surgeon's preference.

3. Frost Procedure: i. For ingrown toenail with "proud flesh" and chronically hypertrophic ungual labia ii. Excise a piece of matrix through an inverse "L" shaped incision iii. Nail and matrix along the problem labia is excised with the second incision iv. Closure is with suture after curettement of the phalanx v. Due to the tissue necrosis that occurs, this procedure requires both primary and secondary wound healing, therefore of little advantage over noncold steel procedures

Figure 1: Illustration of Frost Procedure Clinics in Podiatric Medicine and Surgery: Nail Disorders, Saunders, April 1989, Volume 6:2, with permission

4. Zadek Procedure: Based on the premise that excision of the nail bed was not necessary in preventing regrowth of the nail, therefore Zadik directed his attention only to the nail matrix. i. The incisions utilized are perhaps this procedures greatest contribution ii. Utilized more for total nail excisions in the lesser digits iii. Not recommended for the difficult onychauxic nail (where nail bed removal may also he necessary)

Figure 2: Illustration of Zadek procedure Clinics In Podiatric Medicine and Surgery: Nail Disorders, Saunders, April 1989, Volume 6:2, with permission

5. Kaplan Procedure: The most well documented toenail surgery in the literature. Unlike the Zadek, the Kaplan stressed the need to remove both the nail matrix and nail bed. i. This procedure is indicated for correction of severely onychauxic,

mycotic, or chronically deformed or ingrown toenails. It is also the procedure of choice when the former are combined with painful or deforming subungual exostosis or osteochondroma. ii. The original procedure describes an "H" incision carried out at two tissue depths. The proximal half of the "H" includes only the nail matrix and stresses the preservation of periosteal tissue. The distal half of the "H" is carried directly down to the distal phalanx and involves stripping of the nail bed and thus exposing the distal phalanx. iii. A modified Kaplan has been described, whereby, the "H" incision is replaced by the Zadek-type incision. This allows for maximum exposure of the nail matrix area.

Figure 3: Kaplan Procedure Clinics In Podiatric Medicine and Surgery: Nail Disorders, Saunders, April 1989, Volume 6:2, with permission

Figure 4: Wound closure for Winograd Procedure Clinics In Podlatric Medicine and Surgery: Nail Disorders, Saunders, April 1989, Volume 6:2, with permission

6. Winograd procedure: Dr. Winograd was the first to describe a linear incision into the posterior nail fold with excision and curettage of the nail matrix tissue. The incision he discribed is the same used today. i. Contrary to popular belief, the most important component of wedge resection is wound closure and not whether the entire matrix is encompassed

within the width of the tissue ellipse. ii. When a modified Winograd is considered, 3 preoperative components must be considered:
must be sure that an adequate amount of soft tissue exists for good wound closure.
the length of the ellipse must be at least 3 times the width
wound closure is by primary intention (preferably) 7. Suppan Procedure: i. Frees the eponychial fold and removes the nail ii. Visualizes the nail matrix proximally iii. Cut the lateral borders and the anterior borders iv. Hold tag and remove the proximal attachment v. Curette down to bone into the lateral cul de sac 8. Complications From Nail Surgery: a. Recurrence b. Excessive drainage c. Excessive bleeding d. Poor technique and excessive tissue destruction e. Infection f. Exuberant granulation tissue g. Insufficient amount removed h. Soft tissue migration upward to the dorsum of the toe

Chapter 18: Neurology Neurologic Pathways Presenting Features Assessment of Clinical Problems Tarsal Tunnel Syndrome Classification of Nerve Injuries Neuromuscular Causes of Cavus Foot Types of Nerve Surgery

NEUROLOGY It is not uncommon for a neurologic illness to affect the feet initially, thereby making patients seek podiatric consultations first. This chapter will help you understand disorders affecting the central and peripheral nervous systems with emphasis on the lower extremity.

Neurological Pathways 1. Cerebral Cortex: Divided into frontal, parietal, temporal, and occipital lobes 2. Descending pathways: Divided into corticospinal (pyramidal) and extrapyramidal 3. Thalamus and hypothalamus 4. Cerebellum 5. Brain Stem 6. Spinal Cord 7. Nerve Roots 8. Peripheral Nerves 9. Neuromuscular Junction and Muscle

Presenting Features 1. Presenting Problems: Can include pain, numbness, tingling, weakness, unsteadiness, and involuntary movements. Neurologic disorders should always be suspected in patients with: a. A foot deformity (i.e. pes cavus) b. Leg or foot weakness c. Difficulty in walking d. Pain or paresthesias in the legs 2. The Physical Examination: i History: with children get a developmental history which includes questions such as: When did the child get head and neck control? (normal at 2 months) When was the child sitting independently? (normal at 6 months) When did the child start to walk? (normal by 9-15 months) Low or normal birth weight? Any problems at birth? ii. Motor System (Muscle tone/strength): Specific examination of muscles includes observation, palpation and strength testing. For muscle tone look for atrophy (loss of muscle bulk), fasciculations (brief, fine irregular twitches), and myotonia (decreased relaxation of muscle following a sustained contraction). Sometimes muscle hypertrophy is abnormal To test muscle strength, the specific muscle must be tested against resistance. It is graded from zero (no movement), 1 (trace movement), 2 (movement with the aid of resistance), 3 (movement against gravity), 4 (movement against resistance supplied by the examiner), and 5 (normal strength).

Abnormalities of Movement Fasciculations- visable twitching movements of muscle bundles. Tremors- involuntary rhythmic tremulous movements. Tics- repetitive twitching of muscles often in the face and upper trunk. Chorea- involuntary movements of the face and extremities that are rapid, jerky, and unpredictable. They occur at rest or during any purposeful movement. Athetosis- involuntary movements of the face, extremities that are slower, more twisting and writhing than chorea. They occur at rest or during any purposeful movement. Myoclonus- involuntary, sudden and rapid unpredictable jerks; faster than chorea. Asterixis- involuntary and brief loss of muscle tone in the outstretched fingers and hands, resulting in nonrhythmic flapping of the fingers or the entire hand. (chronic liver disease) Tardive dyskinesia- choreiform movements affecting primarily the tongue, lips, and face, producing repetitive, involuntary grimacing, protrusion of the tongue, opening and closing of the mouth, and deviations of the jaw. iii. Stance and gait: There are specific gait patterns associated with specific diseases.

Abnormal Gait Patterns Spastic gait- Manifested by internal rotation and adduction of the entire limb, with hip/knee/ankle in marked flexion. Seen with cerebral palsy, familial spastic diplegia, paraplegia, and hemiplegia. Dyskinetic gait- A constant movement abnormality with a high degree of variability from patient to patient and gait cycle to gait cycle. It is characterized by motion involving considerable effort, often with deliberate, almost concentrated step. Seen with cerebral palsy. Huntington's chorea, and dystonia musculorum deformans. Ataxic gait- Characterized by a marked instability during single limb stance with an alternating wide/narrow base during double support. During swing phase the limb will swing widely and cross the midline. Seen with multiple sclerosis, tabes dorsalis, diabetic polyneuropathy, Friedreich's ataxia. Waddling gait- A labored walking, exhibiting difficulty with balance, proximal pelvic instability, leading to a lumbar lordosis. May see an associated equinovarus foot type. Seen with Duchenne muscular dystrophy, limb-girdle muscular dystrophy, Beckers muscular dystrophy, spinal muscular atrophy, and congenital dislocated hips. Steppage gait- Gait exhibits a swing phase drop foot. Seen with CharcotMarie-Tooth, polio, Guillain-Barre syndrome, CVA, paralytic drop foot, and fascioscapulohumeral dystrophy. Vaulting gait- Gait changes include a high cadence, increased lateral trunk movement, scissoring and instability from step to step, suggesting a loss of balance. Seen with myotonic dystrophy. Equinus gait- Gait exhibits a swing phase ankle plantarflexion with no heel contact. Seen with cerebral palsy, Charcot-Marie-Tooth, muscular dystrophy, spinal muscular atrophy, schizophrenia, osseous block of the ankle, and habitual toe walking. Festinating gain- Gait changes include loss of reciprocal arm swing, decreased velocity, shuffling, decreased stride length, and increased cadence. Seen with Parkinson's disease. Trendelenberg gait- Stance phase of each step leads to a contralateral tilt of the pelvis with a deviation of the spine to the affected side. Seen with dislocated hip or weakness of gluteus medius. iv. Deep tendon reflexes (DTR's): Assesses the afferent nerve, the synaptic connections within the spinal cord, the motor nerves, and the descending motor pathways. It is important to note right and left asymmetries and the degree of activity, measured from zero to five (zero= no activity, 1= hypotonia, 2= normal, 3= exaggerated response, 4= multiple contractions, 5= sustained contractions). Hyperreflexia indicates a lesion in the corticospinal thalamic tracts. Hyporeflexia indicates a lesion in the lower motor neurons or an intrinsic muscle weakness. The DTR's tested are the:
Biceps/brachioradialis (C5 and C6)
Triceps (C7 and C8)
Patellar (L2, L3, and L4)
Achilles (S1). v. The plantar response, or the Babinski reflex is the response to striking the

sole (extention of the great toe), and when present represents an upper motor neuron lesion of the pyramidal tract. vi. Rossolimo Sign (reflex): involves flicking the plantar aspects of the toes, distally. Flexion response occurs in pyramidal tract disease. This same response may accompany a Babinski reflex. vi. Rhomberg's sign: assesses balance (cerebellar function) and if abnormal the patient will not be able to stand with feet together and eyes closed. Proprioceptive control is lost. vii. Sensory system testing: *Pain and temperature (lateral spinothalamic tract) testing is done with a pin and an ice cube placed on various dermatomes (See Figure 1). *Vibratory testing (posterior columns) is done with a tuning fork (128 cycles/sec) over a bony prominence or joint. *Joint position (posterior columns) is performed by moving the first m.p. joint into either extension or flexion with the patient's eyes closed. *Light touch (anterior spinothalamic tracts) is performed using a nylon filament over various dermatomes. Lower Extremity Dermatomes (Figure 1) L1 and L2 ennervate the anterior thigh. L4 ennervates the lateral thigh, then crosses the patella to innervate the medial anterior calf and foot (medial side of the hallux). L5 ennervates the lateral anterior leg and central aspect of the foot plantarly and dorsally. S1 ennervates the posterior lateral thigh, leg, and lateral border of the foot plantarly and dorsally. S2 ennervates the posterior medial thigh and leg , and the medial-posterior portion of the heel

3. Neurologic Diagnostic Procedures: a. Lumbar Puncture: Tapping of the lumbar subarachnoid space between L3 and L4 provides important information about intercranial pressure and allows a diagnostic analysis of the CSF (the CSF count is abnormal if more than 5 cells are present). b. CT Scan: Rapid noninvasive imaging for the brain, spinal cord and their bony enclosures. c. MRI: Provides extraordinary resolution in imaging of the neural structures without any known risk to the patient. Helpful in identifying brainstem lesions and other abnormalities. MRI cannot be used to examine patients with pacemakers, or patients who are pregnant, who have metal prostheses, and

who are dependent on respirators. d. Electroencephalography (EEG): Voltage vs. time recordings of electrical currents in the brain. Good for detecting epilepsy and metabolic and structural encephalopathies. e. Electromyography (EMG) and Nerve Conduction Velocities: When weakness is clinically difficult to attribute to either nerve, muscle, or neuromuscular junction, electrical studies can establish topographically which nerves and muscles are affected. In EMG, the recording of electrical properties of muscle is displayed on an oscilloscope during needle insertion. Denervated muscle is recognized by fibrillations and fasciculations on the screen. In nerve conduction studies the time for an impulse to travel along the nerve is termed the conduction velocity. If there is an increase in this conduction velocity, there is damage to the particular nerve involved.

Assessment of Clinical Problems Finding the site of the lesion is extremely useful in diagnosing the cause. Once a possible location(s) have been identified, one can review a checklist of disease processes, such as traumatic, vascular, infectious, metabolic, immunologic, neoplastic, and inherited problems that may be responsible. 1. Seizure Disorders: A seizure is a sudden disturbance of cerebral function due to a paroxysmal neuronal discharge in the brain. a. Epilepsy: implies a chronic condition of recurring seizures. Subdivided into two types i. Generalized: Grand mal and petite mal ii. Partial b. Status epilepticus: recurring seizures, one following another without full recovery from the preceding seizure. c. Etiology: may be metabolic (hypoglycemia), hypocalcemia, phenylketonuria, drug toxicity, drug withdrawal, or a focal abnormality of the brain as with trauma or stroke. d. Time sequence: 1. Prodrome: time preceding the seizure that the patient does not feel well. ii. Aura: A symptom or sign signaling the beginning of the seizure (visual, aural or other sensory change) iii. Postictal period: The period after the seizure while the patient returns to normal. e. Management: During the seizure administer first aid, preventing the patient from biting his tongue and keeping the airway open. If the seizure does not stop within 5 minutes, emergency medical care should be instituted (IV's w/ D5W/ diazepam/phenytoin PRN). Control should be achieved with as few anticonvulsants as possible. 2. Cerebrovascular Disorders: Cerebral vascular problems usually appear dramatically with sudden onset and often result in permanent loss of neurologic function. There are two basic types i. Intracranial hemorrhage: (types) hypertensive, ruptured aneurysm, arteriovenous malformations, traumatic, secondary to brain tumor, and

secondary to hematologic disorders ii. Ischemic stroke: (types) thrombotic and cerebral embolism. The prognosis after stroke is usually dependent upon the blood vessel involved and its perfusion territory. 3. Peripheral Neuropathies: In terms of subjective complaints, peripheral neuropathies are the most common causes of foot and toe dysesthesias (burning foot syndrome). In addition patients complain of extremity weakness, muscle atrophy, or both. In addition to motor function, peripheral nerves are responsible for sensory and autonomic function. a. There are three general forms: i. Segmental demyelination: refers to destruction of the myelin segments with survival of the myelin segments with survival of axons until late in the course of the illness. ii. Axonal degeneration: destruction of the axon. iii. Wallerian degeneration: occurs when the nerve is injured or severed at a focal point, and the distal segment breaks down and is reabsorbed. b. Classification of Neuropathies: Remember the mnemonic "Dang Thrapist" D-Diabetic A-Alcoholic N-Nutritional G-Guillain-Barre

T-Toxic H-Hereditary R-Recurrent A-Amyloidosis P-Porphyria I-Infectious S-Systemic T-Tumor i. Diabetic neuropathy: 2/3 of all diabetics show evidence of peripheral nerve dysfunction (clinically or subclinically), which progresses in the face of poor diabetic control. Patients can present with a mononeuropathy, polyneuropathy and can have sensory impairment, or both. At the earliest stage the patient experiences pain, usually worse at night.
Symmetric Distal Polyneuropathy: loss of sensation (predominantly) and motor weakness in a stocking-glove configuration, that occurs bilaterally. The distal portion of the longest nerves are affected first and the feet affected before the hands. Later muscular atrophy can occur with intrinsic muscle wasting.
Mononeuropathies: both cranial and spinal mononeuropathies can occur which includes femoral mononeuropathy (characterized by pain, motor and sensory loss, and absent knee jerk), peroneal mononeuropathy (characterized by a sudden foot drop), and tarsal/carpal tunnel syndrome.
Autonomic Neuropathies: disturbances may be seen in the cardiovascular

system, bowel, bladder, and sexual function. Symptoms include, diarrhea, incontinence, impotence, decreased sweating, and orthostatic hypotension NOTE* The diagnosis of orthostatic hypotension is made by demonstrating a decrease of approximately 25 mm Hg in systolic or 10 mm Hg in diastolic blood pressure after 2 minutes of upright posture without a compensatory increase in heart rate (treated with fluorocortisone or ephedrine).


Neuroarthropathy: foot ulcers occur secondary to neuropathy, microangiopathy, large vessel atherosclerosis, or combinations of these factors. The Charcot joint seen in the lesser tarsus or tarso-metataral area has an unknown etiology. It is unfortunately seen after revascularization procedures of the extremities. The most common bony deformities are the medial convexity, plantar deformity, dorsal midfoot deformity, and plantarflexed metatarsals. A differential diagnosis includes tabes dorsalis, osteomyelitis, leprous neuropathy, and peripheral nerve injuries. Initial treatment for active arthropathy includes 1-2 weeks of bed rest, nonsteroidal anti inflammatory drugs (?), the use of crutches, and a nonweight-bearing cast or splint until the soft tissue swelling and erythema subsides. Gradual weight-bearing can be resumed once radiographic evidence of an arrest is visualized. Patients with fractures of the lower 1 /3 of the tibia are prone to develop ankle arthropathy. Note* Treatment of diabetic neuropathy: For burning pain and dysesthesia (combination of Elavil h.s../ Prolixin t.i.d or Valium t.i.d, Axain topically), lightning-like pain (Tegretol or Dilantin), carpal/tarsal tunnel syndrome (splints/orthotics), itching (diphenhydramine), and diarrhea (codeine).

4. Infectious Diseases: a. Meningitis: Causes symptoms such as fever, neck stiffness, disorders of consciousness, and seizures. 80-90% of cases of meningitis are caused by one of three organisms, H. influenzae, N. meningitis, and D. pneumoniae. Diagnosis is confirmed by lumbar puncture (CSF is cloudy, pressure elevated, WBC > 1000/mm3, and positive CBS). Treatment is usually penicillin G for N. meningitis and D. pneumoniae, and ampicillin for H. influenzae. Positive Brudzinski and Kernig signs clinically. b. Tuberculosis: Can result in multiple cranial nerve palsies. c. Neurosyphilis: Occurs in 25% of patients with syphilis. Diagnosis is by FTAABS test. Penicillin is the treatment of choice. d. Fungal Infections: Cryptococcus neoformans (most common organism) which can produce a subacute meningitis. e. Acute Viral Infections: Poliomyelitis, starts as a flu-like illness, followed by meningitis, and then flaccid paralysis of the limbs and trunk. Herpes zoster (shingles) has a dermatomal distribution of vesicles and demonstrates segmental weakness and pain, sometimes for years.

5. Movement Disorders: Are generally extrapyramidal a. Parkinson's Disease: Characterized by hypokinesia, tremor, rigidity and disorders of gait and balance. On examination there is a "pill rolling" tremor of the hands. The drugs used to treat this disease either act by decreasing cholinergic activity (trihexyphenidyl) or by increasing dopaminergic activity (Ldopa usually combined with carbidopa). NOTE* Neuroleptics such as chlorpromazine and haloperidol may produce a Parkinson-like syndrome. The syndrome stops with withdrawal of the drug. b. Chorea: A variety of neurologic diseases are associated with chorea such as, childhood rheumatic fever (Sydenham's chorea), systemic disorders hyperthyroidism, hypoparathyroidism, and SLE), drugs (oral contraceptives), pregnancy, and hereditary disorders (Huntington's chorea). i. Huntington's chorea: an inherited disease than begins to manifest itself between the ages of 30-40 with. progression to death within 20 years. Manifested by the combination of chorea and dementia. c. Dystonia: Is a movement disorder likely to be seen first by podiatrists, presenting with a slow sustained contraction of muscle groups, resulting in abnormal postures of the trunk and extremities, and of more rapid, twisting movements. i. Dystonia musculorum deformans: a primary hereditary disorder, presents usually with an equinovarus foot. d. Tremor: Essential tremor is a benign disorder that frequently accompanies other neurologic conditions. 6. Tumors: Symptoms depend upon the location of the lesion. 7. Demyelinating and Degenerative Diseases: a. Multiple Sclerosis: characterized by a remitting and exacerbating course of multiple neurologic symptoms, including blindness, diplopia, ataxia, nystagmus, spastic weakness, dysesthesia, and difficulty with bladder and bowel function. Electroimmunodiffusion reveals migration of gamma G immunoglobulin on discrete bands. There is no specific treatment. Corticosteroids can shorten the span of an acute attack. Speech is often explosive. b. Amyotrophic Lateral Sclerosis: a group of diseases characterized by progressive weakness, atrophy, spasticity, hyperreflexia, and fasciculations occurring in a widespread distribution. There is a wide variation in symptoms, with some patients showing more atrophy and some showing more spasticity. Some patients have only cranial nerve involvement. There is no specific therapy. There is an inherited pattern. c. Friedreich's Ataxia: An autosomal-recessive disorder with cerebellar degeneration. Characteristics include gait changes, decreased position and vibratory sense in the legs, absent DTR's, nystagmus, kyphoscoliosis, pes

cavus, and hypertrophic cardiomyopathy. NOTE* Pes cavus is the major foot type associated with neurologic illness. Patients with pes cavus can be divided into four groups: 1. Patients with hereditofamilial disease: Friedreich's ataxia and CharcotMarieTooth disease. 2. Those who have isolated pes cavus but whose family members have one of the aforementioned hereditofamilial neurologic diseases. 3. Those with isolated, or idiopathic, familial pes cavus with no family history of hereditofamilial neurologic disease. 4. Those with familial pes cavus and lymphedema (very rare syndrome). 8. Cerebellar Disorders: These patients present with an imbalance and a difficulty with walking. a. Friedreich's ataxia b. Dandy-Walker deformity c. Arnold-Chiari malformation d. Infections 9. Disorders of Muscles and Nerves: Myopathies are disorders of nerves characterized by progressive weakness. Laboratory tests for diagnosis include measurement of serum muscle enzymes, creatine phosphokinase (CPK), electromyography, nerve conduction studies, and muscle biopsy. a. Muscular Dystrophies: i. Duchenne's muscular dystrophy: An X-linked recessive disorder with a frequent mutation rate, which appears with a slowly progressive proximal weakness beginning in the lower extremities and later involving the upper extremities. It is often associated with early toe walking and causes a waddling gait. The gait changes include decreasing cadences, increasing anterior pelvic tilt, increased hip flexion in swing, decreasing ankle dorsiflexion, and increased shoulder sway. These patients have a progressive muscle atrophy and weakness (there is often pseudohypertrophy of the calf muscles). The serum CPK is markedly elevated in these patients early in the disease and a muscle biopsy establishes a definitive diagnosis. Pathognomonic for this disease is a positive Gower's sign, where the affected child rises from a sitting position on the floor by climbing on his own legs. ii. Becker's muscular dystrophy: Is a more benign form of X-linked muscular dystrophy clinically similar to Duchenne's MD, and is manifested by progressive proximal limb weakness. iii. Facioscapulohumeral dystrophy (Landouzy-Dejerine): A variant of muscular dystrophy with a swing phase drop foot and compensatory increase in hip and knee flexion. This disease gives a "Popeye the sailor" forearm appearance. iv. Limb-girdle muscular dystrophy: Mostly autosomal recessive disorders characterized by progressive proximal weakness. v. Myotonic muscular dystrophy: An autosomal dominant disorder with symptoms that involve a combination of weakness and myotonia (myotonia is a

delayed relaxation of muscle following contraction and is associated with abnormal EMG discharges). vi. Spinal muscular atrophy: An autosomal recessive condition with progressive degeneration of the anterior horn cells. There are three types
Group I: Werdnig-Hoffman disease (most severe, diagnosed in infancy
Group II: intermediate form
Group III: Kugelberg-Welander disease (mildest form). Also called WohlfartKugelberg-Welender disease b. Acquired Myopathies: The following can cause a slow progressive and prominent muscle weakness: i. Endocrine disorders: Hypo/hyperthyroidism ii. Drugs: Corticosteroids, antibiotics, and alcohol. iii. Collagen vascular diseases: Polymyositis, dermatomyositis, scleroderma, RA, and SLE. 10. Perinatal or Gestational CNS Damage Disorders: a. Cerebral Palsy: A nonprogressive brain lesion usually due to a perinatal insult (hypoxia) resulting in a pyramidal tract lesion. There are various types i. Spastic ii. Athetotic iii. Ataxic iv. Rigid b. Familial Spastic Diplegia: Has a strong family history of lower limb spasticity, no perinatal insult, and is progressive. Note* The type of spasticity is based on the anatomical areas involved: Diplegia- all four extremities, primarily lowers Paraplegia- lower extremities only Quadriplegia- all four limbs equally involved Hemiplegia- one side of the body (upper and lower extremities) 11. Disorders of the Spinal Cord and Nerve Roots: a. Spinal Cord Disorders: Localizing the level of a focal lesion of the spinal cord is easier if one remembers the Brown-Sequard syndrome. NOTE* The Brown Sequard syndrome occurs after hemisection of the spinal cord, which results in an ipsilateral spastic paralysis and loss of postural sense, and on the opposite side a loss of pain and temperature sensations i. Spinal cord dysfunction may be acute or chronic
Acute due to: trauma, compression, inflammation, infarction, vascular malformation, and hemorrhage.
Chronic due to: Syringomyelia b. Radiculopathies: i. A fifth lumbar nerve radiculopathy in addition to back pain, often causes radiating pain down the lateral aspect of the leg with numbness or paresthesias of the lateral calf and the dorsum of the foot.

ii. A first sacral nerve radiculopathy characteristically causes radiating pain down the posterior leg with sensory changes on the lateral and plantar aspects of the foot. (absent achilles reflex). 12. Pain Syndromes: a. Reflex Sympathetic Dystrophy Syndrome: Originally termed "causalgia". Other variants include Sudek's atrophy and post-traumatic reflex dystrophy. This syndrome is characterized by disproportionate pain in intensity, duration, location, often from minor or unapparent trauma to an extremity. Clinical diagnosis is difficult due to the vague subjective data and subtle objective signs and symptoms. Early diagnosis is important because early treatment gives the best results. The sympathetic nervous system is always involved and is overactive. Symptoms occur distal to the trauma site. i. Manifestations: (signs and symptoms)
Pain- most prominent characteristic feature Quality of pain: burning, aching or throbbing Severity of pain: mild to excruciating, usually continuous Paroxysmal aggravations: emotional stress, movement, and touch Localized first then spreads Not limited to a dermatome or peripheral nerve distribution
Vasomotor disturbance Vasodilation: warm skin, dry skin, and hypohidrosis Vasoconstriction: cyanosis, cool skin, edema of the part, and hyperhidrosis
Delayed return to function
Trophic changes- are late changes (atrophy, and osteoporosis) Involves the skin, appendages, muscle, bone and joints (RSDS arthropathy) NOTE* The striking feature is that while all signs and symptoms are usually resent, a patient often manifests one out of proportion to all the others. i. There are three grades based upon mode of onset, Intensity, and preponderance of symptoms
Grade 1 (SEVERE): rapid onset, severe burning/knifelike pain, severe vasomotor disturbance, no mobility, atrophy early.
Grade 2 (MODERATE): slow onset, dull/throbbing diffuse pain, aggravated by walking (and relieved with rest and immobilization), edema, atrophy, and osteoporosis.
Grade 3 (MILD): most common type, the border zone between normal response and exaggerated response so is often overlooked, usually seen after surgical procedures ii. There are three stages of the disease divided as per the time frame
Stage 1 (days to weeks): Characterized by Pain Hyperesthesia Hyperalgesia

Localized edema Muscle spasm and tenderness Vasomotor disease No x-ray changes Trophic changes of hair, nails and skin begin In mild cases (GRADE 3) this stage lasts a few weeks and then subsides spontaneously In severe cases (GRADE 1) symptoms become progressively worse
Stage 2 (3-6 months): Gradual decrease of pain Spread of edema, soft to brawny Hair scant, nails brittle/cracked and heavily grooved Muscle wasting X-rays reveal spotty osteoporosis (early), and diffuse osteoporosis (late)
Stage 3 (greater than 6 months): Marked trophic changes which eventually become irreversible Skin is smooth/glassy/drawn/pale or cyanotic with a loss of subcutaneous fat Nail changes Digits are thin and pointed Muscle atrophy, especially interossei Limited ROM of joints Tendon contractions Subluxations Bone atrophy is diffuse and marked NOTE* The goal is to restore functional and anatomical integrity ASAP and break the sympathetic response. NOTE* According to Van Wyngarden and Bleyart in the Journal of Foot Surgery, Volume 31- Number 1, their diagnostic test of choice is a sympathetic and sensory epidural nerve block. If there is a response, then their treatment of choice is frequent sympathetic blocks (bupivacaine+methylprednisolone), in combination with physical therapy, and with oral clonazepam throughout the treatment period. iii. Treatment:
Neurology consult
Psychiatric consult
Anesthesiology consult
Sympathectomy (GRADE 1) -Local blocks (GRADE 2 and 3)
Physical therapy
Systemic steroids (?)
Beta blockers (?)
TENS (?)
Axain + topical lidocaine (?)
Procardia (?)





Analgesics (?) Medication to reduce patients' stress

Innervation of the Lower Extremity Lower extremity innervation is supplied by branches of the sciatic nerve. 1. The sciatic nerve is the interconnection of spinal nerves from L1, L2, L3, L4, L5, S1, S2, and S3 (S2, S3, and S4 make up the pudendal nerve which is localized to the pelvis), passes through the greater sciatic notch, between the greater trochanter of the femur and ischial tuberosity, and rests on the posterior surface of the adductor magnus. In the lower third of the thigh, the sciatic nerve splits into the tibial nerve and common peroneal nerve. 2. The common peroneal splits into the deep peroneal, superficial peroneal and gives off a branch called the lateral sural cutaneous in the popliteal fossa. 3. The lateral sural cutaneous meets with a branch of the tibial nerve (medial sural cutaneous) to form the sural nerve. 4. The deep peroneal nerve (anterior tibial) descends with the vessels anterior to the ankle joint, where it divides into medial and lateral branches. 5. The medial branch of the deep peroneal nerve follows the course of the dorsalis pedis artery and stays lateral to it. This nerve splits in the first interspace where it supplies the adjacent sides of toes 1 and 2. 6. The lateral branch of the deep peroneal nerve passes across the lateral tarsal area where it supplies the extensor digitorum brevis, then splits into three interosseous branches that supply the 2nd, 3rd, and 4th interosseous muscle. 7. The superficial peroneal nerve supplies the peroneal muscles, comes down to the ankle lying between the peroneii and the EDL. It divides into the medial and intermediate (lateral branch) dorsal cutaneous nerves. 8. The medial dorsal cutaneous nerve divides in front of the ankle into two dorsal digital nerves, the medial and lateral dorsal digital nerves. The medial dorsal digital nerve supplies the medial side of the hallux and the lateral dorsal digital branch supplies the adjacent sides of the 2nd and 3rd toes. 9. The intermediate dorsal cutaneous nerve, the smaller branch of the superficial nerve, divides into two dorsal digital branches over the dorsolateral aspect of the foot. The more medial branch supplies the adjacent sides of the 3rd and 4th toes. The lateral branch joins with the terminal branch of the sural nerve to form the lateral dorsal cutaneous nerve. 10. The tibial nerve descends at the back of the thigh to the popliteal fossa, where it passes with the popliteal artery beneath the soleus muscle, and descends to the back of the leg with the posterior tibial vessels. It is located between the FDL medially and the FHL laterally. It enters the lacinate ligament (3rd compartment) and divides into medial and lateral plantar nerves to innervate the sole of the foot. 11. The medial plantar nerve is the larger branch and its branches. It gives off a cutaneous branch to the medial side of the hallux, adjacent sides of the hallux and 2nd toe, the adjacent sides of the 2nd and 3rd toes, and the adjacent sides of the 3rd and 4th toes. The 3rd and 4th common digital nerves communicate in the third interspace and is the site for Morton's neuromas. The muscular attachments are as per Fig. 4. 12. The lateral plantar nerve supplies

the medial and lateral side of the 5th toe and the lateral side of the 4th toe. The muscular attachments are as per Fig. 4.

Tarsal Tunnel Syndrome Is an entrapment or compression neuropathy of the posterior tibial nerve or one of its three branches, the medial and lateral plantar nerves and/or medial calcaneal nerve. 1. Anatomy: Nerve entrapment occurs either in the porta pedis or lacinate ligament a. The flexor retinaculum (lacinate ligament) extends from the medial malleolus to the medial process of the calcaneal tuberosity and the plantar aponeurosis. The deep fibrous septa form four compartments, and converts bony grooves into canals from anterior-medial to posterior lateral: #1 contains tibialis posterior tendon (most superficial), #2 FDL tendon, #3 posterior tibial nerve artery and vein, and #4 FHL tendon. These compartments are unyielding spaces. b. The porta pedis is a canal created by the abductor hallucis muscle belly through which the medial and lateral plantar nerves pass. c. Division of the posterior tibial nerve into its 3 terminal branches may occur proximal to the lacinate ligament, which is most common; within the lacinate ligament, as described in most texts; or distal to the lacinate ligament, which is rare. d. The medial calcaneal nerve is entirely sensory, and innervates the medial and plantar aspect of the heel. It may arise from either the posterior tibial or lateral plantar nerve. e. The medial plantar nerve gives sensory innervation to the plantar aspect of the hallux, second and third toes, medial half of the fourth toe, and the medial half of the plantar aspect of the foot. It gives motor innervation to the abductor hallucis, flexor digitorum brevis, flexor hallucis brevis, and the first lumbrical. f. The lateral plantar nerve gives sensory innervation to the plantar lateral half of the fourth toe, plantar aspect of the fifth toe, and plantar lateral aspect of the foot. Initially it sends motor fibers to the quadratus plantae and abductor digiti quinti before dividing in a superficial and deep branch. Superficial branch supplies motor innervation to the flexor digiti quinti brevis and the dorsal and plantar interossei of the fourth intermetatarsal space. The deep branch supplies the remaining intrinsic muscles of the foot. 2. Pathology: Compression of the nerve initially causes only sensory involvement with possibly partial involvement of motor fibers. Continuation of the irritation, ischemia, and compression may lead to secondary hyperactivity of the autonomic nervous system, manifested by coldness and numbness from the altered sympathetic activity. Eventual structural changes in the nerve result in the development of muscle wasting, paresis, and objective sensory loss. NOTE* Reflexes are unaffected 3. Etiology: In the majority of cases no etiology can be found at the time of surgical decompression. a. Dilated posterior tibial veins: can also cause severe night discomfort. b. Trauma: Fracture, dislocation, sprain, post-traumatic edema and fibrosis. c.

Systemic disease: Gouty arthritis with urate deposits, rheumatoid arthritis, diabetes mellitus, and myxedema. d. Space occupying lesions: Ganglions, neurofibromas, neurilemmomas, and synovial cysts. e. Hypertrophy of abductor hallucis muscle belly. f. Biomechanical: excessive pronation 4. Clinical Symptoms: Symptoms can be either distal to the metatarsal area, or the medial and lateral heel depending on the branch involved. a. Early: i. Intermittent burning pain, numbness and paresthesias over the medial side of the heel, the toes, and the plantar aspect of the foot. b. Late: i. A paresis that will develop into paralysis of the pedal intrinsic muscles. ii. Proximal radiations of pain may develop in the posterior calf. iii. Pain that is proportional to the amount of activity during the day. iv. May develop some sensory loss 5. Diagnosis: Not always easy, as the signs are not always definitive a. History of paresthesias b. History of trauma c. History of systemic disease d. Hoffman-Tinel's sign: A tingling in region of the distribution of the involved nerve with light percussion, results in paresthesias distal to the site of percussion. e. Valleix Phenomena: A nerve trunk tenderness above and below the point of compression, with paresthesias proximal and distal to the point of percussion. f. Turk's test: Application of a venous tourniquet to the lower extremity will elicit positive symptoms on the affected side, by producing a venous occlusion. g. Forced eversion of the foot. h. Positive radiographic evidence of previous injury i. Positive lab studies for any specific disease j. EMG's and nerve conduction studies are only useful for late stage disease. Note* EMG may show fibrillation potentials which indicate denervation of muscle. Nerve conduction studies may reveal an increased distal latency. Placement of nerve conduction study surface electrodes are as follows: 1. Proximal stimulation point: distal aspect of popliteal fossa 2. Distal stimulation point: behind the medial malleolus 3. Recording electrode (for conduction of the medial plantar nerve) through the abductor hallucis ms. belly. 4. Recording electrode (for the lateral plantar nerve) through the abductor digiti quinti muscle belly. 6. Treatment: Conservative a. Local blocks: Posterior tibial nerve blocks with steroids b. Unna boot: can be combined with nerve blocks c. Support hose: for varicosities d. Functional orthoses

7. Treatment: Surgical Decompression (positive EMG's and nerve conduction studies mandate surgical decompression). Involves the complete exploration of the tarsal tunnel with release of the flexor retinaculum and its fibrous bands, and resection and ligation of any dilated veins in the area. The surgical technique is as follows: a. Without a tourniquet, a curvilinear incision is made posterior and inferior to the medial malleolus by 1 cm. b. The subcutaneous tissue is incised and the superficial vessels are ligated as necessary. c. The neurovascular structures superior to the retinaculum are identified, preserved, and retracted (especially the medial calcaneal branch). d. The flexor retinaculum is incised and the posterior tibial nerve or its terminal branches are identified and mobilized. e. The nerve(s) is retracted with a penrose drain. f. The nerve(s) is followed proximally, incising the flexor retinaculum as you go. g. The nerve(s) is followed distally to the point where the medial and lateral plantar nerves pass through the fibrous canals superior to the abductor hallucis ms. belly. h. The abductor hallucis ms. is examined for any abnormality, and any hypertrophy is excised. i. If there are any posterior tibial vein varicosities, they should be ligated. j. The retinaculum is not reapproximated and no deep closure is done. k. The superficial fascia is reapproximated and the skin reapproximated l. Sterile compression dressing and a non-weight-bearing BK cast applied for 3 weeks. 8. Complications: a. Recurrence: due to fibrosis b. Severing the PT artery : if done then tie off and prepare patient for microvascular repair later. c. Severing a nerve d. Tenosynovitis e. Hematoma f. Wound dehiscence

Classification of Nerve Injuries 1. Seddon and Sunderland classified nerve injuries: a. Seddon's classification i. Neuropraxia: (first degree injuries) a conduction disturbance with complete recovery ii. Axonotmesis: (second and third degree injuries) an incomplete division of supportive tissues of the nerve iii. Neurotmesis: (fourth and fifth degree injuries) a complete division of a nerve b. Sunderland's classification i. First degree: only local changes to the myelin ii. Second degree: injury to the axons that is incomplete iii. Third degree: leads to more severe axonal injury with fibrosis

iv. Fourth degree: severe neuronal injury with the axons in complete disarray (no complete neuronal separation) v. Fifth degree: complete transection of the nerve (dismal prognosis)

Neuromuscular Causes of the Cavus Foot The cavus foot is classified according to the level of the CNS that is affected 1. Cerebral Cortex: Hysteria 2. Pyramidal and Extrapyramidal: C.P., athetosis, dystonia musculorum deformans 3. Spinocerebellar Tracts: Friedreich's ataxia, Roussy-Levy syndrome 4. Spinal Cord Level: Polio, myelomeningocele, diastematomyelia, cord tumor 5. Peripheral Nerve or Spinal Nerve Root: C.M.T., polyneuritis-Sotas 6. Muscle: Muscular dystrophy

Types of Nerve Surgery 1. Neurolysis: Frees the nerve from adhesions or scar tissue that obstruct the growth of regenerating axons or block the conduction of nerve impulses. Immature nerve fibers may suffer temporary conduction block with neurolysis. If the entrapped nerve and branches are found in dense scar tissue, the nerve may be rerouted to a more favorable bed which minimizes the risk of subsequent compression a. It is indicated in a complicated first degree injury in which scarring or adhesions have interrupted conduction b. In a second degree injury, the nerve is intact and normal in appearance, but the interfunicular tissue is scarred. Internal neurolysis may be necessary to split the, sheath and release the bundles from the interfunicular scar tissue (difficult) 2. Neurorrhaphy: Nerve repair is justified when conservative care fails and nerve function deteriorates. When it is determined that a traumatized nerve is partially or completely severed neurorrhaphy can be attempted.

The above diagrams A,B, and C show the technique of partial neurorrhaphy. Diagram D shows the exposed nerve with orientation sutures, the ends mobilized, bulbous distal segments removed (E) and epineural sutures inserted circumfrentially (G,H,I) to repair the nerve

Neurons retain for several years the capacity to regenerate a new axon. The regenerative process of the nerve remains intact, and the new axons enter the endoneurial tubes in the stump distal to the trauma. The earlier the reinnervation, the better the prognosis a. If a small nerve is partially or virtually severed, repair of the severed section by partial sutures or resect the damaged segment, mobilize the nerve proximally and distally to gain the added length, and perform an end to end anastomosis b. In a large nerve, if one half is disrupted, partial neurorrhaphy is advisable, and if a neuroma is encountered, resect back to normal tissue and do an endto-end anastomosis c. Whenever a nerve is transected, it retracts approximately 4% of its normal length between excision points 3. Neuroma (Morton's): a. Definition: A neuroma represents hyperplasia of Schwann cells, axonal elements and fibroblasts in an area where proximal elements cannot relocate to their distal pathways b. Histopathology: The term neuroma refers only to nodules that are formed by hyperplasia of axons and Schwann cells. This process is characterized by endoneural and neural edema (early stages); perineural, epineural, and endoneural fibrosis (late stages); and eventually demyelination. It is a reactive lesion, not a tumor. The term 'Morton's Neuroma' refers to a lesion in the third intermetatarsal space only. NOTE* Endoneural edema, fibrosis and demyelination are diagnostic for Morton's neuroma and other types c. Anatomy: lies in the 3rd intermetatarsal space, plantar to the transverse intermetatarsal ligament, where the communicating branch of the lateral plantar nerve joins the communicating branch of the medial plantar nerve d. Signs and symptoms: Burning, radiating, lacinating pain and paresthesia. Can cause calf and heel pain. Palpation can produce pain upon squeezing the intermetatarsal space, and often a "click" is felt upon lateral pressure (Mulder's sign) e. Differential Diagnosis: Metatarsal stress fractures, RA, osteochondritis dissecans (Freiberg's), localized vasculitis, ischemia, tarsal tunnel, nerve root compression syndromes, peripheral neuropathy (especially diabetic neuropathy), and intermetatarsal bursitis f. Etiology: Compression trauma, and stretching of the interdigital nerve, with micro-tears of axons g. Treatment: i. Conservative: Injections, padding, strapping, orthoses, and wider shoes ii. Surgery:
Surgical approach is either dorsal longitudinal, web splitting, plantar longitudinal, and plantar transverse

NOTE* It is important to do the following when doing this procedure a. Achieve meticulous hemostasis b. Identify the digital branches before completing the resection c. Remove the neuroma without damaging the intermetatarsal artery of lumbrical d. Cut the nerve proximal enough to avoid stump neuroma and if possible, bury the cut end in local muscle e. Close the dead space


Other surgical option is decompression of intermetataral neuroma via cutting the transmetatarsal ligament. Can be done open or endoscopically (E.D.I.N., as described by Steven Barret, D.P.M.) h. Complications: The most annoying complication is the formation of a stump or amputation neuroma. The pain perceived is more proximal plantarly on the foot than with the pre-existing neuroma. There is a positive Tinel's sign. This complication does not usually respond to conservative care, and must be surgically resected. The operation should be done under general or spinal anesthesia, with a longitudinal plantar incision. The nerve should be cut back proximally, bathed in steroid, and finally buried in a muscle belly with a nonabsorbable suture. Additionally, nerve caps, and vein grafts have been used successfully. NOTE* Local inflammatory reactions (intermetatarsally) may produce symptoms and signs reminscent of neuroma. These may be chronic, leading to surgical intervention with a clinical impression of neuroma. Histologic studies may reveal vascular fibrofatty tissue with inflammation, but no neuroma

Chapter 19: Pediatrics Evaluation of the Pediatric Patient Pediatric Biomechanics: Normal Values (Newborn to Adult) Congenital Deformities Pediatric Radiology Pediatric Gait Patterns Intoe Gait Pediatric Fractures The Limp in Childhood Juvenile Hallux Valgus Biomechanical Examination of the Child Corrective Casting Techniques in Infants The Toe-Walking Child

PEDIATRICS Evaluation of the Pediatric Patient 1. Examination of the Neonate: a. Apgar score (Dr. Virginia Apgar: 1953): It is based upon observations made at 1 and 5 minutes after birth of the heart rate, respiration, muscle tone, reflex irritability, and skin color (scores of 0-1-2 are given for each). The lower the score the more depressed the infant. Low scores indicate severe acidosis. b. Proportional measurements i. Head circumference (averages 13 inches/slightly larger than the chest) ii. Chest circumference iii. Sitting height (crown rump height roughly equal to the head circumference) c. General postural considerations: depends on the in-utero position i. Cephalic delivery ii. Brow delivery iii. Breech delivery d. Examination of the head and neck i. Check for equal eye movements ii. Head should be held in the midline iii. ROM of the neck tested e. Examination of the upper extremities i. Palpation of the humerus: see if the anterior bulge of the humeral head absent (produces a dislocated shoulder), and check for fracture of humerus. ii. Cleidocranial dysostosis: clavicles absent (this condition is detected later in life due to gait changes from femoral neck deformity). iii. Check ROM shoulders: if limited then possible dislocation iv. Check ROM elbows: if limited possible arthrogryphosis v. Check fingers and nails the absence of which are caused by congenital abnormalities f. Examination of the spine: The infant is placed on his abdomen, and the hand is run over the spine and palpation for scoliosis/kyphosis is performed. i. Congenital scoliosis: is concerned with scoliosis arising in association with congenital vertebral anomalies. Some children with congenital scoliosis show curvature at birth, but many do not. The anomalies and variations in development of the vertebrae may be single or multiple and may be associated with other anomalies, particularly in the ribs, which are frequently combined with spina bifida. ii. Congenital kyphosis: kyphosis at birth is almost always due to congenital anomaly of the vertebral column. iii. Klippel-Feil syndrome: absence of one or more cervical vertebrae, or two or more fused together, with brain stem abnormalities iv. Vertebral agenesis: absence of only the coccygeal segment to absence of all the lumbar and sacral vertebrae. v. Spina bifida: see section Congenital Deformities

g. Examination of the lower extremities i. Gross abnormalities ii. Examination of the hip (dislocation/ femoral rotation/neonatal osteomyelitis) iii. Examination of the knee and leg (dislocation/bowing of tibia/tibial torsion). Bowing of the tibia in the infant is present in achondroplasia. iv. Examination of the foot (metatarsus adductus/calcaneovalgus/ convex pes planus/ talipes equinovarus) h. Examination of CNS (muscle tone/reflexes): Usually, at birth, the infant is limp, but after the first or second cry he develops good muscle tone. i. Shortly after birth, the newborn flexes himself into a position of comfort, the position he occupied in-utero. Motor activity should be observed for symmetry, myoclonic jerks, and convulsive movements. Poor muscle tone in an infant after a few minutes of age is a grave sign. Infants who remain limp longer than a few minutes should be suspected of having anoxia, necrosis, CNS lesions, vascular. collapse, hypoglycemia or mongolism. ii. Some important-reflexes present at birth include:
Blink reflex: which occurs when a bright light is directed to each eye
Rooting reflex: elicited by stroking the angles of the lips with the finger
Normal suck reflex: elicited by placing a sterile nipple in the mouth
Grasp reflex: elicited in the palms and soles by placing a finger at the bases of the fingers or toes
Moro reflex: is very important and is elicited by startling the baby while he is on his back. Normally the infant reacts by first extending his arms, then flexing his arms, clenching his hands, and flexing his knees and hips. The Moro reflex should demonstrate for symmetry and overall vigor. NOTE* Absence of this response in the newborn indicates severe CNS injury or deficiency. Absence of the Moro reflex in one arm indicates a fractured humerus, brachial nerve palsy, or fractured clavicle. Absence of the Moro reflex of one leg indicates lower spinal injury, myelomeningocele, avulsion of the cord, or dislocated hip. A hyperactive Moro reflex indicates tetany, tetanus (not clostridium), or CNS infection. This reflex should disappear by the 5th month. 2. Neurological Examination of the Infant: a. Plantar response i. Either normal or ii. Babinski (should disappear by age 1 year) b. Palmar grasp i. Either normal or ii. Abnormal (should be normal by age 4 months) c. Plantar grasp i. Either normal or ii. Abnormal (should disappear by age 1 year) d. Deep tendon reflexes (hypo or hyperreflexia/absent/symmetrical) i. Patellar

ii. Achilles iii. Biceps/triceps/flexor carpi radialis e. Ankle clonus (absent or present) f. Examination of the anterior fontanelle (should close by age 2 years) i. Bulging indicates excessive cranial pressure ii. Depression indicates dehydration g. Head and neck control (infant should have control by age 2 months) h. Muscle power i. Motor skills of the lower extremities: developmental average landmarks i. Crawls: 3-5 months ii. Creeps: 7-9 months iii. Stands: 9-14 months iv. Cruises: 9-12 months v. Walks: 7-18 months (average is 13 months) 2. Orthopedic examination of the Infant: a. Examination for dislocated hip (discussed under the heading: Congenital Deformities) b. Determination of femoral position (normal=2 x external rotation) c. Frontal plane knee motion d. Transverse plane knee motion e. Determination of malleolar position f. Ankle dorsiflexion/plantarflexion (should be equal) g. Examination of the digits and nails h. Check for spina bifida (check the lower back for any abnormalities) 3. History Taking: a. Pregnancy: i. Maternal trauma ? ii. Any medications? iii. Complications? Hemorrhaging? iv. Delivery: Full-term, premature (<38 weeks- 1500 grams), natural, prolonged, C-section, fetal distress?

Pediatric Biomechanics-Normal Values: Newborn to Adult 1. Chart of normal findings: Part Thigh/Femur/Hip

Birth Position Adult Position Angle of head and neck of femur=150° At age 6 years=125° (angle of Inclination) Externally rotated 60° At age 6 years=0 Femoral torsion (angle declination)=30° At age 6 years=10° Total range of motion=150° Past puberty=100° Knee (Birth) (1&1/2-3yr) (3-6yr) (7-puberty) (puberty-18) (over 18) (over 60) Genu Varum Straight Genu valgum Straight Genu valgum Straight G. valgum Genu Recurvatum=5-10° At age 6 years =0° Externally rotated=30° At age 6 years=0° Frontal plane rotation=5-10° At age 6 years=0-5° Transverse plane rotation=5-15° At age 6 years=0-5° Leg/Tibia Varum(approx. 15°) At age 18 years=0-2° varum Tibial torsion at birth=0° 1 yr=6°, 2-3 yr=10-15°, 5-6 yr=18-23° Malleolar torsion at birth=0° 5-6 yr=13-18° Rearfoot At birth= 10° varus approx. At 6 years=2-5° varus Talocalcaneal angle=30-50° At 6 yrs=25-30° Calcaneal inclination angle=approx. 14° At 6 yrs=20° approx. Talar declination angle=approx. 30° At 6 yrs=21° approx. Calcaneal stance @ 1 yr=5-10° 5 yr=3-8° 8 yr=<2° external rot. After age 18=10V min Dorsiflexion=45° approx. Forefoot Varus 10-15° At age 6=0-2° varus Metatarsus adductus=15-35° Adult=15-22°

Congenital Deformities 1. Dislocated Hip: At birth there may be no clinical sign of dysplasia of the hip, so periodic examinations during the first year are therefore necessary. No clinical sign is diagnostic by itself. This can present with an older child that limps. a. Girls are more susceptible than boys b. Unilateral cases are more common than bilateral, with infants born by breech more at risk. c. Diagnostic tests: i. Ortolani's sign: with adduction of the thighs, a click when the femoral head is either made to enter the acetabulum or emerge from it, or telescoping of the flexed and adducted thigh on the pelvis. ii. Barlow's sign: like Ortolani's sign, except using abduction. iii. Anchor sign: The infant should be examined while on his abdomen and a difference in gluteal folds of the two thighs is checked. A difference in the number of folds can indicate a dislocated hip (not accurate). iv. Galezzi's sign: while the hips are flexed and the knees flexed while the baby is on his back, a dislocated hip results in a lower knee position on the affected side. v. Abduction test: while the infant is on his back, flex the knees and then bring them down to the table in the flexed position. A dislocated hip will have limitation of abduction on the affected side. d. Radiological examination: The value of radiography of the hip of young babies is limited by 3 important factors: that only AP views of the pelvis

can be taken; that much of the hip joint is cartilaginous; and that excessive radiation should be avoided. NOTE* Two AP views should be taken: one with the lower limbs lying together and a second with the hips medially rotated and abducted by 45 degrees. i. Acetabular index: the angle formed by a line touching the inferior margin of the ilium and Hilgenreiner's line. Greater than a 30 degree angle is indicative of a dislocated hip (only useful in a unilateral dislocations). ii. Hilgenreiner's horizontal reference line: across the upper edges of the ischiopubic joint. In the normal child, the metaphysis should lie well below this line, and the epiphysis should only just reach to this line iii. Perkin's vertical reference line: a perpendicular line dropped through the anterior inferior iliac spine at right angles to Hilgenreiner's line. Normally, the femoral epiphysis and the beak-like medial side of the epiphysis on its inner side. iv. Shenton's line: lies along the upper margin of the obdurator foramen and continues outward and downward along the under surface of the femoral neck and the medial aspect of the shaft of the femur. This forms an even curve in the normal baby, but is interrupted in the dislocated hip. v. Simon's line: from the lateral margin of the ilium to the upper and outer edge of the acetabulum, and then continues downwards and outwards along the upper margin of the femoral neck. This forms an even curve in the normal baby, but is interrupted in the dislocated hip. NOTE* Shenton's line and Simon's line can be identified even before the femoral epiphysis is present. When the epiphysis has appeared, then other information can be obtained by drawing Hilgenreiner's line and Perkin's line. vi. Von Rosen's Sign: an AP radiograph is taken with the hips extended and the thighs abducted 45 degrees and medially rotated. A line drawn along the axis of the shaft of the femur running close to the anterior superior iliac spine and crossing the center of the spinal column above the lumbosacral junction constitutes a positive sign for dislocated hip. e. Trendelenberg Gait: seen with bilateral dislocated hips f. There are three forms of congenital hip: i. Acetabulum dysplasia ii. Neuromuscular problems iii. Capsular laxity

Measurements from the above diagram for detection of congenital hip: Keats TE, Lusted LB: Atlas of Roentgenographic Measurements, Yearbook Medical Publishers, Chicago, 1985, with permission

1= Hilgenreiner's line, Y line, or symphyseal line, drawn horizontally through the cotyloid notches of the acetabula 2 & 3= Distances from the apex of the femoral head to Hilgenreiner's line (1), normally these distances are equal 4= Shenton's line. Follows the upper arched contour of the obdurator foramen, thus marking the lower margin of the pubic bone, and is continued as a regularly curved line Into the lower boarder of the femoral neck 5= Break in the continuity of Shenton's line, indicating a dislocation or fracture 6= Fusion of the ischiopubic syndrosis, may be delayed with a dislocation 7= The angle of the acetabulum. If this angle is more than 300 in the newborn and 25° in the one year old it Is said that there is a "steep acetabular roof" and indicative of a dislocation (should decrease to 20° by age 2) 8= The diaphyseal interval, the distance between the diaphysis of the femur and Hilgenreiner's line. This distance should be less than 6 cm 9= If in the newborn the distance of the pivotal point (point of intersection of line 8 and Hilgenreiner's line) from the tip of the acetabular angle Is more than 16 mm, subluxation must be suspected 10= This is the horizontal distance between the vertical line of Ombredanne (Perkin's line) and line 8. This distance is normally less than one-half the epiphyseal width (not illustrated) 11= The vertical line of Ombredanne (Perkin's line) which intersects the upper jutting edge of the acetabular roof and is perpendicular to Hilgenreiner's line. The center of ossification of the normal femoral head lies below the horizontal line and medial to the vertical line. In cases of dislocation this center will be above and lateral respectively 12= The parallelogram of Kopitz. In cases of dislocation a rhomboid will be observed, and the head of the femur will have an eccentric position 13= The guide line of the Y symphysis down from the center of the acetabulum to the center of the head 14= The axis of the neck of the femur 15= The angle between 13 and 14 is normally 120°-125°

2. Spina Bifida: a. Spina bifida occurs in about 1 out of every 1000 live births, the common problem with this deformity is neuropathy (sensory deficit) b. Minor degrees of spina bifida affecting the 5th lumbar vertebrae are insignificant and pose no problems. c. Spina bifida can be grouped into three clinical entities: i. Simple meningocele: which may be present anywhere in the spine, however, most common in the lumbosacral/sacral region, and is caused by a failure of fusion of the vertebral arches with cystic degeneration of the meninges. It presents itself with a swelling in the back covered by skin or a thin membrane. It is flaccid and capable of being transilluminated. The swelling consists of herniation of the dura and arachnoid filled with cerebral spinal fluid. The lower limbs show no deformity or any abnormal reflexes. ii. Open myelomeningocele: most commonly seen in the lumbar/lumbosacral spine. Patients seen at one day old present with an oval area of red glistening tissue at the center of the lesion constituting the dysplastic portion of the spinal cord. The skin is often thin or shows pigmentation in the region adjoining its junction with the membranous area. In 50% of the children born with this there may be one or more abnormalities depending upon the cord level: adduction/lateral rotation of the hip, fixed or limited flexion of the knee or fixed recurvatum, equinus, equinovarus, calcaneus, calcaneovalgus, equinovalgus, vertical talus, and clawtoes. The deformity is always bilateral and symmetrical iii. Closed myelomeningocele and spina bifida occulta: presents with a lipomatous or cystic swelling, abnormal pigmentation, hair, and formation of a dermal sinus. The vertebral arches are unfused, but there is no gross distention of the meninges. This generally occurs at L5 or S1. 3. Congenital Calcaneovalgus: This is the most frequently encountered congenital podiatric deformity. It is the prime cause of the flexible flatfoot deformity. a. It can be unilateral or bilateral, but is usually bilateral, one side being more severe than the other. b. Etiology: i. Abnormal intrauterine position ii. Excessive internal limb rotation in fetal life c. Physical findings: i. The dorsal surface of the foot is in contact with the anterior surface of the lower leg. ii. Redundant skin folds in the lateral malleolar area and tight skin at the anterior ankle. d. Clinical findings: i. The foot lies in acute extention and slight valgus. ii. Forefoot varus iii. Rearfoot valgus iv. Tendo achilles is tight v. Plantarflexion restricted/ dorsiflexion greater than 15 degrees vi. Prominent talar head (plantarmedial prominence) e. Pathology:

i. Talocalcaneal ligaments are relaxed or lacking ii. The navicular is laterally displaced to the talus iii. The distal aspect of the calcaneus is laterally displaced iv. External tibial torsion co-exists in majority of cases NOTE* According to Ganley, in infants, cartilage is stronger than bone and therefore osseous structures do not cause the deformity but rather adapt to the deforming forces. f. Radiological changes: (Lateral View) i. Increased talar declination angle ii. Plantarflexed talus iii. The talar head overlaps the distal superior calcaneal surface iv. The bisection of the talus falls below the cuboid ossification center (D-P View) i. Grossly excessive-talocalcaneal angle g. Treatment: i. Manipulation: the foot is brought down perpendicular to the ankle with the heel in neutral position (5 times per correction, 3 times per day for mild cases) ii. Casting: applying a BK or AK cast, the foot is held in equinus with plantarflexion of the first metatarsal and adduction of the forefoot to align the T-N joint. The rearfoot held in neutral position. Casting weekly for 3-6 months. Following casting, Ganley splints used for 6 months @ 12 hours/day. NOTE* The key to the treatment is gentle, gradual, and persistent correction.

iii. Surgery: reserved when the T-C angle exceeds 30-35 degrees 4. Convex Pes Valgus (Vertical talus/congenital rigid flatfoot): Is a rare condition which presents clinical findings at birth similar to congenital calcaneovalgus, but is very different and more severe. Abnormal radiographic findings consistent with rigid flatfoot will appear with patients at rest and during weightbearing. The range of motion of the subtalar joint is the key clinical finding in the evaluation of this condition. a. Etiology: Talonavicular dislocation where the navicular subluxes over the talus. b. Usually found with other congenital deformities and/or endocrine disturbances. i. Arthrogryposis multiplex congenita ii. Myelomeningocele iii. Cerebral palsy iv. Coarctation of the aorta and high palate v. Congenital dislocation of the hip vi. Clubfoot

vii. Nail-patella syndrome viii. Multiple pterygium syndrome ix. Marfan's syndrome x. Down's syndrome (trisomy 21) xi. Trisomy 13-15, and 18 xii. Neurofibromatosis xiii. Mental retardation c. Clinical Findings: i. A rigid deformity with the heel in neutral/vertical ii. A depression if found anterior to the lateral malleolus iii. A convex plantar aspect (rocker bottom foot) iv. Forefoot is abducted and there is dorsiflexion of the forefoot on the rearfoot. v. Tendoachilles is tight and the anterior muscle group is tight vi. Talar movement is impossible (no supination) vii. Calcaneal equinus d. Pathology: Soft tissue and osseous NOTE* The structures attached to the navicular plantarly will be stretched, while those structures attaching dorsally will be contracted. The tibionavicular, talonavicular, and calcaneofibular ligaments hold the deformity so that the calcaneus cannot be manually inverted. Soft Tissue Pathology: structures contracted, due to dorsiflexion at the midtarsal joint i. Tibionavicular ligament (Deltoid) ii. Talonavicular ligament iii. Anterior ms. group iv. Peroneus brevis/longus v. Triceps surae vi. Calcaneofibular ligament vii. Posterior ankle and subtalar capsule Soft Tissue Pathology: structures stretched i. Spring ligament ii. Tibialis posterior, FDL, and FDB Osseous Pathology: i. Subluxation of the navicular on the talar neck ii. Talus locked in the vertical position iii. Calcaneus in a 20-25° equinus position iv. Talar head subluxed below the navicular v. Talar head has an abnormally flat surface vi. Talar neck is hypoplastic, develops an abnormal facet vii. Talus has an hourglass shape viii. Anterior surface of the calcaneus is deviated laterally ix. Subtalar facets are abnormal due to the abnormal T-C articulation (the anterior facet is absent/middle facet is hypoplastic/posterior facet is malformed x. Calcaneocuboid subluxation (dependent on the type of deformity)

e. Radiographic findings: I. T-C angle increased (usually >45°) ii. Talus perpendicular to the tibial longitudinal axis iii. Equinus calcaneal position iv. Dorsal dislocation of the navicular on the talus v. Lateral forefoot subluxation v. Talocalcaneal overlap vi. Navicular is dorsiflexed and laterally displaced to the talar head (it is usually cartilaginous until age 3 years so its position must be evaluated via position of the talar head and the medial cuneiform f. Treatment: conservative vs. surgical i. Conservative: Serial long-leg casting up to 6 months of age, with the foot in a position of ankle plantarflexion, an inverted heel, forefoot in adduction to reduce the T-N dislocation, and the knee flexed 90°. The key to successful results is lining up the T-N joint. If a proper result occurs, the patient will have an equinovarus foot type which would then have to be corrected. ii. Surgery: Herdon-Hyman and Craig NOTE* Aggressive surgical approach is indicated when the T-N joint is nonreducible 5. Metatarsus Adductus (Metatarsus varus): The latter is the more severe form of this condition. Met. adductus is where the anterior part of the foot deviates medialward and there is a varus angulation at the T-M joints. The heel may be neutral or in valgus and if it is in valgus it is a more severe form., This condition is not usually noticed at birth but about 8 weeks later. The incidence of metatarsus varus has increased 4x in the past 25 years. a. Classification: i. Flexible ii. Rigid iii. Functional dynamic iv. Skew foot b. Etiology: i. Arrested ontogenetic development ii. Uterine pressure iii. Abnormal muscle/tendon insertions of the adductor hallucis/FDB c. Clinical Assessment: i. Degree of inversion/adduction ii. Medical concavity/lateral convexity iii. Associated met primus adductus iv. No rearfoot involvement except with a skew foot v. Use "V" finger test d. Radiographic findings: Angle of met adductus on DP view is normally 15-35° at birth and should decrease to 25°.

NOTE* The metatarsus adductus angle is the angle formed by the intersection of two lines, the bisection of the second metatarsal and the perpendicular of the lesser tarsus. The lesser tarsus is is bisected in the infant using the following technique: 1. A line is drawn from the distal medial talus to the medial base of the 1st metatarsal, and its midpoint marked. 2. A line is drawn from the calcaneus to the base of the 4th metatarsal, and its midpoint marked. 3. A line is drawn connecting the two midpoints from 1 and 2, and this line is bisected. 4. A perpendicular line is drawn at the midpoint of line 3, which is the final reference line that is the bisection of the lesser tarsus. e. Treatment: i. Manipulation ii. Shoe therapy iii. Wheaton Brace (works well in a flexible deformity in child under 1 year old) iv. Serial cast immobilization (cast with the calcaneus in neutral/with an abductory forefoot force) Use 2 sets of casts . v. Orthoses vi. Surgery: Should postpone surgery until after age 2-3 years (HHS: soft tissue; Johnson: cartilaginous; Lepird and Berman 8 Gartland: osseous) 6. Talipes Equinovarus: Clubfoot may be acquired or congenital. At birth, other disturbances such as hip dysplasia/neuromuscular disorders/poliomyelitis/tibial epiphysis abnormality must be ruled out in with patients with clubfoot. a. Incidence: i. 1:1000 births (according to Kite) ii. Increases to 1:35 if a sibling has clubfoot iii. Males to female ratio is 2:1 b. Etiology: i. Arrest of fetal development (Max Bohm: JBJS, 1929) ii. Combination of inheritance and environmental factors (Ruth WyneeDavis: JBJS, 1929) iii. Primary germplasm defect (George Settle: JBJS, 1963) iv. Genetic factors (Palmer) c. Physical findings: i. Medial border concave/lateral border convex ii. Talar head prominent laterally with inversion iii. Palpation of a medially displaced navicular iv. Deep furrowed creases along the medial longitudinal arch area and the posterior ankle. d. Clinical findings: i. Inversion and adduction of the forefoot ii. Inversion of the rearfoot

iii. Talocalcaneal equinus/tibiotalar equinus iv. No dorsiflexion v. Associated with tibial torsion and cavus deformity (with cavus deformity there is also plantarflexion of the forefoot on the rearfoot). e. Types: i. Rigid: usually genetic and very resistant to treatment (seen with small, inverted, plantarflexed calcaneus, and posterior leg atrophy) ii. Flexible: usually due to intrauterine position and usually responds to casting. f. Pathology: i. The major defect is in the talus, with the head and neck medially and plantarly deviated, the superior surface is anterior displaced out of the ankle mortise, and the sinus tarsi is opened as the anterior facet is tilted medially. ii. The T-N and C-C joints face medially and plantarly, with the C-C lying below the T-N joint. iii. Tibia is usually OK, occasionally, tibial torsion involved iv. Soft tissue contractures:
Posterior- ankle capsule, STJ capsule, calcaneofibular ligament, tendoachilles.
Medial- spring ligament, deltoid ligament, ms. TP, FDL, FHL.
Plantar- plantar fascia, abd. hallucis, FHD. g. Radiographic findings: i. DP view reveals S angle of Kite (T-C angle): 0-15° with clubfoot ii. DP view reveals superimposition of talar head and the anterior surface of the calcaneus. iii. DP view reveals ossification center of the navicular is medially displaced iv. Lateral view with dorsiflexion and forced equinus, reveals calcaneal inclination angle of approx. 17° (normal is 45°). v. Lateral view reveals a bisection of talus is above the metatarsals h. Treatment: Conservative vs. surgical i. Serial casting (Kite: JBJS 1963): must be done early and as follows • First, correct the forefoot adduction- Position the forefoot in abduction and push in and up under the calcaneocuboid joint and forcing the forefoot laterally. Abduction is positive and will cause a flatfoot condition • Second, correct the inverted heel- Before the equinus can be corrected these 2 deviations must be treated and corrected first (if not a rockerbottom foot will develop). The cuboid must be brought up to the calcaneus and the navicular must be brought up to the talus. NOTE* Do not attempt to fix the equinus until the foot is mildly flat Third, correct the equinus- By dorsiflexing at the ankle. NOTE* Maintain the casts until a correction is achieved and then follow with a Ganley splint for the same amount of time that casting was utilized

i. Radiographic findings consistent with a failed treatment: i. Forefoot is dorsiflexed on the rearfoot at the midtarsal joint ii. Rocker-bottom deformity iii. Flat-topped talus (can be due to talar head ischemic necrosis from compression) 7. Congenital Deformities of the Forefoot: a. Overlapping lesser toes b. Juvenile hallux valgus: i. Treat with splinting ii. Treat with surgery- (soft tissue/chondrotomy) c. Syndactyly (webbed toes)- usually 2nd and 3rd toe: i. Due to embryonic developmental arrest ii. Associated with Apert's syndrome (acrocephalosyndactyly) iii. Treat with corrective plastic surgery (elective plastic surgery) d. Polydectyly (supernumerary toes): i. Associated with Ellis-van Creveld syndrome (chondroectodermal dysplasia) ii. Treat with surgery: resection of non-functional digit (no muscle/tendon attachments) NOTE* Functional digit articulates with metatarsal head properly and has better blood supply e. Congenital short metatarsals: i. Short 4th metatarsal can be associated with pseudohyperparathyroidism or pseudopseudohyperparathyroidism ii. Treat with metatarsal lengthening procedure f. Ectrodactyly (lobster claw foot): absence of 2 or more metatarsals and their associated phalanges. g. Long toes: Associated with Marfan's syndrome (also seen are visual problems, ligamentous laxity, long fingers, and mitral valve prolapse) h. Edematous feet: Associated with Milroy's disease i. Enlarged or giant toes (macrodactyly): Associated with von Recklinghausen's disease (CT scan of CNS to check for neurofibromas)

Pediatric Radiology 1. Roentgenographic Development of the Foot: a. Important ossification points to remember: i. 1st bone to ossify before birth: calcaneus ii. Last bone to ossify before birth: cuboid iii. 1st bone to ossify after birth: lateral cuneiform iv. Last tarsal bone to ossify after birth: navicular at 3.5 years v. Calcaneal apophysis appears at age 7 years vi. Sesamoids appear at age 12 years b. Ossification at birth: i. Talus ii. Calcaneus

iii. Cuboid (can be absent in the premature baby) iv. Metatarsals v. Proximal phalanges vi. Middle and distal phalanges 2-4 vii. Distal phalanx 1 c. Age 3 months: lateral cuneiform d. Age 4 months: tibial epiphysis e. Age 6 months: cuboid and lateral cuneiform articulate f. Age 7 months: talar neck appears, base of metatarsals widen g. Age 11 months: fibular epiphysis appears h. Age 18 months: phalangeal epiphyses appear i. Age 24 months: medial cuneiform and ossification of epiphysis of metatarsal 1 j. Age 30 months: intermediate cuneiform ossifies k. Age 36 months: ossification of epiphysis of metatarsals 2, 3, and 4 l. Age 3.7 years.: ossification of navicular m. Age 4.2 years: ossification of epiphysis metatarsal 5 n. Age 4.9 years: alignment of tarsal and metatarsal bones NOTE* Boys lag behind girls with regard to skeletal age o. Age 6.7: ossification of calcaneal epiphysis p. Age 12 years: sesamoids appear q. Age 13 years: os trigonum and os vesalianum appear r. Age 14 years: fusion of epiphyses of distal phalanges of toes 2, 3, and 4 s. Age 15 years: epiphyseal fusion of tibia/fibula, metatarsals 2/3/4, and phalanges 1, 3, 4, and hallux. t. Age 17.5 years: epiphyseal fusion complete 2. The Osteochondroses: (also see chapter: The Arthropathies) These are a group of related disorders which effect the primary or secondary centers of ossification. Its etiology probably relates to some type of vascular disturbance to the ossification center, during the time of their greatest developmental activity. a. Osgood-Schlatter's disease (osteochondrosis of the tibial tubercle): i. Clinical appearance: Complaint of pain at the anterior aspect of the knee. Occurs between the ages of 11-15 most commonly in boys who participate in sports. On examination there is enlargement of the tibial tubercle, with a maximum area of tenderness at the insertion of the patellar tendon. ii. Etiology: Tendonitis of the distal portion of the patellar tendon with secondary hypertrophic new bone formation iii. X-ray findings: Soft tissue swelling anterior to the tibial tuberosity (acute stage), irregularity in the ossification center of the proximal tibial tubercle is a normal variation, late stages a prominent/irregular tibial tuberosity with or without a small particle of bone anterior and superior to the tibial tuberosity. iv. Differential diagnosis: Must R/O osteogenic sarcoma v. Treatment: Restriction of excessive physical activities, severe cases

immobilization of the knee. b. Kohler's Disease (osteochondritis of the tarsal navicular): i. Clinical appearance: Affects boys (80%) 3-6 years old. Can be a spontaneous onset (pain and swelling over the navicular) or brought on by injury. A limp (antalgic gait) may be present with the child walking on the lateral side of the foot. ii. Etiology: Abnormalities in ossification of the navicular from compression of the bony nucleus at a critical stage of growth of the navicular. iii. X-ray findings: A disc-like navicular is visualized, with irregular ossification, intermingled plaques and hazy fibrocystic degeneration. There is soft tissue swelling around the bone. iv. Treatment: In mild cases stop strenuous exercises and use rigid orthoses. In severe cases a BK cast in supination for 6-8 weeks. c. Freiberg's Disease (osteochondritis of the second metatarsal): i. Clinical appearance: Usually seen in young active adolescents (after age 13). It is more common in females, and is usually unilateral affecting the 2nd metatarsal head primarily (can affect others). Pain is localized under the affected metatarsal head, with swelling and limitation of motion at the m.p.j. ii. Etiology: Due to a vascular insufficiency from trauma to the epiphyseal area. iii. X-ray findings: Widening of the joint space with effusion and soft tissue swelling in the early stages. Later there is a flattening of the head of the affected metatarsal, a narrowing of the joint space, and subarticular sclerosis. There is never any ankylosis. iv. Treatment: Orthoses to remove pressure from the metatarsal head in mild cases. For severe cases use a BK cast for 4-6 weeks, or if symptoms persist into adult life a metatarsal head resection or total joint replacement. d. Sever's Disease (calcaneal apophysitis): i. Clinical appearance: Seen in children ages 8-14 years. Most common in boys 10-11 with a cavus foot type. Complaints are pain in the heel especially after rigorous activity. Pain is exacerbated by squeezing the medial/lateral epiphyseal margins of the calcaneus. ii. Etiology: Excessive traction on the calcaneal apophysis iii. X-ray findings: Multiple centers of ossification, a moth eaten appearance of bone, and apophyseal sclerosis (all of which also can be seen in a normal apophysis) iv. Treatment: Cessation of rigorous physical activity, stretching of posterior muscles, shock absorbing heel pad, and/or orthoses. If severe then a BK cast.

Pediatric Gait Patterns 1. Parameters of Normal Gait: a. Early independent ambulator (1 year) characteristics: i. Wide base of gait ii. Prolonged hip and knee flexion iii. Arms abducted with elbows extended to increase stability iv. High cadence v. Low velocity vi. Short step length

b. Toddler (1-2 years) characteristics: i. Narrowing base of gait ii. Reciprocal arm swing iii. Increased step length iv. Increasing velocity v. Mild foot drop c. 2 year old characteristics: i. Reduced external rotation during arm swing ii. Decreased pelvic tilt iii. Knee flexion in early stance iv. Knee extention in late stance v. Emerging heel strike vi. Disappearance of mild foot drop d. 3 year old (early mature gait) characteristics: i. High cadence ii. Low velocity iii. Increasing stride length with growth of limb iv. Increasing single support phase e. 7 year old characteristics: i. Decreasing cadence ii. Increasing stride length f. Full mature gait characteristics: i. Increased single support phase ii. Increased velocity iii. Increased stride length iv. Increased ratio of pelvic span to ankle spread v. Decreasing cadence 2. Abnormal Gait Patterns: a. Spastic gait: Manifested by internal rotation and adduction of the entire limb, with hip/knee/ankle in marked flexion. Seen with cerebral palsy, familial spastic diplegia, paraplegia, and hemiplegia. b. Dyskinetic gait: A constant movement abnormality with a high degree of variability from patient to patient and gait cycle to gait cycle. It is characterized by motion involving considerable effort, often with deliberate, almost concentrated step. Seen with cerebral palsy, Huntingtons chorea, and dystonia musculorum deformans. c. Ataxic gait: Characterized by a marked instability during single limb stance with an alternating wide/narrow base during double support. During swing phase the limb will swing widely and cross the midline. Seen with multiple sclerosis, tabes dorsalis, diabetic polyneuropathy, Fredrich's ataxia. d. Waddling gait: A labored walking, exhibiting difficulty with balance, proximal pelvic instability, leading to a lumbar lordosis. May see an associated equinovarus foot type. Seen with Duchenne muscular dystrophy, limb-girdle muscular dystrophy, Beckers muscular dystrophy, spinal muscular atrophy, and congenital dislocated hips. e. Steppage gait: Gait exhibits a swing phase drop foot. Seen with Charcot Marie-Tooth, polio, Guillain-Barre syndrome, CVA, paralytic drop foot, and

fascioscapulohumeral dystrophy. f. Vaulting gait: Gait changes include a high cadence, increased lateral trunk movement, scissoring and instability from step to step, suggesting a loss of balance. Seen with myotonic dystrophy. g. Equinus gait: Gait exhibits a swing phase ankle plantarflexion with no heel contact. Seen with cerebral palsy, Charcot-Marie-Tooth, muscular dystrophy, spinal muscular atrophy, schizophrenia, osseous block of the ankle, and habitual toe walking. h. Festinating gait: Gait changes include loss of reciprocal arm swing, decreased velocity, shuffling, decreased stride length, and increased cadence. Seen with Parkinson's disease. i. Trendelenberg gait: Stance phase of each step leads to a contralateral tilt of the pelvis with a deviation of the spine to the affected side. Seen with dislocated hip or weakness of gluteus medius.

Intoe Gait 1. Evaluation: a. History: i. Onset of the problem: What age? Sudden onset? How long? ii. Severity of the problem: Difficulty walking? Falling? Does not want to play? More pronounced in rigid shoes? iii. Developmental history: as previously discussed iv. Hospitalizations/ injuries v. Family history b. Observation of gait: i. Angle of gait: in-toe or out-toe or rectus ii. Position of the knee at midstance: externally/ internally deviated, straight iii. Presence of a limp? iv. Presence of equinus? v. Early heel lift off? vi. Bouncing gait? vii. Rapid out-toe after midstance? viii. Excessive pronation? No arch present? c. Examination of hips: (performed in younger children: < 2 years) i. Should be able to abduct hips at least 70° (flexing hips and knees) d. Determination of femoral position: i. Mark the center of both knees and position them straight up ii. With the child lying down" and the hip and knee extended, rotate the femur inward (estimate the number of degrees) NOTE* This is done by rotating the knee and visualizing this by noting the numbers on a clock, whereby each hour equals 30°. So if the knee moves from the straight up position to 2 o'clock (external) that equals 60° of external rotation. iii. Rotate the femur outward (estimate the number of degrees of motion) iv. Perform the same examination with the hip flexed an then with the knee

flexed (to eliminate soft tissue elements) NOTE* If the measurements vary with positional changes then the abnormal endings are due to soft tissue tightness. If the measurements are the same then the problem is torsional within the femur. e. Average rotation of the hip joint: i. Up to 1 year old: twice external to internal rotation ii. At 5 years old: internal = external rotation f. Internal femoral position/can produce an in-toe gait: i. Anti-torsion and retroversion External femoral position/can produce an out-toe gait: ii. Retrotorsion and retroversion g. Examination of the knee joint: i. Normal frontal plane motion: birth/5-10°,decreases to 0-5° at 6 years old ii. Normal transverse plane motion: birth/5-15°, 0-5° at years old iii. Pseudomalleolar torsion (pseudolock): excessive transverse plane motion at the knee can result in in-toe gait (usually 15-35°) h. Examination of malleolar position (tibial torsion: add 5° to malleolar torsion): i. measure the malleoli with a goniometer ii. Values: birth/0-5°, 6 years old/13-18° (less than this = in-toe gait) i. Other deformities causing in-toe gait: i. Talar neck adductus ii. Clubfoot iii. Talipes varus iv. Metatarsus adductus v. Spastic posterior tibial ms. vi. Genu varum vii. Tibia varum j. Treatment: i. Not all cases warrant treatment ii. The cases that should be treated are those in which 8° of improvement would not bring their feet into a straight-forward position, those children having difficulty walking, or a destructive foot type iii. Manipulation of the soft tissues by the parent iv. Functional orthoses to control pronation v. Gait plates (child must have a propulsive gait) vi. D-B bar (inhibits abnormal sleeping positions- use 1 " wider than hips) vii. Ganley splint (like D-B bar but neutralizes pronation at the STJ) viii. Plaster cast for pseudolock viii. Surgery Pediatric Fractures 1. Anatomical Considerations: a. Epiphysis i. Pressure epiphysis: At the articular surface, involved with growth ii. Traction epiphysis: Not at the articular surface and not involved with growth

(femoral trochanter, tibial tuberosity, calcaneus, base 5th metatarsal) b. Diaphysis c. Metaphysis d. Epiphyseal plate: Zone between the epiphysis and the metaphyseal plate Microscopic appearance (multiple cell types) i. Resting cells ii. Proliferating cells iii. Endochondral cells e. Points to remember: i. Matrix makes the plate the strongest at areas close to the epiphysis and metaphysis. ii. The zone of provisional calcification, where cells are dividing and calcification begins, is the weakest part of the region, poor in matrix; epiphyseal injuries usually occur at this part. iii. Due to the separation at the middle of the physis, it leaves the proliferating cell zone uninterrupted; thus there is usually no interference in bone growth, as long as circulation to the physis remains intact. iv. Diaphyseal blood supply will nourish the layer of endochondral ossification without crossing the epiphyseal plate. v. Epiphyseal blood supply will enter through the joint capsule and through the perichondrium to the epiphysis zone area of the epiphyseal plate (2 types: intracapsular & extracapsular). vi. When making a diagnosis a minimum of 3 views should be taken and bilateral x-rays should be taken. Note* The physis contains 3 parts: a. Zone of Growth: containing the dividing and resting cells b. Zone of Maturation: for calcification c. Zone of Transformation: for ossification The Zone of Ranvier is a groove surrounding the periphery of the physis and is composed of.. a. Fibroblasts b. Mesenchymal tissue (undifferentiated cells-multipotential) c. Osseous ring of Lacroix (an extention of the metaphyseal cortex) The Zone of Ranvier functions so that longitudinal and latitudinal growth of the physis proceeds in harmony Note* Remember that the periosteum in the child is more vascular, thicker, loosely attached and stronger than in the adult 2. Results of a Swedish study of epiphyseal fractures: a. The risk of fractures increases at ages 11-12 in females and 13-14 in males b. Chance of epiphyseal fracture is 42% till age 16 in males and 27% in females. c. Fractures at the epiphysis peak at 2 years of age and again between 11-14 years of age. d. 13.4% of the fractures occur in the foot and ankle e. 21 % of the injuries are sports related

f. Pathological fractures should be taken into account occurring due to minor trauma in diseases such as: renal disease, cystic fibrosis, growth hormone deficiency, diabetes mellitus, Turner's syndrome. 3. Important points to remember: a. Haversian canal system in children is more extensive as compared to that of adults, especially in the metaphysis. b. Children's fractures can be of compression or tension type; in adults compact bone fails in tension only. c. Incomplete failure in tension results in a greenstick fracture d. In. children, the strongest skeletal segment is the periosteum, the weakest being the growth plate. e. Due to the strong periosteum one rarely sees open fractures in children Intermediate strength is the epiphysis which is protected by joint congruency and cartilage. f. Capsule and ligaments are a continuation of the periosteum, which mostly bypasses the epiphysis, distributing forces to the growth plate and metaphysis. 4. Classifications of epiphyseal fractures: a. Salter-Harris: Is an anatomic classification applicable to most physeal injuries. There are problems associated with this classification: the size of the epiphyseal/metaphyseal fragment is not quantified. There are 5 types: Type 1: complete separation of the epiphysis with no fracture of bone Type 2: fracture along the epiphysis then through the metaphysis producing a triangular fragment Type 3: extends from the joint surface to the epiphyseal plate, along the plate to the periphery Type 4: extends from the joint surface to the epiphysis and plate and through a portion of the metaphysis Type 5: severe crush injury and compression of the plate

NOTE* Type 6 was added by Rang, a bruising of the peripheral growth plate secondary to blunt trauma, resulting in a peripheral osseous bridge causing angular deformity (treat with resection of the osseous bridge with correction of the angular deformity) i. S-H Type 1: Fibular fracture
occurs due to inversion stress
may appear as an isolated injury or in combination with a medial corner injury to the ankle (Salter 3 Tibial)
diagnosis is difficult (there should be at least one cm of lateral soft tissue swelling around the plate area)
these fractures may or may not be displaced
good prognosis
apply short-leg walking cast for at least 3 weeks
occurs in ages < 12

ii.




S-H Type 1: Tibial fracture occurs from shear stress due to external rotation injuries can occur with fibula shaft fracture which is usually transverse may be displaced or nondisplaced





good prognosis treat with closed reduction (prn) and immobilze in NWB A-K cast for 3 weeks plus 2 weeks in a B-K cast

iii. S-H Type 2: Fibular fracture
caused by eversion and external rotation of the foot
treat with 3-4 weeks in a B-K cast
occurs in the older age group where the epiphyseal plate is more bonded (age 13) iv. S-H Type 2: Tibial fracture
caused by eversion (small medial fragment), external rotation (large medial fragment), or plantarflexion (posterior fragment)
associated with a fibular fracture
may be displaced or non-displaced
average age is 13
triangular fragment called Thurston-Holland sign medially
opposite disruption called Lamellar sign laterally, is the overhang of the proximal end of the tibia over its distal end as the fracture shifts laterally
prognosis is good
application of B-K cast for 3-4 weeks and mild manipulation by reversing the mechanism of injury (avoid excessive manipulation because the germinal cells are already damaged) iv. S-H Type 3: Tibial fracture
caused by inversion
may or may not be displaced (take MO x-ray of the ankle to determine amount of displacement)
treat if non-displaced with A-K cast for 3 weeks and a B-K cast for 3 weeks
treat if displaced (by more than 2 mm) with ORIF (the fixation must not cross the plate)
good prognosis if alignment is restored v. S-H Type 4: Tibial fracture
caused by a continuing inversion force greater than that in a Salter 3 injury
treat same as Salter 3 tibial for non-displaced and displaced, except that additional fixation is needed for the metaphyseal fragment (proper anatomical reduction/alignment is necessary)
these are rare
possible growth disturbances vi. S-H Type 5: Tibial fractures
caused by severe axial loading across the plate resulting in multiple fracture lines
these fractures may lead to premature fusion across the whole plate causing a limb length discrepancy
may lead to fusion on one side or from front to back causing asymetrical
angulation of the limb





treat if displaced by ORIF to restore articular congruity prognosis is poor

vii. S-H Type 6:
due to bums or avulsions
loss of growth plate substance
epiphyseodesis can result with premature epiphyseal plate closure with progressive shortening and angular deformity viii. Summary of S-H fractures:
the younger the patient the greater the chance of deformity
type 1 and 2 have a better prognosis than types 3 to 6
a non-displaced epiphyseal fracture has a better prognosis
a compression fracture has the poorest prognosis
blood supply interruption leads to growth arrest
infection in addition to a fracture can be disastrous
reduction (open or closed) should be done gently within 10 days after trauma
healing of epiphyseal injuries takes 3 weeks as compared to 4-6 weeks for bone
the resulting deformity has to be treated surgically
follow-up for growth retardation should be done for at least 3 years
radiological studies with markers indicate 5 types of post-traumatic growth patterns: symmetrical growth, initial/temporary growth stimulation, initial/temporary growth retardation, initial/ progressive growth retardation, and initial/permanent growth arrest.

b. Dias and Tachdjian: Added a classification of physeal injuries based in Lauge-Hansen and Salter-Harris. The first term describes the position of the foot at the time of impact, and the second term refers to the direction of the talus taken by the injuring force. It involves 4 types: i. Supination-plantarflexion
Result in Salter 2 fracture of the distal tibia with the metaphyseal fragment posteriorly ii. Supination-external rotation
Stage 1:Characterized by Salter 2 of the distal tibia
Stage 2: Characterized by a short oblique fibula fracture above the distal fibula physis iii. Supination-adduction
Stage 1:Characterized by Salter 1 or 2 of the distal fibula
Stage 2: Characterized by Salter 3 or 4 of the distal tibia iv. Pronation-external rotation
Stage 1: Characterized by a Salter 1 or 2 of the tibia
Stage 2: Characterized by a fibula fracture above the level of the tibiotalar joint with the metaphyseal fragment lateral c. Juvenile Tillaux fracture: i. An avulsion fracture of the distal lateral tibial tubercle by the anterior tibiofibular ligament due to an external rotation force ii. This fracture is seen on an A-P view as a S-H type 3 fracture of the lateral distal tibial epiphysis, involving from 20-50% of the width of the epiphysis

iii. Usually occurs in ages 12-14, because of closure of the medial half of the epiphysis and not the lateral half iv. Treat if non-displaced with a A-K cast for 6-8 weeks with some internal rotation of the lower end of the cast NOTE* Treatment is ORIF if displaced with lag screw technique from distal lateral to proximal medial (can cross the physis since growth is already completed)

Note* To best view this fracture, take an oblique x-ray in which the fibula is rotated internally to eliminate the overlap of the tibia to better see the entire distal tibial epiphysis

vii. Triplane fractures:
combination of a central vertical Salter 2 and Salter 3 tibial fracture
can be missed on routine x-rays
treat as per Tillaux type

The Limp in Childhood Limp is an exaggeration or deficiency of normal gait which may be painful or painless. It may be associated with paralysis, spasticity, contractures, loss of supporting structures, limb length discrepancy, and ataxia. It should be considered to reflect serious disease until proven otherwise. Except in the most obvious causes, a complete review of history and general physical exam is necessary and if indicated appropriate lab studies, x-rays, and consultations. Looking at limp by age groups is helpful. 1. The Beginning Walker: a. Congenital hip dislocation b. Trauma (always consider abuse) c. Septic joint (diagnosis urgent especially in the hip) d. Osteomyelitis e. Synovitis f. Neuromuscular disorders 2. The Walking Child: a. Congenital dislocated hip b. Cerebral palsy (may only manifest itself as intoeing) c. Discitis (pain on straight-leg raising) d. "Toxic" synovitis (must r/o septic hip, labs are WNL, a small percentage develop Legg-Perthes disease) e. "Growing pains" f. Legg-Calve-Perthes disease 3. Preteens-Teens: a. Congenital dislocated hip b. Slipped proximal femoral capital epiphysis (the patient is usually larger and male; holds leg in internal rotation; in gait patient lurches over the involved hip SUMMARY OF TYPES OF LIMP Age (Yr)

Antalgic

Birth-4

Trauma, infection

5-10

11-14

Paralytic

Short Leg

Cerebral palsy, Congenital, coxa spinal vara, muscular atrophy, CHD, infection spin bifida, hemiatrophy palsy, Trauma, infection, Cerebral Spina bifida, trauma, rheumatoid arthritis, spina CHD, Infection, Legg-Calve-Perthes bifida, muscular dys- rheumatoid arthritis disease, hemophilia, trophy, polio transient synovitis Trauma, synovitis, Muscular dystrophy, infection, trauma, slipped capital femo- polio, peripheral slipped capital femoral epiphysis, infec- nerve trauma, CNS ral epiphysis, neotion, Osgood-Schlat- neoplasm, ischemic plasm ter disease contracture

CHD, Congenital heart disease.

Contracture

Loss of Support

Spina bifida, cerebral CHD, trauma, palsy, CHID, Infecvan, spine I: tion Trauma, CHD, Legg- Trauma, polio, infecCalve-Perthes distion, muscular dysease, infection, rheu- trophy matoid arthritis Infection, trauma, Trauma, slipped capiLegg-Calve-Perthes tal femoral epidisease, slipped capi- physis, inadequate tal femoral epiphysis treatment, CHD

Juvenile Hallux Valgus 1. Classification: a. Congenital: i. Aplasia: small toes, cleft foot, or amputated toes (a secondary HAV/ interphalangeus, no met primus varus) ii. Congenital vertical talus: overgrowth of the medial column iii. Residual met adductus b. Hyperlaxity (hypermobile pes planus): i. Physiologic ii. Pathologic: Down's and Marfan's syndrome c. Adolescent: i. Advanced met primus varus secondary to
trapezoidal medial cuneiform
oblique 1st met-epiphyseal line
oblique 1st met-medial cuneiform joint ii. Associated hypermobile pes planus d. Neurologic: i. Equinovalgus: contracted achilles with overpull of the peroneals ii. Spasticity of the adductor hallucis e. Superimposed factors: i. Extrinsic: shoes, ballet ii. latrogenic 2. Treatment: Treatment depends upon the underlying etiology, age, and clinical findings. a. Akin procedure: for hallux interphalangeus b. Tendon sling with Modified McBride c. Lapidus procedure d. Cotton procedure (sagittal plane opening wedge of medial cuneiform for 1st metatarsal elevatus) e. Hemiepiphysiodesis at the proximal phalanx and base of the first metatarsal f. Proximal 1st metatarsal osteotomies (Austin, Mitchell) good up to 140 IMA g. Distal 1st metatarsal osteotomies 3. Complications: a. The most common complication seen with correction of juvenile bunion is shortening of the first metatarsal. This is a result of interruption of growth of the physis from i. Base wedge osteotomies ii. Epiphysiodesis NOTE* The extent of shortening is dependent on the amount of dissection about the physis and the age of the child b. Avascular necrosis from metatarsal head osteotomies c. Over or undercorrection

Biomechanical Evaluation of the Child 1. The initial visit: a. Perinatal history: i. Was the child full term or premature (premature children are at more risk for neurological problems) ii. Standard delivery, breech delivery (dislocated hip), or cesarean section b. Developmental landmarks: i. When did the child start to ambulate? (the normal range is 9-16 months) If a child is delayed in this then you must explore mechanical pathology, musculoskeletal pathology, and neurologic deficit 2. Gait evaluation: a. Head tilt: Observe the position of the head in gait. An obvious tilt away from the midline would indicate a possible limb length deficit b. Shoulder and pelvis level: If the child walks with an obvious shoulder drop, one should observe the level of the pelvis. NOTE* Generally, an apparent shoulder drop in a young child may be consistent with a shortened limb on that side. In a child under the age of 12 or 13, the shoulder drop is to the shortened side as there is generally no scoliosis present until that age. This is in contrast to the adult where the shoulder drop is typically on the contralateral side from the shortened limb c. Patellar position: An important landmark when exaluating the child with transverse plane deformities of the legs. NOTE* If a child has an adducted gait and the patellar position is internally rotated ("squinting patella") then at least a portion of the deformity is at the femoral level. If the patellar position is normal, this indicates a problem within the knee, tibia, or the foot d. Angle of gait: Typically a child's angle of gait should be more in an external position. If a child's gait is adducted on the transverse plane because of a torsional abnormality, that angle of gait is generally consistent. However, some children demonstrate an angle of gait deformity that varies considerably from step to step. In these cases, special attention should be directed to the amount and direction of transverse plane knee rotation present on the off-weightbearing examination. In other instances, some children will exhibit an "adducting" (rather than an adducted) gait at heel contact which is due to tight medial musculature. e. Calcaneal position: Most children have a pes planus on weight-bearing. A child's calcaneus is normally everted at the onset of ambulation which can persist till the age of 6-7 years old.

NOTE* Calcaneal eversion should reduce approximately 1° per year. Therefore a child with a calcaneal eversion of 6-7° should reduce to perpendicular by the age of 7 (a rough estimate) 3. Off-weight-bearing examination: a. Hip range of motion: External vs. internal rotation measured with the child supine has about a 2:1 ratio for the first few years. The total ROM measures more than 1000. Both the amount of external rotation and the total ROM diminishes over the first few years and essentially becomes symmetrical at the age of 5-6 through adulthood. This is measured with a Martin's goniometer placed on the epicondyles of the femur. If a marked amount of internal hip rotation is noted compared with external rotation, the examination should include evaluation of motion with the hip extended and hip flexed positions (determines whether structural vs. positional) b. Knee range of motion: At birth through 4 years there may be a total of 20-30° of transverse plane rotation available at the knee. This decreases drastically at age 3-4. In a normal child under the age of 3 there should be a symmetrical amount of internal and external rotation of the tibia relative to the femoral segment. However, if there is 300 of external rotation available from a resting position with minimal internal rotation this indicates that the tibia is being maintained in an internally rotated position (congenitally short hamstring or medial head of the gastrocnemius) c. Tibial torsion: This is assessed by measuring malleolar position, by determining the amount of anterior rotation of the tibial malleolus relative to the fibular malleolus (measured by a goniometer placed on the malleolei or tractograph placed on the plantar aspect of the foot). At birth there is no tibial torsion present, however, this gradually increases in an external direction through the first 7-8 years to a normal adult value of 13-18°. Tibial torsion is generally 5° greater than malleolar position. d. Ankle joint dorsiflexion: At birth there is unrestricted ankle joint dorsiflexion (can approach 75°) , reduces to 20-25° by age 3, reduces to 15° by age 10, and reduces to 10° by age 15. When obtaining this measurement the subtalar joint is held in neutral position or the midtarsal joint will unlock thereby introducing additional forefoot dorsiflexion. If dorsiflexion is limited with the knee extended, retake the measurement with the knee flexed. If there is limited ankle dorsiflexion with the knee extended but greater than 150 with the knee flexed, the child has a gastrocnemius equinus. If the limitation is present with the knee extended and flexed then a gastroc-soleus equinus is most likely responsible (an osseous equinus is uncommon in this age group) e. Subtalar joint range of motion: Since a child under the age of 3 has an apropulsive gait, measurement of the STJ ROM is not essential. Only after the age of 3 when a heel-toe propulsive gait is initiated, does a functional orthoses become useful, and therefore so does the STJ measurement. Rangle of motion is accomplished by bisecting the calcaneus and measuring full eversion and inversion. This is generally more than the adult values. The foot must be measured in a slight dorsiflexed position for accuracy. f. Midtarsal joint range of motion: The STJ is placed in neutral position and the

MTJ is locked (in this fashion the 2 axes of the MTJ cross each other and limit extraneous midtarsal joint mobility upon examination). A forefoot varus or valgus deformity upon examination will not be outgrown, and any degree of forefoot deformity should be supported to prevent abnormal compensation 4. Weight-bearing examination a. Relaxed and neutral calcaneal stance position: The calcaneal bisector on weight bearing should be noted. Abnormal calcaneal eversion in the child can be due to compensated forefoot varus (frontal plane), compensated gastrocnemius equinus (sagittal plane), and internal tibial/femoral torsion (transverse plane). b. Tibia varum: The angle that the distal one-third of the tibia makes relative to the ground with the STJ in neutral position is tibial varum (generally 0-5° in the child) c. Genu varum/genu valgum, genu recurvatum: The child demonstrates changes in frontal plane position at the genicular region at different ages . If excessive genu varum is detected and does not reduce with time, the possibility of Blount's disease or juvenile rickets should be investigated. If genu valgum is noted and does not decrease with time, then functional orthoses should be used to reverse the severe pronatory force to the feet. A posterior deflection of the femur into the tibia may be present measuring 5-10° until the age of 5. If any amount greater than this is present before the age of 5, or any amount present at all after 5 should be checked for pathology d. Limb length inequality: This is done by palpating the anterior superior iliac spine, and measuring to the tip of the medial malleolus. Repeat measurement 2-3 times consecutively for consistency. If there is asymmetry in their levels, further investigation is necessary

Corrective Casting in Infants 1. Application of the cast: a. Only gentle force is exerted b. Webril® is utilized and should be no more than 2 layers thick with 3-4 layers at the posterior-of the heel and at the upper limit of the cast. It should be wrapped under a slight stretch making a snug fit. It should extend one-half inch beyond the plaster c. Use extra-fast setting plaster d. Babies usually require only 1 roll of 3 inch plaster and 2 inch rolls for newborns 2. Calcaneovalgus deformity: a. The assistant grasps the thigh and toes and then holds the hip, knee, and foot in the anteroposterior plane with the foot in equinus b. With the foot held in equinus, the metatarsal adducted, apply pressure in three areas: i. The posterior aspect of the heel ii. Over the talus medially iii. Laterally over the 5th metatarsal area

3. Metatarsus adductus: a. Failure to appreciate the rearfoot malalignment (talocalcaneal breach on AP x-ray) will result in failure of treatment and produce a severe flatfoot deformity b. Pressure should be applied in three areas: i. Pressure laterally over the cuboid area ii. Counter pressure medially on the talar head (attempts to close down the T-C angle) iii. Pressure along the 1st metatarsal medially iv. If the hallux is in adduction due to contraction of the abductor hallucis, a strip of plaster is used to hold the hallux in a rectus or slightly abducted position 4. Talipes equinovarus: a. Apply 2-3 casts consecutively,, with the foot in "unlocked" equinus position b. Apply three point pressure: i. Evert the heel by pressure medially ii. Lateral counter-pressure over the talar head in an attempt to open up the TC angle (to try to move the calcaneus laterally from beneath the talar head) iii. Pressure along the 1st metatarsal medially NOTE* Response to this should be a dramatic improvement in the transverse and frontal plane alignment. Later casts are applied with the forefoot to rearfoot in a neutral position and the knee flexed to stretch the posterior structures (equinus is overcome by pulling down on the posterior of the heel and applying dorsiflexion pressure, making sure some of the pressure is on the calcaneocuboid area). Being overzealous will result in a rocker-bottom foot with the calcaneus in an equinus attitude. 5. Tibial torsion: a. The cast is applied from the toes to midthigh with the foot in mild equinus, the knee flexed to at least 300 b. The corrective force is exerted by holding the thigh stable and rotating the foot to the end range of motion (avoid inversion or eversion while doing this)

The Toe-Walking Child Toe-walking may be a result of idiosyncratic or idiopathic factors with no pathological background, or can follow serious neuromuscular, psychological, and skeletal pathologies. Therefore, the etiology of habitual toe-walking is determined by exclusion: 1. Examination: a. Medical history: As above b. Gait Evaluation: c. Physical examination: i. Musculoskeletal ii. Biomechanical iii. Neurologic

2. Differential diagnosis: a. Cerebral palsy: A fixed nonprogressive neurologic deficit acquired before, during or in the months after birth. The spastic form is most likely to produce a toe-walking gait b. Pseudoscissor gait: Must be recognized and differentiated from the scissor gait of CP. This condition occurs when there is a combination of habitual toewalking and adducted limb position due to internal tibial and/or femoral position. The child with a pseudoscissor gait will have more stability than a child with a scissors gait c. Mental retardation: There are behavioral clues to a diagnosis such as dependency on routine, distractibility, fear, lack of spontaneity, poor judgment, and repetitive physical activities that are disturbing to others (rocking, head banging, temper tantrums, etc.) d. Clumsy child syndrome: A behavioral problem characterized by poor control of motor function, impulsiveness, short attention span, and hyperkinesis e. Autism: Autistic children are principally disturbed in their lack of emotional rapport and in their behavioral characteristics. They show seclusiveness, irritability when seclusiveness is disturbed, day dreaming, bizarre behavior, decrease of interest, regression of interpersonal interests, and sensitivity to criticism. There is a gradual withdrawal from affective contact with people f. Dystonia musculorum deformans: A disease of the basal ganglia characterized by slow, powerful twisting and writhing movements g. Delayed maturation of the corticospinal tracts: Results in spastic toewalking due to the lack of inhibition of the stretch reflexes. This condition disappears by the age of 6-8 h. Diastematomyelia: Consists of a partial or complete division of the spinal cord by tissue located in the midline of the spinal canal. There is a mixed upper and lower motor neuron deficit involving the bladder and bowel function and progressive disturbances in gait develop by the age of 2-3 i. Muscular dystrophy (Duchenne and limb-girdle: Toe-walking is the result of a disturbance of antagonistic balances of the variously affected muscle groups. With limb-girdle MD the first symptoms appear in the 2nd decade. With Duchenne's MD the child may walk later than expected with frequent falls when learning to walk j. Peroneal muscular atrophy: This disorder begins in the feet and legs producing difficulty in walking, paresthesias of the legs, and muscle cramps. There is early weakness of the intrinsic muscles of the feet, ankle dorsiflexors, and peroneals. The patellar DTR is lost, vibratory and position sense are diminished k. Gastrocnemius soleus muscle equinus: The most common entity is the habitual toe-walking child. The Silferskjold test first used to differentiate spastic gastrocnemius equinus from spastic gastrosoleus equinus can be usefully applied to evaluate nonspastic short calf muscles. Clinically, a child with a gastrocnemius soleus muscle equinus will stand with an abducted stance angle and will often exhibit a genu recurvatum and significant midtarsal pronation 1. Clubfoot: A deformity in which the leg and foot are said to resemble a club, and is associated with congenital hip dislocation, arthrogryphosis multiplex

congenita, spinal abnormalities, and neuromuscular disease. The form of clubfoot that leads to toe-walking is talipes equinovarus. a. Shoe therapy: Rigid sole high top shoe b. Orthoses therapy: Heel lifts, gait plates, and knee-ankle-foot orthoses c. Short leg casting c. Auditory feedback: A method of cognitive muscle management d. Surgical intervention: With a significant structural gastrosoleus muscle equinus

Chapter 20: Drugs & Drug interactions Introduction to Drug Interactions Antibiotic Drug Interactions Anticoagulant Drug Interactions Antidiabetic Drug Interactions Antihypertensive Drug Interactions Antipsychotic Drug Interactions Cardiac Drug Interactions Diuretic Drug Interactions NonSteroidal anti-inflammatory Drug Interactions Oral Contraceptive Drug Interactions Mechanisms of Drug Interactions Drugs

DRUGS & DRUG INTERACTIONS Introduction to Drug Interactions 1. Types of drug interactions: a. Addition (1 + 1 = 2): The response elicited by combined drugs is equal to the combined responses of the individual drugs b. Synergism (1 + 1 = 3): The response elicited by combined drugs is greater than the combined responses of the individual drugs: c. Potentiation (0 + 1 = 2): A drug which has no effect enhances the effect of a second drug d. Antagonism (1 + 1 = 0): A drug inhibits the effect of another drug 2. Mechanisms of drug interactions: a. Altered absorption b. Altered metabolism c. Plasma protein displacement d. Altered excretion 3. Top 10 interaction drug problem list: a. Antibiotics b. Anticoagulants c. Antidiabetic agents d. Antipsychotics e. Beta blockers f. Digoxin g. NSAIDS h. Oral contraceptives Antibiotic Drug interactions 1. Aminoglycosides with: a. Cephalosporins (parenteral): Effect is increased nephrotoxicity, mechanism unknown b. Penicillins (parenteral): Effect is inactivation of certain aminoglycosides, mechanism is unknown c. Loop diuretics: Effect is increased 8th cranial nerve damage with possible irreversible hearing loss, mechanism is synergistic auditory toxicity 2. Imidazole antifungals (ketoconazole and Itraconazole) with: a. Seldane: Effect is Cardiotoxicity, arrhythmia, death, mechanism is that imidazoles exert a quinidine-like effect with prolongation of Q wave on the EKG b. Hismanal : Same as with Seldane c. H2 antagonists: Effect is inactivation of the imidazoles, mechanism is alteration of the pH by the H2 antagonists and antacids d. Phenytoin: Effect is decreased action of imidazoles, mechanism is increased metabolism by hydantoin induction of hepatic enzymes

3. Macrolide antibiotics (erythromycin, clarithromycin and clindamycin) with: a. Seldane (with erythromycin and clarithromycin): Effect is cardiotoxicity, arrhythmia, death, mechanism is macrolides exert a quinidine-like effect with prolongation of Q wave on the EKG b. Hismanal: Same as with Seldane c. Theophylline (with erythromycin and clarithromycin): Effect is increased theophylline toxicity, mechanism is decreased theophylline renal clearance d. Oral anticoagulants (with erythromycin only): Effect is increased anticoagulant activity with hemorrhage, mechanism is unknown e. Kaopectate (with clindamycin only): Effect is decreased absorption of clindamycin, mechanism is binding absorption of the antibiotic 4. Quinolones with: a. Multivalent cations (antacids): Effect is decreased effects of the quinolones, mechanism is chelation binding decreases the GI absorption b. Theophylline: Effect is increased theophylline toxicity, mechanism is inhibition of hepatic metabolism of theophylline c. Carafate: Effect is decreased effects of quinolones, mechanism is chelation binding decreases GI absorption d. Caffeine: Effect is increased effect of caffeine 5. Miscellaneous antibiotics: a. Penicillins (ampicillin) with allopurinol: Effect is markedly increased rate of ampicillin retention and induced skin rash, mechanism is unknown b. Metronidazole with alcohol: Effect is a disulfiram-like reaction, mechanism is metronidazole inhibits aldehyde dehydrogenase NOTE Disulfiram reaction (with OH) is nausea, vomiting, hypotension, and possible coma later on c. Tetracyclines with multivalent cations: Effect is decreased effects of tetracyclines, mechanism is chelation binding decreases GI absorption d. Ampicillin with oral anticoagulants: Effect is increased anticoagulant activity

Anticoagulant Drug Interactions 1. Anticoagulants (oral) with: a. Aspirin: Effect is increased bleeding and hypoprothrombinemic effects of Warfarin, mechanism is protein binding displacement combined with anti platelet effects b. Erythromycin: Effect is increased anticoagulant activity with hemorrhage, mechanism is unknown c. Cephalosporins: Effect is augmented Warfarin effects, mechanism is antiplatelet effects of certain parenteral cephalosporins d. H2 antagonists:: Effect is increased bleeding with possible hemorrhage, mechanism is inhibition of hepatic metabolism of Warfarin e. Phenytoin: Effect is increase in both bleeding and phenytoin activity,

mechanism is unknown f. Sulfonylureas: Effect is hypoglycemia, mechanism is the hepatic metabolism of the sulfonylureas is inhibited g. Barbiturates: Effect is decreased effect of Warfarin, mechanism is barbiturate induced heptic metbolism of Warfarin h. Griseofulvin: Effect Is decreased effect of Warfarin, mechanism is unknown

Antidiabetic Drug Interactions 1. Insulin with: a. Alcohol: Effect is hypoglycemia, mechanism is inhibition of gluconeogenesis b. Beta Blockers: Effect is hypoglycemia with the masking of hypoglycemic symptoms, mechanism is that beta blockers blunt sympathetic mediated responses to hypoglycemia c. MAO inhibitors: Effect is hypoglycemia, mechanism is inhibition of gluconeogenesis d. Salicylates: Effect is hypoglycemia, mechanism is increased circulating concentration of insulin e. Steroids/Estrogen/Thyroxin: Effect is increased hypoglycemia 2. Sulfonylureas with: a. Alcohol: Effect is hypoglycemia and disulfiram-like reactions, mechanism is decrease elimination and altered metabolism involving aldehyde dehydrogenase b. Anticoagulants: Effect is hypoglycemia, mechanism is inhibition of hepatic metabolism of sulfonylureas c. MAO inhibitors: Effect is hypoglycemia, mechanism is unknown d. NSAIDS: Effect is hypoglycemia, mechanism is protein binding displacement e. Sulfinpyrazone: Effect is hypoglycemia, mechanism is inhibition of hepatic metabolysm of sulfonylureas f. Thiazide diuretics: Effect is hyperglycemia, mechanism is thiazide diuretics decrease insulin secretion

Antihypertensive Drug Interactions 1. ACE Inhibitors with: a. Indomethacin: Effect is decreased hypotensive effect of ACE inhibitor, mechanism is interference with plasma renin activity and vasopressor response b. Potassium supplements: Effect is hyperkalemia, mechanism is unknown c. Capsaicin (Zostrix): Effect is exacerbation of coughing associated with ACE inhibitor, mechanism is unknown 2. Calcium Channel Blockers (Verapamil and Nifedipine) with: a. Calcium salts (with Verapamil): Clinical effect of Verapamil is reversed, mechanism is pharmacologic antagonism b. Quinidine (with Verapamil): Effect is hypotension c. H2 antagonists (with Nifedipine): Effect is hypotension, mechanism is inhibition of hepatic metabolism of nifedipine Antipsychotic Drug Interactions 1. MAO Inhibitors with:

a. Meperidine: Effect is seizures coma apnea, and death, mechanism is unknown b. Tricyclic antidepressants: Effect is seizures, hypotension, coma, and death, mechanism is unknown c. Amine containing foods: Effect is hypertensive crisis or stroke, mechanism is impaired metabolism of tyramine by inhibition of monoamine oxidase 2. Lithium with: a. Iodide salts: Effect is hypothyroidism or goiter, mechanism is pharmacologic synergism b. Thiazide diuretics: Effect is increased lithium toxicity, mechanism is decreased lithium renal clearance c. NSAIDS: Effect is increased lithium toxicity, mechanism is decreased lithium renal clearance 3. Phenothiazines with: a. Meperidine: Effect is excessive hypotension and sedation, mechanism is pharmacologic synergism b. Anticholinergics: Effect is decreased effect of phenothiazines, mechanism is accelerated metabolism of phenothiazines

Cardiac Drug Interactions 1. Beta Blockers with: a. Epinephrine: Effect is initial hypertensive episode, followed by bradycardia, mechanism is beta blockade allowing alpha receptor stimulation increasing BP which stimulates baroreceptors causing bradycardia b. Verapamil: Effect is that the effects of both drugs are increased, mechanism is pharmacologic synergism c. Insulin: Effect is prolonged hypoglycemia with masking of hypoglycemic symptoms (tachycardia), mechanism is that beta blockers blunt sympathetic mediated responses to hypoglycemia d. NSAIDS: Effect is impaired antihypertensive effect of beta blockers, mechanism is NSAIDS inhibit renal prostaglandin synthesis allowing unopposed vasopressor activity e. Theophylline: Effect is antagonistic activity increasing airway resistance, mechanism is pharmacologic antagonism f. H2 Antagonists: Effect is increased effects of beta blockers, mechanism is H2 antagonists can inhibit first pass hepatic metabolism of beta blockers 2. Digoxin with: a. Diuretics: Effect is electrolyte disturbances predispose to digitalis-induced arrhythmias, mechanism is increased loss of potassium affects cardiac muscle action b. Verapamil: Effect is increased digoxin toxicity, mechanism is additive effects c. Erythromycin: Effect is increased digoxin toxicity in about 10% of patients, mechanism is in about 10% of patients, digoxin is metabolized by GI bacteria d. Tetracycline: Effect is the same as above, mechanism is the same as above

e. Quinidine: Effect is increased digoxin toxicity, mechanism is reduced renal and biliary clearance of digoxin f. Quinine: Effect is same as above, mechanism is same as above

Diuretic Drug Interactions 1. Loop diuretics with: a. Aminoglycosides: Effect is increased 8th cranial nerve damage with possible irreversible hearing loss, mechanism is synergistic auditory toxicity b. Phenytoin: Effect is decreased effect of the diuretic, mechanism is decreased absorption and increased metabolism 2. Thiazide diuretics with: a. Lithium: Effect is increased lithium toxicity, mechanism is decreased lithium renal clearance 3. Potassium sparing diuretics with: a. Potassium supplements: Effect is hyperkalemia. mechanism is decreased elimination of the potassium ion 4. Spironolactone with: a. Salicylates: Effect is blockage of spironolactone-induced diuresis, mechanism is blockage of the renal tubular secretion

Non Steroidal Anti-Inflammatory Drug Interactions 1. NSAIDS with: a. Anticoagulants: Effect is increased bleeding and hypothrombinemic effects of Warfarin, mechanism is protein binding displacement combined with antiplatelet effects b. Beta Blockers: Effect is impaired antihypertensive effect of beta blockers, mechanism is NSAIDS inhibit renal prostaglandin synthesis allowing unopposed vasopressor activity c. Lithium: Effect is increased lithium toxicity, mechanism is decreased lithium renal clearance d. ACE inhibitors (Indomethacin): Effect is decreased hypotensive effect of ACE inhibitors, mechanism is interference with plasma renin activity and vasopressor response e. Methotrexate: Effect is increased methotrexate toxicity, mechanism is decreased renal clearance of methotrexate

Oral Contraceptive Drug Interactions 1. Oral contraceptives with: a. Phenytoin: Unintended pregnancy b. Barbiturates: Unintended pregnancy c. Griseofulvin: Unintended pregnancy d. Corticosteroids: Effect is therapeutic and adverse actions of corticosteroids are enhanced

Mechanisms of Drug Interactions 1. Alteration of Intestinal Absorption: a. Antacids diminish absorption of: (Antacids contain Ca++, Mg++, or Al +++) i. Phenylbutazone ii. Sulfonamides iii. Barbiturates iv. Salicylates v. Oral anticoagulants vi. Indomethacin vii. Ampicillin/penicillin viii. Tetracycline ix. Cipro® b. Antacids increase the absorption of: i. Talwin® ii. Antihistamines iii. Phenergan® iv. Darvon® c. Drugs that alter vitamin K levels: i. antibiotics (penicillin, ampicillin, erythromycin, and tetracycline) reduce vitamin K production, therefore may increase anticoagulant activity. d. Drugs that alter GI motility: i. Decrease motility: codeine, morphine, and other opiates ii. Increase motility: milk of magnesia, cathartics 2. Competition for Plasma binding protein: a. Oxacillin/cloxacillin/dicloxacillin/nafcillin can displace uric acid which can precipitate a gouty attack. b. Dicoumarol can sustain tolbutamide activity (causes severe hypoglycemia) 3. Metabolism or Biotransformation Alteration: a. Inhibition of metabolism: i. Anticholinesterases inhibit metabolism of ester-type local anesthetics resulting in a prolonged effect of the drug. ii. Oral anticoagulants prolong the effects of tolbutamide and increase the toxicity of diphenhydramine by inhibiting metabolism. b. Acceleration of metabolism: i. Phenobarbital accelerates the metabolism of coumadin, anticoagulants, steroids, and griseofulvin. Note* Patients on anticoagulants and barbiturates must be carefully monitored when the barbiturate is discontinued, as prolonged hemorrhage can result.

4. Alteration of Electrolytes: a. Hypokalemia may be caused by long term usage of digoxin, thiazide, and furosemide diuretics, and corticosteroids. b. Hyperkalemia may result from ACE inhibitors 5. Alteration of Renal Excretion: a. Probenecid inhibits renal secretion of penicillin and other medications (see #6, this chapter) b. Salicylates (in small doses) interfere with the uricoscuric action of probenecid 6. Drugs With Opposing Actions: a. Thiazide diuretics elevate blood glucose levels. This may partially counteract the hypoglycemic action of an antidiabetic drug, necessitating adjustment of the dose. b. Many diuretics produce hyperuricemia, requiring dose adjustments 7. Drug Interactions That Can Be Life Threatening: a. Warfarin + phenobarbital b. MAO inhibitor + wine and cheese (tyramine) c. Neomycin + succinylcholine d. Tolbutamide + dicumarol e. Digitalis + thiazide diuretic f. Seldane or Hismanil + macrolide antibiotics g. Seldane or Hismanil + Imidazole antifungal agents 8. Potential Drug Interactions During the Perioperative Period: a. Increase anesthetic requirements (Halothane/enflurane/isoflurane) on the following: i. Patients on MAO inhibitors ii. Alcoholism iii. Cocaine b. Decrease anesthetic requirements: i. Alcoholism ii. Alpha-methyldopa iii. Clonidine iv. Verapamil c. Potentiate neuromuscular blockers: i. Magnesium ii. Aminoglycoside antibiotics iii. Lithium iv. Lidocaine v. Quinidine 9. Other Drug Interactions: a. Tagamet®: Interacts with benzodiazepines: sedation may be enhanced b. Morphine and meperidine: Interacts with CNS depressants: enhanced

sedation c. Valium®: Interacts with alcohol, antihistamines, barbiturates, narcotics: increased CNS depression 10. Possible adverse reactions to antibiotics in the elderly: a. Pen G potassium: Hyperkalemia in patients with renal insufficiency b. Pen G sodium: Sodium retention, volume overload c. Carbenicillin: Pulmonary edema, hypokalemia associated with serious arrhythmias, postop hemorrhage d. Ticarcillin: Pulmonary edema, neurotoxicity e. Tetracyclines: Exacerbation of pre-existing abnormal renal function f. Minocycline: Vestibular disorders (nausea, vomiting, dizziness, vertigo) g. Cephalothin: Nephrotoxicity, acute renal failure h. Aminoglycosides: Nephrotoxicity, ototoxicity i. Clindamycin: Pseudomembranous colitis j. Chloramphenicol: Bone marrow suppression, aplastic anemia k. Trimethoprin-sulfamethoxazole: Blood dyscrasias in patients with borderline folate stores

Drugs 1. Topical antibacterials: a. Muprocyn (Bactroban®): Effective against gram (+) cocci b. Iodochloroquine (1 % cream/ointment): Effective against gram (+) and (-) organisms c. Gentamycin (Garamycin®): An aminoglycoside effective against gram (+) and (-) organisms d. Chloramphenicol (Chloromycetin®): Effective against gram (+) and gram (-) organisms. Blood dyscrasias have been reported 2. Topical antiseptics: a. Povidone-lodine (Betadine): Antibacterial and antifungal scrub b. Chlorhexidine (Hibiclens: Antibacterial and antifungal, and nonallergenic c. Hexachlorophene (Phisohex: Antibacterial and antifungal, a neurotoxin (especially in infants) d. Benzalkonium Cl (Zephiran Chloride®): A quaternary ammonium compound. Antifungal and antibacterial depending on the concentration e. Dakin's Solution (sodium hypochlorite): Active ingredient of commercial liquid bleaches 3. Astringents: Have drying effects secondary to evaporation. Astringents precipitate protein, thereby decreasing oozing a. Burrow's solution: 5% aluminum acetate b. Domeboro's powder (Pedi-boro®/Bluboro®): Aluminum sulfate and calcium acetate c. Dalibour solution: Copper and zinc sulfates with camphor d. Silver nitrate (0.1-0.5%): Also has antiseptic effects e. Acetic acid (1-2%): May decrease pseudomonas colonization

4. Drugs to treat Rheumatoid Arthritis; a. Hydroxychloroquine (Plaquenil®): Can cause muscle weakness that can affect the DTR's b. Penicillamine (Cuprimine): Cytotoxic and immunosuppressant (cytotoxic to lymphocytes and can cause bone marrow depression) c. Gold salts: Toxicity may affect the CBC with a lowering of the Hb, WBC, and platelets. Skin reaction in sun-exposed areas i. Parenteral: Solganal®, Myochrysine® ii. Oral: Auranofin® d. Cytotoxics/lmmunosuppressants: Cytotoxic to lymphocytes and can cause bone marrow suppression, making patients more susceptible to infections i. Methotrexate (Rheumatrex) ii. Azathioprine (Imuran®) e. Glucocorticoids 5. Adrenocorticosterolds: a. Control mechanism: Corticotropin (ACTH) released from the anterior pituitary stimulates the adrenal cortex to secrete glucocorticoids (cortisol) and other corticosteroids. The release of ACTH is affected by corticotropin releasing factor (CRF) from the hypothalamus. ACTH and CRF are subject to negative feedback inhibition by cortisol/glucocorticoids. ACTH is at its highest level in the early morning b. Actions/Side effects of glucorticoids: Any dose of glucocorticoids may exert a physiologic (replacement) or pharmacologic (anti-inflammatory, immunosuppressive) effect. Adverse effects can result from too rapid withdrawal, manifesting as acute renal insufficiency. Glucocorticoids inhibit the early and the late phases of the inflammatory response. The physiologic antagonism of histamine, prostaglandin, and kinin-induced vasodilation occurs. There is an inhibition of prostaglandin and leukotriene synthesis. Also, leukocyte adherence, chemotaxis, and bacteriocidal/fungicidal activities are reduced. An inhibition of interleukin1 and T-cell lymphokine release occurs: i. Hepatic gluconeogenesis/glycogen deposition ii. Suppression of the HPA axis (after 5-7 days of high dose therapy) iii. Decrease resistance to infection (signs of infection may be masked) iv. Possibility of perforation in patients with peptic ulceration or inflammatory bowel -disease v. Myopathy: characterized by weakness of proximal muscles of the arms and legs (tendon rupture) vi. Osteoporosis (postmenopausal females are at greatest risk), fractures, aseptic necrosis of the femoral head vii. Fluid and electrolyte imbalances (sodium and water retention, hypokalemia) viii. May increase blood pressure and exacerbate K+ sensitive arrhythmias ix. Exacerbation of diabetes mellitus x. Impaired wound healing and skin fragility xi. Increased frequency of subcapsular cataracts or glaucoma xii. With high doses, psychologic disturbances (steroid psychosis) may occur

c. Agents: i. Short-acting:
Betamethasone sodium phosphate: Celestone®,
Dexamethasone sodium phosphate: Decadron®, Hexadrol® ii. Long-acting:
Hydrocortisone:
Dexamethasone acetate: Decadron-LA®
Triamcinolone acetonide: Kenalog®
Methylprednisolone acetate: Depo-Medrol® iii. Mixtures:
Betamethasone acetate and phosphate: Celestone Soluspan® 6. Drugs to treat gout: a. Colchicine: This inhibits PMN migration and phagocytosis of urate crystals, PMN lactic acid production is reduced. Colchicine is used to treat acute gout. It can be used IV for a more rapid response when there is gastric intolerance precluding oral therapy (oral dose is .5-1.2 mg followed by .5-1.2 mg every 1-3 hours until pain is relieved or GI distress develops. No more than 8 mg should be given) (IV dose is 2 mg administered slowly over 2-5 minutes, followed by .51.0 mg every 6 hours. No more than 4 mg should be given in 24 hours). This medication inhibits spindle formation during mitosis, therefore decreases DNA activity (DNA activity is a source of urates) b. Uricosuric agents: i. Probenecid (Benemid®): inhibits renal tubular absorption of urate, approximately doubling the daily excretion of uric acid ( also inhibits the tubular excretion of most penicillins/cephalosporins, naproxen, indomethacin, methotrexate, and oral hypoglycemics NOTE* In diabetics using probenecid, a false positive test may result for urinary glucose using Clinitest® reagents may be observed ii. Sulfinpyrazone (Anturane): similar to probenecid in action c. Xanthine oxidase inhibitors: i. Allopurinol (Zyloprim): Inhibits xanthine oxidase which converts xanthine into uric acid. This drug is contraindicated in an acute attack (acts as a competitive

inhibitor of the enzyme) d. NSAIDs: Used for symptomatic relief of acute gouty arthritis 7. NSAIDs: a. Actions: i. Analgesia ii. Anti-inflammatory iii. Antipyresis iv. Gastric symptoms v. Inhibition of platelet aggregation (reversible) vi. Exacerbation of symptoms of aspirin-intolerant patients vii. Other: CNS symptoms, hepatic injury with elevation of serum transaminase, cutaneous reactions b. Indications: i. Arthritis ii. Tendonitis iii. Soft-tissue inflammation iv. Mild to moderate pain NOTE* The action of NSAIDs are compared to aspirin in reducing symptoms

c. Groups: i. Salicylates:
Diflunisal (Dolobid®) ii. Propionic acids:
Ibuprofen (Motrin®) iii. Acetates:
Naproxen (Naprosyn®/Anaprox®)
Fenoprofen (Nalfon®)
Ketoprofen (Orudis®)
Etodolac (Lodine®)
Flurbiprofen (Ansaid®) iv. Pyrole acetic acids:
Indomethacin Indocin®)
Sulindac (Clinoril®)
Tolmetin (Tolectin®)
Nabumetone (Relafen®) v. Oxicams:
Piroxicam (Feldene®) vi. Phenylacetic acids
iclofenac (Voltaren®) vii. Pyrazoles:
Phenylbutazone (Butazolidin®) viii. Fenamates:
Meclofenamic acid (Meclomen®) d. Drug interactions with NSAIDs:

i. Anticoagulants: May prolong prothrombin time ii. ACE inhibitors: Reduce the antihypertensive effect iii. Beta Blockers: Reduce the antihypertensive effect iv. Lithium: Lithium levels increased v. Loop diuretics: Effect of diuretics decreased vi. Methotrexate: Increased risk of methotrexate toxicity v. Thiazides: Decreased antihypertensive/diuretic actions vi. Probenecid: Increased concentrations of NSAIDs 8. Laxatives/Antidiarrheals: a. Laxatives: Are used for the treatment of constipation secondary to the use of opiate analgesics for postoperative pain relief. Are classified by differences in mechanism (active or passive), intensity of effect, and time to the onset of action i. Passive (24-72 hours): Metamucil®, Colace®, Chronulac® ii. Active (6-8 hours): Ex-lax®, Senokot®, Dulcolax® iii. Saline cathartics (30 minutes-3 hours): Magnesium citrate, Milk of Magnesia®) iv. Suppositories (15 minutes-1 hour): Glycerin, Dulcolax b. Antidiarrheals should not be used for the treatment of acute diarrhea associated with broad-spectrum antibiotics because of possible exacerbation of pseudomembranous colitis i. Passive (non-opiate): Kaopectate®, Pepto-Bismol® ii. Opiates and others (decrease GI motility): Lomotil®, Imodium® 9. Muscle relaxants: Decrease skeletal muscle tone for use in acute muscle spasms. Can be used after muscle or tendon transfer. All agents cause a degree of sedation or CNS dysfunction. Most agents are combined with acetominophen or aspirin a. Centrally acting agents: i. Metaxalone (Skelaxin®): contraindicated in patients prone to hemolytic anemia ii. Carisoprodol (Soma®): Contraindicated in acute intermittent porphyria iii. Cyclobenzaprine (Flexeril®): Contraindicated in patients who have cardiac pathologies or those receiving MAO inhibitors iv. Orphenadrine (Norflex®): Contraindicated in glaucoma or prostatic hypertrophy v. Chlorzoxazone (Paraflex®) 10. Antiemetics: May be required postoperatively to control nausea and vomiting. Drug-induced vomiting is believed to be mediated by dopamine impulses within the chemoreceptor trigger zone of the CNS, therefore dopamine receptor antagonists are generally effective a. Phenothiazines: These drugs exert dopamine-receptor antagonism, plus provide variable blockade of alpha-adrenergic (hypotension), chlolinergic (atropine-like), and histamine receptors. Therefore these drugs should be used with caution in patients with cardiovascular disease i. Prochlorperazine (Compazine®) ii. Chlorpromazine (Thorazine®)

iii. Promethazine (Phenergan) b. Nonphenothiazines: i. Trimethobenzamide (Tigan®): Contraindicated in patients who have hypersensitivity to local anesthetics ii. Benzquinamide (Emete-Con): May increase blood pressure, especially in patients receiving epinephrine or other pressure agents iii. Hydroxyzine (Atarax®/Vistaril®): 11. Opioid analgesics and antagonists: Opioid analgesics exert their actions by combining with one or more subtypes of opioid receptors within the CNS, peripheral nervous system, or smooth muscles. The receptors designated mu, kappa, or sigma are the most significant. Opioid analgesics are classified into 3 groups based on the action at these receptors

12. Morphine/Morphine-like agents/Antagonists: Morphine exerts its actions largely through agonistic behavior at the mu and kappa receptors a. Actions: i. Analgesic response characterized by a reduction in the sensory intensity and the emotional response to pain ii. Sedation and euphoria (behavioral) iii. Depression of autonomic reflexes yields respiratory depression, pupillary constriction, suppression of cough reflex, orthostatic hypotension iv. Peripheral effects: constipation, increased urethral tone, weak bronchoconstriction b. Precautions: i. Contraindicated in diarrhea characterized by pseudomembrane formation ii. Use cautiously in patients with bronchial asthma, chronic obstructive pulmonary disease or cor pulmonary c. Drug interactions:

i. May potentially affect other CNS depressants ii. May cause toxic reactions in patients receiving MAO inhibitors d. Agonists-Antagonists: i. Agonists: Dependence/abuse are less with these, and withdrawal symptoms are less than with morphine-like drugs ii. Antagonists (Naloxone/Narcan®): this antagonizes the mu, kappa, and sigma receptors, thereby preventing or reversing opiate-induced respiratory depression, sedation, hypotension and psychomimetic effects of sigma agonists such as pentazocine. Should be used to achieve complete or partial reversal of opiate induced CNS depression and can be used to diagnose suspected opioid overdose 13. Analgesic combinations: The analgesic effect of the opioids can be enhanced by the concurrent administration of a non-narcotic analgesic. Also these may contain caffeine, antacids, or barbiturates a. Codeine combinations: Tylenol® with codeine, empirin with codeine, APC with codeine, Fiorinal® b. Oxycodone combinations: Percodan®, Tylox®, Percocet® c. Hydrocodone combinations: Vicodin®, Lortab®, Dolo-Pap® d. Pentazocine combinations: Talwin Compound®, Talacen® e. Propoxyphene combinations: Darvon® with ASA, Darvon-N® with ASA, Darvocet-N 50/ N-100®, Darvon Compound® 14. Antidepressants for chronic pain syndromes: Any antidepressant may be used to treat pain but the heterocyclic compounds are more popular. The dosages are generally 1 /2 of those used for the treatment of depression a. Amitryptyline (Elavil®): 25-100 mg b. Doxepin (Apadin): 25-100 mg c. Imipramine (Tofranil®): 50-100 mg 15. Antihistamines: Nearly all mammalian tissue contain histamine, with the highest concentration found in the lungs, skin, and stomach. Histamine is also stored in the mast cells and in circulating basophils where it is released by antigenic stimuli or indirectly by organic bases. Responses to stimuli are mediated by 2 distinct populations called H1 and H2. Antihistamines are H1receptor antagonists a. Actions: i. Reduce prominent vasodilation, vasodilation, increased microvascular permeability, and bronchoconstriction caused by histamine ii. Variable anticholinergic, antipruritic, sedative, and antiemetic effects iii. Since related to local anesthetics, demonstrate local anesthetic activity b. Indications: I. Adjunct in the treatment of pruritus and allergic reactions ii. Nocturnal leg cramps iii. As local anesthesia in patients allergic to amides and ester-linked compounds

iv. Perioperative medication

16. Anxineytics (Sedative-Hypnotics): Benzodiazepines a. Major effects: i. Anxiolytic action (that is distinguished from the effects of reduced conscious excitability) ii. Sedation/sleep induction iii. Skeletal muscle relaxation iv. Anticonvulsant action v. Antiemetic effect b. Indications: i. Perioperatively, for the relief of anxiety
Valium®- 10 mg PO or IM
Ativan®-0.05 mg/kg IM up to 4 mg
Librium®- 50-100 mg PO or IM 1 hour before surgery ii. Conscious sedation iii. Sleep induction:
Dalmane®- 15-30 mg
Restoril®- 15-30 mg


Halcion®- .25-.5 mg
Ativan®- 2-4 mg iv. Skeletal muscle relaxation:
Valium®- 5-10 mg 3-4 times daily v. Termination of acute seizures
Valium®- 5-10 mg IV, repeated every 10-15 minutes prn, or 2-3 mg IV repeated every 5 minutes c. Precautions: i. Contraindicated in acute narrow angle glaucoma ii. IV administration may result in apnea or hypotension

Chapter 21: Surgery of the Congenital Foot Flatfoot Surgery (flexible) Subtalar Joint Blocking Procedures: (Arthroereisis and Arthrodesis) Flatfoot Surgery (rigid): Convex Pes Piano Valgus Metatarsus Adductus Surgery Cavus Foot Surgery Clubfoot Surgery

SURGERY OF THE CONGENITAL FOOT Flatfoot Surgery (Flexible), 1. Etiology of Flexible Flatfoot (pes planovalgus): a. Rare syndromes: (Down's, Ehler's-Danlos, Marfan's, and Morquio's syndromes) b. Calcaneovalgus: (not all cases) c. Biomechanical: i. Forefoot varus ii. Forefoot valgus iii. Equinus iv. Torsional abnormalities v. Muscle imbalance (weakness of the supinators) vi. Ligamentous laxity d. Neurotrophic feet (early stages) e. Enlarged or accessory navicular f. Limb length inequality 2. Biomechanical alterations: a. The subtalar joint is pronated b. The midtarsal joint becomes unstable and unlocked: this is because the STJ is in a pronated position with the calcaneus everted, the T-N joint and the C-C joint become divergent from each other, their axes become more parallel. This allows for independent range of motion of each of these joints and increases the range of motion of the MTJ itself. The pronated STJ allows for compromised function of the peroneus longus and tibialis posterior muscles. This results in loss of osseous stability as the heel comes off the ground. The reactive force of gravity produces a dorsiflexory force on the forefoot. The following are the changes to the foot: i. Arch fatigue ii. Hypermobile first metatarsal iii. Subluxation of the first ray iv. Contraction of the digits v. A medial distribution of body weight when the calcaneus everts beyond 4-5° of eversion. vi. Collapse of the MTJ vii. The axis of the STJ in the normal patient is approx. 42° from the transverse plane 16° from the sagittal plane. Any change in this will result in changes to motion on the various planes. In clinically examining each patient, it may be necessary to estimate the primary plane of motion of the STJ to predict the ability (biomechanically or surgically) to control the STJ. In examining the ROM of the joints of the foot, the predominant axis of motion can be estimated.

NOTE* IF frontal plane motion (inversion/eversion) is predominant the joint axis will be more horizontal. If transverse plane motion (abduction/adduction) is more predominant, the joint axis is more vertical. If sagittal plane motion (dorsiflexion/plantarflexion) is more predominant, the axis will lie closer to the frontal and horizontal planes. 3. Radiographic Alterations: a. If transverse plane dominance: i. Increase in the dorsoplantar T-C angle ii. Increase in the cuboid abduction angle iii. Decrease in the percentage of T-N congruency b. If frontal plane dominance: i. Widening of the lesser tarsus on dorsoplantar view ii. Decrease of the first metatarsal declination angle iii. Decrease in the height of the sustentaculum tall c. If sagittal plane dominance: i. Increase in the talar declination angle ii. Naviculocuneiform breach iii. Increased T-C angle on the lateral view iv. Decreased calcaneal inclination angle d. The stress dorsiflexion lateral view (charger view) is used to determine osseus blocks of the ankle joint. e. Harris-Beath views are helpful in determining T-C coalitions (taken from posterior and superior with the x-ray beam at 35°, 40°, and 45° to the perpendicular). 4. Evaluation, Criteria. and Goals: a. First ascertain the available range of motion: then differentiate rigid vs. flexible flatfoot. Note* Procedures that are effective for flexible flatfoot are usually ineffective for rigid flatfoot, and the foot with bony adaptation secondary to forefoot varus/supinatus also requires a different approach b. Determine the planar dominance: because the foot that presents a high degree of transverse plane motion is extremely difficult to control nonsurgically. c. Surgery must be avoided in the normal low arched foot (pes planus), which must be distinguished from the collapsing pes planovalgus deformity as we are describing. d. Consider the age of the patient and the percentage of bone growth remaining. e. Consider the presence of other related medical conditions f. Consider the presence of other superstructural deforming forces (tibial torsion) g. Other surgical criteria for flexible flatfoot: i. Symptoms are resistant to conservative therapy ii. The unstable foot is not controllable by mechanical devices iii. Secondary changes are present or can be definitely predicted

h. Goals of surgery: i. Relief of pain ii. Biomechanical control of excessive pronation iii. Prevention of progression of the deformity 5. Soft Tissue Approaches: (Medial Column Procedures) a. Kidner procedure: i. Requires the removal of an accessory navicular (changes the leverage of the tibialis posterior ms.). ii. Removal of any hypertrophied tuberosity of the navicular iii. Transposition of the insertion of the tibialis posterior tendon into the underside of the navicular. b. Lowman procedure: i. Achilles tendon lengthening ii. T-N wedge arthrodesis iii. Rerouting the tibialis anterior tendon under the navicular and suture to the spring ligament. iv. Tenodesis of the medial arch with a slip of the Achilles tendon, which is left attached to the calcaneus and folded forward along the medial arch as an accessory ligament (this helps maintain the calcaneus and forefoot in adduction). v. Desmoplasty of the T-N ligaments

c. Young procedure: i. Tendoachilles lengthening ii. Rerouting of the tibialis anterior tendon through a slot in the navicular without detaching the tendon from its insertion. iii. Tibialis posterior reattachment beneath the navicular

6. Osseous Approaches: (medial column procedures) a. Hoke arthrodesis: i. Tendo achilles lengthening ii. navicular to the medial and intermediate cuneiform Note * The Hoke procedure is now used as an adjuctive procedure in combination with a TAL, calcaneal osteotomy, or arthroereisis. It is utilized in the presence of severe N-C sagging, and is reserved for patients whose bone growth is complete and when secondary changes. have occurred in a joint b. T-N arthrodesis: i. Generally used in combination with other procedures (TAL, calcaneal osteotomies, medial column tendon balancing ii. Blocks all MTJ motion and almost all STJ motion iii. When the T-N joint is wedged the procedure can reduce some forefoot varus deformity, and can be combined with an Evans calcaneal osteotomy. iv. Most useful in degenerative joint changes/severe collapse at the T-N joint, part of a repair of a ruptured tibialis posterior, and paralytic deformity. c. Miller procedure: i. Lengthening of the tendo achilles ii. Raising an osteoperiosteal flap left in place proximally, along the medial arch (this includes the spring ligament and tibialis posterior tendon insertion) and reattaches in an advanced position.

iii. Arthrodesis of the navicular-medial cuneiform joint iv. Arthrodesis of the 1st metatarsal-medial cuneiform joint d. Osteotomies of the talus: i. Stokes: ii. Perthes: closing wedge at the talar neck e. Osteotomies of the medial cuneiform: i. Anderson and Fowler: plantar flexory wedge in conjunction with an Evans calcaneal osteotomy. ii. Cotton: opening wedge to produce plantarflexion of the medial column 7. Osseous Approaches: Calcaneal osteotomies (3 types): Calcaneal osteotomies allow some margin for error, because joint motion is still present. You must be specific in choosing procedures for the appropriate problem. You must correct the etiology, not the symptoms. During the procedure, dorsiflex the foot and make sure it is in neutral in all planes before being satisfied on wedge size and fixation. These procedures are basically designed to replace the triple arthrodesis and allow maintenance of joint motion after the foot is corrected. a. Extra-articular: i. Chambers:
A procedure to limit STJ motion by placing a bone graft under the sinus tarsi (similar to arthroereisis) ii. Baker-Hill: (to reduce heel valgus and excessive pronation)
A refined Chambers concept for use in patients with CP
They used a vertical-lateral approach to perform a horizontal osteotomy inferior to the posterior facet of the STJ
A wedge shaped graft is inserted. iii. Selakovich:
Through a medial approach performing an osteotomy and grafting of the sustentaculum tali
Tightening of the spring ligament
Repositioning of the tibialis posterior
Transfer of all/part of the tibialis anterior into the navicular b. Anterior: i. Evans (refined by Ganley): good when the forefoot abducts severely when the STJ is in neutral. This procedure is contraindicated in neurological disorders that may generate spasticity and varus due to functional overcorrection. The rationale for this procedure is that as the lateral column is lengthened, the entire forefoot is forced to pivot around the head of the talus, effectively adducting the forefoot and tightening the structures of the arch NOTE* If there is excess lengthening of the lateral column, an equinus may be produced (talus abducts and dorsiflexes)


Due to scarring the incision has been changed, to one parallel to the skin tension lines in an oblique/transverse fashion on the lateral side of the foot





over the C-C joint (avoid the sural nerve inferiorly and the intermediate dorsal cutaneous nerve superiorly; they are found at the extreme poles of the incision) The peroneals are retracted inferiorly Reflection of the EDB ms. dorsally while preserving the dorsal calcaneocuboid ligament NOTE* This ligament is critical in limiting the dorsal shift of the anterior beak of the calcaneus






Osteotomy of the calcaneus parallel and 1.5 cm proximal to the C-C joint from lateral to medial insertion of tibial bone graft or bone bank iliac crest, which is tapped into position, and any void filled with bone chips Suture the EDB back into place: impossible to achieve good closure of this muscle layer Note* This procedure straightens the lateral column with reduction of heel valgus. In most cases it is still necessary to reduce the amount of forefoot varus and stabilize the medial column by doing a T-N fusion, wedge osteotomy of the cuneiform, naviculocuneiform fusion, or medial arch tenosuspension (predominant)




Complications include undercorrection/overcorrection, delayed/nonunion, and if there is a met. adductus present It will be made worse. Note* One of the most difficult pes planovalgus foot types to treat is one with a vertical STJ axis. This foot compensates for deforming forces mainly in the transverse plane. This foot is recalcitrant to mechanical control and medial column procedures. Lateral column lengthening procedures are indicated (Evans procedure)




When the Evans procedure is done in conjunction with a medial arch tenosuspension the cuboid abduction angle is decreased, the forefoot abduction angle is decreased by an average of 170 and the calcaneal inclination angle is increased by 7°. c. Posterior (varus producing osteotomies): Are designed to place the weightbearing surface of the calcaneus in neutral or varus, preserve STJ motion while changing the ratio of available inversion/eversion i. Gleich
Oblique calcaneal osteotomy displaced anteriorly, helps increase the calcaneal inclination angle ii. Dwyer
Most commonly performed as an opening wedge (can be closing wedge also) from the lateral side
Slightly overcorrect with the osteotomy

iii. Silver
Lateral opening wedge osteotomy with the direction from just posterior to the posterior facet running inferiorly. iv. Koutsogiannis
Lateral approach with a transection osteotomy of the calcaneus (oblique) Posterior fragment is medially displaced until it lies below the sustentaculum tali Note* Posterior calcaneal osteotomies are most useful in the least prevalent type of pes planovalgus, where there is frontal plane dominance. These osteotomies are most useful in conjunction with medial column procedures v. Additional procedures:
Sullivan (a dorsal anterior sliding osteotomy of the posterior aspect of the calcaneus to treat equinus)
Moeller (triplane closing wedge osteotomy of the lateral cortex, for cavus foot)
Keck and Kelly (dorsal closing wedge osteotomy just anterior to the achilles; it will decrease the inclination angle and remove pressure from a Haglund's deformity)
Reinhart (for pes cavus deformity where a through and through osteotomy is done) 8. Ancillary Procedures: a. Tendo Achilles lengthening: is indicated in almost all of the above flatfoot procedures 9. Rearfoot Arthrodesis: Is usually used with severe DJD, severe triplane deformity with pain, paralytic deformity, or for long-standing rupture of the tibialis posterior, with collapse of the foot. a. Subtalar arthrodesis: Restores the appropriate T-C relationship while preserving midtarsal motion i. The procedure involves resection of the sinus tarsi with packing with autologous bone chips, and screw fixation. ii. Objections to this procedure include:
Fusion of one portion of the STJ results in DJD of the other joints
No correction occurs in the forefoot which is usually in varus
Potential for fatigue failure of the screw
Long term loss of the correction b. Triple arthrodesis: Because this is a long-standing and reliable procedure, it will be discussed in great detail. i. Definition: fusion of the T-C, C-C, and T-N joints ii. History: originally used for paralytic deformities, modified by Ryerson in 1923 with a two incision approach/internal fixation/above knee casting. iii. Indications: pain, instability, structural deformity (rigidity) iv. Specific etiological conditions:
Valgus foot deformity







vi.



v.











Collapsing pes valgus deformity Ruptured posterior tibialis tendon Tarsal coalitions Tarsal arthritis Cavus foot Talipes equinovarus Preoperative considerations: Procedure must be delayed until the patient reaches skeletal maturity Patient must have adequate ankle dorsiflexion available Due to the amount of dissection prophylactic antibiotics should be considered Hemostasis necessary during the procedure Surgery: The dissection is started laterally passing between the sural and the intermediate dorsal cutaneous nerves. The contents of the sinus tarsi are vacated, the extensor digitorum brevis muscle is reflected distally, and the peroneals are mobilized and protected from the lateral surface of the calcaneus. This gives exposure to the posterior facet, the C-C joint, and the lateral aspect of the T-N joint. The medial incision is dissected down to the dorsomedial aspect of the T-N joint. The periosteum and posterior tibial tendon are dissected inferiorly off the navicular, and the periosteum is reflected off the dorsal surface of the navicular and the head and neck of the talus until it connects with the lateral incision. If a subtalar wedge is to be taken, the medial incision dissection is carried posteriorly, reflecting the periosteum and the deltoid ligament of the sustentaculum tali, exposing the anterior and middle facets. A minimal amount of bone is resected off all joint surfaces. The MTJ -is resected first, which relaxes tissues and makes it easier to manipulate the foot. Any wedging of the MTJ should be done after the STJ is resected and temporarily fixed. In any wedging of the STJ, the most bone should come off the calcaneus. The rearfoot and forefoot must be fixed in slight valgus, because a valgus foot can be accommodated to be comfortable and a varus foot can rarely be made comfortable. If inadequate dorsiflexion is available at the ankle then jamming of the anterior ankle will occur causing development of chronic synovitis and degenerative destruction of the foot. Too much resection posterior to the STJ will cause dorsiflexion of the ankle joint and jamming. Anterior displacement of the talus on the calcaneus will plantarflex the forefoot, while posterior displacement of the talus will dorsiflex the forefoot. Plantarflexion of the forefoot will cause more ankle joint dorsiflexion and jamming of the ankle. The forefoot can be rotated on the rearfoot to accommodate frontal plane problems. Temporary fixation is achieved with K-wires or Steinmann pins. The STJ is fixated first. Rigid compression fixation gives more constant joint fusion. A 6.5mm cancellous or cannulated screw is used to fixate the STJ. Using screws in the MTJ is difficult due to the angulation, and so staples may be used for fixation of the T-N and C-C joints. Fluoroscopy or intraoperative xrays must be taken to assure proper position.

vi. Postoperative management:
Jones compression cast for 2-3 days
Drain pulled at 48-72 hours
A B-K NWB cast is applied for 8 weeks
Change cast and suture removal at 2-3 weeks
Change cast every 2-3 weeks thereafter
Take serial x-rays to evaluate healing every 4 weeks
A B-K WB cast is then used for 4 weeks
Physical therapy continued for 3 months
Goal is a return to normal function 6 months postoperatively vii. Complications:
Fracture
Wound dehiscence
Peroneal tendonitis
Entrapment neuropathy
Nonunion viii. Postoperative gait pattern:
Abducted gait
Shorter stride
Difficulty in going down stairs

Subtalar Joint Blocking Procedures (Arthroereisis and Arthrodesis) for Flatfoot There are 2 major categories: extra-articular arthrodesis which actually fuses the joint by means of a bone graft eliminating all motion, and arthroereisis which limits excessive valgus motion of the STJ and retains the varus range of motion. 1. Arthrodesis: a. Grice Green (EASTA: extra-articular subtalar joint arthrodesis): This procedure allows you to fuse the STJ without disturbing growth. i. Indications
Paralytic instability and equinovalgus
Peroneal spastic flatfoot
Unresectable tarsal coalitions
Age bracket 3-14 years old ii. Contraindications
Ankle valgus flatfoot iii. Procedure
Use corticocancellous graft placed at 900 to the STJ axis 2. Arthroereisis: a. Indications i. To see if a patient needs an arthroereisis: have the patient stand on the toes, the heel must supinate ii. Age is 4-8 years iii. Cavovalgus foot iv. A foot that has been unresponsive to treatment for 2 years

v. Eversion of the heel at least 8° vi. Predominant frontal plane deformity vii. Flexible forefoot varus deformity above 10° b. Contraindications i. Rigid flatfoot ii. Significant arthritis/trackbound tarsal joints iii. Ankle valgus iv Equinus (must be released) v. Skewfoot vi. Torsional problems vii. Frontal plane knee deformity c. 3 types i. Self-locking wedge
Viladot
Valenti
Addante
Valgus stop ii. Axis altering (not for adults): elevates a low STJ axis
STA-peg iii. Direct impact (can be used for all ages)
Sgarlato
Pisani d. Anatomical placement i. Sinus tarsi
Valgus stop
STA-peg
Sgarlato ii. Canalis tarsi
Valenti
Viladot e. Postoperative care i. Cast for 2 weeks ii. Orthoses and high top sneakers for 1 year f. Complications i. Extrusion of the implant ii. Fracture of the implant iii. Fracture of the calcaneus iv. Improper placement of the implant v. Over/undercorrection vi. Infection vii. Erosion of the bone-implant interface

Flatfoot Surgery (rigid): Convex Pes Planovalgus 1. Etiology of Rigid Flatfoot: a. Vertical talus b. Congenital T-N dislocation c. Arthrogryphosis d. Tarsal coalition/peroneal spastic flatfoot

e. Tarsal arthrosis caused by trauma f. Cerebral palsy g. Spina bifida h. Improper correction of clubfoot i. Post-traumatic j. Neurotrophic (late stages) 2. Clinical Presentation of Convex Pes Planovalgus (vertical Talus): (see pediatrics) a. Rocker-bottom deformity with prominent talar head bulge on the medial and plantar aspect of the foot. b. The forefoot may actually touch the anterior surface of the tibia c. Valgus rearfoot that is in equinus

3. Radiographic Presentation of Convex Pes Planovalgus: a. Definitive diagnosis when it is evident that the tarsal navicular is dorsally dislocated on the neck of the talus even when the foot is maintained in a stress plantarflexed attitude (forced plantarflexion and inversion will not reduce the dislocation of the T-N joint in a true convex pes piano valgus deformity). b. Talus is vertical, lying parallel to the longitudinal axis of the tibia c. Calcaneus is in an equinus position d. T-C angle is abnormally increased on the D-P view 4. Pathology of Convex Pes Planovalgus: a. Severe dislocation of the T-N joint (navicular is articulating with the dorsal aspect of the talus b. Neck of the talus is hypoplastic c. Talar head is flattened d. Calcaneus is displaced posteriolaterally e. Calcaneus is convex on its plantar surface f. The tibialis posterior and peroneals are located anterior to their normal

position and are contracted g. The tibialis anterior, EHL, EDL, and the triceps surae are contracted h. The tibionavicular ligament and dorsal talonavicular ligament are contracted (the problem in the repair of this foot type) Surgery of the Convex Pes Planovalgus Foot: Surgery is dependent upon patient's age, clinical and radiographic features, type and degree of previous treatment, and experience of the surgeon. The common objective of all procedures is release of all soft tissue contractures, establishment of a rectus forefoot to rearfoot relationship, and the production of equal medial and lateral foot columns. a. Talar procedures: resect the head and neck of the talus b. Navicular procedures: naviculectomy c. Tendon transfers: transfer of the tibialis anterior/posterior and peroneals d. Open surgical reduction: T-N joint reduction along with a peritalar release, heel cord lengthening, extensor and peroneal tendon lengthening, STJ and ankle joint capsulotomy, calcaneocuboid joint reduction, and transfer of the tibialis anterior into the navicular (K-wires removed at 6 weeks and A-K cast removed at 3 months)

Metatarsus Adductus 1. Indications a. Failure to respond to conservative treatment b. Residual deformity after treatment of talipes equinovarus c. Newly diagnosed metatarsus adductus deformity 2. Considerations: (see section Pediatrics) a. Age of patient b. Osseous development c. Severity of deformity d. Presence of concomitant deformities e. Extent of malfunction and disability 3. Soft Tissue Surgery: a. Heyman, Herndon, and Strong: i. Indications:
For flexible met. adductus which is reducible on manipulation (stress x-ray)
Usually children less than 5 years old
Deformity present at Lisfranc's joint, without significant bowing present in the proximal portion of the metatarsal bones themselves ii. Procedure:
2 or 3 longitudinal dorsal incisions, or a transverse incision
Release of the dorsal, interossei, and plantar ligaments of the tarsometatarsal joints and intermetatarsal joints
Preserve the plantar-lateral ligaments, especially 5th metatarsocuboid articulation and the peroneus brevis tendon
Manipulate the foot into abduction
K-wire fixation of the first met-cuneiform joint and 5th met-cuboid joint
Release of the naviculocuneiform and intercuneiform joints is rarely needed


Consider abductor hallucis release or tenotomy in conjunction with HH&S iii. Precautions
Avoid damage to the 1st metatarsal epiphyseal growth plate (do not confuse this with the met-cuneiform joint)
Be careful not to introduce latrogenic dorsal dislocations at the metcuneiform joints iv. Postop care
Cast for 6-12 weeks
Manipulate the foot and recast every 3-4 weeks depending upon the severity
Monitor the foot carefully for the development of a flatfoot deformity v. Complications
Dorsal dislocation
Degenerative arthritis
Damage to the growth plates b. Thompson procedure (modified): i. Indications
Congenital hallux varus primarily
Flexible met. adductus secondarily
Hyperactivity of the abductor hallucis ms. ii. Procedure
Medial longitudinal 1st m.p.j. skin incision approach
Dissection to level of deep fascia over the abductor hallucis muscle
Transection of the abductor hallucis tendon with resection of a segment of the tendon and portion of the distal muscle
Consider lesser m.p.j. release medially if lesser digits are also adducted
Release of the medial head of the flexor hallucis brevis if adduction of the hallux is still present iii. Precautions
Do not reduce varus of the hallux without insuring correction of any adduction deformity of the first metatarsal
Place the medial incision over the 1st m.p.j. strategically; if too superior or inferior, may damage the medial neurovascular bundle
Avoid the procedure as a primary mode of correction for met. adductus unless clinical findings and x-rays strongly support hyperactivity of the abductor hallucis as the primary etiology iv. Postoperative care
Weightbearing in a surgical shoe for 3-6 weeks
Splinting of the hallux and the first ray v. Complications
Hallux abductovalgus
Hallux hammertoe (hallux malleus) c. Johnson osteochondrotomy: cartilaginous procedure i. Indications
Met. adductus deformity in children between the ages of 5-8 years (can be younger) ii. Procedure






3 dorsal longitudinal incisions Closing abductory base wedge osteotomy of the 1st metatarsal Wedge resection of cartilage and bone from the bases of the lesser metatarsals, distal to the proximal articular surface (base is lateral with the apex medial)
Fixation of the osteotomies with stainless steel wire, k-wires, or staples iii. Precautions
Avoid damage to the epiphyseal growth plate of the 1st metatarsal
Overcorrection/undercorrection of individual ray segments iv. Postoperative care
Non-weightbearing with cast immobilization for 6-8 weeks
Serial x-rays to assess healing 4. Osseous Surgery: a. Modified Berman-Gartland procedure: i. Indications
Met. adductus in the child older than 6-8 years old
Residual deformity following treatment of talipes equinovarus ii. Procedure
3 dorsal longitudinal incisions
Transverse or oblique-type closing abductory wedge osteotomy of the 1st metatarsal
Similar type of osteotomies of the lesser metatarsals with the cortical hinge medially
Fixation of osteotomies with SS wire, K-wires, staples, AO screws or combinations iii. Precautions
Avoid damage to growth plate of 1st metatarsal
Meticulous subperiosteal dissection is critical to avoid heavy callus formation and undesirable synostosis between adjacent metatarsals
Preservation of the medial cortical hinge is important to insure stability
Careful planning to avoid over/undercorrection iv. Postoperative care
Non-weightbearing cast immobilization 6-8 weeks
Convert the cast to posterior splint and start PT
Orthotics when patient resumes weightbearing
Serial x-rays to assess bone healing at 6 weeks, 12 weeks, 24 weeks and 1 year v. Complications
Over/undercorrection
Delayed union/nonunion/pseudoarthrosis
Fracture of cortical hinge
Damage to growth plate
Elevatus of metatarsals
latrogenically induced flatfoot deformity b. Lepird procedure: i. Indications
Met. adductus in the child greater than 6-8 years old


ii.



Residual talipes equinovarus deformity Procedure 3 dorsal longitudinal incisions Oblique closing-abductory wedge osteotomy (Juvara type) of the 1st metatarsal with AO/ASIF screw fixation
Rotational osteotomy of each lesser metatarsal with AO/ASIF screw fixation (2.7 mm cortical used mostly) perpendicular to the plane of the osteotomy
An oblique closing wedge osteotomy may be used on the 5th metatarsal in place of the rotational type (if preferred)
Rotational osteotomies are performed from dorsal-distal to plantarproximal with temporary preservation of the cortical hinge (facilitates fixation). The osteotomy is approximately 45° from the weightbearing surface. The precise angle will depend on the declination of the metatarsal segment. As the declination of the metatarsal increases, the osteotomy will be more parallel to the weightbearing surface of the foot
Area of the cortical hinge preserved is most commonly proximal/plantar
The screws are then removed and the osteotomy is completed
The screws are reinserted, the distal fragments are rotated laterally, and the screws are tightened
The alignment of the foot is assessed; if realignment is necessary the screw(s) can be loosened and the bone adjusted iii. Postoperative care
Same as Berman-Gartland iv. Complications
Same as Berman-Gartland
if the osteotomy is performed too vertically the rotation of the osteotomy will be around the longitudinal axis of the metatarsal bone itself, resulting in inversion/eversion of the bone itself v. Advantages
This procedure is amenable to rigid internal fixation and primary bone healing
Over/undercorrection can be corrected during surgery
Biplanar correction can be achieved
Eliminates pin tract infections 5. Ancillary Procedures: a. Equinus Deformity i. TAL ii. Gastrocnemius recession b. Flatfoot Deformity: i. STJ arthroereisis ii. Evans calcaneal osteotomy iii. Modified Young's tenosuspension/ Modified Kidner procedure iv. T-N joint arthrodesis/ N-C arthrodesis

Cavus Foot Type 1. Description: Pes cavus is primarily a sagittal plane deformity and can best be described by the area of involvement.

a. Anterior pes cavus: Types i. Metatarsus cavus (at Lisfranc's joint) ii. Lesser tarsal cavus (lesser tarsus) iii. Forefoot cavus (Chopart's joint) iv. Combined anterior cavus (occurring at 2 or more of the aforementioned areas) b. Rearfoot cavus: may not truly be a separate cavus deformity. It may be a compensation for anterior cavus. It etiology is: i. Pseudoequinus: reverse buckling of the ankle joint ii. Muscle weakness/spasticity iii. Congenital c. Combined: both rearfoot and forefoot Note* The apex of the deformity should be located on a lateral x-ray 2. Etiology: a. Neuromuscular: 66% Note* Because there is such a high correlation between neuromuscular disease and pes cavus, and because the cavus foot is often an early manifestation of such disease, a neurology consult is mandatory prior to any surgical intervention i. Muscle lesion: muscular dystrophy ii. Peripheral nerve lesion: Charcot-Marie-Tooth, polyneuritis, traumatic lesion iii. Spinocerebellar tract: Friedreichs ataxia iv. Anterior horn cell: poliomyelitis, cord tumors v. Pyramidal/extrapyramidal: cerebral palsy vi. Cerebral cortex: hysteria b. Congenital i. Pes arcuatus (rare) ii. Spina bifida iii. Myelomeningocele iv. Clubfoot v. Congenital syphilis c. Idiopathic: 33% i. Trauma ii. Infection iii. Ledderhose's disease iv. Spinal cord tumors 3. Classification: a. Flexible deformity (mild): Non-weight bearing, contracted digits, high arch and varus deformity of the heel may be noticed. With loading, digits appear normal, arch is flattened and heel may go into valgus. Minimal clinical symptoms at this point

b. Semi-rigid deformity (moderate): Weight-bearing does not completely reduce the contracture of the digits, arch appears higher and heel is in more varus attitude. Soft tissue contractures and bony adaptation begin to take place. Symptoms are more prominent. c. Rigid deformity (severe): Joint motion is limited. The foot is similar in appearance both weight/non-weight bearing. Digits are contracted dorsally and painful keratomas are present. Difficult to fit shoes. d. Progression of deformity: Often progresses from flexible to rigid as the patient gets older. 4. Compensation for Anterior Cavus: a. Retraction of the toes at the m-p joints (due to extensor substitution) b. Reverse bucking of the m-p joints c. Forefoot reduction of the "flexible" anterior cavus d. Ankle joint dorsiflexion 5. Associated Conditions: a. Forefoot varus b. Forefoot valgus c. Plantarflexed 1st ray d. Metatarsus adductus e. Rearfoot pseudoequinus f. Rearfoot varus 6. Principles of Surgical Judgement: a. The presence of neurological disease will dictate what types of procedures you can and cannot do. You must determine whether the disease is progressive b. For idiopathic pes cavus the following flow chart from McGlamry ED (ed) Comprehensive Textbook of Foot Surgery , 2 ed, Williams & Wilkins, (with permission) illustrates the surgical decision making plan best. c. You must determine whether the deformity is flexible or rigid and follow the preceding flow chart d. You must consider the age of the patient (soft tissue procedures are best in the child) 7. Preoperative Evaluation: a. Neurology consult b. Spinal x-rays c. EMG's and nerve conduction studies d. X-rays of the foot (lateral) i. Calcaneal inclination angle > 30° ii. Talar-1st metatarsal angle > 6° (Meary's angle) iii. Increased pitch of the 5th metatarsal iv. Note apex of the deformity v. Cyma line broken posteriorly (can be normal) vi. Sinus tarsi is clear and accentuated vii. Coalition views should be used to assess the subtalar joint viii. An axial view of the calcaneal angle should be taken to rule out a structural

varus

8. Pathogenesis: a. With weak tibialis anterior the long extensors substitute for ankle dorsiflexion, causing hyperextension of the MPJ's and retrograde pressure on the metatarsal heads (extensor substitution) b. Weak peroneus brevis and strong posterior tibial ms. will create a varus heel c. Paralysis of intrinsics causes the development of clawtoes d. Weak gastrocnemius causes flexor substitution which causes clawtoes. 9. Surgery: Soft tissue a. Plantar release i. Subcutaneous fasciotomy ii. Steindler stripping: through a medial incision the abductor hallucis, -flexor digitorum brevis, and the abductor digiti quinti are stripped from the periosteum of the calcaneus. The plantar fascia is released and the long plantar ligament is released. iii. Tachdjian: describes a plantar medial approach used with a fixed anterior cavus. Includes releasing the long/short plantar ligaments, spring ligament (calcaneonavicular), the calcaneonavicular portion of the bifurcate ligament, and the plantar fascia. Lengthening of the long flexors and the tibialis posterior is performed if on intraoperative reduction of the cavus foot bow-stringing of these tendons is noted iv. Complications:
Plantar fasciitis
Forefoot may become splayed (Note * These procedures are followed by serial casting b. Tendon transfers (give best results when the patient is > 10 years old) i. Jones suspension: transfer of the extensor digitorum longus to the neck of the 1st metatarsal with i.p.j. fusion Complications:
Transfer lesion to the 2nd metatarsal if 1st ray is raised too high
Hallux limitus
Tendon may not hold the correction
Failure of the fusion site ii. Heyman procedure: transfer of all five extensor tendons to their respective metatarsal heads. Complications:
Clawtoes may result
Tendonitis of the EDL
Tendons may not hold the correction
Same as Jones complications iii. Hibbs procedure (modified): transfer of the long extensors to the second and third cuneiform, a Jones transfer of the EHL, anastomosis of the distal stumps of the long extensors to the EDB tendons. This procedure helps load the midtarsal joint in dorsiflexion.

Note* Although the Hibbs procedure is a classic procedure described for the correction of anterior cavus, it should not be performed for pes cavus, because it fails to provide the dynamic force necessary to elevate the metatarsal heads iv. Split tibialis anterior tendon transfer (STATT): the lateral half of the tibialis anterior tendon is sectioned and anastomosed to the peroneus tertius tendon near its insertion into the base of the 5th metatarsal. v. Peroneus longus tendon transfer vi. Tibialis posterior tendon transfer Note* The above procedures are utilized with flexible deformities

10. Surgery: Osseous a. Cole procedure: dorsal wedge tarsal osteotomy to reduce a fixed anterior cavus, which extends from the cuboid laterally through the naviculocuneiform joints medially. The width of the wedge is determined by the severity of the deformity.

Note* The disadvantage of the Cole procedure is that it can result in a shorter, wider, and thicker foot b. Japas procedure: a midtarsal V-osteotomy (apex of the V is proximal and at the highest point of the cavus). The lateral limb of the V extends through the cuboid, and the medial limb of the V extends through the cuneiform Note* Difficult to control the amount of correction Note* The primary difference in indications between the Cole and Japas is that the Cole is for more severe deformities and is only performed in the skeletally mature foot c. 1st ray Dorsal Wedge Flexory Osteotomy d. DWFO all metatarsals Complications: i. If 1st metatarsal is done alone, may get transfer lesion to 2nd ii. May decrease ROM of 1st MPJ iii. May get a metatarsal on different planes e. Truncated tarsometatarsal wedge osteotomies: first described by Jahass, excision of a truncated wedge of bone. across the tarsometatarsal articulations. This procedure is contraindicated in subtalar joint abnormalities, moderatesevere rearfoot varus, or muscular imbalance secondary to Charcot-MarieTooth disease f. McElvenny-Caldwell procedure: elevation of the first metatarsal by fusing the 1st met-cuneiform joint. If the deformity is too severe then fusion of the N-C joint is added. g. Calcaneal osteotomies (Dwyer: opening or closing and biplane): Note* The biplane osteotomy permits reduction of the calcaneal inclination angle or sagittal plane deformity, as well as frontal plane varus h. Triple arthrodesis: previously described under Section: Flatfoot Deformity i. Hoke procedure: a combination of subtalar arthrodesis with a resection/reshaping/reimplantation of the head and neck of the talus j. Dunn procedure: a tarsal arthrodesis that obtained posterior displacement of the foot by excising the navicular and part of the head and neck of the talus Note* The Dunn and Hoke procedures are useful when posterior displacement of the calcaneus beneath the talus is needed

Talipes Equinovarus (clubfoot) The reason to treat a clubfoot is to obtain a pliable, plantargrade, cosmetically acceptable foot in a short treatment time with minimal risk. The indications for operative treatment are incomplete correction of the varus and equinus components, and you may see the bony pathology progressing if continued conservative treatment is followed. When surgery is done early there is less

deformity to the talus 1. Types: a. Rigid b. Non-rigid c. Neural component foot with joint problems Idiopathic: only the foot is deformed, the musculoskeletal system is otherwise normal. In this foot type you will probably go on to surgical intervention before a non-idiopathic foot since the disorder should be known and the progression of the disease should be known. You should wait to treat this foot till the full deformity has developed as the treatment is more effective Non-idiopathic: the deformity is a local manifestation of a systemic skeletal syndrome. The foot deformity and associated skeletal anomalies are due to the same etiologic factors that caused the failure of normal musculoskeletal development. Can be caused by: a. Congenital diseases: congenital constricting band syndrome (Streeter disease), hereditary onycho-osteodysplasia (nail-patella syndrome), arthrogryphosis multiplex congenita b. Neurologic diseases: meningomyelocele, spina bifida, hydrocephalus, CP c. Myopathy: muscular dystrophy 2. Etiology: a. Unknown- but many theories (see Chapter: Pediatrics) 3. Anatomical Presentation: a. The talus is supinated over the top of the distal calcaneus so that the calcaneus is plantarflexed and inverted b. Master Knot of Henry is the deforming force on the medial side of the foot. It is the fibrous junction of the FHL/FDL sheaths to the navicular and fascia of the FHB. It must be severed to allow the navicular to re-establish itself laterally with the calcaneus c. The talus is usually deformed: the head and neck are medially displaced and downward (this is consistent in rigid clubfoot) d. The T-N joint is subluxed with the navicular medially e. Posterior medial structures are tight along with the STJ tissues f. Cuboid is displaced inwardly along with the navicular at the M-T joint and the anterior calcaneus following to go down and under the talar head g. The anterior surface of the calcaneus faces more medially, so the lateral column must be corrected to give a rectus foot h. Two accessory joints are regularly found i. The navicular rests on the anterior portion of the medial malleolus ii. The posterior-lateral calcaneus rests on the posterior fibular malleolus i. The tendo achilles is slightly medial on the calcaneus j. The most consistent bony deformity is at the talar neck. It is short and medially deviated k. Arteriography: i. PT artery is most prominent (so must protect during surgery)

ii. Deep plantar arch is supplied primarily by the PT not the DP (as in the normal foot) iii. A majority of the TEV feet develop without the DP artery l. The calcaneofibular and posterior talofibular ligaments are tight due to the equinus position m. The medial submalleolar skin is contracted and heals poorly 4. Pre-operative Evaluation: a. Angle of Kite (normal= 20-40°) approaches 00 b. A-P view shows talar bisection lateral to 1 st metatarsal c. If foot has marked forefoot adductus, corrective surgery is indicated for this d. Flat-top talus may be present due to aggressive conservative treatment, which may later produce osteochondral fracture and later arthritis e. Preoperative vascular assessment is important to determine the amount of correction able to be done: the limiting factor to any correction is the stress placed on the medial soft tissue and the neurovascular bundle f. Make sure the preoperative x-ray is taken with the knee/leg/foot vertical and not abducted g. A lateral stress dorsiflexion view is the most accurate judge of a clubfoot correction h. The long axis of the talus is directed downward toward the 3rd met instead of medial to the 1st metatarsal as in the normal foot i. Should consider a plantar release in children older than 6 due to cavus deformity that progresses from accommodation contractures of the plantar fascia, abductor hallucis, intrinsic toe flexors, and abductor digiti minimi j. Talus is too far forward in the mortise, therefore, increased equinus and decreased dorsiflexion k. Tibia shows increased lateral torsion l. Ossification centers usually appear later in the clubfoot m. Parallel talus and calcaneus n. No overlap of the anterior ends of the talus and calcaneus o. In the normal foot the T-C angle increases with dorsiflexion, but with the clubfoot this angle does not change p. If surgery is delayed till after the age of 10, many adaptive changes will have taken place, and a triple arthrodesis may be the procedure of choice 5. General Symptoms: a. Lateral callosities b. Tiring easily c. Thin calf ms. on the affected side d. Smaller foot e. Small 1st metatarsal with larger 4th and 5th metatarsals f. Limb length difference with adaptive scoliosis g. Hyperextended knees h. Metatarsus adductus i. No wrinkles over the achilles insertion (this helps diagnosis idiopathic from non-idiopathic as so if wrinkles are present the foot did have plantar/dorsiflexion at one time indicating a non-idiopathic clubfoot)

j. Genu valgum k. External rotation of the leg

6. General Order of Surgical Corrections: a. Posterior release b. Posterior medial release c. Plantar release d. Subtalar release e. Metatarsus adductus procedure f. Tendon transfers g. Calcaneal osteotomies h. Triple arthrodesis with soft tissue release i. Amputation (if all else fails) 7. Surgical Treatment (soft tissue): Performed after 3 months of failed conservative care- the next step. a. Posterior Medial Subtalar Release (TURCO procedure) i. Skin incision is classically a hockey stick incision from the base of the 1st metatarsal continuing under the medial malleolus and partially up the medial aspect of the leg. Due to severe skin necrosis from this, a linear incision is now used

ii. Isolate the posterior tibial ms., FHL, FDL, neurovascular bundle, and medial achilles iii. Loosen the abductor hallucis from the medial calcaneal tuberosity iv. Release the Master Knot of Henry (this obstructs a good view of the medial side of the foot) v. Posterior release is done first to allow good visualization of anatomical structures







Inferior/posterior achilles release with sagittal plane Z TAL Release FHL sheath and retract with the neurovascular bundle medial and anterior Apply dorsiflexory pressure and transect ankle and STJ capsule Resect calcaneofibular and posterior talofibular ligaments Resect posterior superficial part of the deltoid ligament (talotibial) Lengthen the FDL to prevent clawtoe deformity

vi. Medial release now tries to reposition medially displaced navicular laterally onto the talar head




Posterior tibial ms. is sectioned retaining good control of the distal segment to help isolate the T-N joint and medial structures Resect the calcaneofibular ligament (spring) Resect the superficial part of the deltoid leaving the deep tibiotalar intact anteriorly

vii. Plantar release




incise the plantar fascia incise the first layer of intrinsics incise the long plantar ligament

viii. Subtalar release allows the anterior calcaneus to move lateral-dorsal so the talus may reposition to a more appropriate pronated position
Evert the heel and intersect the interosseous talocalcaneal ligament
May need to sever the bifurcate ligament to help reposition the talus and calcaneus ix. After all soft tissue releases and the foot is corrected, the T-N and T-C joints should be stabilized with K-wires x. Resected tendons should now be repaired except the posterior tibial xi. Skin closure: may need skin graft in the severely deformed foot or overly corrected foot xii. If metatarsus adductus present now do HHS procedure

Note* Turco states that best results are obtained when: a. the child is 1-2 years old b. Good results decrease with age c. Good results if the child is walking due to Wolfs Law to help bone remodel d. Previous surgery is a hindrance b. Tendon transfers: usually done as an adjunctive procedure, and not primary ones. Transfers are only useful to help hold the correction of the flexible foot i. Stewart TAL ii. STATT iii. Anterior tibial transfer iv Posterior tibial transfer 8. Surgical Treatment (osseous): Usually done after the child is 4 or if soft tissue surgery has failed a. Evans calcaneal osteotomy (corrects the anterior medial position of the anterior calcaneal surface-an adaptive change) b. Dwyer calcaneal osteotomy (tries to establish a perpendicular heel and a weight bearing center of gravity) c. Triple arthrodesis is the procedure of choice when all else fails d. Talectomy is a possibility in the severely deformed foot e. Amputation can be a viable alternative when most other procedures fail. With the aid of bracing, many times the extremity is more functional with a good device as compared to a very deformed and painful foot 9. Postoperative Evaluation: a. Calcaneus is rotated out of plantarflexion to dorsiflexion b. Posterior tubercle moves down when the anterior process moves up and laterally away from under the talus c. T-C angle now approx. 400 (lateral x-ray) and 250 on A-P view d. Intraoperative lateral should shoe dorsiflexion of the calcaneus, overlap of the talus on the anterior calcaneus if correction achieved Note* Failure of the calcaneus to dorsiflex is evidence of incomplete subtalar correction regardless of what the A-P x-ray and clinical exam reveal 10. Postoperative Care: a. Cast in neutral b. Prophylactic antibiotics given c. Change cast every month, first cast change at 3 weeks-remove sutures d. At second cast change, remove K-wires e. Weight bearing allowed when wires removed f. Straight last shoes used for 1 year g. Physical therapy 11. Complications: a. Rocker bottom foot if conservative treatment of equinus is corrected before

the varus component or if the internal fixation is removed too soon b. Flap/skin necrosis c. Inability to close the skin after reduction d. Damage to growth plates e. Relapse of the deformity f. Loss of the longitudinal arch g. Stiffness h. Hammertoe deformities i. Skewfoot can develop secondary to a valgus correction of the forefoot 12. General Facts: a. Treatment must be related to the type of clubfoot and age b. The first step in the correction of clubfoot should be the replacement of the navicular on the talus c. Soft tissue procedures will fail if secondary bony changes are present d. In the older child an adaptive contracture can produce a cavus foot. This is different from the average cavus foot because the calcaneus is plantarflexed in clubfoot-cavus and usually dorsiflexes in idiopathic or neuromuscular cavus. This is due to plantar contracture of the aponeurosis, abductor hallucis, intrinsics, and deep plantar ligaments

Chapter 22: Generalized Disease Conditions of Bone Soft Tissue Overgrowth Abnormalities of Alignment General Increased Bone Density Osteopenia Marrow Abnormalities The Dysplasias

GENERALIZED DISEASE CONDITIONS OF BONE Soft Tissue Overgrowth 1. Acromegaly: An acquired condition resulting in excess of growth hormone due to a pituitary eosinophilic adenoma. Radiographically, it is characterized by overgrowth of bone, cartilage, and soft tissue. With adult onset the hands and feet demonstrate the most pronounced skeletal changes 2. Pachydermoperiostosis (Idiopathic Osteoarthropathy): A hereditary condition transmitted as an autosomal dominant gene. It manifests itself in adolescence as overgrowth of the soft tissues, periostitis, and synovitis. Clinically, this is characterized by thickening of the skin, clubbing of the terminal digits, and painful swollen joints. It does resemble Acromegaly except the terminal tufts tend to be reabsorbed rather than enlarged. The scalp demonstrates cutis verticus gyrata-longitudinal wrinkles. 3. Neurofibromatosis-1 (von Recklinghausen's Disease): An autosomal dominant multisystem disease. Neurofibromas of the skin, bones and. soft tissues result in grotesque deformities. Neurofibromas occur on the peripheral and cranial nerves and have the potential for sarcomatous degeneration. "Cafeau-lait" spots are present on the skin. Half of these patients develop skeletal abnormalities which include kyphoscoliosis, scalloping of the vertebral bodies, rib notching, and a characteristic defect of the orbit of the eye. The peripheral skeleton can develop overgrowth of the soft tissues and bones or overtubulation, giving the bones a thin bowed appearance. 4. Macrodactyly: A localized enlargement of the soft tissues of a digit, which can be idiopathic or non-idiopathic.

Abnormalities of Alignment 1. Ehlers-Danlos Syndrome: A group of inherited connective tissue disorders resulting in hyperelasticity of the skin and fragility of blood vessels. Ligamentous and capsular laxity as well as muscular weakness lead to subluxation and dislocation. In the feet pes planus is very common. Atrophic scarring occurs: There are 9 subtypes. Types I, II, and III are the most common, and are autosomal dominant types. 2. Marfan's Syndrome: An inherited autosomal dominant connective tissue disorder resulting in abnormal elastic tissue and collagen production and excessive laxity. Hyperextensible joints and ligamentous laxity result in hallux valgus and pes planus, and kyphoscoliosis. The most serious complication of Marfan's syndrome is a dissecting aneurysm of the aorta. The radiographic hallmark of Marfan's is exaggerated length of the bones. The lens of the eye Is also displaced usually upward.

General Increased Bone Density

1. Osteopetrosis (Albers-Schonberg Disease): An inherited bone disease causing diffusely dense bones. The basic defect is a failure of osteoclasts to absorb primary spongiosa during enchondral bone formation. This leads to a "bone-within-a-bone" appearance. The bone is actually very weak. 2. Melorrheostosis: An acquired condition causing cortical thickening. Its etiology is unknown. The cortical thickening is smooth and thick and involves the periosteal surface or the endosteal surface, encroaching on the medullary canal. 3. Osteopoikilosis: A hereditary "spotted" bone disorder transmitted as an autosomal dominant. There are multiple round or oval bone densities occurring in the spongiosa of bone. There is a predilection for the tarsus in the foot. There is no uptake with this via bone scan (differential for blastic metastases). 4. Bone Islands: Are histologically identical to osteopoikilosis but occur as single lesions. 5. Paget's Disease of Bone: The destruction of bone with subsequent repair results in thickened, disorganized trabeculae and increased size of bone, giving the appearance of increased density. Usually the tibia is affected, but can involve the bones of the feet. The coarse trabeculae often have a different appearance from blastic metastases and melorrheostosis. Malignant degeneration is a rare complication (malignant fibrous histiocytoma, osteosarcoma, fibrosarcome, chondrosarcoma-all called "Paget's sarcoma" if they occur in a setting of Paget's Disease of Bone).

Osteopenia 1. Rickets and Osteomalacia: Due to deficient mineralization of bone specifically due to insufficient vitamin D from malabsorption, renal disease, lack of adequate sunlight, liver disease, and metabolic disorders. In the child this can cause widening of the growth plate, cupping of the epiphyses, and bowing of the legs. The pathognomonic sign of osteomalacia is the presence of Looser's lines or pseudofractures. These lucent lines are perpendicular to the cortex, are often bilateral and symmetrical. 2. Osteoporosis (decreased bone mass): Loss of trabeculae and thinning of the cortex i. Scurvy: Lack of vitamin C results in failure to produce intracellular substances, therefore, osteoporosis of the adjacent metaphysis, seen as a transverse radiolucent bands. This is called the scurvy line. Fractures can occur through this zone with complete separation of the epiphyseal plate. The vascular endothelium is abnormal, which leads to hemorrhage. Subperiosteal bleeding causes wide separation of the periosteum, and healing manifests as a thin shell of peripheral periosteal new bone. It takes a minimum of 4 months of lack of vitamin C for the disease to become apparent. This is very rare today in developed countries.

ii. Osteogenesis Imperfecta (Ekman-Lobstein disease): A generalized connective tissue disorder that is inherited as an autosomal dominant gene. A deficiency of osteoblasts results in severe generalized osteoporosis, the long bones are overtrabeculated and bowed, and protrusio acetabuli are frequently seen. Additionally there is abnormal dentition, blue sclerae and early deafness. iii. Disuse: Diffuse, severe osteoporosis accompanies disuse or immobilization, with changes resulting in thinning of the cortex and loss of trabeculae giving the bone a ground glass appearance. iv. Reflex Sympathetic Dystrophy Syndrome (Sudek's Atrophy): Generally follows minor trauma, with severe pain and soft tissue swelling and rapid demineralization. Rapid loss of mineral results in a patchy"motheaten" pattern of demineralization. (see Chapter: Neurology).

The basic radiological changes inherent to all the marrow affecting disorders includes expansion of the marrow cavity, thinning of the trabeculae, and the appearance of rectangular, osteopenic bone.

Marrow Abnormalities 1. Anemias: i. Thalassemia major: causes microcytic/hypochromic anemia. Generalized involvement of all the bones of the feet occurs as mentioned above. ii. Sickle cell disease: produces changes similar to thalassemia. Those changes can sometimes be mistaken for osteomyelitis. Can cause infarctions in bone due to vascular blockage by abnormal RBC's. 2. Storage Diseases: i. Glycogen storage diseases (Von Gierke's disease) ii. Cerebrosides (Gaucher's disease and Niemann-Pick disease) iii. Mucopolysaccharides (Hurler's, Hunter's, Sanfiiippo's. Morquio's, Scheie's, and Maroteaux-Lamy syndromes) 3. Fibro-Osseous Dysplasia: i. Fibrous dysplasia: A developmental anomaly that results in fibrous tissue replacement of the marrow cavity 4. Granulomatous Diseases: i. Sarcoidosis: a systemic granulomatous disease of unknown etiology that can affect the bones in a small percentage of cases, and when involved, almost always is seen in the phalanges causing small punched-out defects. Severe involvement may result in cortical destruction, fractures, and collapse of bone, giving an arthritis mutilans scenario. ii. Tuberculosis: Granulomatous disease due to hematogenous spread of the TB bacillus. Acid fast stains show TB bacilli, which are not seen in Sarcoid. 5. Infarction: Any type of vascular obstruction may result in marrow

infarction. The radiographic changes are frequently those of bone destruction. i. Pancreatic disease

The Dysplasias Dysplasia is a disturbance in the formation and modeling of bone; it is usually hereditary and most commonly occurs as a result of inborn errors in metabolism. Foot dysplasias are an expression of a generalized skeletal anomaly. 1. Spondyloepiphyseal Dysplasia (Morquio-Brailsford disease) 2. Multiple Epiphyseal Displasia (Fairbank's disease) 3. Chondrodysplasia punctata (Conradi's disease) The Occurence of Cone Shaped Epiphyses a. Normal variant b. Chondroectodermal dysplasia (Ellis-van Crevald syndrome) c. Cleidocranial dysostosis d. Dyschondrosteosis e. Hand-foot-uterus syndrome f. Oto-palato-digital syndrome g. Osteopetrosis h. Pycnodysostosis i. Tricorhinophalangeal syndrome Occurence of Tarsal Coalition a. Isolated variant (usually in the hindfoot) b. Juvenile rheumatoid arthritis c. Apert's syndrome d. Arthrogryphosis multiplex congenita e. Hand-foot-uterus syndrome f. Oto-palato-digital syndrome (Taybi's syndrome) Occurence of Polydactyly a. Arthrogryphosis b. Basal cell nevus syndrome c. Cleidocranial dyostosis d. Ellis-van Crevald syndrome e. Gorlin-Chaudhry-Moss syndrome f. Larsen's syndrome g. Myositis ossificans progressiva h. Rubenstein-Taybi syndrome i. Trisomy 13-15 (Perth's syndrome)

Occurence of Syndactyly a. Normal variant b. Apert's syndrome c. Carpenter's syndrome d. Bloom's syndrome e. Down's syndrome f. F syndrome g. Laurence-Moon-Biedl syndrome h. Taybi's syndrome i. Popliteal pterygium syndrome j. Prader-Willi syndrome k. Silver's syndrome l. Trisomy 13 Occurence of Short Hallux a. Myositis ossificans progressiva b. Taybi's syndrome c. Hand-foot-uterus syndrome d. Apert's syndrome e. Larsen's syndrome f. Popliteal pterygium syndrome g. Franconi's syndrome h. Holt Oram's syndrome Occurence of Short Metatarsals a. Normal variant b. Enchondromatosis c. Juvenile RA d. Osteochondromatosis e. Pseudohypoparathyroidism f. Pseudopseudohypoparathyroidism g. Trauma h. Turner's syndrome* *Turner's syndrome is-one of the more common chromosomal syndromes resulting in a sex chromosome" abnormality that causes a XO pattern. Important clinical findings are coarctation of the aorta, horseshoe kidneys, short neck, and hypogonadism. Radiographically, a short 4th metatarsal is commonly found.

Chapter 23: Radiology Standard Radiographic Techniques Specific Radiographic Studies Anatomic Angles Common Structural Measurements (Diagrams) Pediatric Radiology The Osteochondritities The Accessory Bones of the Foot

RADIOLOGY Standard Radiographic Techniques of the Foot and Ankle The standard of our profession's technique (especially for pre-operative planning) is a weight-bearing x-ray of each foot individually, in the angle and base of gait, with proper shielding to the patient. This allows us to reproduce the same bony architectural relationships consistently. 1. Dorsoplantar Projection: X-ray tube angled 15° from vertical and aimed at the lateral aspect of the navicular. 2. Weight-bearing Lateral Projection: X-ray tube angled at 900 from vertical 3. Non-weight-bearing Medial Projection: Useful in examining the talus, calcaneus, and lesser tarsal bones for the effects of trauma. 4. Lateral Oblique Projection: Gives a magnified and slightly distorted representation of the bones of the foot. Gives the most accurate picture of the shape of the proximal phalanx of the fifth toe. 5. Medial Oblique Projection: Has limited value in examining the foot. 6. Axial Sesamoidal Projection: Good for examining the plantar aspect of the sesamoids and their relationship with the 1st metatarsal head. 7. Axial Calcaneal Projecton: Useful when examining the calcaneus for fractures, abnormalities of shape, or neoplasms 8. Harris and Beath (ski jump/coalition) Projection: Useful in examining the STJ (T-C coalitions of the posterior or middle facets), Calcaneal fractures, and sustentaculum tali. 3 exposures taken with the x-ray tube set at 35°, next at 40°, and then at 45° 9. Ankle Mortise Projection: The ankle is internally rotated 15° with the xray tube at 90° from vertical. Good for evaluating the joint space. The view for measuring the angles of the ankle (see Anatomic Angles below). 10. Lateral & Oblique Projections of the Ankle: Used in looking for the effects from trauma. 11. Stress Inversion Projection of the Ankle: Usually taken following inversion sprains. With the ankle joint anesthetized, bilateral views should be taken in plantarflexion and at right angles. It can sometimes be difficult to correlate the number of degrees of talar tilt with the number of ligaments ruptured.

Note* Some feel that a tilt of 159= rupture of the anterior talo-fib ligament, 15309= rupture of the anterior talo-fib ligament and calcaneofib ligaments, and over 30° of talar tilt= all three ligaments ruptures (this is a guide, not a hard and fast rule) 12. Anterior Drawer Projection: Is taken following trauma to the ankle joint, with a distraction force placed on the forefoot. (looking for an anterior excursion of the talus out of the mortise). If the excursion is greater than 4 mm. as compared to the opposite side, then disruption of the anterior talofibular ligament is assumed. 13. Stress Dorsiflexion Projection: Can be useful for the evaluation of talipes equinovarus (measure the T-C angle). 14. Isherwood Projections: Consist of 3 projections to fully visualize the STJ. They are: the lateral oblique, medial oblique axial, and lateral oblique axial. Positioning is very difficult with these positions, so better use tomograms or CT. 15. Broden Projections: For examination of the STJ (Broden #1 examines the posterior facet & Broden #2 examines the sinus tarsi). Consists of 4 views with the beam angled at 10°, 20°, 30°, and 40° while centering the x-ray tube on a point 2 cm anterior and distal to the tip of the lateral malleolus. Has generally been replaced by tomography and CT. 16. Anthansen Projections: To view the medial and posterior facet of the STJ.

Specific Radiographic Studies 1. Bone Scanning: Bone scintigraphy using technetium-99m MDP is excellent for screening as it provides extremely good sensitivity but at the expense of being very nonspecific. Increased tracer uptake occurs as a result of hyperemia. A positive bone scan does not necessarily represent an osseous lesion, because juxtacapsular joint lesions, periosteal inflammation, or inflammation at tendonous insertions can also produce positive results. The predominant scintigraphic finding is a "hot spot" (increased tracer localization). The exception to this are "cold spots" which is due to NO delivery of the tracer as a result of poor circulation, necrosis, or a fulminant destructive osteomyelitis not accompanied by significant reparative processes which is also due to poor circulation. To obtain good-quality scintigraphic results the following guidelines should be followed: Request close up views of the foot and ankle with multiple angles of view (not whole body shots), and have the studies supervised by a radiologist who can ensure that the images are filmed at appropriate densities (this avoids white-outs or black outs). a. 99m Technetium-MDP is currently the most frequently used radionuclide. b. It is renally excreted c. Has a half-life of 6 hours, d. MDP chemiadsorbs to bone with the hydroxyapatite crystal (99mTc is just a

label) e. Provides more anatomic information with less time, exposure and expense than Gallium 67 imaging. f. May continue to show abnormal isotope accumulation after infection subsides as a result of continued bone repair. g. Uptake of technetium 99m MDP will occur in any focus of increased bone turnover, whether due to physical stress (osteoarthritis), repair (fracture, reactive periostitis, rheumatoid arthritis, plantar fasciitis), or tumor (primary or secondary; multiple myeloma is a relative exception) h. When to order: Persistent pain with negative x-rays, osteomyelitis from overlying soft tissue infection (x-ray negative), extent of osteomyelitis, progress of healing of osteomyelitis and fracture, osteomyelitis ve Charcot, and unexpected x-ray or MRI abnormality Three Phase Bone Scan: is used to differentiate OM from cellulitis. Phase 1: at time of injection shows an immediate radionuclide angiogram or dynamic blood flow, OM and cellulitis both show increased uptake at this point. Phase 2: 10 minutes after injection looking for focal increases (blood pool image) cellulitis and OM are still positive at this point. Phase 3: 4 hours after injection (delayed static scan or bone image), cellulitis becomes quiescent at this point- ONLY CLASSICALLY Phase 4: 24 hours later used for patients with poor vascular flow and the 3rd phase looks almost exactly like the 2nd phase (increased sensitivity for detecting osteomyelitis in the diabetic foot)

NOTE* False negatives have been reported in infants and children

Osteomyelitis has intense and focal in all 3 phases NOTE* Bone scans are a good indicator if the uptake Reflex Sympathetic Dystrophy patient will be responsive to treatment 2. Gallium Scanning: The isotope, Gallium-67 citrate, was originally developed as a marker for certain tumors, i.e. lymphoma, and is considered an imaging marker for inflammation. It is less dependent upon blood flow than technetium. a. There are 3 mechanisms for Gallium-67 localization: i. Leukocyte localization or incorporation ii. Direct lactoferrin and transferrin binding at the site of infection (also Gallium binds to the siderophores of bacteria) iii. Direct bacterial uptake by phagocytes b. The usual dosage of is 3-5 mCi, and is usually performed 24 hours after injection

NOTE* Gallium is more reliable in differentiating benign from malignant tumors, assessing subacute and chronic infections. The only tumor Gallium is specifically used for is lymphoma c. Combination of gallium scanning following technetium scanning by 24 hours (due to the short half life of Tc-99m)is helpful in distinguishing chronic from acute OM, and cellutitis from OM. d. Gallium is valuable in monitoring disease activity and response to treatment in patients with chronic osteomyelitis (gallium is not as sensitive to bone remodeling as technetium) e. Gallium imaging is for chronic infection, predominantly lymphocytes 3. 111 Indium White Cell Scanning (Indium is just the label): This scan is much more specific for infection (especially acute infections) and involves predomininantly granulocytes. With this scan, the patient's white blood cells are labeled with the tracer and injected intravenously. This technique was developed to detect leukocyte accumulation at sites of inflammation and abscess formation. Scans are performed 24 hours after injection. A positive scan is defined as a focal accumulation of leukocytes that is higher than the surrounding bone activity. This technique is reserved for complicated posttraumatic or post-surgical patients with equivocal conventional bone scans, in cases where 99mTc MDP scanning reveals false positive results because of rapid turnover. Therefore, it may be more accurate in detecting acute infections. VIII. Limitations of Scans: Some patients show multiple hot spots at an early stage of S. aureus septicemia but do not progress to OM. You can have a negative scan with a confirmed OM due to impaired blood supply (false-negative). You can have difficulty in differentiating OM from cellulitis. You can have difficulty in differentiating normal bone repair from bone infection (false-positive). 4. Xeroradiography: A process in which an image is produced on a seleniumcoated plate. This process tends to emphasize the characteristics of borders between tissues, making detailed information more easily seen. It is sensitive enough to visualize non-metallic foreign bodies. (no longer readily available) 5. Fluoroscopy: An imaging modality in which x-rays are produced continuously on demand to give a real-time, dynamic image that is displayed on a television screen. The C-arm fluoroscope is the usual unit used intraoperatively. 6. MRI: MRI gathers information (imaging the nucleus of the atom) in the form of low energy radiowaves and transduces this energy into images with the use of computers. Four components are necessary for the production of such images:
Magnetic nuclei (the sample)
The strong magnetic field
Coils to transmit and receive radio frequency waves
Magnetic gradiance (small magnetic fields with known, carefully

controlled spatial variation) NOTE* Protons spin on their long axis, making a magnetic field. In the human body, these protons spin randomly. When the body is placed in the MRI machine, most (or more) of the protons line up parallel to the magnetic field of the machine. Feeding radiowaves into the body (RF), the protons are excited and energy is released producing an image. Most clinical MR imaging is performed with spin-echo pulse sequences. A spin-echo sequence consists of a 90° pulse followed after a time period by a 180° pulse, with a consequent production of a signal (echo). The echo-time (TE) is the time elapsed from the beginning of the 90° pulse to the peak of the echo. The repetition time (TR) is the time elapsed between successive 90° pulses. In typical MRl foot ankle studies the spin echo sequence is performed twice (referred to as 2 averages or excitations) By varying both TR and TE, images that primarily reflect TI-relaxation, T2relaxation, or proton density may be obtained. a. A signal that reflects primarily T1 images is produced by using a spin-echo sequence of a short TE (20-30 msec) and short TR (300-800 msec) b. T2 images are produced with a long TE (60-120 msec) and long TR (15003000 msec) c. A proton image (or balanced image containing properties of both T1 and T2) is produced with a short TE and long TR With all other factors being equal, imaging time is directly proportional to TR, with T2 images taking the longest time to obtain (prone to degradation due to motion by the patient) a. On T1-weighted images, tissue characterized by a short T1 relaxation time produces a high-intensity signal, whereas, long T1 tissue yields a low-intensity signal. Conversely, on T2-weighted images, a long T2 relaxation time which results in high signal intensity, and a short T2 results in low signal intensity. NOTE* Adequate characterization of musculoskeletal disease usually requires both T1 & T2-weighted images, because each provides complimentary information in terms of soft tissue contrast and anatomic detail. b. T1-weighted images provide the best signal-to-noise ratio, resulting in superior anatomic definition. A typical T1 weighted image : repetition time of 500 millisec and echo time of 30 millisec (TR500/TE30). These numbers can be seen to the right of the image on the film, which allows you to determine if the image is T1 or T2 or or a proton image. c. T2-weighted images provide the best soft tissue contrast, and are therefore, best for many pathologic processes, such as neoplasms and inflammation. d. High density (bright) areas most often reflect a high density of mobile protons or tissues with a short T1 or a long T2 (bone marrow and subcutaneous tissues

that contain large amounts of fat). Low intensity (dark) areas have fewer mobile protons (cortical bone and tendons). Most soft tissue tumors (with the exception to those composed of fat) have an appearance to those of muscle (low to intermediate signal intensity) on T1 weighted images, but can be differentiated from muscle on a T2 weighted image. NOTE* Evaluation of T1 weighted images: a. Dark (black) areas are: tendons, subchondral cortex of bone, blood vessels with moving blood, ligaments, muscles, tumors b. Light (white) areas: fat (whitest), medullary bone, stationary blood Evaluation of T2 weighted images: a. Dark areas: ligaments, compact bone b. Intermediate areas (gray): subcutaneous fat, bone marrow, muscle c. Light areas: stationary blood, tumor Evaluation of proton image: a. Intermediate (gray): fluid , muscles

NOTE* There are other MRI Stues: STIR mage wcs gooor tumors anGradient echo (also known as magnetic resonance angiography) which is good for hyaline cartilage e. Benefits of MRI: i. MRI is better than CT in evaluating bone tumors of the medullary canal (CT has higher resolution for tumors of the cortex). It permits better delineation of the tumor and has superior soft tissue contrast

NOTE* MRI cannot predict malignancy vs. non-malignancy ii. MRI is excellent in diagnosing trauma with patients that have preexisting metallic implants. iii. MRI is the imaging modality of choice for avascular necrosis. iv. MRI gives direct multiplanar imaging capabilities in any desired plane (sagittal, axial, and coronal) NOTE* When ordering an MRI you must specify what you are trying to look for, and if you want a certain view, you must specify this too f. Precautions: i. MRI not to be done in the first trimester of pregnancy (no studies showing fetal abnormalities with MRI to date) ii. MRI should be avoided with cerebral aneurysm clips (may become dislodged), cardiac pacemaker (interfere with function), and implanted metallic objects near the orbit of the eye) iii. Patients with claustrophobia may require sedation

7. CT Scanning: Can establish the presence, nature, size, margination, and

exact location of tumors. Muscle and soft tissue involvement can be determined. If a tumor is located next to blood vessels, a contrast medium is needed to enhance its identification. Is excellent to evaluate metabolic bones diseases (osteoporosis, aseptic necrosis, osteomalacia). It is excellent in evaluating trauma especially the calcaneus and STJ. The CT can dictate whether open reduction would be beneficial and whether one or a twosided approach is indicated to effect the reduction. CT is excellent in the diagnosis of tarsal coalition and degenerative changes of the tarsus or lesser tarsus where superimposition has always been a problem. 8. Arthrography: Following the injection of contrast medium into a joint, x-rays are taken. Good for the diagnosis of capsular or ligamentous tears. Has been replaced by MRI when available. Contrast media can cause anaphylactic reactions 9. Tomography: This procedure requires a complex reciprocal motion of both the radiographic tube and cassette around the patient. It requires a relatively large number of radiation exposures and demands exacting technique, but has the advantage of providing excellent bony detail in areas of complex osseous anatomy. The most useful applications of tomography are in the evaluation of osteochondral fractures in the dome of the talus; arthritic changes or loose bony fragments of the STJ and the tarsometatarsal joints, stress fractures of the navicular, union vs. non-union of an arthrodesis site, and the status of metallic implants (metallic implants affect the quality of CT and MRI). 10. Tenography: Is most often used on the ankle tendons. It can also document calcaneofibular ligament tears, because this ligament is contiguous with a part of the peroneal tendon sheath. It has been used to identify irregularities of the peroneal tendons themselves. Has generally be replaced with MRI (non-invasive). a. Tenogram shows narrowing and irregularity of the involved tendon b. Is only useful in tendons that go around a bone (like the malleoli) c. Tenography of the posterior tibial tendon reveals 3 types of pathology: central swelling, thinning of the tendon, and rupture d. The results of tenography can be: i. Normal ii. Mild marginal irregularity iii. Moderate marginal irregularity iv. Marked marginal irregularity v. Occlusion of the tendon sheath e. Contrast is injected into the proximal portion of the tendon sheath (Conray 43®) mixed 50/50 with Xylocaine®. Upon completion of the tenogram, a steroid is injected

Anatomic Angles 1. Angles of the Ankle: Are helpful when evaluating ankle trauma. on the D-P projection.

2. Angular Relationships on the D-P Projection: a. Talocalcaneal Angle or Angle of Kite (normal for ages 0-5 years= 35-50° & ages 5-adult= 15-35°): Has long been used as an index of relative foot pronation and supination. It is a measure of the transverse plane angular relationship between the longitudinal bisectors of the talus and calcaneus. It becomes increased with STJ pronation and reduced with supination. b. Cuboid Abduction Angle (normal= 0-5°): Lines along the lateral surfaces of both the cuboid and calcaneus. With pronation (increased abduction: Lenoire's sign) the angle increases. This is important with serial casting. c. Forefoot Adductus Angle (normal=0-15° In the rectus foot): Is the angle formed by the longitudinal reference of the rearfoot and the bisection of the second metatarsal. d. Metatarsus Adductus Angle (normal= 0-15°): The relative position of the forefoot to the rearfoot. It is measured on D-P view by comparing the

longitudinal bisection of the second metatarsal, with the bisection of the lesser tarsus. An increase of the angle results in medial deviations of the first metatarsal. e. Metatarsus Primus Adductus Angle or First Intermetatarsal Angle (normal in rectus foot--8-1 2° and 8-10° In adductus foot): Represents the medial deviation of the first metatarsal relative to the second. The angle is measured on D-P view by the intersection of longitudinal bisections of the first metatarsal and second metatarsal. NOTE* In general, angular increases up to 15° are correctable by distal osteotomies, while increases greater than 15° require proximal osteotomies f. Tibial Sesamoid Position (positions 1-3 can be considered normal): This position is sometimes used to decide the necessity for fibular sesamoid removal during HAV surgery. The change in sesamoid position occurs relative to the 1 st metatarsal head. TSP is measured relative to the 1 st metatarsal bisector. There are 7 positions. NOTE* A severely dislocated fibular sesamoid becomes a strong deforming force maintaining the hallux in the laterally rotated position, and impeding correction of a high metatarsus primus adductus angle NOTE* Removal of the fibular sesamoid plus cutting the adductor tendon will result in a hallux varus. Prior to its removal a plantar-axial view should be evaluated, and if there are no degenerative changes and lateral subluxation is not severe then the sesamoids can be relocated. g. Hallux Abductus Angle (normal= 10-15°): Represents the transverse plane position of the hallux relative to the long axis of the first metatarsal. This angle is produced by the intersection of the first metatarsal and first proximal phalangeal bisectors. This measurement quantifies the lateral deviation of the hallux in HAV. h. Hallux Interphalangeal Angle (normal= 0-10°): Represents the lateral hallux deviation at the level of the IP joint. It is the measurement of the angle produced by the intersection of the proximal and distal phalangeal bisectors. Increases in this value produce a lateral curvature of the hallux that become clinically significant, and becomes an important assessment of HAV when attempting to determine whether a proximal or distal Akin or Akin arthrodesis should be performed. i. Proximal Articular Set Angle (normal= 7.5°): An angle formed by a perpendicular to a bisection of the 1 st metatarsal and a line representing the effective articular cartilage. This represents the effective cartilage in relation to the shaft of the metatarsal. Any increase in the PASA is pathological and may either add to a structural deformity or combined deformity (lateral deviation of the cartilage).

j. Distal Articular Set Angle (normal= 7.5°): The angle that measures the relationship of the effective articulating cartilage of the base of the proximal phalanx to a mid-line bisection of the proximal phalanx of the hallux. If the DASA is highly abnormal, this may indicate the need for some type of osteotomy to reduce the angulation of the proximal phalanx. k. Metatarsal Protrusion distance (normal = +/- 2 mm.): The measure in the difference on length between the 1st and 2nd metatarsals. This parameter is of primary concern when 1 st metatarsal surgery is being considered on a patient with an abnormally increased negative protrusion distance. I. Metatarsus Quintus Abductus Angle (normal = 8-10°): The angle created by the intersection of the 4th and 5th metatarsal bisectors. This angle is increased with a splayed foot. NOTE* The intermetatarsal angle between the 4th and 5th metatarsals can also be drawn using a line parallel to the proximal medial portion of the 5th metatarsal as the lateral arm and bisected the 4th metatarsal as the medial arm of the angle NOTE* When examining for lateral bowing of the 5th metatarsal an angle calledthe lateral deviation angle of the 5th metatarsal is examined. This angle isformed by a line bisecting the head and neck of the 5th metatarsal and the line previous described to simulate the proximal 5th metatarsal shaft. Normal= 2.640 With pathology of the 5th metatarsal this number usually = 8°. When this is present the structural deviation should be considered as a significant contributing factor in the tailor's bunion deformity, and addressed surgically. m. Metatarsal Parabola (normal= 142.5°): The angle formed by the intersection of lines touching the 1 st and 2nd metatarsal heads intersecting with 2nd-5th metatarsal heads. 3. Angular Relationships on the Lateral Projection: a. Calcaneal Inclination Angle (normal= 18-21°): Is a measurement of the sagittal plane position of the calcaneus as seen on the lateral x-ray. This angle is increased in rearfoot cavus deformities and decreased (or negative) in flatfoot deformities. b. Talar Declination Angle (normal=21°): Is the angle formed by the plane of support and the column tali axis (bisector of the head and neck of the talus). This axis will be colinear with the 1st metatarsal declination axis. This angle increases with pronation and decreases with supination. Note* The Talar Declination Angle and the Calcaneal Inclination Angle are inversely proportional

c. Cyma Line: A lazy S curve formed by the T-N and C-C joints (Chopart's joint). Pronation causes the T-N joint to be anteriorly displaced, and supination causes the T-N joint to be posteriorly displaced. d. Sinus Tarsi: In the normal foot it is seen on lateral view as an oval area of decreased bone density, separating the posterior from middle subtalar facets. When pronation occurs, as the talus rides anteriorly on the calcaneus and plantarflexes, the sinus tarsi is obliterated. e. Fowler-Phillip Angle (normal=44-69°): This is used to evaluate the posterosuperior tuberosity of the calcaneus (Haglund's deformity). Symptoms are common when this angle exceeds 700 f. Talocalcaneal Angle (normal=15-35°): Compares the long axis of the head and neck of the talus to the inferior surface of the calcaneus. This angle is decreased in the supinated foot and increased in the pronated foot. It is useful in determining the treatment with talipes equinovarus. g. Bohler's Angle (normal=25-40°): Is used to describe the calcaneal architecture by defining the contour of the dorsal calcaneal surface. The angle is decreased in joint compression and beak fractures of the calcaneus as well as with Haglund's deformity. h. Talometatarsal Angle or Meary's Angle (normal 0-10°): The angle formed from the bisection of the talus and the bisection of the first metatarsal. Is used in evaluating whether a plantarflexed or hypermobile ray is present. i. Critical Angle of Gissane (normal=120-145°): This angle is created by the subchondral bone of the posterior calcaneal facet and of the middle and anterior calcaneal processes, as seen on the lateral view. It is utilized when evaluating calcaneal injuries. j. Neutral Triangle: For reference, the sparsely trabeculated neutral triangle occurs just below, and posterior to the apex of the Critical Angle of Gissane. 4. Arthromorphic Variants: In HAV surgery there are further considerations that must be given to the structural anatomy of the 1st MPJ and the shape of the 1 st metatarsal head. a. Congruous joint: The measurement of the articulating cartilage of the head of the 1st metatarsal and proximal phalanx is parallel b. Deviated joint: The lines intersect outside the joint c. Subluxed joint: The lines intersect within the joint d. Dislocated joint: see diagram to follow d. Round head: The weakest variant and deviates easily.

e. Square head: A more stable shape of joint f. Square head with a central ridge: The most stable variant. It is believed that the central ridge is an extention of the plantar crista. 5. Hallux Abductus Deformity: a. Structural Deformity (bony): A deformity in which there is osseous change in either the PASA the DASA or both. The structural deformity has as its characteristics the congruous joint. The HA deformity is also equal to the summation of the PASA and the DASA. b. Positional Deformity (soft tissue): There is an abnormality in the HA angle. The PASA and DASA are normal. The joint is either deviated or subluxed. The summation of the PASA and DASA are less than the HA angle. c. Combined Deformity: Has elements of both structural and positional deformities. Either the PASA or the DASA or both are abnormal, and when added together they do not equal the HA angle. The joint is either deviated or subluxed.

Common Structural Measurements (diagrams to follow)

Common Structural Measurements (A to W) A: Metatarsus adductus angle (normal 15°) B: Metatarsus adductus angle (alternate) C: Metatarsus primus adductus angle (normal 8-12°) D: Proximal articular set angle (normal 0-10°) E: Distal articular set angle (normal 5.2°) 1st MPJ articulation: (F-I) F: Congruous G: Deviated H: Subluxed

I: Dislocated J: Hallux abductus angle (normal 10-15°) K: Hallux abductus interphalangeal angle (normal 0-10°) L: Metatarsal protrusion distance (normal +/- 2mm) M: Tibial sesamoid position N: Tangential angle to the second axis +5° to -5° O: Metatarsus quintus abductus angle (normal 7°) P: 1st metatarsal declination angle Q: Calcaneal inclination angle (normal 18-21°) R: Fowler-Phillip angle (normal 44-69°) S: Bohler's angle (normal 28-40°) T: Critical angle of Gissane (normal 120-145°) U: Dorsoplantar talocalcaneal angle (Kite) (normal 20-40°) V: Lateral talocalcaneal angle (normal 35-50°) W: Anterior cyma line

Pediatric Radiology 1. Roentgenographic Development of the Foot: a. Important ossification points to remember: i. 1st bone to ossify before birth: calcaneus ii. Last bone to ossify before birth: cuboid iii. 1st bone to ossify after birth: lateral cuneiform iv. Last tarsal bone to ossify after birth: navicular at 3.5 years v. Calcaneal apophysis appears at age 7 years vi. Sesamoids appear at age 12 years b. Ossification at birth: i. Talus ii. Calcaneus iii. Cuboid (can be absent in the premature baby) iv. Metatarsals v. Proximal phalanges vi. Middle and distal phalanges 2-4 vii. Distal phalanx 1 c. Age 3 months: lateral cuneiform d. Age 4 months: tibial epiphysis e. Age 6 months: cuboid and lateral cuneiform articulate f. Age 7 months: talar neck appears, base of metatarsals widen g. Age 11 months: fibular epiphysis appears h. Age 18 months: phalangeal epiphyses appear i. Age 24 months: medial cuneiform and ossification of epiphysis of metatarsal 1 j. Age 30 months: intermediate cuneiform ossifies k. Age 36 months: ossification of epiphysis of metatarsals 2,3, and 4 l. Age 3.7 years: ossification of navicular m. Age 4.2 years: ossification of epiphysis metatarsal 5 n. Age 4.9 years: alignment of tarsal and metatarsal bones NOTE* Boys lag behind girls with regard to skeletal age o. Age 6.7: ossification of calcaneal epiphysis p. Age 12 years: sesamoids appear q. Age 13 years: os trigonum and os vesalianum appear r. Age 14 years: fusion of epiphyses of distal phalanges of toes 2, 3, and 4 s. Age 15 years: epiphyseal fusion of tibia/fibula, metatarsals 2/3/4, and phalanges 1, 3, 4, and hallux. t. Age 17.5 years: epiphyseal fusion complete 2. The Talocalcaneal Angular Relationships in the Diagnosis of Normal and Pathological Conditions:

3. Secondary Centers of Ossification: a. Metatarsals 2-5: at the metatarsal heads b. Metatarsal 1: at the base c. Phalanges: at the bases

d. Calcaneus: only constant tarsal bone

The Osteochondritities 1. These are a group of related disorders which effect the primary or secondary centers of ossification. Its etiology probably relates to some type of vascular disturbance to the ossification center, during the time of their greatest developmental activity.

2. The radiographic findings of lucency and fragmentation of the articular surface with collapse of a wedge shaped fragment of epiphysis and subsequent sclerosis are the manifestations of ischemic bone. 3. Originally classified together as a spontaneous osteonecrosis, but are a heterogenous group of entities with several different etiologies. 4. The Aseptic Necroses: a. Freiberg- metatarsal heads b. Kohler- navicular c. Bunchke/Buckman/Lewin/Wagner- cuneiforms d. Theimann- phalanges e. Sever- calcaneus (apophysis) f. Diaz/Mouchet- calcaneus

g. Lance- cuboid h. Iselin- base of 5th metatarsal i. Relander- tibial sesamoid (1st metatarsal) j. Lewin/Wagner/Theimann- epiphysis of toe phalanges k. Legg-Calve'-Perthes- femoral capital epiphyses 1. Mandl/Buchman- greater trochanter of femur m. Felix/Monde- lesser trochanter femur n. Kohler/Sindins/Larsen- patella o. Osgood-Schlatter- tibial tuberosity p. Blount- proximal tibial epiphysis

The Accessory Bones of the Foot

Illustration of oblique and A-P projection with most common accessory bones: 1. Os trigonum 2. Os sustentaculi 3. Os tibiale externum 4. Os supranaviculare 5. Pars peronaea metatarsalis primi 6. Os intermetatarseum 7. Calcaneus secundarium 8. Cuboides secundarium

9. Os vesalianum

Chapter 24: Hallux Valgus & Related Disorders Goals of HAV Surgery Anatomical Facts of the 1st MPJ Predisposing Factors Biomechanics Etiology of HAV Deformity Types Radiological Measurements for HAV Physical Examination Preoperative Considerations Arthroplasty Procedures Capsule-Tendon Balancing Procedures Implant Arthroplasty Procedures Arthrodesing Procedures Proximal Phalangeal Osteotomies Distal Metatarsal Osteotomies Proximal Metatarsal Osteotomies Shaft Osteotomies Combination Procedures Other Procedures Hallux Rigidus and Limitus Hallux Varus Hallux Hammertoe Diff. Diagnosis of Pain in the Sesamoid Area Complications of HAV Surgery HAV Procedure Chart and Their Indications

HALLUX VALGUS AND RELATED DISORDERS Goals of Hallux Valgus Surgery 1. 2. 3. 4. 5.

Pain free joint IM angle less than 100 Congruent joint Good range of motion Sesamoids in good position (TSP 3 or less) 6. Cosmetic result acceptable

Anatomical Facts of the 1st M.P. J. 1. The articular surface of the base of the proximal phalanx is larger plantarly than dorsally. 2. The medullary canal of the proximal phalanx Is dorsal to middle of the proximal articular surface; this is due to the concave nature of the plantar curvature. 3. The bony prominence on the dorsum of the proximal phalanx is for the EHB. 4. 1st metatarsal has cristae on the plantars 5. The nutrient foramen on the lateral aspect of the shaft is 2.7cm from the M.PJ.urface of the head to separate the sesamoids. 6. The epiphysis is on the base, so head osteotomies are permissible on children; but watch the nutrient artery. 7. The ligaments of the 1 st MPJ are: a. Medial collateral: intracapsular b. Lateral collateral :intracapsular c. Tibial plantar sesamoidal d. Fibular plantar sesamoidal e. Tibial sesamoidal: intracapsular f. Fibular sesamoidal: intracapsular g. Inter-sesamoidal: intracapsular h. Deep transverse metatarsal i. Capsule 8. The capsule itself: a. The sesamoids are invested in the capsule through which the FHB runs b. The capsule blends with the periosteum and may be removed easily from the base with an elevator c. The capsule is strongly attached to the metatarsal head d. There are medial and lateral collateral ligaments 9. EHL attaches through the hood ligament and lifts the proximal phalanx into extention (the EHB is under the hood ligament).

10. The hood ligament attaches the dorsal to plantar structures 11. The capsularis is actually a branch of the tibialis anterior 12. The only structure that never changes is the interosseous ligament 13. The bunion bump Is the abnormal position of the cartilaginous surface 14. Blood Supply to the 1st MTP and 1st metatarsal are via the 1st dorsal and plantar metatarsal arteries and the superficial branch of the medial plantar artery

Predisposing Factors 1. Biomechanical a. Primarily genetic in nature b. Acquired factors

2. Arthritic a. RA b. Psoriatic arthritis 3. Neuromuscular a. Cerebral palsy 4. Traumatic (primarily hallux limitus and hallux rigidus) 5. Genetic: a. Down's syndrome b. Ehler-Danlos syndrome c. Marfan's syndrome

Biomechanics 1. The first metatarsal dorsiflexes due to hypermobility and when dorsiflexed it also inverts (the 1st ray axis is medial/proximal/dorsal to plantar/lateral/distal). NOTE* There is almost no transverse plane motion due to the horizontal positioning of the axis 2. A foot with a low axis to the transverse plane gets a small amount of abduction/adduction of the first ray as does a rectus foot. This type will develop more of a dorsal bunion. The metatarsus adductus foot with a higher 1st ray axis gets a more medial bunion. 3. As the 1st metatarsal dorsiflexes and inverts, the hallux which is held to the ground by muscle power, is everting and dorsiflexing as well as subluxing laterally due to adduction of the first metatarsal. 4. Due to poor weight bearing of the 1st metatarsal, the second gets transfer lesions and the 1st develops a dorso-medial metatarsal head hypertrophy to form a bunion. 5. This is an acquired condition due to abnormal pronation in an adducted foot type or inflammatory disease of the joint which changes mechanics and muscle direction around the joint due to edema. 6. There must be a propulsive phase of gait for HAV to develop. 7. A hypermobile 1st ray is the primary cause due to a pronatory force and weakening of the peroneus longus. 8. Pronatory problems may develop from neuromuscular pathology, but a neuromuscular problem may not show bunion development even with pronation due to poor propulsion.

9. The loss of the normal tibial sesamoid position or excision of the tibial sesamoid will hasten the development of HAV. 10. Factors that affect the rate of progression of HAV are: a. The amount of pronation during propulsion b. The amount of adduction of the forefoot c. The amount of calcaneal eversion (a flatter STJ axis increases eversion and hastens HAV development) d. The amount of STJ and MTJ subluxation e. The presence of inflammation of the 1 st MTPJ f. The angle and base of gait g. The stride length (amount of time in propulsion) h. Obesity i. Terrain h. Poor fitting shoe gear 11. If you see HAV prior to age 3-4 suspect an anatomical anomaly or neuromuscular problem (there is no active propulsion In this age group) 12. The hallux is prevented from following the metatarsal head due to the need for ground purchase, therefore, at the 1st MTPJ torque is formed to sublux the joint. A normal 1st MTPJ does not have frontal plane motion, so as the metatarsal dorsiflexes and inverts, the stable hallux dorsiflexes and everts, and subluxation begins. 13. The hallux loses stability at weightbearing due to the hypermobile base, causing the lesser mets to carry more of the load. 14. Lateral subluxation of the hallux occurs due to weakening of the peroneus longus and dorsiflexion of the metatarsal with the transverse head of the adductor pulling on the hallux and enhancing its lateral migration. 15. The sesamoids migrate laterally to change the abductory forces on the hallux. This causes bony adaptation on the plantar metatarsal head so that the crista is gradually worn away, to allow further lateral shift of the sesamoids. 16. Bony adapation shows medial deposition and lateral absorption of the metatarsal head. 17. The metatarsal head develops a groove (sagittal groove) where the phalanx now articulates. This allows for normal plantar/dorsiflexion in the plantar part of the metatarsal head, but on the dorsal part you get abduction and eversion due to the new bony adaptation. 18. As metatarsus adductus increases, HAV develops. The angulation in

the met-cuneiform joint helps this progression. 19. If the bunion develops lateral pressure on the lesser toes look for: a. Onychocryptosis of the fibular nail groove of the hallux b. Interdigital soft corn c. Hammertoes and underlapping digits. 20. A stable hallux against the second digit causes the retrograde muscle contraction to cause the 1st ray to adduct, therefore, the IM angle Increases (this causes the met-cuneiform split). 21. As long as you have a propulsive gait the HAV worsens. It stops when you have a plodding type of gait. 22. After a long time of dorsiflexion of the 1st ray, there is an adaptation of the 1st ray into a position of elevatus that is somewhat rigid. 23. The medial branch of the superficial peroneal nerve may develop neuritis due to trauma. 24. Rheumatoid complications that help the development of HAV are: a. Intra-articular swelling causes the long tendons to migrate laterally b. Intrinsic muscle spasm causes the sesamoids to migrate laterally c. Pain of the lesser metatarsals may cause excess pronation to get the weight off the painful area

Etiology of Hallux Abducto Valgus 1. Excessive pronation during stance phase results in a. Hypermobile 1st ray due to loss of proper P. longus mechanics i. Results in dorsiflexion/varus of the 1st MTPJ and mild adduction of the metatarsal ii. A stretching and loosening of the medial sesamoid ligaments and adaptive tightening of the fibular sesamoid ligament (also some lateral subluxation of the hallux)(GRADE 1) iii. Valgus hallux due to continuation of 1st metatarsal medially and abnormal lateral tracking of the sesamoid iv. Crista starts to erode and transverse adductor helps pull hallux over along with increased ground reaction force from hypermobile first ray v. Abductor hallucis becomes displaced plantarly, as the crista continues to erode and the sesamoids move laterally to change the mechanical advantage of the adductor hallucis and flexor hallucis brevis to decrease the stability of the hallux vi. The hallux moves laterally and buttresses the second toe (GRADE 2) vii. The IM angle becomes increased due to the retrograde force from the abductor hallucis position (GRADE 3)

viii. The PASA increases adaptively, the crista erodes more as the joint pain increases and the lateral metatarsal head degenerates ix. Eventually there is complete erosion of the crista and fast exacerbation of the HAV deformity x. The hallux becomes subluxed and dislocated on the 1st metatarsal (GRADE 4) xi. Marked HAV deformity NOTE* The longer it takes to change from one stage to the next, the less severe the resultant deformity will be b. Tibial sesamoid tracking problems i. Crista erodes NOTE* When the crista erodes you can transfer the adductor hallucis to the tibial sesamoidal ligament to hold the sesamoids in the proper position ii. Chondromalacia iii. Osteoarthritis iv. Fibrosis of the 1st MTPJ v. Marked HAV deformity

1. Structural Deformity (bony): A deformity in which there is osseous change in either the PASA the DASA or both (so either the PASA or DASA are abnormal). The structural deformity has as its characteristics the congruous joint. The HA deformity is also equal to the summation of the PASA and the DASA. 2. Positional Deformity (soft tissue): There is an abnormality in the HA angle. The PASA and DASA are normal. The joint is either deviated or subluxed. The summation of the PASA and DASA are less than the HA angle.

3. Combined Deformity: Has elements of both structural and positional deformities. Either the PASA or the DASA or both are abnormal, and when added together they do not equal the HA angle. The joint is either deviated or subluxed. NOTE* Structural deformities may exist at levels other than the 1st metatarsophalangeal joint and contribute to the metatarsophalangeal deformity

Radiological Measurements For HAV 1. Hallux abductus interphalangeal angle = normal 0-10° i. When abnormal, a structural abductus deformity of either the head of the proximal phalanx or the distal phalanx base or both may be present. However, the abnormality is most often seen at the head of the proximal phalanx, and regardless of the site is corrected via osteotomies. Valgus rotations falsely affect the HAI 2. Hallux abductus angle= normal 15° i. Significance: This measurement is the prime method of quantifying the abductus in a HAV condition. Can be either structural, positional, or combined NOTE* The HA angle is a combination of PASA+DASA+JOINT DEVIATION 3. Distal articular set angle= normal 0-10° i. Significance: DASA is a structural component of HA. When abnormalities are detected with this measurement, osteotomies of the hallux proximal phalanx are indicated 4. Proximal articular set angle= normal 7.5° i. Significance: PASA represents a structural component of hallux abductus, and is an attempt to quantify the structural adaptation of the 1st MTPJ NOTE* Situations exist where PASA of 12° is normal. Functional vs. Dysfunctional PASA: PASA remains functional so long as PASA is less than the IM angle or Dysfunctional PASA= PASA - IM Therefore, if the PASA exceeds the IM angle, the PASA should be corrected by at least the number of degrees difference between the two angles. In cases that require correction of the IM angle by base/shaft procedures, the anticipated postoperative IM angle must be determined. 5. 1st Metatarsal Declination Angle = normal 15-20° i. Significance: Gives information regarding sagittal plane position 6. Joint position: The 1st MTPJ is either parallel, deviated or subluxed

7. Metatarsus primus adductus angle (intermetatarsal angle)= normal 8-12° in the rectus foot and 8-10° In the adductus foot i. Significance: When the angle is abnormally increased the condition may be termed metatarsus primus adductus. The MA angle may determine the significance of the IM angle. Adducted foot types require correction of the IM at a lesser angle, therefore, the adducted foot type will require a base/shaft procedure at lower degrees than a rectus foot type. 8. Metatarsus adductus angle (MA)= normal under 15° i. Significance: The MA determines the significance of other measurements (IM, HA, and PASA). MA is influential in the choice of procedures. MA feet tend to develop HAV more rapidly than rectus feet 9. Metatarsal protrusion distance (MPD)= normal +2 mm. to -2 mm. i. Significance: An excessively long metatarsal may be the etiologic factor in hallux limitus or HAV, and an excessively short metatarsal can cause 2nd metatarsalgia. Procedures should be selected that avoid shortening the MPD or if unavoidable combine with a plantarflexing procedure 10. Tibial sesamoid position= normal 1-3 1. Significance: TSP documents the stage of progression of HAV. The plantaraxial view is best to determine the exact position of the sesamoids with regard to their position in their respective grooves 11. First metatarsal base gapping= normal Is less than a 2mm gap

Physical Examination 1. The foot of the patient is evaluated on a weightbearing and on a nonweightbearing attitude: a. Weightbearing: i. EHL contracture ii. Hallux purchase iii. Hallux position with regard to resting calcaneal stance position/neutral calcaneal stance position iv. Radiographic analysis (including mineralization, osteophytes, and cysts) b. Nonweightbearing: i. 1st ray ROM ii. Manual reduction of IM iii. 1 st MTPJ ROM, quality of motion, and axis of motion iv. Location of pain v. Location of bunion vi. Hallux position relative to 2nd toe vii. Calluses viii. EHL contracture (rare) ix. Associated deformities (2nd hammertoe, etc.) x. Trackbound (position the toe in a rectus position and dorsiflex and plantarflex- there is inability for adequate ROM with resultant pain)

2. A complete vascular, neurologic, dermatological, and biomechanical examination should additionally be performed.

Preoperative Considerations (planning) 1. Decide upon the right choice of procedure based upon radiological and clinical assessment 2. Remember that capsulotomies will not correct a structural deformity 3. Use a template in preoperative planning if you are unsure 4. Use fixation method which you are most comfortable with and that will provide the best stability 5. Try to minimize complications with proper execution of procedure and normal postoperative recovery period 6. Review the risks and consequences thoroughly with the patient

Arthroplasty Procedures 1. Keller a. Indications i. HAV with degenerative joint disease ii. Second and third degree hallux rigidus Note* Second degree hallux rigidus a. Established arthrosis b. Painful ROM c. Loss of central articular cartilage d. Proliferation and enlargement of peripheral osteophytes e. Ankylosis Third degree hallux rigidus a. Complete disappearance of the joint space b. Ankylosis of the MTPJ c. Sign (cant hypertrophy of the joint d. Irregular hypertrophic osteophytes iii. Geriatric bunion b. Advantages i. Relief of pain ii. Establish/restore 1st MTPJ ROM iii. IM reduction of 3-5° iv. Minimal rehabilitation v. Early return to shoes c. Disadvantages i. Short hallux ii. Loss of purchase iii. Sesamoid retraction iv. Altered gait v. Limited ROM vi. Limited IM reduction

d. Complications i. Hallux extensus ii. Loss of purchase iii. Retraction of the hallux with loss-of joint space iv. Metatarsalgia/stress fracture 2nd metatarsal and/or 3rd metatarsal v. Edema/telescoping of the hallux base e. Modifications i. Reattachment of the flexor brevis ii. EHL lengthening iii. Purse-stringing the capsule iv. Capsular flap v. K-wire splinting vi. Implant arthroplasty vii. Anchor the FHL to the sesamoids and the base of the proximal phalanx 2. Hueter: Complete resection of the 1 st metatarsal head, usually performed as part of the Hoffman-Clayton 3. Mayo: Resection of one-quarter inch of the 1 st metatarsal head and medial eminence. 4. Stone: Remodeling of the 1st metatarsal head. An oblique plane resection of the head, leaving a three-quarter inch space at the 1st MTPJ 5. Regnauld: Resection of a portion of the base of the proximal phalanx with the fashioning of a "hat-shaped". inverted, or "cork shaped" autogenous graft. This procedure besides shortening a long proximal phalanx and increasing ROM in the presence of DJD, will also correct a mildly abnormal DASA, mildly abnormal HIA by angling the surface of the base of the proximal phalanx. 6. Valenti "V" Resection: a. Indications i. Hallux valgus ii. Hallux limitus in the elderly iii. Nonactive patient iv. Hallux rigidus in cases of implant salvage b. Surgical technique: A "V" shaped osteotomy at the head of the 1st metatarsal and the base of the proximal phalanx (a 45° angular resection of the metatarsal and phalanx) on the dorsal and plantar aspect. A dorsal U-shaped capsular flap perserves intrinsic attachments at the base of the proximal phalanx. EHL lengthening c. Advantages: i. Restoration of ROM ii. Preservation of hallux purchase iii. Immediate weightbearing

Capsule-Tendon Balance Procedures

1. McBride: Originally described with an incision lateral to the EHL, excision of fibular sesamoid, medial eminence removed, adductor tendon transferred to the lateral side of the metatarsal head, and the medial capsule and adductor tendon shortened (several modifications to date) a. Criteria: Structural deformities of the 1st ray should not be present unless corrected by other procedures i. Normal HIA ii. Normal DASA iii. Normal PASA iv. Normal IM angle v. Hypertrophied medial eminence vi. Deviated to subluxed 1st MTPJ vii. Deviation of sesamoids >4 (fibular sesamoid may be arthritic) viii. Increased HA angle b. Surgical technique: i. A 6 cm. dorsolinear incision parallel and medial to the ii. Inverted "L" capsulotomy iii. Medial eminence removed drilling with .045 k-wire to produce fibrocartilage iv. If erosions in the cartilage are found then perform subchondral v. Removal of the fibular sesamoid only if it is acting as a deforming force and an adductor transfer is not being done (just freeing the attachments is not enough) vi. Release OR transfer of the Adductor tendon
The tendon is pulled over the 1st metatarsal neck and sutured into the medial capsule. This repositions the sesamoids
The tendon is tied into the metatarsal neck and into the medial capsule (this helps close the IM angle vii. Cut EHB NOTE Do not cut the adductor and remove the fibular sesamoid, you will predispose to a hallux varus b. Contraindications: i. Structural deformities ii. Hallux rigidus iii. DJD c. Complications: i. Stiff joint ii. Undercorrection of the deformity iii. Hallux varus 2. Silver: a. Indications: i. Hypertrophied medial eminence ii. Mild HA angle iii. No other structural abnormalities

b. Surgical technique: Removal of the medial eminence c. Complications: i. Stiff joint ii. Increase on HA angle following surgery due to cutting of medial stabilizing structures 3. Hiss: Like the Silver, plus the abductor hallucis is repositioned on the medial aspect of the 1st MTPJ (trying to balance the abductory component)

Implant Arthroplasties Implants utilized for the 1st MTPJ are static spacers which relieve pain, allow for limited painless motion, and give some internal stability to the joint. Ideally, biocompatibility requires the implant to be:
Chemically inert or free from biodegradation and sterile
capable of withstanding stresses imposed upon it
Durable or possess an integrity of structure without modification of its physical properties because of the biological environment
Non-irritation, eliciting only a benign local tissue response General indications for 1 st MTPJ implant arthroplasty:
Hallux valgus with subluxation and painful limited ROM
End stage hallux rigidus
Revisional surgery
Rheumatoid arthritis
Painful DJD
Gouty arthrosis/arthritis
Osteochondral fractures
Intra-articular fractures General contraindications for Implant arthroplasty:
infection
Salvagable joint 1. Hemi implant: a., Criteria: i. Joint pain ii. Adequate bone stock of the proximal phalanx iii. Normal IM angle unless reduced by another procedure iv. Normal articular cartilage of the head of the 1st metatarsal (no DJD) v. Adequate capsular tissue to allow for implant coverage b. Complications: i. Implant instability: Pistoning can occur from removal of too much bone as well as axial rotation of the implant ii. Implant failure: Mechanical stress can produce microfragmentation with migration of the silicone particles into the lymphatic system. With this there will be obvious loss of function and possible deformity. Not so with titanium implants iii. Foreign body reaction: lymphadenopathy which is reminiscent of metastatic

Ca clinically iv. Osteochondritis dessicans: From excessive stripping of the periosteum and resultant avasular necrosis v. Detritic synovitis reaction: The surgical area will become red and swollen with a chronic low grade pain. Once infection is ruled out the patient can be treated with NSAIDS or remove the implant device (less chance of this with titanium implants) vi. Infection: Implant must be removed and not replaced for at least 6 months to 1 year. If gram negative infection was present, implant should not be replaced for longer period of time if at all vii. Pistoning of the implant into cancellous bone (if implant chosen is too small) viii. Chronic edema c. Contraindications: 1. DJD of the 1st metatarsal head contraindicates a hemi implant ii. Severe osteoporosis of the involved bones iii. Inability to correct a high IM angle iv. History of a prior joint infection within the last 6 months v. History of allergic reaction to implant material 2. Hemi-angled Implant (Well): for accommodation up to 15° lateral deviation of the 1st metatarsal articular surface NOTE* This device eliminates the "lateral gap sign" as seen with the standard hemi-implant, which is. the nonarticulation between hemi- implant and lateral metatarsal articular surface a. Criteria: As above plus i. Abnormal PASA ii. Revisional surgery for hallux varus (reverse the implant) b. Complications: As above 3. Total Swanson Implant: Manufactured by Dow-Corning Wright, comes in 7 anatomical sizes plus the addition of titanium grommets. A central hinge in a "U" configuration allows for dorsiflexion. An intramedullary stem on both sides of the implant stabilizes the implant within the medullary canals. There is no angulation of the stems in the sagittal or transverse plane. There is a short stem version available in 6 sizes

a. Criteria: As above plus i. Good bone stock of the 1 st metatarsal head ii. Degenerative changes of the 1 st metatarsal head iii. Abnormally low metatarsal declination angle b. Complications: As above c. Contraindications: As above 4. Total Lawrence Implant: Manufactured by Sutter Biomedical and is marketed In 4 sizes. The proximal stem is angled 150 dorsally in the sagittal plane to allow for normal 1 st metatarsal declination, without sacrificing excursion of the implant to compensate for this. It is designed for a ROM of 85° of dorsiflexion

a. Criteria: As above plus i. Normal 15° declination angle b. Complications: As above c. Contraindications: As above 5. Total LaPorta Implant: Manufactured by Sutter Biomedical, comes in right, left, and neutral, referring to the deviation of the stems on the transverse plane. The right and left implant show a 100 angulation (lateralward) on the transverse plane. It is designed for a ROM of 60° a. Criteria: As above plus i. Normal 150 declination angle or use a neutral LaPorta implant for an abnormally low metatarsal declination angle. ii. Can be used for a mildly elevated IM angle without performing a procedure to reduce it, due to the 100 transverse plane abduction built into the proximal stem b. Complications: As above c. Contraindications: As above 6. Total Bioaction Implant: Newer two-piece device made of high density polyethelene, cobalt steel and titanium. a. Criteria: As per total Swanson implant b. Complications: As above c. Contraindications: As above 7. Kinetic Great Toe Implant: Two piece titanium/cobalt chromium implant with an anatomic dorsal flange providing an anatomic range of motion

a. Criteria: as above b. Complications: as above c. Contraindications: as above NOTE* This device also may be used to replace previous implants that have failed. This system offers implants that are anatomically and biomechanically accurate, with instrumentation that is precise to aid in its installation. The system consists of four phalangeal components which articulate with all six metatarsal (three left/three right) components. The metatarsal component is made from cobalt chromium (CoCr) which is the same material used for the femoral component of the total knee inn plant. The phalangeal component is made form titanium alloy as the backing to a high molecular weight polyethylene bearing surface NOTE* It is mandatory that all patients after receiving the implant arthroplasty be advised that prior to any invasive procedure (medical/ dental) that the patient be given prophylactic antibiotics, as is the case with all implanted prosthetic devices

Arthrodesis 1. McKeever Type (fusion of the 1st m.p.j.): Originally described as a peg-inhole 1st mpj fusion. a. Criteria: i. Flail toe ii. Failed implant arthroplasty Iii. Arthritis/gout iv Severe hallux valgus deformity v. Loss of extensor and/or flexor function vi. Intra-articular fractures with post-traumatic arthritis vii. Previously failed bunion procedures viii. Failed Keller arthroplasty procedure ix. Prior infection/septic arthritis x. Hallux limitus/rigidus xi. Rheumatoid arthritis xii. Charcot joint/osteoarthropathy xiii. latrogenic hallux varus xiv. Tumor b. Ideal position of fusion i. Slight dorsiflexion (5-10° from the ground supporting surface) ii. Slight abduction (parallel to the 2nd toe) or 10-15° on the transverse plane iii. No frontal plane valgus or varus rotation NOTE* Position will vary depending on activity, lifestyle, and shoe gear c. Surgical technique: i. Cartilage denuding

ii. Metatarsal head resection ( as part of pan-metatarsal head resection) iii. With bone grafting (i.e. failure of implant cases) d. Possible ancillary procedures: i. Tibial or fibular sesamoidectomy ii. IPJ arthrodesis (most common) iii. Relocation and arthrodesis of the lesser toes iv. Possible metatarsal osteotomies v. Possible Hoffman-Clayton vi. EHL lengthening vii. Excision of ipj sesamoid viii. CBWO/ Lapidus/ OBWO e. Fixation types: i. Insertion of crossed .045 k-wires ii. Monofilament 28 gauge wire loops iii. 4.0 cancellous screw iv. 3.5 Cortical screw in a lag technique v. 2.7 mm. screw in a lag technique vi. Herbert screw f. Advantages: i. Preserves adductor, short flexor, and EDB ms. function ii. Improved cosmetic appearance iii. Improved stability iv. Improved overall balance and gait vi. Improved position of lesser toes vii. Restores and maintains weightbearing function to the 1st ray viii. May be converted to Keller or implant arthroplasty ix. Relief of pain x. Simultaneous reduction of IM angle xi. Recurrence of the deformity is unlikely g. Disadvantages: i. May promote arthritic changes at the ipj ii. Optimum position may be difficult to achieve as it is technically difficult to perform iii. May require autogenous graft iv. May limit shoe gear v. May result in gait alterations v. Difficulty in kneeling h. Complications: i. IPJ arthritis of the hallux ii. Delayed union/non-union/malunion/pseudoarthrosis iii. Fracture iv. Onychocryptosis v. Medioplantar calluses vi. Hallux flexus vii. Impaired gait viii. Balance problems ix. Possible subluxation of toes 2 and 3 x. Improper positioning

2. Lapidus Type (fusion of the 1st metatarsal-cuneiform joint): a. Anatomy: i. The joint is arthrodial with its own synovial membrane ii. The medial cuneiform distal articular surface is reniform in shape with a convex medial border and concave lateral border iii. The surface is elongated in the vertical direction with an inferior and medial inclination iv. The proximal articular surface of the 1st metatarsal is reniform with upper and lower parts v. There is a variable articulation between the 2nd metatarsal at its proximal medial aspect and the first metatarsal at its proximal lateral aspect vi. Dorsal and plantar 1st metatarsal-1st cuneiform ligaments are present vii. There are no interosseous ligaments between the base of metatarsals 1 and 2 viii. There is a strong interosseous ligament between the 1st and 2nd cuneiform and between the 1st and 2nd cuneiform and 2nd metatarsal ix. Tibialis anterior tendon inserts at the proximal junction of the medial and inferior surfaces of the 1st metatarsal x. Peroneus longus tendon inserts at the proximal junction of the lateral and inferior surfaces of the first metatarsal b. Indications: i. Extreme hypermobility associated with HAV ii. Correction of sagittal plane deformity iii. Correction of severe metatarsus primus adductus associated with a hypermobile or structurally medially deviated M-T-C joint iv. Repair of fracture or dislocation v. Hypermobile flatfoot with medial column sag c. Surgical technique: Via a dorsal longitudinal incision medial to the EHL tendon, with capsular incision dorsal linear or transverse. Articular cartilage is resected from the joint surfaces. The metatarsal is then adducted and slightly plantarflexed and then fixated appropriately with a compression screw, staple or k-wires. A BK NWB cast is applied until radiographic signs of fusion and stability are seen. Originally, Lapidus fused the 1st and 2nd metatarsal bases, but this is rarely necessary. Modifications of this procedure include i. Transfixation of the 1st to 2nd metatarsals with a threaded k-wire ii. Fusion of the 1st to 2nd metatarsal base with bone graft obtained from the medial exostosis of the metatarsal head

NOTE* There exist 3 surgical alternatives for extreme hypermobility cases: a. Cartilage abrasion and subchondral perforation, manual reduction, temporary fixation followed by bone screw fixation b. Joint wedge resection, minimal bone resection, lateral plantar wedge with bone-screw fixation and -stress receiving graft c. Joint resection, minimal bone removal with temporary reduction of the lengthening by means of allogeneic bone, double screw fixation, and occasional temporary plates. With each, there must be at least two points of fixation

d. Complications: i. Prolonged healing time ii. Malalignment in the frontal, sagittal or transverse planes iii. Severence of the vascular structures in the proximal intermetatarsal space iv. Non-union and pseudoarthrosis

Proximal Phalangeat Osteotomies The Akin-type procedures are generally combined with other types of bunion procedures to correct deformities around the 1st MTPJ, however, the cylindrical Akin is often used independently to shorten a long proximal phalanx 1. Proximal Akin: It is a medial closing wedge osteotomy at the metaphysis of the proximal phalanx. Is used to correct a high DASA. There should be adequate bone stock and adequate length of the proximal phalanx. The IM and HA angles will be unaffected. The lateral hinge is kept intact and the osteotomy should be fixated. 2. Distal Akin: It is a medial closing wedge osteotomy of the distal part of the proximal phalanx used to correct a high HI angle. IM angle unaffected. a. Indications: i. Pressure of the hallux on the 2nd digit ii. Epiphysis may be open iii. Good bone stock iv. HIA > 100 v. Adequate length of proximal phalanx vi. DASA is normal vii. Congruous 1st mpj unless corrected by another procedure b. Disadvantages: i. Long healing phase ii. Fixation needed iii. Elimination of propulsive phase of gait for 3-6 weeks c. Complications: i. Poor correction ii. Pain postop due to poor fixation iii. Non-union iv. Short hallux v. Hallux elevatus from FHL damage 3. Cylindrical Akin: Removal of cylindrical section to shorten a long proximal phalanx. The proximal osteotomy is one and one-half cm. from the base of the proximal phalanx, and the second osteotomy is made distally to the first cut. 4. IPJ fusion: Used to correct a hallux hammertoe or injury to the ipj. Must have good ROM of the 1st MTPJ. 5. Kessel-Bonney: A dorsal wedge osteotomy of the base of the proximal phalanx, used for hallux limitus. This extends pre-existing joint motion more dorsally. a. Advantages:

i. Allows the hallux to be in a dorsal position at the propulsive phase of gait ii. Allows for immediate ambulation b. Disadvantages: i. Requires an osteotomy with fixation ii. Does not really increase overall 1 st MTPJ ROM iii. Often creates a lack of toe purchase iv. Does not correct the underlying etiology of the deformity v. Requires elimination of the propulsive phase of gait for 3-6 weeks

Distal Metatarsal Osteotomies The major criteria for all distal osteotomies of the 1st metatarsal head are adequate bone density, adequate ROM, and arthritis-free joint. The potential complication for all distal 1st metatarsal osteotomies is avascular necrosis. 1. Austin: a. Criteria i. Normal to mildly abnormal PASA ii. Increased IM angle (max 14°/depends on other factors) NOTE* 1 mm in lateral shift of the capital fragment equals a reduction of 1° of IM angle.

NOTE* One can safely shy the metatarsal head laterally one-third of the width of the bone. So if the metatarsal head measures 21 mm. across, you can safely shy the bone 7 mm. and thereby close the IM angle 7° (since the wider the bone the more lateral shifting you can perform) iii. Normal metatarsal declination b. Surgical technique: V osteotomy with 60° angular cuts, originally described with no fixation, but commonly fixation devices utilized. c. Advantages i. Reduces the IM angle ii. Performed in cancellous bone iii. Stable in the sagittal plane allowing early ambulation iv. Avoids the sesamoids d. Disadvantages i. Technically challenging (easier with Reece osteotomy guide) ii. Dislocation potential e. Complications i. Dislocation of capital fragment ii. Intra-articular fracture iii. Aseptic necrosis

NOTE* It has been reported in the literature that an unusual sequel of this procedure has been for the capital fragment to pop out of the wound and fall on the operating room floor. The suggested protocol for this is to: a. Pick up the fragment with a sterile forceps and place in a basin containing 1 liter of sterile saline + 1 cc. Neosporin G. U. irrigant + 1:100, 000 Bacitracin for 5 minutes. b. Then transfer to another basin with the same type of solution for another 5 minutes. c. Then transfer to a third basin containing the same solution and swirl for an additional 1 minute and replace back into the foot with fixation. d. Advise the patient of the occurrence. e. Prophylaxis with 1 gm IV Cefadyl at 8, 16, and 24 hours postoperatively. 2. Austin/Kalish modification: As above but with a smaller angular cut to allow for longer dorsal wing for placement of 2-2.7mm screws or one 3.5 mm screw 3. Austin/Youngswick modification: a. Criteria i. Normal to slightly abnormal PASA ii. Increase IM angle (mild) iii. Metatarsus elevatus iv. Limited ROM b. Operative technique: Similar to other Austin procedures except with removal of rectangular wedge from dorsal arm of the 600 angle of the V. Additionally the wedge can be placed in the plantar arm of the V cut for additional plantarflexion of the capital fragment. c. Advantages i. Plantarflexes ii. Shortens- relaxes the tension around the joint, thereby increasing ROM iii. Stable if fixated iv. Done in cancellous bone d. Disadvantages i. Potential displacement ii. Difficult to perform iii. Needs fixation iv. Should be non-weight bearing 4-6 weeks e. Complications i. Intra-articular fracture ii. Excessive shortening iii. Dorsal displacement iv. Metatarsalgia 4. Austin/Bicorrectional modification: a. Criteria i. Abnormal PASA

ii. Increased IM angle iii. Normal metatarsal declination b. Operative technique: Same as traditional Austin except another cut is made which is thicker medially so as to remove a trapezoidal wedge of bone from the dorso-medial metatarsal head. When! the capital fragment is shifted laterally and impacted the IM and PASA is subsequently reduced. c. Advantages: i. Same as the Austin plus ii. Reduces the PASA d. Disadvantages i. Technically challenging (more so than the traditional Austin) ii. Dislocation potential e. Complications i. Same as the traditional Austin 5. Reverdin: a. Criteria i. Increased PASA ii. Normal IM angle iii. Normal metatarsal declination b. Advantages: i. Reduces the PASA ii. Performed in cancellous bone iii. Fixation optional iv. Good visualization c. Disadvantages: i. Potential sesamoid trauma ii. No IM angle reduction or sagittal plane reduction d. Complications: DJD 6. Reverdin-Green (distal "L" osteotomy): This is identical to the Reverdin except with an additional plantar osteotomy cut made parallel to the weightbearing surface to protect the sesamoids 7. Reverdin-Laird: Adds transposition of the metatarsal head to the ReverdinGreen procedure, with reduction of the IM angle 8. Reverdin-Todd: Combined with the Reverdin-Green and Reverdin-Laird, this modification adds correction of the sagittal plane deformity of the 1st metatarsal 9. Hohmann: Its modifications are the Mitchell and the DRATO a. Criteria: Sagittal and transverse plane deformities i. Increased PASA ii. Increased IM angle iii. Elevatus b. Precautions: Cannot be used for frontal plane deformities, in the presence of degeneration of the crista or any DJD

c. Advantages: i. Reduces PASA ii. Reduces IM angle iii. Plantarflexes d. Disadvantages: i. Highly unstable ii. Needs 2 point' fixation iii. Cast required iv. Extracapsular v. Performed in cortical bone vi. Does not remove the medial eminence e. Complications: i. Dislocation ii. Delayed or non-union iii. Metatarsus elevatus 10. Mitchell: A step down transpositional/angulation osteotomy at the metatarsal neck a. Criteria: i. Normal PASA ii. Moderate increase in IM angle iii. Positive metatarsal protrusion iv. Metatarsal elevatus b. Advantages: i. Reduces the IM angle ii. Removes the medial eminence iii. Plantarflexes the met head iv. Avoids the sesamoids v. More stable than the Hohmann c. Disadvantages: i. No PASA correction ii. Shortens the metatarsal iii. Performed in cortical bone iv. Dislocation potential 11. DRATO: a. Criteria: i. Abnormal PASA ii. Mild increase of IM angle iii. Valgus rotation of the metatarsal head iv. Sagittal plane deviation of 1st metatarsal head articular cartilage (facing either plantarward or dorsalward) b. Advantages: It addresses 4 deformities in one procedure (PASA, sagittal plane 1st met head, valgus rotation, and IM angle) c. Disadvantages: i. Very difficult to perform ii. Done in cortical bone iii. Cast/ NWB 6-8 weeks

d. Complications: Same as with other procedures of this type 12. Waterman: Distal metaphyseal dorsal wedge osteotomy that raises the declination of the metatarsal head. Utilized for hallux limitus. a. Disadvantages: i. Does not actually increase the 1st MTPJ ROM ii. Can create a lack of hallux toe purchase iii. Does not correct the underlying etiology iv. Requires removal of the propulsive phase of gait for 3-6 weeks postop. 13. Wilson: An oblique displacement osteotomy that shortens the 1st metatarsal and decreases the IM angle. 14. Peabody: Similar to the Reverdin except performed more proximally. 15. Lambrinudi: A plantarfiexory osteotomy of the 1st metatarsal. Reserved for the younger active individual without severe joint disease with hallux limitus complaints.

Proximal Metatarsal Osteotomies: These procedures are used when the true IM angle should be reduced (greater than or equal to 140 in the rectus foot) and/or when a sagittal plane deformity of the first ray needs to be corrected. These procedures are performed transversely across the metatarsal, perpendicular to the long axis, and 1-1.5cm distal to the met-cuneiform joint. 1. Trethoan (opening base wedge): Used when the metatarsal is relatively short. Must utilize a bone graft (best to fixate with a staple to avoid compression of the bone graft). 2. Louisan-Balacescu (closing base wedge): A transverse closing base wedge osteotomy. Fixated with a staple. osteoclasp, K-wires, or monofilament wire. Complications have been elevatus of the metatarsal, non-unions, and delayed unions. The Juvara modifications allows for AO fixation. 3. Juvara Type A: Oblique base/shaft osteotomy from medial-proximal to lateral-distal, a wedge of bone removed to close the IM angle, medial hinge is kept intact, and screw fixation utilized. NOTE* For screw fixation the osteotomy cut is performed obliquely and must be at least twice as long as the width of the metatarsal shaft 4. Juvara Type B: As in type A, a wedge is removed for IM angle reduction, also the hinge is broken after screw insertion for sagittal plane rotation. 5. Juvara Type C: No wedge is removed but the hinge is broken, so that

sagittal plane rotation is possible and axial transposition is possible (lengthening or shortening). NOTE* Biomechanics of the Axis: a. When the axis lies in the plane, no motion occurs in that plane. b. Motion around an axis occurs in a plane that is perpendicular to the axis. c. An osteotomy hinge will act as an axis of rotation. d. A hingeless osteotomy may be rotated in the plane in which the osteotomy lies (an axis of rotation will exist perpendicular to the plane of the osteotomy) e. A hinge should be made perpendicular to the weight bearing surface to prevent subsequent dorsiflexion of the metatarsal. f. More significant sagittal plane errors will occur when the hinge erroneously deviates in the frontal plane g. Virtually any combination of planal deviations may be obtained if the hinge (or in the case of hingeless osteotomies) the plane of the osteotomy is correctly manipulated (the problem is achieving the exactly desired deviation on each plane).

6. Arcuate (Weinstock): A proximal dome shaped osteotomy that reduces a high IM angle and sagittal plane deformity. No cortical hinge is left intact. Its benefit

is that it avoids shortening the metatarsal. Its drawback is that it is unstable and occasionally difficult to fixate.

7. Van Ness: Plantar closing base wedge osteotomy for reduction of metatarsal elevatus. K-wire fixation utilized. NOTE* Fixation studies of proximal metatarsal osteotomies revealed: a. Dorsal loop: failed at 1 lb pressure b. Dorsal loop with .062 k-wire: failed at 3.5 lb pressure c. Right angle loops: failed at 6 lb pressure d. Crossed. 062 k- wires: failed at 6 lb pressure e. 4 mm. cancellous screw: failed at 8 lb pressure f. 3.5 mm. cortical screw: failed at 9.5 lb pressure g. Two 2.7 mm. cortical screws: failed at 10 lb pressure (gives better and more even compression) h. Right angle loops with .062 k-wires: failed at 10 lbs pressure Shaft Procedures 1. Offset V (Vogler): a. Criteria: i. IM angle of 17-18° ii. PASA between 8-30° NOTE* It has been reported that there is an average reduction in IM angle of 9.1° and PASA of 7.99° iii. Minimal to no joint pain iv. No excessive DJD b. Operative technique: A long V osteotomy that extends almost to the met-

cuneiform joint enabling reduction of the IM angle and PASA. The apex of the V is more proximal than the standard Austin (done at the metaphysealdiaphyseal junction) with the angle measured at 35°. The dorsal arm is longer extending between midshaft and the proximal one-third of the metatarsal. Fixation is achieved with 1 K-wire or 2.7 mm. screw. b. Complications: As per most osteotomies of this type 2. Scarf: a. Criteria: i. Increased IM angle ii. Increased PASA b. Operative technique: A long Z osteotomy that reduces the IM angle and the PASA. Modifications of this procedure include: i. A medially based incision ii. The length of the horizontal osteotomy is in direct proportion to the width of the IM angle iii. The direction of the osteotomy has been modified such that approx. two-thirds of the width of bone is dorsal to the osteotomy, proximally, and one third is plantar, in order to prevent stress fractures from occurring c. Advantages: i. The long plantar fragment possesses stability in two planes ii. Lends itself to AO fixation (tension band effect) d. Disadvantages: i. Difficult to perform ii. Possible vascular compromise iii. Performed in diaphyseal bone e. Complications: i. Aseptic necrosis 3. Mau (Gudas modification for screw fixation): An oblique shaft osteotomy from plantar-proximal to dorsal-distal. Indicated for IM angle reduction. 4. Ludloff (Engelman modification for screw fixation): An oblique shaft osteotomy from dorsal-proximal to plantar-distal

Combination Procedures 1. Stamm (opening base wedge + Keller) 2. Logroscino (closing wedge + Reverdin)

Other Procedures 1. Cotton (1st cuneiform opening wedge osteotomy): a. Criteria: i. Metatarsus primus adductus ii. Pronounced obliquity of the 1st met-cuneiform joint iii. Whenever a double osteotomy is indicated b. Contraindications: i. Excessive bony bridging at the opposing surfaces of the osteotomy c. Operative technique: A wedge is removed from the 1st cuneiform. The cut is

made parallel to the joint and does not enter the met-cuneiform joint plantarly, and is placed tibial to the intercuneiform joint at the bases of the 1st and second metatarsals. The 1st cuneiform osteotomy is then performed on the distal 1/3 of the bone. The more distal the osteotomy the more effect it has on the joint direction. The graft comes from the medial eminence and is fashioned prior to removal of the cuneiform wedge. NOTE* Dissection of the 1st cuneiform must be done carefully to avoid avascular necrosis of this bone d. Complications: i. Inadequate reduction of the deformity ii. Malalignment of the osteotomy iii. latrogenic tenotomy of the FHL iv. Metatarsus primus elevatus e. Advantages: i. This procedure can be added if the distal metaphyseal osteotomy proves to be inadequate to repair the deformity ii. Postoperative recovery is far easier than a closing base wedge or Lapidus iii. No cast is required and partial weight bearing can begin several days postoperatively iv. Allows surgery in the presence of a short 1st metatarsal as this procedure lengthens the 1st ray 2. Cheilectomy: Removal of osteophytes from the 1st MTPJ

Hallux Rigidus and Hallux Limitus 1. Etiology: a. Dorsiflexed 1st metatarsal secondary to abnormal pronation and hypermobility of the 1st ray. b. Dorsiflexed 1st metatarsal secondary to muscle imbalance affecting the 1st ray. c. Dorsiflexed 1st metatarsal secondary to sagittal plane structural malalignment of the 1st metatarsal. d. Abnormally long 1st metatarsal. e. Prolonged 1st MTPJ immobilization. f. Arthritic conditions of the 1st MTPJ either traumatic or metabolic g. latrogenic secondary to previous foot surgery affecting the 1st ray.

2. Preoperative Symptoms: a. Spasms or tendonitis of the EHL. b. Inability to move the hallux normally and or pain on motion. c. Inability to wear high heeled shoes. d. Painful hyperkeratotic lesion under the IPJ of the hallux. e. Painful hallux nail plate. f. Enlargement over the dorsal aspect of the 1st MTPJ 3. Preoperative signs: a. Dorsal bunion with or without skin irritation. b. Limited or absent 1st MTPJ motion c. Hallux extention distal to the IPJ d. Deformation of the hallux nail plate e. Weakness of the peroneus longus and/or hyperactivity of the anterior tibial ms. f. Crepitation and/or pain with 1st MTPJ ROM. 4. Preoperative radiographic signs:

a. Dorsal osteophytic proliferation b. Dorsiflexed 1st metatarsal relative to talar bisection c. Narrowing of the 1st MPJ joint space d. Flattening of the 1st metatarsal head e. Arthritic changes of the 1st MPJ f. Subchondral sclerosis 5. Biomechanical considerations: One must determine if there is a functional component that is producing the deformity, as a functional limitus is a common finding in the patient with significant uncontrolled pronation producing hypermobility of the 1st ray. To determine this examine the patient in a relaxed vs. neutral calcaneal stance position. A functional limitus only occurs in the relaxed position. 6. Conservative treatment: a. Orthoses b. Metatarsal bar c. Rocker-bottom shoes 7. Surgical treatment- Joint preservation techniques: a. Soft tissue release: Should be followed by immediate ROM excercises i. Release of fibrosis on the dorsal aspect of the joint ii. Release of the dorsal capsule iii. Release of the medial capsule if previously overcorrected iv. Release of the plantar adhesions between the sesamoid apparatus and the plantar aspect of the metatarsal head b. Cheilectomy: The osseous proliferation around the joint is excised i. Advantages:
Easily performed
Reduces the dorsal enlargement
Allows for increase in ROM in many cases
Creates minimal postoperative disability
Allows for immediate postop propulsive phase ambulation ii. Disadvantages:
Potential for capsulodesis
Does not correct the underlying etiology

c. Kessel-Bonney osteotomy: i. Advantages:
Allows the hallux to be in a dorsal position at the propulsive phase of gait
Allows for immediate postoperative ambulation ii. Disadvantages:
Requires an osteotomy with no fixation
Does not actually increase the overall ROM
Often creates a lack of hallux purchase
Does not correct the underlying etiology
Requires the elimination of the propulsive phase of gait for 3-6 weeks postop d. Mitchell-type osteotomy: This produces shortening and plantarflexion of the metatarsal head i. Advantages:
Allows for correction of an abnormally long metatarsal
Allows for mild plantarflexion of the 1st metatarsal
Increases overall 1st MTPJ motion by relaxing tension around the joint produced by a long metatarsal
Allows for mild correction of an abnormal IM angle
Does not interfere with an open epiphysis ii. Disadvantages:
Requires an osteotomy with fixation





Allows only minimal plantarflexion of the head Requires non-weightbearing for 4-6 weeks postop

e. Watermann osteotomy: i. Advantages:
Allows the hallux to become more dorsal without using any additional joint motion ii. Disadvantages:
Does not correct the underlying etiology of the deformity
Can create a lack of toe purchase, and requires the elimination of the propulsive phase of gait for 3-6 weeks postop f. Austin-Youngswick osteotomy: This procedure produces a shortening and plantarflexion of the head i. Advantages:
Allows for correction of an abnormally long 1st metatarsal
Allows for mild plantarflexion correction
Relaxes tension around the joint via the shortening
Allows for immediate postoperative ambulation
Can be utilized to correct abnormal IM angle
Does not interfere with an open epiphysis ii. Disadvantages:
Requires an osteotomy
Allows only minimal plantarflexion
Requires elimination of the propulsive phase of gait for 3-6 weeks postop g. Plantarflexory wedge osteotomy (Van Ness): A wedge of bone is removed from the plantar aspect of the 1st metatarsal base i. Advantages:
Allows for true correction of a structurally dorsiflexed 1st metatarsal
Increases overall 1st MPJ ROM ii. Disadvantages:
Requires non-weightbearing with immobilization for 6 weeks postop
Does not allow for easy repositioning of the 1st ray intraoperatively if too much bone is resected h. Juvara type C osteotomy: i. Advantages:
Allows for true correction of a structurally dorsiflexed 1st metatarsal
Increases overall 1st MTPJ ROM
Does not require removal of a bony wedge
Can be modified for reduction of an high IM angle
Allows for easy intraoperative repositioning of the 1st metatarsal on the sagittal plane ii. Disadvantages:
Requires non-weightbearing with immobilization for 6 weeks postop
Requires the use of two cortical screws for fixation 8. Surgical treatment- Joint destructive procedures: a. Keller arthroplasty

i. Advantages:
Elimination of joint pain
Allows for increase ROM
Easily performed
Allows for immediate propulsive-type gait ii. Disadvantages:
Destroys the joint
Creates instability of the 1st ray
Does not correct the underlying etiology
Creates lesser metatarsalgia b. Arthroplasty with joint prosthesis: c. Arthroplasty with joint prosthesis and proximal plantarflexory osteotomy d. Arthrodesis: i. Advantages:
Eliminates joint pain
Creates significant internal stability of the 1st ray ii. Disadvantages:
Eliminates all motion of the 1st MTPJ
Requires fixation for 6-8 weeks with immobilization
Restricts the type of shoes which can be worn postoperatively depending upon hallux position in the sagittal plane

Hallux Varus 1. Etiology: a. Congenital and often accompanied by other congenital abnormalities b. Most commonly latrogenic following surgical treatment of HAV i. Excessive resection of the medial eminence ii. Excision of the fibular sesamoid and release of the adductor tendon iii. Overcorrection of the IM angle iv. Overtightening of the medial capsule v. Overcorrection of the PASA 2. Preoperative Symptoms of latrogenic Hallux Varus: a. Inability to wear conventional shoe gear comfortably b. Pain along the medial aspect of the hallux c. Pain along the medial side of the arch (ms. contracture) d. Pain may be present at the MPJ with or without shoes NOTE* Capsulitis of the 2nd MPJ may be the only initial complaint 3. Preoperative Signs of latrogenic Hallux Varus: a. Presence of an adducted positioned hallux b. Contracture of the hallux IPJ (sometimes) c. Contracture of the EHL (sometimes)

d. Contracture of the abductor hallucis (sometimes) e. Pain and crepitation may be present at the 1st MTPJ f. Hallux limitus may be present at the 1st MTPJ 4. Preoperative Radiographic Signs: a. The hallux will be in an adducted position at the 1st MTPJ b. The IM angle will usually be reduced c. The head of the 1st metatarsal may be staked d. The fibular sesamoid may be absent e. The evidence of a previous osteotomy on the 1st metatarsal may be seen f. A negative PASA may be present g. Arthritic changes may be present at the 1st MTPJ h. Arthritic changes may be present at the hallux IPJ 5. Operative Considerations: a. The deformity should be corrected as soon as possible to prevent DJD of the joint b. There is no one surgical procedure. The causative factor(s) must be determined and corrected along with any secondary changes that had developed, by selecting the proper procedures (i.e. reverse Austin, reverse Akin, reverse hemi-angulated implant , soft tissue balancing, arthrodesis, and Keller/total implant arthroplasty)

Hallux Hammertoe (etiology) 1. 2. 3. 4. 5.

Cavus foot (extensor substitution) Removal of the sesamoids Detachment of the flexor tendons Overzealous HAV surgery Plantar hallux IPJ sesamoid

Differential Diagnosis of Pain in the Sesamoid Area 1. 2. 3. 4. 5. 6. 7. 8.

Joplin's neuroma Sesamoiditis Osteochondritis of the sesamoids Ruptured bipartite sesamoid DJD with an eroded crista Hypertrophic sesamoid Fractured sesamoid Tumor of the sesamoid (a giant cell tumor has been reported)

NOTE* Most bipartite sesamoids are tibial, 75% are unilateral, and ossification of the sesamoids occurs at age 8-10 years

Complications of HAV Surgery (General) 1. Staking the metatarsal head and producing hallux varus 2. Hallux hammertoe

3. Longitudinal fracture when removing the exostosis 4. Sesamoiditis from invasion of the met-sesamoid articulation by tumor 5. Fracture of the articular cartilage of the MTPJ 6. Unstable osteotomy 7. Non or delayed union 8. Damage to the neurovascular structures 9. Elevatus and iatrogenic hallux rigidus 10. Over or undercorrection 11. Osteoporosis from disuse 12. Infection 13. Problems with the fixation devices 14. Hallux limitus/rigidus 15. Avascular necrosis

Chart of Procedures and Their Indications Abbreviations: HI= Hallux Interphalangeus IM= Intermetatarsal Angle DASA= Distal Articular Set Angle MP= Metatarsal Protrusion PASA= Proximal Articular Set Angle SES= Sesamoid Position HA= Hallux Abductus Angle D/PF= Motion of the 1st ray (dorsi/plantarflexion) JNT= Condition of the 1st m.p. joint TYPE= Type of Procedure N= Normal I= Increased D= Decrease G= Good P= Positional S=Structural A= Arthritic

Chapter 25: Trauma Medical Management and Assessment of the Polytrauma Patient Assessment of Lower Extremity Injury General Evaluation and Treatment of Fractures Calcaneal Fractures Talar Fractures Osteochondral Fractures Navicular Fractures Cuboid Fractures Cuneiform Fractures Fifth Metatarsal Base Fractures Metatarsal Fractures (1st, 2nd, 3rd & 4th) Tarsometatarsal Joint Dislocations/Fractures Subtalar Joint Dislocations Ankle Fractures Ankle Inversion Sprain Deltoid Ligament Ruptures Compartment Syndrome Open Fracture Classification System and Treatment Soft Tissue Injuries Crush, Gunshot, and Lawnmower Injuries Puncture Wounds Epiphyseal Plate Injuries (also see chapter 19, Pediatrics) Digital Fractures and Dislocations 1st MPTJ Trauma Nail Bed Trauma Toe Tip Injuries With Tissue Loss Dog and Cat Bites

TRAUMA Medical Management and General Assessment of the Trauma Patient 1. First Priorities: a. Evaluate and establish an appropriate airway and ventilate with 100% oxygen (intubate if ventilation is inadequate, but stabilize cervical spine with Philadelphia collar) b. Control external hemorrhage c. Inspect patient for skin color, alertness, chest wall motion, and extremity motion d. Auscultate the chest for breath sounds and establish adequate ventilation (if suspect pneumothorax with respiratory distress, insert chest tube without waiting for x-ray confirmation) e. Obtain vital signs NOTE* Carotid pulse is palpable at systolic BP of 60 mm Hg, femoral pulse at 70 mm Hg, and radial pulse at 50 mm Hg f. If pulselessness/hypotensive from blunt trauma to chest or a penetrating wound of precordium with distended neck veins not relieved by thoracostomy tube, open chest for effective CPR g. Establish IV lines and begin infusion (if patient is hypotensive use femoral lines via cutdown in conjunction with upper extremity infusion). Use crystalloid, colloid and/or blood as indicated (lactated Ringer's is preferred because it prevents metabolic acidosis) NOTE* In general, blood transfusions should be instituted when crystalloid infusion exceeds 50 ml/kg

NOTE* If systolic BP is less than 100 mm Hg, place IV in both antecubital spaces, and if inaccessible do greater saphenous cutdown h. If patient still hypotensive insert arterial line to monitor BP and blood gases i. Initiate EKG monitoring j. Assess neurologic status by Glasgow coma scale i. Check pupillary response, extremity posturing, and response to commands ii. Evaluate motor function of all extremities and trunk iii. If sensory and/or motor deficit, establish spinal cord level of functional changes k. Obtain admission blood work (CBC and coagulation profile, arterial blood gases, urinalysis, and venous blood chemistries) 2. Second priorities: a. Obtain a H&P if possible

b. Secondary examination of the head, chest, abdomen, pelvis, and extremities with attention paid to life threatening injuries c. Obtain appropriate x-rays (cervical, chest, etc.) d. Place a Foley catheter and check for occult blood in the urine e. Place a NG tube and check for occult blood in the GI tract f. Splint extremity fractures g. Complete neurologic examination h. Tetanus prophylaxis i. Culture and sensitivity of open wounds j. No antibiosis unless specific indication is apparent k. Perform emergency surgery if required 3. Third priorities: a. Systematic evaluation of the body b. Specialty radiology (CT, angiograms) c. Specialty consultations d. Invasive monitoring (Swan-Ganz) e. Urgent Surgery

Assessment of Lower Extremity Injury 1. Examination: a. Rapid neurovascular assessment NOTE* Lower extremity injuries are of low initial priority unless there is frank bleeding. With an arterial injury, there is a pulsatile flow or spurt of bright red blood. if present exert manual pressure initially, surgical repair later b. Quantity and quality of pulses c. Observe motor function d. Inspect for lacerations, swelling, deformities e. Joints palpated NOTE* Signs of ischemia are pain, pallor, paresthesias, paralysis, pulselessness. You have 6 hours to reverse before permanent pathological changes occur 2. Traumatic limb or digital amputation salvage: a. The avulsed part should be placed in sterile saline soaked gauze, sealed in a plastic bag, and immersed in ice water b. The avulsed part that has been properly cooled may last up to 24 hours c. The avulsed part that is not cooled within about the first 8 hours has a poor chance of being replanted

General Evaluation and Treatment of Fractures 1. Determine type of fracture: a. Classification of fractures: i. Transverse ii. Oblique iii. Spiral

iv. Comminuted b. Stable or unstable: i. How much bone to bone contact is there? ii. Are the fragments well aligned? iii. Is the area subject to movement? iv. How extensive is the soft tissue involvement? v. How is the blood supply to the fractured segment? vi. What kind of bone is involved in the fracture? c. Open or closed d. Intraarticular or extraarticular d. Cortical or cancellous bone involvement NOTE* Characteristics of cortical and cancellous bone Cortical Osteogenic properties poor Fractures surfaces small Soft tissue support poor (few) Vascularization poor Inherent stability poor

Cancellous good large good good good

e. Description of a fracture based upon the 4 basic relationships (described by the mnemonic LARD): i. Length and location ii. Angulation iii. Rotation iv. Displacement 2. Treatment of fractures: After determining the location and evaluating the patient's physiological status, a treatment regimen is tailored to the patient's needs: a. Rest, Ice, Immobilization, Compression, Elevation b. Closed reduction (with or without internal fixation). The mechanisms of closed reduction are: i. Step 1- Increase the deformity ii. Step 2- Distract the fragments iii. Step 3- Reverse the mechanism of injury c. Open reduction (with or without internal fixation) d. Excision of fracture fragments e. Amputation

Calcaneal Fractures A disabling injury of the foot. There are a number of associated injuries when dealing with a calcaneal fracture including: compression fracture of the lumbar vertebrae, laceration of the kidney-renal damage, fractures of the lower extremity, and compartment syndrome 1. Anatomical considerations: a. The largest tarsal bone that has a thin cortical shell enclosing cancellous

bone that contains traction trabeculae radiating from the inferior cortex and pressure lamellae converging to support the posterior and anterior facets. b. The calcaneus articulates with the talus through 3 facets, the largest being the posterior c. The middle and anterior facet have a common joint cavity with the TN joint and are separated from the larger posterior facet by the sulcus calcaneus. d. The lateral end of the tarsal canal gives attachment to the bifurcate ligament, the EDB, and the inferior extensor retinaculum. e. Boehler's tuber joint angle overlies the posterior articular facet and is a measurement of the sagittal plane between the anterior and posterior aspect of the calcaneus (normal 20-400) f. Gissane's critical angle is the position that abuts with the lateral process of the talus and which under compression force acts as a wedge creating the primary fracture line in the calcaneus

2. Radiological Examination a. Plain film x-rays NOTE* Evaluating integrity of the bone plus Boehler's angle and the Critical angle of Gissane is essential in the diagnosis i. A-P view ii. Lateral view iii. Anthensen's view (demonstrates medial and posterior facets of the STJ) iv. Isherwood views:
Oblique lateral (anterior process and calcaneocuboid)


Medial oblique axial (medial and posterior facet)
Lateral oblique axial (posterior facet) v. Broden's projections
Broden 1 (shows the posterior facet from anterior)
Broden 2 (shows the sinus tarsi to posterior) b. Tomography c. CT scanning (The Gold Standard) 3. Classification: Due to the fact that two types of fractures exist (intraarticular and extra-articular) the classification that is best used is a combination of the Rowe (inclusive for extra-articular) and Essex-Lopresti (inclusive for intra-articular, replacing Rowe 4 8 5) a. Rowe: i. Type 1a: Fracture of the tuberosity ii. Type 1b: Fracture of the sustentaculum tali iii. Type 1c: Fracture of the anterior process (most common; female patients predominate, mostly related to wearing high heeled shoes) iv. Type 2a: Beak fracture v. Type 2b: Avulsion fracture involving the tendo Achilles insertion vi. Type 3: Oblique body fracture not involving the STJ vii. Type 4: Body fracture involving the STJ viii. Type 5: Joint depression fracture with comminution b. Essex-Lopresti: i. Fractures not involving the STJ: Tuberosity fractures
Beak type
Avulsion medial border -Vertical
Horizontal ii. Fractures involving the calcaneal-cuboid joint:
Parrot-nose type
Various iii. Fractures involving the STJ:
Without displacement
Tongue-type with displacement
Centro-lateral depression of the joint
Sustentaculum tali fracture alone
Comminuted NOTE* The primary fracture line is vertical from the vertex of the critical angle of Gissane to the plantar aspect. The secondary fracture line is determined by the direction of the force c. Sanders: A new classification that utilizes CT scanning rather than plain radiographs for its identification. This is the first system to have a prognostic value i. Type 1: nondisplaced ii. Type 2: two part posterior facet fracture (a) Fracture through the lateral column

(b) Fracture through the central column (c) Fracture through the medial column iii. Type 3: three part posterior facet fracture with central depression (ab) Fracture through lateral and central columns (the bone between FX a and b is depressed) (ac) Fracture through lateral and medial columns (the bone between FX a and c is depressed (bc) Fracture through the central and medial columns (the bone between FX b and c is depressed) iv. Type 4: Four part posterior facet fracture

4. Mechanism of injuries: a. Torque injuries (extra-articular fractures) i. Anterior process fx ii. Avulsion fx iii. Sustentacular fx b. Direct impaction (extra-articular fractures) i. Tuberosity fx ii. Beak fx c. Falls from a height (intra-articular fractures) d. Concussive force from below (intra-articular fractures) 5. Clinical Diagnosis of Calcaneal Fractures: a. Anterior process fractures: i. Swelling- well defined 3-4 cm. anterior to the lateral malleolus

ii. Inversion and adduction increase pain NOTE* Must R/O 5th metatarsal base fractures b. Beak and avulsion fractures: i. "Pop" sound heard/felt on the heel with sudden pain ii. Pes planus antalgic gait iii. Weakness of plantarflexion iv. Edema, ecchymosis, bullous lesions (Mondor's sign) c. Fractures of the medial and lateral process: i. Heel thickens, edema, and ecchymosis ii. ROM of ankle, STJ, and MTJ within normal limits d. Fracture of the body no STJ involvement i. Inability to bear weight ii. Edema/ecchymosis iii. Generalized pain around the heel iv. Pain with ROM of ankle and STJ e. Fracture of sustentaculum tali i. Pain and edema on the medial aspect of the foot 1 inch below the medial malleolus ii. Pain inferior to medial malleolus on dorsiflexion (FHL) iii. STJ ROM decreased and painful iv. Ankle joint ROM WNL f. Tongue depression fractures i. Rapid edema and severe pain and inability to bear weight ii. Severe bleeding under fascia iii. Discoloration of the heel extending to the calf iv. Blister formation v. Flattened arch vi. Decreased plantarflexion (Hoffa's sign) vii. Widened heel viii. R/O compression fracture of lumbar vertebrae and ankle (10% occurrence) 6. Treatment: a. Anterior process fractures: i. Small fragment fractures
Soft cast NWB for 2-4 weeks (early mobilization important) ii. Large displacement fragment
RIF or excision (it is recommended to wait 1 year before excision) b. Beak or avulsion fractures: i. Beak fractures
BK cast 4-6 weeks (weight bearing if fragment not displaced)
If fragment displaced closed reduction followed by BK NWB cast for 6 weeks in plantarflexion with gradual weightbearing
RIF (screw) if closed reduction unsuccessful followed by BK NWB cast ii. Avulsion fractures
ORIF followed by screw fixation followed by BK NWB cast in plantarflexion

for 4 weeks followed by a neutral position BK cast for 2 weeks c. Fractures of the medial and lateral process: i. For nondisplaced treat with compression dressing/ice/elevation NWB. After edema subsides, follow with well molded BK cast for 4 weeks iii. For displaced fragment closed reduction followed by BK NWB cast for 6 weeks d. Fracture of the body not involving the STJ: i. For non displaced use compression dressing/ice/elevation with ROM exercises immediately (NWB 4-6 weeks) ii. If displaced, closed reduction with BK NWB cast 6-8 weeks (Steinmann pin can be used with proximal displacement) e. Fracture of the sustentaculum tali: i. Compression dressing/ice/elevation ii. ROM excercises immediately for FHL iii. BK cast with progressive weightbearing iv. Firm shoe with orthoses v. If displaced closed reduction followed by BK cast 4 weeks NWB followed by weight-bearing 2 weeks f. Tongue and joint depression fractures: i. Closed reduction ii. Open reduction (extensive)

NOTE* Treatment for significant calcaneal fractures has traditionally been conservative (either closed reduction or posterior percutaneous pin fixation). However, calcaneal fractures treated by these methods resulted in a marked disability that gradually resolved to a tolerable level but with many sequelae (widening of the heel, significant malalignment in varus or valgus, and lateral impingement syndromes). If the talus was left impacted into the posterior facet region, anterior ankle arthritis developed. Because of this, new techniques have been advocated. Open Reduction Technique: The lateral approach is used most for the primary incision. The medial approach is used when needed for more accurate reduction and rigid stabilization, or when CT scan demonstrates that most of the pathology lies medial in the fracture. A wide lateral flap is made incorporating the peroneal tendons and sural nerve, down to the subperiosteal layer. Timing is important to give a satisfactory result. Some advocate waiting 4-7 days to allow the swelling to resolve, but immediate fixation can also be done if the fracture is open or is associated with a compartment syndrome Several technical options are available with regard to hardware: a. Either 3.5 mm. cortical or 4.0 mm. cancellous screws can be used to fix the reduced posterior facet to the sustentacular fragment b. Neutralize the entire calcaneus with 3.5 mm. reconstruction plates, flattened 1/3 tubular plates (possible in combination), or cervical plates (plates are recommended for neutralizing the interfragmental screw repair and for holding the lateral wall

c. A transverse K-wire is inserted through the calcaneus to attach a Kirschner traction device for manipulation (traction reduces the medial wall) d. A bone graft would not be necessary if adequate lateral to medial wall reduction is performed. However, some feel that a bone graft is necessary under the posterior facet after it has been elevated from the body of the calcaneus

b. A plate stabilizing the lateral wall (the plate is the key in preventing the posterior heel from drifting into varus) c. A transverse K-wire or Schanz screw is inserted into the posterior body and helps reduce the Medial wall indirectly to pull the heel out of varus, and lock in the medial cortices before the lateral-to-medial lag screws are inserted 7. Further considerations of treatment of intra-articular fractures: a. Displaced intra-articular calcaneal fractures require open reduction in order to restore joint congruency b. The Essex-Lopresti maneuver can be used in elderly patients with intraarticular tongue-type fractures who cannot tolerate surgery

NOTE* The Essex-Lopresti maneuver is a technique of reduction. The patient is taken to the OR and using fluroscopic control, a Steinmann pin is driven into the posterior tuberosity from the posterior aspect of the heel. The pin is then used as a lever to elevate the impacted and depressed joint surface and tongue portion. This is accomplished by pushing the protruding portion of the pin downward toward the plantar aspect of the heel. If the articular surface and posterior tuberosity are noted to fall into proper alignment the pin is advanced into the anterior calcaneus to fixate the fracture. A second pin may be driven parallel to the first for added fixation. A BK cast is applied

c. Summary of correction: If there is visual congruency of the subtalar joint, visual alignment of the fracture through Gissane's angle, and radiographic absence of an intra-articular step off at the posterior facet with reduction of the medial wall on the axial view, then reduction must be considered anatomic NOTE* The 4 areas to consider when evaluating the intra-articular fracture of the calcaneus are posterior facet disruption, medial wall (determines height), lateral wall blow out (determines width) and calcanel cuboid joint a. Posterior facet: Indication for ORIF is with more than a 3 mm step off involving the posterior facet or if there is an angulation of the tuberosity fragment greater than 10 0 b. Medial wall pathology: 1 cm or more displacement of the medial wall is indicative of increased shortening and increased width, and should be treated with ORIF c. Lateral wall pathology: Lateral wall disruption can cause sural nerve irritation and peroneal tendon dysfunction, therefore should be reduced d. Calcaneal cuboid joint: Involvement can be treated with closed reduction 8. Surgical incisions: a. Medial approach: The main advantage of this approach is in the direct visualization of the reduction of the posteriolateral fragment and the superiomedial fragment and sparing the peroneals and sural nerve i. McRenolds horizontal incision ii. Stephenson vertical incision iii. Zwipp medial "L" incision b. Lateral approach: Gives expansile exposure to the lateral wall of the calcaneus, the calcaneocuboid joint and most importantly the posterior facet (site of major pathology) i. Modified -Kocher incision ii. Oilier incision iii. Right angle incision (consists of a vertical and horizontal arm; an excellent expansile incision which exposes the entire lateral rearfoot complex via a subperiosteal flap, and can be extended proximally if a concomitant ankle fracture is present)

NOTE* The most advantageous approach includes the use of a primary lateral incision with an ancillary medial incision if there is difficulty reducing the posteriolateral and superiomedial fragments 9. Complications of Calcaneal Fractures: a. Heel pain b. Peroneal tendonitis c. Osteoarthritis of the STJ, MTJ, and ankle joint d. Heel pad damage e. Bony prominence f. Flexor tenosynovitis g. Sural or posterior nerve entrapment h. Calcaneus gait (weak plantarflexion) i. Rigid pes planus j. Reflex sympathetic dystrophy k. Infection NOTE* In cases of severe comminution, the question of primary subtalar fusion or triple arthrodesis is still debated

Talar Fractures 1. Anatomy: a. 2nd largest tarsal bone with more than 1 /2 the surface being cartilage b. No muscular or tendinous attachments c. The 3 main parts are the head, body and neck. The neck deviates medially 15-200 and is its most vulnerable part d. The FHL lies within a groove on the posterior talar tubercle held by a retinacular ligament e. Inferiorly 3 facets are present; between the posterior and middle is a transverse groove which (with the calcaneus) forms the tarsal canal that exits laterally into the sinus tarsi 2. Blood supply: a. Extraosseous blood supply comes from: i. Posterior tibial (#1) ii. Anterior tibial (#2) iii. Perforating peroneal (#3) b. The talar neck is supplied by an anastamosis of 2 vessels: i. Artery of the tarsal sinus ii. Artery of the tarsal canal 3. Classification: a. Chips and avulsions b. Compression fractures c. Fractures of the body: i. Non displaced ii. Displaced

iii. Comminuted d. Fractures of the neck (Hawkins' classification): All caused by some fall or accident resulting in a severe dorsiflexory force to the foot i. Group 1: Vertical fracture of the neck that is undisplaced
One of the three sources of the blood supply is disrupted (a 13% chance of avascular necrosis has been reported) ii. Group 2: Vertical fracture of the neck that is displaced, the STJ is subluxed or dislocated, and the ankle joint is WNL
Two main sources of blood supply are interrupted (a 42% chance of avascular necrosis has been reported)
Prognosis is related to the development of avascular necrosis iii. Group 3: A vertical fracture of the neck that must be displaced and the body of the talus must be dislocated from both the ankle and subtalar joints
All three sources of blood supply are disrupted (91 % chance of avascular necrosis) iv. Group 4: The fracture of the talar neck is associated with dislocation of the body from the ankle and the subtalar joints with an additional dislocation or subluxation of the head of the talus from the T-N joint
Avascular necrosis reported in 100% of cases NOTE* Early anatomical reduction in displaced fractures yields the most favorable long term results

NOTE* Hawkins' sign is an area of translucency of subarticular or subchondral bone seen on x-ray, following injury, which indicates healing is occurring e. Fractures of the talar dome (Berndt and Harty): see section Osteochondral fractures f. Dislocations: i. Anterior dislocations ii. Posterior dislocations iii. Lateral dislocations iv. Medial dislocations v. Total dislocation 4. Treatment: a. Talar neck: i. Group 1:
BK/NWB cast for 6-12 weeks, followed by NWB with no cast for an additional 2-5 months with ROM ankle excercises (prognosis is excellent)
ii. Group 2:
Closed reduction with BK/NWB cast until evidence of union
Early ORIF when and if closed reduction fails or the original reduction is unstable (prognosis related to the development of avascular necrosis) iii. Group 3:
ORIF with accurate anatomical reduction must be achieved followed by





BK/NWB cast for 3-4 months (prognosis is poor) iv. Group 4: As per Group 3 NOTE* If the talus must be removed, a Blair procedure is recommended NOTE* Arthrodesis procedures have been stated to give better results as a secondary procedure than a talectomy alone NOTE* Hawkins grades 3 and 4 fractures were thought to be unsalvagable but with modem ORIF techniques there are improved chances of restoring normal function after injury.

a. The operative incision to the talus must not inflict any additional harm to the arteries bringing blood to the body and the neck the most critical blood supply coming from the posterior tibial in the deltoid: ligament attachment. An additional blood supply courses into the undersurface through the talocalcaneal ligament b. The talus must be reduced as quickly as possible to protect any remaining blood supply by untwisting and reducing tension in the deltoid ligament, and to encourage revascularization c. An atraumatic operative approach is needed that allows adequate visualization for anatomic reduction (Oilier lateral incision, transverse Cincinnati incision or a posterolateral vertical incision work well)

b. Lateral process: i. Undisplaced:
BK cast partial weight bearing 4 weeks i. Displaced:
Excision of bone fragment if symptomatic c. Total talar dislocations (out of the ankle mortise and STJ, anterior to the fibula, head directed medially, talus rotated on the longitudinal axis so its inferior aspect points posteriorly): i. Manipulation:
Usually not successful but should be attempted ii. Skeletal traction:







Steinmann pin through calcaneus attached to traction apparatus to achieve an open space between the tibia and calcaneus. The assistant inverts and plantarflexes the foot, as the surgeon presses both thumbs on the posterior aspect of the talus by inward and backward movement to rotate the talus. Afterward, the pin is removed and the foot is immobilized in an anterior and posterior splint for 7 days with the knee bent to 300 and ankle at 90°. This is followed by a BK cast for 6-8 weeks. Avascular necrosis is inevitable. If there is an open wound treat appropriately.

Osteochondral Fractures 1. Classification (Berndt and Harty): a. Stage 1: A small area of compression of subchondral bone b. Stage 2: A partially detached osteochondral fragment c. Stage 3: A completely detached osteochondral fragment remaining in the defect. d. Stage 4: A displaced osteochondral fragment NOTE* It has been found that 44% are lateral and anterior, and 56% are medial and posterior. Lateral lesions are shallow wafer shaped and medial lesions are deep cup shaped 2. Mechanism of injury: a. Lateral lesions: Inversion and dorsiflexion b. Medial lesions: Inversion, plantarflexion and lateral rotation of the tibia on the talus 3. Diagnosis: a. Stage 1: i. Usually no symptoms, and has been diagnosed as an ankle sprain ii. ROM of the ankle is WNL and painless b. Stage 2: i. Painful with associated collateral ligament damage
Lateral dome lesions have pain over the lateral collateral ligaments
Medial dome lesions have pain over the deltoid ii. Ankle ROM may be limited due to traumatic synovitis c. Stage 3 8 4: i. Pain is more severe ii. Decreased ROM of the ankle, joint locking or crepitus, and/or instability of the collateral ligaments Note* The diagnosis can be made on x-ray (the A-P view shows the medial talar dome clearly, the lateral dome is obscured but can be visualized in the medial oblique), but the use of tomograms or CT are best 4. Treatment: a. Conservative: For stage 1, 2, 3 medial lesions via NWB BK cast for 6 weeks followed by a patellar-bearing brace until the fracture heals

b. Surgical: For stage 3 lateral and 4, surgery to remove fragment, or stabilize fragment using K -wire or Herbert screw NOTE* Review of the literature reveals that surgically treated patients have better results in preventing post-traumatic arthritis. However, conservative vs. surgical treatment depends upon the size/location/stage of the fracture fragment

Staging System for Osteochondral Lesions T2W-MRI

Arthroscopy

Stage 1

Normal

Radiographs

Marrow edema (diffuse high signal intensity

Stage 2

Semicircular fragments

Low signal line surrounds fragment

Normal or irregularity and softening of cartilage Articular cartilage breached, definable but nondisplaced fragment

Stage 2A

Subcortical lucency

Stage 3

Semicircular fragment Loose body

High-signal fluid within fragment High signal line surrounds fragment Defect talar dome

Stage 4

Displacable fragment Loose body

Navicular Fractures Fractures of the navicular are easily missed,, and are important to diagnosis quickly as a delay in treatment could lead to traumatic arthrosis of Lisfranc's joint as well as the T-N joint. Isolated fractures are uncommon, and usually occur in conjunction with Lisfranc's dislocations and fractures of the rearfoot. Stress fractures of the navicular have been seen in runners but more frequently in basketball players, and this problem is often misdiagnosed as anterior tibial tendonitis 1. Anatomy: a. Cancellous bone which is convex distally where it articulates with the three cuneiforms and is concave proximally to accomodate the talar head b. The dorsal navicular surface is roughened and serves as an attachment for the dorsal talonavicular ligament, cuneonavicular ligaments and the cubonavicular ligament c. The plantar surface is so roughened and is invested by the plantar calcaneonavicular ligament (spring ligament) d. The lateral surface serves the attachment for the navicular portion of the bifurcate ligament e. The navicular tuberosity provides the major attachment site for the posterior tibial tendon f. The blood supply is from the dorsalis pedis and the medial plantar artery which form an arcade of 6-8 randomly arranged vessels that penetrate the navicular surface (the central 1 /3 is relatively avascular) 2. Navicular Fracture Classification by Watson-Jones a. Type I- Fracture of the tuberosity i. Relatively common as compared to other types ii. The mechanism of this fracture is acute eversion of the foot causing an avulsion-type fracture, caused by increased tension placed on the tibialis posterior tendon iii. These fractures are generally non-displaced because of the multiple soft tissue attachments to the tuberosity iv. Best demonstrated radiographically on the AP and oblique x-ray with the foot in moderate equinus v. It is important to differentiate this fracture from a type II accessory navicular vi. If the type I fracture is severely displaced you should suspect calcaneocuboid involvement vii. The combination of a severely displaced fracture and compression fracture of the cuboid and/or calcaneus is referred to as the NUTCRACKER SYNDROME vii. Treatment is with an Unna-type boot of BK partial weight-bearing cast x 4 weeks. viii. If a symptomatic non-union occurs it is recommended that the fragment be

removed and reattachment of the tibialis posterior performed

b. Type II- Fracture of the dorsal lip

i. Most frequent fracture of the navicular and is intraarticular ii. The mechanism of injury is plantarflexion of the foot followed by either forced inversion or eversion iii. Best seen on the lateral x-ray iv. Can be confused with 2 accessory ossicles in the same area, the os supratalare and os supranaviculare v. Treatment is with a BK partially weight-bearing cast for 4-6 weeks

vi. If late problems such as a painful dorsal prominence occurs, excision of the fragment is recommended c. Type IIIA - Fracture of the body without displacement d. Type IIIB - Fracture of the body with displacement

i. A severe injury that causes disruption of the talonavicular and cuneonaviclar joints ii. Can be either displaced (type A) or nondisplaced (type B) iii. The mechanism of injury can result from either direct crush or blow, or indirect from a fall from a height with the foot in a marked plantarflexion position at the moment of impact iv. These fractures are usually intraarticular v. DP, lateral, and oblique x-rays will demonstrate the fracture vi. A differential diagnosis for a type Ill navicular fracture include a bipartite tarsal navicular and lithiasis of the navicular vii. Treatment of nondisplaced fractures is with a BK walking cast for 6-8 weeks viii. Treatment of displaced fractures is with ORIF and a BK non-weightbearing cast for 6-8 weeks e. Type IV- Stress fracture of the navicular

i. Usually an athletic injury, most commonly track and field ii. Symptoms are increased pain with activity, and decreasing pain following the activity iii. Usually intraarticular iv. Usually found with either a bone scan, CT scan, or MRI v. Early diagnosis is important to prevent a complete fracture and an eventual nonunion v. Treatment is a BK non-weight-bearing cast for 4-6 weeks if nondisplaced, and if displaced ORIF with a BK non-weight-bearing cast for 6-8 weeks NOTE* Watson-Jones navicular fracture classification described 3 types: Type 1 (tuberosity fx), Type 2 (dorsal lip fx), and Type 3 (transverse body fx)

Cuboid Fractures The cuboid is a key bone in the rigid lateral column of the foot. Its position is stabilized by several structures to ensure its structural and functional integrity 1. Anatomy: a. The cuboid is locked in articulation with 5 bones of the foot (4th and 5th metatarsals, calcaneus, lateral cuneiform, and a fibrous articulation with the navicular) b. Primarily cancellous c. Dorsally, the bifurcate ligament attaches the calcaneus to the cuboid, the dorsal cuneocuboid ligaments tether the cuboid to the lesser tarsus d. Dorsolaterally, the dorsal tarsometatarsal ligaments attach the cuboid to the metatarsal bases e. Plantarly, the long and short plantar ligaments attach to and cross the cuboid while adding to the maintenance of the longitudinal arch f. The sural nerve and lesser saphenous vein cross over the cuboid area g. The peroneus longus courses plantarly under the peroneal groove in the cuboid

h. The arterial supply is made up of an arterial rete system supplied by the lateral malleolar artery, the lateral tarsal artery and the arcuate artery 2. Classification system: a. Type 1: Stress fracture b. Type 2: Avulsion fractures (a) Bifurcate ligament area (b) Tarsometatarsal ligament area c. Type 3: Body fracture, nondisplaced d. Type 4: Indirect crush fracture or nutcracker fracture e. Type 5: Plantar dislocation f. Type 6: Direct crush 3. Avulsion Fractures: a. Most common on the lateral aspect at the calcaneocuboid joint and the 5th met-cuboid articulation. b. Avulsion fracture of the tuberosity due to tension on inferior calcaneocuboid ligament. c. Adduction of the cuboid on the calcaneus will result in avulsion due to tension on lateral calcaneocuboid ligament. NOTE* Avulsion fractures of the cuboid must be differentiated from os cuboid secondarium, os peroneum and/or os vesalianum d. Treatment is closed reduction with casting 4. Fractures of the body of the cuboid: a. Due to axial rotary forces while the foot contacts the ground in a plantarflexed position- usually associated with fracture of the base of the 5th metatarsal and calcaneus b. Crush fracture as above mechanism but with more force (a nutcracker effect) c. Treatment is closed reduction with BK cast 6-8 weeks or arthrodesis in case of crush fracture 5. Stress fractures: a. Should be suspected if concerned about peroneus longus tendonitis, calcaneocuboid arthritis, dropped cuboid, and capsulo-ligamentous strain in the cavus foot type. b. Treatment: BK cast 6-8 weeks (first 2 weeks NWB)

NOTE* In general, treatment for type 1, 2, and 3 injuries is usually NWB BK cast for 6-8 weeks. Avulsion fractures are sometimes opened if the dislodged fragment is felt to be intraarticular or will cause impingement on the peroneal tendons. Type 5 dislocations must be reduced, with closed reduction under general anesthesia attempted first with an inversion-adduction force on the forefoot while pushing the cuboid up from the arch. If this fails, open reduction is advised. Type 4 fractures usually require autogenous bone grafting for anatomic alignment of the calcaneocuboid and tarsometatarsal joints

Cuneiform Fractures 1. Avulsion fractures: a. Usually located on the medial aspect of the internal cuneiform as an avulsion due to pull of the tibialis anterior 2. Fractures of the body: a. Mechanism: Either by direct trauma or rotational force 3. Stress fractures: a. Diagnosed by bone scans, CT, or tomography b. Treated with BK WB cast 4. Treatment: Requires traction to reduce the dislocation and allow anatomical reduction of the cuneiforms to prevent chronic pain and arthritis NOTE* a. Cuneiform fractures are usually associated with Lisfranc dislocations b. The mechanism of the dislocation and fractures of the cuneiforms involves the forefoot and rearfoot acting as levers, with the lesser metatarsals displaced laterally and dorsally c. Fracture of the 2nd metatarsal base is an important factor in causing dislocation or fracture of the middle cuneiform d. Lisfranc's ligament interruption has an effect on a middle cuneiform fracture/dislocation Fifth Metatarsal Base Fractures Fractures of the 5th metatarsal are commonly associated with inversion sprains of the ankle, therefore, with any ankle inversion injury, the 5th metatarsal base should always be evaluated. This is the Stewart Classification

1. Type 1: A true Jone's fracture which occurs between the epiphysis and diaphysis (metaphyseal level). a. Usually oblique or transverse in nature b. Situated at the distal end of the articular capsule above the intermetatarsal ligaments c. The mechanism of injury is internal rotation of the forefoot while the base of the 5th metatarsal remains fixed, The capsule is only stretched and the peroneus brevis takes practically no part on the injury d. Upon physical examination, extreme mobility of the shaft of the 5th metatarsal is found e. This is an unstable fracture with a very poor blood supply and because of this, this fracture has a very high propensity for non-union f. Treatment is with a non-weight-bearing cast BK cast for 4-6 weeks, or If displaced, then ORIF

2. Type 2: Intraarticular fracture of the 5th metatarsal base with one or two fracture lines a. A result of shearing force caused by the internal twisting of the forefoot while the peroneus brevis is contracted b. Displacement of the fragments depends upon the extent of the damage to the capsule and ligaments c. Treatment is with an Unna-type boot or BK non-weightbearing cast for 4-6 weeks, or if nonreducible, then ORIF

3. Type 3: This is an avulsion fracture of the base of the 5th metatarsal a. This is oftentimes mistaken in the literature for a Jones fracture. It is the most proximal injury, where a small fragment is torn away, the fracture is extraarticular, and the fracture line is usually at right ankles to the long axis of the metatarsal base a. The mechanism of injury is primarily a sudden sharp contraction of the peroneus brevis when the ankle is in plantarflexion

b. The treatment is with an Unna-type boot of BK non-weightbearing cast for 46 weeks, or if nonreducible then ORIF with tension bend wiring or screw fixation. If the fragment is too small for fixation, then excision of the fragment and reattachment of the peroneus brevis tendon is recommended

4. Type 4: This is a comminuted intraarticular fracture of the 5th metatarsal base a. The mechanism of injury is similar to Type 2, but in this case the 5th metatarsal base gets crushed between the cuboid and the ground causing fragmentation b. There is a high rate of non-union c. Treatment is an Unna-type boot or a BK non-weight-bearing cast for 46 weeks, or if fracture fragments are severely displaced, bone grafting and ORIF may be required

5. Type 5: A fracture that occurs in children, where there is a partial avulsion of the epiphysis with or without a fracture line or hairline crack as seen in Type 2. This fracture can also be classified as a Salter-Harris I. a. The treatment is a BK non-weight-bearing cast for 4-6 weeks

Metatarsal Fractures (1st and 2nd-3rd-4th) 1. Classification: a. Site: i. Epiphyseal ii. Diaphyseal iii. Metaphyseal b. Type: i. Incomplete separation of the bony fragments ii. Complete separation iii. Greenstick fracture iv. Buckle type fracture c. Configuration: i. Transverse

ii. Spiral iii. Oblique iv. Comminuted v. Stress fracture d. Relationship of the fragments: i. nondisplaced ii. Displaced:
Shifted sideways
Rotated
Distracted
Overriding
Angulated
Impacted e. Relationship to outside environment: i. Simple ii. Compound NOTE* If, wound is open treat accordingly :(check blood loss, shock etc) tetanus prophylaxis, antibiotic therapy, skin coverage as necessary, rigid reduction of fracture, and fluid replacement as necessary NOTE* Salter devised a classification system describing fractures of long bones 1. Location of the fracture: diaphysis, metaphysis, physis, epiphysis, intraarticular 2. Extent of the fracture: complete or incomplete 3. Arrangement of the fracture: transverse, spiral, oblique, compression, comminuted 2. Treatment: a. Closed reduction with BK NWB cast 4-6 weeks b. Open reduction: i. Monofilament wire ii. K-wires iii. AO technique NOTE* Complications include pseudoarthrosis, avascular necrosis, and malposition NOTE* Radiographic diagnosis of this fracture should not be confused with the normal apophysis present in children (closed b age 15 in boys and 12 in girls). and Iselin's disease (osteochondrosis) Also differentiation should be made between an avulsion fracture and an os vesalianum and os perineum

NOTE* Radiographic evidence of chronicity is manifested by a wide radiolucent fracture line, periosteal reaction, thickening of the lateral margin of the cortex adjacent to the fracture with or without callus, and intramedullary sclerosis 3. First metatarsal fractures: a. Anatomy: i. Articulates laterally with the 2nd metatarsal, proximally with the medial cuneiform, and distally with the base of the proximal phalanx of the hallux ii. 2.7 cm proximal to the head of the 1 st metatarsal (on the lateral aspect) is the foramen for the nutrient artery iii. Plantar surface is concave, causing this side to be under tension during weight bearing iv. Holds the sesamoids, the tibial being larger separated by the crista or central ridge (if more than 2 sesamoids, bipartite indicating multiple ossification centers) v. Muscles around the 1st metatarsal:
Peroneus longus: involved in 1st metatarsal base avulsion fractures
Tibialis anterior
EHL
EHB
Adductor hallucis
Abductor hallucis
FDB
Tibialis posterior vi. Arterial supply is the dorsalis pedis and 1 st plantar metatarsal b. Classification: a. Salter classification is based on 6 categories i. Site: anatomical location ii. Configuration: transverse, oblique, spiral, etc. iii. Open or closed iv. Location v. Extent: complete or incomplete vi. Relationship of the fracture fragments to each other: displaced, angulated, rotated, etc. c. Treatment: i. Simple fractures with no displacement are treated NWB BK cast for 6-8 weeks ii. Displaced fractures should be anatomically reduced (usually open reduction ORIF) iii. Open fractures: treated as per open fracture classification

4. External fixator device for metatarsal fractures: A miniature external fixation device can be utilized in the treatment of metatarsals. Maintains the normal metatarsal parabola pattern a. Indications: When a metatarsal fracture is severely comminuted or when a significant loss of bone stock is present (gunshot) b. This supplies rigid fixation giving stability to the fracture and can be combined with other forms of fixation c. It is capable of both compression and lengthening the metatarsal fragments and can be combined with bone grafting as needed d. Should be reserved for patients for whom reduction by any other means cannot be obtained 5. Internal metatarsal fractures (metatarsals 2-3-4): Treated like the other metatarsal fractures

A: Is a diaphyseal fracture with straight plate fixation without lag screw B: is a diaphyseal/metaphyseal neck fracture with application of L plate with lag screw fixation C: Is a metaphyseal base fracture with application of T-plate with lag screw fixation

Ankle Fractures 1. Classifications: a. Lauge-Hansen: A two-word description indicating the position of the. foot at the time of injury, and the direction of the talus. Five types of injuries listed: i. Supination-Adduction ii. Pronation-Abduction iii. Supination-External Rotation iv. Pronation-External Rotation v. Pronation-Dorsiflexion

NOTE* The major advantage of the classification is to enable the examiner to assess the stability of the ankle from the x-rays by predicting ligamentous injuries In external rotation injuries, the progression of lesions simply follows the anatomic sequence around the ankle joint: deltoid-medial malleolus complex, anterior syndesmosis, fibula, and posterior syndesmosis. In supination injuries, the sequence starts with the anterior syndesmosis, and in pronation injuries, with the deltoid-medial malleolus complex. b. Danis-Weber: Based on the location of the fracture of the fibula and is useful for determining the appropriate form of treatment for ankle fractures. i. Type A: Below the joint level ii. Type B: At the level of the joint iii. Type C: Above the level of the joint 2. Lauge-Hansen: a. Supination-Adduction: NOTE* The hallmark of this injury is an avulsion fibular fracture at the level of the ankle or below. i. Stage 1: Transverse fracture of the lateral malleolus usually below or at the level of the ankle mortise or lateral collateral ligamentous rupture (pulloff) ii. Stage 11: Stage I plus an oblique fracture of the medial malleolus (pushoff) NOTE* Variants of Stage If S -A injuries are: rupture of the deltoid ligament rather than fractures of the lateral malleolus, concomitant damage to the tibiofibular syndesmosis with fracture of the medial and lateral malleolus, avulsion fracture of the lateral malleolus proximal to the A.T.F. with damage to the lateral collateral ligament, S-A fracture of the medial malleolus without injury to the lateral side, NOTE* Healing is more favorable with supination injuries (less overall damage)

b. Pronation Abduction: 1. Stage I: Fracture of the medial malleolus or tear of the deltoid ligament ii. Stage II: Stage I plus rupture of the anterioinferior tibiofibular and posterioinferior tibiofibular ligaments and transverse tibiofibular ligament, with fracture of the posterior lip of the tibia iii. Stage III: Stage II plus an oblique supramalleolar fracture of the fibula (the anteroposterior tibiofibular ligaments tear but the interosseous ligament does not)

c.

Supination-External Rotation: NOTE* This is the most common fracture of the ankle, and its hallmark is a spiral fracture of the fibula

i. Stage I: Rupture of the anteroinferior tibiofibular ligament, sometimes with avulsion of the bony fragment between the tibia and fibula. (tibia: Chaput, fibula: Wagstaff) ii. Stage II: Stage I plus a spiral oblique fracture of the lateral malleolus. iii. Stage III: Stage 11 plus a fracture of the posterior lip of the tibia (Volkmann's fracture) iv. Stage IV: Stage III plus a fracture of the medial malleolus

d. Pronation-External Rotation: NOTE* 'The hallmark is a high fibular fracture. i. Stage I: Fracture of the medial malleolus or a tear of the deltoid ligament. ii. Stage II: Stage I plus a tear of the anteroinferior tibiofibular ligament and interosseous ligament. iii. Stage III: Stage II plus an interosseous membrane tear and a spiral fracture of the fibula 7-8 cm. proximal to the tip of the lateral malleolus iv. Stage IV: Stage III plus a fracture of the posterior lip of the tibia.

e. Pronation-Dorsiflexion: i. Stage I: Fracture of the medial malleolus ii. Stage II: Fracture of the anterior inferior aspect of the tibia iii. Stage Ill: Supramalleolar fracture of the fibula (transverse) iv. Stage IV: Fracture of the posterior aspect of the tibia (Pilon fracture) Reudi and Allgower divided these into:
Grade I: Cleavage fracture of the distal tibia with no disruption of the internal surface
Grade II: Internal surface disruption with no comminution
Grade III: Impaction and comminution NOTE* In a fall from a height, where there is pronation-dorsiflexion injury, axial compression is present, which will result in the following fractures of the tibial plafond: a. if the talus is dorsiflexed upon impact, anterior portion of tibial plafond is fractured b. if the talus is plantarflexed upon impact, posterior portion of the tibial plafond fractures c. if the talus is in neutral position upon impact, central shattering of the articular surface of the tibial plafond takes place

3. Danis-Weber fractures: a. Type A (Supination-adduction Lauge-Hansen): The fibular fracture occurs below the level of the tibial plafond and therefore below the level of the syndesmotic ligaments. It is associated with a vertical fracture of the medial malleolus. b. Type B (Supination-external rotation or Pronation-abduction LaugeHansen): An avulsion fracture of the medial malleolus and fracture of the fibula that begins at the level of the tibial plafond. The posterior rim of the tibia might also be fractured c. Type C (Pronation-external rotation Lauge-Hansen): Characterized by rupture of the syndesmosis and a fibular fracture that is located above the tibial

plafond. Associated injuries are an avulsion fracture of the medial malleolus or deltoid ligament rupture and a large or small posterior malleolar fracture. 4. Other fractures: a. Tillaux fracture: Fracture of the anterior tubercle of the tibia due to tension of the IATF ligament. Also a type 3 epiphyseal injury of the anterolateral distal tibia. b. Wagstaff-Lefort fracture: Vertical fracture of the anterior margin of the lateral malleolus due to an avulsion of either the anteroinferior tibiofibular or anterior talofibular ligaments. c. Maisonneuve fracture: Fracture of the proximal fibula , associated with tibiofibular diastasis. d. Pankovich classification of Wagstaff fractures: i. Type l: Avulsion fracture and fibular fragments remaining attached to the anterior talofibular ligament and IATF ligament ii. Type Il: Oblique fracture with fragment remaining attached to the IATF ligament iii. Type III: Oblique fracture of the fibula in addition to a fracture of the anterior tibial tubercle e. Bosworth fracture: Fibular oblique fracture caused by external rotation but the fracture occurs after posterior dislocation of the fibula. This causes closed reduction to be impossible. f. Frost. fracture: A triplane fracture which is a combination of Tillaux and Salter-Harris Type 2 occurring at the distal tibia g. Pott's Fracture: A fracture of the distal fibula and disruption of the deltoid ligament (or medial malleolar fracture) h. Cooperman's fracture: This is a Salter-Harris triplane type 4 epiphyseal ankle fracture which consists of 2 fragments: the first is composed of the tibial shaft, medial malleolus, and the anteromedial portion of the epiphysis; the second consists of the remainder of the metaphysis, epiphysis, and attached fibula. i. Chaput's tubercle: The anterolateral tubercle of the distal tibia j. Shepherd's fracture: Fracture of the posterolateral tubercle of the talus. k. Volkmann's fracture: A fracture of the posterolateral corner of the distal tibia (Volkmann's triangle), medial malleolus, fibular shaft, and tibiofibular diastasis. l. Ashurst's sign: The overlap of the anterior tibial tubercle and the medial 2/3 of the distal fibula normally is found on the A-P x-ray of the ankle. Ashurst's sign is present with a lessening of this overlap due to widening of the ankle mortise due to disruption of the anterior tibiofibular ligament m. Thurston-Holland sign: The spike of metaphyseal bone attached to the fractured epiphysis seen with Salter-Harris 2 fractures. 4. Treatment of ankle fractures: a. General considerations: A decision to perform surgery takes in account all aspects of the patient's condition. In general, the best long term results in terms of restoration of function and avoidance of posttraumatic arthritis are directly related to treatment that restores anatomy and allows for early

range of motion and early weight-bearing. Early ORIF should be done provided that the initial evaluation of the patient reveals a satisfactory .neurovascular status and skin condition of the foot. Early ORIF reduces swelling by stabilizing the fracture and also reduces bleeding. If the fracture is open, the wound should be cultured and broad spectrum IV antibiotics started, followed by wound debridement, irrigation, and ORIF as indicated. The wound is left open and delayed primary closure is performed at least 5 days later. Closed reduction of displaced ankle fractures rarely accomplishes restoration of normal anatomy without repeated forced manipulations, and does not allow for early ambulation and range of motion. NOTE* ORIF is indicated for all ankle fractures with a greater than 2 mm. lateral or posterior displacement of the lateral or medial malleolus b. Absolute criteria: i. Fractures and dislocations must be reduced immediately ii. All joint surfaces of the ankle must be anatomically reduced iii. Reduction must be maintained while the fractures are healing iv. Motion of the joints should be started as soon as possible c. Other criteria: i. ORIF of the fibula should precede fixation of the medial malleolus because it provides a buttress to the talus, which tends to displace laterally and pull along the medial malleolus. Shortening of the fibula must be prevented (see chapter 29: Ankle Conditions, Nonunion of Malleoli) ii. Repair of the deltoid is difficult and rarely necessary, and should be reserved for more severe injuries in which soft tissues around the ankle are damaged. iii. Large displaced fragments of the anterior and posterior processes of the tibia, which are present in some indirect ankle fractures, should be anatomically reduced (if at least 1 /4th the weight-bearing surface) in order to restore congruity of the articular surface (reduction of these fragments prevents subluxation of the talus) iv. Fracture of Chaput tubercle and Wagstaff fractures should always be reduced and fixed v. A displaced yet essentially intact fibula requires syndesmotic screws for proper reduction NOTE* Stability of the syndesmosis is tested by pulling the fibula laterally with a bone hook. When there is more than 2-3 mm of lateral displacement of the fibula, instability is present and the use of a syndesmotic screw(s) is indicated. It is desirable to insert this screw 2-3 cm above the tibial plafond. When there is a plate attached to the fibula, one cortical screw can be removed and replaced with a syndesmotic screw. When drilling for a syndesmotic screw, the direction must be anteromedial to avoid inserting the screw posterior to the tibia

NOTE* Observe for tendon dislocations, i.e. posterior tibial tendon into the ankle joint d. Fixation of the fibula: Should be fixed prior to the medial malleolus i. AO Technique: Interfragmentary screws are inserted most often from the anterior edge in a posteroinferior direction
Overdrilling is unnecessary and may cause comminution of the fragment
3.5 mm cortical screws are most often used ii. Cerclage Wiring:
It is useful in comminuted fractures while a plate is being applied to the lateral side of the fibula
Can be used as an adjunctive device for an oblique fracture of the fibula while an intramedullary nail is being used iii. Inyo Nails:
Excellent for transverse fractures of the distal fibula
Useful in osteoporotic bone but requiring cerclage wiring of an oblique fracture of the fibula prior to insertion
When inserting the nail, it is critical to reduce the fracture anatomically in order to avoid penetration outside the bone e. Fixation of the medial malleolus: Requires fixation with a device that provides compression between the fracture fragments I. AO technique:
Essentially only 4.0 mm cancellous screws should be used for fixation of the medial malleolus (self-tapping 4.5 mm malleolar screws are not practical because the head of the screw is too large and prominent after insertion)
A screw usually 40-45 mm in length is usually used
In osteoporotic bone a washer would be used to prevent penetration of the head of the screw head
A second screw is used when the malleolar fragment is large (a K -wire can be used first to prevent rotation of the fragment and retained for additional stability) f. Closed reduction: i. The main advantage of closed reduction is lack of postoperative wound complications ii. Closed reduction is contraindicated in unstable ankle fractures in which both malleoli are fractured iii. Closed reduction is acceptable in fractures when open reduction is contraindicated (vascular compromise, neglected open fractures, pyoderma, skin necrosis or contusion) iv. Gravity is utilized by positioning the leg horizontally and in external rotation while holding the foot in one hand with the heel resting in the palm. This effectively produces internal rotation and adduction of the talus and in that way reduces the fibula and brings in position the medial malleolus
A short leg cast is first applied while the fracture is being reduced, then is extended to a long leg cast with the knee in 30° of flexion. A minimum of 6 weeks of immobilization is required

5. Factors that result in irreducible fractures: a. Interpositon of the deltoid ligament b. Trapping of the tibialis posterior tendon c. Trapping of the medial tendon(s) d. Dislocation and fracture-dislocation of the fibula behind the tibia

6. Soft tissue complications of fractures and dislocations of the ankle: a. Skin: Blistering, decubitus breakdown, slow wound healing b. Massive Edema: Treat with compression immediately, cold application, elevation, rigid internal fixation and early ROM c. Fracture blisters: Direct result of edema. ORIF must be delayed for 3-7 days d. DVT's: Due to plaster immobilization, venous insufficiency, sickle-cell. Treat casted patients with sub-Q heparin 2500-5000 units Q 8-12 hours if they are at risk e. Chondrolysis of the ankle (cartilage necrosis): Leads to posttraumatic arthritis f. Avascular necrosis of the talus g. Infection following open fractures (5-30%) h. Nerve injuries

i. Nerve disruptions (complete and incomplete) ii. Reflex sympathetic dystrophy syndrome i. Arterial injuries j. Tendon injuries k. Ligament injuries i. Medial deltoid ii. Lateral ligament (chronic thickening, local tenderness, inversion instability, anterior subluxation) 7. Bony complications of fractures and dislocations of the ankle: a. Fractures of the lateral malleolus: i. Non-union and malunion (external rotation) with chronic swelling and widening of the ankle b. Fractures of the medial malleolus: i. Non-union: More common than the lateral malleolus due to soft tissue interposition between the fragments
Chronic diastasis
Loose bodies
Arthritic changes c. Fractures of the posterior tibial margin: Greater than 25% margin renders the ankle unstable leading to posterior subluxation i. Posterior subluxation
Medial and lateral malleoli and syndesmosis torn ii. Malunion with posterior subluxation
Most common complication d. Fractures involving the distal tibiofibular syndesmosis: i. 2nd only to plafond injuries, leads to arthrodesis of the ankle ii. Mortise widening e. Vertical or Pilon fractures of the distal tibia: i. Varus or valgus deformity ii. Traumatic arthritis iii. Articular incongruity f. Epiphyseal injuries: i. Articular incongruity is the main concern ii. Vascular embarassment iii. Posttraumatic arthritis iv. Varus or valgus deformity of the ankle v. Angular deformity vi. Leg length discrepancy vii. Bone and joint sepsis

Midtarsal Joint Dislocations The talonavicular and the calcaneocuboid joints function as a single unit in movements (functions with STJ in inversion and eversion) so are considered together as the MTJ. Injuries are rare 1. Classification (Main and Jowett): Midtarsal joint injuries are defined according to the direction of the force producing the dislocation. a. Medial force results in three grades of injuries: i. Fracture sprain of calcaneus, talus, navicular, or cuboid

ii. Fracture/subluxation or dislocation with medial subluxation or dislocation of forefoot while the talocalcaneal relationship remains normal iii. Swivel dislocation with only the T-N joint dislocating b. Longitudinal force injuries: i. Fracture of the navicular takes place c. Lateral force injuries: i. Fracture sprain of the navicular tuberosity, dorsal chip of the talus or navicular, and lateral fracture of the cuboid ii. Fracture/subluxation will result in T-N lateral subluxation and nutcracker fracture of the cuboid iii. Swivel dislocation with the talus dislocating laterally relative to the navicular d. Plantar force injuries: i. Result in dorsally dislocated talus and calcaneus relative to the navicular, and cuboid chip fractures also present dorsally, as well as anteroinferior calcaneal fractures e. Crush injuries: Have variable patterns. Usually associated with open wounds 2. Treatment: a. Medial force injuries: reduced by traction and reversal of the mechanism of injury with casting (WB or NWB) b. Lateral force injuries: closed reduction first. C-C fusion is recommended for persistent symptoms. Triple arthrodesis has been the traditionally recommended treatment if conservative care has failed

Tarsometataral Joint Dislocations/Fractures (Lisfranc dislocation) This type of injury occurs in conjunction with high energy trauma (equestrian injuries) as well as minor twisting injuries, which are also associated with injuries to the cuneiforms, cuboid, and the navicular. The key to understanding this injury is the structural integrity provided by the slotting in the base of the second metatarsal, which is surrounded by 5 adjacent bones that create a tight mortise. There is no ligament between the base of the 2nd and 1st metatarsals, but a ligament extends from the medial base of the 2nd metatarsal obliquely to insert into the medial cuneiform. Soft tissue loss and vascular impairment can be a major problem in this setting The 2nd metatarsal is the key to stability of Lisfranc's joint. The dorsal tarsometatarsal ligaments are weaker than the plantar tarsometatarsal ligaments. 1. Mechanism of injury: a. Abduction and plantarflexion: 2nd metatarsal is fractured, the remaining ligaments give way and the forefoot is subluxed laterally b. With continued abduction, there may be a nutcracker-like fracture of the cuboid.

2. Classifications: a. Hardcastle et. al. i. Type A: Total incongruity (the metatarsals displace in a unit in one plane ii. Type B; Partial incongruity ( at least one of the tarso-metatarsal joints is not displaced) iii. Type C: Divergent (the 1 st metatarsal is displaced medially and the other metatarsals are displaced laterally) b. Quenu and Kuss c. Myerson: Further subdivided Hardcastle's classification i. Type A: Total incongruity ii. Type 131: Partial incongruity, medial metatarsals iii. Type B2: Partial incongruity, lateral metatarsals iv. Type C: Divergent patterns v. Type Cl: Partial displacement vi. Type C2: Total displacement 3. Diagnosis: Via x-ray (A-P & lat)/tomography (A-P)/CT scan a. Widening between the base of the 1 st and second metatarsals or the middle and medial cuneiforms is often present. This widening can also be between the base of the second and third metatarsals or middle and lateral cuneiforms. b. An avulsion fragment referred to as the "FLECK SIGN" is often present between the base of the 1st and 2nd metatarsals or middle and medial cuneiforms. c. Projected lines from the base of the metatarsals should not intersect the corresponding cuneiforms or cuboid. d. Angulation of the metatarsals can occur without apparent fracture at the base. e. Widening between the base of the 5th metatarsal and the cuboid can occur. NOTE* Due to the spontaneous relocation that this fracture dislocation can produce, x-rays do not usually show the true magnitude of the severity of this injury 4. Treatment: Includes splinting, casting, closed reduction and casting, closed reduction and percutaneous pinning, or open reduction and percutaneous pinning (according to type) a. If instability is present but alignment is anatomic with release of the force, immobilizing the extremity in a BK NWB cast is appropriate. b. If instability is present and alignment is not anatomic with release of force, then pinning (open or closed) is mandatory followed by casting. c. If severely unstable, then open anatomic reduction with heavy gauge K wires or screw fixation is the procedure of choice. d. With severe joint comminution, primary arthrodesis may be considered

NOTE* Pin placement according to Myerson classification type: a. Type A: 2 Kwires (medial and lateral) b. Type B 1: 2 medial K-wires c. Type B2: 1 wire laterally d. Type C: 3 or more wires The medial pin should go across the 1st metatarsal-cuneiform joint, the 2nd pin should go across the 3rd and 4th tarsometatarsal joints, and a 3rd pin across the 2nd ray articulation. The pins should remain in place for a minimum of 6 weeks

NOTE* Always pin the 2nd metatarsal base

NOTE* Most feel that stability and anatomic reduction depends upon the 2nd metatarsal, so that if the 2nd metatarsal relocates, all the other metatarsals will follow if there is no damage to the intermetatarsal ligaments 5. Complications: a. Amputation b. Sepsis c. Thrombophlebitis d. Compartment syndrome e. Neuroma formation (either traumatic or postsurgical “amputation” type) f. Post-traumatic arthritis

Ankle Inversion Sprain Also see Chapter 29, Ankle Conditions: Chronic Lateral Ankle Instability Definition: A sprain is a disruption of fibers, a strain is plastic deformation with elongation Inversion sprains by definition involve lateral ligament disruption. The anterior talofibular ligament resists internal rotation, plantarflexion, and anterior subluxation of the talus. The posterior talofibular ligament functions to reinforce the ankle joint and the calcaneofibular ligament functions to resist adduction forces. 1. Anatomy: a. Lateral ligaments: i. Anterior talofibular (ATFL) (intracapsular): The primary stabilizing structure preventing anterior displacement of the talus (fan shaped). ii. Calcaneofibular (CFL) (extracapsular) iii. Posterior talofibular (PTFL) (intracapsular/extrasynovial): The thickest and strongest and the least likely to be injured iv. Lateral talocalcaneal ligament NOTE* PTFL is 20-45° posteroinferior to the fibular bisection so allows STJ range of motion. NOTE* Inversion of the ankle is resisted primarily by the ATFL when the ankle is plantarflexed and by the CFL when the ankle is dorsiflexed.

NOTE* Angular relationships between the ATFL and the CFL is 100° in the frontal plane and 105° in the sagittal plane. This sagittal plane angle decreases with STJ supination and increases with STJ pronation. The angular relationship between these two lateral ligaments is very d cult to attain during reconstructive ankle stabilization repair tending to cause a decrease in allowable STJ supination at the expense of attaining stability against inversion stress. 2. Ligament composition: a. 67% water b. Remaining 33%: 90% collagen type 1, elastin, and glycosaminoglycans 3. Causative Factors: a. Tibial varum b. Calcaneal varum c. Plantarflexed -1st ray d. Rigid forefoot valgus e. STJ varum f. Uncompensated equinus g: Muscle imbalance (peroneal insufficiency) h. Previous sprains (elongated ligaments no longer restrain inversion) i. Torsional abnormalities j. Short leg syndrome k. Ankle varus 4. Mechanism of injury: a. Internal rotation, plantarflexion, and adduction of the talus beyond normal physiologic limits 5. Classifications of inversion ligamentous injuries (mechanism of injuries): a. Leach (1983) i. 1 st degree (ATFL rupture) ii. 2nd degree (ATFL, CFL, and capsule rupture) iii. 3rd degree (all three ligaments and capsule) b. Diaz (1st word describes the position of the foot and ankle and the second word the direction of the force applied: similar to Lauge Hansen classification) i. Supination-inversion (with a plantarflexed ankle or a neutral ankle) ii. Supination internal rotation iii. Supination plantarflexion NOTE* Additionally, ankle sprains can be classified into: Type I: stretching of the ligaments or tearing of the ATFL Type II: a partial rupture or tearing of the ATFL and CFL Type III: a total rupture of the ATFL, CFL, PTFL, and capsule or tearing of the ligaments 6. Diagnosis:

a. Scout films b. Stress views (local anesthesia: peroneal block + local ankle infiltration): Can use a Telos® apparatus for better quality control i. Inversion stress: A 5-6° difference between the injured and uninjured ankle signifies ligamentous rupture NOTE* Always take bilateral inversion stress films when examining a patient radiographically with potential grade III ruptures

NOTE* Degree of talar tilt is not a true indication of which ligament is ruptured ii. Push-pull stress (anterior draw sign): The ability to pull the ankle out of the mortise more than 4 mm. usually indicates a rupture of the anterior talofibular ligament NOTE* There are certain situations where the stress test may be invalid: genetic ligamentous laxity, history of chronic ankle instability, inability to achieve adequate anesthesia, or inability to properly maneuver the uninjured ankle. In these cases, ankle arthrography would be indicated NOTE* The main indication for ankle arthrography in a soft tissue injury is to evaluate a possible ankle diastasis and to confirm ligament tears c. Ankle arthrography: In performing this test you must consider the following i. The patient must have no allergy to iodine ii. The injection should be administered at the anterior-medial aspect of the ankle (to prevent confusion from the actual injury) iii. The test must be performed within the first 5-7 days following the injury iv. Dye that is found within the normal anatomical confines of adjacent tendon sheaths and not within the surrounding soft tissue should be considered a normal anatomical variant d. Peroneal tenography: A diagnostic technique for evaluation of the calcaneofibular ligament. If dye is injected into the peroneal tendon sheath and is found to enter the ankle joint but no dye is seen in the soft tissue surrounding the ankle, a negative test. NOTE* For some patients there is a normal communication between the peroneal tendon sheath and the ankle joint capsule: gives a false positive 7. Differential diagnosis and associated findings: a. 5th metatarsal base fractures (avulsion and Jones) b. Stieda's process fracture (talar posterior process) c. Calcaneal avulsion of the EDB

d. Calcaneal anterior process fracture e. Talar dome fractures (medial or lateral) f. Sinus tarsi syndrome g. Peroneal stenosing synovitis h. Peroneal tendon dislocations i. Peroneal neuropathy NOTE* A Jones fracture is a transverse fracture secondary to a triplane load with pull of the peroneus brevis

8. Treatment: a. Symptomatic therapy: Used for patients with negative stress x-rays, patients with a significant medical history which would contraindicate more definitive therapy,. geriatrics with a sedentary lifestyle, and patients who present to treatment 3-4 weeks following injury. i. Elastic compression ii. Ice iii. Analgesics iv. Weight-bearing to tolerance v. Physical therapy (proprioceptive excercises and strengthening) NOTE* TEMPER is an acronym for ankle sprain rehabilitation: T: Timely diagnosis/temporary immobilization E: Edema reduction M: Muscle strengthening P: Proprioceptive excercises E: External stabilizing devices R: Return to activity b. Definitive therapy: Either immobilization (preferred) or surgery i. Immobilization:
48 hours following the injury a BK weightbearing cast is applied for 3-6 weeks
This is followed by an Aircast® for an additional 3 weeks (for athletes this is continued for 6-9 weeks)
Stress x-rays should be repeated in 6 months to evaluate the treatment ii. Surgical treatment 2-3 days following injury (must be young and athletic who need complete stability):
Single ligament rupture: Watson-Jones*: This uses the peroneus brevis, which passes through the fibula from posterior to anterior, through the neck of the talus from dorsal to plantar, back through the fibula, from anterior to posterior, and sutured back onto itself. Lee Procedure (modified Watson-Jones)*: This uses the peroneus brevis tendon, which is then passed through the fibula, from posterior to anterior, and then sutured back onto itself. Evans*: This utilizes the peroneus brevis through an oblique hole through the fibula sutured back onto the belly of the peroneus brevis. Storren Nilsonne Pouzet Haig Castaing and Meunier Dockery and Suppan


Double ligament rupture: Elmslie*: Originally described as using the fascia lata and passed through a drill hole in the lower aspect of the fibula, through the calcaneus, back through the same drill hole, and tied onto itself, after passing through the neck of the talus. Chrisman and Snook*: This uses the split peroneus brevis, which is passed through the fibula from anterior to posterior through a flap in the calcaneus, and is then sutured back to the peroneus brevis tendon. Stroren Hambly Winfield Gschwend-Francillon
Triple ligament rupture: Spotoff Rosendahl and Jansen 8. Inversion injuries can result in the following: a. Sprains of the STJ ligaments b. Medial STJ subluxation c. Dislocation of the talus d. Osteochondral fractures of the talar dome e. Shear fractures of the head of the talus medially f. Shear fractures of the navicular laterally g. Avulsion fractures of the posterior aspect of the talus h. Avulsion fracture of the base of the 5th metatarsal i. Fracture of the cuboid j. Avulsion fracture of the lateral malleolus 9. Complications: a. Inappropriate diagnosis and lack of treatment b. Early complications i. Painful hemarthrosis ii. Hematoma iii. Rarely, gangrene of the skin of the lateral ankle in cases of rupture of the perforating peroneal artery c. Neuropraxia in grades II and III with damage to the intermediate dorsal cutaneous nerve NOTE* With greater than 20% of stretching, fascicular interruption may occur, causing permanent neurotmesis of the intermediate dorsal cutaneous nerve and producing a profound lateral foot and ankle sensory loss d. The most common surgical complication of primary ankle repair, involves the intermediate dorsal cutaneous nerve i. Entrapment neuropathy ii. Laceration

e. Late complications of surgical repair result from overzealous tightening of the lateral ankle structure (grade III ankle sprains should be fixed in neutral not in eversion f. Painful sinus tarsi can occur later from an everted ankle position

LIGAMENTOUS INJURIES Lateral

Medial

Common Adduction (inversion) Type I (Anterior Talofibular Ligament) palpable tenderness Talus Stable - Anterior drawer sign - Inversion stress - X-Ray (Bilateral)

Rare Rarely alone Abduction or External Rotation Edema (occhymosis in deltoid area)

Treatment

1 strap 2 physical therapy

Type II Anterior Talofibular Ligament Palpable tenderness Calcaneal Fibular Ligament diffuse ankle pain If plantar flexion • possible anterior deltoid ligament rupture Talar stability + Anterior drawer - Inversion stress - X-Ray Treatment 1. strap (occ. B. K.. W.B. cast) 2. physical therapy 3. youth - possible ligament

Deltoid ligament ruptured to variable degree assesment made as per Close (1956) 1. Mortise view 2. If lateral displacement of talus 2mm + Type I 3mm + Type II 4mm + Type III Treatment 1. Type I strap 2. Type II 3. Type III -cast B, K., W. B.

Type III AnteriorTaloflbular ligament Calcaneofibular ligament Post Deltoid if plantar flexion 1. Talar stability + Anterior drawer + Inversion stress - X-Ray

Syndesmotic Treatment (usually occurs in young athlete) 1. ligament repair with cast 2. physical therapy

Rare Rarely alone Abduction external rotation Edema ecchymosis -in syndesmotic area

Anterior + Post Tibiofibular ligament interosseous ligament usually with Maisonneuve fracture Treatment 1. Dap. on other assoc injury 2. Mild -cast B.K., W.B. 3. Severe, A.O. Fixation

Deltoid Ligament Ruptures 1. Anatomy: The deltoid takes origin off the medial malleolus, which ends structurally in two colliculi (one anterior and one posterior), divided by an intercollicular groove. There is a superficial and a deep deltoid: a. Superficial deltoid i. Naviculotibial ii. Calcaneotibial (strongest) iii. Superficial talotibial b. Deep deltoid i. Deep anterior talotibial ii. Deep posterior talotibial 2. Mechanism of Injury: Solitary injury to the deltoid is rare, it is usually accompanied by other ligament injuries or fractures. NOTE* Most common are fractures of the fibula and ruptures of the tibiofibular ligaments a. Types of injuries: i. Supination-external rotation ii. Pronation-external rotation iii. Pronation-abduction 3. Signs and symptoms: a. Pain and swelling on the medial and anterior aspects of the ankle b. Since there are usually associated injuries, the usual presentation is a completely edematous and ecchymotic ankle that is being splinted 4. Diagnosis: a. Scout films (with pronation injuries a high fibular x-ray) b. Stress x-ray (local anesthesia): Can be done by hand or using a Telos® apparatus i. Mortise view of the ankle where the foot is abducted and everted in relation to the leg ii. Lateral view where the foot is anteriorly displaced in relation to the leg NOTE* Stress views are done bilaterally and the clear space is what is compared Note* A clear space of 1 cm. or greater is diagnostic of a complete rupture, and a displacement of 3mm. or more means tearing of part of the deltoid

5. Treatment: a. Usually closed reduction and with BK NWB cast with the foot in inversion is sufficient for 3-6 weeks, followed by a BK weight-bearing cast for another 3-6

weeks. b. Surgical repair is indicated if closed reduction does not replace the talus to its proper position. NOTE* This can occur if the deltoid gets rolled up or inverted, or if the posterior tibial tendon gets trapped.

Compartment Syndrome Usually diagnosed in the arm and leg, also occurs in the foot, and can follow several types of injuries, most commonly multiple fractures or crushing injuries. This entity should be considered in the differential diagnosis in patients presenting with a painful swollen foot post trauma 1. Definition: Increased compartmental pressure resulting in decreased perfusion and ultimate ischemic changes to the tissues on the compartment. This can eventually result in contractures and poorly functioning limbs, a. Physiology: At rest the intramuscular pressure is approximately 5 mm Hg. During a muscular contracture the pressure can increase up to 150 mm Hg or more. At relaxation, the compartment pressure rapidly drops, and within 5-10 minutes, has returned to baseline. With a compartment syndrome, there is no drop of pressure 2. Types of compartment syndrome: a. Acute: Occurs when the resting pressure in the compartment exceeds the available perfusion pressure. This is usually the result of trauma with hemorrhage or gross muscular edema causing the increased compartmental pressure. If untreated tissue necrosis is inevitable b. Chronic: Occurs when the resting pressure is higher than the normal resting pressure but not so high as to cause hyperprofusion. Following excercise, the time for pressure to return to baseline is protracted. This results in a relative prolongation of the ischemic time resulting in symptoms during or following excercise. Actual muscle necrosis is unusual 3. Diagnosis: Measurement of an increased intramuscular pressure in the compartment via a wicks catheter (usually greater than 30 mm Hg) Two criteria must be fulfilled for this diagnosis to be made: a space that is limited by fascia, skin, or bone must be present; second increased compartment pressure caused by a decrease in compartment size or an increase in the size of the contents within that compartment must be present Any injury with a pressure greater than 30 mm Hg should undergo an immediate fasciotomy Note* The patient might still present with a pulse because the vascular collapse occurs first at the arteriolar level 4. Compartments of the foot:

a. Medial compartment: Its borders are the medial and lateral intermuscular septum, the medial portion of the plantar aponeurosis, the tarsus (proximally) and shaft of the first metatarsal (distally). It contains the abductor hallucis flexor hallucis brevis, and the FDL tendon b. Central compartment: Its borders are the medial and lateral intermuscular septum, the central portion of. the plantar aponeurosis, the tarsus (proximally) and interosseous fascia (distally). It contains the flexor digitorum brevis, FDL tendon with lumbricals, quadratus plantae, adductor hallucis, PT and peroneal tendons c. Lateral compartment: Its borders are the lateral intermuscular septum, lateral portion of the plantar aponeurosis, and the associated osseous components. It contains the abductor digiti minimi, flexor digiti minimi, and opponens digiti d. Interosseous compartment: Its borders are the metatarsals and the interossei fascia. It contains the interossei 5. Clinical Findings: a. Pain out of proportion to the clinical findings b. Paresthesias c. Pulselessness d. Or none of the above 6. Treatment: a. Fasciotomy i. Double dorsal technique:
Midfoot and forefoot: 2 dorsal longitudinal incisions, one over the 2nd metatarsal and the other over the 4th (deepened down to the metatarsal shaft) where a hemostat is passed into each adjacent interosseous space. The wound is closed secondarily in 5 days. ii. Extensile medial incision iii. Combined approach 7. Associated complications: a. Comminuted fractures b. Severe soft tissue injuries c. Post-ischemia swelling d. Intramuscular hematomas associated with bleeding diasthesis e. Crush injuries

Open Fracture Classification System and Treatment 1. Gustillo and Anderson described an open fracture classification system: This depends upon the mechanism of injury, degree of soft tissue damage, the configuration of the fracture, and the level of contamination a. Type 1: i. Wound less than 1 cm long and clean ii. Minor soft tissue damage is present ii. Fracture is simple, transverse, or short oblique with minimal comminution

b. Type 2: i. Wound more than 1 cm. long without extensive tissue damage, flaps or avulsions ii. There is a slight crushing injury, moderate comminution of the fracture ill. Moderate contamination c. Type 3: Extensive soft tissue damage, including muscles, skin, and neurovascular structures, with a high degree of contamination (high velocity injuries, farm injuries) i. Type 3A: Open fractures with adequate soft tissue coverage of bone despite extensive soft tissue laceration ii. Type 3B: Open fractures having extensive soft tissue loss with periosteal stripping and bone exposure. Severe contamination and severe comminution. Usually a local or free flap is needed for bony coverage iii. Type 3C: Open fractures are associated with arterial injury requiring microvascular repair, regardless of the soft tissue coverage 2. General principles of treatment: a. Tetanus history and therapy administered b. Thorough H & P conducted (blood loss measured-CBC,HCT, Hb) with neurological, musculoskeletal, and vascular assessment of the lower extremities c. Complete x-rays d. Appropriate antibiosis should be administered in the E.R. (cultures and gram stains should be taken) NOTE* The primary bacteria encountered in open fractures is Staph. aureus. However, the choice of antibiotic is determined by the extent of the soft tissue injury. Gustillo and Anderson recommend cefazolin for type 1 and 2 open fractures (2 gm initially followed by 1 gm Q 6 hr for 3 days). For type 3 injuries a cephalosporin plus an aminoglycoside (1.5 gm/kg body weight then 3 to 5 gm/kg body weight in divided doses) is used. Penicillin is added for farm injuries to cover Clostridium sp. e. Immediate debridement and irrigation, with repeat debridement and irrigation in 24-48 hours NOTE* The irrigant can contain either 1 gm cefazolin in 1 liter of sterile saline, or 50,000 units of bacitracin and 1 million units of polymyxin B in 1 liter of sterile saline. f. All foreign debris should be excised g. All marginal, macerated skin, and soft tissue should be debrided h. Fluorescein (non-toxic dye) may be used to assess the viability of the soft tissue structures i. The wound should be kept moist and re-evaluated in 48-72 hours, with repeated debridements, especially if soft tissue coverage is necessary

NOTE* 10-15 mg/kg of fluorescein is injected IV and observed under UV light after 10-20 minutes. Vascularized tissue will fluoresce yellow-green and nonvascularized tissue will appear dark blue j. For type 1, 2, and 3A open fractures delayed primary closure, using skin grafts within 5-7 days k. For type 3B and 3C open fractures, the soft tissue loss is so great that the use of skin flaps is necessary and a delay in using them becomes apparent because of the repeated debridements l. External fixation should be used for all type 3 and unstable type 2 fractures The advantages of external fixators include the ease of application without additional trauma, allows for daily wound inspections and care, allows for grafting procedures, accomplishes compression/reduction of the angulation/ stabilization of the fracture without much surgical trauma m. Internal fixation (screws, plates, pins, etc.) should be used for articular and metaphyseal open fractures. This is done preferably within 8 hours of the injury NOTE* An open fracture untreated in the initial 7-8 hours (golden period) is generally considered to convert from a contaminated wound to an infected wound 3. Absolute indications for open reduction: a. Irreducible fractures where function and alignment can not be obtained otherwise b. Displaced intra-articular fractures where incongruity will lead to degeneration of the joint c. Displaced epiphyseal fractures with a large potential for growth disturbance d. Major avulsion fractures with muscle ligament attachments e. Nonunions that do not have the capacity to unite (pseudoarthrosis and avascular nonunions 4. Antibiotic considerations: a. Limiting the duration of the initial antibiotic therapy is important to minimize the emergence of resistant nosocomial bacteria b. Type 1 fractures are treated with Cefazolin 2 gm STAT followed by 2 gm Q 8 h for 48 to 72 hours c. Type 2 and 3 are treated with combined therapy, using cefazolin as above, plus an aminoglycoside (Gentamycin or Tobramycin) dosed at 1.51.7 mg per kg on admission, followed by 3.0 to 5.0 mg per kg per day in divided doses. The duration of therapy is 3 days unless overt infection develops d. Administer 10 million units of Pen G if the injury was sustained on a farm, to cover for Clostridium sp.

Soft Tissue Injuries

1. Classification: a. Tidy wound: Surgical incision, laceration b. Untidy wound: Crush, avulsion, abrasion c. Wound with tissue loss: Excision, burn, ulcer, avulsion d. Infected wound: Established (cellulitis, lymphangitis, abscess, bum, or vasculitis) or Incipient (bum, contaminated wound, abrasion) 2. Treatment (general): a. Tetanus prophylaxis b. Antibiotic prophylaxis c. H 8 P, including vascular, neurological, musculoskeletal and integumentary status d. Inspection of the wound under local or regional anesthesia e. Initial gentle cleansing of the wound with a mild soap (no strong antiseptics that can cause tissue damage) f. X-rays, CBC, and urinalysis as necessary g. Primary wound care: remove all foreign and devitalized material copious flushing, atraumatic tissue handling, avoid tourniquet h. Skin closure when appropriate 3. Treatment (specific): a. Tidy wound: Once debrided, can be closed after appropriate skin cleansing (skin edges may be freshened) b. Untidy wound: Deep damage must be repaired and skin closure should be delayed until wound demarcation has progressed to the point where viability is reasonably assured. Secondary or delayed primary closure may be indicated. Swelling within closed compartments may indicate the need for the release of damaged fascia or skin c. Wound with tissue loss: Must prevent the wound from drying out and must cover exposed vital structures using biological dressings, porcine xenografts, or appropriate autograft f. Infected wound: Prior to closure the wound must be debrided and converted to a contaminated wound, and then a clean wound (check with C&S and colony counts: less than 105 bacteria per millimeter means contamination)

Crush Gunshot and Lawnmower Injuries 1. General protocols: a. Priority is given to prevention of infection especially Clostridia sp. b. Therefore tetanus prophylaxis is given (see chapter Infectious Disease) c. Antibiotic therapy is started after cultures are taken d. Debridement and copious lavage under local/regional, or general anesthesia e. Depth and extent of the wounds carefully explored and inspection with removal of all foreign bodies and all non-viable tissue and packed open f. The wound is reexamined under regional/general anesthesia in 24-48 hours, and after further debridement the wound is packed open g. The wound should not be closed before 5-7 days (check cultures and use clinical judgement)

NOTE* The most important criterion is the clinical appearance of the wound in the decision to close a wound. The number 105 bacteria present in the wound is mentioned as a criteria of active infection, as it has been seen on the board exams (this is unreliable) h. Use xenograft as necessary to prevent further contamination i. Use split thickness skin flap immediately on the dorsum of the foot if the tendons are exposed without the paratenons (this is the only time immediate coverage is utilized) j. Rigid stabilization of fractures

Puncture Wounds These wounds deserve special attention because they characteristically have a benign presentation that can rapidly progress to OM if not treated appropriately. Complications run as high as 10%. Pseudomonas is the most common pathogen isolated 1. General protocols: a. Tetanus prophylaxis b. Remove all foreign material, leave wound open, do C&S c. Start broad spectrum antibiotics d. If no improvement in 3 days suspect a gram (-) infection e. If bone or joint is penetrated or if wound is deep, surgical exploration and debridement are necessary f. If pain persists after 4 days of treatment use bone/gallium scans, sed rate, WBC to follow patient progress

Epiphyseal Plate Injuries: Also see section: Pediatrics (Pediatric Fractures) 1. Anatomic differences: Since the growth plate is radiolucent, acute injury can only be inferred from widening of the growth plate or from displacement of the adjacent bones on plain x-ray. The periosteum is stronger, thicker, and produces callus more quickly than in adults 2. Biomechanical differences: Pediatric bone is less dense, more porous with a smaller lamellar content than adult bone. It also will fail not only in tension, as adult bone, but in compression as well. Hence there are certain pediatric fracture patterns: buckle fractures, plastic deformation of bone, and greenstick fractures 3. Physiological differences: Growth provides the basis for a greater degree of remodeling than is possible with the adult (a bump of a malunion is corrected by periosteal resorption; a concavity is filled out by periosteal new bone). This is an example of Wolff's Law. Also, a fracture through the shaft of long bone stimulates longitudinal growth (increased nutrition of the growth cartilage),

which can result in a longer bone as a result of a fracture. Because of this, pediatric fractures can be treated more conservatively than with an adult 4. Growth plate injuries: Problems after injury are rare, but when growth is disturbed, the reason is from avascular necrosis of the plate, crushing or infection of the plate, formation of a bone callus bridge between the bony epiphysis and metaphysis, and hyperemia producing local overgrowth. There are 2 types of growth plates, epiphyseal (those that form under pressure) and apophyseal (those that form under traction) 5. Anatomy: The growth plate is a cartilagenous disc situated between the epiphysis and the metaphysis. The germinal cells are attached to the epiphysis and their blood supply is from the epiphyseal vessels. As the germinal cells multiply, the cell population of the plate increases. The plane" of separation in the physis is most frequently at the junction of the calcified and uncalcified cartilage, known as the zone of transformation. With an epiphyseal separation, most of the important germinal part of the plate usually remains with the epiphysis. If much of the germinal layer is disturbed, growth may be affected 6. Classification: Salter-Harris a. Type 1: A complete separation of the growth plate at the zone of transformation, no disruption of growth, treated with closed reduction and immobilization for 3 weeks b. Type 2: Separation of the growth plate with extention of the fracture line into the metaphysis. This extension creates the 'Thurston Holland Sign'. There is usually no growth disturbance and it is treated the same way as type 1 c. Type 3: Separation of the growth plate with extension of the fracture line into the epiphysis so that it is intraarticular. Potential for growth disturbance as the fracture line crosses the entire growth plate, and must not be left displaced by ORIF d. Type 4: A fracture from the metaphysis through the growth plate and into the epiphysis, and can result in growth disturbance. This fracture is unstable and requires ORIF e. Type 5: A crush type injury usually with subsequent growth disturbance. Treated with closed reduction (if displaced) and immobilization 3-6 weeks NWB f. Type 6: A scooping out of a portion of the growth plate, via some type of projectile causing osseous and soft tissue damage. Any large fragments of bone are reduced. Bony bridging causing growth disturbances can be a complication here. Treat the bony bridge with resection and interposition of fat or silicone rubber g. Type 7: An intraarticular fracture that does not involve the physis. Very difficult to diagnosis in the very young. Treat with immobilization if nondisplaced and ORIF if the fragment is large and displaced (or excision of the fragment if too small to reduce) 7. Apophyseal Injuries: Either an inflammatory process secondary to traction vs. a Salter-Harris fracture type 1 a. Calcaneal apophysitis: Involves reduction of stress to the apophysis, (heel

lifts, orthoses, and local anti-inflammatory measures) with severe cases requiring BK casting. Later calf muscle stretching is helpful b. Tuberosity of 5th metatarsal: Injury from direct impact or forced inversion of the foot. If the tuberosity is displaced, closed reduction with immobilization for 3 weeks 8. Treatment: Always advise of the long term sequelae of the fracture 9. Internal fixation devices: Smooth K-wires should be employed and should be buried to avoid infection of the plate which can cause an autolysis of the plate. Never use threaded pins or screws across a growth plate 10. Specific ankle fractures: a. Tillaux fracture: A Salter-Harris type 3 of the tibia involving the lateral aspect of the tibia. This fracture is unique to the age group of 12-13 year olds. Treatment is ORIF if displaced or unstable, and closed reduction with immobilization for 6 weeks if stable and in anatomic alignment b. Triplane: A Salter-Harris type 4 fracture of the tibia. Diagnosis is made by visualizing the fracture on at least 2 views. An unstable fracture, requiring ORIF

Digital Fractures and Dislocations 1. Fractures of the hallux: a. Communited fracture of the distal phalangeal tuft i. Mechanism: Direct trauma ii. Treatment:
Local anesthesia and prep
Avulse the nail atraumatically
If closed fracture reduce any gross prominences, replace nail plate as part of compression dressing, patient instructed to check vascular status frequently, Reece© shoe, ice packs
If open fracture, tetanus prophylaxis, IV antibiotics, debride necrotic tissue and loose exposed bone leaving no prominences, irrigate copiously, open drainage, Reece© shoe, and follow appropriately b. Intra-articular dorsal avulsion fracture of the distal phalangeal base: i. Mechanism: Forced plantarflexion of the hallux IPJ (stubbing) resulting in avulsion of the EHL insertion ii. Treatment of displaced fracture (most common): ORIF followed by Reece© shoe iii. Treatment of nondisplaced (uncommon): Closed reduction with slipper cast, or BK cast (with or without percutaneous pinning) c. Hallux IPJ intra-articular fractures of the distal or proximal phalanx: i. Mechanism: Transverse plane torque (stubbing) resulting in a push-off fracture of the medial or lateral condyle of either the distal phalangeal base or the head of the proximal phalanx ii. Treatment of displaced fracture (most common): First attempt closed

reduction, and if successful pad 1st interspace with felt or cotton and tape to the 2nd toe. If closed reduction fails, ORIF larger fragments and excise smaller fragments. Reese© shoe for 4-6 weeks d. Proximal phalanx shaft fracture: i. Mechanism: Direct or indirect trauma resulting in a transverse oblique fracture ii. Treatment of displaced fracture: Closed reduction (with or without percutaneous pinning), splinting, Reese© shoe iii. Treatment of nondisplaced fracture: Buddy splinting to 2nd toe and Reece© shoe e. First MPJ intra-articular condylar fractures of the proximal phalanx: i. Mechanism: Transverse plane torque resulting in avulsion of the insertion of the medial or lateral intrinsics ii. Treatment of displaced fracture: ORIF followed by Reece© shoe for 6 weeks (smaller fragments maybe excised and the intrinsics reinserted) iii. Treatment of nondisplaced: If no change in hallux abductus, then buddy splint to the 2nd toe, if the hallux abductus changed, consider surgical repair. 2. Fractures of the lesser toes: a. Fractures of the distal and intermediate phalanges: Rare unless crush type b. Non-articular proximal phalangeal fractures: i. Mechanism: Direct or indirect trauma (stubbing most common) resulting in a transverse, oblique or spiral fracture appearing sub-capitally, mid-shaft, or at the base or epiphysis ii. Treatment of displaced fracture (less common): Closed reduction followed by buddy splinting, or ORIF for gross reduction failures iii. Treatment of nondisplaced fractures (common): Buddy splinting c. PIPJ intra-articular proximal phalangeal fractures: i. Mechanism: Usually a stubbing injury with axial forces resulting in an oblique push off or comminuted fracture ii. Treatment of displaced and non-displaced fractures: Closed reduction aimed at restoring alignment, followed by buddy splinting. If failure then primary arthroplasty. d. MPJ intra-articular proximal phalangeal fractures: i. Mechanism: Usually a stubbing injury ii. Treatment of displaced fracture: ORIF depending on the size of the fragment and comminution iii. Treatment of nondisplaced fracture: Reece© shoe for 6 weeks

1st MPJ Trauma 1. Turf Toe: a. Mechanism: Hyperdorsiflexion, hyperplantarflexion, hyperadduction, or hyperabduction stress resulting in a - 1st MTPJ sprain without alignment

changes b. X-ray evaluation: Rule out dislocation, osteochondral injury, or sesamoid fracture (take MO, LO, Lateral, AP, plantar axial) c. Treatment: Ice, rest, Reece© shoe, modify the athletic shoe. 2. First MTPJ dislocation: a. Mechanism: Hyperdorsiflexion b. X-ray evaluation: Rule out osteochondral fracture and sesamoid fracture (take AP, lateral, plantar axial) c. Classification (Jahss): i. Type 1:
Joint capsule torn transversely under the metatarsal neck
Proximal phalanx, plantar capsule, and sesamoids dislocated dorsally on the first metatarsal head
First metatarsal protrudes through the capsule, depressed plantarly by the retrograde forces of the hallux
Hallux IPJ is flexed
Usually not reducible by closed technique ii. Type 2A:
Same as type 1 except that rather than the entire plantar capsule and sesamoid apparatus dislocated dorsally, the intersesamoidal ligament ruptures and the sesamoids sublux to each side of the metatarsal head
Easier to reduce than type 1 iii. Type 2B:
Same as type 2A except sesamoid fractures occur instead of the intermetatarsal ligament rupturing
Easier to reduce than type 1 3. Treatment: a. Type 1: Open reduction NOTE* Closed reduction can be tried under anesthesia as follows: traction and increase dorsiflexion, then push the proximal phalanx into contact with the metatarsal head, then push (don't pull) the proximal phalanx into the reduced position, maintaining contact with the metatarsal head b. Type 2A: Closed reduction followed by Reece shoe or BK walking cast c. Type 2B: Closed reduction followed by Reece shoe or BK NWB cast (sesamoid may have to be excised at a later date prn symptoms) or open reduction with excision of the fractured sesamoid 3. Sesamoid fractures: a. Mechanism: Fall from a height, repetitive direct trauma (dancing), and repetitive indirect trauma (traction of the intrinsics) b. Presentation: i. Sesamoid involved: Tibial more than fibular (tibial is larger), rarely both injuried, almost never bilateral

ii. Clinical presentation: Pain on direct palpation and pain on hallux dorsiflexion iii. Differential diagnosis of pain in the sesamoid area: Joplins neuroma, sesamoiditis, osteochondritis dissecans, osteochondrosis, ruptured bipartite sesamoid, turf toe, DJD/eroded crista, hypertrophic sesamoid, and fractured sesamoid c. X-ray evaluation: Order bilateral AP, lateral and plantar axial (MO for tibial and LO for fibular sesamoid) 75% of bipartite sesamoids are unilateral. Bone scan if in doubt d. Normal sesamoids:
Ossification appears at 8-10 years
Bipartite sesamoids more common in tibial than in fibular
Sesamoids may be multipartite

Nail Bed Trauma 1. Classification (S. Malay): a. Primary onycholysis: i. A separation of the nail plate from the bed ii. Partial avulsions cause posterior nail fold friction injury, subungual bleeding, and digital sepsis especially in compromised patients iii. Removal of the nail plate, antisepsis, and antibiotics (prn) iv. No adverse sequelae b. Subungual hematoma: i. Blood clot under the nail plate ii. Must check for fractures of the plate from impaction iii. Treat like open fractures, the nail plate must be removed from the tissue to decompress the area iv. X-rays should be taken to r/o fracture v. The nail plate can be removed if the hematoma comprises more than 25% of the nail plate vi. Drill holes can be made if feasible c. Simple nail. bed laceration: i. Tetanus coverage ii. Systemic antibiotics iii. Surgical cleansing and lavage (no epinephrine utilized in seriously traumatized digits) iv. If you are avulsing a salvagable nail plate, remove it in one piece and save for subsequent splinting v. Nail bed injuries are usually repaired with a 6-0 absorbable suture on an atraumatic needle vi. The root and the bed must be accurately aligned on the toe vii. Periosteal irregularities must be debrided viii. Reusing the nail plate involves scraping all soft tissue from the nail plate, drilling holes through the body, then soaked in Betadine until the bed repair is accomplished, and then the nail plate is replaced on the nail bed and anchored with Steri-strips® ix. Avulsive lacerations of the bed are treated with intermediate thickness skin graft

d. Complex nail bed laceration: As above plus i. If a major segment of the proximal nail fold over the matrix is avulsed with a skin defect, rotational flaps are utilized e. Nail bed laceration with phalangeal fracture: As above plus i. Subungual fractures must be accurately reduced ii. Remove all bone spicules and nail fragments 2. Complications: a. Split nail b. Adhesions of the skin fold to the nail root c. Chronic ingrown nails d. Widening of the nail e. Narrowing of the nail f. Protruding or non-adherent nail g. Malaligned nail

Toe Tip Injuries With Tissue Loss These injuries are secondary to crush forces, and should be considered and treated like open fractures. Tissue loss increases the likelihood of poor cosmetic result 1. Classification (Rosenthal): According to the level and direction of tissue loss a. Level of nail bed tissue loss i. Zone 1: distal to bony phalanx ii. Zone 2: distal to the lunula iii. Zone 3: proximal to the distal end of the lunula b. Direction of tissue loss i. Dorsal oblique ii. Transverse guillotine iii. Plantar oblique iv. Tibial or fibular axial v. Central or gouging 2. Treatment: a. Zone 1: i. Flush, debridment and appropriate wound closure (usually secondary intention) ii. Occasionally skin graft large defects (split thickness less durable, full thickness more durable) b. Zone 2: i. Reduction of bone with debridement of necrotic tissue ii. Coverage of nail bed and phalanx tip usually achieved by local neurovascular advancement flap c. Zone 3: i. Not suitable to initial treatment in ER or office ii. Usually complete nail bed loss iii. OR debridement of necrotic tissue and matrix

iv. Delayed revision of the digit v. Attempt to maintain tendon function v. Terminal Symes may be necessary

Dog and Cat Bites Both dog and cat bites are susceptible to infection because of direct inoculation of bacteria from the animals into the bite wound. In addition to tearing of tissue, dogs can also cause a crushing injury. Most patients with bite wounds harbor bacteria, so that aggressive therapy should be undertaken initially. 1. Pasturella multocida (gram negative bacillus) is present in 50% of cat bites and 25% of dog bites Other organisms should also be considered: Pseudomonas, Staphylococcus, and beta streptococcus 2. Some authors believe that the culture of the bite wound offers little information because of the multiplicity of organisms found and the absence of an established infection 3. X-rays of the involved area should be obtained 4. Thorough and aggressive debridement and irrigation (manual lavage using Ringer's lactate or dilute Betadine®) 5. Elevation and immobilization with the ankle at 900, and after 72 hours improvement occurs, then initiate ROM and adjunctive PT 6. Leave any potentially contaminated wound open for 4-6 days, and at that time, if the wound is clean, without redness or swelling, it is reasonably safe to perform primary closure 7. The use of prophylactic antibiotics is still controversial a. For cat bites, dicloxicillin, penicillin, or Augmentin® is recommended (erythromycin in penicillin allergy) b. For dog bites dicloxicillin, cephalexin, or Augmentin® is adequate (one study showed a 95% cure of infected dog bites with cephadrine) 8. Rabies is of concern with any animal bite. See Chapter 6, Infectious Disease, section on Rabies

Chapter 26: Digital Deformities and Surgery Hammertoe Syndrome Mallet Toe Syndrome Claw Toe Overlapping 5th Toe Hallux Hammertoe Hallux Interphalangeal Arthrodesis Lesser Digital Arthrodesis Overlapping 2nd Toe Syndactlyization Digital Implants Floating Toe Syndrome Blue Toe Syndrome Polydactylism

DIGITAL DEFORMITIES AND SURGERY Hammertoe Syndrome There is a necessity for surgical procedures not only to relieve symptoms, but also to preserve function. The toe functions to decelerate the foot, stabilize, help in propulsion, and for kinesthetic sensation. To prevent a recurrence, it is necessary to investigate and neutralize the deforming forces for full correction of the deformity 1. Definitions: a. Hallux hammertoe: This is a deformity whereby there is a dorsal contracture of the 1st MTP joint and a plantar contracture of the hallux IPJ. There is a dorsal contracture of the MTP joint capsule and plantar contracture of the hallux IPJ capsule b. Lesser hammertoe: Plantarflexion of the PIP joint with dorsiflexion of the MTP joint. c. Clawtoe: Dorsiflexion of the MTP joint and plantarflexion of the DIP and PIP joints. d. Mallet toe: Plantarflexion of the DIP joint e. Clinodactyly: Curly toe (transverse plane deviation) f. Digiti quinti varus: Overlapping 5th toe 2. Classification: Digital deformities are classed according to their flexibility. This is determined by dorsiflexing the MTP joint and noting the amount of reduction of the digit (Kelikian push up test) at the MTPJ a. Flexible: Reducible on weight bearing and with the push up test b. Semi-rigid: Slightly reducible by hand c. Rigid: No change in the deformity when examiner attempts manual correction 3. Anatomy: Electromyographic studies have shown that the long flexor fires approximately at 15% of stance phase, the short flexor at 60%, the EDB at 40%, the EDL during swing and heel contact, and the intrinsics (interossei) at 50%. a. Extensors: i. The EDL goes to each lesser digit by a separate tendon ii. The EDB goes to the middle three lesser toes
EDL and EDB form a common tendon that passes over the proximal phalanx to split into three slips. The middle slip goes to the middle phalanx and the lateral two rejoin to insert over the distal phalanx
The sling apparatus is part of the extensor hood. The sling mechanism wraps around the base of the proximal phalanx and attaches to itself. It can lift up on the proximal phalanx like a sling. There are no specific attachments of the extensor apparatus into the proximal phalanx
The EDL and EDB dorsiflex the MTP joint by the sling and cause weak extension of the DIP and PIP joints, but in vivo cause passive flexion due to the passive stretch on the fibers.

b. Flexors: i. Goes to each digit to insert on the distal phalanx after passing deep and superficial through the FDB under the proximal phalanx. It has the quadratus plantae attached to its lateral border to help align its pull and the four lumbricals attached distally and medially. ii. The FDB is a 1st layer muscle that goes to each toe and inserts on the middle phalanx.
Flexor tendons do not insert on the proximal phalanx






Action of the FDL and FDB gives active flexion of the IPJ's and secondary passive extension of the MTP joint from the passive pull on the extensor complex These are stance phase muscles that help in stabilization and propulsion of the foot and digits Predominant action of the brevis vs. longus may determine whether the PIPJ or DIPJ is contracted

c. Intrinsics: i. There are 4 dorsal interossei. They abduct the digits around a central ray. Their insertion is on the medial side of the 2nd and the lateral side of the 2nd, 3rd, and 4th proximal phalanx. There is also a point of attachment of both plantar and dorsal interossei to the plantar plate under the MTP joint. ii. Plantar interossei are 3 in number. They adduct the 3rd, 4th and 5th digits toward the 2nd by attaching to the medial side of the phalanx and plantar plate.
The interossei run dorsal to the deep transverse metatarsal ligament, but inferior to the axis of flexion of the MTP joint, and both function to plantarflex the MP joint and extend the PIPJ and DIPJ
When both interossei on each side of the MTP joint fire concurrently, transverse plane abduction/adduction is stabilized
These are stance phase muscles that help prevent buckling of the toes due to the mechanism of the sling and production of passive stretch on the longer extrinsic muscles iii. Lumbricales are 4 muscles that originate from the medial side of each of the 4 FDL tendons, run beneath the deep transverse intermetatarsal ligament to insert into the base of the proximal phalanx and form the distal extent of the extensor expansion.
They plantarflex the MTP joint and dorsiflex the PIPJ's and DIPJ's
Not recorded on EMG
By limiting dorsiflexion of the MTP joint they help hold the digit in a more rectus position iv. Quadratus plantae is attached to the FDL laterally coming off the calcaneus. Its proximal pull helps align the FDL pull to reduce the adductovarus component to the lateral digits. d. Arterial and venous supply: i. The majority of the arterial supply is via the medial plantar artery digital branches to each digit. ii. Dorsally the digits are supplied by the dorsal digital proper branches iii. The venous supply runs parallel to the arterial supply e. Neurological supply: Divided into plantar and dorsal i. Dorsal aspect:
Saphenous nerve runs on the medial aspect of the foot to the 1st MTP joint
The deep peroneal nerve supplies the adjacent sides of the lateral and medial aspects of the 1 st and 2nd toes
The medial dorsal cutaneous branch of the superficial peroneal nerve supplies the medial aspect of the hallux and the contiguous sides of the 2nd and 3rd digits



The intermediate dorsal cutaneous nerve from the superficial peroneal nerve supplies the adjacent sides of the 3rd and 4th digits, and the 4th and 5th digits The sural nerve supplies the lateral aspect of the dorsum of the foot and the lateral aspect of the 5th digit

ii. Plantar aspect:
The medial plantar nerve of the posterior tibial nerve supplies the hallux, 2nd, 3rd, and medial aspect of the 4th digit
The lateral plantar nerve supplies the lateral aspect of the 4th and 5th digit f. Summary: i. Stance:
FDL and FDB are deforming digital forces, but the FDB is the primary deforming force
Interossei and lumbricales have the potential for stabilizing the MTP joint and neutralizing the deforming forces
With intrinsic pathology, hammertoes form
When the intrinsics function properly, stable digital function ensues
Interossei are stance phase, lumbricales are not well documented (swing phase hypothesized) ii. Swing:
EDL and EDB are active deforming forces that could create a hammer toe in swing phase by creating MTP joint dorsiflexion and passive plantarflexion of the IPJ's
It is assumed in normal foot function, that lumbricales prevent hammertoes from occurring

4. Etiology: The etiology of the hammertoe will depend to a degree on the time in the gait cycle when the toe becomes initially deformed. There are 3 basic mechanisms. NOTE* These all have a common mechanism: abnormal extention of the proximal phalanx and secondary passive stretch of the flexors and flexion of the PIPJ's and DIPJ's a. Flexor stabilization: Is an increased pull of the long flexors as they gain mechanical advantage over the intrinsics due to i. Early flexor firing to help stabilize the hypermobile and flat foot ii. Intrinsic pathology
This is a stance phase condition seen from midstance on
The foot is flexible and forefoot abducted







The long flexors are firing early and longer to stabilize a pronated mobile forefoot The intrinsics are not able to counter the deforming forces so hammertoe deformities develop The flattened foot may come from forefoot varus, equinus, calcaneal valgus, torsional problems, muscle imbalances, ligament laxity, and neuromuscular problems Adducto-varus deformity of the 5th and sometimes the 4th toes

b. Extensor substitution: Is a swing phase condition due to weak anterior muscles (due to ankle equinus, weak lumbricales, and spastic EDL) i. Marked dorsiflexion of the MTP joint that may straighten on ground contact. The extensor tendons and the metatarsal heads are prominent ii. Progresses to a rigid deformity with time iii. The extensors gain a mechanical advantage over the intrinsics (lumbricales) when the anterior muscles are firing to dorsiflex the foot at the ankle in swing to gain ground clearance and at heel contact to prevent foot slap iv. Patients may be diagnosed NWB by having them dorsiflex their foot. Normally the digits will dorsiflex approximately 300 at the MTP joints. With extensor substitution there will be more dorsiflexion of the proximal phalanx v. Extensor substitution can occur in an equinus foot. There is an increased declination of the front part of the foot vi. Even though the digits are rectus on weight-bearing, during swing they curl vii. Results in an anterior pes cavus viii. Whatever will allow the long extensors to fire early or gain a mechanical advantage over the lumbricales will result in extensor substitution c. Flexor substitution: Occurs where there is weakness of the triceps surae. i. The posterior deep muscles and the peronei attempt to produce heeloff in place of the weakened triceps. This may be due to overlengthening of the achilles or a congenital problem. ii. A calcaneal gait is common iii. Produces a hammertoe deformity without the adductovarus component iv. A supinated high arch foot type is seen 5. Preoperative considerations: a. If the Kelikian push-up test allows the digit to straighten, then the EDL and MTP capsule is not so taut so that only a flexor tenotomy may be done b. 90% of the hammertoe deformities are a result of FLEXOR STABILIZATION compensation secondary to hypermobile flat feet. Therefore following surgery orthoses must be used to neutralize the etiology c. With EXTENSOR SUBSTITUTION an arthroplasty would only be temporary due to lack of neutralization of the deforming forces, soft tissue releases would only add a little time, and orthoses function during stance phase and won't work here. Therefore an arthrodesis is the procedure of choice. A Hibbs procedure would only be useful in a flexible deformity d. With FLEXOR SUBSTITUTION strengthening of a weakened triceps by tendon transfer and fusion of the digits would be in order

6. Surgical procedures: a. Post procedure: Arthroplasty with proximal head resection b. Lambrinudi procedure: Fusion of PIP and DIP joints c. Young-Thompson procedure: Peg-in-hole fusion d. Gotch procedure (or Gotch and Kreuz): Resection of the base of the proximal phalanx and syndactylization of the digits e. Girdlestone procedure: Transfer of the flexor tendons to the dorsum of the proximal phalanx f. Sgarlato procedure: Transfer of the FDL dorsally with capsular resection through a 3 incision approach g. Taylor procedure: PIPJ arthrodesis using a K-wire h. Hibbs procedure: A tenosuspension transferring the EDL to the met heads or base conjointly i. Collins procedure: Repositioning of the medial and lateral extensor slips dorsally on the digits j. Suppan CAP procedure: Indicated for hammertoe correction in children. Two transverse semielliptical incisions are made over the head of the proximal phalanx, skin section and tendon and capsule removed, the collaterals are left intact, metaphyseal osteotomy performed with cylinder of bone removed. The capital fragment will fit snugly against the shaft of the proximal phalanx and held snugly by the skin repair 7. Correction of the non-reducible hammertoe: Know the etiology and neutralize it and follow a stepwise approach during surgery. a. Arthroplasty to release PIPJ pressure and reduce the corn. Now do the Kelikian push up test. (If the toe still does not straighten go to the next procedure) b. Extensor recession for release of the hood and sling fibers to slacken the extensor apparatus to the proximal phalanx: If the toes still does not straighten go to the next procedure NOTE* When doing this do not cut the lumbricales to the base of the proximal phalanx

c. Hood release or EDL lengthening: If no straightening go on to the next procedure d. Capsulotomy of the MTP joint: If no straightening go on to the next procedure e. Plantar hood release f. If a problem still exists fuse the PIPJ with a K-wire and extend through the MTP joint held in a rectus position: Allows the digit to function as a rigid beam and the deforming flexor to pull the entire toe into plantarflexion

NOTE* Test the proximal phalanx for any dorsal resistance after each step. If the proximal phalanx springs dorsally after it is placed in a corrected position, go on to the next step

8. Correction of reducible hammertoe deformity: a. Flexor tenotomy: When there is a flexion at the PIPJ which can be reduced, the long flexor tendon may be the only pathological entity which needs correction. If the skin is contracted, it is done through a plantar incision, otherwise done through a medial or lateral approach. b. Extensor tenotomy and capsulotomy: When the extensor tendons are contracted along with the dorsal capsule of the MTP joint, this may be the only pathological entity which needs correction. Care is made not to injure the cartilage of the joint. The toe is splinted for 4-6 weeks. NOTE* It is important to lengthen both the long and short extensors c. Repositioning of the extensor slips: In digits in which the PIPJ is buckled but completely reducible, the medial and lateral extensor slips may be repositioned dorsally on the digits. NOTE* By performing this procedure, one avoids resection of bone, shortening of a digit, and flailness. The toe becomes straight, but very little motion is present at the IPJ. 9. Complications: a. Floppy digit with phalangeal base resection b. Edema and sausage toe c. Floating toe with metatarsalgia d. Short toe e. Regeneration of the phalangeal head f. Infection g. Decreased sensation h. Blue toe secondary to venous congestion i. White toe secondary to arterial spasm NOTE* The difference between a floppy (flail) toe and a floating toe is that a floating toe does not purchase the ground while a floppy toe may purchase the ground however it is unstable.

Mallet Toe Syndrome A sagittal plane deformity in which the distal phalanx is flexed on the middle 1. Surgery (adults): a. Two semi-elliptical incisions encompassing the middle phalangeal head will allow good access for resection of this deformity b. Must be careful of the neurovascular structures with this procedure

c. Usually the deforming forces emanate from the contracture of the FDL or

abnormal morphology of the bony middle phalanx 2. Surgery (children): a. Suppan CAP procedure: Performed similar to the hammertoe procedure, except the metaphyseal osteotomy is done at the head of the intermediate phalanx, and no subcutaneous sutures are used

1. Definition: Dorsiflexion of the proximal phalanx with plantarflexion of the

middle an distal phalanx 2. Surgery of severe claw toe with MPJ deformity: a. Incision from DIPJ to metatarsal neck (curving across the metatarsal neck) b. Z-plasty EDL and retract c. Prepare bone for arthrodesis (now do Kelikian push up test) d. Extensor hood release (Kelikian test) e. Capsulotomy at MPJ f. Fuse toe with K-wire across the MPJ g. Repair EDL h. If medial or lateral dislocation of the flexor plate present, you will need capsulorrhaphy on one side of the MPJ

Adductovarus 5th Toe Deformity (overlapping 5th toe This condition is usually hereditary and present most often bilaterally. Before a procedure is done it is necessary to determine if any functional adaptation has taken place in the 5th MTP joint. If this has occurred it is then necessary to perform an osseus procedure (adults only). If there is any skin contracture, a plastic release must be additionally performed 1. Etiology: a. Proximal phalangeal base removed b. Intrauterine position c. Result of tailor's bunion procedure (tissue contracture) d. Short EDL e. Hammertoe toe repair sequelae 2. Diagnosis: a. Adduction of the toe b. Contracture of the MTP capsule c. Medial contracted EDL d. Varus rotation e. Extention of MTP joint f. Subluxed MTP joint 3. Surgical planning: a. Skin incisions: i. Z-plasty or V-Y NOTE* The central arm of the Z-plasty is in line with the direction you want to lengthen the skin

ii. Plantar elliptical iii. Plantar V-Y iv. Longitudinal incisions with dog ear resection v. Syndactylization b. Tendon/soft tissue: i. Release and lengthening of the EDL ii. Capsulotomy iii. Plantar capsule release iv. Transfer EDL to distal stump of abductor digiti quinti

v. Suspend EDL tendon around the metatarsal neck v. FDL split and reattached dorsally c. Bony procedures: i. Resect 5th metatarsal head ii. Proximal phalangeal head removal iii. Removal of the base of the proximal phalanx iv. Abductory wedge removal of phalanx v. K -wire to hold position 4. Procedures: a. Lapidus procedure: Extensor tenotomy with transfer of the distal stump under the proximal phalanx to attach to abductor digiti quinti b. Kelikian procedure: Syndactyly of the 4th and 5th after capsule release and

arthroplasty of the 5th toe c. Ruiz Mora procedure: Resection of the proximal phalanx and semieliptical plantar crease incisions to hold in corrected position d. Lanzonis procedure: Extensor tenosuspension of the 5th metatarsal head and fusion of the PIPJ and MTP capsulotomy e. Goodman-Swisher procedure: A V-Y plasty, Z-tenotomy and capsulotomy f. Butler procedure: Two concurrent racket shaped incisions completely encircling the toe so to derotate and plantarflex g. McFarland procedure: Proximal phalangeal head removed, Jones suspension and syndactylization h. Jahss procedure: Ruiz Mora incision with diaphesectomy of the proximal phalanx NOTE* In a child osseous procedures usually do not have to be performed. A Zplasty or V-Y plasty may be utilized to release the skin contracture. An extensor tenotomy at the level of the MTP joint and capsulotomy are performed. A plantar skin wedge can be removed. Toes are splinted for 4 weeks

NOTE* In adults it is usually necessary to perform an osseous procedure at the level of the MTP joint. If the base of the proximal phalanx is resected, then syndactylism of the 4th and 5th digits should be performed. If a partial metatarsal head resection is performed, then a Z-plasty or V-Y skin plasty is performed. Some also advocate the removal of a transverse skin ellipse plantarly to help hold the toe in position

Hallux Hammertoe Deformity 1. Etiology: a. Muscle imbalance seen with a cavus foot type b. Following surgical procedures of the 1 st MTP joint i. Especially with removal of both sesamoids ii. Detachment of the flexor brevis tendons at their insertion onto the base of the hallux tendons iii. Overzealous HAV surgery with medial subluxation of the tibial sesamoid c. In the presence of IPJ sesamoids which bind down the long flexor tendon in a shortened position 2. Flexible deformity: An IPJ fusion with EHL lengthening may be done, approached through 2 semi-eliptical incisions, NOTE* Fixation for fusion is either with 2 K-wires, AO fixation (4-0 cancellous, 3.5 cortical, 2.7 cortical), or 28 gauge monofilament wire loops NOTE* AO fixation of the IPJ cannot be used with a total joint replacement unless 2.7 mm cortical screw modification is utilized, but can be difficult

NOTE* Monofilament wire fixation and crossed K-wires are the best choices when planning to utilize a total joint replacement NOTE* When doing an IPJ fusion, the propulsive phase of gait should be eliminated for 6 weeks 3. Rigid hammertoe deformity: Jones tendon transfer plus IPJ fusion 4. Rigid hammertoe deformity plus rigid plantarflexed 1st ray: IPJ fusion plus dorsal wedge osteotomy of the 1st metatarsal 4. Postoperative complications: a. Non-union b. Hallux limitus or rigidus c. Hallux extensus d. Elevatus of the first metatarsal with IPK sub 2nd metatarsal

Hallux Interphalangeal Arthrodesis 1. Fixation techniques: a. Stainless steel monofilament wire, 28 gauge b. Two 0.045 Kirschner wires c. 4.0 cancellous screw d. 3.5 cortical screw (lag) e. 2.7 cortical screw (lag) 2. Indications for fusion: a. Semi or non-reducible IPJ contracture b. Hyperkeratosis overlying the IPJ c. Transverse or frontal plane deformity of the hallux d. Clawtoe deformity e. Abnormally long or short toe Lesser Digital Arthrodesis 1. Biomechanics: a. Flexor substitution b. Extensor substitution 2. Signs and symptoms: a. Semi-rigid or rigid deformity b. Dorsal hyperkeratosis c. Transverse plane deformity may be present d. Clawtoe deformity may be present e. Abnormally long or short toe may be present f. Painful PIPJ motion may be present g. Flail toe secondary to previous surgery 3. Fixation: a. Stainless steel monofilament 28 gauge wire loops

b. 0.045 K-wire c. Reese arthrodesis screw d. Orthosorb® NOTE* Fusion of the 2nd toe will not stop the formation of a hallux abductus deformity Overlapping 2nd Toe 1. Etiology: a. Chronic biomechanical forces b. Intra-articular steroid injections c. Inflammation of the joint capsule (seen with RA) 2. Surgery: a. Resection of phalangeal base b. Flexor tendon transfer c. Proximal IPJ arthrodesis d. Partial met head resection e. Relocation of the flexor plate f. Freeing the base of the proximal phalanx from attachments and freeing the metatarsal head from attachments and fixating with K-wire g. Repositioning of a 2nd MTP capsular flap h. Total implant arthroplasty

Syndactylization 1. Classification: a. Type 1 (zygodactyly): Most common i. 2nd and 3rd digits most frequently involved (followed by the 3rd and 4th digits) ii. Asymptomatic and requires repair primarily for cosmetic reasons b. Type 2 (synpolydactyly): i. Associated with duplication of a part or entire digit (the duplicated digit usually intervenes between two essentially normal digits) ii. 3rd and 4th digits primarily affected, followed by the 4th and 5th toes iii. Usually discomfort due to shoe irritation when the 5th toe is involved c. Type 3: Fingers only d. Type 4: Fingers only e. Type 5 i. Syndactyly with concomitant metatarsal (or metacarpal) synostosis 2. Surgery: Plastic flap repairs (see following diagram)

Digital Implants 1. Signs: a. Deformity involves the 2nd and or 3rd toe at the PIPJ b. Semi-rigid or rigid hammertoe deformity c. Painful PIPJ motion may be present d. Hyperkeratosis may be present e. Involved toe is of normal or shortened length when placed in its proper position f. Absence of significant MTP joint or DIP joint contracture of the involved toe g. Absence of significant frontal plane deformity of the involved toe h. Normal skin condition, vascular status, and neurological status 2. Radiographic findings

a. Adequate bone stock to receive the stems of the implant b. Adequate width of the proximal and intermediate phalanx to receive the stems of the implant c. Adequate length of the intermediate phalanx to receive the stem of the implant d. Absence of MTP and/or DIPJ contracture e. DJD of the PIPJ may be present 3. Implant product selection: a. Silastic H.P. 100, (Swanson Type) Weil Design, Dow Corning Wright: A double stemmed flexible implant with cylindrical central body b. Sutter Lesser Toe Proximal Interphalangeal Joint Prosthesis (Sgarlato Design), Sutter Biomedical: A double stemmed very flexible implant with a central hinge and rectangular stems with a polyester mesh internal fabric for reinforcement c. Sgarlato Hammertoe Implant Prosthesis, Sgarlato Labs: The newest device, also a double stemmed with a trapezoidal solid central portion

4. Implant procedure: a. Two longitudinal semi-elliptical incisions (to prevent fat toe syndrome) b. The dorsal tendinous structure is dissected free from the base of the distal phalanx to the middle of the shaft of the proximal phalanx, and is retracted medially or laterally c. The PIPJ is entered by severing the capsular ligaments d. The head of the proximal phalanx is excised at the surgical neck (a little more bone is removed than with a traditional arthroplasty) e. The proximal phalangeal stump is reamed first, and the middle phalangeal stump is reamed f. The implant is inserted, and there should be a 2-3 mm space between the implant and each bone (very important) g. The tendon and skin are then repaired

5. Advantages of digital implants: a. Relief of pain b. Maintenance of toe stability c. Maintenance of toe length d. Restoration of function e. Allows for PIPJ motion and plantar gripping power of the toe f. Minimal postop disability and early toe motion 6. Disadvantages (versus regular arthroplasty): a. Cannot be performed in an abnormally big toe b. Difficult to perform in the 4th and 5th toe due to small bone stock NOTE* The Sgarlato (S.H.I.P.) and Sutter device have been used in the 5th toe due to their size.. The Sutter which has the advantage of having a small central portion whose thickness is less than its width, can be placed either angled or vertical to prevent pressure from the shoes or adjacent tissues. The S.H.I.P. can be placed normally c. Need good bone stock and adequate width of bone d. Need to have normal. sagittal plane position of the MTP joint e. Needs specialized equipment f. Cannot be used with frontal plane deformity g. Need to remove implant if infection occurs h. The Silastic Swanson design could permit lesion recurrence and digital swelling due to the large diameter central portion i. The Sgarlato implant is also available in a longer stemmed version which is useful in revisional surgery as well as digits with longer phalanges 7. Contraindications: a. Nonreducible contracture of MTP joint and/or DIPJ of the involved toe b. Inadequate bone stock c. Infection d. Inadequate vascular status e. Significant frontal plane deformity f. Presence of an implant at the MTP joint of the involved toe g. Inadequate skin coverage

Floating Toe Syndrome 1. Etiology: a. Bradymetatarsia b. Excessively elevated metatarsal c. Dislocated flexor plate d. Procedures which reduce the internal cubic content of the joint e. Resection of the base of the proximal phalanx 2. Surgery: a. Correct the underlying etiology

b. PIPJ fusion c. Total joint replacement

Blue Toe Syndrome 1. Definition: Blue toe syndrome/purple toe syndrome results from atheromatous embolization, which can eventually lead to gangrene if the cause is not eliminated 2. Causes: a. Atherosclerosis (most common) i. Thrombosis formation, b. Infection i. Microthrombi formation ii. Secondary syphilis c. Atheroembolism i. Cholesterol emboli from ulcerated plaques in the more proximal vessels ii. Mural wall thrombi iii. Endocarditis iv. Myxoma v. Vascular surgery vi. Angiography vii. Meningitis d. Anticoagulation i. Coumadin e. Thrombolytic activity i. Tissue plasminogen activator ii. Streptokinase f. Drugs i. Dopamine ii. Beta blockers iii. Steroids iv. Epinephrine (in local anesthetics) g. Hyperviscosity syndromes i. Cryoglobulinemia ii. Cold agglutinins iii. Polycythemia vera h. Hypercoagulable states i. Malignancies ii. Diabetes mellitus i. Vasculitis i. Polyarteritis nodosa group ii. Hypersensitivity group ii. Wegener's granulomatosis group iv. Giant cell arteritis j. Foot surgery 3. Signs and Symptoms:

a. Pain b. Bluish mottling of the digit c. Pedal pulses tend to be present d. Can be either bilateral or unilateral 4. Origin of the Emboli: a. Bilateral signs and symptoms in the toes suggests ulcerated plaques in the aorta. b. Unilateral signs suggests ulcerated plaques in the iliac, femoral, of popliteal arteries. 5. Treatment: a. Angiography to determine the location of the plaque b. Photoplethysmography of the digits c. Removal of the atheromatous plaque d. Endarterectomy d. Risk factor modification e. Amputation as necessary f. Medical therapy as needed (i.e. D/C anticoagulant or other suspected causative agent, use of antibiotics or other drug)

Polydactylism A hereditary malformation, transmitted as an autosomal dominant trait. It may occur as a single deformity in the foot (nonsyndromatic) or may be associated with accessory digits in the hand, and there may be other congenital malformations as well (syndromatic). The digital deformities may be pre-axial (hallux) or post-axial (5 toe) or central toes 2,3,4). The duplication of the toe may be complete or involve the distal phalanx or the distal and middle phalanx. The metatarsal may be partially or completely duplicated. Duplicated digits may share a common metatarsal. Shoe fit is the major problem. 1. Classification (Temtamy and McKusick): Adapted from the classification of the hand (less applicable to the foot) a. Pre-axial: i. Type 1 to type 4 b. Post-axial: i. Type A: A fully developed accessory digit that articulates with either the 5th metatarsal or with a duplicated 5th metatarsal ii. Type B: Characterized by an accessory digit devoid of osseous tissue which represents a vestigal digit NOTE* Venn-Watson further divided postaxial polydactyly into 5 specific morphological patterns, based on the degree of metatarsal duplication 1. Surgical tenets: a. The most rudimentary digit (least important) should be excised when possible leaving 5 toes b. Try to achieve a normal functioning foot as well as a cosmetically pleasing

one c. Avoid scar on the medial or lateral side of the foot where shoe pressure will irritate them 2. Surgical excision of lateral pre-axial toe: a. If any other congenital deformities are present, they should be corrected first

b. The above diagram shows an accessory pre-axial great toe that is in varus secondary to a metatarsus adductus. The metatarsus adductus is treated first via casting (which will help stretch the medial skin of the hallux prior to surgery). In the above case it is best to remove the lateral toe so the scar line is on the lateral aspect. Redundant soft tissue can be excised from the 1st interspace, and the adductor hallucis stump from the amputated toe is sutured to the base of the remaining proximal phalanx, and the intermetatarsal ligaments are repaired. This helps straighten the toe and close the intermetatarsal angle 3. Surgical excision of a medial postaxial toe: a. The following diagram illustrates the lesser developed medial 5th toe. Excision is made via two longitudinal eliptical incisions around the accessory 5th toe which meet at approximately midshaft of the 5th metatarsal

Chapter 27: Muscle and Tendon Pathology Muscle Physiology Principles of Tendon Repair Tendon Lengthening and Tenotomy Tendon Transfers Tendon Grafts Posterior Tibial Tendon Rupture Posterior Tibial Tendon Dysfunction (Acquired Adult Flatfoot Syndrome) Peroneal Tendon Pathology Achilles Tendon Rupture Lateral Ankle Stabilization Procedures Postoperative Care and Training Following Tendon Transfer Tenosynovitis

MUSCLE AND TENDON PATHOLOGY Tendon repair and tenoplasty are integral parts of many podiatric procedures, thus it is imperative that the podiatric surgeon be familiar with the principles of tendon healing and repair. Knowledge about tendon healing will allow the surgeon to make appropriate decisions concerning the procedure performed, materials used, postoperative care, and potential complications

Muscle Physiology 1. Anatomy: a. Connective tissue surrounding the muscle i. Intact muscle enclosed by the epimysium ii. Muscle fascicles enclosed by perimysium iii. Individual muscle fiber enclosed by endomysium b. Muscle's structural and functional subunits: i. Fasciculus ii. Muscle fiber iii. Myofibril: The myofibrils complex protein structure is the basic contractile unit:
Actin: Thin protein filament containing contractile proteins tropomysin and troponin
Myosin: Thick protein filament iv. Sarcomere: the smallest functional unit of the muscle fiber extending from one "Z" line to the next
The myofibril is composed of alternating "A" bands corresponding to the thick myosin filaments and "I" bands corresponding to the thin actin units
The "A" band encloses the "H" band (where cross bridges are absent) and in the middle of the "I" band is the "Z" line
T-tubules are invaginations of the sarcolemma which form an interconnected network
The sarcoplasmic reticulum extends from one T-tubule to the next forming the terminal cisternae v. Myoneural junction:
The axon gives rise to several terminal twigs, the end of each is dilated and unmyelinated vi. Organelles:
Mitrochondria are found between the myofibrils and appear in varying amounts depending upon the type of muscle fiber
Cytochromes for oxidation, and glycogen appear in varying amounts c. Tendons: i. Dense connective tissue between connective tissue in muscle, and insertion area ii. Golgi tendon organs transmit information concerning tendon tension 2. Physiology of muscle fiber: a. Muscles function according to the Sliding Filament Theory of Muscular contraction: rest, excitation coupling), contraction, recharging, and relaxation b. Initiation of contraction:

i. The axons released acetylcholine which initiates an action potential along the sarcolemma ii. The action potential is propagated into the depths of the myofibril via the T-tubule system iii. This in turn mediates a release of calcium from the sarcoplasmic reticulum (the sarcoplasmic reticulum has an active pump to recover calcium once it is released) iv. In the presence of repeated neural stimulation calcium will remain in the sarcoplasm v. Following the action potential is an absolute refractory period, during which no action potential may be initiated vi. Next follows a relative refractory period during which a greater than normal neural stimulus may initiate another action potential in the sarcolemma c. Myofibril contraction (the ratchet mechanism): i. In the absence of calcium, tropomycin blocks the myosin-binding sites on the F-actin ii. When calcium is released by the sarcoplasmic reticulum into the sarcoplasm, it bonds to the Tn-C portion of the troponin, which mediates a conformational change in tropomyosin which uncovers the myosin binding sites iii. ATP binds to heavy meromycin (form of myosin), which releases it from the actin. The ATP-ase activity of the heavy meromysin then cleaves the phosphate, and the myosin can once again bind to actin iv. Upon binding with actin, the heavy meromysin changes conformation, thereby pulling the actin along v. As calcium is reabsorbed by the sarcoplasmic reticulum, the myofibrils again relax NOTE* Motor unit response is an all or nothing d. Fast twitch vs. slow twitch muscle Feature # of type 1 fibers # of type 2 fibers Speed of response Strength Stamina Major energy source

Fast Twitch + +++ +++ + + anaerobic

Slow Twitch +++ + + +++ +++ aerobic

e. Type 1 vs. Type 2 muscle Feature Color Myoglobin content Mitochondrial content

Type 1 RED +++ +++

Type 2 WHITE + +

Glycolytic enzymes Glycogen content Complexity of T-tubules Speed to respond to stimulus

+ + + +

+++ +++ +++ +++

f. Energy system function: i. Phosphagen system (anaerobic)
ATP and phosphocreatine
Availability of energy is rapid
Small amounts of energy available for a few seconds (30 seconds)
Utilized in sprinting, jumping, swimming etc.
Primary source of energy muscle storage ii. Glycolytic system (anaerobic)
For activities 30 seconds to 1.5 minutes
No oxygen required
Formation of lactate takes place
Lactate accumulation results in oxygen debt and muscle fatigue iii. Aerobic phosphorylation
For activities greater than 1.5 minutes
Carbohydrates, proteins and fats utilized through the Krebs cycle and electron transport system (oxidative phosphorylation)
Site of energy formation is the mitochondria -No lactate formation NOTE* Sport activities require all 3 sources of energy but in different proportions depending on the sport characteristics NOTE* Rigor mortis occurs due to exhaustion of A TP in the presence of calcium (in the absence of ATP, myosin becomes tightly bound to actin) 3. Training programs: a. Most training programs are an adaptation of sprinting and endurance training i. Endurance training results in hypertrophy of type 1 fibers ii. Sprint training results in hypertrophy of type 2 fibers NOTE* Fiber type can change in response to training programs, but there is no proof that one fiber can transform to another fiber type iii. Training results in cardiac hypertrophy, increase in cardiac stroke volume, and decrease in heart rate 4. Types of training: a. Isometric excercises: i. Contraction in which a muscle maintains a constant length ii. Contraction against stationary objects iii. Maximal isotonic contraction increases strength to a greater extent than

submaximal contractions iv. Isotonic training does not require a long time of excercising v. Maximal strength gained is very specific for the joint angle at which the training is performed vi. Motor performance is not increased by isotonic exercise vii. Isometrics are static excercise viii. Strength gained by isometrics decrease the maximal speed of a limb b. Isotonic excercises (concentric): Implies constant tension i. During isotonic excercise the amount of force exerted on a weight being lifted depends on the acceleration of that weight (Newton's 2nd law: F+W+MA) ii. In case of isotonic training, voluntary maximal contraction (VMC) takes place somewhere during training iii. The maximal lift is really the weakest point in the ROM of the joint. If the weight could be lifted quickly on each repetition, the VMC would be possible to perform through the entire ROM iv. Motor performance is increased v. There is an increase in lean body mass and a decrease in body fats c. Eccentric excercises: Negative weight training i. A contraction in which the muscle lengthens upon contraction ii. Strength gained is not different than in concentric or isotonic contraction iii. Less effort is required to gain the same strength as in concentric training iv. Tension developed in the muscle during eccentric contractions (as compared to concentric contraction) utilizing equal weights indicates that more tension is developed during concentric contraction v. To cause equal tension as that during concentric training, more weight has to be used during eccentric training vi. Eccentric training has the following disadvantages:
Muscular soreness
Trainer is necessary to use heavier weights
Weight handled can be hazardous
Training time is longer than with other training methods d. Isokinetic excercises: Constant velocity excercise i. The machine is set at a constant velocity but the resistance is not set; whatever force the trainee applies to the machine set at a certain velocity, is offered as a resistance to the trainee by the machine ii. The above allows the VMC throughout the entire ROM iii. To be strong at fast speed of movement, the athlete should be training at fast speed of movement iv. Isokinetics increases motor performance v. Motor performance is increased to a greater extent at fast speed than at slow speed vi. Muscular soreness is minimal vii. No weight is lifted vii. Length of the workout is decreased e. Variable resistance exercises:

i. Percentage of increase in resistance that an individual can tolerate and complete a particular movement depends upon the following variables:
Limb length
Muscle length
Point of attachment of the tendons on the bone
Bony position ii. Motor performance increases with variable resistance machinery (high cost) f. i.




Comparisons Isotonic vs. isokinetics: Strength increase is greater in isokinetic as compared to isotonics Isokinetic contractions are preferred over isotonics Isokinetic training increases isokinetic and isotonic strength more than isotonics
Isokinetic training (at fast speeds) increases motor performance more than isotonics
Isokinetics is as effective as isotonics in decreasing fat and increasing lean body mass
Less muscle soreness with isokinetics over isotonics ii. Isokinetics vs. isometrics:
Isokinetics causes a greater increase in isometric and isokinetic strength than does isometrics iii. Isotonics vs. Isometrics:
Motor performance is Improved to a greater extent with isotonics than isometrics iv. Variable resistance vs. isometrics:
Probably better motor performance with variable resistance NOTE* The strength training choice will depend upon the cost of the equipment, amount of strength gains, and motor performance increase

Principles of Tendon Repair 1. Histology: a. Tropocollagen: The most basic molecular unit of tendon NOTE* Successive molecules of tropocollagen are assembled and eventually form collagen fibers. These longitudinally anastomosed fibers constitute a tendon b. Tendons are composed of 3 anatomical coverings: i. Endotenon: Surrounds groups of collagen fibers and forms units called fascicles ii. Epitenon: This covers groups of fascicles. It is also the visceral layer and is responsible for the intrinsic repair response iii. Paratenon: A loose filmy structure that covers the entire tendon and has a rich vascular supply that communicates with the, tendon itself. The paratenon allows the tendon to glide

NOTE* Without the paratenon, the tendon would stick to the surrounding tissue, so care must be made during surgery not to damage this structure 2. Tendon healing: a. 4 stages each taking approx. one week i. Stage 1: The severed ends being joined by a fibroblastic splint. At the end of this stage the repair site is in its weakest state consisting of serous material and granulation tissue (termed zone of degeneration) ii. Stage 2: Shows an increase in paratenon vascularity and collagen proliferation. Immobilization is still necessary. iii. Stage 3: Collagen fibers begin to form longitudinally and give the tendon a moderate degree of strength. At this time controlled passive motion is beneficial to decrease the formation of fibrous adhesions (CPM) iv. Stage 4: Exhibits fiber alignment which imparts increased strength to the tendon. At this point active mobilization can be initiated b. Tendon lengthenings will often result is a loss of muscle strength roughly equal to one grade of manual examination once healed 3. Suture selection: Plays a vital role in uneventful tendon surgery a. Surgilon®: This non-absorbable non inflammatory suture allows for increased strength during the end of stage 1 when the tendon is the weakest b. Stainless steel: Excellent to anchor tendon to bone and then removed when healing occurs. It is the strongest and least reactive, and best in contaminated wounds. Its drawbacks are it can "kink" up and "saw" through a tendon. c. Silk: Was used for years but has been replaced with less reactive nonabsorbable and absorbable sutures. d. Tevdek®/Ticron®: Nonabsorbable braided polyester that retains greater ability to resist gap-producing forces at 3 weeks than either nylon or polypropylene e. Vicryl®/Dexon®: Absorbable polygalactic acid and polyglycolic acid usually provide strength long enough for the repair 4. Methods of tendon repair: tendon to tendon suture techniques (see following diagrams) a. Bunnell end-to-end: Excellent technique but can cause tissue restriction b. Double right angle: Good for quick repair of small tendons c. Lateral trap: Firmly grips the outside of the tendon without constricting the microcirculation in the center. The central mattress suture acts as a temporary anchor. d. Chicago: A simple x-stitch described by Mason and Allen e. Robertson: An excellent method of anastamosing tendons of unequal diameter f. Interlace: Another method for attaching smaller to larger tendons as in tendon grafting g. Herringbone stitch and insertion: A method of grafting one tendon into the

center of another h. Bunnell pull-out suture: A pull-out stitch is a non-absorbable suture that anchors a deep stitch to the outside of the skin so it can be removed once healing it complete. Anchored to the outside with a button.

NOTE* Side-to-Side anastamosis of a transferred tendon provides the most physiological pull, the greatest danger is that of slippage, so the adjoining surfaces should be roughened and the epitenon scraped free (encourages fibrous union) and then sutured

NOTE* When suturing a tendon it is important to preserve the microcirculation and therefore not encircle or strangle large amounts of tendon tissue. Close apposition is important but the tendon ends must not bunch or overlap excessively. Tendon-to-tendon approximation must be equal otherwise fibrous tissue extrusions will bind to the surrounding tissues. Necrotic ends must be debrided

5. Securing tendon to bone: Most secure form of fixation a. Trephine plug: Using a Michele vertebral trephine a hole is drilled into the bone with the tendon pressed inside and the resultant plug is later tapped into place securing the tendon b. Three hole suture (see diagram prior page): Anchoring the transposed tendon with a double armed suture and placing it in a drill hole. The sutures (a nonabsorbable polyester suture is recommended) are then tied into 2 adjacent small drill holes. c. Buttress and button anchor: For tenodesis using a nonabsorbable suture (stainless steel) that is removed once the healing is complete d. Tunnel with sling: Can only be used with a tendon with sufficient length. Made via a tunnel in a bone with the tendon passed through and sutured on itself. Used with a Jones suspension of the EHL e. Screw and washer (cleated polyacetyl): Useful where there is little soft tissue for the transferred tendon can be sutured. f. STATAC Device (Zimmer® Inc.): Titanium implant that is drilled into the bone with non-absorbable sutures attached that can be threaded to Keith needles and sewn through a tendon. 6. Objectives of tendon transfer: a. To improve motor function where weakness and imbalance exist and thereby prevent contractures and further deformity b. To eliminate deforming forces c. To provide active motor power d. To provide better stability e. To eliminate the need for bracing f. To improve cosmesis 7. Principles of tendon transfers: a. Select suitable cases, do not create a new imbalance b. Understand the anatomy and physiology c. Correct the fixed or structural deformities first d. Select the proper timing (age of patient) e. Select a suitable tendon for the transfer (adequate length and strength) f. Provide a direct or mechanically efficient line of pull g. Perform stabilizing procedures first (if needed) h. Preserve the gliding mechanism i. Use atraumatic technique j. Preserve blood supply and innervation

k. Provide adequate muscle-tendon tension on fixation l. Use secure fixation techniques m. Provide detailed postoperative management 8. Grading system of manual muscle testing: 5 Normal Full resistance at end range of motion 4 Good Some resistance at end ROM 4+ Moderate resistance at end ROM 4Mild resistance at end ROM 3 Fair Able to move against gravity alone 2 Poor Able to move with gravity eliminated 1 Trace Can palpate or visualize muscle contraction 0 Zero No evidence of muscle contraction

Tendon Lengthening and Tenotomy Tendon lengthening and tenotomy have limited indications when abnormal contracture of a musculotendinous unit compromises normal function. Absolute tenotomy has few applications in reconstructive foot surgery (severing the adductor tendon in HAV surgery, the FDL for mallet toe, and tenotomy for lengthening of the Achilles tendon) 1. Common procedures: a. Strayer technique (distal recession): Modification of the Volpius-Stoffel procedure. Lengthening the gastrocnemius ms., requiring the complete severence of the aponeurosis, suturing the retracted proximal aponeurosis to the underlying soleus, and casting the foot in neutral to allow for healing at the new length b. Silverskiold procedure (proximal recession): Release of the muscular heads of the spastic gastrocnemius from the femoral condyles and reinsertion to the proximal tibial area (a 3 joint muscle is converted to a 2 joint muscle) c. Fulp and McGlamry tongue-in-groove procedure (distal recession): Modified Baker procedure. The tongue-in-groove cuts are inverted in the gastrocnemius

NOTE* These procedures are utilized for the correction of non-spastic ankle equinus secondary to gastroc. shortening. If a spastic gastroc. equinus is present then you must also perform a concomitant excision of the central soleus aponeurosis

d. White tenotomy: Tenotomy of the anterior 2/3 of the distal end of the Achilles tendon and the medial 2/3 of the tendon, performed 5-7.5 cm proximal to the insertion (presumption of torque) e. Hoke's tenotomy: A triple tenotomy of the Achilles tendon starting 2.5 cm from the insertion and the others at 2.5 cm intervals extending proximally f. Hibbs procedure: Tendo Achilles lengthening via a lateral skin incision, with the medial 2/3 of the tendon divided proximally and then split longitudinally in the distal direction at the lateral end of the incision. The lateral 2/3 of the tendon is then divided near the point insertion and it is split longitudinally in the proximal direction at the medial end of the incision g. Sliding Z-plasty: Can be used for the Achilles (Hauser or White procedures) or extensor tendons h. Abductor hallucis tenotomy: Tenotomy of the abductor hallucis in the treatment of congenital hallux varus and metatarsus adductus. NOTE* Tendon lengthenings (once healed) will often result in a loss of muscle strength roughly equal to one grade of manual examination

Tendon Transfers 1. Common procedures: a. Murphy modification (for advancement of the tendo Achilles): Is utilized in young patients with CP where the spasticity of the triceps is causing ankle equinus. This procedure is performed by transecting and rerouting the achilles tendon into the calcaneus distally just proximal to the subtalar joint b. Peroneus brevis tendon transfer: This muscle is transferred to aid in dorsiflexion via rerouting the tendon medially into the 3rd cunieform. c. Peroneus longus tendon transfer: This muscle is transferred when additional dorsiflexory power is needed via rerouting the tendon medially into

the 3rd cuneiform. It can also be rerouted into the posterior calcaneus when paralytic calcaneal deformities are present NOTE* The peroneus longus tendon transfer to the cuneiform is utilized with a drop foot deformity and weakness or paralysis of the anterior muscle group d. Tibialis posterior tendon transfer: Has the potential to be a good dorsiflexor when replacement is needed via rerouting the tendon laterally, and inserting it into the 3rd cuneiform NOTE* The tibialis posterior tendon transfer is indicated when a weak or paralyzed anterior muscle group is present, equinovarus deformity, drop foot, Charcot-Marie-Tooth deformity, and permanent peroneal nerve palsy e. Tibialis anterior tendon transfer: To reduce the supinatory forces in the foot via detaching the tibialis anterior over the navicular and rerouting it laterally into the 3rd cuneiform. NOTE* Tibialis anterior tendon transfer can be used for recurrent clubfoot, flexible forefoot equinus, drop foot, and Charcot-Marie-Tooth deformity

f. Split tibialis anterior tendon transfer (STATT): Its goal is to increase true dorsiflexion of the foot by balancing its power laterally via splitting the tibialis anterior and suturing the lateral portion to the peroneus tertius (see chapter 21, Surgery of the Congenital Foot) NOTE* The STATT is recommended for spastic rearfoot varus, fixed equinovarus, excessive invertor power, forefoot equinus with swing phase extensor substitution and claw toes, flexible cavovarus deformity, and dorsiflexory, weakness h. Hibbs tenosuspension: Is performed to release the retrograde bucking at the MPJ's causing the flexible forefoot equinus, is done via detaching all 4 tendons of the EDL distally enough and fused at the base of the 3rd metatarsal to the. corresponding EDB NOTE* EDL slips 4 and 5 must be attached to EDB tendon 4 i. Jones suspension: Used for treatment of a cocked-up hallux by transecting the EHL at the IPJ of the hallux and rerouting it through a medial to lateral drill hole in the head of the 1st metatarsal

NOTE* The Jones suspension has been utilized for flexible cavus foot flexible plantarflexed 1st ray (with or without hammered hallux), and prophylaxis when both hallucal sesamoids are removed j. Young procedure: A tendon transposition (rerouted through a "keyhole" in the navicular) for flatfoot (see chapter 21, Surgery of the Congenital Foot) k. Kidner procedure: Advancement of the tibialis posterior either inferior to the navicular bone or modified by attachment to the medial cuneiform to increase its adductory influence on the forefoot (see chapter 21, Surgery of the Congenital Foot) l. Lowman procedure: For flatfoot, a rerouting of the a medial band of the tibialis anterior tendon under. the navicular and sutured to the spring ligament and transfer of a section of tendo Achilles (see chapter 21) m. Heyman procedure: A panmetatarsal suspension for equinus foot via suturing the EDL to their respective metatarsal heads (see chapter 21, Surgery of the Congenital Foot) n. Flexor digitorum longus transfer: Transferring the FDL to the proximal phalanx of the involved digit will convert it into a strong plantarflexor of the MPJ o. Peroneal anastomosis: Involves securing the peroneus longus to the peroneus brevis at the level of the midcalf (for pes cavus deformity to decrease the plantarflexory force on the 1st ray and to increase the eversion force to the foot) p. Joplin sling procedure: To narrow the forefoot (used with children where you do not want to do an osseous procedure). It is done via cutting the EDL tendon 5 and passing it through and underneath the 5th MPJ joint capsule to the abductor hallucis and back around and over the EHL suturing it to the 1st MPJ joint capsule. The EDL tendon 4 is sutured to stump of the EDL 5. The adductor is transected. 2. Healing for tendon transfers: a. Casting for 4 weeks (foot in neutral position and at right angles to the leg) b. Early passive ROM at about 3 weeks by bivalving the cast c. Later, progressive weight-bearing excercise (isometrics)

Tendon Grafts 1. Donor tendons: Are usually from the plantaris, peroneus tertius, strips of the Achilles, and slips of the EDL or EDB 2. Carbon Implants: The carbon acts as a scaffold on which new tendon can develop, which makes it appropriate for filling large gaps as can be present in the Achilles tendon (experimental as of now) 3. Silastic sheets: Used to protect a tendon anastomosis in one study 4. Silicone rod Implant: Used in staged gliding tendon transplant in patients where the gliding bed has been damaged. This creates a pseudosheath for delayed tendon grafting

5. Tendon xenografts: Bovine grafts are experimental at this point 6. Dacron mesh (Dacron Cooley graft): The dacron vascular graft is split to provide a band of material of the desired length that can be woven through or around a ruptured Achilles tendon as a lattice for further healing, In the same manner as the plantaris tendon is used

Posterior Tibial Tendon Rupture 1. Anatomic considerations: a. Deep posterior compartment muscle b. Originates from the tibia, fibula and interosseous membrane c. Extrinsic insertions into all bones of the midfoot except the talus, 1st and 5th metatarsal d. Passes retromalleolarly with the flexor retinaculum and functions as a two pulley system (medial malleolus and navicular) providing a mechanical advantage to the tendon 2. Functional considerations: a. Open kinetic chain: i. Supination (plantarflexion-,adduction-inversion) b. Closed kinetic chain: i. Deceleration of STJ pronation ii. Acceleration of STJ and oblique MTJ supination in midstance phase of gait iii. Rigid lever for gastro-soleus function 3. Etiology: a. Traumatic forces and injuries b. Progressive degeneration due to excessive demand (severe forefoot varus, equinus, obesity) c. Severe degeneration secondary to systemic disease (RA, mixed connective disease, DM, etc.) d. Neoplasms 4. Subjective findings: a. Medial arch and/or ankle pain b. Diffuse swelling and tenderness along the course of the TP tendon c. Symptoms aggravated by proloned weightbearing and ambulation d. May be more painful on initial arising in the AM (post-static dyskinesia) e. Progressive flatfoot deformity f. Sedentary/decreased activity 5. Clinical findings: a. Edema and increased warmth of the medial aspect of the foot and ankle b. Palpable tenderness along the course of the tibialis posterior tendon c. Tenosynovitis may be present d. Collapse of the medial arch e. Palpable defect with complete ruptures f. Increased heel valgus and midfoot abduction

g. Decreased muscle strength with guarding h. Positive single heel rise test i. Apropulsive/antalgic gait without resupination j. Flexible to rigid depending upon the duration 6. Radiographic findings: a. DP view: i. Increased T-C angle (angle of Kite) ii. Increased calcaneocuboid angle (cuboid abduction angle) iii. Degenerative arthritic changes b. Lateral view: i. Decreased calcaneal inclination angle (can be normal) ii. Increased T-C angle iii. Increased talar declination angle iv. Significant medial column faulting v. Forefoot supinatus vi. Degenerative arthritic changes c. Special studies: i. MRI: T1-weighted images provide images about the tendon itself, T2 weighted images are useful to highlight fluid within the tendon sheath or adjacent edema NOTE* MRI is most revealing. Three patterns of rupture have been reported: a. Type 1: Intrasubstance tears noted on MRI with longitudinal splits and hypertrophy of the tendon (increased signal on T1) b. Type 2: Progression of intrasubstance tears noted on MRI as decreased girth and attenuation of the tendon c. Type 3: Complete rupture (noted as discontinuity of the tendon on MRI) ii. CT iii. Tenogram 7. Conservative treatment: Not usually helpful a. NWB cast 4-6 weeks b. Shoe modifications/orthotic devices c. NSAIDS 8. Surgical treatment: Depends upon the time since the rupture, degenerative changes taken place, rigidity of the deformity, and expected functional demands a. Soft tissue procedures: i. Early tendon repair:
Excision of all scar tissue
Excision of inflamed synovium
Z-plasty shortening repair technique or transfer of tibialis anterior
Primary reattachment to the navicular tuberosity ii. Delayed primary repair with tendon free graft and desmoplasty iii. Delayed primary repair with tendon transfer and desmoplasty

iv. Evans type procedure NOTE* The indications for primary soft tissue repair alone are limited b. Osseous procedures: i. Isolated STJ arthrodesis ii. Evans calcaneal osteotomy iii. Talonavicular arthrodesis iv. Combinations of above v. Triple arthrodesis vi. Ankle arthrodesis vii. Pantalar arthrodesis viii. Talonavicular arthrodesis with lateral column lengthening c. Ancillary procedures: i. TAL ii. Gastrocnemius recession iii. Medial column suspension procedures iv. Bone grafting v. Subtalar joint arthroereisis

Posterior Tibial Tendon Dysfunction (acquired adult flatfoot syndrome) 1. Etiology: a. Tenosynovitis of tendon b. Shallow or absence of malleolar groove c. Attenuation of tendon d. Rupture 2. Differential diagnosis: a. Residual calcaneal valgus b. Torsional abnormalities c. Limb length discrepancy d. Post-traumatic arthritis e. Charcot arthropathy f. Lisfranc dislocation 3. Signs and symptoms: a. Pain b. Edema c. Abducted forefoot d. Apropulsive gait e. Loss of inversion power f. Progressive flatfoot g. Antalgic gait h. Difficulty on toe raising i. Heel not inverting with standing on toes 4. Diagnostic studies:

a. Tenogram b. CT c. MRI 5. Treatment (conservative) a. BK cast immobilization in equinovarus x 4 weeks b. Orthoses c. NSAIDS 6. Treatment (Surgery): a. Tendon repair b. FHL tendon transposition c. Secondary stabilization: i. Medial column fusion ii. Modified Young procedure iii. STJ arthroereisis iv. Evans calcaneal osteotomy v. Triple arthrodesis NOTE* Posterior tibial inflammation can be divided into peritendonitis, chronic tenosynovitis, and stenosing tenosynovitis. a. Peritendonitis: elicits pain at the musculotendinous junction, and is consistant with an overuse syndrome. Treatment is physical therapy and orthoses b. Chronic tenosynovitis: elicits pain around the tendon between the tip of the malleoli and the navicular (seen with rheumatic disease patients), requiring orthoses and steroid injections c. Stenosing tenosynovitis: elicits pain around the malleoli, and requires surgical intervention

Peroneal Tendon Pathology 1. Types of pathology: a. Dislocation: i. Etiology:
Eversion/dorsiflexion trauma
Congenital absence of groove in the lateral malleolus
Direct blow to the lateral ankle with the ankle inverted ii. Signs and symptoms:
Ankle edema
Tendonitis
Pain
“Clicking” sound
Avulsion flake from the fibula noted on x-ray i. Treatment:
Strapping (acute and chronic cases)
Cast immobilization 3--6 weeks (acute)




Surgical repair (acute and chronic) followed by BK cast x 4 weeks and physical therapy

b. Stenosing Tenosynovitis: i. Etiology:
Direct trauma
Lowgrade/chronic trauma
Enlarged peroneal tubercle
Calcaneal fracture
Arthritis ii. Signs and symptoms:
Pain
Trigger point pain
Thickened tendon sheath
Pain with ankle inversion
Chronic edema iii.Diagnostic studies:
X-ray (calcaneal axial view)
CT
MRI
Peroneal tenogram

iv. Treatment:
Surgical repair of osseous pathology
Surgical repair of the tendon sheath
Iontophoresis
Physical therapy c. Tendon rupture: i. Etiology:
Laceration Chronic degeneration ii. Signs and symptoms
Pain
Edema
Loss of eversion strength
Inability to plantarflex the 1st ray
Increased soft tissue mass iii. Diagnostic studies:
Peroneal tenogram
MRI
CT iv. Treatment:
Cast x 6 weeks
Surgical repair (either primary repair or secondary with a graft)

Achilles Tendon Rupture In most cases rupture results in longitudinal tearing of the tendon tissue into irregular strips either at the musculotendonous junction (younger patient) or at the point of insertion into the calcaneus (middle-aged people), the 2 most common sites of rupture. The areas most susceptible to rupture are areas of decreased circulation, myotendonous junctions, and the area 4-6 cm proximal to the tendo Achilles insertion 1. Etiology: a. Direct blow b. Laceration c. Abnormal muscle pull 2. Clinical diagnosis: a. Pain at the site b. Palpable tendon gap c. Increased soft tissue mass d. Loss of plantarflexory strength e. Inability to walk on toes f. Doherty-Thompson Test (+) (or just Thompson Test): The patient attempts to plantarflex the foot while the calf is being squeezed. The inability to perform this plantarflexion is a strong indication of Achilles tendon rupture

NOTE* Plantaris rupture often mimics tendo Achilles rupture but with this the Thompson test is normal, and the pain is usually located along the course of the ruptured plantaris tendon 3. Radiographic findings: a. Obliteration of Kager's triangle b. Increased soft tissue density c. Toyger's angle (130-150°) d. CT scan e. MRI 4. Treatment: Partial rupture a. BK cast x 3-4 weeks in plantarflexion b. Followed by another BK cast with less plantarflexion x 4 weeks 5. Treatment : Complete rupture (24 hours-5 days) a. Full equinus BK cast x 3 weeks, followed by b. Gravity equinus BK cast x 3 weeks, followed by c. Heel lifts 6. Treatment: Complete rupture (5 days or longer) a. Surgical repair b. BK NWB cast x 3 weeks, followed by c. BK weight-bearing cast x 3 weeks, followed by d. Heel lifts (19 mm to 13 mm to 6 mm) NOTE* If a diagnosis of a distal rupture is made within 10 days, the Lynn procedure is ideal. Lynn procedure: A 7 inch medial/longitudinal incision parallel to the medial border of the TA. The paratenon is opened in the midline and with the foot held in 20° plantarflexion, and without excising the irregular ends, the TA is sutured using an absorbable suture. If the plantaris is intact, its insertion at the calcaneus is divided and the tendon is fanned out to form a membrane, which is then placed over the TA repair and sutured into place (covering the TA 1 inch above and below the repair). The TA paratenon and skin are closed. Cast applied NOTE* If a diagnosis of a proximal rupture is made within 10 days, a McLaughlin procedure is preferred.

McLaughlin's procedure: A midline incision curving laterally is made. The frayed tendon edges are trimmed back to healthy tissue. A drill hole is made medially to laterally through the calcaneus, and a stab wound is made at its point of emergence. A long screw is passed through the drill hole in the calcaneus. A wire suture is inserted into the proximal tendon fragment, which is then pulled into position by the 2 ends of the wire suture which are fastened to the projecting ends of the screw. With retraction thus counteracted, the trimmed tendon ends are sutured together. The superfluous portion of the screw is cut free and removed. A twisted wire with a split lead shot (for palpable localization of the mattress suture) is attached to the proximal portion of the wire suture. Cast applied.

NOTE* The Bosworth procedure or the Lindholm procedure is used for late repair of a rupture. Bosworth procedure: Ruptured tendon exposed through a posterior longitudinal midline incision from the calcaneus to the proximal 1/3 of the calf. Excision of scar tissue at the ruptured ends. Free up from the medial raphe of the gastrocnemius a strip of tendon 1/2 inch wide and 7 inches long, leaving this strip attached just proximal to the rupture site. The strip is turned down and passed transversely through the proximal tendon and then passed transversely through the distal tendon, and then passing the tendon through the distal end from anterior to posterior, while holding the knee at 90° and the ankle in plantarflexion. Once again the strip is brought proximally and passed through transversely and sutured onto itself. Cast applied Lindholm procedure: A posterior curvilinear incision is made from the midcalf to the calcaneus. The rupture is exposed, the ragged ends are debrided and apposed with a box-type mattress of heavy silk or other non-absorbable suture. From the proximal tendon and gastrocnemius aponeurosis, 2 flaps are fashioned, each approx. 1 cm wide and 7-8 cm long. These flaps are left attached at a point 3 cm proximal to the site of rupture,- and each flap is twisted 1800 on itself so that its smooth external surface lies next to the subcutaneous tissues as it is turned distally over the rupture. Each flap is sutured to the distal stump of the tendon and to the other flap, completely covering the site of the rupture. Wound closed. Cast applied.

5. General surgical principles:

a. Functional length restoration b. Approximation of clean ends c. Avoid the sural nerve d. Preserve the tendon sheath e. Evacuate the hematoma f. Use proper anchoring sutures for the tendon g. Tendon graft as necessary 6. Complications: a. Nonoperative i. Occurs from long term cast immobilization in equinus (needs aggressive isokinetic rehabilitation). At the 10-15 week mark atrophy of the triceps occurs b. Operative: i. Intratendinous hemorrhage and irreparable damage to the paratenon ii. Every attempt must be made to cover the newly repaired tendon with the paratenon complex, because if not, this will become immobile and nongliding iii. Rerupture iv. Infection, wound dehiscence, sinus tarsitis, and STJ damage

Lateral Ankle Stabilization Procedures (tendon transfers) Single ligament rupture: Watson-Jones*: This uses the peroneus brevis, which passes through the fibula from posterior to anterior, through the neck of the talus from plantar to dorsal, back through the fibula, from anterior to posterior, and sutured back onto itself. Lee Procedure (modified Watson-Jones)*: This uses the peroneus brevis tendon, which is then passed through the fibula, from posterior to anterior, and then sutured back onto itself. Evans*: This utilizes the peroneus brevis through an oblique hole through the fibula sutured back onto the belly of the peroneus brevis. Storren Nilsonne Pouzet Haig Castaing and Meunier Dockery and Suppan Double ligament rupture: Elmslie*: Originally described as using the fascia lata and passed through a drill hole in the lower aspect of the fibula, through the calcaneus, back through the same drill hole, and tied onto itself, after passing through the neck of the talus. Chrisman and Snook*: This uses the split peroneus brevis, which is passed through the fibula from anterior to posterior through a flap in the calcaneus, and is then sutured back to the peroneus brevis tendon.

Stroren Hambly Winfield Gschwend-Francillon Triple ligament rupture: Spotoff Rosendahl and Jansen

NOTE* In the case of lateral instability, both the Watson-Jones and the Evans procedures are utilized. a. The Watson-Jones restores the function of the calcaneofibular and talofibular ligaments by rerouting the peroneus brevis tendon. The chief drawback of this procedure is that it involves drilling a hole through the neck of the talus (difficult to accurately accomplish). A second problem can arise with this technique if the peroneus brevis is too short to be threaded through the tunnels fashioned to receive it. b. The Evans technique, which was designed to obviate the potential difficulties of the Watson-Jones, has the disadvantage of involving reconstruction of only the calcaneofibular ligament.

c. The Chrisman and Snook procedure was designed to repair the anterior talofibular and inferior calcaneofibular ligaments, with preservation of the peroneus brevis tendon

Postoperative Care and Training Following Tendon Transfer 1. Age of the patient at the time of the transfer: a. Should be old enough to cooperate in training (>4 years old) b. Earlier transfer is indicated when delay would result in structural deformity 2. Support In overcorrected position: a. Until full function is restored and no tendency for reccurrence b. Bivalved cast will help hold tendon in relaxed position during this period 3. Preoperative training to localize contracture In muscle to be transferred 4. Instruct patient to contract transferred muscle: a. Voluntary contracture through the original arc while guiding the part in the direction provided by the transfer b. Initially palpate the belly of the ms. and tendon to ensure proper contraction c. Initially excercises are performed in the bivalved cast d. Mild gentle tension on the transferred tendon may be used to assist patient in "finding" the transfer e. Electrical stimulation may also be used to assist patient in "finding" transfer 5. Establish motion in the new function provided 6. Development of motor strength: a. Once motor strength becomes fair, the bivalve cast is gradually discontinued during the day b. Controlled activities are permitted to develop function c. Resistance excercises are begun to develop strength when a normal ROM and fair strength are established d. Important to excercise antagonistic muscles also 7. Incorporation of the transfer into the new functional pattern: a. Action of the transfer may be good through full range and moderate resistance and yet during walking, voluntary control is lost b. Use of crutches during this period is helpful c. Careful supervision is required d. Walking periods are gradually increased until gait pattern becomes a conditioned reflex 8. Use of bracing: a. Should be judicious and for specific reasons b. Standing and walking excercises must also be performed without a brace to

stimulate function in the transfer 9. Bivalved casts: a. Prolonged use is very important b. Continue until the muscle has developed full strength and balanced function with no tendency for reccurrence of the original deformity 10. Triple arthrodesis: a. If dynamic balance can be established prior to the development of structural deformity, arthrodesis can be avoided b. Perform the osseous correction/stabilization and then perform tendon transfer and muscle reeducation after bone union has taken place

Tenosynovitis An inflammation of the synovial lining of the tendon sheath 1. Etiology: a. Acute infectious tenosynovitis: Caused by a pyogenic organism. The bacterial invasion and the resultant purulent exudate can involve the entire length of the tendon sheath. Treatment with antibiotics must be prompt, I and D may be necessary when the purulent material organizes b. Chronic infectious tenosynovitis: Caused by diseases such as syphilis and TB. The synovial wall becomes thickened and there is a fibrinous exudate which affects the peroneal and extensor tendons most frequently. c. Acute simple synovitis: Results from overuse most commonly affecting the EHL, TA, and tendo Achilles d. Chronic simple tenosynovitis: Caused by continuous shoe friction on the extensors or Achilles tendon e. Stenosing tenosynovitis: Usually affects the anterior and posterior tibial, EDL, and the peroneals below the lateral malleolus and in the inferior retinaculum. Caused by friction with-in the "pulley system" of the ankle within the fibrous sheath. In digits, "trigger toe" occurs. f. Hemorrhagic tenosynovitis: Caused by trauma in which the epithelial lining of the sheath is ruptured followed by hemorrhage and clot formation (excision of the hematoma is recommended) g. Paratendonitis: Results from excessive friction between the tendon and the paratenon caused by overuse, crepitation can occur h. Acute tenosynovitis caused by rheumatoid arthritis: Nodular masses can form within the tendon sheath, which may be rheumatoid nodules.

Chapter 28: Lesser Metatarsal Surgery Anatomy (Metatarsals 2-3-4) Differential Diagnosis of Metatarsalgia Surgical Treatment of the IPK Lesser Metatarsal Joint Replacement Panmetatarsal Head Resection Metatarsus Adductus Freiberg's Disease Tailor's Bunion Splayfoot Brachymetatarsia (Brachymetopody) Skewfoot

LESSER METATARSAL SURGERY The central 3 metatarsals are usually grouped together because they do not have individual axes of motion.

Anatomy (Metatarsals 2-3-4) 1. The deep transverse metatarsal ligament attaches to the plantar pad and head of the central metatarsals on both sides. This affords greater stability to the metatarsals 2-4 rather than to metatarsals 1 & 5

2. The plantar plate attaches to the metatarsal heads and the extensor hood runs from dorsal to plantar to join at the inferior junction of the hood, capsule, and deep transmetatarsal ligament 3. Blood supply to a long bone is via 3 sources: a. Nutrient b. Metaphyseal: In the metaphyseal region, there is an additional advantage of having metaphyseal vessels adding a vascular system to bone c. Periosteal: overlap entirely with the nutrient artery and so in most places there is at least two supplies 4. Surgical neck is distal to the anatomical neck, and the condyles are directly

plantar to the flare between the two 5. There is a normal declination of the metatarsal of approximately 15°

Differential Diagnosis of Metatasalgia, 1. Local factors: a. Stress fractures b. Neuroma or neuritis c. Intermetatarsal bursitis d. Freiberg's infraction e. Biomechanical factors: i. Abnormality of metatarsal parabola resulting in plantarflexion, shortening or elevation of a metatarsal ii. Pes planus or pes cavus g. Tumors h. Arthritis (local as well as systemic) i. Sesamoiditis j. Tendonitis 2. Referred or systemic etiology: a. Compression neuropathy of spinal cord L5-S3 b. Compression neuropathy of tarsal tunnel c. Peripheral neuropathy d. Ischemia

Surgical Treatment of the IPK One should try to biomechanically evaluate why a lesion is present so that the chances for return are reduced after correction of both the actual lesion and the underlying cause. 1. Etiology of plantar lesions (metatarsals 2-4): a. Biomechanical forces: Equinus, rearfoot varus, FF varus/valgus, adductory twist b. Hammertoe syndrome: Causes a retrograde plantarflexory force on the metatarsal head. As the MPJ dorsiflexes due to muscular imbalances around that articulation, the dorsal sling mechanism causes the proximal phalanx to dorsiflex and apply a downward vector to the metatarsal. As time progresses, there is a soft tissue contracture of the area and the metatarsal is exposed to abnormal stresses c. Atrophy or displacement of the plantar fat pad d. Long or short metatarsal (even at the same declination angle) e. Sagittal misalignment (abnormal declination angle): Abnormal plantarflexed position, abnormal adjacent metatarsal, hypermobility f. Abnormal bone shape (prominent plantar condyle) 2. Etiology of plantar lesions (metatarsal 5): a. Biomechanical: Rearfoot varus, rigid forefoot valgus, forefoot varus b. Sagittal malalignment: Abnormal plantarflexed 5th metatarsal, plantarflexed cuboid, dorsiflexed 4th metatarsal

c. Congenitally long 5th metatarsal or short 4th metatarsal d. Abnormal bone shape or size (prominent plantar lateral condyle) e. Fat pad atrophy 3. Differential diagnosis: a. Verruca plantaris: pinpoint bleeding, usually not directly on weightbearing area, fast development, skin lines surround the lesion b. Inclusion cyst: history of trauma (foreign body, puncture) c. Scar tissue (history of trauma) d. Foreign body 4. Preoperative considerations: a. Mark the lesion with a x-ray opaque marker b. Take x-ray in the angle and base of gait in full weight-bearing c. Evaluate the metatarsal parabola (141.5°) d. Check the axial view to evaluate the condyles e. Look at the morphology of the metatarsal head and the relative position of the fat pad 5. Summary of procedures: Can be done at the head, shaft, or the. base of the metatarsal. It is a good idea to enucleate the lesion prior to, or at the time of surgery to hasten recovery of the plantar skin. a. Procedures at the neck or head: i. Percutaneous metaphyseal osteotomy (PMO):
Osteotomy at the metaphyseal region where the capital fragment is dorsiflexed
Done so that the capital fragment is forced to the appropriate level when walking
The deep transverse ligament helps hold the the head in the correct position, not allowing it to dislocate dorsally
The cut is dorsal-distal to plantar-proximal to avoid the condyles and lift the entire distal segment (fixation at the proper level) ii. Transverse osteotomy:
Similar to the PMO but done visually
May be modified to shorten a metatarsal or fixated to control position iii. "V" osteotomy:
Done at the anatomical neck
Gives good transverse and frontal plane stability due to the "V" cut
Cut must include the condyles
Apex is distal so the head and the phalanx act as one unit, so the head is not free to dislocate
Ambulation is allowed to force the head into the appropriate position
Must debride or excochleate the lesion preop to avoid forcing the head too high
May impact on the shaft to control position iv. Dorsiflexory wedge osteotomy (DFWO): A tilt up osteotomy •Done at the anatomical neck or at the base (1 cm from the metatarsal-

cuneiform joint)
Apex is plantar and the base-is dorsal
Shortens the metatarsal
Must be proximal to the condyles at the neck
Must fixate
Ambulation in a Reese® shoe v. Arcuate osteotomy:
Bone at the neck or base
Special blade is needed (1800 arc)
Allows for transverse and sagittal motion
Must be fixated vi. McKeever peg-in-hole:
Shortens the metatarsal significantly
Technically difficult vii. Cylindrical stepdown osteotomy:
For long metatarsal
A cylindrical segment of bone is removed to cause shortening of the metatarsal that needs fixation and NWB viii. Chevron:
A double "V" osteotomy with section removed used to shorten the metatarsal
Fixation must be used
Cannot take too much bone due to the soft tissue attempting to maintain length
Cuts must be parallel and congruent ix. Osteoclasis:
Surgical fracture at the anatomical neck by forceps
Semi-free floating head
No heat from the power equipment, therefore, little bone necrosis x. Metatarsal head resection and condylectomy:
Helpful for subluxed and/or deformed joint
Joint is basically removed xi. Metatarsal head resection:
For deformed or destroyed MPJ
Shortens the ray
Allows contracture of the toe but the pain from the lesion disappears
Best done in the elderly
Close and purse string the capsule xii. Plantar condylectomy:
Open the MPJ and elevate the metatarsal head to allow access to the plantar condyles
Condyles are resected and area rasped smooth
Osteoarthritis can develop and joint limitus may develop as disruption of the integrity of the MPJ is necessary
No bone healing needed, therefore, early ambulation b. Procedures at the shaft: i. Giannestras step down osteotomy:
For a long metatarsal




Z" shortening of the metatarsal that needs fixation

c. Procedures at the base: i. Cresentic: As described above ii. DFWO: As described above 6. Complications of metatarsal osteotomies: a. Transfer lesions develop (so try not to overcorrect by indiscriminate elevation) b. Dorsal bump develops from too much elevation without having remodeled the head c. Floating toe develops from destroying the internal cubic content of the joint d. Non-union occurs if ischemia is produced or no fixation or stabilization of the osteotomy site exists e. Flail toe from transection of the musculotendonous tissues surrounding structures f. Dislocation of the metatarsal head and deformed position of the head or toe g. Edema h. Return of the original deformity due to not enough elevation of the metatarsal segment

Lesser Metatarsal Joint Replacement 1. Indications: a. Inflammatory arthritides: RA b. Degenerative arthrosis secondary to: i. Osteochondral fractures ii. Osteochondritis dissecans iii. Orthopedic deformity iv. Joint subluxation v. Malaligned fractures of the foot vi. Trauma vii. Previous surgery viii. Congenital deformity c. Congenital deformity- Brachymetatarsia d. Flail toes e. Floating toes f. Revisional surgery 2. Types: a. Swanson flexible hinge toe implant b. Sgarlato double-stem cup implant (hinge avoided) c. Swanson condylar implant 3. Surgical technique: a. Lazy "S" Incision over the MPJ (less skin contracture) b. Linear or "U" shaped capsulotomy

c. Preoperative soft tissue contractures eliminated via extensor/flexor tenotomies and/or plantar plate/hood release d. Bony resection (mostly metatarsal head) e. Reaming the medullary canals (caution in the proximal phalanx) f. Sgarlato recommends centralizing the flexor tendons via a drill hole in the plantar portion of the phalangeal base and attaching the tendon by suture g. Check fit with a sizer h. Flush copiously i. Wound closed in layers 4. Complications: a. Implant instability: Pistoning can occur from removal of too much bone as well as axial rotation of the implant b. Implant failure: Mechanical stress can produce microfragmentation with migration of the silicone particles into the lymphatic system. With this there will be obvious loss of function and possible deformity c. Foreign body reaction d. Osteochondritis dissecans: From excessive stripping of the periosteum and resultant avasular necrosis e. Detritic synovitis reaction: The surgical area will become red and swollen with a chronic low grade pain. Once infection is ruled out the patient can be treated with NSAIDS or remove the implant device f. Infection: Implant must be removed and not replaced for at least 6 months to one year. If gram negative infection was present, implant should not be replaced for longer period of time if at all g. Pistoning of the implant into cancellous bone (if implant chosen is too small) h. Chronic edema i. Fracture of the base of the proximal phalanx 5. Contraindications: a. Severe osteoporosis of the involved bones (seen with RA) b. History of a prior joint infection within the last 6 months c. History of allergic reaction to implant material d. Medically compromised patient (diabetic neuropathy, Charcot joint)

Panmetatarsal Head Resection This procedure can be gratifying but must be performed only when the proper criteria are met. 1. Historical: a. Hoffman (1911): Transverse plantar approach b. McKeever (1952): Dorsal longitudinal approach c. Clayton (1963): Transverse dorsal approach for metatarsal head and phalangeal base resections 2. Preoperative signs: a. IPK's under most metatarsal heads b. Atrophy of plantar fat pad c. Ability to palpate prominent metatarsal heads

d. Dorsally contracted toes at the MPJ's e. Possible contracted toes and proximal interphalangeal joint or distal interphalangeal joint with associated lesions f. Range of motion at the MPJ may be limited or painful or may be absent g. Range of motion of the MPJ may elicit crepitus h. Signs of degenerative disease and deformity i. Patient ambulates with an apropulsive type gait j. Ulceration of sub-metatarsal head area 3. Preoperative symptoms: a. Moderate to severe pain on the plantar aspect of the forefoot when the patient ambulates with or without shoes b. Painful multiple hyperkeratotic lesions c. Painful plantar ulcerations under the metatarsal heads area d. Patient may complain of painful dorsally contracted toes when wearing shoes e. Patient complains of pain when most of the MPJ's are moved f. Patient may complain that the toes cannot be straightened g. History of metabolic disease (RA, psoriatic arthritis, etc.) 4. Preoperative x-ray evaluation: a. Evidence of DJD b. Dorsally contracted MPJ c. Most of the MPJ's show evidence of DJD d. Bone loss evident secondary to severe DJD e. Proliferation of bone at the MPJ's f. Loss of normal joint space g. Cystic and erosive changes in the metatarsal heads h. Generalized osteoporosis i. Moderate to severe angulation deformity of the toes and metatarsals may be present 5. Surgical procedure of choice: a. 5 dorsal linear incisions: 3 dorsal linear incisions; or transverse incision b. Maintain normal metatarsal parabola: The second is the longest, followed by the 1st and third, followed by the 4th, and finally the 5th c. The 1st metatarsal head is resected more medially than laterally d. The lesser extensor tendons are usually tenotomized e. Angulate the dorso-plantar cuts on all the metatarsal heads in order to remove more bone plantarly than dorsally g. Release the tourniquet prior to closing to prevent hematoma formation h. K-wires can be used (helps eliminate the need for syndactylism) i. Betadine soaked gauze can prevent postoperative edema and infection and helps keep the toes in an aligned position 6. Advantages: a. Eliminates painful MPJ's b. Ability to ambulate without pain c. Allows patient to wear regular shoes

d. Allows reduction of dorsally contracted toes in most cases e. Elimination of plantar pressure points 7. Disadvantages: a. Loss of propulsive gait b. Flail toes postoperatively c. Incidence of hematoma formation with resulting fibrosis d. Destroys the function of the MTPJ's e. Loss of digital stability NOTE* if one excises a large amount of the metatarsal and one is already dealing with short toes (especially the 5th), then syndactylism will aid in achieving some stability of the area distally in the forefoot. This procedure can be an adjunct to panmetatarsal head resection

Metatarsus Adductus 1. Clinical evaluation: a. Adducted forefoot in the transverse plane with the apex of the deformity at LisFranc's joint b. Medial border concave with a deep vertical skin crease c. Hallux widely separated from the 2nd toe d. The lesser digits will be adducted at their bases e. Occasionally the abductor hallucis may be palpably taut 2. Radiographic evaluation: a. Increase in metatarsus adductus angle (greater than 200)

NOTE* Not always accurate as the lesser tarsal bones in the neonate are not measurable as they are radiographically "silent", and in many cases the T-C relationship is abnormal. Therefore It is best to use the calcanealsecond metatarsal angle (normal parameters pending) 3. Indications for surgery a. Failure to respond to conservative treatment b. Residual deformity after treatment of talipes equinovarus c. Newly diagnosed metatarsus adductus deformity 4. Considerations: (see section Pediatrics) a. Age of patient b. Osseous development c. Severity of deformity d. Presence of concomitant deformities e. Extent of malfunction and disability 5. Soft Tissue Surgery: (current procedures will be discussed in detail) a. Heyman, Herndon, and Strong: i. Indications:
for flexible met. adductus which is reducible on manipulation (stress x-ray)
usually children less than 5 years old
deformity present at Lisfranc's joint, without significant bowing present in the proximal portion of the metatarsal bones themselves ii. Procedure:
2 or 3 longitudinal dorsal incisions or transverse incision
release of the dorsal, interossei, and plantar ligaments of the tarsometatarsal joints and intermetatarsal joints
preserve the plantar-lateral ligaments, especially 5th metatarsocuboid articulation and the peroneus brevis tendon
manipulate the foot into abduction
K-wire fixation of the first met-cuneiform joint and 5th met-cuboid joint
release of the naviculocuneiform and intercuneiform joints is rarely needed
consider abductor hallucis release or tenotomy in conjunction with HH&S iii. Precautions:
avoid damage to the 1st metatarsal epiphyseal growth plate (do not confuse this with the met-cuneiform joint)
be careful not to introduce iatrogenic dorsal dislocations at the metcuneiform joints iv. Postop care:
cast for 6-12 weeks
manipulate the foot and recast every 3-4 weeks depending upon the severity
monitor the foot carefully for the development of a flatfoot deformity v. Complications:
dorsal dislocation
degenerative arthritis




damage to the growth plates

b. Thompson procedure (modified): i. Indications:
congenital hallux varus primarily
flexible met. adductus secondarily
hyperactivity of the abductor hallucis ms. ii. Procedure:
medial longitudinal 1st MTPJ skin incision approach
dissection to level of deep fascia over the abductor hallucis muscle
transection of the abductor hallucis tendon with resection of a segment of the tendon and portion of the distal muscle
consider lesser MTPJ release medially if lesser digits are also adducted
release of the medial head of the flexor hallucis brevis if adduction of the hallux is still present iii. Precautions:
do not reduce varus of the hallux without ensuring correction of any adduction deformity of the first metatarsal
place the medial incision over" the 1st MTPJ strategically; if too superior or inferior, may damage the medial neurovascular bundle
avoid the procedure as a primary mode of correction for met. adductus unless clinical findings and x-rays strongly support hyperactivity of the abductor hallucis as the primary etiology iv. Postoperative care:
weightbearing in a surgical shoe for 3-6 weeks
splinting of the hallux and the first ray v. Complications:
hallux abductovalgus
hallux hammertoe (hallux malleus) c. Johnson osteochondrotomy: cartilaginous procedure i. Indications:
met. adductus deformity in children between the ages of 5-8 years (can be younger) ii. Procedure:
3 dorsolongitudinal incisions
closing abductory base wedge osteotomy of the 1st metatarsal
wedge resection of cartilage and bone from the bases of the lesser metatarsals, distal to the proximal articular surface (base is lateral with the apex medial)
fixation of the osteotomies with stainless steel wire, K-wires, or staples iii. Precautions:
avoid damage to the epiphyseal growth plate of the 1st metatarsal
overcorrection/undercorrection of individual ray segments iv. Postoperative care:
non-weightbearing with cast immobilization for 6-8 weeks
serial x-rays to assess healing

6. Osseous Surgery: a. Modified Berman-Gartland procedure: i. Indications:
met. adductus in the child older than 6-8 years
residual deformity following treatment of talipes equinovarus ii. Procedure:
3 dorsolongitudinal incisions
transverse or oblique-type closing abductory wedge osteotomy of the 1st metatarsal
similar type of osteotomies of the lesser metatarsals with the cortical hinge medially
fixation of osteotomies with SS wire, K -wires, staples, AO screws or combinations iii. Precautions:
avoid damage to growth plates of 1st metatarsal
meticulous subperiosteal dissection is critical to avoid heavy callus formation and undesirable synostosis between adjacent metatarsals
preservation of the medial cortical hinge is important to insure stability
careful planning to avoid over/undercorrection iv. Postoperative care:
non-weightbearing cast immobilization 6-8 weeks
convert the cast to posterior splint and start PT
orthotics when patient resumes weightbearing
serial x-rays to assess bone position and healing at 3 weeks , 6 weeks, 12 weeks, 24 weeks and 1 year v. Complications:
over/undercorrection
delayed union/nonunion/pseudoarthrosis
fracture of f cortical hinge
damage to growth plate
elevatus of metatarsals
iatrogenically induced flatfoot deformity b. Lepird procedure: i. Indications:
met. adductus in the child older than 6-8 years
residual talipes equinovarus deformity ii. Procedure:
3 dorsolongitudinal incisions
oblique closing-abductory wedge osteotomy (Juvara type) of the 1st metatarsal with AO/ASIF screw fixation
rotational osteotomy of each lesser metatarsal with AO/ASIF screw fixation (2.7 mm cortical used mostly) perpendicular to the plane of the osteotomy
an oblique closing wedge osteotomy may be used on the 5th metatarsal in place of the rotational type (if preferred)
rotational osteotomies are performed from dorsal-distal to plantar proximal with temporary preservation of the cortical hinge (facilitates fixation). The osteotomy is approximately 45° from the weightbearing surface. The precise

angle will depend on the declination of the metatarsal segment. As the declination of the metatarsal increases, the osteotomy will be more parallel to the weightbearing surface of the foot
area of the cortical hinge preserved is most commonly proximal/plantar
the screws are then removed and the osteotomy is completed
the screws are reinserted, the distal fragments are rotated laterally, and the screws are tightened
the alignment of the foot is assessed; if realignment is necessary the
screw(s) can be loosened and the bone adjusted iii. Postoperative care:
same as Berman-Gartland iv. Complications:
same as Berman-Gartland
if the osteotomy is performed too vertically the rotation of the
osteotomy will be around the longitudinal axis of the metatarsal bone itself, resulting in inversion/eversion of the bone itself v. Advantages: this procedure is amenable to rigid internal fixation and primary bone healing
over/undercorrection can be corrected during surgery
biplanar correction can be achieved
eliminates pin tract infections 7. Ancillary Procedures: a. Equinus Deformity: i. TAL ii. Gastrocnemius recession b. Flatfoot Deformity: i. STJ arthroereisis ii. Evans calcaneal osteotomy iii. Modified Young's tenosuspension/ Modified Kidner procedure arthrodesis/ N-C arthrodesis

Freiberg's Disease Also known as osteochondrosis of the metatarsal head or avascular (aseptic) necrosis of the bone, most commonly affects the 2nd metatarsal 1. Etiology: a. Trauma (or trauma followed by fracture) b. Ischemia c. Prominent plantar metatarsal head with excessive loading with a compromise to the circulation to the subchondral bone d. Often appears after age 13, affecting women 3 times more frequently than men 2. Signs and symptoms: a. Pain in the MPJ (usually dorsally), either sharp, dull, or aching In character b. Edema with increased activity c. Limitation of motion of the involved digit and MPJ d. Palpable irregularities may be present dorsally e. Distal distraction of the toe will cause pain

f. Adjacent MPJ hyperkeratoses may be present as the Involved metatarsal bears less weight 3. X-ray evaluation: a. The initial findings include a joint space widening 3-6 weeks after the onset of symptoms b. This is followed by increased density of subchondral bone c. As the disease progresses, a zone of rarefaction develops surrounded by a sclerotic rim d. With time, the epiphyseal bone weakens and collapses with the formation of spicules and loose bodies e. Flattening of metatarsal head with osteophytic lipping f. Joint narrowing g. Peripheral soft tissue swelling h. Bone margins are sclerotic 4. Treatment: a. Directed toward preventing further damage and displacement of the MPJ (casting and cortisone shots followed by orthoses)) b. Later stages: i. Implant arthroplasty: If symptoms are due to joint arthritis ii. Metatarsal head remodeling (must preserve the alignment of the toeuse splint 3 months postoperatively) iii. Bone grafts (Smillie): To restore the contour of the metatarsal head by inserting a cancellous graft (good for stage 1-3) iv. Rotational osteotomies (Gauthier and Elbaz): Rotates the lower aspect of the metatarsal head dorsally after a section of damaged cartilage has been excised. This allows the plantar cartilage to articulate with the proximal phalanx

NOTE* Dr. Freiberg's only surgical treatment involved removing the loose bodies

5. Classification (by Smillie into 5 stages):

a. Stage 1: Fissure fracture b. Stage 2: Absorption of bone. Central aspect of bone is sinking into the metatarsal head c. Stage 3: Further. progression with projections remaining on either side of the metatarsal head. The plantar articular cartilage remains intact d. Stage 4: Fractures and loose bodies may occur. Plantar cartilage no longer intact e. Stage 5: Flattening of the metatarsal head. Tailor's Bunion 1. Etiology: a. Any uncompensated varus position of the forefoot or rearfoot in a fully pronated foot b. A congenital plantarflexed 5th ray deformity c. A congenital dorsiflexed 5th ray deformity

d. Idiopathic e. Lateral deviation or wide 5th metatatarsal head f. Combined influences 2. Clinical findings: a. Prominence over the 5th metatarsal head with pain b. Hyperkeratosis and erythema over the 5th metatarsal head area c. 5th toe assumes a varus or adducto varus attitude NOTE* Must determine if a splayfoot deformity is present. Evaluate on weight-bearing and x-ray. Radiographically, splayfoot deformity is characterized by an IM angle between the 1st and 2nd metatarsal of greater than 12° and between the 4th and 5th metatarsals of greater than 8°. In association with varus of the 1st metatarsal, the slant of the distal articular surface of the medial cuneiform is more than 105°

3. Radiological findings:-6 types according to the findings a. Rotation of the lateral plantar tubercle into a lateral position b. Increased IM angle (normal 6.47°): People with tailor's bunion have an IM of 8.71 or greater (Fallat and Buckholz) c. Increased lateral deviation angle (normal 2.64°) People with tailor's bunion have a lateral deviation angle of 8.05° (Fallat and Buckholz) d. A large "dumbell-shaped" 5th metatarsal head e. Arthritic changes resulting in exostosis formation at the 5th MPJ f. Any combination of the above conditions, the 1st three being most common 4. Surgical management: 1. Hohmann osteotomy: Single transverse osteotomy at the level of the metatarsal neck with medial displacement of the capitol fragment b. Oblique osteotomy from distal lateral to proximal medial with displacement of the capital fragment proximally and medially (reverse Wilson procedure) c. Modified Mitchell: Step down osteotomy d. Austin type osteotomy: 2 mm of medial transposition e. Mercado osteotomy: Medially based closing wedge osteotomy at the metatarsal neck f. Yancy osteotomy: Midshaft medially based closing wedge osteotomy g. Gerbert et al osteotomy: Proximal diaphyseal closing wedge osteotomy h. Buchbinder osteotomy: DRATO i. McKeever: Partial metatarsal head resection j. Kelikian: Partial metatarsal head resection with syndactylization of the 4th and 5th toes k. Distal oblique osteotomy with intramedullary K-wire fixation

NOTE* Excessive 5th metatarsal head resection results in laxity of the internal cubic content of the joint leading to further varus or adducto varus malalignment of the 5th toe, and more retrograde pressure on the 5th metatarsal head

Splayfoot As this deformity consists of high IM angles for the 1 st and 2nd , and 4th and 5th, surgical repair is focused on reducing the IM angles. This is accomplished via a closing base wedge osteotomy of the 1 st metatarsal with AO fixation, and distal oblique osteotomy of the 5th metatarsal with K-wire fixation.

Brachymetatarsia (Brachymetapody) 1. Etiology: a. Congenital: Premature idiopathic closure of the distal epiphyseal growth plate

NOTE* The congenital pattern has also been associated with neonatal hyperthyroidism, pseudohypoparathyroidism, pseudopseudohypoparathyroidism, malignancy, Down's syndrome, Albright's syndrome, myositis ossificans, Turner's syndrome, sickle-cell anemia, Still's disease, and enchondromatosis b. Traumatic c. Infectious 2. Clinical presentation: a. Symptoms usually appear in adolescence when full growth discrepancy is most apparent b. In the younger patient the only complaint will be the appearance of a shortened or "floating" toe c. The adjacent toes underlap the involved toe d. Calluses under the adjacent metatarsal heads with metatarsalgia e. The amount of associated disability typically depends upon the amount of weight that Is transferred to the adjacent metatarsal heads f. A deep sulcus is present underneath the short metatarsal NOTE* The iatrogenic and traumatically induced types of brachymetatarsia are usually more acute and severe in their presentation 3. Radiological findings: a. Short, underdeveloped metatarsal with deficient bone content b. Osteoporosis of the metatarsal head 4. Operative planning: a. Consider the amount of length needed to restore the normal metatarsal parabola b. Must consider whether to lengthen and plantarflex the involved metatarsal or shorten and dorsiflex the adjacent metatarsals c. Soft tissue mobility and neurovascular status of the involved ray d. Use of a bone graft either autogenous or allogeneic 5. Procedure: a. Bone lengthening procedure (frontal plane "Z" osteotomy) b. Insertion of corticocancellous bone graft c. Extensor tenotomy d. " V" to "Y" skin plasty e. BK NWB cast until osseous healing 6. Complications: a. Risk of neurovascular compromise b. Non-union

c. Absorption or collapse of the graft d. Painful pseudoarthrosis e. Painful limitation of motion at the joint

Skewfoot 1. Description: A metatarsus adductus forefoot-type with a pathological rearfoot valgus component 2. Etiology: a. After serial casting for metatarsus adductus in which the rearfoot was in a pronated position b. Untreated metatarsus adductus which has compensated by excessive subtalar joint pronation c. Congenital metatarsus adductus with associated calcaneovalgus 3. Clinical evaluation: a. The metatarsals are angulated medially b. The base of the 5th metatarsal is prominent c. A large space is noted between the hallux and 2nd toe d. A metatarsus varus may be present e. The digits are abducted in stance f. Talar bulging (ptosis) on weight-bearing with low medial arch g. Abducted midfoot position with internal rotation of the malleoli h. Rearfoot equinus may be present 4. Types: a. Simple skewfoot: An adducted forefoot with an abnormally pronated rearfoot b. Complex skewfoot: An adducted forefoot, abducted midfoot, and abnormally pronated rearfoot

5. Radiological evaluation: a. Increased metatarsus adductus angle (MA angle greater than 21 °) b. Increased cuboid abduction angle (greater than 5°)

6. Indications for surgery: a. Too old for correction by conservative means b. Deformity is increasing despite conservative treatment c. Deformity is obviously not manageable by conservative means d. Deformity is beginning to cause secondary deformities e. Patient is experiencing painful compensatory symptoms f. Patient is accommodating to life style because of related symptoms g. Increased difficulty with standard shoegear 7. Surgical repair: As this Is a complex deformity, multiple procedures must be employed as necessary a. Equinus correction: Gastrocnemius recession or TAL as indicated b. Pes valgoplanus correction: Evans opening calcaneal osteotomy and medial arch tenosuspension. The Evans osteotomy lengthens the lateral column and therefore, realigns the midtarsal joint NOTE* This procedure can unmask a previously unappreciated metatarsus adductus c. Metatarsus adductus correction: Modified Berman-Gartland or Lepird d. Subtalar joint instability and bony adaptation: STJ arthrodesis

Chapter 29: Ankle Conditions Differential Diagnosis of Chronic Ankle Pain Tarsal Tunnel Syndrome Sinus Tarsi Syndrome Peroneal Subluxation Ankle Arthrodesis Lateral Ankle Instability Chronic Lateral Ankle Instability Chronic Medial Ankle Instability Ankle Equinus Malunion and Nonunion of the Malleoli

ANKLE CONDITIONS AND TREATMENT Differential Diagnosis of Chronic Ankle Pain 1. Lateral: a. Peroneal tendon and nerve: i. Peroneal tendon stenosing tenosynovitis ii. Peroneal dislocation iii. Peroneal neuropathy b. Sural nerve injury 2. Dorsolateral a. Sinus tarsi syndrome b. Extensor digitorum brevis (myositis, avulsion) c. Calcaneus anterior process fracture 3. Intracapsular: a. Talar posterior (lateral) process fracture b. Talar dome (osteochondral) defects c. Intra-articular fibrous bands, hypertrophic synovitis, meniscoid bodies 4. Medial: a. Tarsal tunnel syndrome b. Posterior tibial tendon tendonitis, rupture c. Flexor hallucis longus tendonitis d. Os trigonum fracture 5. Other: a. Ligamentous injury (instability) b. Traumatic DJD of STJ or ankle

Tarsal Tunnel Syndrome This is an entrapment or compression neuropathy of the posterior tibial nerve or one of its three branches, the medial and lateral plantar nerves and/or medial calcaneal nerve. 1. Anatomy: Nerve entrapment occurs either In the porta pedis or lacinate ligament a. The flexor retinaculum (lacinate ligament) extends from the medial malleolus to the medial process of the calcaneal tuberosity and the plantar aponeurosis. The deep fibrous septa form four compartments, and converts bony grooves into canals from anterior-medial to posterior lateral: #1 contains tibialis posterior tendon (most superficial), #2 FDL tendon, #3 posterior tibial nerve artery and vein, and #4 FHL tendon. These compartments are unyielding spaces. b. The porta pedis is a canal created by the abductor hallucis muscle belly through which the medial and lateral plantar nerves pass. c. Division of the posterior tibial nerve into its 3 terminal branches may occur proximal to the lacinate ligament, which is most common; within the lacinate

ligament, as described in most texts; or distal to the lacinate ligament, which is rare. d. The medial calcaneal nerve is entirely sensory, and innervates the medial and plantar aspect of the heel. It may arise from either the posterior tibial or lateral plantar nerve. e. The medial plantar nerve gives sensory innervation to the plantar aspect of the hallux, second and third toes, medial half of the fourth toe, and the medial half of the plantar aspect of the foot. It gives motor innervation to the abductor hallucis, flexor digitorum brevis, flexor hallucis brevis, and the first lumbricalis. f. The lateral plantar nerve gives sensory innervation to the plantar lateral half of the fourth toe, plantar aspect of the fifth toe, and plantar lateral aspect of the foot. Initially it sends motor fibers to the quadratus plantae and abductor digiti quinti before dividing in a superficial and deep branch. Superficial branch supplies motor innervation to the flexor digiti quinti brevis and the dorsal and plantar interossei of the fourth intermetatarsal space. The deep branch supplies the remaining intrinsic muscles of the foot. 2. Pathology: Compression of the nerve initially causes only sensory involvement with possibly partial involvement of motor fibers. Continuation of the irritation, ischemia, and compression may lead to secondary hyperactivity of the autonomic nervous system, (manifested by coldness and numbness) from the altered sympathetic activity. Eventual structural changes in the nerve result in the development of muscle wasting, paresis, and objective sensory loss. NOTE* Reflexes are unaffected 3. Etiology: In the many cases no etiology can be found at the time of surgical decompression. a. Dilated posterior tibial veins: can also cause severe night discomfort. b. Trauma: Fracture, dislocation, sprain, post-traumatic edema and fibrosis. c. Systemic disease: Gouty arthritis with urate deposits, rheumatoid arthritis, diabetes mellitus, and myxedema. d. Space occupying lesions: Ganglions, neurofibromas, schwannomas, synovial cysts, etc. e. Hypertrophy of abductor hallucis muscle belly. f. Biomechanical: excessive pronation 4. Clinical Symptoms: Symptoms can be either distal to the metatarsal area, or the medial and lateral heel depending on the branch involved. a. Early: i. Intermittent burning pain, numbness and paresthesias over the medial side of the heel, the toes, and the plantar aspect of the foot. b. Late: i. A paresis that will develop into paralysis of the pedal intrinsic muscles. ii. Proximal radiations of pain may develop in the posterior calf. iii. Pain that is proportional to the amount of activity during the day.

iv. May develop some sensory loss 5. Diagnosis: Not always easy, as the signs are not always definitive a. History of paresthesias b. History of trauma c. History of systemic disease d. Hoffman-Tinel's sign: A tingling in region of the distribution of the involved nerve with light percussion, results in paresthesias distal to the site of percussion. e. Valleix Phenomena: A nerve trunk tenderness above and below the point of compression, with paresthesias proximal and distal to the point of percussion. f. Turk's test: Application of a venous tourniquet to the lower extremity will elicit positive symptoms on the affected side, by producing a venous occlusion. g. Forced eversion of the foot. h. Positive radiographic evidence of previous injury i. Positive lab studies for any specific disease j. EMG's and nerve conduction studies are only useful for late stage disease. Note* EMG may show fibrillation potentials which indicate denervation of muscle. Nerve conduction studies may reveal an increased distal latency. Note* Placement of nerve conduction study surface electrodes are as follows: 1. Proximal stimulation point: distal aspect of popliteal fossa 2. Distal stimulation point: behind the medial malleolus 3. Recording electrode (for conduction of the medial plantar nerve) through the abductor hallucis ms. belly. 4. Recording electrode (for the lateral plantar nerve) through the abductor digiti quinti muscle belly. 6. Treatment: Conservative a. Local blocks: Posterior tibial nerve blocks with steroids b. Unna boot: can be combined with nerve blocks c. Support hose: for varicosities d. Functional orthoses 7. Treatment: Surgical Decompression (positive EMG's and nerve conduction studies mandate surgical decompression). Involves the complete exploration of the tarsal tunnel with release of the flexor retinaculum and its fibrous bands, and resection and ligation of any dilated veins in the area. The surgical technique is as follows: a. A curvilinear incision is made posterior and inferior to the medial malleolus by 1 cm. b. The subcutaneous tissue Is Incised and the superficial- vessels are ligated as necessary. c. The neurovascular structures superior to the retinaculum are identified, preserved, and retracted (especially the medial calcaneal branch). d. The flexor retinaculum is incised and the posterior tibial nerve or its terminal branches are identified and mobilized.

e. The nerve(s) is retracted with a penrose drain. f. The nerve(s) is followed proximally, incising the flexor retinaculum as you go. g. The nerve(s) is followed distally to the point where the medial and lateral plantar nerves pass through the fibrous canals superior to the abductor hallucis ms. belly. h. The abductor hallucis ms. is examined for any abnormality, and any hypertrophy is excised. i. If there are any posterior tibial vein varicosities, they should be ligated. j. The retinaculum is not reapproximated and no deep closure is done. k. The superficial fascia is reapproximated and the skin reapproximated i. Sterile compression dressing and a non-weight-bearing BK cast applied for 3 weeks. 8. Complications: a. Recurrence: due to fibrosis b. Severing the PT artery : if done then tie off and prepare patient for microvascular repair later. c. Severing a nerve d. Tenosynovitis e. Hematoma f. Wound dehiscence

Sinus Tarsi Syndrome 1. Symptoms: A diffuse deep aching pain on the dorso-lateral aspect of the foot over the sinus tarsi. Relief of the discomfort after an injection of anesthesia deep into the sinus tarsi while maintaining superficial sensation is a diagnostic feature. 2. Etiology: a. Post traumatic: i. Inversion ankle sprain ii. Fibular fracture iii. Calcaneal fracture iv. Talar neck fracture NOTE* Arthroscopic studies of the posterior facet showed an absence of the normal synovial recesses in front of the talocalcaneal interosseous ligament. This may indicate synovial hyperplasia, scarring, and/or synovitis b. Biomechanical fault: i. Pes piano valgus (stretching of the cervical ligament) ii. Pes cavus c. Systemic arthritic/metabolic: i. RA ii. Gout iii. Seronegative arthropathies 3. Findings:

a. Subjective: i. Diffuse pain on the lateral side of the foot ii. Feeling of rearfoot instability especially on uneven terrain iii. Dramatic relief of symptoms with an anesthetic block b. Objective: i. Pain reproduced with direct pressure over the sinus tarsi ii. Discomfort with forced inversion and plantarflexion iii. X-rays normal iv. Ankle joint is WNL v. STJ motion painful but not limited vi. MTJ motion mostly pain free vii. Palpation of the intermediate dorsal cutaneous nerve and sural nerve uneventful viii. Palpation of the anterior talofibular and calcaneofibular ligaments is uneventful ix. Elicit pain by digital pressure on both sides of the sinus tarsi simultaneously c. Diagnostic: i. X-rays ii. Diagnostic anesthetic block iii. Arthrography of the posterior facet of the STJ iv. Ankle stress films (to RIO ankle instability) v. 3 phase bone scan to R/O fracture vi. MRI to evaluate the soft tissues, fracture, and infectious disease or arthritic process vii. CT scan to R/O coalitions 4. Differential diagnosis: a. Entrapment neuropathy of the intermediate dorsal cutaneous nerve b. Entrapment neuropathy of the sural nerve c. Damage to the anterior talofibular ligament d. Damage to the calcaneofibular ligament e. Peroneal tenosynovitis f. DJD of the STJ (posterior or middle facet) g. Coalition h. Talar neck fracture i. RA, gout, seronegative arthritides j. Talar dome fractures k. Space-occupying lesion 5. Treatment: a. Conservative: i. Injection of series of local anesthetic/steroid, once every 2 weeks x 3 times ii. NSAID's iii. Tape immobilization iv. BK cast v. Foot orthoses (if biomechanical) vi. Physical therapy b. Surgery: Sinus Tarsi evacuation as follows: 1. Transverse incision over the sinus tarsi 4 cm.

ii. Resection of portions of the extensor retinaculum, a fatty plug, the cervical ligament, and a synovectomy of the adjacent middle and posterior articulations of the STJ for a total distance of 2 cm. iii. Evaluation of the STJ articulations (ATFL, CFL, and peroneals) iv. Postop: Orthopedic shoe for 2 weeks, followed by physical therapy NOTE* if the pain persists despite appropriate care then a STJ fusion or triple arthrodesis is indicated 6. Complications: a. Entrapment neuropathies b. Avascular necrosis c. Subtalar instability

Peroneal Subluxation 1. Clinical presentation: a. Post-traumatic state: Evident after acute injury or later with a history of recent antecedent trauma. The post-traumatic state represents: i. Either a subperiosteal dissection of the superior peroneal retinaculum or ii. An avulsion fracture of the fibula with the adherent superior peroneal retinaculum and deep fascia b. Chronic subluxing state with an insidious progression of pain about the peroneals (not necessarily associated with trauma). This state represents: i. A stretching, redundancy, or pouching of the superior peroneal retinaculum and deep fascia permitting displacement of the peroneal tendons within an intact compartment NOTE* The key difference between the two forms of tendon dislocation is based upon the relationship of the deep fascia and superior peroneal retinaculum to the peroneal tendons and the distal fibula 2. Classification of peroneal injuries (Eckert and Davis):

3. Surgical technique (one type): A reduction of the deep fascial redundancy with insertion Into the fibula a. 8 cm incision placed posterior to the palpable posterior division of the anterior border of the fibula overlying the peroneal compartment b. Incision into the superficial and deep fascia c. Periosteal incision just superior to the posterior division of the anterior border of the fibula d. 5 drill holes into the fibula from the lateral surface to the posterior surface, with the most distal drill hole just overlying the peroneal groove area e. Redundant deep fascia containing the peroneals is plicated f. Sutures inserted (twice around) with the knots below the deep fascia g. BK weight-bearing cast applied for 6 weeks NOTE* A Jones procedure for peroneal stabilization involves detaching a small strip of Achilles tendon proximally, and rerouting it from posterior to anterior through a drill hole in the fibula, then sutured onto itself

Arthrodesis of the Ankle 1. Indications: This procedure is indicated primarily in patients with severe pain and deformity, Including: DJD, RA, talar collapse, failed ankle joint prostheses, infection of the ankle joint, drop foot, invasive tumors, and congenital deformities 2. Preoperative evaluation: a. Patients selected for ankle fusion should be those for whom it will be reasonable to expect a significant reduction in pain and deformity, and an increase in activity b. Evaluate integrity of adjacent joints (STJ and forefoot): To R/O the necessity for a secondary STJ fusion or triple arthrodesis c. Ankle joint is fused at right angle to the leg, and compensation for heel height must then come from plantarflexion at the midtarsal and tarsometatarsal joints d. Stability at the knee joint is important in those patients undergoing a pantalar fusion e. Good bone stock a necessity 3. Surgical approaches: Dictated by the exposure necessary to perform the desired technique a. Transverse anterior approach (Charnley): Severs the extensor tendons and anterior neurovascular bundle b. Midline longitudinal anterior approach: Inadequate visualization of the posterior ankle joint c. Lateral approach via hockey-stick incision: When combined with a fibular osteotomy this approach gives good exposure of the posterior, lateral, and anterior aspects of the ankle d. Medial malleolar approach: When combined with medial malleolar osteotomy gives good exposure of the anteromedial, medial, and posteromedial aspects of the ankle joint NOTE* Procedure of choice for good visualization is the lateral hockeystick incision plus medial incision 4. Surgical technique categories: a. Articular wedging with or without grafting b. Anterior arthrodesis with inlay grafting c. Articular wedging combined with malleolar osteotomy d. Dowel or other subtotal fusions e. Compression arthrodesis 5. The requirements for a successful fusion: a. Complete removal of all the cartilage, fibrous tissue, and any other material that may prevent contact of raw bone to raw bone b. Accurate and close fitting of the fusion surfaces c. Optimal position of the ankle joint

d. Maintenance of the bone apposition in an undisturbed fashion until fusion is completed

Chrenshaw AH (ed): Campbell's Operative Orthopedics, Volume 2, CV. Mosby, St.Louis, 1971, p. 1126, with permission

Lateral Ankle Instability 1. Plantar flexion inversion injury classification (Leach): a. 1st degree: ATFL b. 2nd degree: ATFL, CFL, and capsule c. 3rd degree: ATFL, CFL, PTFL, and capsule 2. Factors which predispose to recurrent ankle sprains: a. Tibial varum b. Ankle varum c. Calcaneal varum d. STJ varus e. Plantarflexed 1st ray f. Rigid forefoot valgus g. Uncompensated equinus h. Muscle imbalance i. Weak peroneals ii. Overactive tibialis anterior and tibialis posterior i. Previous ankle sprains j. Torsional abnormality k. Short leg syndrome

Chronic Lateral Ankle Instability Many surgical procedures have been devised to reconstruct the lateral ligaments, but because of their unique configuration, accurate anatomic reconstruction is nearly impossible.

The above diagram shows the relationship of the anterior talo-fibular ligament to the calcaneoflbular ligament. This relationship is hard to recreate with any surgical procedure. This is why there is limitation of STJ range of motion following stabilization surgery

1. Etiology: a. Post-traumatic ligamentous disruption b. Osteochondral dome fractures c. Degenerative joint disease d. Peroneal subluxation e. Muscular weakness or paralysis f. Talofibular meniscoid g. Generalized ligamentous laxity h. Tibio-fibular diastasis i. Non-union of previous fracture j. Poorly reduced/healed fracture k. Fixed calcaneal varus l. Tibial varum m. Rigid plantarflexed 1st ray

2. Anatomy of the lateral ankle: a. The peroneal muscles terminate in tendons proximal to the ankle joint and a common synovial sheath surrounds the peroneals at this point above the ankle and contains them in a fibro-osseous tunnel b. Posterolaterally, they are contained by the superior peroneal retinaculum and medially by the lateral ankle joint ligaments c. At the level of the ankle joint the peroneus brevis lies anterior and deep against the fibular groove, with the peroneus longus posterior d. As the peroneus brevis tendon passes distally, below the tip of the fibula, it turns anterior, plantar, and lateral, crossing the CFL superficially e. As the peroneus longus passes distally it runs plantar and anteriorly, then passes in an inferior tunnel formed by the inferior peroneal retinaculum at the level of the peroneal tubercle of the calcaneus. The peroneus brevis tendon lies in a similar tunnel superior to the tubercle on the calcaneus f. The ATFL is intracapsular g. The CFL, PTFL, and fibulotalocalcaneal (not always present) are extracapsular NOTE* Due to the angular relationships of the ATFL and the ankle, inversion of the ankle is primarily resisted by the ATFL when the ankle is plantarflexed, and by the CFL when the ankle is dorsiflexed 3. Clinical and radiographic evaluation: a. Common complaints: persistent instability, pain, edema, weakness, and associated insecurity on uneven surfaces b. Radiology: Talar tilt and anterior draw test (need comparison views of the contralateral ankle), arthrography, tenography, and MRI NOTE* Controversy exists over the interpretation of inversion stress views. The anterior draw test is most useful in assessing the ATFL integrity (0-5 mm of anterior displacement is normal, 8-10 mm consistent with a single ligament rupture, 10-1.5 mm consistent with a double ligament rupture, and greater than 15 mm anterior displacement is consistent with a triple ligamentous rupture). These two tests are complementary. They should be done under common peroneal and sural nerve block. A Telos® stress device is used for more of a constant/gradually applied force.

4. Surgical Procedures: Stabilization procedures depend upon the patient's needs a. Delayed primary repair: Suturing of the ATFL/CFL with a non-absorbable suture (0 or 2-0), with NWB BK casting for 6 weeks b. Delayed secondary repairs (utilizing fascial grafts): Are categorized according to the number of ligaments ruptured

i. Single ligament rupture: • Watson-Jones*: This uses the peroneus brevis, which passes through the fibula from posterior to anterior, through the neck of the talus from plantar to dorsal, back through the fibula, from anterior to posterior, and sutured back onto itself. • Lee Procedure (modified Watson-Jones)*: This uses the peroneus brevis tendon, which is then passed through the fibula, from posterior to anterior, and then sutured back onto itself. • Evans*: This utilizes the peroneus brevis through an oblique hole through the fibula sutured back onto. the belly of the peroneus brevis. • Storren • Nilsonne • Pouzet • Haig • Castaing and Meunier • Dockery and Suppan ii. Double ligament rupture: • Elmslie*: Originally described as using the fascia lata and passed through a drill hole in the lower aspect of the fibula, through the calcaneus, back through the same drill hole, and tied onto itself, after passing through the neck of the talus. • Chrisman and Snook*: This uses the split peroneus brevis, which is passed through the fibula from anterior to posterior through a flap in the calcaneus, and is then sutured back to the peroneus brevis tendon. • Stroren • Hambly • Winfield • Gschwend-Francillon iii. Triple ligament rupture: • Spotoff • Rosendahl and Jansen NOTE* A Split Peroneus Brevis Lateral Ankle Stabilization Procedure was developed at Doctor's Hospital, which has proven to have minimal morbidity and to be dependable, especially for the athletic individual The surgical procedure is as follows: a. Patient lying in the lateral position with thigh tourniquet b. Single incision beginning approx. 10-12 cm proximal to the lateral malleolus, extending distally just posterior to the fibular malleolus c. A subperiosteal channel is created from the neck of the talus to the base of the 5th metatarsal, and a wire loop is placed within the channel to facilitate passage of the tendon later d. The peroneal retinaculum is incised just posterior to the fibula, peroneals retracted posteriorly, CFL exposed, and a 4 mm hole is made from the anterior edge of the fibula, angled slightly inferiorly (bone plug is saved)

e. A 6 mm hole is made in the body of the calcaneus adjacent to the insertion of the CFL f. A final subperiosteal channel is made from the posterior fibula to the hole created in the calcaneus, and a wire loop is inserted for later passage of the tendon g. The peroneus brevis tendon is then split (at the start of the muscle belly), tagged with a suture and pulled distally within its tendon sheath to the base of the 5th metatarsal h. The tendon is brought through the 1st subperiosteal channel to the neck of the fibula and passed through from anterior to posterior, sutured to the anterior fibula i. The tendon is brought through its 2nd subperiosteal channel and buried into the hole created in the calcaneus NOTE* Either dacron mesh (Dacron Cooley graft) or Marlex surgical mesh (porous film) can be used as an adjunct in the repair of the lateral ligaments 5. Complications after reconstruction: a. Questions that should be asked to determine problems: i. Is there still a sense of ankle instability and repeated inversion injuries? ii. Is the primary problem chronic pain? If the problem is the former, then reconstruction is the problem.. If the problem is the latter then there might be a secondary lesion b. A varus rearfoot can contribute to reinjuring the ligament and causing a failed reconstruction over time. Also subtalar instability can cause failure (if this is the reason, the patient might. require additional surgery involving the calcaneofibular ligament) c. If pain is the patient's main complaint you must rule out a coexistent lesion such as an osteochondral fracture, tarsal coalition, ankle arthrosis, chronic tear in the peroneal tendon, or postoperative neuroma of the sural nerve

Chronic Medial Ankle Instability Deltoid injuries are rare and occur when the foot is forcibly everted on the leg (see chapter 25: Deltoid Injuries). If an external rotary component is also present, a concomitant fibular fracture with disruption of the T-F syndesmosis will occur. Therefore, when confronted with an unstable medial ankle check for a displaced fibular fracture or T-F diastasis 1. Anatomy: a. Superficial deltoid: Tibiocalcaneal b. Deep deltoid: Anterior tibiotalar, tibionavicular, and posterior tibiotalar 2. Surgical repair: a. Delayed primary repair

Ankle Equinus

Primary neuromuscular spasticity of the posterior muscle group needs to be approached differently than a secondary acquired contracture of the gastrocnemius. The goal of the surgery will also depend on the etiology. The resulting gains in ankle joint dorsiflexion must be weighed against the loss of a grade of muscle strength 1. Patient complaints: a. Low back pain b. Calcaneal apophysitis in children c. Heel spur syndrome in adults d. Arch pain e. Inability to stand for long periods without pain/fatigue f. Juvenile HAV g. Digital contractures 2. Anatomy: a. The gastrocnemius is a muscle spanning two joints, and forming the belly of the calf attached by two heads to the femoral condyles, the medial head being larger b. The gastrocnemius and soleus are innervated by the tibial nerve from S1 and S2 c. The soleus is a broad flat muscle deep to the gastrocnemius, arising from the back of the head and the upper fourth of the posterior surface of the fibula. d. The soleus joins with the gastrocnemius to form the tendo Achilles. At the insertion, the gastrocnemius component usually comprises the lateral side of the superficial surface and a small portion of the lateral aspect of the deep or anterior surface of the tendon e. Superficial to soleus are gastrocnemius and plantaris; deep are flexor digitorum longus, flexor hallucis longus, tibialis posterior, and the posterior tibial vessels and tibial nerve, all separated from soleus by the deep transverse fascia f. The plantaris arises in close association with the lateral head of the gastrocnemius, has a small fusiform belly, that ends in a long slender tendon, which crosses obliquely between gastrocnemius and soleus and runs along the medial border of the tendo Achilles,-to be inserted with it. The plantaris limits dorsiflexion of the ankle g. The tendo Achilles is the thickest and strongest human tendon, surrounded by a paratenon (highly vascular areolar tissue which bathes the tendon in synovial fluid). The tendo Achilles attaches to the posteriorsuperior surface of the calcaneus h. The anatomy of the ankle joint is a modified ginglymus joint because in full plantarflexion, the narrow posterior aspect of the trochlear surface of the talus allows the frontal plane motion of inversion and eversion to occur in the mortise (normal dorsiflexion should be 10-200, normal plantarflexion 30-500) 3. Muscular activity: a. The muscles of the calf are the major plantarflexors, the gastrocnemius also extends the knee, and the soleus steadies the leg on the foot in standing b. Phasic activity of the triceps is from shortly after heel contact until just

before toe-off, all functioning to extend the knee during a normal gait cycle (it does this through the soleus, by slowing the forward progression of the tibia, thus allowing the femur to rotate over it, extending the knee joint) c. The soleus fires at about 15%-20% of the stance phase of gait, slightly ahead of the gastrocnemius 4. Pathomechanics: a. In normal function, with the knee fully extended and the STJ in neutral position, at least 100 of dorsiflexion of the foot to the leg are needed b. When there is pronation past perpendicular, this shortens the origin to insertion distance of the gastrocnemius (the distal aspect of the calcaneus lowers, the midtarsal joint lowers to the ground, the calcaneal inclination angle decreases) and over a period of time there is secondary adaptation, and the amount of dorsiflexion is limited c. With a primary equinus deformity at 50%-60% of midstance, with the hip and knee extended, you cannot get 100 of dorsiflexion and, therefore, the subtalar joint and midtarsal joints pronate to give more dorsiflexion (the oblique axis of the MTJ gives more dorsiflexion than any other joint in the foot as it compensates for the equinus d. This midtarsal joint pronation will also induce the forefoot into a supinatus deformity NOTE* Tendon lengthening should not be done unless the etiology of the equinus is absolutely certain because there will be an automatic loss of 10% of its strength 5. Classification: a. Uncompensated: The STJ remains supinated, therefore, the lack of dorsiflexion at the ankle joint cannot be compensated by abnormal STJ and MTJ pronation (the CP patient) b. Fully compensated: Presents with STJ and MTJ pronation, seen as the hypermobile flatfoot, with the rearfoot maximally everted to the floor and the forefoot everted on the rearfoot (the most severe symptom complex). Creates a spinal lordosis, excessive transverse plane motion about the knee, low back pain, chondromalacia, exaggerated genu valgum, juvenile bunions, and digital contractures c. Partially compensated: The patient has sufficient combination of ankle joint dorsiflexion and dorsiflexion about the oblique axis of the MTJ to permit heel contact during the early portion of the stance phase of gait. However, there is insufficient dorsiflexory motion to permit the leg to angulate 100 to the floor later in stance. Early heel-off is seen during gait. Generally, with a partially compensated equinus, the calcaneus will strike the floor but will evert only minimally, and then will rapidly achieve an early heel-off 6. Etiologies: a. Muscular (gastrocnemius equinus, gastrosoleus equinus)

ii. Congenital shortness: Toe walker for 1 st 6 months iii. Acquired shortness: From casts, high-heeled shoes, excessive pronation b. Osseous i. Osseous equinus: Dorsal exostosis of the talar neck from a flat top talus (can be from treatment of a clubfoot) ii. Pseudoequinus (cavus foot type) 7. Clinical findings:

a. With the patient supine and the knee extended and the STJ in neutral position, the foot is dorsiflexed. If dorsiflexion is less than 100 an ankle equinus to exists b. Silverskiold test is then used to differentiate gastrocnemius equinus from the remaining types of posterior equinus: by flexing the patient's knee to a right angle and again dorsiflexing the patient's foot. If more than 100 of dorsiflexion is found a gastrocnemius equinus still exists. Thus after performing the Silverskiold test there is still limitation of ankle joint dorsiflexion, other sources of ankle joint dorsiflexion remain to be evaluated (either gastrosoleal equinus or osseous equinus). NOTE* To help evaluate osseous equinus a stress dorsiflexion lateral x-ray is used. Comparison is made with the regular lateral view and checked for 2 items: a. The excursion of the tibia over the talus b. How much motion of the tibia and talus is occurring as a unit 8. Surgical procedures: See Chapter 27, Tendon pathology: Tendon Lengthening and Tenotomy a. Distal recession (Volpius and Stoffel) b. Slide lengthening (White) c. Distal recession (Strayer) d. Lengthening the apneurotic tendon of. the gastrocnemius (Baker) e. "Z" plasty (Sgarlato) f. Frontal plane "Z" plasty (McGlamry) g. Modified Baker tongue and groove (Fulp and McGlamry): For nonspastic gastrocnemius equines

Malunion and Nonunion of the Malleoli According to Ramsey and Hamilton, 1 mm of ankle asymmetry causes a 42% decrease in contact area between the talus and the tibia. Therefore, because stress per unit area increases as the total contact area decreases, even mild malunion of the fibula and the ensuing talar instability can result in significant disability 1. Malunion of the fibula: a. Might not become symptomatic for several years, with the patient complaining of a dull ache over the anterior aspect of the ankle which worsens with use, swelling, onset of arthritis, and a limp b. Radiographic criteria used to diagnose a malunion of the lateral malleolus are similar to those used in evaluating acute ankle fracture i. Evaluation of the tibiofibular articulation ii. Fibular length and rotation iii. Ankle mortise symmetry iv. Talar tilt v. Bimalleolar angle: measures the exact amount of fibular shortening (comparison of both ankles is necessary, and a 10 change in the angle corresponds to a 1 mm change in fibula length).

NOTE* Three views should be used (AP), (LAT), and 15° internally rotated mortise view

c. Conservative treatment: i. AFO ii. NSAIDs iii. Injections d. Surgical treatment: When conservative measures fail, reconstruction can be attempted. If that fails. then a fusion can always be done. i. The concurrent presence of a medial malleolar malunion makes reconstruction more difficult. A malleolar malunion has no substantial effect on stability of the ankle and only needs to be corrected if symptomatic or- with a step-off in the weight-bearing joint surface of more than 2 mm. ii. A concomitant malunion of a large posterior malleolar fragment (more than 30% of the joint) usually precludes reconstruction (posterior displacement of the talus, soft tissue scarring, and osteoporosis of the displaced piece make reduction difficult) iii. The fundamentals are that there is a shortened and externally rotated lateral malleolus, with lateral subluxation. The procedure to accomplish correction is as follows: • The fibula must be freed leaving only the collateral ligaments intact • An oblique or transverse osteotomy is made at the level of the malunion and an AO compression device set in the distraction mode (to increase fibular length)

• •

A plate is fixed to the fibula The syndesmosis is held in reduction with a 4.5 mm cortical screw

2. Nonunion of the medial malleoli: a. Occurs more frequently in fractures that are treated with closed reduction b. Surgery for a nonunion should only be considered if the clinical examination, including pain, tenderness at the fracture site, correlates with the radiographic findings c. Nonunion of the medial malleolus can occur anywhere but proximal lesions nearer the weight-bearing aspect of the tibial plafond are more likely to be symptomatic d. If a malunion is present it should be taken down and anatomically reduced with compression screws and a local cancellous bone graft from the metaphysis of the distal tibia e. If the nonunion is in anatomic alignment, it can be left in place with a trough trough created across the nonunion site and packed by a cancellous bone

3. Nonunion of the lateral malleoli: a. Similar approach should be taken as with medial malleolar nonunions, although these are more prone to produce a malunion and instability b. A small, distal, non-united fragment (smaller than 1 cm) should be excised rather than trying to obtain osseous union. The collateral ligaments should be carefully reattached

Chapter 30: Heel Conditions Anatomy of the Heel Radiological Evaluation of the Calcaneus The Heel in Systemic Disease Seronegative Arthritis and Heel Pain Heel Spurs and Heel Spur Syndrome Tumors of the Heel Tarsal Coalitions Sever's Disease Haglund's Deformity Causes of Heel Pain (a summary)

HEEL CONDITIONS Anatomy of the Heel 1. Blood supply:

2. Attachments: a. The plantar calcaneal tuberosity consists of 2 smaller tubercles, the larger, the medial process, and the smaller the lateral process, separated by a sulcus. b. The plantar aponeurosis is made up of a medial, central, and lateral band (the central band being divided into a superficial and a deep plantar fascia). c. The central band is attached to the medial process of the plantar tuberosity, posterior and plantar to the origin of the flexor digitorum brevis. d. The band divides into 5 slips as it approaches the digits (the superficial stratum inserts into the skin of the transverse sulcus separating the digits from the sole, and the deeper stratum divides into two slips which embrace the sides if the flexor tendons and blend with the sheaths of these tendons). e. The abductor hallucis originates from the medal tubercle of the calcaneal tuberosity and plantar aponeurosis and extends along the medial side of the foot until it inserts into the medial side of the proximal phalanx of the hallux. f. The FDB attaches at the medial calcaneal tubercle just superior to the plantar aponeurosis, and extends along the aponeurosis where it sends tendon slips to the 4 lateral digits, with each tendon splitting into 2, allowing the FDL to pass between them on its way to the distal phalanx (these medial and lateral slips insert into the base of the middle phalanx)

g. The abductor digiti minimi originates at the medial and lateral tubercles of the calcaneal tuberosity and plantar aponeurosis and extends along the lateral aspect of the foot to insert into the lateral side of the base of the proximal phalanx of the 5th toe h. The long plantar ligament attaches at the medial and lateral tubercles of the calcaneal tuberosity and extends across the plantar aspect of the calcaneus where it branches into 4 ligamentous slips to the bases of the 4 lesser metatarsals i. Dorsally interconnecting the talus and calcaneus and in reinforcing the functional subtalar joint are the interosseous talocalcaneal ligament (located in the sinus tarsi) and the cervical ligament (located lateral to the sinus tarsi j. Other ligaments include: the lateral, medial, and posterior talocalcaneal ligaments, and the calcaneotibial and calcaneofibular portions of the collateral ligaments of the ankle joint k. The calcaneal dorsal surface has 3 facets, anterior, middle and posterior. The posterior is the largest, separated from the middle by the sulcus calcanel (or sinus tarsi when including the sulcus tali of the talus) 3. Innervation: a. The tibial nerve gives off the medial calcaneal branches that innervates the heel while continuing through the tarsal tunnel, and as it exits the tunnel it divides into the medial and lateral plantar nerves b. The lateral plantar nerve runs along the medial side of the lateral plantar artery where it innervates the quadratus plantae and abductor digiti minimi ms., and then divides into superficial and deep branches. The lateral plantar nerve travels deep to the plantar aponeurosis as it leaves the tibial nerve from the tarsal tunnel to travel distally and laterally and crosses the aponeurosis where it inserts into the calcaneal tuberosity c. The inferior calcaneal nerve branches from the lateral plantar nerve just distal to the bifurcation of the tibial nerve into medial and lateral plantar nerve, and courses between the abductor hallucis ms. and medial head of the quadratus plantae ms., and continues laterally remaining 5.5 cm anterior to the calcaneal tuberosity coursing between the FDB and long plantar ligament. It finally crosses over the lateral head of the quadratus plantae and terminates in the abductor digiti minimi ms.

Radiological Evaluation of the Calcaneus

The Heel in Systemic Disease Many diseases manifest themselves in the heel. These include the following: 1. Rheumatoid arthritis: a. Sources of heel pain in RA have been attributed to plantar and posterior spurring, calcaneal erosions, valgus deformity of the STJ and heel, associated sites of soft tissue inflammation (Achilles tendonitis, plantar myofasciitis, inferior and posterior calcaneal bursitis), or the presence of rheumatoid nodules b. Most commonly affected sites in the heel are the posterior surface near the insertion of the Achilles tendon and the inferior surface near the origin of the

plantar fascia c. Bony changes involve bony proliferation or spurring, erosive changes, sclerosis, and osteoporotic changes NOTE* Rheumatoid arthritis according to a study by Resnick et al, produces erosive bony changes at the posterior/superior surface and the posterior surface of the calcaneus immediately above the site of attachment of the Achilles tendon. It also produces well-developed posterior and plantar spurs at the posterior surface at the site of insertion of the Achilles, and the plantar surface anterior to the site of attachment of the plantar aponeurosis 2. Gout: a. The calcaneus may be affected in gout by pressure erosion from adjacent tophaceous deposits penetrating bone, classically producing wellmarginated bony erosions with sclerotic margins and over-hanging edges b. Mineralization of the calcaneus in gout is unaffected 3. Calcium pyrophosphate dihydrate deposition (CPPD): a. This disorder mimics acute gouty attacks, and rarely affects the calcaneus, however, can affect the talocalcaneonavicular region producing an osteoarthritis profile demonstrating joint space narrowing, and subchondral cyst formation. This is sometimes called chondrocalcinosis. 4. Osteoporosis: a. It is estimated that 30% of bone must be lost before osteoporosis can be identified radiographically b. It has been suggested by numerous authors that the calcaneus be used in the evaluation of osteoporosis by grading changes (as bone mass diminished, there was a reproducible change in the trabecular appearance which was progressive as bone became more porotic) 5. Diffuse idiopathic skeletal hyperostosis (DISH): a. This is recognized as an ossifying diathesis, most commonly encountered in middle-aged males, characterized by areas of hyperostosis at points of attachment of tendon, ligament or fascia to bone (axial spinal symptoms predominate). b. Pedal conditions involve the talus (beaking), heel pain, and plantar and retrocalcaneal spurs. The spurs are large, irregularly shaped, with well defined margins, without reactive sclerosis, periosteal reaction, or erosions producing a noninflammatory appearance (calcification of the plantar fascia may be seen) 6. Diabetes mellitus: a. Periarticular calcifications of the calcaneus b. Calcifications of the long plantar ligament c. Osteophytosis of the calcaneus d. Diabetic osteoarthropathy e. Pathologic fractures

7. Hypertrophic osteoarthropathy: a. Involves the clinical triad of clubbing of the nails, periostitis with new bone formation, and arthritis. Often seen secondary to pulmonary neoplasms or pulmonary suppurative conditions, bowel disorders, heart disorders, thyroid disorders, and other conditions (some genetic) b. It has been reported that the calcaneus has been involved with this disease, manifesting itself with a band of increased density elevated from the lateral aspect of the tuberosity, in the region of the calcaneo-cuboid joint (acute periostitis with subperiosteal new bone formation) 8. Paget's disease of bone (osteitis deformans): a. This condition involves accelerated bone resorption and destruction followed by disorganized repair, leaving an irregular mosaic pattern of well defined mature and immature bone b. The calcaneus has been seen to be involved, with the chief symptom of pain in the heel c. Radiographic demonstration of areas of decreased density with widening, destruction, and disorganization of the calcaneal trabecular pattern amid irregular, patchy, sclerotic areas creating the typical irregular mosaic type pattern 9. Sarcoidosis: a. Is a multisystem, multiorgan disorder of a autoimmune etiology and with associated immunologic abnormalities, typified by the development of noncaseating granulomas in various organs b. Increased observance of HLA B8 antigen c. Sarcoid arthropathy occurs 3-15%, and presents as an acute polyarthritis d. This disease can affect the calcaneus with the symptom of heel pain. Radiographically there can be cortical defects or cyst formation 10. Sickle cell anemia: a. An autosomal dominant disorder characterized by an abnormality in hemoglobin, producing hemolytic crises and a variety of clinical complications related to vascular occlusive phenomena. b. Calcaneal involvement has been reported manifested by aseptic necrosis documented by Tc-99m bone scans (decreased uptake), and an erosive process on the superior surface of the calcaneus (may be pathognomonic for sickle-cell) 11. Acromegaly: a. Occurs secondary to an excessive amount of growth hormone present after epiphyseal closure which results in excessive growth of various body parts, (hands, feet, jaw, internal organs, etc.) b. Clinical there is thickening of the skin (increased heel pad thickness)

Seronegative Arthritis and Heel Pain Patients who do not respond to conservative treatment or present with an atypical picture might cause the clinician to consider some of the less common

causes of heel pain as these. 1. General features of the seronegatives: a. Unlike RA, these disorders have a greater affinity for the spinal and sacroiliac areas, and involve the insertions of tendons and ligaments on bone which produce painful enthesopathies (these are thought to produce the heel pain associated with the seronegatives) b. Increased incidence of HLA B27 NOTE* HLA B27 is thought to be linked to genes that regulate new bone formation 2. Ankylosing spondylitis (Marie Strumpell disease): Peripheral arthritis may be the initial presentation and the heel may be involved. 3. Reiter's Syndrome: Involvement of the enthesis of the calcaneus, presenting with mild, moderate swelling without redness. 4. Psoriatic arthritis 5. Treatment: a. NSAIDs usually work well b. Methotrexate may be used in severe cases of Reiter's syndrome and psoriatic arthritis c. Physical therapy d. Orthoses

Heel Spurs (Heel Spur Syndrome) 1. Etiology: a. Disease processes b. Biomechanical abnormalities (physiologic reaction to constant stress forming new connective tissue which eventually converts to bone) includes all types of feet with an abnormal pronation component and even supinated foot types

NOTE* A heel spur (exostosis) need not be painful; it is only significant that the patient has pain at the anatomic site and that we determine the pain is caused by a mechanical abnormality and not to any other sources of heel pain (heel spur syndrome). Abnormal pull of the plantar calcaneal periosteum at the tuberosity causes separation of periosteum from bone and an inflammatory reaction (hence pain). The pulled periosteum fills in forming the spur. Hence, it is an adaptive response. No pull=no separation=no inflammation=no pain. Once a spur forms and there is no new pull, etc., there is no pain despite the presence of a spur (barring fractures, etc.). Pronation and supination place a twisting pull on the calcaneal periosteum at the tubercles, hence spurs form.

2. Diagnosis: a. Radiographically b. Palpation with execution of the Hubscher maneuver over the medial band of the plantar fascia 3. Treatment: Heel spurs should only be treated if symptomatic a. Orthoses b. Oral anti-inflammatory medications and steroid injections c. Shoe accomodations d. Strappings e. Physical therapy f. Surgery: i. Surgical approaches: • Medial horizontal incision (DuVries) • Posterior horizontal "U" incision (Griffith) • Transverse plantar incision (Michetti) • Longitudinal plantar incision • Lateral horizontal incision • Minimal incision approach (Mercado) • Endoscopic Plantar Fasciotomy (Barrett and Day) ii. Whatever the approach, careful dissection is mandatory to avoid transection of the lateral plantar nerve iii. Other complications • Wound dehiscence • Hematoma • Phlebitis • Infection • Fracture

NOTE* Endoscopic Plantar Fasciotomy by Barrett and Day has been reported to give excellent results via the transection of a portion of the plantar fascia. The bony exostosis is left intact. This procedure utilizes two small incisions with a slotted canula passed just inferiorly to the fascia. Through one end of this canula a camera (scope) is passed and through the other end a small knife is passed.

Tumors of the Heel As the largest bone in the foot, the calcaneus has many anatomic features which make it unique and potentially more prone to develop tumors and tumorlike conditions. Internally, it has an abundant vascular supply, which may explain the increased incidence of metastatic malignant lesions. Also the large cancellous component may sequester these tumors for long periods of time before they become symptomatic. Externally, the extensive surface area of the calcaneus and the numerous points of attachment of intrinsic and extrinsic muscles, tendons, and ligaments lend themselves to a vast array of tumors. Pain has been shown to be the primary complaint of patients presenting with tumors. 1. Pseudotumors: a. Inclusion cysts: in the soft tissues b. Traumatic neuromas: in the soft tissues c. Ganglionic cysts: in the soft tissue or bone d. Keloids: in soft tissues e. Foreign body granulomas: in soft tissues f. Piezogenic papules (protrusions of adipose tissue surrounding the heel) g. Rheumatoid nodules: in soft tissues 2. Skin and soft tissue tumors: a. Verrucae b. Molluscum contagiosum c. Keratoacanthoma d. Squamous cell carcinoma e. Plantar fibromatosis (Ledderhose's or Dupuytren's disease) f. Lipomas g. Eccrine poroma h. Leiomyoma i. Glomus tumor j. Malignant melanoma k. Kaposi's sarcoma l. Many others 3. Bone tumors: a. Solitary bone cyst: Most frequently seen bone lesion other than the heel spur, found in the anteroinferior and lateral regions of the calcaneus. Can be found as a result of pathologic fracture of the thin wall (“Fallen Fragment” sign on x-ray)

b. Ewing's sarcoma and other sarcomas c. Osteoid osteoma d. Intraosseous lipoma e. Giant cell tumor of bone

f. Multiple myeloma: the most common primary bone malignancy g. Aneurysmal bone cyst h. Chondroblastoma i. Osteoblastoma

j. Chondromyxoid fibroma k. Hemangioma l. Osteogenic sarcoma Tarsal Coalitions It is usually a congenital anomaly that represents a failure of differentiation and segmentation of primitive mesenchyme, which results in failure of joint formation. These coalitions cause a limitation or absence of motion of the involved joint and can affect the entire foot in gait 1. Classifications: a. Intra-articular vs. extra-articular (usually accessory bone fusion) b. Fibrous, cartilaginous, or osseous c. Developmental pattern d. Congenital or acquired (acquired cases include trauma, previous surgery, infection, RA, and OA). 2. Types: a. Talocalcaneal (fuses between the ages of 12-16): Talar beaking; broadening lateral talar process; middle subtalar joint not visualized; asymmetric anterior subtalar joint; "ball and socket" ankle joint. Usually the middle facet. b. Calcaneonavicular (fuses between the ages of 8-12): Close approximation of the calcaneus and navicular; irregularity and indistinctness of cortical surfaces; hypoplastic head of the talus c. Talonavicular d. Calcaneocuboid (rare) 3. Pathognomonic Signs and Symptoms: a. Peroneal Spasticity (peroneal spastic flatfoot) b. Talonavicular beaking c. Halo sign (in cases of T-C coalition, occasionally this sign can be observed on the lateral projection, seen around the sinus tarsi) d. Broadening and flattening of the lateral process of the talus e. Decrease in ROM of the subtalar joint f. Sudden onset of pain after excessive activity g. Children begin to complain between the ages of 12-15 (with T-C bars) h. Sinus tarsi syndrome i. If an osseous bar is present then there will be no motion at the STJ and no pain over the bar but pain can be present distally j. Adults may be asymptomatic but show degenerative changes 4. Radiological Diagnosis: a. Normal Harris Beath projections: the posterior and middle facets should be present and parallel to each other. With a subtalar coalition the facets are no longer parallel. b. CT scanning provides the best diagnostic tool (it is the gold standard) c. Calcaneonavicular coalitions can best be seen on the 45° medial oblique xray d. Talonavicular and calcaneocuboid coalitions can be seen on the lateral view 5. Treatment: Surgery

a. Calcaneonavicular coalition: i. A modified Oilier approach ii. Origin of the extensor digitorum brevis muscle belly is detached proximally and reflected distally (bar now exposed) iii. An osteotome or saw is used to resect the osseous segment (at least 1 cm of bone is removed) iv. The EDB belly is now placed Into the defect created and then sutured to the plantar medial aspect of the foot using Keith needles, nonabsorbable suture, and button fixation v. The wound is closed in layers vi. A BK cast is applied for 4 weeks

NOTE* The calcaneonavicular bar resection is contraindicated in the presence of degenerative changes In the talonavicular joint with accompanying talar beaking, with complete ossification of the bar, and when there is a second coalition between the talus and calcaneus. If this procedure fails, a triple arthrodesis may be indicated to relieve the patient's symptoms

b.

Talocalcaneal coalition: i. Conservative therapy 1 st since most of these are asymptomatic and when symptomatic respond to conservative care. • BK walking casts for 3-6 weeks • Injection into the sinus tarsi with steroids • Orthoses ii. Surgery (resection of the bar vs. triple arthrodesis) •Medial Incision for resection of middle facet coalition, with the incision starting just behind the medial malleolus and following the top of the calcaneocuboid joint • The posterior tibial and FDL are retracted superiorly; the FHL and

neurovascular bundle are retracted inferiorly • K-wires are used to locate the joint • A rotary drill with a burr is used to resect the coalition • If successful there will be an immediate increase in motion c. Associated Conditions: (Tarsal coalitions have been reported to be associated with the following) i. Phocomelia and hemimelia ii. Nievergelt-Pearlman syndrome iii. Arthrogryposis multiplex congenita

Sever's Disease Sever's disease was first described by Haglund who noted irregularities of the calcaneal apophysitis, similar to those observed in osteochondrosis of the tibial tuberosity. It is the only bone in the body whose epiphysis assumes the entire weight before it is ossified 1. Secondary ossification: a. First appears in females (ages 4-6) and later in males (ages 7-8) b. It can be divided into a bipartite or tripartite apophysis c. Fusion takes place as early a 12 years old in females and 15 years old in males 2. Etiology: a. Tension from the Achilles tendon and plantar fascia (equinus) b. Acute and chronic trauma c. Infection d. Embolism e. Stress fracture f. Obesity g. Congenital and hereditary factors h. Endocrine disturbances i. Diet disturbances 3. Symptoms: a. Increased pain with activity especially sports b. Demonstrable pain when the posterior aspect of the heel is squeezed from side to side when direct pressure is exerted on the lower one-third of the posterior calcaneus 4. Treatment: Always conservative a. Rest and cessation of sports b. Heel lifts c. BK cast in resistant cases d. Follow-up with an orthoses e. Stretching excercises (NOTE* The symptoms will resolve when the apophysis fuses

Haglund's Deformity Haglund's syndrome, a common cause of pain in the posterior heel, consists of a painful swelling of the local soft tissues with or without the prominence of the calcaneal. bursal projection. 1. Clinical presentation: It is a chronic, sometimes painful condition, characterized clinically by a tender swelling in the region of the Achilles tendon near its insertion and radiographically by an osseous proturberance at the superio-posterior aspect of the calcaneus 2. Radiographic analysis: a. Fowler-Phillip angle: 44°-69° is normal (>75° is pathologic) NOTE* Since the calcaneal inclination angle can influence the usefulness of the Fowler-Phillip angle, the C-I angle should, therefore, be taken into account (see the following diagram)

b. Using the following diagram is more accurate to represent this disorder 3. Treatment: a. Conservative: Removing pressure either with a heel lift or orthoses b. Surgical: i. Resection of the posteriosuperior border of the calcaneus and bursa ii. Wedge (osteotomy with the base dorsally) is removed from the proximal half of the calcaneus posteriorly to the posterior articular facet (the vertical cuts to be two-thirds the height of the calcaneus, but through and through from medial to lateral) NOTE* The incision most commonly employed for both procedures is a lateral para-Achilles tendon approach with the incision being linear, lazy "L", or reversed "J" shaped

Causes of Heel Pain (a summary) 1. Inflammatory: a. Juvenile RA b. Rheumatoid arthritis c. Ankylosing spondylitis d. Reiter's syndrome e. Gout 2. Metabolic: a. Migratory osteoporosis b. Osteomalacia 3. Degenerative: a. Osteoarthritis b. Atrophy of fat pad 4. Nerve entrapment: a. Tarsal tunnel syndrome b. Entrapment of the medial calcaneal branch of the PT nerve

c. Entrapment of the nerve to the abductor digiti quinti 5. Traumatic: a. Calcaneal fractures b. Calcaneal malunions c. Traumatic arthritis d. Rupture of the fibrous septae of the fat pad e. Puncture of the fat pad 6. Overuse syndromes: a. Plantar fasciitis b. Stenosing tenosynovitis of the FDL and FHL c. Calcaneal apophysitis d. Subcalcaneal bursitis e. Periostitis f. Calcaneal stress fractures g. Achilles tendonitis h. Haglund's deformity 7. Infectious: a. Osteomyelitis 8. Other: a. Tumors

Chapter 31: Amputations General Surgical Technique Digital Amputations MPJ Amputations Transmetatarsal Amputations Tarsometatarsal Amputations (Lisfranc's) Midfoot Amputations (Chopart's) Amputation of the Ankle (Syme's, Boyd, Pirogoff) Below Knee Amputation

AMPUTATIONS Amputation that includes disarticulation is an ancient surgical procedure, with techniques that have evolved over the centuries. In the last 20 years research and advances in surgical technique have led to a more scientific approach, so that the indications are more exact, and the level of amputation is more distal. The combined approach of vascular surgeon, podiatrist, and plastic surgeon have helped prevent major amputations, or allowed amputations to be performed more distally on the extremity, resulting in less morbidity and lower mortality.

General Surgical Technique 1. Before surgery the general condition of the patient must be stabilized (control of infection, blood sugar, hydration, etc.) 2. Surgical handling of skin must be meticulous 3. A tourniquet is used except in the presence of vascular disease, and the limb is exanguinated if no infection or tumor is present 4. Flaps should be planned to provide sensate skin over the stump 5. The scar must not adhere to the underlying bone 6. Blood vessels should be carefully ligated and nerves divided as proximally as possible under gentle traction to allow them to retract (these divided nerves should not lie close to the bone) 7. The bone end should be rounded and beveled appropriately 8. Drainage of the stump is mandatory 9. If infection is present, and the viability of the tissues is in question, the wound should be left open

Digital Amputations 1. Indications: a. In gangrene of the toes (need adequate proximal arterial flow) b. Malignant or large, deforming, benign tumors of the digits 2. Effects of digital amputation: a. Amputation of all the toes allows the patient to have a normal gait while walking slowly b. Amputation of the 2nd toe alone results in the hallux going into a valgus position c. Amputation of the hallux only does not alter gait when the patient is walking slowly but causes a limp with a quick walk because of loss of push-off 3. Procedure: a. Short dorsal flap at the level of the bone resection and a long plantar flap can then be reflected over the stump

b. The tendons and nerves should be sectioned after gentle traction to allow them to retract c. Round the bone end to prevent a distal keratoma

MPJ Amputations 1. Indications: a. Severe trauma b. Gangrene 2. Procedure: a. A long posterior flap should be used and the dorsal incision made approximately 1 cm distal to the MPJ b. Specifically in the 1st ray, the flexor and extensor tendons and intrinsic muscles should be sutured over the metatarsal head to prevent retraction of the sesamoids to stabilize the 1 st ray (groove the met head to hold the tendons) c. If the sesamoids are not present the prominence on the underside of the 1st metatarsal head should be removed d. After the articular cartilage of the 1st metatarsal is removed, the metatarsal is beveled medially to provide better shape to the final amputation stump e. Also the lateral third of the 5th metatarsal head should be removed with this disarticulation f. If there is a sub-metatarsal callus or ulceration present, a plantar condylectomy should be performed

Transmetatarsal Amputations 1. Indications: a. Ischemia b. Gangrene c. Osteomyelitis d. Frostbite e. Trauma 2. Procedure: a. Can be single ray resection for the treatment of infection, and is most successful in the 1 st and 5th ray b. A racket incision with a dorsal limb c. The metatarsals should be sectioned at the level of the dorsal skin incision, in a line curving proximally from the medial side d. Careful attention should be given to the digital nerves, and must be seen to retract or a painful "stump" neuroma can develop e. The plantar surface of the metatarsals should be beveled to allow better weight distribution

1. Complications: This procedure has fallen into disfavor because muscle imbalance resulted in severe equinus deformity. A tendo Achilles lengthening and reattachment of the extensor tendons is recommended to prevent this

2. Procedure: Reattachment of the extensors should be considered. The base of the second metatarsal should be left in place in line with the medial and lateral cuboid joints

1. Complications: This amputation has a greater tendency to result in an equinus deformity because of loss of the insertion of the tibialis anterior tendon and toe dorsiflexors 2. Procedure: The tibialis anterior tendon must be dissected free as distally as possible and anchored through or around the neck of the talus. A tendo Achilles lengthening is a useful adjunct. The intrinsic muscle bellies can be used to cover the distal stump

Amputation at the Ankle (Syme's, Boyd, Pirogoff) 1. Syme's amputation: a. Indications: A Syme's through-ankle amputation is indicated in some congenital deformities, tumors, and management of the diabetic foot. Protective sensation to the heel pad must be present because this is the end stump. The heel pad must be stable and adhere to the the end of the tibia to prevent migration b. Procedure: The skin is 1st marked 1 cm below the lateral malleolus and 2 cm below the medial malleolus. These marks are joined by a horizontal skin incision. A vertical skin incision is then made to joint these points. The incisions are deepened cutting structures to expose the calcaneus and the neck of the talus. After the anterior capsule of the ankle joint is sectioned, the foot is forcibly plantarflexed and the talus pulled forward and downward. The collaterals are sectioned. The Achilles once exposed is divided near its insertion

near the calcaneus. The calcaneus is dissected free from the soft tissues. A transverse saw cut is made through the lower end of the tibia and lateral malleolus. The anterior tibial, posterior tibial and greater saphenous are ligated. The calcaneal nerve branch of the posterior tibial nerve must be preserved

2. Boyd amputation: Part of the calcaneus is retained and fused to the lower end of the tibia 3. Pirogoff amputation: A technique based on rotation of the calcaneus 90° and a fusion of the calcaneus to the lower end of the tibia

Below Knee Amputation 1. Indications: a. Vascular disease b. Trauma c. Tumor d. Diabetes complications e. Infection

2. Procedure: Suitable flaps should be planned. The stump should measure between 12.5 cm-17.5 cm depending upon body height. The anterior surface of the tibia should be beveled, and the fibula should be cut 3 cm proximal to this

Chapter 32: Biomechanics Normal Values Criteria of Normalcy in the Lower Extremity Adult Biomechanical Examination Common Structural Variations Planes of Motion Axes of Joint Motion Angular and Axial Deformities Anatomy of Gait: Activity of Muscles Observation of Gait Subtalar Joint Measurements Subtalar Joint Function Midtarsal Joint Function

BIOMECHANICS Normal Values 1. Quick reference chart of normal biomechanical findings: Part Thigh/Femur/Hip (frontal plane)

Birth Position Angle of head and neck of femur=150° (angle of Inclination)

Adult Position At age 6 years=125°

At age 6 years=0 Externally rotated 60° At age 6 years=10° Femoral torsion (angle declination)=30° Past puberty=100° Total range of motion=150° Knee (Birth) (1&1/2-3yr) (3-6yr) (7-puberty) (puberty-18) (over 18) (over 60) Genu Varum Straight Genu valgum Straight Genu valgum Straight G. valgum Genu Recurvatum=5-10° At age 6 years =0° Externally rotated=30° At age 6 years=0° Frontal plane rotation=5-10° At age 6 years=0-5° Transverse plane rotation=5-15° At age 6 years=0-5° Leg/Tibia Varum(approx. 15°) At age 18 years=0-2° varum Tibial torsion at birth=0° 1 yr=6°, 2-3 yr=10-15°, 5-6 yr=18-23° Malleolar torsion at birth=0° 5-6 yr=13-18° Rearfoot At birth= 10° varus approx. At 6 years=2-5° varus Talocalcaneal angle=30-50° At 6 yrs=25-30° Calcaneal inclination angle=approx. 14° At 6 yrs=20° approx. Talar declination angle=approx. 30° At 6 yrs=21° approx. Calcaneal stance @ 1 yr=5-10° 5 yr=3-8° 8 yr=<2° external rot. Dorsiflexion=45° approx. After age 18=10V min Forefoot Varus 10-15° (birth) At age 6=0-2° varus Metatarsus adductus=15-35° (birth) Adult=15-22° (transverse plane)

Criteria of Normalcy in the Lower Extremity 1. Nonwelghtbearing: a. Malleolar torsion should be 13°-18° externally rotated b. Ankle joint dorsiflexion should be at least 100 with the knee extended c. Ankle joint plantarflexion should be at least 20° d. Total STJ ROM should be 30° (with 20° of inversion and 10° of eversion) e. When the STJ is in neutral position, the calcaneal bisection should be parallel to the bisection of the lower 1/3 of the leg and perpendicular to the supporting surface f. When the MTJ is maximally pronated and locked the forefoot should be perpendicular to the calcaneal bisection and parallel to the supporting surface and the knee on the frontal plane with the hip neutral at 0° g. There should be equal excursion dorsally and plantarly (5mm) of the 1st ray from a level equal with the 2nd metatarsal when the STJ is in its neutral position and MTJ maximally pronated h. The 5th ray should have equal excursion dorsally and plantarly from a level equal with the central 3 metatarsals when the STJ is in its neutral position and MTJ maximally pronated 2. Weightbearing: a. The distal 1 /3 of the leg should be vertical b. The knee, ankle, and STJ should lie in transverse planes parallel to the supporting surfaces c. The STJ should rest in its neutral position

d. A bisection of the posterior surface of the calcaneus should be vertical e. The MTJ should be locked in a maximally pronated position about both its axes f. The plantar plane of the forefoot and rearfoot should be parallel to each other and to the supporting surface g. The central 3 metatarsals should be completely dorsiflexed and describe a plane parallel to the supporting surface h. The 1st and 5th metatarsals should describe a common transverse plane with the central 3 metatarsals

Adult Biomechanical Examination 1. Non-weightbearing assessment: a. Ankle dorsiflexion: i. Taken with the patient supine ii. The minimum ankle joint dorsiflexion that is necessary for normal ambulation is 10° with the knee extended. iii. Dorsiflexion is also measured with the knee flexed NOTE* If the amount of dorsiflexion is less than or equal to 100 whether the knee is extended or flexed, then there is an osseus or soleus equinus; if the amount of dorsiflexion is decreased only with extention, then there is a gastrocnemius equinus b. Subtalar joint ROM: to calculate neutral position i. The posterior calcaneus is bisected as is the posterior /distal 1 /3 of the leg ii. The foot is dorsiflexed to resistance, the MTJ is pronated and locked against the rearfoot, and the rearfoot is supinated maximally and pronated maximally. The total ROM is measured with a goniometer (or tractograph) placed parallel to the bisection of the lower 1/3 of the leg iii. The STJ neutral position is defined as that point that divides the medial 2/3 of motion from the lateral 1/3 of motion NOTE* Calculated neutral position= eversion - total ROM-3 For example: From an examination there is revealed to be: 20° inversion + 10° eversion = 30° total ROM. So following the formula from above: Neutral position= eversion (100)- TROM-3 (100)= 0 ° A positive number means a valgus or neutral position, while a negative number means a varus or neutral position iv. The minimal STJ ROM is 8-12° for normal ambulation c. Midtarsal (forefoot): i. The foot is held by the 5th metatarsal and dorsiflexed to resistance and then slowly everted until the STJ reaches neutral position ii. The plantar plane of the rearfoot should be perpendicular to the calcaneal bisector

d. First ray: i. Dorsiflex the foot to. resistance and bring the STJ into its neutral position, stabilize the 2nd-5th metatarsal heads and grasp the 1st metatarsal head and move it in a dorsal to plantar direction to resistance (this distance should be about 5 mm or 100 to either side of its resting position and its resting position should lie on the same transverse plane as the lesser metatarsals) e. Malleolar torsion: i. Reference marks are placed on the malleoli, the knee placed on the frontal plane, and a measurement made with a gravity goniometer ii. Normal malleolar torsion is 13-18° externally rotated f. Hip motion (transverse plane): internal and external rotation of the femur i. The hip joint functions around its neutral position, in a transverse plane, with the femur rotating the same number of degrees from a neutral position (same with the hip flexed and extended). Total range of internal and external rotation must be equal to be considered normal ii. Mark the patella or the femoral condyles and measure internal and external rotation with a goniometer iii. A normal hip rotates 45° internally and 45° externally from a zero degree starting point. This results in a total ROM of 90° and a neutral position of zero (from the neutral position, the hip rotates 45° in each direction) NOTE* Other examples of hip ROM: a. Internal rotation = 55° external rotation= 35° Total ROM= 90° 90-2= 45°, 55°(int)-45= 10° therefore, neutral position= 100 internal (from neutral position, the hip rotates 45° in each direction) b. Internal rotation=10° external rotation= 40° Total ROM= 50°, 50-2=25° 10°(int)- 25°=-15° therefore, neutral position= 15° external (from neutral position, the hip rotates 25° in each direction)

NOTE* When there is a variance in the degree of neutral position between the flexed and extended hip position, this indicates soft tissue abnormality limiting hip rotation. This abnormality is called internal or External Femoral Rotation Example of a 15° internal femoral position: Internal rotation with hip extended= 45° external rotation with the hip extended= 15°, total ROM=60° therefore, neutral position with the hip extended=15° internal Internal rotation with the hip flexed=45° external rotation with the hip flexed=45°, total ROM=90° therefore neutral position with the hip flexed=0

NOTE* Lack of symmetry in total ROM between the flexed and extended positions results in asymmetry of the neutral position measurement. This indicates soft tissue abnormality at the hip. 2. Weight-bearing assessment: a. Angle and base of gait: i. The angle and base of gait are necessary to measure NCSP, RCSP and tibial varum. This allows for standardization and reproducibility of values ii. The angle of gait is the number of degrees that the foot is deviated from the line of progression of gait (mid-sagittal plane of the body). Normally the foot is between 7°-10° abducted from the line of progression iii. The base of gait is defined as the space between the malleoli during midstance (normally 1 & 1 /2 inches) b. Neutral calcaneal stance position (NCSP): i. Defined as the angular relationship between the calcaneus and the ground with the STJ in its neutral position and the patient standing in the angle and base of gait ii. The calcaneus is bisected, the foot is placed in STJ neutral position, and the angular relationship between the calcaneus and (perpendicular to) the ground is assessed c. Resting or relaxed calcaneal stance position (RCSP): This is measured with the patient standing in the angle and base of gait with the STJ in a relaxed position. A measurement is taken of the number of degrees the calcaneal bisector deviates from perpendicular with the ground d. Tibial varum: Measured by placing the goniometer on the bisection of the lower 1 /3 of the leg, with the feet in angle and base of gait, and the foot placed in the NCSP e. Gait evaluation: Things to look for i. What is the position of the calcaneus at heel strike? ii. Does the foot pronate excessively? iii. What is the position of the calcaneus and foot at midstance? iv. Is the heel lifting at the proper time? v. In propulsion: • Is it vigorous and active? • Does the hallux participate? • Does the foot roll medially? • Is there a plantarflexion of the ankle? vi. Is the knee joint on the frontal plane at heel strike, internally deviated, or externally deviated? vii. Does the knee joint flex and extend normally or not? viii. Does the pelvis function around the transverse plane or tilt excessively to one side? ix. Does the patient lead with one side excessively?

x. Do the arms swing symmetrically? xi. Are the trunk and head in the sagittal plane?

Common Structural Variations: Signs and Symptoms 1. Rearfoot varus: A condition in which the calcaneus is inverted relative to the ground with the STJ in its neutral position. Symptoms: a. Callus, plantar 4th and 5th metatarsal heads b. Tailors bunion c. Haglund's deformity d. Inversion ankle sprains e. Adductovarus 4th and 5th hammertoes f. Mild HAV deformity NOTE* With rearfoot varus the changes during gait are as follows: The knee would function fully extended both at heel contact and during midstance. The leg may be somewhat internally rotated at heel contact, and some internal rotation would occur if STJ motion were available from this point. During the latter half of stance phase normal external rotation of the leg occurs. Position of the heel at contact would be inverted. If the rearfoot varus is not fully compensated, the heel remains in an inverted position. The STJ is normally supinated at heel contact NOTE* Rearfoot varus is not a major pronator. It only allows pronation until the heel is vertical 2. Rearfoot valgus: A condition in which the calcaneus is everted relative to the ground with the STJ in its neutral position. Symptoms: a. Callus, plantar 2nd metatarsal head (occasionally) b. Fatigue muscle of foot and leg c. Arch pain d. HAV deformity 3. Forefoot varus: A structural abnormality in which the plantar plane of the forefoot is inverted relative to the supporting surface and a vertical bisection of the posterior surface of the calcaneus when the STJ is in its neutral position and the MTJ is maximally pronated and locked (rearfoot is normal). Symptoms: a. Callus, plantar 2nd, 4th, and/or 5th metatarsal heads b. Muscle fatigue in foot and leg c. Tailor's bunion d. AdductovaruS 4th and 5th hammertoes e. HAV deformity f. Plantar fascitis/heel spur syndrome

NOTE* With forefoot varus the changes to the gait cycle are as follows: During gait the individual with compensated forefoot varus functions with the knee internally rotating during forefoot loading (contact). The external rotation of the knee that occurs later in stance phase is decreased. There may be some reduction in the amount of flexion of the knee during stance phase because of the pronated position of the foot. The knee would be fully extended at heel contact and midstance. Following heel contact, normal ankle joint plantarflexion occurs with smooth contact of the forefoot. At heel contact the calcaneus is inverted. The heel everts during the stance phase of gait as the forefoot loads. The STJ will be in a pronated position through the rest of the stance phase of gait 4. Forefoot valgus (plantarflexed 1st ray with compensation by MTJ longitudinal axis supination): A structural abnormality in which the plantar plane. of the forefoot is everted relative to the supporting surface and the posterior bisection of the rearfoot when the STJ is in its neutral position and the forefoot is maximally pronated and locked about both MTJ axes (the rearfoot is normal). Symptoms: a. Callus, plantar to 1st and 5th metatarsal heads b. Tibial sesamoiditis c. Muscle fatigue in foot and leg d. Flexion contractures of the lesser digits e. Lateral knee strain 5. Forefoot valgus (plantarflexed 1st ray with compensation by supination of the STJ and MTJ longitudinal and oblique axes): Symptoms a. Callus, plantar to the 1st and 5th metatarsal heads b. Tibial sesamoiditis c. Flexion contraction of the lesser digits d. Lateral knee strain e. Inversion ankle sprains f. Haglund's deformity g. Intoe gait seen in children 6. Metatarsus primus elevatus: A structural abnormality in which the 1st ray has a resting position above the plane of the lesser metatarsals. Symptoms: a. Callus, plantar 2nd metatarsal and hallux IP joint b. Fatigue of muscles of the foot and leg c. Dorsal bunion d. Hallux limitus/rigidus 7. Equinus deformity (adults): Symptoms: a. Corn, 5th toe b. Adductovarus deformities of the 4th and 5th toy c. Fatigue of the muscles of the foot and leg d. HAV deformity e. Plantar fasciitis/heel spur syndrome

f. Neuroma symptoms g. Contracture of all the digits (extensor substitution) NOTE* The gait variations seen are as follows: The compensatory changes for equinus are an early heel-off with the knee slightly flexed throughout the stance phase of gait. The knee will be somewhat flexed at heel contact, the flexion might increase during midstance, but it never fully extends at heel lift. As the leg swings forward, it actually becomes hyperextended relative to the femur and then begins to flex, and is flexed by the time the heel contacts the ground. Rather than being an actual compensatory mechanism for equinus, this seems to protect the knee from abnormal stress in a fully extended position. In severe equinus the knee may go into hyperextention during the stance phase of gait (back-knee function). The ankle will be at 90° at heel contact unless the equinus is severe. Following foot flat, the ankle will then dons flex to the limit of its ROM, at which time heel-off will occur (the earlier the heel lift, the sooner the load to the forefoot, the more stress induced symptomatology there is. The STJ will typically be neutral or slightly inverted at heel contact. 8. Forefoot supinatus: A relatively fixed supinated position of the forefoot relative to the rearfoot with the STJ in its neutral position and the forefoot maximally pronated and locked about both MTJ axes, caused by soft tissue adaptation. The MTJ ROM is typically decreased secondary to soft tissue contracture

Planes of Motion There are three planes of motion in the body, one perpendicular to the other two, corresponding to the three dimensions in space. The position is one with the body erect, elbows extended, palms facing forward, _and feet slightly separated and parallel 1. Sagittal plane: A vertical plane passing through the body from front to back, dividing it into right and left half. The cardinal plane divides the body into equal symmetrical halves 2. Frontal plane: A vertical plane passing through the body from side to side, dividing it into a front and back half. The cardinal frontal plane passes through the center of gravity dividing the body into equal but asymmetrical halves 3. Transverse plane: This is a horizontal plane, which passes through the body from side to side and from front to back, dividing it into an upper and lower half. The cardinal transverse plane passes through the center of gravity and divides the body into equal but asymmetrical halves NOTE* It is these planes of motion that are used as coordinates to describe where the axis of motion lies and what motion will occur around the axis

Axes of Joint Motion 1. Either single or triplane joint motion: a. An axis can be defined as an invisible line around which all motion takes place b. The axis of motion is always perpendicular to the plane in which the motion takes place (the motion takes place in one plane and the axis lies in the other 2 planes) c. The frontal-transverse axis is horizontal (its motion is sagittal plane), the sagittal-transverse axis is horizontal (the motion is frontal plane), and the frontal-sagittal axis is vertical (the motion is transverse plane) d. The majority of joints in the lower extremity are hinge-like, therefore when motion occurs around a joint it occurs by rotation about an axis 2. Position of the joint axes: a. Single joint motion: The plane of motion is perpendicular to the axis of motion b. Triplane joint motion: The amount of motion that can occur in that plane will depend upon the degree of angularity the joint axis makes to each individual body plane

NOTE* The greater the amount of degrees (up to 90°) between an axis of motion and a cardinal body plane, the greater the amount of motion that will occur in that body plane 3. Motion of specific joints: a. Hip: i. Transverse plane axis (controls sagittal plane motion): Controls the movements of flexion and extension. The range of hip flexion depends upon the position of the knee: • When the knee is extended the hip can flex 90° (active flexion) and 140° (passive flexion) • With the knee flexed the hip can be flexed 120° (active flexion) and 120° (passive flexion) ii. Anteroposterior axis: lies in the sagittal plane and controls the movements of abduction and adduction iii. Vertical axis (controls transverse plane motion): controls internal and external rotation b. Knee: i. Frontal plane axis (controls sagittal plane motion): Controls the motion of flexion and extension • Active flexion of the knee with the hip joint extended can result in 120° of flexion, and 140° with the hip joint flexed • Passive flexion of the knee may attain a range of 160° ii. Longitudinal plane axis (controls transverse plane motion): Motion of internal and external rotation • Active internal rotation has a range of 30°, while active extended rotation has a range of 40° c. Ankle: The primary motions at the' ankle joint are flexion and extension in the sagittal plane i. The axis of the ankle joint passes lateral, plantar, and posterior to medial, dorsal, and anterior passing through the tips of the malleoli. It is deviated from the frontal plane due to malleolar torsion • The range of dorsiflexion available at the ankle joint is 20-30°, while the range of plantarflexion is 30-50° NOTE* Due to slight deviations in the transverse frontal axis of the ankle joint we will see transverse plane motion of abduction and adduction d. Subtalar: The axis is oblique to all 3 body planes which allows for triplanar motion (pronation and supination). Pronation allows the motion of abduction, eversion, and dorsiflexion. Supination allows for adduction, inversion, and plantarflexion

i. Subtalar joint axis passes from a plantar, posterior, lateral direction to a dorsal, anterior, medial direction. It enters the heel and exits through the dorsomedial surface of the talar neck ii. The axis is directed 42° from the transverse plane and 16° from the sagittal plane iii. As the axis is deviated 42° from the transverse plane positioning it approximately equidistant from being completely vertical or completely horizontal, and equal amount of transverse and frontal plane motion will occur (i.e. Equidistant from both the frontal and transverse planes) iv. Additionally, as the axis is deviated 16° from the sagittal plane, this allows a minimal amount of dorsiflexion and plantarflexion v. The normal values for passive ROM from neutral is 20-35° of inversion to 1015° of eversion for a total ROM of 30-35° e. Midtarsal: Has 2 axes of motion which allow for triplanar motion i. The longitudinal axis passes 150 from the transverse plane and 9° from the sagittal plane. It passes dorsal, anterior, medial to plantar, posterior and lateral. It enters the calcaneus and exits medially through the 1st metatarsalcuneiform joint. Since the longitudinal axis is more longitudinal (close to the transverse-sagittal axis) its permits frontal plane motion of inversion and eversion. The normal ROM is 4-6°

ii. The oblique axis passes 52° from the transverse plane and 57° from the sagittal plane. It enters the lateral aspect of the calcaneus (plantarly) and exits the talonavicular joint (dorsally). The motion that occurs is adduction and abduction, and dorsiflexion and plantarflexion. Inversion and eversion does occur, but is minimal f. First ray: Consists of the 1st metatarsal and medial cuneiform

i. The axis of motion passes dorsal, medial, posterior (enters the medial aspect of the talonavicular joint) to plantar, lateral, anterior (exits third metatarsallateral cuneiform area ii. It angles approximately 45° to both the frontal and sagittal planes and slightly from the transverse plane. It is a triplanar axis, with most of the motion in the sagittal and frontal planes in a 1:1 ratio iii. When the first ray dorsiflexes, it inverts and when it plantarflexes it everts. For every degree the first ray dorsiflexes it also inverts 1°. The first ray axis is now a pronatory axis. The ankle, STJ, MTJ (longitudinal and oblique) and fifth ray all possess pronatory-supinatory axes. The 2nd, 3rd, and 4th rays as well as the digital IPJ's are all uniplanar and produce sagittal plane motion only

NOTE* The digital MPJ's contain 2 axes, a transverse and a vertical. While the vertical axis allows for transverse plane motion, it is the transverse axis which allows for dorsiflexion/plantarflexion to occur. The transverse axis moves in a dorsal-proximal direction with MPJ dorsiflexion. The first MPJ must allow for 65% of joint dorsiflexion. The joint acts as a ginglymus joint for the initial 25° of dorsiflexory motion, and acts as arthrodial joint with the first metatarsal plantarflexing for and MPJ dorsiflexion after the Initial 25° iv. The average ROM is 5 mm for dorsiflexion and 5mm for plantarflexion NOTE* The term "degrees of freedom" refers to the number of axes a joint has. While the ankle and most joints of the foot have one degree of freedom, the MPJ's and the MTJ each have 2 axes and thus 2 degrees of freedom

g. Fifth ray: Consists of the 5th metatarsal

i. It has an axis of motion from proximal inferior, lateral to distal, superior medial and angles to all body planes ii. It angles 20° from the transverse plane and 35° from the sagittal plane, therefore exhibiting triplane motion. The degree of sagittal and frontal plane motion is large, and transverse plane motion is minimal iii. When the 5th ray dorsiflexes it also everts and abducts (pronatory axis) h. Lesser rays: The central 3 rays along with the IPJ's, have axes that are parallel with the frontal and transverse planes, therefore will have motion only in the sagittal plane

Angular and Axial Deformities of the Lower Extremity in Children 1. Definitions: a. Torsion: is the twisting of a long bone on its longitudinal axis b. Rotation is an axial change in the limb due to changes at the joint c. Anteversion is an anterior axial change in the femur with relation to the head and neck to the distal condyles (refers to rotational and positional changes of the limb at the hip) d. Antetorsion (femoral): Refers to twists in the axis of bone. It is a twisting of the head and neck of the femur on its own body axis while the portion of the femur on its own body axis entering Into the knee joint area remains (more or less) in a fixed position, lining up with the lower leg NOTE* Normally, antetorsion at birth is approximately 390, and eventually untwists to 12° by adulthood. If antetorsion is greater than it should be (femur does not untwist enough), then we have one of the factors influenceing a pigeontoe gait

NOTE* While the bony femur is untwisting after birth, there is a simultaneous inward rotation of the thigh (anteversion) in the region of the hip. The bony external twisting (torsion) is being neutralized by the inward rotation of the thigh to align the extremity for forward progression e. Retroversion: Is a lack of normal torsion in the femur, less than normal by 10-12° 2. Axial Deformities: a. Tibial torsion: Normally 18-23° (external) in the adult. Measured by malleolar torsion which is 5° less i. Etiology: Soft tissue origin? osseous origin ? ii. Treatment: The decision whether to treat or not is determined by the degree of the deformity (if any), and the age of the child. In the infant with rigid tibial torsion, serial-above knee casting is effective, followed by maintenance with a Ganley splint or D-B bar NOTE* The actual amount of tibial torsion cannot be measured, so therefore we measure malleolar torsion. From birth to 1 year it measures 0° to 10° (external), 1 year to 5 years it measures 8°to 13 ° (external), and 6 years to adult it measures 13-180 external torsion 3. Femoral torsion: a. Anteversion (medial femoral torsion): Is an axial deformity within the neck and shaft of the femur, resulting in a medial functioning knee

i. Normal femoral alignment at birth is approximately 35-40° of anteversion, which gradually derotates to the adult alignment of 12-15° ii. Any delay in this progression should be considered abnormal and treated owing to positional imbalance caused by soft tissue constraints and the adaptability of the epiphysis to external forces. It is usually seen is the older female child and manifested by the "reverse tailor's" sitting position iii. With this, there is a persistent medial effect of the femoral growth plate iv. Examination reveals excessive medial angle of the femur associated with a limited lateral range of motion suggestive of femoral anteversion v. Treatment: • In the older child who presents with a knock knee conformation and who, on examination, shows excessive medial femoral ROM, treatment initially consists of change in sitting habits • Later (if necessary) a Ganley femoral derotation splint (this splint is of benefit in the 4-8 year child with excessive medial ROM) • In true persistent osseous anteversion in the older child a femoral derotation osteotomy or epiphyseal stapling may be necessary NOTE* The treatment approach to femoral problems has been difficult since any splinting device attached to the feet or legs is nullified once the knee flexes

b. Retroversion (lateral femoral torsion): Felt to be a continuation of lateral rotated position of the femur in infancy. Lateral ROM is excessive. Often found in females, usually obese with heavy thighs. The gait effect is knock-knee 4. Angular deformities: a. Knock knee (genu valgum): An angular problem found more often in the obese female child, it also may be associated with coxa vara, and is often the visual result of the proximal axial problems of medial and lateral femoral torsion. These changes are often associated with torsional changes of the lower leg and valgus foot deformity. Depression of the lateral tibial condyle in

persistent knock-knee in the older child may also lead to soft tissue strain often reflected as quadriceps and calf pain. This can lead to DJD in the adult i. Etiology: • Physiologic • Medial femoral torsion • Lateral femoral torsion • Anteversion syndrome (Kleiger) • Trauma: microtrauma (Hueter-Volkman law of epiphyseal response to pressure states that increased pressure across the epiphyseal plate will decrease the rate of growth), direct trauma, infection b. Bowleg (genu varum): May, be associated with coxa valga i. Types: • Physiologic: noted at birth • Rickets: result of vitamin D deficiency causing a disturbance in the metabolism of phosphorous and calcium • Osteochondritis deformans tibiae (Blount's disease): an angulation is noted only at the proximal tibia causing a characteristic "beaking" of the medial tibial plateau. This disease shows fragmentation of the proximal tibial metaphysis and may not become evident before 24-30 months of age. Additionally, infants with a metaphyseal-diaphyseal angle of 110 or greater (created from the intersection of a bisection of tibial and a bisection of the femur) will eventually develop Blount's disease

Anatomy of Gait: Phasic Activity of Muscles The human body has evolved bipedalism as the most efficient means of locomotion. Bipedal gait is a repetitive sequence of alternating movements of the lower limbs; one complete sequence represents a gait cycle 1. Subdivisions of the gait cycle: a. Stance phase (62% of gait): The period of ground contact and weight support of the foot i. Contact period (27% of stance and 17% of the entire gait cycle): initiated by heel strike, the fully dorsiflexed foot Is lowered to the ground as the body moves from a posterior position to one more directly over the foot. The key locomotor events of contact are: • Subtalar joint pronation (for shock absorption) which is normal pronation • Subtalar supination (closed chain, begins at the end of contact) • Internal rotation of the leg and femur (concurrent with STJ pronation) • Full loading of the metatarsus is completed by the end of contact • Peak vertical ground reactive forces occur for the first time at the end of contact (the first of the two periods where the ground reactive force rises above body weight during late contact phase • The foot functions as a mobile adaptor in contact • Internal leg rotation initiates STJ pronation • At the end of contact the STJ begins supinating and it is initiated primarily by the posterior tibial and is aided somewhat by the other calf supinators and leg external rotators

NOTE* At the beginning of weightbearing, during the entire contact period, the STJ pronates in order to make the foot more flexible and, as such, a better mobile adaptor to variances in terrain. ii. Midstance period (40% of stance): Foot flat begins midstance, when it singly bears the body weight (single support), and the alternate foot is in the swing phase. The key locomotor events of midstance are: • Conversion of the foot from a mobile adaptor to a rigid lever for propulsion. The primary condition for a rigid lever to occur is STJ supination (when this does not occur you have all types of problems (i.e. flatfoot). This leads to a poor propulsive unit • A decrease in vertical ground reaction force to about 75% of body weight, but begins to increase again prior to heel lift • Continued external leg rotation • The contralateral limb is in swing phase • STJ supination as a result of external leg rotation and the supinating calf muscles (especially the posterior tibial and swinging limb). The foot passes through STJ neutral shortly before heel lift. From this point on, the STJ is supinated NOTE* During midstance the STJ is still pronated but starts supinating to convert the foot to a rigid lever iii. Propulsive period (33% of stance): Continuation of the forward shifting body results in heel lift and the initiation of the propulsive period, whereby the weight is shifted to the forefoot and at the end, opposite foot regains contact with the ground by heel strike. The key locomotor events of propulsion are: • Continued STJ supination which increases skeletal rigidity and creates a rigid lever • Continued external leg rotation • Second peak vertical ground reaction force (about 125% of body weight) • Shift of forefoot weightbearing from lateral to medial • The opposite foot begins to bear weight just after lateral to medial shift and by toe-off the opposite foot is in full contact phase b. Swing phase (38% of gait): That portion of the gait cycle when the foot is off the ground. During swing the foot pronates first and then supinates. The key events of swing phase are: • During swing, the foot is transported from one step to the next • The leg continues to externally rotate momentarily after toe-off. Then it begins an internal rotation during the swing • Pronation of the foot to aid ground clearance and then resupination to prepare for contact • Ankle joint dorsiflexion, and hip/knee flexion to shorten the length of the leg (there would be a tremendous amount of pelvic motion during gait if there

were no mechanisms to flex and shorten the leg length) c. Double support: Both feet are in ground contact at the beginning and end of each stance phase in the walking gait. Both feet are on the ground 25% of the gait cycle (0-12% and then again from 50-62% of the entire gait cycle) NOTE* In running gaits, the swing phase proportionally increases in duration, an instead of stance phase overlap, the limbs overlap in off-ground motion in a period of float; i.e. there is no double support phase during running, also there is an airborne phase with no ground contact and there is never more than one foot in ground contact at one time

2. Hip and knee motion: a. Motions in gait: At toe off, both the hips extended and knee is flexed while the limb Is posterior to the body. At heel strike the hip is flexed, the knee extended and the limb forms a lever for the movement of the body onto the heel. During stance the limb extends at the hip as the body moves over the stationary foot. Internal rotation of the limb continues from swing phase into the contact period of stance. In midstance, the limb begins external rotation as the opposite side of the pelvis and hip shift forward and medially rotate during swing phase of the opposite limb b. Swing phase muscle action: i. Hip flexors: • The primary flexor of the hip is the iliopsoas which is activated shortly after toe off: it is comprised of the iliacus and the psoas major to form a common muscle belly ii. Hip stabilizers and rotators: In swing phase, the hip on- the swing side has lost support from the ground; it needs to shift body weight medially to the stance limb and to resist downward tilt. The unsupported hip, therefore, needs greater muscular stabilization in swing phase than it does when supported in stance • Transverse stabilization of the unsupported hip is produced by the erector spinae on the swing side • The hip abductors (gluteus medius and minimus) pull down the pelvis on the supported side, and lift and level the pelvis op the swing side. Their primary function on the swing side is to abduct the-thigh • The medial hip adductors (adductor longus, adductor brevis, adductor magnus, and pectineus), stabilize the hip and thigh (with the abductors) in both stance and swing, and they contribute to flexion, extension, and internal and external rotation of the hip iii. Knee extensors: • The quadriceps femoris (rectus femoris, vastus medialis, vastus lateralis, vastus intermedius) is a biarthrodial muscle acting on hip flexion and knee extension at the same time. The quadriceps is the only extensor of the leg, and in the walking gait, extends the leg near the end of swing (this extention is decelerated by the hamstrings (semimembranosis, semitendinosis, biceps femoris)

iv. Knee flexors and hip extensors: • The hamstrings, prior to heel strike, exert a flexor force on the leg, decelerating ongoing extension, and extend the hip in early stance. The semimembranosus and semitendinosus medially and biceps femoris laterally, are synergists of each other in stabilizing rotation at the knee at heel contact. The hamstrings also stabilize both the hip and knee joints at heel strike NOTE* The gluteus maximus (the largest and most powerful of lower extremity muscles) contributes to hip extensor stabilization c. Stance phase muscle action: In the contact period, those muscle groups that decelerated and stabilized these joints at heel strike continue to perform these functions until the foot achieves full foot support. At midstance most of the weight-support functions are managed by bone and ligament, requiring little primary muscular action. As. the body moves over the standing foot, the limb externally rotates in all segments down to the ankle. This rotation is a reaction both to subtalar supination and to medial rotation of the opposite limb swing phase. After the stance limb passes beneath the hip joint, the hamstrings are again activated to help extend it 3. Ankle motion: a. Motions in gait: Functions on a pronatory/supinatory joint axis with the majority of motion consisting of sagittal plane dorsiflexion and plantarflexion. Any rotation of the leg carries the talus with it when the foot is off the ground, and any subtalar action involving the talus affects leg rotation when the foot is weight bearing b. Dorsiflexors: Dorsiflexion occurs from late contact to the propulsive period, whose action is the result of kinetic forces of the body moving over the limb. The 4 anterior crural tendons pass anterior to the transverse axis of the ankle joint, and therefore dorsiflex the ankle. Distally, the tendons pass to either side of the subtalar and midtarsal joint axes where the tendon passing medially (tibialis anterior) exerts an inverting force, supinating the STJ and MRJ axes. The tendons passing laterally (EDL, peroneus tertius) exert an everting force (these apply a pronatory force to the STJ and MTJ longitudinal axes). The anterior crurals function mainly during swing to dorsiflex the foot to clear the ground. The toe extensors begin to act at the end of the propulsive. period, when they help stabilize the toes. They are joined by the tibialis anterior and peroneus tertius, and together lift. the foot at toe off. After heel strike, they decelerate the foot while it is lowered to the ground. NOTE* The tibialis anterior is the main dorsiflexor because of its insertion at the base of the first ray, and acts together with the EHL in elevating the first ray and hallux above the groung during swing (its insertion is also medial to the STJ and MTJ axes making it an effective supinator, and invertor during dorsiflexion)

NOTE* Summary of anterior aural function: They become active at toe-off to dorsifex the foot. They remain active throughout swing, and show a peak activity at heel strike as they decelerate the forefoot as it strikes the ground. They are active for the first 10% of stance c. Plantarflexors: Consist of 6 muscles divided into superficial and deep groups (superficial: gastrocnemius, soleus, plantaris) (deep: tibialis posterior, FDL, FHL). The tendo Achilles passes 2 cm posterior to the STJ axis giving it more leverage to act on the ankle than any other muscle (supinates the ankle). The combined action of the triceps surae (2 heads of the gastroc and the soleus.) together with the deep plantarflexors, produce 4 times as much power as the combined dorsiflexors, and mainly act on the fully loaded limb in single support. The tibialis posterior is the strongest invertor and adductor of the foot. The plantarflexors begin to function in the contact period and continue through midstance and into propulsion. They act to decelerate the momentum of the body as it moves across the fixed foot dorsiflexing the joint. The gastrocnemius also resists hyperextension of the knee prior to heel lift NOTE* Summary of posterior aural function: The, triceps surae are active during the middle of stance phase. They begin to fire during contact and terminate during propulsion in order to achieve heel-off 4. Tarsal joint motion: a. Motions in gait: The definitive feature of the contact period is progressive loading of the foot from its initial contact at the heel, along the lateral border, to full foot support. At this stage, the foot is undergoing pronation, and the leg continues to rotate internally. These joints are characterized by their flexibility (if the MTJ is unlocked, the 1 st ray is not stabilized). By midstance, the weight is progressively more medially distributed as the body center of gravity continues to move over it. From the lateral border of the foot, weight is shifted medially along the metatarsal heads. The stresses on the foot now require rigidity in tarsal structure to transfer weight to the forefoot. As the STJ begins to supinate, the leg, with the hip and the thigh, externally rotate. This supinatory process involves the windless effect as the foot proceeds through propulsion. b. Tarsal stabilizers: In midstance, the soleus, gastrocnemius, and tibialis posterior are the prime movers to supinate the foot with concurrent external rotation of the leg. The peroneus brevis and longus (lateral crural ms.) are inactive in the contact period and only begin to act well into midstance and early propulsion. The peroneus brevis is the prime evertor (pronator) of the foot. The peroneus longus exerts a force on the first ray, pressing the first metatarsal to the ground as well as on the intervening tarsals. The combined result is a compact tarsus. The continuing secondary action of the soleus and supinating tendons from the posterior compartment, maintain pressure on the lateral border of the foot. This maintains a fixed position of the cuboid, which acts as a pulley for the peroneus longus tendon. At the end of midstance, the heel is lifted, and the cuboid is released, permitting the peroneus longus to act more

directly on the 1st ray as body weight is lifted from the lateral metatarsal heads 5. Forefoot motion: a. Motions in gait: Stability in the forefoot begins to develop in the latter part of midstance when the foot is supinating, the MTJ is locked, and the tarsal and metatarsal bones are in a close packed position. At heel lift, the foot forms a lever from the plantarflexing ankle joint to the met heads that form its fulcrum. The MPJ's are transversely stabilized while the toes are firmly braced against the ground forming a stable platform for the fulcrum. The loaded extension at these joints activates the windless effect of the plantar fascia, which is stretched by its attachment to the MPJ and hallux b. Extrinsic muscle action. The FHL continues to act almost until toe off as the hallux is the last part of the foot to leave the ground and requires a longer period of stabilization than do the lesser toes. The tibialis posterior and the peroneals compress the metatarsal bases as well as the tarsal bones. The peroneus longus stabilizes the 1 st ray through the propulsive period c. Intrinsic muscle action: The main function of the intrinsic muscles of the foot is to transversely and axially stabilize the digits against the metatarsal heads and against ground reaction forces. All intrinsic muscles begin to contract in midstance and most continue throughout the propulsive period. Transverse stabilization of the toes is accomplished by the plantar and dorsal interossei. The dorsal interossei are bipennate and 4 in number, originating from the corresponding adjacent sides of their respective intermetatarsal spaces. The first dorsal interosseous attaches medially into the base of the proximal phalanx of the second toe while the 2nd, 3rd, and 4th attach laterally into digits 2, 3, and 4. The plantar interossei are unipennate. These three muscles attach medially into the 3rd, 4th, and 5th digits and originate from the medial aspect of their respective metatarsals. Their combined action resists displacement of the toes to either side. Transverse stability of the hallux is provided by the abductor hallucis on one side and adductor hallucis on the other side. The abductor digiti minimi mimics the function and attachment of the dorsal interosseus on the lateral side of the 5th toe. The FHB, FDB and flexor digiti minimi brevis act synchronously with the long flexors, stabilizing the toes against the ground. The flexor digiti minimi brevis attaches laterally into the 5th toe, as a unipennate muscle and functions with the interossei to provide transverse plane digital stability. The interossei are stance phase muscles and function to plantarflex the MPJ's against the retrograde dorsiflexing buckling force that accompanies the FDL and FDB contraction. The axial tension of the FDL is aided by the quadratus plantae. The lumbricals are 4 muscles originating from the medial aspect of the corresponding FDL slip, and attaching medially into the base of the extensor hood of the lesser toes, as they pass plantar to the deep transverse metatarsal ligament. These have been described as swing phase muscles, stabilizing the MPJ's plantarly while assisting in extending the PIPJ's and DIPJ's, limiting excessive swing phase contraction. This provides a stable insertion to allow the EDL to be an important dorsiflexor of the ankle during swing phase of gait

NOTE* The greatest combined effect of all these muscles is achieved in conjunction with the extensor expansion mechanism, which links the IPJ's & the MPJ's in each toe so that tension on the long extensor extends a row of digital joints at a time

NOTE* Summary: The abductor digiti minimi and EDB become active at about 30% of stance, the FHB, abductor hallucis, and FDB become active at about 40%, 50% and 60% of stance respectively, and the interossei become active at about 25% of stance. Activity of all these muscles ceases near toe-off

d. Muscles acting on the 1st ray and hallux: During supination in the midstance period, the peroneus longus is uniquely significant in plantarflexing the 1st ray. The FHL assists in supination during the earlier part of midstance, plantar stabilization of the, metatarsal head together with the action of the peroneus longus, and stabilization of the hallux in propulsion 6. Summary of joint motion during gait: a. Hip joint motion-sagittal plane: i. Contact: hip extends from flexed position ii. Midstance: hip continues to extend iii. Propulsion: hip flexion b. Hip joint motion-transverse plane: i. Contact: internal rotation of the thigh in the pelvis, corresponding to internal leg rotation with STJ pronation ii. Midstance and propulsion: external rotation of the thigh on the pelvis c. Knee joint motion sagittal plane: i. Contact: flexion (the major shock absorbing mechanism of the body) ii. Midstance: body weight passes over the knee, so there is extension iii. Propulsion: the knee flexes again for pushoff d. Knee joint motion-transverse plane: Corresponds to supination and pronation in the STJ i. Contact: with STJ pronation comes internal rotation of the tibia ii. Stance: external rotation of the tibia on the femur e. Ankle joint motion-sagittal plane: i. Contact: plantarflexion until midcontact ii. Late contact to midstance: dorsiflexion iii. Propulsion: plantarflexion f. Subtalar joint motion: i. Contact: pronation

ii. Midstance and propulsion: supination g. Midtarsal joint motion: There are 2 separate axes Longitudinal axis i. Contact: Supinated ii. Midstance: Fully pronated by heel lift* Ill. Propulsion: Remains pronated and locked

Oblique axis Pronated Pronated Supinates

NOTE* Longitudinal axis pronation during midstance* is very important for normal propulsion. Negative plaster casts are taken of the feet with the longitudinal axis of the MTJ in pronation

Observation of Gait 1. Stance phase: a. Posterior view: i. Contact: • Heel contact is inverted but rapidly everts • Contact is slightly lateral to the midline of the heel i. Midstance: Posterior bisection of the posterior of the heel goes from everted to vertical i. Propulsion: • Posterior bisection of the heel inverts as heel lifts b. Lateral view: i. Contact: • Posterior portion of the heel strikes the ground with the foot dorsiflexed on the ankle • Plantarflexion of the ankle begins slightly after contact • At contact the knee is extended and flexes rapidly for shock absorption ii. Midstance: • Ankle dorsiflexion of 5°-10° as the body weight passes over the planted foot • Knee returns to full extension • Late midstance heel lifts as the trunk passes over the planted foot, literally peeling the heel up from the floor iii. Propulsion: • Ankle plantarflexes to facilitate toe-off • Knee flexion as the trunk advances further c. Anterior view: i. Contact: • Forefoot is markedly inverted as the heel contacts the ground • Leg is slightly inverted ii. Midstance: • Forefoot has everted bringing the metatarsals to the ground. The forefoot is loaded 5-4-3-1-2 or 5-4-3-2-1- depending upon the metatarsal length and

muscle functioning • Leg is slightly internally rotated iii. Propulsion: • Marked dorsiflexion of the MPJ's • Lateral digits lift-off first • Body weight passes through the center of the hallux • Leg externally rotated 2. Swing phase: a. Lateral view: i. Trunk muscles advance the leg forward ii. Ankle dorsiflexion to decrease leg length iii. Hip and knee flexion to assist in shortening

Subtalar Joint Measurements 1. Open kinetic chain measurement and neutral position calculation: In the non-weightbearing patient, the bisection of the posterior distal 1 /3 of the leg is the point from which calcaneal inversion and eversion are measured. a. Example 1: The calcaneus can evert 80 from the leg bisection and invert 22° from the lebisction. The total STJ ROM is 30°

To find the neutral position of this STJ we need to find the point from which there is twice as much supination as there is pronation. In this case the neutral position is 2° inverted, as from this point there is 100 of pronation and 20° of supination available Total STJ ROM X 2= Inversion from neutral position 3 Inversion from the leg -MINUS- Inversion from neutral= Neutral position

30°(total ROM) X 2= 20° 22°(inversion from leg)- 20°= 20 varus 3 b. Example 2: Calcaneal inversion= 32°, calcaneal eversion= 7°, total ROM= 39° 39°+ 3 x 2= 26° inversion from neutral, 32°-26°=6° varus NOTE* Another method for calculation is: Total ROM- Eversion = Neutral 3 If the resulting number is (+), then there is a varus or neutral position If the resulting number is (-), then the resulting number is valgus or neutral 2. Closed kinetic chain measurement and neutral position calculation: a. Example 1: Maximum calcaneal inversion 12° (right), 150 (left), maximum calcaneal eversion 6° (right), 3° (left), tibial varum 1 ° bilaterally i. To calculate neutral position: Total ROM 18° bilaterally 18+ 3 x 2= 12° 12°- 12°= 00 (right), 15°- 12°= 30 varus (left) ii. To calculate NCSP: Add the tibial varum component to the neutral position measurement Tibial varum is 1 ° (left) + 30 varus (left)= 40 rearfoot varus (left) Tibial varum is 1 ° (right) + 0° (right)= 1° rearfoot varus (right) iii. To calculate the RCSP: Since these values indicate a rearfoot varus component, this individual will compensate at the STJ to bring the calcaneus perpendicular to the ground, by using all STJ pronatory ROM that it needs (the pronatory ROM of the STJ is 1/3 the total ROM or 6°). On the right the NCSP= 1° varus so the RCSP= 0° On the left the NCSP= 40 varus, so the RCSP= 0° (using 2/3 available pronatory ROM) b. Example 2: Maximum calcaneal inversion 16° (right), 15° (left), maximum calcaneal eversion 2° (right), 3° (left), tibial varum 30 (right), 2° (left) i. Calculate the neutral STJ position: Total ROM (right)= 18° Total ROM (left)= 18° 18-3 x 2= 12° (bilateral) inversion from neutral 16°- 12°= 40 varus (right), 15°- 12°= 30 varus (left) neutral position ii. To calculate the NCSP: Tibial varum 3° (right) + 4° varus neutral (right)= 7° rearfoot varus NCSP (right) Tibial varum 2° (left) + 3° varus neutral (left)= 50 rearfoot varus NCSP (left) iii. To calculate the RCSP: Know that 1/3 the total STJ ROM is 6°. 7° rearfoot varus (right)- 6° (1/3 available pronation)= 1° RCSP (right) 5° rearfoot varus (left)- 6° (1/3 available pronation)= 0° RCSP (the STJ still has 1° more of available compensatory motion left)

NOTE* Forefoot varus is compensated (mostly) by STJ pronation, and minimally by some MTJ pronation. If the amount of forefoot varus is 3° or less, the STJ will only compensate that sped lc number of degrees. lf, however, the forefoot varus is greater than 3° the STJ will (usually) maximally pronate to the end of its ROM. Therefore it will pronate more than the number of degrees required to bring the forefoot's medial surface into contact with the ground. The reason the STJ maximally pronates with a forefoot varus deformity greater than 3° is that once the calcaneus is everted more than 3° the force of the body's weight pushes it to the end of the STJ's pronatory ROM. If, however, the STJ cannot completely compensate the forefoot varus deformity, then and only then will the MTJ pronate to help with the compensation (on the longitudinal axis), leading to first ray dorsiflexion and inversion NOTE* In a rearfoot valgus greater than 2° the body weight on the everted calcaneus will cause the STJ to pronate to the end of its ROM. A rearfoot valgus of less than 2° does not change the STJ position from the NCSP. If a greater than 10° rearfoot valgus exists, the head of the talus will usually plantarflex toward the ground before the STJ completely pronates. While this produces a severe flatfoot, the STJ may not be pronated to the end of its ROM

Subtalar Joint Function During the gait cycle, the STJ functions during the weightbearing (closed kinetic chain) and nonweightbearing portions (open kinetic chain). 1. Open kinetic chain (OKC): a. During the 1st half of the swing phase, the STJ pronates, and during the last half of swing the STJ supinates b. In OKC function, the STJ pronatory and supinatory components are exhibited exclusively by the calcaneus (with OKC pronation, the calcaneus abducts, everts, and dorsiflexes) c. In OKC motion, the calcaneus moves around the talus, which functions as an immobile extension of the leg 2. Closed kinetic chain (CKC): a. In CKC the STJ motion, the calcaneus and talus both move, the calcaneus moves only in the frontal plane (inversion and eversion), and the talus moves in the transverse and sagittal planes NOTE* The bones of the STJ move around the STJ's axis of motion, and if any motion takes place in a bone which is proximal to that axis, the motion will be in the opposite direction of the named major motion. b. In CKC STJ pronation, the calcaneus will still evert, but the talus will plantarflex and adduct c. In CKC STJ supination, the calcaneus will invert and the talus dorsiflex and abduct (the talus abducts and dorsiflexes because it is proximal to the STJ joint

axis) (transverse plane talar excursion reflects the transverse plane movement of the leg) NOTE* During the contact period (STJ pronation) the calcaneus is everting, while the talus is plantarflexing and adducting. During midstance and propulsion the calcaneus is inverting while the talus abducts and dorsiflexes (STJ supination) d. Internal rotation of the tibia is associated with CKC STJ pronation, and the converse is true with CKC STJ supination e. The 2 major functions of CKC pronation are shock absorption and adapting to uneven terrain 3. Measurement of STJ motion: a. There is really no good way to measure STJ motion in all 3 planes, therefore, the frontal plane motion of the calcaneus is used as an index of STJ motion (a bone distal to the STJ axis) b. From the STJ neutral position, the normal foot can supinate twice as much as it can pronate. The average total ROM for the STJ is about 30° of calcaneal frontal plane motion (minimum normal STJ ROM is 8-12° for normal ambulation)

Midtarsal Joint Function Although triplane motion occurs about both the MTJ axes, some planes of motion are so small as to be clinically insignificant 1. MTJ function: a. Motion about the longitudinal axis will occur primarily in the frontal plane (inversion and eversion) b. The oblique axis allows primarily for sagittal and transverse plane motion NOTE* Since 2 planes of motion occur about the MTJ oblique axis, it is necessary to know which motions are coupled. As the axis is a pronatory/ supinatory axis, the following occurs by necessity: a. With plantarflexion: adduction also occurs b. With dorsiflexion: abduction also occurs NOTE* The MTJ's total ROM is dependent upon the STJ's position. The axes of the articular facets are just about parallel when the STJ is maximally pronated. This allows for a certain congruity to the 2 joints (T-N and C C joints). As the STJ goes from a maximally pronated position toward a more supinated position, the axis of the 2 joints progressively diverge from one another, congruity is lost, and with it ROM decreases

c. The MTJ longitudinal axis has an average ROM of 4°-6° (ROM of the oblique axis is unknown) d. When the STJ is maximally pronated, the MTJ's ROM is increased and the forefoot becomes mobile. When the STJ is maximally supinated the MTJ's ROM is decreased and the forefoot inverts with the rearfoot

Chapter 33: Anatomy Neuroanatomy Angiology Myology Arthrology

ANATOMY Neuroanatomy 1. Femoral nerve: a. Formed from the ventral rami of lumbar nerve roots (L2, L3, and L4) b. Divides into anterior and posterior division (the posterior division gives rise to the saphenous nerve which supplies cutaneous innervation to the medial leg and foot) 2. Sciatic nerve: a. Formed from the ventral rami of lumbar and sacral nerve roots (L4, L5, S1, S2, and S3) b. The largest nerve of the body c. Divides into its terminal branches, the tibial and common peroneal nerve d. Supplies all musculature of the leg and foot (except 'for that supplied by the saphenous nerve) 3. Common peroneal nerve (L4, L5, S1, S2): a. One of 2 terminal branches of the sciatic nerve, and winds superficially around the neck of the fibula b. Gives off the sural communicating near the head of the fibula, which joins with a communicating branch of the tibial nerve to form the sural nerve c. Terminal Branches: i. Deep peroneal nerve: This nerve runs with the anterior tibial artery (laterally) in the lower leg to give muscular innervation to the EDL, EHL, TA, peroneus tertius, EDB, and ends in the first interspace ii. Superficial peroneal nerve: In the distal 1 /3 of the leg, the nerve pierces the anterolateral intermuscular septum and deep fascia to become cutaneous, and divides into 2 branches, the medial and intermediate dorsal cutaneous nerves before reaching the ankle. This gives innervation to the peroneus longus and brevis 4. Tibial nerve (L4, L5, S1, S2, S3): a. The larger of the 2 branches of the sciatic nerve b. Travels between the two heads of the gastrocnemius to leave the popliteal fossa, descends along the back of the leg with the posterior tibial artery and veins c. The nerve lies medial to the blood vessels in the upper 1 /3 of the leg and lateral to them in the lower 1 /3 of the leg d. The nerve supplies the gastrocnemius, popliteus, tibialis posterior, FHL, and FDL e. Terminates into medial and lateral plantar nerves at the level of the lacinate ligament (prior to this, gives off medial calcaneal branch) 5. Sural nerve (L5, S1,S2): a. Formed by union of medial sural cutaneous (tibial) and sural communicating branch of the lateral sural cutaneous of the common peroneal b. Pierces the deep fascia to become cutaneous at the upper mid-calf region, travels distally near the lateral side of the achilles with the small saphenous vein, and passes forward below the lateral malleolus

e. Becomes the lateral dorsal cutaneous nerve on the lateral aspect of the foot 6. Saphenous nerve (L3,L4): a. This is the only nerve in the foot that originates from the lumbar plexus (comes off the posterior division of the femoral nerve and is its longest branch) b. Travels with the greater saphenous vein along the medial side of the leg c. It divides into 2 branches in the lower 1 /3 of the leg giving sensory innervation to the skin of the medial ankle and medial side of the foot (it may reach distally as far as the metatarsophalangeal joint) 7. Deep peroneal nerve (L4, L5, S1): a. Travels with the anterior tibial artery and lies lateral to it in the foot b. Divides into its terminal branches and passes into the dorsum of the foot in the middle compartment c. Its terminal branches are the lateral terminal nerve (passes across the tarsal area to innervate the EHB) and the medial terminal nerve (to the 1st interspace) where this divides into 2 dorsal digital nerves (2nd dorsal digital proper nerve & 3rd dorsal digital proper nerve) 8. Superficial peroneal nerve (L5, S1, S2): a. Primarily a cutaneous nerve with 2 terminal branches, the medial and intermediate dorsal cutaneous nerves b. Medial dorsal cutaneous nerve divides into a medial and lateral branch. These supply the medial side of the hallux, lateral side of the 2nd toe, and the medial side of the 3rd toe. c. Intermediate dorsal cutaneous nerve divides into medial and lateral branches. These supply the lateral side of the 3rd toe, medial side of the 4th toe, lateral aspect of the 4th toe, and the medial aspect of the 5th toe 9. Lateral dorsal cutaneous nerve (S1, S2): a. A continuation of the sural nerve below the ankle, and communicates with the intermediate dorsal cutaneous nerve, and divides into 2 branches (one to the lateral side of the 5th toe, and the other anastomoses with branch of the superficial peroneal nerve)

10. Medial calcaneal nerve (S1, S2): a. Last branch given off by the tibial nerve before dividing into medial and lateral plantar nerves b. It perforates the lacinate ligament and divides into anterior and posterior branches (posterior branch supplies the heel) c. The anterior branch continues distally into the plantar aspect of the foot, where it anastomoses with the lateral calcaneal branch of the sural nerve laterally, anastomoses with the saphenous nerve anteromedially and anastomoses with the lateral and medial plantar nerves distally 11. Lateral Calcaneal Nerve (S1, S2): a. Given off before the sural nerve goes around the lateral malleolus b. Supplies the cutaneous innervation to the lateral aspect of the heel and sensory innervation to the lateral proximal aspect of the plantar surface of the foot

12. Medial plantar nerve (S3): a. Larger of the 2 terminal branches of the tibial nerve running in the 3rd compartment of the lacinate ligament b. Enters the foot at the porta pedis and emerges from between the abductor hallucis and FDL c. Supplies the cutaneous innervation to the medial plantar aspect of the midfoot, abductor hallucis, FDB d. Its terminal branches are the 1st plantar digital nerve and 1st, 2nd and 3rd common plantar digital nerves

]

13. Lateral plantar nerve (S2, S3): a. Smaller of the 2 terminal branches of the tibial nerve, lying posterior to the posterior tibial artery, eventually lying medial to the lateral plantar artery with which it travels into the plantar aspect of the foot b. The nerve passes through the porta pedis lying between the FDB and quadratus plantae. Between the FDB and abductor digiti minimi the nerve divides into its 2 terminal branches, superficial and deep c. Superficial branch comes off the main branch at the level of the 5th metatarsal and supplies the flexor digiti minimi brevis, opponens digiti

minimi (when present), 3rd plantar interosseous, and 4th dorsal interosseous d. Deep branch follows along with the lateral plantar artery between the 3rd and 4th muscle layers (deep to the adductor hallucis and superficial to the plantar interossei) and supplies the transverse/oblique heads of the adductor hallucis, lateral 2 (or 3) lumbricales, and interosseous muscles of the 2nd and 3rd intermetatarsal space (2nd and 3rd dorsal, 1st and 2nd plantar), and 1st dorsal interosseous NOTE* The 1st and 2nd dorsal interossei receive additional innervation from the deep peroneal nerve

Angiology 1. The arteries: Blood flows from the left ventricle of the heart, through the ascending aorta, aortic arch, descending aorta, thoracic aorta, and abdominal aorta. In the lower abdomen, the aorta divides into paired common iliac arteries. Each common iliac artery divides distally into internal and external iliac arteries. The external iliac artery becomes the femoral artery as it passes under the inguinal ligament, a. Femoral artery: Courses through the medial thigh through the femoral triangle into the adductor canal b. Deep femoral (profunda femoris): The last branch of the femoral artery before leaving the femoral triangle c. Popliteal: When the deep femoral crosses over the medial femur it then becomes the popliteal and continues to the lower border of the popliteus where it divides into anterior and posterior tibial (before its bifurcation it gives off a sural branch which is the only source of blood to the gastrocnemius) d. Anterior tibial: Branches off the popliteal artery at the level of the soleal line, travels into the anterior compartment of the leg, lies between the tibialis anterior and EDL muscle bellies in the proximal 1/3 of the leg. Immediately above the the ankle joint the EHL tendon crosses over the anterior tibial artery and at this level the artery is found between the EHL and EDL. The anterior tibial artery can terminate as the dorsalis pedis or becomes insignificant before reaching the ankle joint, and if this happens, the dorsalis pedis will be absent or arise as a branch of the perforating peroneal artery

i. Branches of anterior tibial artery • Posterior recurrent tibial • Anterior recurrent tibial • Muscular branches (to the tibialis anterior, EDL, EHL, peroneus tertius, and muscles of the deep posterior compartment of the leg) • Anterior medial malleolar (superficial and deep branches) • Anterior lateral malleolar (transverse portion meets with branches from perforating peroneal; descending portion anastomoses with the descending retromalleolar branch of the peroneal artery) e. Dorsalis pedis: Begins as it crosses the ankle joint continuous with the anterior tibia] artery, and gives off branches i. Branches of the dorsalis pedis • Medial branches (medial tarsal arteries) • Lateral branches (artery to the sinus tarsi, lateral tarsal, arcuate, anterior perforating, 4th dorsal metatarsal, and 1 st dorsal metatarsal artery) f. Posterior tibial: Branches off the popliteal artery at the level of the soleal line, remains within the posterior compartment of the leg, runs superficial to the tibialis posterior proximally and over the FDL distally as it descends into the medial ankle into the 3rd compartment of the flexor retinaculum, and bifurcates into medial and lateral plantar arteries while in the 3rd compartment deep to the muscle belly of the abductor hallucis

i. Branches of the posterior tibial artery • Circumflex fibular • Peroneal (gives off muscular branches, perforating branch, communicating branch, posterior peroneal, anterolateral transverse branch, collateral branch, and recurrent calcaneal branches) • Nutrient artery (supplies the tibia)

NOTE* This is the largest nutrient artery in the body • Muscular branches (to the soleus, FDL, FHL, and tibialis posterior) • Communicating artery • Posterior Medial malleolar • Medial calcaneal • Artery of the tarsal canal g. Medial plantar: Smaller of the 2 terminal branches of the posterior tibial and gives rise to 2 branches (supplies the abductor hallucis, FDB, 1st dorsal interosseous) i. Branches of the medial plantar artery: • Superficial branch (gives rise to medial marginal plantar artery of the hallux and the common plantar digital artery) • Deep branch (divides into a medial and lateral branch) h. Lateral plantar: Travels into the intermediate compartment laterally and distally between the quadratus plantae and FDB muscle bellies, and terminates by connecting the perforating branch of the dorsalis pedis NOTE' This artery serves as a landmark, separating the 3rd and 4th muscle layers of the plantar aspect of the foot i. Branches of the lateral plantar artery: • 3 posterior/perforating arteries • 4 plantar metatarsal arteries • Proper digital arteries 2. The veins: Two sets of veins are found in the lower extremity, superficial and deep. Most arteries are associated with a pair of deep veins (venae commitantes). Valves are present in the veins, but are more numerous in the deep veins. The valves are located at the termination of the great and small saphenous veins, above and below the knee and ankle joints, and in the leg. Perforating veins connect superficial veins to deep veins a. Superficial veins: i. Dorsal digital veins ii. Dorsal venous arch iii. Superficial plantar veins iv. Greater saphenous vein v. Lesser saphenous vein b. Deep veins: i. Deep dorsal venous network ii. Deep venous plantar network iii. Medial and lateral plantar vein iv. Femoral vein 3. The lymphatics: a. Lymph nodes: The largest group of lymph nodes are found in the inguinal

region, and are divided into superficial and deep i. Superficial nodes: There are 2 groups of superficial nodes totalling 1525 in number ii. Deep nodes: 1 to 3 in number, found in the femoral canal and occasionally medial to the femoral vein, where the great saphenous vein drains into it

Myology 1. Osteofascial compartments of the leg a. Anterior i. Boundaries: Anterior and laterally by the crural fascia, medially by the tibia, posteriorly by the fibula. and interosseous membrane ii. Contents: tibialis anterior, EHL, EDL, peroneus tertius, anterior tibial artery and veins, deep peroneal nerve b. Lateral i. Boundary: Laterally is the crural fascia, posteriorly by the peroneal septum, medially by the fibula, and anteriorly by the anterior peroneal septum ii. Contents: peroneus longus and brevis c. Posterior (divided into superficial and deep) i. Superficial • Boundaries: Medially/laterally/posteriorly by the crural fascia, and anteriorly by the deep transverse intermuscular septum • Contents: Gastrocnemius, soleus, and plantaris ii. Deep • Boundaries: Posteriorly by the deep transverse intermuscular septum, laterally by the fibula, and medially by the tibia • Contents: FDL, FDB, tibialis posterior, posterior tibial artery and vein, and tibial nerve 2. Retinacula of the ankle: Thickened portions of crural fascia which bind tendons of extrinsic muscles of the foot closely to bone. They are considered to be superficial ligaments of the ankle a. Extensor Retinaculum: Is divided into two distinct portions, superior portion (transverse crural ligament) and inferior portion (cruciate crural ligament)

i. Transverse crural: • Located entirely on the leg (attached to the tibia and fibula above the malleoli) • Separates the tendons of the EDL, the peroneus tertius, and EHL from each other ii. Cruciate crural: • Forms a transverse "Y", with a lateral stem and 2 medial arms • Lateral stem attaches to the lateral surface of the calcaneus, deep fascia, and talus • The superior arm is separated into superficial and deep layers by the EHL which runs through it • The inferior arm passes around the medial side of the foot to blend with the deep fascia of the sole, and attaches to the medial aspect of the plantar fascia near the tuberosity of the navicular. Medially, the fibers bifurcate to envelope the muscle belly of the abductor hallucis, forming a tunnel b. Flexor Retinaculum (lacinate ligament): i. Forms (in part) the tarsal tunnel ii. The apex is attached superiorly to the crural fascia and the anteromedial portion of the medial malleolus. The base it attached inferiorly to the medial surface of the calcaneus, the medial process of the calcaneal tuberosity, and tendo Achilles iii. Contents of the tarsal tunnel: • 1st (medial compartment): tibialis anterior crosses the medial surface of the talus and deltoid ligaments • 2nd compartment: flexor digitorum longus crosses the posteromedial tubercle of the talus and passes over the medial surface of the sustentaculum tali • 3rd compartment: tibial vessels (the nerve runs deep to the artery and vein) • 4th (lateral) compartment: flexor hallucis longus grooves the inferior surface of the sustentaculum tali c. Peroneal Retinaculum: Divides into superior and inferior surfaces i. Superior peroneal retinaculum: • Is quadrilateral in shape • Splits to enclose the tendons of the peroneus longus and brevis ii. Inferior peroneal retinaculum; • Continuous with the main stem of the inferior extensor retinaculum where it attaches to the lateral surface of the calcaneus • Some fibers bind to the peroneal tubercle, forming a septum that separates the 2 peroneal tendons 3. Extrinsic muscles of the foot: a. Muscles of the anterior compartment: i. Tibialis anterior: • Origin: Lateral condyle of the tibia, the upper 2/3 of the lateral surface of the shaft of the tibia, the interosseous membrane, the deep surface of the

crural fascia, and the intermuscular septum • Insertion: Into the medial and plantar aspects of the medial cuneiform (90%) and the medial and plantar aspects of the base of the 1st metatarsal (10%) • Vascular supply: Anterior tibial artery • Innervation: Deep peroneal nerve • Functions: Statically in dorsiflexion of the foot on the leg, and dynamically to accelerate and decelerate the foot during gait, assist in dorsiflexion at toe off, dorsiflex the 1 st ray during swing, resists plantarflexion of the foot at heel strike, prevents excessive pronation during swing, and supinates the midtarsal joint around its longitudinal axis prior to heel strike ii. Extensor hallucis longus: • Origin: Anterior surface of the fibula at its middle half (medial to the origin of the EDL) and the interosseous membrane • Insertion: Inserts at the base of the distal phalanx of the hallux • Vascular supply: Anterior tibial • Innervation: Deep peroneal nerve • Functions: Statically it dorsiflexes the foot on the leg, extends the hallux, extends the distal phalanx on the proximal phalanx, and assists in inverting the foot. Dynamically, during stance it creates a "rigid beam effect" for the hallux by stabilizing the 1st MTPJ and the IPJ, and during swing it acts as the strongest dorsiflexor of the foot and accelerates the foot immediately after toe off iii. Extensor digitorum longus: • Origin: Lateral condyle of the tibia, upper 3/4 of the lateral condyle of the tibia, upper 3/4 of the anterior surface of the tibia, upper lateral part of the interosseous membrane, deep surface of the crural fascia, and the anterior peroneal septum • Insertion: It divides into 4 tendons at various distances proximal to the ankle joint, and sends a tendon to each lesser toe. Near the metatarsal heads, each tendon forms a membranous expansion (extensor hood) which covers the MTPJ dorsally and laterally and receives tendons of insertion from the lumbricales and interossei muscles to the lesser toes. Tendons to the 2nd, 3rd, and 3rd toes receive tendons from the EDB on their lateral sides. The EDL tendons to each toe then divide into 3 parts distal to the extensor hood apparatus at the head of the proximal phalanx • Vascular supply: Anterior tibial artery • Innervation: Deep peroneal nerve • Functions: Statically the EDL dorsiflexes the foot on the leg, extends the lateral 4 toes, and extends the phalanges of the toes upon each other. Dynamically, it stabilizes and accelerates the foot during gait, and during the propulsive period of gait it helps create a "rigid beam effect" in each lesser toe by assisting the lumbricales in rigidly extending the IPJs during propulsion. During swing phase it assists in dorsiflexion iv. Peroneus tertius: • Origin: From the lower border of the anterior surface of the fibula, and adjoining portion of the interosseous membrane

• Insertion: On the dorsum of the base of the 5th metatarsal • Vascular supply: Anterior tibial • Innervation: Deep peroneal nerve • Functions: Statically in flexion of the foot on the leg and eversion of the foot. Dynamically it assists in dorsiflexion of the foot for clearance of the toes during swing, and helps prevent excessive supination of the foot during swing b. Muscles of the lateral compartment: i. Peroneus longus: • Origin: From the head and upper 1/2 of the lateral surface of the fibula, the crural fascia, and the anterior/posterior septa • Insertion: Posterolateral inferior angle of the base of the 1st metatarsal (90%) and the adjacent portion of the medial cuneiform (does give a slip that gives origin to the 1st dorsal interosseous muscle) • Vascular supply: Anterior tibial and peroneal arteries -Innervation: Superficial peroneal nerve • Functions: Statically in plantarflexion of the foot on the ankle, eversion of the foot. Dynamically it is a stance-phase muscle by stabilizing the base of the 1st ray against the tarsal bones, stabilizes the 1st metatarsal head plantarly against the ground, resists the adductory force exerted on the first ray by the tibialis posterior, and assists (with the peroneus brevis) in transferring body weight from lateral to medial side of the forefoot during propulsion ii. Peroneus brevis: • Origin: from the lower 2/3 of the lateral surface of the fibula and the anterior/posterior personeal septa • Insertion. Lateral aspect of the tuberosity of the 5th metatarsal • Vascular supply: Peroneal artery • Innervation: Superficial personeal nerve • Functions: Statically it plantarflexes the foot on the leg and everts the foot. Dynamically it is a stance phase muscle by assisting the peroneus longus in producing an abductory stabilizing force on the foot during midstance and propulsion, stabilizes the lateral column during midstance and propulsion, resists supination of the foot and external rotation of the leg by the calf muscles, provides a pronatory force at the subtalar and midtarsal joints and assist the peroneus longus in transferring body weight from the lateral to the medial forefoot c. Muscles of the posterior compartment (divided into superficial and deep compartment) i. Gastrocnemius (superficial): • Origin: The medial head (larger) of the gastrocnemius from the posterior portion of the medial condyle of the femur, the lower part of the supracondylar line, and the posterior aspect of the knee joint capsule. The lateral head from the posterior portion of the lateral condyle of the femur and the lower part of the lateral supracondylar line

NOTE* The tendon of the lateral head of the gastrocnemius may contain a sesamoid bone (fabella) The soleus attaches to the medial 2/3 of the deep surface of the tendo- Achilles The plantaris is absent 7% of the time The tendo Achilles is 15 cm in length The gastrocnemius passes across 3 joints (knee, ankle, STJ) The soleus passes across 2 joints (Knee and ankle) • Insertion: Fuse with the soleus to form the Achilles tendon • Vascular supply: Sural branch of the popliteal artery to each head entering the origin of the muscle • Innervation: Tibial nerve • Functions (swing phase): Prevents hyperextension of the knee, assists in deceleration if the internal rotation of the leg toward the end of contact, to prevent torque forces from developing in the knee, assists in developing supination of the STJ during midstance and early propulsion, and flexes the knee and lifts the heel to initiate propulsion ii. Soleus (superficial): • Origin: From the upper 1 /3 of the posterior portion of the fibula, posterior surface of the fibula, posterior portion of the head of the fibula, soleal line on the posterior surface of the tibia, and the middle 1 /3 of the medial border of the tibia • Vascular supply: Posterior tibial artery, peroneal and sural arteries Innervation: Tibial nerve • Functions (stance phase): Stabilizes the lateral forefoot against the ground during late contact and midstance, assists in decelerating knee flexion, assists in decelerating STJ pronation and internal leg rotation at the end of contact, assists in extending the knee during midstance, assists in heel lift during propulsion by stopping ankle joint dorsiflexion iii. Achilles tendon: • The thickest and strongest tendon in the body in the lower 1 /4 of the leg. The fibers of the soleus are anterior to those of the gastrocnemius proximally, and as the tendon passes distally, the gastrocnemius fibers take a lateral turn to become lateral to the soleus fibers iv. Plantaris (superficial): • Origin: From the lateral supracondylar line of the femur, slightly medial to the lateral head of the gastrocnemius • Insertion: Into the medial edge of the tendo Achilles -Vascular supply: Sural arteries • Innervation: Tibial nerve • Functions: Statically it flexes the leg on the thigh and plantarflexes the foot on the leg. Dynamically, it assists the gastrocnemius in its function during locomotion v. Flexor digitorum longus (deep):

• Origin: From the posterior surface of the tibia below the popliteal line and medial to the vertical line and from the fascia of the tibialis posterior muscle belly • Insertion: Into the middle of the bases of the distal phalanges of the lateral 4 toes plantarly • Vascular Supply: Posterior tibial artery • Innervation: Tibial nerve • Functions: Statically, plantarflexing the foot on the leg, flexes the lateral 4 toes upon their metatarsals, and flexes the phalanges of each toe upon each other. Dynamically (stance phase) assists with deceleration of STJ pronation and internal leg rotation during contact, assists with deceleration of the forward motion of the tibia during midstance, assists with STJ supination and external leg rotation during midstance, assists with deceleration of ankle joint dorsiflexion (contributes to heel lift), maintains stability of the lesser digits against the ground during propulsion, assists in plantarflexion of the foot upon the leg during propulsion, and assists the abductor hallucis and FHL in supination of the MTJ about its oblique axis during early propulsion vi. Flexor hallucis longus (deep): • Origin: From the lower 2/3 of the posterolateral portion of the posterior surface of the fibula, posterior peroneal septum, deep transverse intermuscular septum • Insertion: Into the base of the distal phalanx of the hallux, plantarly • Vascular supply: Peroneal and posterior tibial • Innervation: Tibial nerve • Functions: Flexes the hallux at the MTPJ and IPJ, and plantarflexes the foot on the leg. Dynamically it assists with deceleration of the forward momentum of the tibia during midstance, assists with STJ supination and external leg rotation during midstance, assists in deceleration of forward momentum of the tibia, maintains stability of the hallux against the ground during propulsion, assists in posterior stabilization of the phalanges on each other against the 1st metatarsal head, and assists the abductor hallucis and FDL with supination of the MTJ about its oblique axis vii. Tibialis posterior (deep): • Origin: From the posteriomedial surface of the fibula, posterior surface of the interosseous membrane between the tibia and fibula, posterior surface of the tibia • Insertion: Primarily onto the tuberosity of the navicular, however, insertions reach all the tarsal bones except the talus • Vascular supply: Sural, peroneal, and posterior tibial arteries innervation: Tibial nerve • Functions: Plantarflexes the foot on the leg and inverts the foot. Dynamically it is a stance phase muscle that decelerates STJ pronation and internal rotation of the leg during the contact period, assists with deceleration of forward momentum of the leg during the contact and midstance periods, accelerates STJ supination and external rotation of the leg during midstance, assists in heel lift by decelerating forward motion of the tibia in ankle joint dorsiflexion

4. Plantar aponeurosis and plantar compartments of the foot: a. Plantar aponeurosis/Plantar fascia: Is divided in 3 portions (central, lateral, and medial) i. Central portion: Is the thickest and strongest, triangular in shape, with its apex attached to the posteromedial portion of the tuberosity of the calcaneus. It extends distally and separates into 5 bands. At the level of the metatarsal heads, each band divides into a deep and superficial process. NOTE* There are several aponeurotic structures in the distal forefoot associated with the superficial processes: a. Natatory ligament: Made up of 6-8 bands of transversely oriented aponeurotic tissue deep to the superficial portion of the plantar aponeurosis. It divides the area between the web spaces and dermis in the plantar aspect of the metatarsal head region b. Fasciculus aponeurotica transversum c. Sagittal septa d. Vertical fibers e. Mooring ligaments

f. Superficial transverse metatarsal ligament b. Plantar compartments of the foot: Are divided into medial, central and lateral i. Central compartment: Is the largest and contains 4 fascial spaces • Contains tendons of the FDL, tibialis posterior, peroneus longus, and FDB, flexor accessorius, 4 lumbricales, and adductor hallucis ii. Medial compartment: • Contains the tendons of insertion of the tibialis posterior and FHL and muscle bellies of the adductor hallucis and FDB iii. Lateral compartment: • Contains the abductor digiti minimi, flexor digiti minimi brevis, and opponens

5. Intrinsic muscles of the dorsum of the foot: a. Extensor digitorum brevis: i. Origin: From the tubercle at the lateral end of the calcaneal sulcus and cervical ligament ii. Insertion: To the lateral side of the EDL to toes 2, 3, and 4. It runs superficial to the dorsalis pedis artery

iii. Vascular supply: Dorsalis pedis (lateral tarsal branch/perforating peroneal) iv. Innervation: Lateral terminal branch of the deep peroneal and occasionally the superficial peroneal v. Functions: Extends toes 2, 3, and 4 and extends the phalanges on each other. Dynamically it is a stance phase muscle that stabilizes the MTJs oblique axis in a pronatory direction during propulsion, and stabilizes the 2nd, 3rd, and 4th metatarsals against the lesser tarsus in a posterior direction, assists the lumbricales and EDL in extending the 2nd, 3rd, and 4th toes during propulsion b. Extensor hallucis brevis: This is the medial portion of the EDB muscle belly i. Origin: From the tubercle at the lateral end of the calcaneal sulcus and cervical ligament ii. Insertion: Onto the dorsal aspect of the proximal phalanx of the hallux or the lateral aspect of the EHL tendon iii. Vascular supply: Dorsalis pedis (lateral tarsal branch perforating peroneal) iv. innervation: Lateral terminal branch of the deep peroneal, and occasionally the superficial peroneal v. Functions. Extends the hallux at the MTPJ and extends the distal phalanx on the proximal phalanx of the hallux. Dynamically the EHB is a stance phase muscle that stabilizes the 1st metatatarsal against the lesser tarsus during midstance and propulsion, and assists in stabilizing the hallux against the 1st metatarsal in a posterior and abductory direction

6. Intrinsic muscles of the plantar aspect of the foot: a. First layer (superficial): i. Abductor hallucis: • Origin: Medial process of the calcaneal tuberosity, lacinate ligament, plantar aponeurosis • Insertion: Mainly to the plantar part of the MTPJ joint capsule and the medial sesamoid • Vascular supply: Medial plantar artery • Innervation: Tibial nerve • Functions: Statically it flexes and abducts the hallux. Dynamically (stance phase) it stabilizes the hallux in an abductory direction, assists in stabilizing the proximal phalanx against the 1st metatarsal head, plantarflexes the 1st ray, and stabilizes the oblique axis of the MTJ in a supinatory direction during propulsion against the pronatory force of the ground reaction ii. Flexor digitorum brevis: • Origin: Medial process of the calcaneal tuberosity, and the deep surface of the plantar aponeurosis • Insertion: Into the medial and lateral portions of the plantar aspect of the middle phalanx of each lesser toe NOTE* Just proximal to the MTPJ the tendon to each toe divides longitudinally to allow passage of the FDL. It reunites to form a grooved channel for the FDL under the proximal phalanx, and then divides again at the head of the proximal phalanx into 2 tendons • Vascular supply: Medial plantar artery • Innervation: Medial plantar nerve • Functions: Statically it flexes the lesser toes and flexes the middle phalanx upon the proximal phalanx. Dynamically (stance-phase) it stabilizes the oblique axis of the MTJ in a supinatory direction, stabilizes the 2nd, 3rd, and 4th rays posteriorly and plantarly, plantarflexes the lesser rays during propulsion, assists the FDL in maintaining the stability of the lesser digits iii. Abductor digiti quinti (minimi): • Origin: Lateral process of the calcaneal tuberosity, plantar surface of the calcaneus, plantar aponeurosis • Insertion: The lateral side of the base of the proximal phalanx of the 5th toe plantarly with the tendon of the flexor digiti quinti brevis • Vascular supply: Lateral plantar artery • Innervation: Lateral plantar nerve • Functions: Statically it flexes and abducts the 5th toe. Dynamically (stance phase) stabilizes the 5th toe posteriorly, plantarly, and in an abductory direction b. Second layer: i. Quadratus plantae: Has 2 heads with the medial head being larger. The 2 heads come together to form a sheet-like 4 sided muscle • Origin: The medial surface of the calcaneus (lateral head originates anterior to the lateral process of the calcaneus on its plantar surface from the

long plantar ligament) • Insertion: Attaches to the lateral aspect of the FDL tendon, before it divides • Vascular supply: Lateral plantar artery • Innervation: Lateral plantar nerve • Functions: Statically it aids in flexing the 4 lateral toes by assisting the FDL. Dynamically it stabilizes the oblique axis of the MTJ in a supinatory direction during midstance and propulsion, stabilizes the tendons of the FDL, and stabilizes the lesser metatarsals

ii. Lumbricals: Are numbered 1-4 from medial to lateral • Origin: 1 st from the medial margin of the FDL to the 2nd toe. 2nd from adjacent sides of of the 1st and 2nd FDL tendons. 3rd from adjacent sides of 2nd and 3rd FDL tendons, 4th from adjacent sides of 3rd and 4th FDL tendons Insertion: Into the medial aspect of middle of proximal phalanges • Vascular supply: Plantar metatarsal artery • Innervation: 1st lumbrical L5 and S1 (medial plantar nerve), the rest via roots S1 and S2 • Functions: Statically they function to flex the 4 lesser toes, adduct the

lesser toes toward the hallux and extend the phalanges of each toe. Dynamically they function to extend the IPJs of each lesser toe, assist in stabilizing the proximal phalanx of each lesser toe against the ground NOTE* All intrinsic muscles of the 2nd layer are related to tendons of the FDL which pass through it c. Third layer: i. Flexor hallucis brevis: Has a "Y" shaped configuration • Origin: Originates from the medial aspect of the plantar surface of the cuboid (stem), the lateral and plantar aspects of the 3rd cuneiform (lateral arm), peroneus longus sheath, (lateral arm), tibialis posterior to the 3rd cuneiform and cuboid (lateral arm), and tendinous slips of the tibialis posterior to the metatarsal bases (medial arm) • Insertion: 2 heads of insertion into the plantar plate of the 1st MTPJ and sesamoid area, then passes forward to insert with the tendon of the abductor hallucis into the base of the proximal phalanx • Vascular supply: 1st plantar metatarsal artery • Innervation: Medial plantar nerve • Functions: Statically it aids the hallux in flexion. Dynamically (stance phase) it stabilizes the base of the proximal phalanx of the hallux against the ground during propulsion, assists in stabilizing the entire hallux against the ground, and assists in stabilizing the 1st, 2nd, and 3rd metatarsals at the metatarsocuneiform joints during propulsion ii. Adductor hallucis: This consists of 2 different muscle bellies of origin (oblique and transverse heads) • Origin: Oblique head from the medial sides of the shafts and bases of metatarsals 2-4, adjacent portions of associated cuneiforms, and peroneal sheath. The transverse head originates from the deep transverse metatarsal ligaments, plantar plates, joint capsules, and plantar metatarsal ligaments 3-5 MTPJs • Insertion: Both heads insert by a common tendon which inserts into a bony prominence on the inferolateral aspect of the base of the proximal phalanx of the hallux with the tendon of the lateral head of the FHB • Vascular supply: 1 st plantar metatarsal artery • Innervation: Deep branch of the lateral plantar nerve • Functions: Statically flexes hallux. Dynamically the oblique head is a stance-phase muscle that stabilizes the hallux in an adductory direction as well as a posterior direction against the metatarsal head and assists in stabilizing the proximal phalanx against the ground during propulsion. The transverse head is a stance-phase muscle that prevents elongation of the deep transverse metatarsal ligament, and transverse stability to the forefoot at the MTPJs during propulsion iii. Flexor digiti quinti (minimi) brevis: • Origin: From the base of the shaft of the 5th metatarsal, crest of the cuboid, and peroneal sheath • Insertion: To the base of the proximal phalanx of the 5th toe laterally and

plantar (along with the tendon of the abductor digiti quinti) • Vascular supply: Lateral plantar artery • Innervation: Superficial branch of the lateral plantar nerve • Functions: Statically it abducts and flexes the 5th toe. Dynamically it functions as an interosseous muscle during gait

d. Fourth layer: i. Plantar interossei: Three in number • Origin: 1 st from the base and medial surface of the shaft of the 3rd metatarsal. 2nd medial surface of the shaft and plantar surface of the base of the 4th metatarsal. 3rd from the plantar aspect of the base and medial surface of the shaft of the 5th metatarsal • Insertion: 1st inserts into the 3rd toe medially near the base of the proximal phalanx, and the medial side of the 3rd MTPJ capsule. 2nd is into the 4th toe medially near the base of the proximal phalanx, and the medial side of the 4th MTPJ capsule. 3rd inserts medially into the 5th toe near the base of the proximal phalanx, and the medial side of the 5th MTPJ capsule • Vascular supply: 2nd, 3rd, and 4th plantar metatarsal arteries

• Innervation: Lateral plantar nerve • Functions: Statically the plantar interossei aid in flexing the toes into which they are inserted and aid in extension of the IPJs. Dynamically they draw the toes medially toward the 2nd digit

ii. Dorsal interossei: Four in number • Origin: 1st from the adjacent surfaces of the first and second metatarsals. 2nd from the adjacent surfaces of the second and third metatarsals. 3rd from the adjacent surfaces of the third and fourth metatarsals. 4th from the adjacent surfaces of the fourth and fifth metatarsals • Insertion: 1st inserts into the membranous expansion of the EDL to the 2nd toe and the medial side of the base of the proximal phalanx of the 2nd toe. 3rd into the membranous expansion of the EDL to the 3rd toe and the lateral side of the base of the proximal phalanx to the 3rd toe. 4th into the the membranous expansion of the EDL to the 4th toe, and the lateral side of the base of the proximal phalanx of the 4th toe • Vascular supply: 2nd, 3rd, and 4th plantar metatarsal arteries

• Innervation: Lateral plantar nerves (superficial and deep) • Functions: Statically they aid in flexing the toe to which they insert and in extending the IPJs. Dynamically these are stance-phase muscles that stabilize the bases of the proximal phalanges posteriorly and transversely against their metatarsal heads

7. Extensor hood expansion: a. It is a membranous sheet covering each lesser toe from the MTPJ to (and including) the distal phalangeal joint b. It receives contributions from the: i. EDL tendon ii. Plantar and dorsal interossei tendons iii. Tendons of the lumbricales iv. EDB tendon (toes 2-4) v. Deep process of the plantar aponeurosis c. The hood apparatus provides a means for the EDL to extend the proximal phalanx without having a direct connection to it by controlling the actions of the interossei and lumbricales muscles d. The hood apparatus is made up of 2 parts that are continuous with each other, the sling and wing e. The sling is more proximal, and the wing is more distal f. The action of the lumbricales and interossei of the phalanges is intergrated with that of the EDL by the extensor apparatus attachments

Arthrology 1. Tibiofibular joints: The tibia and fibula are joined in 3 areas proximal, distal, and crural interosseous a. Proximal tibiofibular joint: A plane synovial joint between the facet on the medial aspect of the head of the fibula and the fibula facet on the lateral condyle of the tibia i. Anterior superior tibiofibular ligament

ii. Posterior superior tibiofibular ligament b. Distal tibiofibular joint: A syndesmosis between the distal ends of the tibia and fibula i. Interosseous tibiofibular ligament ii. Anterior inferior tibiofibular ligament iii. Posterior inferior tibiofibular ligament

c. Crural interosseous membrane (middle tibiofibular joint): A sheet of fibrous connective tissue between the interosseous borders of the tibia and fibula d. Functional anatomy of the tibiofibular joint: i. Motion is limited to slight rotation and gliding ii. In ankle dorsiflexion, the talus is forced into the ankle mortise, separating the 2 bones (adding stability). Distal separation is limited by the fibrous syndesmosis of the distal joint and the crural interosseous membrane 2. Ankle joint (talocrural): A modified ginglymus or hinged synovial joint. In addition to dorsiflexion/plantarflexion, a small amount of abduction/adduction as well as eversion/inversion a. Articular surfaces (superior concavity): The ankle mortise

i. Distal end of the tibia (tibial plafond): wider anteriorly (produces stability in stance) ii. Comma shaped facet on the lateral surface of the medial malleolus iii. Triangular shaped facet on the medial surface of the lateral malleolus iv Anterior tibiofibular ligament b. Medial collateral ligaments (deltoid): Fans out into one deep and 3 superficial portions, with attachments to the talus, calcaneus, and navicular i. Anterior tibiofibular ligament: Deepest ii. Posterior tibiofibular ligament iii. Tibiocalcaneal ligament: Blends with the spring ligament iv. Tibionavicular ligament c. Lateral collateral ligaments: 3 subdivisions i. Anterior talofibular ligament: Intracapsular, blends with the ankle joint anteriorly, shortest lateral ligament, deep ii. Posterior talofibular ligament: Strongest, intracapsular but extrasynovial iii. Calcaneofibular ligament: Extracapsular, found deep to the tendons of the peroneals NOTE* This ligament crosses the ankle and STJ as does the tibiocalcaneal ligament

d. Fibrous capsule: Surrounds the ankle joint and is attached to the margins of the articular surfaces

e. Synovial capsular membrane: i.Closely attached to the fibrous capsular membrane medially and laterally ii. Bulges are seen at the anterior tibiofibular ligament and parts of the lateral ligament iii. Synovial membrane is exposed near the medial malleolus iv. Loose fold of synovial membrane is present in the ankle mortise between the articulation of the lateral malleolus and inferior surface of the tibia (allows for accommodation of the talar dome) f. Functional anatomy: i. Oblique axis of motion running from posteroinferolaterally to anterosuperomedially (pronatory/supinatory) ii. The axis changes as the foot moves with dorsiflexion and plantarflexion 3. Subtalar joint (anatomic): A modified ginglymus joint NOTE* The "anatomic" STJ is defined as the synovial articulation between the posterior talar facet on the superior surface of the calcaneus and the posterior calcaneal facet on the inferior surface on the body of the talus. The 'functional" STJ includes the middle and anterior facets The anterior and middle facets of the calcaneus are part of the talocalcaneonavicular, a separate Synovial joint.

a. Articular areas: The posterior facets are roughly triangular in shape. The articular surface of the the talus is concave, and the calcaneal surface is convex alond its longitudinal axis b. Sinus tarsi: Formed by the articulation of the sulcus calcanei between the posterior and and anterior-middle facets of the calcaneus and the sulcus tali on the inferior surface of the talar neck. It is wider laterally c. Fibrous capsule: Completely surrounds the joint and reinforced by capsular ligaments d. Capsular ligaments: i. Posterior calcaneal ligament: "Y" shaped. Medial band forms a roof over the groove for the FHL tendon ii. Lateral talocalcaneal ligament iii. Medial talocalcaneal ligament

iv. Anterior talocalcaneal ligament v. Interosseous talocalcaneal ligament (ligament of the tarsal canal): Located within the tarsal canal and strengthens the STJ posteriorly vi. Cervical ligament: Found laterally in the sinus tarsi, and resists supination of the STJ e. Functional anatomy: • Most important STJ supinators are the tibialis anterior and tibialis posterior • Most important pronators are the peroneus longus and peroneus brevis • The long axis of the posterior talar facet of the calcaneus is at an angle of about 40° to the long axis to the foot 4. Talocalcaneonavicular joint: The head of the talus fits into a socket formed by the posterior articular surface of the navicular and the anterior and middle talar articular facets of the calcaneus, as well as the plantar calcaneonavicular ligament a. Classification: A modified condylar joint (capable of gliding and rotatory motion) b. Articular surfaces: i. Head of talus: • Convex in all directions ii. Acetabulum pedis (joint socket): • Anteroinferior portion: Concave in all directions, and formed by the posterior surface of the navicular • Posterior portion: Formed by the anterior and middle articular facets of the calcaneus • Inferomedial portion: Formed by the plantar calcaneonavicular ligament NOTE* The articular area of the talar head is greater than the socket, and as a result, in normal anatomic position, the head protrudes slightly dorsally at the joint c. Capsular ligaments: i. Dorsal talonavicular ligament ii. Plantar calcaneonavicular ligament (spring): Important in supporting the talar head iii. Calcaneonavicular portion of the bifurcate ligament: "Y" shaped with the stem attached to the calcaneus and one arm attached to the cuboid and the other arm to the navicular d. Synovial membrane: Lines the fibrous capsule e. Functional anatomy: i. Some gliding and rotational movements are possible, but the TCN joint cannot act independently ii. Any motion at the STJ causes motion in the TCN joint. Additionally, motion between the talus and navicular also involves the C-C joint

5. Calcaneocuboid joint: Formed by the articulation of the posterior surface of the cuboid and the anterior surface of the calcaneus a. Classification: A saddle-shaped synovial joint b. Fibrous capsule: Surrounds the entire joint and has 3 capsular ligaments i. Dorsal calcaneonavicular ligament ii. Lateral calcaneocuboid ligament iii. Calcaneocuboid portion of the bifurcate ligament c. Extracapsular ligaments: i. Long plantar ligament (long calcaneocuboid): • Superficial and deep fibers • Longest ligament in the foot • Posterior fibers attached to plantar surface of the calcaneus and runs distally to bases of metatarsals 2-5 d. Synovial capsule: Lines the entire joint e. Functional anatomy: Has two axes of rotation i. One axis through the calcaneal process ii. One axis through the head of the talus • Pronation results in the plantar, dorsal, and lateral ligaments being taut • Supination results in the opposite

6. Great tarsal joint: Made up of the following joints a. Cuboideonavicular joint: i. Classification: Syndesmosis or planar synovial ii. Fibrous capsule: Present only when a synovial joint is present. Has 3 capsular ligaments • Dorsal cuboideonavicular • Interosseous cuboideonavicular • Plantar cuboideonavicular i. Function: Very limited motion, but the motion that does occur is with pronation/supination of the STJ b. Cuneonavicular joint: i. Classification: Planar in configuration, with a slight convexity in the navicular ii. Fibrous capsule: Continuous with all 3 navicular facets, but absent laterally. Has 3 main capsular ligaments • Dorsal cuneonavicular • Medial cuneonavicular • Plantar cuneonavicular (divided into 3 ligaments) c. Intercuneiform joints: Forms part of the transverse pedal arch, with the intermediate cuneiform being the highest point of the arch i. Classification: Planar synovial ii. Articular areas: • Medial intercuneiform joint • Lateral intercuneiform joint • Cuneocuboid joint iii. Fibrous capsule: Blends with the cuneonavicular capsule d. Cuneocuboid joint e. Tarsometatarsal joints (2nd and 3rd) f. Intermetatarsal joints (bases of 2nd and 3rd) 7. Tarsometatarsal joints (LisFranc's joint): Formed by the articulations between the anterior surfaces of the cuneiforms and cuboid proximally and posterior surfaces of the metatarsals distally. The 2nd metatarsal base is recessed proximally for added stability and restricted motion. a. Classification: Has 3 synovial joints i. Medial tarsometatarsal joint: Between the base of the 1st metatarsal and medial cuneiform ii. Intermediate tarsometatarsal joint: Between the base of the 2nd and 3rd metatarsals and intermediate and lateral cuneiforms iii. Lateral tarsometatarsal joint: Between the bases of the 4th and 5th metatarsals and cuboid

b. Fibrous capsule: Each T-M synovial joint has its own capsule c. Capsular ligaments: i. Dorsal tarsometatarsal ligaments ii. Plantar tarsometatarsal ligaments d. Inferior surface of the medial cuneiform to the base of the 1st metatarsal i. Interosseous tarsometatarsal ligaments (attach the cuneiforms or cuboid to the metatarsal bases) • Medial interosseous ligament (LisFranc's ligament): Strongest, runs from the lateral surface of the medial cuneiform to medial surface of the 2nd metatarsal base, and is important for stability of the T-M joint • Intermediate interosseous ligament (2nd) • Lateral interosseous ligament (3rd) e. Function: Slight gliding motion of the lesser metatarsal on their adjacent tarsal bones

Chapter 34: SOFT TISSUE TUMORS Soft Tissue Tumors

SOFT TISSUE TUMORS Soft tissue tumors are those originating in the supportive and connective tissues of the body, other than bone or cartilage. Benign and malignant forms occur. In addition, there are tumor-like lesions (“pseudotumors”) that may clinically suggest a neoplasm. The difference is based upon a good history, examination and biopsy

Soft Tissue Tumors 1. Scar (cicatrix), Hypertrophic scar, Keloid: a. Reactive connective tissue lesions, secondary to penetrating trauma, and therefore secondary lesions (see Chapter 13, Dermatology) 2. Fibroma: a. A benign, self-limiting proliferation of fibroblasts, producing collagen, most being subcutaneous single lesions b. They occur at any age c. Koenen's Periungual Fibromas are seen on the hands and feet of about onethird of patients with tuberous sclerosis NOTE* Patients with tuberous sclerosis show an acneform facial rash whose lesions are called adenoma sebaceum, but which are angiofibromas. Some patients also are epileptic due to intracranial calcifications. This form of tuberous sclerosis is called Epiloia. Fibromas may develop independent of other diseases and are firm, discrete lesions. Sometimes other elements are involved, e.g. fibrolipoma, fibrokeratoma, angiofibroma, fibromyxoma, xanthofibroma, neurofibroma, etc. Lesions may recur after excision 3. Fibromatosis: This is a group of diseases demonstrating infiltrative growth that makes them less discreet than fibromas a. Lesions are frequently multiple, and patients may have more than one type b. Plantar fibromatosis usually affects the medial fascial slip, but any area may be affected. This is correctly called Ledderhose's or Dupuytren's disease c. A cure may be impossible because the lesion is infiltrative so that residual unseen lesion is always left behind after excision d. Variants affecting the feet may include juvenile hyalin fibromatosis, extraabdominal desmoid tumors, infantile digital fibromatosis, and juvenile aponeurotic fibromatosis of Keasbey (which also occurs in adults) e. Desmoids also occur in Gardner's syndrome f. Fibromas may histologically resemble well diferentiated fibrosarcoma g. Older Keasbey lesions may become chondrified or ossified. Fibroosseous pseudotumor of the digits affects the fingers and toes, showing soft tissue ossifications. It is not the same as a Keasbey lesion

NOTE* A differential diagnosis of fibrosarcoma vs. plantar fibromatosis should be kept in mind on initial examination of the foot 4. Myxomas: a. Are soft tumors of fibrous origin that show a loose fibrous stroma and much mucin and mucopolysaccharide within b. This group includes digital mucus cysts and the synovial cysts such as ganglion (only when the tendon sheath is present, hence, never distal to the tarsus), and bursa c. Synovial cysts can also be intraosseous lesions d. This group are pseudotumors 5. Fibrosarcoma: a. A malignant, collagenous, metastatic tumor that can occur at any age and which is uncommon in the foot b. They may be deep or intradermal c. They also may be well differentiated or poorly differentiated d. They may show a histologic "herringbone" pattern of cellular arrangement 6. Histiocytomas: a. Are similar to fibromas, but show less collagen b. The histiocyte is considered a facultative fibroblast, a cell state (rather than a true cell type) c. There are 3 major groups: i. Fibroblastic fibrous: includes the following types • Dermatofibroma • Xanthomas (some) • Myxomas • Dermatofibrosarcoma protuberans (malignant): show a storiform pattern histologically ii. Histiocytic fibrous: • Giant cell tumor of soft tissue (and bone) • Xanthogranuloma • Pigmented villonodular synovitis • There are also malignant forms recognized iii. Pleomorphhic fibrous: A group of unusual xanthomas, xanthogranulomas, and atypical fibroxanthomas NOTE* Tendon xanthomas may suggest lipoproteinemia. Necrobiotic xanthogranulomas may be associated with multiple myeloma. Multicentric reticulohistiocytosis may be a cause of polyarthritis 7. Synovial Chondromatosis (loose bodies, joint mice, joint rice, osteochondritis dissecans): a. A rare condition that follows trauma to synovium of large joints such as the ankle b. Some of the bodies may ossify

c. X-rays and scans are helpful in the diagnosis 8. Synovial sarcoma (tendosynovial sarcoma): a. A highly malignant tumor of synovial tissues, often not arising from a joint b. Young people are affected c. They may be slow or fast in growing and are very metastatic, especially if 5 cm or larger in size d. Radiographic techniques and biopsy aid in the diagnosis e. Treat aggressively (chemotherapy, surgery, irradiation) f. This is one of the few tumors for which there is no benign equivalent (i.e. there is no synovioma) 9. Subcutaneous Nodular Fat Necrosis (pancreatic panniculitis): a. Consists of reddish, tender nodules on the feet and ankles often accompanied by ankle arthralgias b. This accompanies pancreatitis and pancreatic carcinoma c. Elevated blood levels of trypsin increase vascular permeability so that elevated serum lipase escapes and damages the fat, causing inflammatory tumor-like nodules d. If biopsy proven, these lesions suggest need for immediate consultation 10. Lipogranulatomatosis (Farber's disease): a. Very rare, recessively inherited sphingolipidosis, showing periarticular and tendon masses, especially at the wrists and ankles b. Other organs are affected and patients rarely live beyond the first year c. The masses may, therefore, be diagnostic, requiring immediate consultation 11. Piezogenic Papules: a. Represent cystic herniations of subcutaneous heel fat into the dermis b. They are seen on weightbearing in obese patients c. They may be painful and can undergo necrosis d. Control with heel cupping devices and diet 12. Lipoma: a. A benign tumor of adipose tissue and multiple lesions may occur b. These may be present independently or as part of Gardner's syndrome and neurofibromatosis-1 c. Lipomas do not reduce in size as fat is lost due to diet or illness d. Variants include fibrolipoma, angiolipoma, and myelolipoma (producing myeloid hematopoietic cells) e. They can be excised locally without recurrence f. Tendon sheath lipomas (endovaginal lipomas) may occur in the feet and/or hands g. Lipoblastoma may affect the feet of children 13. Liposarcoma: a. Is a malignant, metastatic tumor of fatty tissue b. It is probable the most common lower extremity sarcoma in adults, but it is

uncommon in the feet c. There are gradations from well to poorly differentiated d. They may be slow growing and asymptomatic until a nerve or other tissue is sufficiently affected to result In pain or altered function e. These are deep seated tumors that should be excised followed by chemotherapy and irradiation 14. Myositis Ossificans (Munchmeyer's disease): a. A benign reactive lesion deep in striated muscle resulting from trauma b. Early stages may be hard to tell on x-ray and histologically from the parosteal or extraosseous forms of osteogenic sarcoma c. Older lesions appear fully ossified and may be excised if they impede function or cause pain d. Myositis ossificans progressiva is a rare hereditary disease of children and young adults in which ossified lesions affect many tissues and are not related to trauma (patients may show shortened digits, absent thumbs and great toes, or hallux valgus bilaterally) 15. Rhabdomyoma: a. Is a benign tumor of striated muscle and has not been reported in the foot b. Patients showing signs and symptoms of tuberous sclerosis (see Fibroma section this chapter) may have cardiac rhabdomyoma and should, be sent for examination 16. Supernumerary Muscles: a. Have been reported in the ankle region and may simulate tumors 17. Rhabdomyosarcoma: a. Very malignant metastatic tumor of striated muscle b. Rare in the foot, there have been reported cases c. There are 2 main types: i. Embryonal: seen in mostly younger persons ii. Pleomorphic: seen in older persons d. These tumors are fast-growing and they erode bone e. Amputation, chemotherapy, and irradiation are all treatment methods NOTE* Probably the most common lower extremity malignant tumor of children 18. Leiomyoma: a. Is a benign tumor arising from smooth muscle NOTE* The sources of smooth muscle in the feet are the arrector pill muscles associated with pilosebaceous units in the dorsal skin of the feet and toes, and blood vessels (frequently veins) anywhere in the foot. b. The tumors are pilar leiomyomas and angioleiomyomas c. These lesions are often painful

19. Leiomyosarcoma: a. A malignant smooth muscle tumor rare (but does occur) in the ankle or foot area b. Lesions may be superficial (dermal in origin) or deep (subcutaneous) c. Metastases from other sites may occur in the foot 20. Neuromas: a. Are not tumors b. They are reactive lesions arising as a result of trauma c. Rudimentary (supernumerary) digits may contain neuromatous tissues 21. Schwannoma: a. Is the benign peripheral nerve sheath tumor seen in the lower extremities b. It is considered a more accurate term than the older "neurilemoma" or "neurinoma" c. Slow growing, sometimes painful and mainly occurring on the flexor surfaces d. They may fluctuate due to cystic changes e. These fall into the peripheral nerve sheath tumor (PNST) group f. Histologically one sees Verocay bodies that may be well developed (Antoni type A) or that may show myxoid degeneration (Antoni type B) g. The "ancient schwannoma" is one that shows cystic degeneration and/or calcification h. These lesions can be excised and are not recurrent i. In association with neurofibromatosis-1 there may be multiple schwannomas j. The neurothekeoma is a benign peripheral nerve sheath tumor 22. Neurofibroma: a. A benign, slow-growing, solitary, superficial, usually asymptomatic nodule b. Excision is curative c. Most cases occur in women d. Neurofibromatosis-1 (von Recklinghausen's disease, multiple neurofibromatosis) is a hereditary malformation involving neural, cutaneous, and fibrous elements i. Many organ systems may be involved ii. There are strict criteria for diagnosis of neurofibromatosis-1 that involve cafeau-lait spots iii. Patients show a high rate of development of unrelated malignant tumors iv. There is a high risk of transformation of neurofibromas to neurofibrosarcomas in neurofibromatosis-1 v. Diseases associated with neurofibromatosis-1 include: • Scoliosis • Erosions of bone (due to neurofibromas) • Frohlich's syndrome • Addison's disease • Endocrine tumors • Increased incidence of malignant melanoma • Connective tissue tumors • Multiple lipomas

•

Meningocele and syringomyelia

23. Malignant Peripheral Nerve Sheath Tumors (MPNST): a. These include malignant schwannoma and malignant neurofibrosarcoma b. These are extremely rare in the feet but are a risk in the patient with neurofibromatosis-1 (when present there is a high mortality rate c. These tumors may also arise as a result of overexposure to irradiation (therapeutic or occupational) d. These tumors are metastatic and may be painful e. Treatment consists of amputation (improvements in chemotherapy and irradiation are still being assessed) f. Malignant triton tumor is a malignant schwannoma with evidence of concurrent rhabdomyosarcoma 24. Malignant Neuroepithelioma (adult peripheral neuroblastoma, primative neuroectodermal tumor): a. Rare in the feet but has been reported b. Neuroectodermal tumor of infancy (pigmented neuroectodermal tumor of infancy, melanotic progonoma) is also extremely rare in the foot but has been reported 25. Granular Cell Tumor (Abrikossoff tumor): a. Occurs in benign and malignant forms and is uncommon b. It was once thought to be a tumor of muscular origin, but has been shown to be of peripheral nerve origin c. It does occur in the foot 26. Angiomas:. a. May arise from the endothelium of blood vessels and/or lymphatic vessels b. Predominant picture based on the presence of blood cells determines whether the lesion is a hemangioma or a lymphangioma 27. Congenital Hemangiomas: a. May be localized or may involve large areas of limb and or other organs b. Most are capillary hemangiomas and after what appears to be a spurt of rapid growth (in the first 6 months of life) most involute within a year or two c. Patients should be checked to determine whether a larger (venous) hemangioma underlies the surface lesion d. There are rare cases in which capillary hemangiomas in infants are accompanied by thrombocytopenia (Kasabach-Merritt syndrome) 28. Acquired Tufted Hemangioma: a. Is the adult form of congenital capillary hemangioma b. Verrucous hemangioma (angiokeratoma circumscriptum) underlies hyperkeratoses and may clinically resemble warts or angiokeratoma c. Cherry angiomas (De Morgan spots, senile angiomas) are tiny papular angiomas that arise (mostly on the trunk) after adolescence d. Nevus flammeus (nevus telengiectaticus, “port wine stain”) is a dermal lesion

with many dilated capillaries that usually suggests an underlying vascular anomaly such as arteriovenous malformation and/or varicosities in the ParkesWeber syndrome (osteohypertrophic hemangiectasia, Klippel-Trenauney syndrome). The A-V malformations usually produce bruits audible with a stethoscope, local temperature changes, limb hypertrophy, and a risk of “high output” heart failure 29. Cavernous Hemangiomas: a. Composed of arterial and venous channels and are deep, large, diffuse lesions that may clinically feel like a “bag of worms” b. X-rays may show intravascular calcifications called phleboliths (associated with thrombi) c. Venous hemangiomas are clinically similar but do not show the arterial elements i. These types of hemangiomas are seen in the blue rubber bleb nevus, Maffuci (Kast-Maffuci) syndrome, ataxia telangiectasia, von Hippel-Lindau disease, and Sturge-Weber syndrome 30. Angiokeratoma: a. The name given to a number of syndromes that affect the feet (and other areas) showing dilated capillaries (ectasias) with secondary epidermal hyperplastic changes b. There are various types, all (except the Fordyce type) affecting the feet i. Mibelli type ii. Papular type iii. Fabry type NOTE* Angiokeratoma of Fabry is a storage disease whereas the others are not c. Cobb's syndrome involves a cutaneous hemangioma in a dermatomal distribution resembling angiokeratoma and associated with a spinal cord angioma 31. Angioma Serpiginosum: a. Consists of red, flat, grouped, asymptomatic, dilated capillaries, forming netlike or macular patterns b. Most occur in postadolescent women 32. Pyogenic Granulomas: a. Eruptive hemangiomas that are friable, easily traumatized, and that may become secondarily infected b. Most are on a stalk 33. Glomus Tumors (glomangiomas, angiomyoneuromas): a. Arise in the digits as a tiny, painful and tender, frequently subungual tumors b. They arise from the Suquet-Hoyer canal, the shunts arising from arterioles

that bypass the capillary network to the venules c. They may be red to purple and may be accompanied by thrombocytopenia (hence a variant of the Kasabach-Merritt syndrome) d. Most occur as single lesions e. Glomangiosarcoma is extremely rare, but has been reported 34. Synovial Hemangiomas: a. Arise in joints and tendon sheaths b. Rare and difficult to excise c. There is pain, swelling, joint effusion and hemarthrosis 35. Hemangiopericytoma: a. Rarely occurs in the feet b. There are benign and malignant forms, and histologic characteristics do not necessarily correlate with the benign or malignant nature of the lesion c. The patients must be watched for recurrence and/or metastases 36. Lymphangiomas: a. As a group are rare b. They may arise in the context of chronic and extensive lymphedema, e.g. Milroy's disease, elephantiasis due to Wucheria infestation, etc. c. Cystic hygroma represents a cavernous lymphangioma 37. Papillary Endothelial Hyperplasia (Masson's pseudoangiosarcoma): a. An intravascular proliferation of endothelial cells in association with a thrombus, and usually follows trauma b. It is not common c. Most cases show single lesions and these may be difficult to differentiate histologically from angiosarcoma 38. Ectasias (vascular dilatations): a. May occur in the feet and be mistaken for angiomas b. The most common is the “spider nevus” (spider angioma, nevus araneus) 39. Angioendothelioma: a. The name given to group of lesions that are considered by some to be of intermediate malignancy b. Types: i. Spindle cell type: • Is most apt to occur on the lower extremities • Uncommon, seen frequently in young males ii. Reactive proliferating angioendotheliomatosis: • A vascular, benign lesion in response to infection, (especially subacute bacterial endocarditis) that truly involves endothelial proliferation • Usually clears n 6-24 months • AIDS patients may develop this lesions n response to cat scratch fever organisms (Rochalimaea henselae) iii. Malignant angioendothelioma:

• A malignant intravascular lymphoma and not an angioma or angiosarcoma 40. Angiosarcomas: a. Very rare in the lower extremities b. Very malignant endothelial tumors, usually occurng in the elderly c. They may be associated with chronic edema d. They may grow rapidly and may metastasize e. Most cases are fatal f. Amputation a good distance proximal to the tumor is the surgical approach g. Irradiation has not been very effective h. Some superficial forms (not the deep forms) have been treated successfully with carbon dioxide laser i. Patients must be checked for recurrences and metastases 41. Kaposi's Sarcoma (multiple idiopathic hemorrhagic sarcoma): a. Is related to immunodeficiency, occurs n older patients, AIDS patients, and patients on chemotherapy or post-transplant immunosuppression therapy b. May occur n the presence of leukemias and lymphomas c. Lesions may appear as purpuric macules, papules, patches, nodules, plaques, and tumors d. Silent visceral lesions may be present e. It is presently divided into the following types: i. Classic (sporadic) epidemic (non AIDS) • Attributed to the elderly eastern and southern European men • Skin associated lesions frequently begin on the feet ii. African- affects adults and children and not restricted to the feet iii. Allograft-associated (immunosuppression) iv. Epidemic (AIDS-associated) NOTE* On occasion, malignant lower extremity tumors may develop that cannot be clearly identified as to tissue of origin. These include the alveolar soft-part sarcoma, the mesenchymoma, and any undifferentiated malignant soft tissue tumor 42. Nodules of Metastatic Lymphoma (non-Hodgkins) or Myeloid Leukemia (granulocytic sarcoma, chloroma): a. May occur n the dermis as metastatic site to feet b. Biopsy is diagnostic c. Mycosis fungoides is a T-cell lymphoma originating n the skin i. Woringer-Kolopp disease: Is the localized epidermotropic form formerly called Pagetoid reticulosis ii. Sezary syndrome: is the systemic form • Circulating abnormal lymphoid cells • Peripheral lymphadenopathy • Erythroderma • Intense pruritus

43: Mastocytomas: a. Are tumors formed by mast cells b. Some localize to the dermis others are systemic c. Dermal lesions urticate (Darier's sign) d. Pruritis and flushing may occur due to local vasodilatory effects of mastcell derived histamine shock e. A single local lesion is known as urticaria pigmentosa 44. Metastatic Cancers: a. Metastatic cancers from visceral organs may occur in the dermis b. They are usually rapidly growing, multiple (various sites) and otherwise nonspecific clinically c. A history if malignant tumor (even years ago) is a clue, but not always present d. Even with such a history, a new lesion may be an independent entity

Chapter 35: Physical Medicine and Rehabilitation for the Management of Foot Conditions Physical Modalities and Diseases

PHYSICAL MEDICINE AND REHABILITATION FOR THE MANAGEMENT OF FOOT CONDITIONS Physical medicine can broadly be defined as that element of health care that utilizes physical agents such as light, heat, cold, water, electricity, mechanical agents such as excercises, aids to ambulation, gait training, tests and measurements in the diagnosis and treatment of disease. Physical Modalities and Diseases 1. Physical modalities (used for foot conditions) a. Ultrasound b. Short wave diathermy c. Infrared lamps d. Radiant light bakers e. Whirlpool f. Contrast baths g. Paraffin baths h. Massage i. Ultraviolet radiation j. Electrical stimulation k. Hi-lo galvanic current l. Faradic current m. Sinusoidal current n. Transcutaneous electrical nerve stimulation (TENS) o. Cold packs p. Lasers q. Traction r. Intermittent compression s. Exercise i. Passive ii. Active assistive iii. Voluntary active iv. Active resistive v. Coordinative t. Gait training u. Crutches/walkers/canes/braces/parallel bars v. Prosthetics/orthotics w. Activities of daily living x. Diagnostic procedures and tests 2. Chronically disabling conditions which usually present with pedal manifestations: a. Arthritis b. Burns c. Cerebral palsy d. Cerebral vascular accidents e. Congenital deformities

f. Dermatomyositis g. Degenerative spinal cord disease h. Joint deformities i. Muscular contractures j. Muscular atrophy k. Paraplegia l. Quadraplegia m. Peripheral nerve injuries n. Peripheral vascular disease o. Anterior poliomyositis p. Polymyositis q. Polyneuritis r. Residuals of severe trauma s. Scleroderma t. Spina bifida u. Spinal cord injuries v. Stasis dermatitis w. Ulcerations x. Chronic renal failure y. Alcohol/drug abuse z. Chemical dependency 3. Treatment considerations: Examples of conditions which involve the foot that benefit from the use of physical medicine and rehabilitation a. Adhesive capsulitis b. Antalgic gait c. Arthritis (acute or chronic) d. Arthritis with nerve root pressure e. Ataxic gait f. Atrophy g. Burns h. Bursitis i. Causalgia j. Capsulitis k. CVA's l. Compression syndromes (entrapments) m. Contractures n. Contusions o. Degenerative joint disease p. Dislocations q. Fasciitis r. Fibrosis s. Foot drop (peroneal palsy) t. Fractures u. Hemiplegia v. Inflammation (acute or subacute) w. Multiple sclerosis x. Muscle spasm (acute. or severe)

y. Muscular dysfunction z. Myositis A. Nerve palsy B. Neuralgia C. Neuritis D. Osteoarthritis (acute or severe) E. Osteomyelitis F. Osteoporosis G. Pain H. Paralysis from nerve disease or injury I. Paraplegia J. Parkinson's disease K. Periostitis L. Peripheral neuritis M. Peripheral neuropathy N. Post joint surgery O. Quadriplegia P. Radiculitis Q. Scleroderma R. Sesamoiditis S. Severe or generalized weakness T. Severe osteochondritis dissecans U. Sprains/strains V. Sudeck's atrophy W. Synovitis X. Tendonitis/tenosynovitis Y. Trauma/post-trauma Z. Ulcerations

Therapeutic Modalities and Procedures 1. Therapeutic cold: a. Indications: i. To reduce pain and edema following trauma ii. To reduce pain iii. To create a reactive hyperemia iv. To help reduce inflammatory reactions v. To provide for local tissue destruction vi. To decrease local tissue metabolism vii. To help facilitate muscle contraction in some forms of neurogenic weakness b. Basic contraindications and precautions: i. Hypertension ii. Raynaud's disease or phenomenon iii. Vascular disease iv. History of frostbite or pernio v. Rheumatoid arthritis vi. Cold hypersensitivity vii. Any condition that produces a cold pressor response c. Methods of application:

i. Immersion ii. Cold packs iii. Ice Massage iv. Cryokinetics v. Contrast applications with heat 2. Therapeutic Heat: a. Physical agents (superficial heat): These modalities cause a rise in tissue temperature generally limited to the skin and subcutaneous tissue. The effect is increased circulation, with histamine release and enhanced phagocytosis and lymph flow. Also there is a sedative type effect and increased connective tissue extensibility i. Hot water ii. Hot air iii. Infrared iv. Radiant light v. Whirlpool vi. Paraffin vii. Hot packs b. Physical agents (deep heat): These modalities cause the same physiological effects as with superficial heat agents, but they also have the ability to heep deep structures such as muscle and joint capsule. These modalities are extremely useful for helping regain lost motion in contracted joints or shortened muscles i. Short wave diathermy: NOTE* High frequency electrical energy extends from electrode to electrode through human tissue causing a heating effect. The diathermy may be either short wave (heating within a magnetic field) or microwave energy beamed from an "antenna" to, an area of the body ii. Microwave diathermy: not to be used if a patient has a pacemaker iii. Ultrasound: NOTE* High frequency sound produced from the vibration of a piezoelectric crystal. Sound energy is passed directly through the skin and causes heating at interfaces such as junctions between different tissues. An example of this is the junction between bone and muscle. c. Primary physiologic effects: i. Hyperemia ii. Sedation iii. Analgesia iv. Increased regional vascularity v. Increased tissue temperature vi. Increased metabolic rate vii. Arterial dilatation

viii. Increased capillary flow and hydrostatic pressure ix. Increased collagen extensibility x. Increased tissue inflammatory response xi. Increased edema d. Indications: i. Analgesia ii. Increased local vascular cutaneous flow iii. Sedation iv. Hyperemia v. Accelerate the suppurative process vi. Muscle spasticity vii. Joint stiffness vii. Contractures e. Contraindications and precautions: i. Tendency to hemorrhage ii. Active hemorrhage iii. Impaired sensation to pain and temperature iv. Ischemia and vascular impairment v. Non-inflammatory edema vi. During the immediate (24-48 hour) post trauma period vii. Known malignancies viii. Patients with coma or paralysis ix. Use with extreme caution if there is a threat of hemorrhage, in the very old or the very young, and in those patients who have debilitated or insensitive conditions f. Modalities for superficial therapeutic heat: i. Baths ii. Electric heating pads iii. Hot packs iv. Hot water bottles v. Compresses vi. Paraffin vii. Radiant heat viii. Lamps ix. Bakers g. Modalities for superficial heat by convection: i. Hot air baths ii. Moist air baths iii. Agitated water baths or whirlpool h. Modalities for deep heat: i. Short wave diathermy ii. Microwave diathermy (caution in patients with pacemakers) iii. Ultrasound i. Infrared radiation: i. Superficial heat source ii. Bulbs iii. Bakers iv. Heat lamps

v. Heated carborundum rods vi. Glowing wire coils with proper reflectors j. Infrared radiation indications: i. Subacute and chronic inflammation ii. Contusions (if no threat of hemorrhage) iii. RA iv. Early joint stiffness v. Degenerative or osteoarthritis vi. Sprains/strains vii. Neuritis viii. Myositis k. Infrared contraindications and precautions: i. Acute inflammation ii. Malignancy iii. Ischemia iv. Impaired sensation (pain and temperature) v. The very young/elderly who are unable to respond to the effects of heat l. Deep heat (short-wave diathermy) contraindications and precautions: i. Hemorrhage or suggestion of hemorrhage ii. Sensory loss iii. Application over moist dressings iv. Malignancy v. TB vi. Areas of ischemia vii. Arteriosclerosis viii. Thromboangiitis obliterans ix. Metal implants x. Foreign bodies xi. Pregnancy/menstruation xii. Suppuration xiii. Special care in patient with pacemakers xiv. Special care in the geriatric and pediatric patient xv. Metal contact with skin or other tissues xvi. Epiphyseal and developing bone m. Deep heat indications: i. Post trauma (after the threat of hemorrhage) ii. Analgesia iii. Pain and spasm iv. Inflammation (subacute or chronic) associated with: bursitis, periostitis, arthritis, neuritis, neuralgia, myositis, capsulitis, postfracture care, fibrositis, tenosyovitis, tendonitis, sprains, strains v. Rheumatoid arthritis vi. Postdislocation vii. Reflex vasodilation n. Microwave diathermy contraindications and precautions: i. Ischemia ii. Hemorrhagic areas iii. Tumors

iv. Impaired sensation v. Debilitation vi. Edema vii. Use over wet dressings viii. Metallic implants ix. Pregnancy x. Use over adhesive dressings xi. Special care over bony prominences xii. P.V.D. xiii. Synovitis with excessive areas of synovial fluid xiv. Systemic and local infections xv. Patients with pacemakers xvi. Care in the pediatric/geriatric patient o. Microwave diathermy indications: i. Deep heating of subcutaneous tissue and superficial musculature ii. Musculoskeletal system for joint diseases (DJD, RA, bursitis and tendonitis) iii. Post trauma if no threat of hemorrhage iv. Strains/sprains v. Neuritis p. Ultrasound indications: i. Joint contractures associated with immobilization, trauma, scarring, RA and DJD ii. Pain iii. Muscle spasm iv. Tendonitis v. Acute inflammation due to trauma vi. Adjunct to exercise therapy vii. Phonophoresis with indicated drugs viii. Subacute sprains/strains ix. Calcific bursitis x. Resolution of hematomas xi. Neuroma/neuritis q. Ultrasound contraindications and precautions: i. Basic contraindications for all forms of deep heat ii. Avoid large fluid areas iii. Hemorrhagic diseases iv. Decreased sensation and insensitivity v. Vascular insufficiency vi. Tumors v. Malignancies vi. Over epiphyses vii. Pacemakers viii. With caution over implants both from a thermal and mechanical concern r. Hydrotherapy indications: i. Muscle weakness ii. Following amputation iii. Following joint injury iv. Paraplegia

v. Burns vi. Selected post-surgical debridement vii. Selected spastic palsy viii. Selected flaccid paralysis s. Whirlpool bath indications: i. Chronic post-traumatic conditions ii. Early joint stiffness iii. Pain iv. Painful scars v. Adhesions vi. Neuritis vii. Arthritis viii. Tenosynovitis ix. Strains/sprains x. Painful stumps xi. Preliminary to massage, exercise and electrical stimulation x. Burns xi. Post CVA xii. After fracture care xiii. Vascular insufficiency xiv. Decubitus ulcers xv. Industrial medicine xvi. After peripheral nerve injuries xvii. Dermatologic debridement xviii. Sports and dance medicine xix. Post surgical rehabilitation t. Whirlpool bath contraindications/precautions: i. Acute phlebitis ii. Osteoporosis (caution) iii. Cardiac (caution) iv. Immediate trauma v. Excessive edema vi. Vascular or neurologic impairment vii. Non-inflammatory edema viii. Caution in the geriatric/pediatric patient u. UV radiation precautions: i. Photo-ophthalmia of patient and operator ii. Hypersensitive areas (skin folds) iii. Unusual skin sensitivities iv. Photosensitive drugs (sulfonamides, tetracyclines, green soap, dyes, coal tar preparations, oral hypoglycemics, chlorthiazide diuretics, phenothiazines) v. UV radiation indications: i. Local UV radiation for its anti bacterial /fungicidaI effects for superficial ulcers, infections, dermatophytosis, and sterilization of fresh wounds ii. Decubitus ulcers iii. Boils/carbuncles/furunculosis iv. Burns

v. Eczema vi. Contact dermatitis v. Erysipelas vi. Felon vii. Granulating tissue viii. Infectious eczemoid dermatitis ix Intertrigo x. Psoriasis xi. Leukoderma and vitiligo xii. Urticaria ix. Diabetic ulcerations (caution) w. UV radiations contraindications/precautions: i. Excessive exposure ii. Photosensitivity iii. Encapsulated pus without drainage iv. Acute generalized dermatitis v. Drug photosensitivity vi. Malignancies vii. Sarcoidosis viii. Lupus erythematosus ix. Herpes simplex x. Caution with the cardiac, renal or with hepatic insufficiency 3. Manual modalities: a. Massage indications: Classical massage, transverse friction massage i. Relief of pain ii. Arthritis iii. Periarthritis iv. Bursitis v. Neuritis vi. Fibrositis vii. Mobilization of contracted tissue viii. Reduction of swelling and induration b. Massage contraindications: i. Infection ii. Cutaneous inflammation iii. Tumors iv. Burns v. Skin diseases in relation to contamination and irritation vi. Clotting disorders vii. Fractures viii. Thrombophlebitis ix. Aneurysms x. Thrombosis xi. Fever xii. Acute systemic disease c. Manipulation indications: i. Loss of range of motion

ii. The residuals of long periods of immobilization iii. The residuals of trauma and/or capsular inflammation d. Manipulation contraindications: i. Immediate post trauma ii. Joint effusion iii. Acute inflammation iv. Ligamentous rupture v. Dislocation (unless used for repositioning) vi. Fracture (unless used for repositioning) 4. Kinetic Procedures a. Therapeutic excercise: Prescribed to increase and maintain joint and soft tissue mobility, prevent adhesions and fibrosis, and to aid in soft tissue healing i. Techniques: • Resistive: Isotonic, isometric, and isokinetic (Kin-Com, Cybex, and Biodex) • P.N.F.: Proprioceptive neuromuscular facilitation (exercise which employs combined neuromuscular training techniques • Neuromuscular re-education (secondary to nerve injury) ii. Indications: • Preventing joint contractures • Preventing joint adhesions • Increasing joint range of motion due to trauma, muscle spasm, disease, or states that limit function and mobility and prevent activity • Arthritis and related conditions • Post-amputation • Neuromuscular and collagen diseases that produce contractures and limited ranges of motion • Paresis due to multiple conditions, such as CVA, • Weakness and atrophy due to disuse and/or after immobilization • Muscular weakness • To strengthen muscles iii. Contraindications/precautions/limitations: • Acute active inflammation • Active post-trauma • Severe cardiovascular disease • Severe pulmonary disease • Metastatic malignancies • Nonunion fracture sites (caution) • Pain in the arthritides (caution) • Severe joint and/or muscle pain (caution) • Infection b. Range of motion exercise: i. Active: patient exercises on their own ii. Passive: Joint mobilization or manipulation iii. Active assist

5. Electrical modalities: This group of modalities delivers an electrical current to the patient with various physiological effects. Among these effects are pain relief, reduction of swelling, and muscle stimulation for enhancement of strengthening or retardation of atrophy. a. TENS: Used for reduction of pain. The Gate Control theory of pain states that stimulation of large diameter nerve fibers may effect transmission of a noxious stimuli before it reaches the cortex. This theory was used to explain TENS for many years. More recently, other theories of central modulation have been used to explain why TENS causes a reduction of pain i. Indications: • Chronic pain • Acute pain associated with postoperative control • Arthritis • Bursitis • Sprains/strains • Tenosynovitis • Metatarsalgia and related foot pain • Painful motor and sensory nerve lesions • Post amputation pain including phantom pain • Peripheral neuritis ii. Contraindications: • Cardiac pacemakers • Carotid sinus • Insulin pump • In the presence of electronic life support systems • Over denuded skin b. Iontophoresis: An electrical generator with DC current used for ion transfer of medication into areas beneath the skin. This is often used for the purpose of infliltrating a tendon, ligament or joint capsule with an anti-inflammatory or anesthetic c. Electrical stimulation: Is a high frequency current used primarily for enhancement of shortening exercised i. Indications: • Injury to the muscles/tendons/joints • Paralysis • Sprains/strains • Postfracture and after dislocation to help retard atrophy and restore muscle function • To help restore muscle tone and strength • To help provide tissue contraction to milk tissues of excess fluids • To relieve muscle spasm from trauma and associated muscle conditions • Muscle pain and spasm • Myositis • Metatarsalgia • Post polio • Muscle re-education • Following surgery to help prevent clots and embolism

• With ultrasound for trigger points and pain • Denervated muscles • To help retard muscle atrophy • Synovitis • Disuse • Fibrositis • Contractures • Pain with ankylosis • Stress and anxiety ii. Contraindications/precautions: • Individual patient reactions • Allergy • Placement of electrodes over malignancies • Severe inflammation • The head area • Cardiac area • Pacemakers • Pregnancy • Special concerns in the presence of vascular and/or neurologic deficiencies d. Galvanic currents: i. Indications: • Reduce pain • Reduce swelling • Increase local circulation • Aid in nerve regeneration • Soften scar tissue e. Hi-volt: This high voltage, low amperage modality is used for pain reduction, swelling reduction and muscle stimulation. Tissue impedance is overcome more easily due to the high voltage, allowing deeper penetration of current. Some theories state that inflammation may also be reduced by using this modality f. Interferential: This modality relies on an extremely high frequency (25004000Hz) to allow deeper penetration for the purpose of stimulation of nerves for pain relief. MODALITY Electrical Stimulation Monophasic D/C High volt or interferential

Electrical Stimulation Low voltage Monophasic

Electrical Stimulation

INDICATIONS

PRECAUTIONS

Pain reduction Muscle reeducation and strengthening Muscle pump for edema reduction Increase ROM Acute inflammation Fracture healing Wound healing Fracture healing lontophoresis Pain reduction

Pacemakers Thrombophlebitis Malignancy Skin sensitivity Pregnancy

As above

Pacemakers

Pulsed Biphasic A/C TENS TEAM

Muscle spasm Increase ROM

Skin sensitivity

Diathermy

Improve circulation Increase local metabolic activity Increase tissue temperature Reduce muscle guarding or spasm Reduce chronic inflammation Facilitate wound healing Analgesia/sedation Increase connective tissue stentibility Acute inflammation Chronic inflammation Vasoconstriction Control edema Analgesia Reduce muscle guarding or spasm Improve ROM Reflex vasodilation Decrease local metabolic activity Vasodilation Analgesia/Sedation Reduce muscle guarding or spasm Increase metabolic activity Facilitate tissue healing Chronic inflammation Increase connective tissue distensibility Deep tissue involvement Increase circulation Increase metabolic activity Reduce chronic inflammation Reduce muscle guarding or spasm Improve healing Phonophoresis Decrease edema Reduce acute bleeding Acne Wounds (septic or aseptic) Folliculitis Tinea Pedis Pityriasis rosea

Metal implants Pacemakers Malignancy Wet dressings Decreased sensation Acute inflammation Poor circulation Pregnancy Over the eyes

Short wave Micro Wave

Cryotherapy Ice CO2 Cold Compression

Superficial Heat Whirlpool Paraffin Hot Packs Infrared

Ultrasound

Intermittent Compression Ultra Violet

Cold hypersensitivity Cold urticaria Poor circulation Healing wounds Hypertension

Acute inflammation Poor circulation Malignancy

Infection Malignancy Acute inflammation Epiphyseal areas Early fractures Thrombophlebitis Poor circulation Poor sensation Over the eyes Over the pregnant uterus Medication allergies Pain Circulatory impairment Poor circulation Generalized dermatitis Renal or hepatic insufficiency Hyperthyroidism

Psoriasis

Lupus Pellagra Herpes Eczema Diabetes Psoriasis Sensitizing medications

Chapter 36: Arthroscopy Ankle Arthroscopy

ARTHROSCOPY The most important indication for an arthroscopic procedure is less disability than an open joint procedure. The advantages of arthroscopy are its use as a diagnostic tool to see the pathology present when there is pain or disability in the absence of a positive on MRI or CT, and ability to simultaneously correct the condition. Hence it is a diagnostic and therapeutic procedure

Ankle Joint Arthroscopy 1. History: a. Takagi (1918): First use in cadaveric knee- Tokyo, Japan b. Bircher (1921): First arthroscopic knee examination (meniscus) c. Burman (1931): First use in the USA (a cadaveric knee) d. Takagi (1939): First successful ankle arthroscopy e. Watanabe and Takagi: First operative procedure f. Watanabe (1945): Developed smaller scopes to be used in joints g. Heller and Vogler (1982): Podiatric applications of ankle arthroscopy 2. Patient evaluation and selection: Arthroscopy of the foot and ankle should only be done after all conservative measures have been exhausted a. Diagnostic indications: i. Unexplained pain ii. Swelling iii. Stiffness iv. Instability v. Hemarthrosis vi. "Popping" b. Therapeutic indications: i. Debridement of osseous bodies ii. Repair of the ATFL iii. Irrigation iv. Septic joint (flush out bacteria) v. Osteochondral defects vi. Soft tissue impingement vii. Synovitis viii. Arthrofibrosis ix. Arthrodesis c. Contraindications: i. Cellulitis and local infections ii. Fused joint iii. Moderate DJD with restricted range of motion iv. Severe edema v. High risk medical patients 3. Instrumentation: a. Arthroscopes: 2.7 mm, 4.0 mm with 30° viewing b. Trochars, canulas and obturators c. Accessory instruments (biopsy forceps, scissors, grasping forceps, suction punch, meniscal knives, cutter, shavers, probes, suture delivery systems) d. Irrigation system (normal saline, Ringer's lactate or acetate) e. Other: Electrosurgical units, lasers, distraction devices (noninvasive or

invasive) 4. Ankle portals: a. Anteromedial: i. Medial to the anterior tibial tendon, saphenous nerve and vein ii. Visualization of the medial gutter, medial transchondral bone margins b. Anterolateral: i. Lateral to the peroneus tertius and EDL ii. Care must be taken to preserve the superficial peroneal nerve iii. Visualization of the lateral gutter c. Anterocentral: i. Lateral to the EHL ii. Care must be taken to preserve the anterior tibial artery and deep peroneal nerve d. Posterolateral: i. Patient is usually prone ii. Incision is lateral to the Achilles tendon iii. Care must be taken to preserve the sural nerve and lesser saphenous vein e. Posteromedial: i. Medial to the Achilles tendon ii. Care must be taken to preserve the posterior tibial artery and nerve iii. Visulalization to the posterior process of the talus and transchondral lesions to the back of the talus f. Accessory portals 5. Anatomy: a. Anterior joint pouch: i. Medial gutter: • Medial malleolus • Adjacent talar medial articular surface • Anterior tibiotalar ligament (floor of the gutter) • Posterior tibiotalar ligament (with valgus stress)

a. Anterior ankle (continued): i. Medial bend • Anterior tibial lip • Medial talar shoulder • Tibial plafond

a. Anterior ankle (continued): i. Anterior joint line • Sagittal groove of the talus • Synovial recess (tibia) • Capsular reflection (tibia)

a. Anterior ankle (continued): i. Lateral talar shoulder • Tbiofibular synovial recess • Tibiofibular synovial fringe • Anterior inferior tibiofibular ligament

b. Anterior ankle (continued): i. Lateral gutter • Mdial fibular articular surface • Anterior talofibular ligament • Posterior talofibular ligament (with varus stress deep in the lateral gutter)

b. Posterior ankle: i. Posterior joint pouch: • Posterior tibial lip • Posterior talar dome • Sagittal groove of the talus • Psterior tibiofibular ligament • Labrum of the posterior tibiofibular ligament • Medial bend • Medial malleolus • Posterior tibiotalar ligament

b. Posterior ankle (continued): i. Posterior ankle via an anterior view • Posterior tibiofibular ligament • Posterior capsule wall • Medial bend • Medial gutter • Posterior dome of the talus

6. Ankle Pathology: a. Soft tissue: i. Synovitis ii. Fibrous bands iii. Meniscoid bodies • Wollins lesion iv. Adhesive capsulitis b. Cartilage: i. Subchondral erosions ii. Chondromalacia: • Collins classification: Grade 1 : Fraying Grade 2: Fibrillation, fissuring Grade 3: Extensive fissuring Grade 4: Cartilage loss • Goodfellows classification (superficial degeneration): Type 1 : Superficial erosion Type 2: Loss of superficial layer Type 3: Exposed subchondral bone Type 4: Deep matrix exposed • Goodfellows classification (basal degeneration):

Stage 1 : Cartilage softening Stage 2: Blister formation Stage 3: Exposed matrix Stage 4: Bone exposed iii. Chondral lesions: • Bauer and Jackson classification: Type 1: Linear crack Type 2: Stellate lesion Type 3: Cartilage flap Type 4: Avulsed with exposed bone Type 5: Fibrillation Type 6: Fibrillation plus subchondral erosion c. Osseous pathology: i. Osteochondral bodies ii. Subchondral bone cysts 7. Specific ankle joint pathology: a. Osteochondral lesions b. Avulsion fractures of the ankle: i. Anterior/posterior tibial lips ii. Ligamentous insertions c. Medial impingement lesions d. Transchondral ankle fractures: i. Berndt and Harty classification: Stage 1: Compression Stage 2: Partially detached Stage 3: Totally detached Stage 4: Avulsed e. Tibial lip fractures f. Impingement exostosis 8. Specific procedures done arthroscopically: a. Ankle arthrodesis b. Lateral ankle stabilization 9. Post-operative care and rehabilitation: a. With exploration and general debridement: compressive dressing and immediate weightbearing b. With ligamentous repair: range of motion within 24 hours, patient in an aircast 6 weeks post-weightbearing c. With debridement for chondral defect: non-weightbearing 8 weeks with active range of motion d. With arthroscopic arthrodesis: 8 weeks in hard non-weightbearing cast followed by 2 weeks in weightbearing splint 10. Complications of ankle arthroscopy: a. Scope breakage

b. Infection c. Cartilage injury or creation of multiple small bodies d. Hemarthrosis due to trochar damage e. Compartment syndrome f. Polyneuritis of the ankle g. Venous laceration h. Painful scar i. Nerve laceration j. Recurrence of symptoms

Chapter 37: Laser Applications in Podiatric Surgery Lasers and Laser Physics Fundamentals Tissue Interraction Laser Safety Clinical Applications in Podiatric Surgery The CO2 Laser The Nd: YAG Laser The ARGON Laser The KTP Laser Other Surgical Lasers

LASER APPLICATIONS IN PODIATRIC SURGERY

Applications of lasers to medicine and surgery have increased exponentially over the past decade. This technology has become established in the medical community and has become the standard of care for many procedures. Lasers have justified their utilization by the improved clinical outcome in the delivery of comparably more traumatic and invasive procedures. Some procedures are not possible without the precision or uniqueness of this modality. There are a great variety of laser types and delivery systems, each having indications unique to the desired tissue response. Fundamental to the surgeon in selecting the wavelength, power and control to produce the intended effect, with safe handling of the instrument, is a knowledge of laser physics for this tissue interaction. LASERS AND LASER PHYSICS HISTORY 1. The Quantum Theory: Max Planck 1910 Light is quantified in Photon units the basic unit of light (6.625 x 10-27 erg sec (cm2/sec)) 2. Stimulated Emission Theory: Albert Einstein 1917 Basis of laser light 3. First laser developed, demonstrated and patented Theodore Maiman Ruby Laser 1960 UNITS OF MEASUREMENT 1. Frequency Expressed in Cycles per Second (CPS) Hertz (Hz) 2. Wavelength The measurement of one crest to another of a particular frequency 3. Length

4. Time

5. Power

Meter = the basic measurement unit Prefix centi (cm) = 1 x 10-2 meters = .01 meters -3 mili (mm) = 1 x 10 meters = .001 meters micro (um) "micron" = 1 x 10-6 meters = .000001 meters nano (nm) = 1 x 10-9 meters = .000000001 meters Second = the basic measurement unit Prefix mili (ms) = 1 x 10-3 seconds = .001 seconds micro (us) = 1 x 10-6 seconds = .000001 seconds -9 nano (ns) = 1 x 10 seconds = .000000001 sec pico (ps) = 1 x 10-12 seconds = .000000000001 sec Watts (W) = The basic measurement unit Power density = Watts per centimeter squared (W/cm2) Joules (J) = Watts x Seconds of power on tissue

FUNDAMENTALS 1. The wavelength is the key to tissue absorption, laser delivery systems and to laser safety. 2. Comparison with other modalities: Scalpel --> Mechanical pressure. Local effect. Controlled crushing. Electrocautery --> Electrons. Conduction through isotherms. Global effect. Radiosurgery --> Radio Frequency transmission. Local effect. Laser --> Photon absorption. Specific to tissue content. Thermal precision. 3. The mnemonic "LASER": L ight A mplification by S timulated E mission of R adiation 4. Laser frequencies most commonly used are in the infrared and visible spectra. 5. These are non-ionizing photonic radiation. 6. No lead shielding is required. 7. Exception: Excimer (UV) lasers are ionizing. 8. Laser light is NOT a natural phenomena. UNIQUE CHARACTERISTICS OF LASER LIGHT Coherent Monochromatic Collimated Coherent = All crests of wavelengths line up. Crests and troughs are equidistant in time and space. This eliminates wavelengths canceling each other out and producing interference patterns which would decrease its intensity. This enables very efficient power production. Coherent light, (compared with incoherent, conventional light) can be focused to an exact single point. ie: 200 W of incoherent conventional light will illuminate a room. 200 W of coherent laser light will rapidly carve through the cement wall of the room. Monochromatic = Pure, single color. Responsible for the interaction of tissue chromophores producing a specific effect. ie: CO2 laser to incise and ablate amelanotic tissue, Nd:YAG for deep tissue penetration, Argon penetrates epidermis. Collimated = Emitted stream of photons is linear, and does not diverge. This also eliminates wavelengths producing interference patterns reducing power. COMPONENTS OF A LASER 1. Partially reflecting mirror 97% 2. Fully reflecting mirror 100% 3. Lasing media 4. Xenon flash lamp

5. high frequency Switching system 6. High voltage power supply 7. Delivery system - Articulating Arm, Fiberoptic, waveguide 8. Lense 9. Aiming Laser (HeNe), if required, depends on laser type

Conventional light radiation + Multiwavelength - polychromatic + Divergent + Coherent + Spontaneous Emission THEORY of LASER OPERATION 1. Spontaneous Emission (conventional) 2. Stimulated Emission (laser)

Laser light radiation + Pure - monochromatic + Collimated + In phase + Stimulated Emission

CREATION OF LASER LIGHT V. CONVENTIONAL LIGHT 1. Lasers are classified by the type of active media used in the laser tube. ie: CO2 laser tube filled with CO2 (excitable media), N2, and He gasses. Nd:YAG is a Yttrium, Aluminum and Garnet crystal doped with Neodymium as the excitable media. 2. Atoms are stimulated to rise from a lower energy shell to a higher shell, 3. Then fall back to emit a specific monochromatic wavelength of light. 4. These waves reflect in the laser media randomly at first, then become coherent together by being amplified by reflecting between the mirrors. 5. Once their energy exceeds the threshold of transmission through the partially reflecting mirror, laser radiation is emitted in a linear, collimated, array. 6. Frequency doubling media is also used to change laser wavelength. ie: Tunable dye or KTP (Potassium, Titanium, Phosphate) laser. The KTP crystal pumps a KTP crystal. Efficiency drops to about 30% of input. Nd:YAG Laser -----------> KTP Crystal------------> output 1060 nm 532 nm DELIVERY MECHANISMS 1. Low frequencies = longer wavelengths = far- and mid-infrared. Articulating arms, or internally reflecting waveguides are used. 2. At near-infrared, 2100 nm and above (Ho:YAG laser) fiberoptics contain these frequencies having a higher index of refraction. 3. Fiberoptics are constructed of quartz (Aluminum dioxide), silicon dioxide or silver halides, coated with a plastic sheath. 4. Lenses, or contact light scalpels of selective focal lengths, can be integrated into the terminal end of the fiberoptic system. 5. The bare fiber is also used for free beam ablation work.

TRANSMISSION MODES 1. Desirable laser energy distribution energy follows a Gaussian curve. 2. Energy decay falls exponentially on either side of the curve.

TEM00 has a narrow spot size true Gaussian curve. 0.2 mm diameter spots appropriate for cutting

TEM01 small spot 0.3 mm at best called "near Gaussian" not desirable can be used for ablation.

TISSUE INTERACTION 1. This is THE most important aspect of lasers in medical science. 2. Tissue interaction with the specific laser wavelength is the KEY to laser selection. TRANSMISSION CHARACTERISTICS THROUGH TISSUE 1. reflection 2. transmission 3. scattering 4. adsorption ** Absorption of specific wavelength by specific chromophores is key.

CLINICAL TISSUE INTERACTION PHENOMENA The effect on tissue by thermal lasers commonly used in Podiatry is both: 1. power and 2. time dependent: POWER DENSITY 1. Is the standard of expression in documenting laser power to tissue. 2. Expressed in W/cm2. 3. P.D. maybe constant while tissue spot size and power varies.

This allows physicians to communicate standard terminology, allows for preference. It is the STANDARD OF CARE: in operative reports describing laser use It is necessary for communicating standard measurement in the scientific community. A typical example using 14 Watts with a 0.2 mm diameter contact tip or spot size (which is 0.1 mm radius) Traditional Algebraic: WATTS 14 4.46 446 ----------- = --------------------- = ----------------- = --------------------- = 44,600 0.12 0.01 0.01 pi x r2 3.14 x --------102 100 where: 0.1 is the radius 10 is the conversion factor of 10 mm/cm a shortcut algebraic: WATTS 127 x ----------- = d2

14 127 x --------- = 0.22

44,450

WATTS PER CM2 Chart WATTS

TIP DIAMETER (mm) or CO2 Spot Size (mm) 0.1 0.2 0.4 0.6 0.8 1.0 2.0 3.0 ----------------------------------------------------------------------------------------------------------------------4 50,955 12,739 3,185 1,415 796 510 127 57 5 63,694 15,924 3,981 1,769 995 637 159 71 6 76,433 19,108 4,777 2,123 1,194 764 191 85 7 89,172 22,293 5,573 2,477 1,393 892 223 99 8 101,911 25,478 6,369 2,831 1,592 1,019 255 113 9 114,650 28,662 7,166 3,185 1,791 1,146 287 127 10 127,389 31,847 7,962 3,539 1,990 1,274 318 142 11 140,127 35,032 8,758 3,892 2,189 1,401 350 156 12 152,866 38,217 9,554 4,246 2,389 1,529 382 170 13 165,605 41,401 10,350 4,600 2,588 1,656 414 184 14 178,344 44,586 11,146 4,954 2,787 1,783 446 198 15 191,083 47,771 11,943 5,308 2,986 1,911 478 212 16 203,822 50,955 12,739 5,662 3,185 2,038 510 226 2,166 541 241 17 216,561 54,140 13,535 6,016 3,384 18 229,299 57,325 14,331 6,369 3,583 2,293 573 255 19 242,038 60,510 15,127 6,723 3,782 2,420 605 269 20 254,777 63,694 15,924 7,077 3,981 2,548 637 283 21 267,516 66,879 16,720 7,431 4,180 2,675 669 297 22 280,255 70,064 17,516 7,785 4,379 2,803 701 311 23 292,994 73,248 18,312 8,139 4,578 2,930 732 326 TIME The gating of the flash lamp may be: 1. C.W. Continuous Wave - Continuously on 2. Single Pulsed - Continuous on for a preset period 3. Superpulsed - Rapid pulsing at peak power at 250 - 1000 Hz. Average power is determined by 1. pulse width and 2. repetition rate This allows tissue to undergo "thermal relaxation" 4. Ultrapulsed - Much higher RF (Radio Frequency) switching nanosecond pulse width. More thermal precision. 5. Q-switched - Very high peak power with picosecond pulse width THERMAL RELAXATION = Interval between pulses to allow dissipation of energy. Minimum interval is 1:10 ratio on-off.

LASERS APPLICABLE TO PODIATRIC SURGERY WAVELENGTH 10,600 um Far IR

USE IN PODIATRY Noncontact: Dissection Derm.Pathologies Nail Pathologies

DEPTH OF PENETRATION 0.1 mm

FUNCTION Cutting Ablation Coagulation

Nd:YAG

Bare Fiber Deep tumor destr.

6-8 mm

Ablation Coagulation

Nd:YAG

Contact-tip: Dissection

50-200 u

Cutting

2,100 um Mid IR

Ho:YAG

Near-contact: Cartilage and bone

0.4-0.6 mm

Ablation

4881514 um

Argon

Noncontact Verruca

Dermal vessels

Photoablation

532 um

KTP

Noncontact: Cutaneous vascular Verruca Contact: Dissection

Dermal vessels

Photoablation Cutting

Noncontact: Cutaneous vasc. lesions

Dermal vessels

1,060 um Near IR

478 urn

CO2

CopperVapor

1-2 mm Photoablation

ie: CO2 is strongly absorbed by water, therefore superficial penetration. Holmium is absorbed by water but not as much as

C02, so deeper tissue penetration. Argon and KTP are absorbed by Hb and chromophores. Nd:YAG (bare fiber) is not absorbed by anything, so it penetrates. LASER SAFETY 1. Reference: "ANSI 136.3 Publication" on laser safety 2. Four Classes of Lasers: Class I - No ocular damage with direct viewing Class II - Ocular damage with prolonged exposure Class III - Ocular damage to the eye before the eye can blink Class IV - Medical lasers. Great potential and hazard to the eye and skin. Ignites combustible materials. Beam = fire hazard. 3. Dedicated laser nurse in O.R. controlling use and monitoring laser safety 4. Key operated, controlled access. 5. Room shields to outside personnel. 6. Eye protection for patient and all OR personnel. 7. Wavelength specific eye protection hung outside the door so that people can enter the room safely. 8. Adequate smoke evacuation appropriate to tissue atomization. 9. Dual stage filtration, carbon and 0.2 um filter. 10 Coaxial visible aiming beam for use with invisible light lasers. 11 Proper filtering mask. EYE PROTECTION 1. Impact is direct or reflective. 2. Minimal hazard zone is determined to be 6 feet away from the reflected zone. 3. O. D. = Optical Density, expressed as an exponent of power of 10. ie: O. D. of 5 is 100 x as absorbent as O. D. of 3 4. Always expressed as an O.D. at a specific wavelength 5. Recommended to surgeon (direct viewing field) - minimum O.D. of 5 @ wavelength. 6. Recommended to OR personnel (indirect) - minimum O.D. of 3 @ wavelength. 7. Conventional glass or plastic glasses will stop CO2 8. Recommend UV coating to stop the ultraviolet fluorescence off carbonization. 9. Eye protection still necessary for endoscopic procedures, fibers could break. 10. High density filters on endoscopes, arthroscopes, waveguides. 11. The reflected light transmits directly back to the surgeon. CO2 - corneal burn. Surgeon's cornea replaceable. Argon, KTP - retinal damage,

Irreversible. Nd:YAG absorbed in the vitreous humor causing posterior cataract formation. Reversible? Doubtful.

DRAPING FOR LASER SURGERY 1. Surgical site draping for CO2 laser use should be wet towels. 2. Drapes should be dry for the Nd:YAG procedures. (Water is a transmitter at the YAG frequency and absorbed at CO2 frequency.) 3. Laser nurse - laser on standby when not immediately using the instrument avoids accidental discharge. 4. Multiple foot switches - Bovey, power saws, table, can be confused with the laser. 5. A defocused beam has more of a tendency to start fires. 6. A focused beam will have a tendency to drill. 7. A prefocused beam will have a tendency to accelerate the hole it is drilling. The power density increases approaching the focal point. 8. Always have water on hand, to extinguish a potential flame. 9. Anodized instruments (blackened or roughened) are helpful to diffuse the beam, minimizes reflections but does not eliminate. 10. Endotracheal tubes should be coated with Mirasil (noncombustible material). HAZARDS OF THE LASER SMOKE PLUME 1. Epidermis with the CO2 laser creates a great deal of smoke. 2. The shock waves backscatter verrucoid particles which can be inhaled. 3. Vaporized tissue and debris is liberated by tissue atomization 4. Studies show live intact DNA recovered from the laser plume. 5. Hazard in AIDS and hepatitis patients Hazard in patients with infectious lesions, i.e. warts. 6. Lesions have been reported by Dermatologists, Podiatrists, and Gynecologists. 7. Formaldehyde also produced, large number of other carcinogens. High power plume evacuators are required with dual stage filters. 1. Charcoal filter for carcinogens, smell. 2. Filtering down to 0.2 microns to filter out virus a. The key is good technique in smoke evacuation. b. Keep the smoke evacuator close to the area of surgery. c. A laser mask will filter down to 0.3 microns. d. These measures reduce nearly all of the hazards of the viral particles

II - CLINICAL LASER APPLICATIONS IN PODIATRIC SURGERY STANDARD OF CARE

1. OPERATIVE REPORT - Include laser type power density calculation. ie: "Procedure: Austin Bunionectomy, left foot (Soft tissue with CO2 laser): With the CO2 laser set at 33,000 W/cm2 power density, a linear incision was ..." 2. CONSENT FORM - Include the laser type or wavelength used and the intended application of the laser if there is conventional instrumentation used. ie: "(Usual description of surgery), soft tissue with CO2 laser" 3. ETHICS IN ADVERTISING - Differentiate the application of the laser ie: "Laser assisted" bunionectomy, or "Laser for soft tissue" Advertise straightforward what laser procedures (warts, nails) are done if also advertising conventional procedures (bunionectomy) that are not performed with laser assistance. Public misconceptions: No incision, laser cuts bone. You will never lose a patient because of an honest disclosure of a procedure.

THE CO2 LASER

PROPERTIES OF THE CO2 LASER 1. Active media is C02, helium, nitrogen Carbon dioxide is the excited media Helium and neon are catalysts 2. High absorption in water, Tissue mostly water therefore superficial absorption "What-you-see-is-what-you-get" Low scattering in tissues 3. Invisible beam at 10,600 nm far-infrared, helium-neon aiming beam necessary ADVANTAGES OF USING THE CO2 LASER 1. Thermal precision Maximum impact on target and minimum damage to adjacent tissue 2. Absolute hemostasis minimizing postoperative edema. Coagulates small blood vessels, lymphatics (<0.5 mm diameter) Minimizes pathways spreading malignant cells 3. Accelerated healing of internal tissue because of lack of mechanical trauma. Fibroblasts are less stimulated. therefore skin sutures need to be left in tissue a few days longer, however internal scarring is less tissue remodeling is minimized due to little scar formation. earlier joint range of motion. 4. Minimal postoperative pain sealing axonal tubules in small cutaneous nerves 5. Pain may increase several days postoperatively if patient weightbearing sealed exoplasm from nerve endings is under increased hydrostatic pressure electrolytes stimulate neural discharge 6. Sterilization of the target sight Inactivate any bacteria, fungi, or virus 7. No foreign body reaction

8. Versatile - Operates in CW or pulse mode to vaporize or incise tissue 9. Portable and inexpensive relative to other lasers 10. Minimal amount and cost of disposable laser items per case. 11. Handpieces easily sterilizable 12. Least expensive laser

SELECTION OF LASER PARAMETERS 1. Appropriate power, spot size, power duration, and angle to tissue 2. Ablational work: spot size less than 2-3 mm in diameter 3. Incisional work: spot size less than 0.3 mm in diameter DISADVANTAGES 1. Cost, power, alignment, control, additional informed consent 2. Smoke evacuation system 3. Combustible materials risk, extra drapes, higher protection 4. Special training for physician/staff 5. Learning curve 6. Credentialling process/extension of privileges if hospital use PROCEDURES PERFORMED USING THE CO2 LASER ASSIST 1. Plantar Verruca Ablation 2. Porokeratoma Ablation 3. Nail Matrixectomy Ablation 4. Fungal Nail Treatment - Drilling through nail plate 5. Heel Fissure Debridement 6. Ulcer Debridement/Sterilization 7. Incisional Procedures for soft tissue component (of neuroma, bunion, etc.) THEORY OF CO2 LASER TISSUE INTERACTION 1. Controlled, highly localized vaporization. 2. Energy is absorbed by water. 3. High conductivity minimal to adjacent tissue damage. 4. Avoid tissue carbonization - increases and conducts thermal effects Immediately seen. Worse problem at low power densities. Global tissue temperature and thermal conductivity. Wipe this off with a damp gauze.

CO2 LASER PROCEDURES TECHNIQUE OF CO2 LASER ABLATION

1. Power Density over 1000 W/cm2 2. Larger spot size- 2-3 mm The following diagrams, illustrate two methods: linear and circular overlap. The goal is an evenly ablated surface. 1. Circumscribe lesion by 2 mm peripherally 2. Curette representative area and send biopsy for pathology. 3. Deep channels should be avoided. 4. Do not penetrate dermis in verrucoid lesions. 5. If you have a 0.2 mm spot size at focal point, defocus to 1.0 mm. For example, 20 watts with a 1 mm spot size equals 2540 watts/cm2 power density. Scarring results from dermal penetration IPK's and porokeratosis are focally penetrated to the dermis. 1. Need to lase to subdermal fat. 2. 75% cure rate, somewhat higher than conventional applications. 3. Little scarring. 4. More focal treatment is required at higher power levels. 5. Remove char by lavage or sponge

TECHNIQUE OF CO2 LASER FOR INCISION/EXCISION 1. Power density greater than 6,000 watts/cm2 preferred 2. Small spot size, maximum 0.3 mm diameter, 3. TEM01 lasers are not able to produce less than 0.3 mm spot at focal point. Thus they are not appropriate for making incisions. 4. TEM00 lasers are available to deliver 0.1 mm, but commonly 0.2 mm. Example: a. 20 watts with 0.2 mm spot size equals 63,500 watts/cm2 power density. b. Technique: smooth rapid continuous motion c. In focus d. Traction and countertraction perpendicular to incision. 5. Traction/countertraction of the incised area will enable smooth tissue plane delineation. 6. Retrace path to achieve desired depth. 7. Important: Characteristics of individual lasers vary greatly.

8. Test on a tongue blade first. Depth should be a little over halfway through with minimal charring. NOTES: 1. A TEM00 laser produces a very different effect compared to a TEM01 machine 2. A superpulsed laser has a variety of pulse settings to achieve the same P. D. 3. The ultrapulsed lasers cut faster at lower power settings. 4. These are characterized by very short duration RF pulsed power supplies Power densities are a general rule of thumb and should be adjusted to 1. each wavelength, 2. the particular instrument and 3. the type of tissue undergoing surgery. HEMOSTASIS 1. By Coagulation: Defocus to a spot size greater than twice the vessel diameter Use a Power density less than 1500 watts/cm2 Technique: defocus beam to increase spot size and direct beam at site 2. By Dessication (thermal contraction): Spot size 1 mm Power density as with coagulation Technique: direct beam to tissue immediately adjacent FOCUSED, FREE BEAM LASER APPLICATIONS 1. In Focus: Incision 2. Defocus: Debulking 3. Greatly defocused: Coagulating 4. Prefocused: Avoid altogether OVERLASING Significant problem to inexperienced user is "Overlasing" Definition: delivery of an inappropriate amount of laser energy to target tissue or to the surrounding tissues producing unintended tissue destruction. (Immediately visualized with CO2 lasers.) CAVERNOUS HEMANGIOMA 1. Considered ablative surgery requiring high power densities. 2. This is a highly vascular tumor. 3. Nd:YAG (bare fiber) is appropriate for deep penetration 4. Causes deep thermal vascular stenosis. 5. CO2 is not good for coagulation for these tumors, but it can be used. 6. KTP and Argon are more appropriate for superficial vascular lesions. KELOID AND HYPERTROPHIC SCAR 1. Excellent indication for CO2 laser excision because of lack of fibroblast stimulation. 2. Superficial epidermal incision with the CO2 laser, NOT with the steel scalpel.

3. Avoid charring, will delay healing. 4. Refer to technique for incision/excision LASER ASSISTED OSSEOUS PROCEDURES 1. Advertise as laser assisted bunionectomy. 2. Lasers used for soft tissue dissection only. 3. Not FDA approved for osseous work. 4. Used for incision, soft tissue dissection and capsular work. 5. Result is less postoperative pain, edema, and earlier range of motion. 6. Fascial layers - very little water content therefore is more transmissible at this wavelength 7. Excellent for capsular incision. Earlier ROM. contraindicated for periosteal dissection hemostasis of ALL vessels. This seals the metaphyseal arteries and slows periosteal healing 8. Remember the delayed skin healing effect 9. Leave the sutures in a few days longer 10. Fibroblast stimulation is minimal thus scar formation is minimal 11. Better cosmetic result. BONE AND CARTILAGE 1. Accidentally hitting the bone cortex will take 16-20 weeks to heal. Solution: Debride damaged cortex immediately. Damage is usually superficial. 2. Carbonization in a joint will set up severe chronic inflammation. Solution: Lighten up on capsular dissection in this area Irrigate thoroughly postoperatively, as always 3. Excellent application for subchondrodesis procedures Instead of using K-wire to drill use CO2 at high P.D. for 0.5 seconds. Space closer together with less mechanical disturbance to cartilage LASER TREATMENT OF VERRUCA 1. CO2, Nd:YAG, Argon, KTP 532 can be used. 2. Selection or combination treatments depend upon clinical presentation. The technique is to ablate in a layering method 1. Anesthesia, avoid epinephrine. Avoid directly sublesional. 2. Drape area using moist towels or laser safe drapes. 3. Power density CO2 laser: 6,000 to 21,000 watts/cm2. Decrease for light skinned and thin skinned individuals Also reduce power density for thin areas on dorsal areas of the foot 4. Circumscribe lesion taking 2 mm min border of normal appearing tissue at the periphery. Viable verruca in this tissue. 5. Do this in focus. 6. Submit representative biopsies. 7. Plow multiple interspersing furrows and crosshatch these to an even base. 8. Next wipe area with a sterile, moist gauze to remove char. Avoid relasing char. 9. Repeat lasing and wiping until dermal/epidermal separation occurs. Epidermis will appear to peel away from the dermis. 10. Several passes are required on the plantar surface of the foot. Desired depth is papillary dermis.

11. Healing will occur from basal cells in the dermal papillae. 12. Relase superficial areas until an homogeneous depth is encountered to rete ridges. 13. Photocoagulate in a defocused mode. Coagulate the surface to a very light haze. This also sterilizes the surgical bed of viral particles. 14. Work is complete. Do not revaporize. Inspect with magnification. 15. Silvadene cream and sterile dressing for 24 hours. Avoid occlusive dressings. Extra strength Tylenol for small lesions Hydrocodone 2.5 mg i-ii Q 4 h prn for large masses 16. Expect moderate drainage for 3 days to 1 week. Wound closes completely in 1 month entirely healed. In 2 months no signs of treatment are usually visible. * Treat lesions less than 1 cm from each other as one lesion * Do not leave a bridge of healthy skin between. Handling large lesions: i.e. large, mosaic verruca. 1. Keep depth of penetration even. 2. Circumscribe and divide the lesion into quadrants. 3. Lase each quadrant individually. 4. If the patient is supine, work from posterior to the anterior If bleeding is encountered be sure it does not drain over the surgical site. 5. Be prepared with extra smoke evacuation filters. To accomplish hemostasis, if needed:: 1. reduce the power density and "brush" hemorrhagic area. 2. Power density can be reduced by backing off to a defocused mode. 3. Suction blood away first - laser does not coagulate free blood Postoperative Care: 1. Patient seen 3 days to 1 week 2. Patient allowed to clean twice daily with H202 and bandaid exception: large lesions require redressing until drainage decreases. 3. Normal bathing after first redressing. Accommodative pad if needed. 4. Stop dressing when drainage ceases, no dressing at night. 5. Monitor patient for at least 6 months due to the nature of HPV. 6. Success rate easily 90% after learning curve reached. Complications: 1. Infection--rare, laser sterilizes the bed. 2. Overlasing NOTES: 3. Increased pain--result of overlasing. 4. Increased bleeding--result of overlasing

5. Increased scarring--result of overlasing 6. Scarring--Penetration of dermis

LASER NAIL MATRIXECTOMY

1. No epinephrine 2. No tourniquet - will have good hemostasis 3. Avulse the nail, do not ablate with laser 4. Power settings: 0.2 mm spot size, 125 mm focal length lense, 10 watts CW 5. Aim at 45 degrees, under proximal nail fold for acisional technique 6. Outline matrix and circumscribe to periphery of distal phalanx condyle avoid lasing bone. 7. Lase the matrix in layers achieving a uniform layer of desiccated tissue. Debride with a dermal curette to the next layer of matrix. Stop when coming close to bone. Several passes are necessary 8. Keep site very dry and free from blood. 9. Dilute phenol may be used as an adjunct, but the laser replaces the blade. 1. Techniques for missing part of the matrix are just a probable with laser or blade 2. Characterized as a blind procedure. 3. Burning bone may result in periostitis, very rare. 4. Recurrence after learning curve partial permanent procedure, hallux, 0.5%. 5. These rate of results after learning curve reached. 6. Usually recurrence is keloid, hypertrophic scar formers, and psoriatic patients 7. Patients with high epidermal growth turnover 8. Total permanent if recurrent in these patients POSTOPERATIVE CARE 1. Leave sterile dressing on 24 h Patient to change at home Patient to clean twice daily with H202. No soaks. 2. Some tissue necrosis 1 week 3. Patient to keep dry for 3 days 4. Patients seen 24 hours - 3 days postop 5. Bandaid dressing 6. Normal healing 7. Discontinue dressing and soaks when drainage ceases, generally 2 weeks 8. Allow it to drain 1-3 weeks until it stops draining spontaneously. 9. Total permanent drain more on the 3 week margin, lesser digit partials for a week or so.

COMPLICATIONS 1. Increased pain 2. Increased drainage 3. Delayed healing 4. Soft tissue infection 5. Thermal osteitis 6. Osteomyelitis 7. Overlasing is generally the culprit of all those complications. PREVENTION OF COMPLICATIONS 1. Use appropriate power density 2. Keep the hand piece moving or apply power with periodicity 3. Keep exposure time on a given spot to a minimum 4. Don't relase over char 5. Always know where the beam is going, especially these blind procedures FROST AND WINOGRAD TECHNIQUE 1. Do not use lasers to cut the nail- excessive heat. Use incisional power densities as described for incisional procedures 2. Laser is 90 degrees to the skin, P.D.= 40,000 W/cm2 Then decrease when performing matrixectomy 3. Incision would be the same otherwise as the Winograd please refer to that section within this review book 4. Laser incision is made straight back past the eponychium Second curvlinear incision around soft tissue pathology Remove hypertrophied nail lip and granuloma tissue. 5. Closure with 4-0 Nylon suture. 6. Tourniquet is not necessary. LASER TREATMENT OF ONYCHOMYCOSIS 1. No anesthesia required 2. Laser "mottling" techniques 3. Object is to punching holes in the top nail plate 4. This allows topical medications to penetrate a. Laser settings to just barely fire through a tongue depressor. b. These settings should be just subthreshold for patient feeling any heat c. Laser must be in a pulsed mode d. holes drilled 4-5 mm apart e. Three separate treatments 6 weeks apart. f. Topical antifungal applied BID SUBTOTAL MATRIXECTOMY 1. Anesthesia as before 2. The plate is always removed conventionally 3. Lasing is performed on the total matrix 4. however only scanned to 50% of the depth 5. The idea is to remove only part of the nail matrix to result in a thinner nail

SUBUNGUAL HEMATOMA 1. No anesthesia 2. Same procedure as mottling technique 3. Slightly higher power Density may be used 4. Lase a couple of holes until the nail plate is penetrated. 5. Hematoma will isolate thermal effects. LASER TREATMENT OF GRANULOMAS These respond very well to laser treatment 1. Ablate the granuloma in a crisscross pattern, the same as verruca 2. Alternate with a moist gauze until normal tissue is encountered 3. Good hemostasis should be encountered throughout the procedure 4. No chemocautery, bovey, or hemostatic solutions are necessary 5. Once the granuloma is gone the minimal bleeding encountered stops 6. Defocus, relase, apply sterile dressing. 7. Home treatment and followup as with verruca. CAUTION IN REVISIONAL PROCEDURES Scar tissue, if encountered, has less water content. Therefore reduce power density when you relase this type of tissues. Otherwise excess vaporization penetrating tissue planes may occur.

THE Nd:YAG LASER GENERAL DESCRIPTION 1. 1060 nm, near-infrared, separate HeNe aiming beam 2. Most frequently used laser besides the CO2 laser 3. This is a general surgical instrument used most of the time by general, thoracic, plastic, and urologic surgeons 4. See absorption chart - Nd:YAG is centered between other common medical lasers 5. Unique characteristic - the "window" of low absorption and high transmissibility YAG is poorly absorbed by hemoglobin, chromophores, protein, or water. 6. 99% of Podiatric use is with contact laser scalpels 7. Able to coagulate vessels < 0.2 mm diameter 8. User friendly, but tip selection, type and size must be understood 9. Power settings are very important 10. Endoscopically/arthroscopically compatible MODES OF OPERATION 1. Non-contact mode - used for debulking and treating deep tumors. higher power levels required ie: 40 W 2. Contact-tip mode - highly localized scalpel form similar to CO2 laser lower power ie: 12-16 W (frosted tip) 4-6 W (nonfrosted) 3. Contact-tip is very superficial absorption, cutting only at the tip. "What-you-see-is-what-you-get"

Noncontact is indicated for deep Contact is used for incision and excisional work.

tumors.

THE INSTRUMENT 1. Instrument is portable, conventional nondedicated power OK 2. C.W. mode only 3. Flashlamp excites Neodymium-doped crystal of Yttrium, Aluminum, Garnet 4. Fiberoptic delivery system, air or water cooled within the sheath 5. Large variety of handpieces, general surgical one is used 6. Large variety of contact tips, fiber and handpiece combinations THE CONTACT TIP 1. Developed for 3-dimensional feedback, feels similar to a conventional scalpel Better control of dissection 2. Converts light energy from a laser into heat energy. 3. Very precise hot knives, tissue effect 50-200 microns 4. Types of conical tips: Frosted, clear, ceramic, titanium coated There are many combinations of tips: 1. Sapphire scalpels interchangeable - screw onto handpiece 2. Integrated quartz tips with fiber and handpiece also used 3. Scalpel must be in contact with tissue when power on or flare out of expensive tip will occur 4. Flare-out threshold temperature: Sapphire scalpel - 2000 degrees F Quartz scalpel - 1000 degrees F 5. Tip shapes - Chisel, flat, round, cylindrical, hook a. Long or short conical used in Podiatry b. Tapered conical tip concentrates energy c. Polished lense at distal end d. Available radii are 0.2-1.2 mm diameter

i. when calculating P.D. don't forget diameter -> radius ii. and mm to cm conversions 6. Frosted and nonfrosted available a. Frosted - distal end roughened to allow lateral radiation except at lense and allows coagulation during dissection b. Nonfrosted - tip is clear i. radiation only at distal lense ii. appropriate for very fine dissection at low power levels c. Procedures are scalpel specific SURGICAL APPLICATIONS LASER SCALPEL Rapid dessication Seals small nerves Seals small vessels Cell necrosis is small Cuts with Light Energy High precision

STEEL SCALPEL Controlled crushing Smears small nerve endings No microcoagulation Cell necrosis is moderate Cuts with physical pressure Normal tactile feedback

ADVANTAGES OF Nd:YAG OVER SCALPEL 1. Less postoperative pain 2. Less bleeding of smaller vessels/lymphatics - less swelling 3. Sterilizes surgical site reducing chance of infection 4. Less cell necroses 5. Less fibroblastic stimulation - faster tissue remodeling Nd:YAG MEDICAL INDICATIONS 1. Situations contraindicating tourniquet particularly where a dry field is essential 2. Dissection of delicate tissue planes in all axis requiring contact 3. Patients where surgical trauma may stimulate adverse reactions Collagen-vascular disease (ie: SLE), gout, R.A., etc. 3. Patients with platelet, hematogenous and vessel disease, sickle cell, phlebitis 4. Elderly patient exhibiting capillary fragility PODIATRIC MEDICAL INDICATIONS FOR Nd:YAG SCALPEL 1. The Nd:YAG laser scalpel decreases the surgical pathophysiology of a. edema in a dependent extremity b. leakage of intravascular fluid in the surgical site of the foot from hydrostatic pressure c. nerve microtrauma and axonal depolarization d. local surgical cell necroses (v blade) e. scar formation f. nosocomial infection 2. Extremity surgery a. Hydrostatic pressure, terminal perfusion. weightbearing b. structure undergoing reconstructive surgery are all

c. factors complicating foot and ankle surgery 3. Hypertensive patient with peripheral edema 4. Plastic reconstruction 5. Wet cases 6. Cases where visualization must be optimized ie: Nerve decompression within ganglion complex 7. Any situation where cell necrosis must be minimized CONTRAINDICATIONS Defer these cases until the learning curve plateau is reached 1. Digital surgery - cannot justify utilization Instrument overkill for procedure 2. Revisional surgery - actually indicated but these surgeries carry a higher risk by default If successful laser gets the credit If not successful surgeon gets blammed Public expectations of lasers are high 3. Any bone work - not FDA approved This is not a wavelength for this 4. Medical-Legal cases - Same idea as revisional Surgery 5. Amputation - Same idea as revisional surgery 6. PVC cases - Same idea 7. Acute Trauma cases - no time to call in laser team INDICATIONS FOR FROSTED AND NONFROSTED CONTACT TIPS PROCEDURE Nerve releases and Neuroma Neurectomy Bunionectomy (soft tissue) Ganglions

CONTACT-TIP Nonfrosted Nonfrosted Frosted Nonfrosted

Tendon transplants/lengthening Heel spur (soft tissue) Plantar Fasciotomy General Podiatric Surgery dissection

Nonfrosted Frosted Nonfrosted Frosted

INAPPROPRIATE Nd:YAG PROCEDURES 1. Wrong tip = wrong procedure ie Neuroma sx with frosted tip Induces thermal periostitis in adjacent metatarsals This can be done with frosted at short power applications 2. Nail matrixectomy = burns periosteum use CO2 3. Warts = can use, but it's more easily treated with CO2 4. See contraindications

COMMENT Thermal Radiation Lateral Radiation Limit capsular dissection Particularly those adjacent to muscle Long remodeling time Excellent visualization Around calcaneus only Coagulation during

GENERAL CONSIDERATIONS IN APPLICATION OF THE Nd:YAG LASER 1. Drapes are dry. Water transmits this wavelength. 2. Separate mayo stand for fiberoptics with expensive tips and power equip 3. Notch filter glasses are the best eyewear protection, best visibility 4. Select general surgery handpiece 5. Select tip size and frosting based on presurgical plan 6. Laser nurse will connect fiberoptics to launch pad on laser 7. Calibrate instrument and hand off calibration cone, now contaminated Select power level, C.W. mode 8. Incision is made with a steel blade only to the dermis When you see the whiteness of the dermis - stop Contact tip is held 45 degrees to tissue New frosted tips need 2 seconds at full power to "age" 9. Traction - countertraction throughout procedure 10. Room suction be used for the minimal smoke plume much less than CO2 laser 11. Deeper dissection now before using forceps Use traction - countertraction 12. Dissect in linear strokes. Avoid burying the tip. This laser needs less pressure than a steel blade Tactile feel is like a hot knife through butter So let the laser do the work 13. Repeat dissection strokes until each plane of tissue complete 14. Dissection may be adjacent to vessels, stay 3-4 mm from nerves at high power levels 14-16 W 15. Hemostasis of larger vessels can be with the laser alternate on either side, observe coagulation 16. Capsular dissection may be made right over cartilage with no damage to cartilage 17. Dissect only the periosteum/capsule you intend to discard Good hemostasis, but seals off periosteal vessels 18. Remainder of capsule/periosteum done with blade 19. Bone work with conventional power instrumentation 20. Watch on-time during intermetatarsal neuroma surgery Avoid thermal periostitis in adjacent metatarsals 21. Seal nerve endings in neuroma sx. with the contact tip Prevents stump neuroma formation 22. Minimal char formation seen Very dry and atraumatic surgical site seen 23. Closure is conventional, dressings conventional 24. Sutures remain in a few days longer Expect macroscopic bleeding due to tourniquet reflux hyperemia REALISTIC EXPECTATIONS 1. Learning curve is steeper than CO2 Laser 2. Postoperative bruising still seen 3. Swelling, and pain still seen - although diminished 4. Macroscopic bleeding present but diminished 5. Be ready for the unexpected New technology presents new situations 6. Do simple cases first

THE ARGON LASER GENERAL DESCRIPTION 1. Dual wavelength output: Blue 488 nm Green 514 nm very close to KTP 532 nm (pure green) 2. 1 to 2 mm depth of penetration. 3. Operates as a coagulation device, not used for cutting 4. Argon and KTP pass epidermis to absorb in the dermal hemoglobin selectively Nd:YAG and CO2 do not absorb in the region of the Hb curve 5. Fiberoptic delivery system 6. collimated handpiece, freebeam fiber, contact 7. Aiming beam is a low power argon beam, hard to see through OD 3 or 5 glasses 8. 30 degree divergence on the KTP fiber, 2 degree divergence on the Argon fiber. 9. 488 nm filter is used to filter out green component 10. Hemoglobin Absorption is a bimodal curve 11. Ideally the wavelength should fall on the peak absorption of this curve and be maximally transmissible through other tissues MECHANISM OF ACTION 1. Chromophores on the bottom of the foot are minimal 2. They pose little problem because the epidermis, dermis basal layer is transparent to this wavelength 3. Absorption at this wavelength is low first absorbed in the hemoglobin within the vessels of the reticular dermis 4. vessels are stenosed via selective photoablation. a. Able to coagulate vessels less than 1 mm in diameter. b. Indicated for tissue coagulation and necrosis procedures (acisional) c. KTP laser, 532 nm can be used also for vascular stenosis. d. Deeper dermal structures, such as capillary hemangioma, other lasers are indicated for this such as the free beam Nd:YAG. EYE PROTECTION 1. Optical Density (O.D.) minimum of 5 at 488 nm. 2. Unfortunately, these glasses block out the aiming beam The aiming beam is a low level intensity treatment beam. 3. Visible light eye protection radically alters the colors of the surgical field SURGICAL APPLICATIONS INDICATIONS FOR THE ARGON LASER 1. This treatment is very useful for incisionless surgery It is highly favored by the patient, particularly in the large verrucae on the plantar aspect of the foot and the posterior aspect of the heel normally a CO2 laser would leave an ulcerative defect Immediate shoe gear 2. Multiple disseminating lesions or mosaic warts on the plantar foot 3. Vascular lesions of a superficial nature 4. Patients having communicable diseases when a bloodless field is desired

5. It is not indicated for highly fibrotic and scarred verrucoid lesions. Scar tissue transmits this frequency giving a painful result ADVANTAGES 1. Minimal exposure to blood--this is an incisionless procedure. 2. Decreased laser plume about 5% of that with CO2 laser A smoke evacuator is still required 3. Good treatment for immunocompromised patients 4. Faster than CO2 laser, i.e. a 45 minute procedure for the CO2 laser for verruca plantaris would take 5 minutes with the Argon laser 5. It is repeatable 6. Sterile preparation unnecessary. Surgeon still should be gloved for isolation from lesion contaminants. ARGON LASER DESTRUCTION OF VERRUCA 1. Object = delivery of energy to the superficial dermis - papillary plexus These are the vessels feeding the wart. The wart is an epidermal structure, not a dermal structure. It is however fed by vessels from the dermis. 2. Anesthesia peripheral to lesions and without epinephrine 3. Thick sections of epidermis should be debrided previous to treatment This minimizes epidermal carbonization. 4. Inject peripherally - do not blanch skin from the injection pressure 5. Collimated handpiece is used with 600 nm to 1 mm diameter fiber 6. 5 degree to 30 degree divergence. Focusing handpieces are available. 7. Bare fiber is held 1-2 cm from tissue 8.2-4 mm spot, 5.5 watts, 0.5 seconds for the plantar foot. May be used continuous mode and brushed when a good technique is adapted. 9. Selection of appropriate power density is very important. 3 watts for thin skin, 6.5 watts for thick skin 10. Include 2 - 3 mm border peripheral to the wart, 11. Carefully check this tissue for a "blanching effect". 12. Allow for a 3 to 5 second delay in this blanching 13. This is a result of the coagulation of the superficial dermal vessels. No vaporization occurs NOTES: 1. Some carbonization is normal in thick epidermis Avoid charring this by continuous circular motions. 2. When blanching occurs, this is the proper setting. Also the proper rate of hand piece movement. 3. This is a time dependent phenomena.

4. After the vasculature is coagulated the chromophores have absorbed the wavelength. 5. If blanching is not encountered, do not increase power, do not slow down handpiece movement. 6. Repeat the same movement of the handpiece over the area. 7. When proper parameters are determined, continue treatment beyond the test area. 8. The result is not only power and spot size, giving P.D., but time dependent. POSTOPERATIVE CARE 1. Accommodative pad prn No dressing necessary. Patient can put his shoe and sock on and walk out of the operating room. 2. Hydrocodone 2.5 mg i-ii Q 4-6 h prn pain 3. Blistering likely to occur in 3 to 5 days. Patient may incise and drain this at home. After I&D, patient is to leave the skin on, for a protective barrier. 4. At one week a black necrotic skin component will form This lasts 3 weeks and spontaneously sheds. 5. Check patient in 3-4. Recheck in 10 weeks. 6. Should fully heal within 4 to 5 weeks. No scarring should be seen. A slight hypopigmentation may be observed. 7. Ulceration is not possible with this laser as the chromophores, hemoglobin and oxyhemoglobin stops the absorption in the superficial papillary plexus.

THE KTP LASER

GENERAL CHARACTERISTICS 1. Very similar to Argon laser. Single wavelength 532 nm (v. 514 nm Argon). 2. Difference: KTP can cut tissue, contact mode 3. Very useful in selected tissue (below) 4. A frequency doubled Nd:YAG laser 5. Blanching of the skin also seen similar to the Argon laser 6. Note indications for vascular tumors: Argon superficial KTP moderate Nd:YAG (bare fiber) deep 7. Absorption coefficient is slightly increased over the Argon A.C. - The distance it takes for the radiation to diminish 90% in tissue. 8. Contraindicated in surgery in close proximity (0.5 cm) to thin cortical bone Vessels of the bone will absorb this wavelength, necrose vascular supply 9. Contact mode and free beam mode FIBER PREPARATION Fiber preparation is done previous to each case 1. Fiber must be cleaved: a. Optical fibers have a crystalline nature b. A cleaver is used to penetrate the sheath and score the fiber cortex this sets up a stress riser so the fiber can be snapped c. the end of the fiber is inspected for a flat, even surface emitted laser light should be circular and symmetrical

d. The sheath must be stripped. e. 4 mm recommended by manufacturer, but emits too much lateral light f. so strip 2-3 mm instead, but enough so the sheath doesn't melt g. So leave it to Cleaver to strip off the sheath for fiber preparation

SURGICAL APPLICATIONS

KTP TREATMENT OF VERRUCA 1. Same as for Argon 2. Treatment is slightly deeper 3. Blanching is similar but has more significance of penetration depth KTP APPLICATIONS TO PLANTAR FASCIOTOMY 1. MECHANISM OF ACTION a. KTP is a nonthermal laser b. Selective wavelength absorption c. Operates in contact mode by specific photoablation of protein and hemoglobin. d. Pericalcaneal tissue = adipose, muscle, and plantar fascia Advantage - transmission through clear adipose. Advantage - plantar muscle contact - very little bleeding e. Muscle is highly vascular and plantar fascia is separated off Usually muscular bleeding is considerable Absorption in muscle is superficial - stopped by Hb f. Lower power levels required 2.. THERMAL LASER PROBLEMS INDICATING KTP LASER a. Thermal lasers, C02, Nd:YAG --> adipose photohydrolysis and liquefaction b. This water and fat liquefaction interferes with laser cutting c. Disadvantage CO2 laser - strongly absorbed by water and no cutting occurs d. Disadvantage Nd:YAG laser - water transmits and energy is disseminated. e. Surgical site in heel spur work is deep and visibility must be optimized Particularly with endoscopic size incisions 3. DISADVANTAGES OF KTP LASER a. Retinal hazard b. Fiber preparation before every case c. Cannot dissect in close proximity to bone d. Inefficient laser - requires dedicated 220 V 50 A line e. Larger zone of necrotic damage and zone of coagulation than the CO2 f. Takes a long time to dissect through vertical septa and plantar fascia g. Must take care not to deliver much energy into muscle (well absorbed) h. Learning curve

OTHER SURGICAL LASERS

Other medical lasers available with properties, delivery systems unique to each Podiatry is already using these, but be familiar with basic lasers first Ho:YAG LASER 1. a near-contact laser being used for resecting calcaneal spurs 2. good for endoscopic and arthroscopic work 3. transmits through water 4. also indicated for cartilage ablative procedures for joint restoration COPPER VAPOR LASER 1. Known largely for treating port wine stain and congenital cutaneous vascular pathologies 2. Two wavelengths - yellow and green 3. yellow for superficial vascular 4. green for deeper vascular 5. dermatological surgery 6. very inefficient, large laser, long warmup period Q-SWITCHED LASERS 1. used to be used in ophthalmic procedures 2. Q-switched Ruby and Q-switched Nd:YAG for tatoo removal 3. no anesthesia necessary 4. multiple treatments necessary 5. little scarring results, mild hypopigmentation EXCIMER LASER 1. UV laser, 0.2 mm absorption 2. Ionizing radiation 3. Cardiac catheterization, osteotomy, corneal sculpting 4. High frequency, short wavelength means high precision Er:YAG LASER 1. Mid infrared, 0.1 mm absorption 2. Bone surgery 3. Difficulty in fiberoptic delivery - fragile and toxic

BIBLIOGRAPHY 1. Arndt, Kenneth A., "Argon Laser Therapy of Small Cutaneous Vascular Lesions", Journal of the American Academy of Dermatology, vol. 118, April 1982, pp. 220-224. 2. Borovoy, Mathew; Fuller, Terry A.; Elson, Lawrence M.; Laser Safety in Podiatry", The Journal of Foot Surgery, 1985, vol. 24, no. 2, pp. 136-138. 3. Borovoy, Mathew; Klein, Jeffery T.; Fuller, Terry A.; "Carbon Dioxide Laser Methodology for Ablation of Plantar Verrucae", vol. 24, no. 6, 1985, pp. 431-437. 4. Cacciaglia, G.B.: Reigelhaupt, R.W.; "Effectiveness of Lasers on Plantar Papillomas: A Preliminary Study", Journal of Foot Surgery, vol. 24, no. 1, 1985, pp. 477-481. 5. Carlson, Bruce A., and Pyrcz, Robert A., "Lasers in Podiatry and Orthopaedics", Nursing Clinics of North America, v. 25, No. 3, September 1990, Pg. 719-723. 6. Carlson, Bruce A.; Pyrcz, Robert; "Human Papilloma Virus-Induced Lesions: Their Treatment and the Evolution of an Alternative Laser Application", Current Podiatric Medicine, November 1989, pp.9-12. 7. Carlson, Bruce A., "Complications Associated with Laser Surgery", Clinics in Podiatric Medicine and Surgery, vol. 4, no. 4, October 1987, pp. 823-828. 8. Chromey, Paul A., "The Significance of Power Density in Applying the CO2 Laser", Current Podiatric Medicine, September 1986, pp. 20-22. 9. Chromey, Paul A., "The Application of CO2 Laser to Soft Tissue Tumors", Current Podiatric Medicine, May 1986, pp.24-27. 10. Collis, Sheldon; Rowland, Roberta N.; "Lasers For Podiatry Principles and Language", Current Podiatry, April 1984, pp. 33-34. 11. Kaplan, Isaac, "The CO2 Laser In Clinical Surgery: Past, Present, and Future", Journal of Clinical Laser Medicine and Surgery, pp. 341-343, vol. 9, no. 5, 1991. 12. Kelly, Peter F.; "Nd:YAG Contact-Tip Laser Reduces Pain from Foot Surgery", Clinical Laser Monthly, Volume 10, No. 1, January, 1992. 13. Kelly, Peter F., "Nd:YAG Contact Tip V. Cold Steel Applications in Podiatric Foot and Ankle Surgery", American Society for Laser Medicine and Surgery, Supplement 4, 1992. 14. Kelly, Peter F.; "The Light Scalpel - Nd:YAG Laser Contact-Tip", Issue 24, 1992, The Laser Letter, International Society of Podiatric Laser Surgery, Doylestown, PA. 15. Kelly, Peter F.; "The Nd:YAG Laser for the Podiatric Surgeon", The Laser Letter, Issue 25, 1992, International Society of Podiatric Laser Surgery, Doylestown, PA.

16. Kelly, Peter F.; "KTP Laser Application to Calcaneal Spur Surgery", Clinical Laser Monthly; Volume 11, No. 3, April, 1993. 17. Kelly, Peter F., "KTP Laser Application to Calcaneal Spur Resection and Plantar Fasciectomy", American Society for Laser Medicine and Surgery, Supplement 5, 1993 18. Landsman, Mark J.; Mancuso, John E.; Abramow, Steven P.; "Laser's Use in Bone and Joint Surgery, Clinics in Podiatric Medicine and Surgery, vol. 9, no. 3, July 1992, pp. 721-737 19. McDowell, Brian A., "Carbon Dioxide Laser Excision of Benign Pedal Lesions, Clinics in Podiatric Medicine and Surgery, vol. 9, no. 3, July 1992, pp. 617-632. 20. Mueller, Terrance J.; Carlson, Bruce A.; Lindy, Marc P.; "The Use of the Carbon Dioxide Surgical Laser for the Treatment of Verrucae", Journal of the American Podiatry Association, vol. 70, no. 3, March 1980, pp. 136-141. 21. Nicholson, Ronald A., "Two Techniques Described using C02 Laser for Matrixectomy", Laser Practice Report, vol. 7, no. 7, pp. 1 S-2S. 22. Pyrcz, Robert A.; Carlson, Bruce A.; "Lasers in Podiatry and Orthopedics", Nursing Clinics of North America, vol. 25, no. 3, September 1990, pp. 719-723. 23. Wasserman, Gerald, "Treatment of Morton's Neuroma with the Carbon Dioxide Laser", Clinics in Podiatric Medicine and Surgery, vol. 9, no. 3, July 1992.

SPEED-READING BIBLIOGRAPHY 1. "Continued efforts to enhance the utilization of laser technology and the ability of laser education at teaching hospitals are key for the future." Lanzafame, Raymond, J.; Hinshaw, Raymond, J.; "Laser Education, Laser Usage, and Surgical Attitudes: A Challenge for the Future", Pg. 279-81, Journal of Clinical Laser Medicine and Surgery, Volume 10, No. 4, 1992. 2. "It (the CO2 laser) routinely provides a bloodless surgical field as well as unusual surgical precision." Fairhurst, Mark V.; Roenick, Randall K.; Brodland, David G.; Subspecialty Clinics: Dermatology, "Carbon Dioxide Laser Surgery for Skin Disease", Mayo Clinical Proceedings, Vol. 67, Pg. 49-58, 1992. 3. "Thermally induced tissue destruction is accurate with little damage to surrounding normal tissue because the coherent, collimated, monochromatic beam of light can be focused to a very tiny point using an optical lens system. Histologically, the area of tissue necrosis adjacent to the laser incision is less than 0.1 mm, usually 50-70 microns. This facilitates healing with reduced scarring. The zone of cellular damage varies from 0.3 to 0.5 mm." Chromey, Paul A., Current Podiatric Medicine, September 1986, Pg. 2022.

4. "Carbon dioxide laser offers many advantages demonstrated in this study, including minimal bleeding, improved healing, reduced edema, improved postoperative discomfort, minimal scarring and minimal infection." Cacciaglia, G.B., Reigelhaupt, R.W., "Effectiveness of Lasers on Plantar Papillomas: A Preliminary Study", Journal of Foot Surgery, Vol. 24, No. 1, 1985, Pg. 477-481. 5. "Since the beam affects well defined areas of the skin, there is minimal necrosis of adjacent tissue; consequently, postoperative pain, edema, and scarring are minimized." Mueller, Terrance J.; Carlson, Bruce A.; Lindy, Mark P.; "The Use of the Carbon Dioxide Surgical Laser for the Treatment of Verrucae", Journal of the American Podiatry Association, Vol. 70, No. 3, March 1980, Pg. 136-141. 6. "Podiatry started using the laser for the excision of Morton's neuroma and for incisional approaches to bunionectomy and other podiatric procedures." "The same advantages were found to be present for incisional procedures: less bleeding, pain, and postoperative edema." Peyrcz, Robert A., Carlson, Bruce A., "Lasers In Podiatry and Orthopedics", Nursing Clinics of North America, Vol. 25, No. 3, September 1990, Pg. 719-723. 7. "Utilizing the CO2 laser in neuroma surgery for making incisions and sealing the nerve stump decreases postoperative pain and healing, allowing patients to resume normal ambulation faster than with conventional scalpel surgery." Wasserman, Gerald, Clinics in Podiatric Medicine and Surgery, "Treatment of Morton's Neuroma With the Carbon Dioxide Laser", Vol. 9, No. 3, July 1992, Pg. 671-686. 8. "The contact method of performing endoscopic and open surgery with the Nd:YAG laser opens a new era in laser surgery ... with cutting capabilities previously only seen with the CO2 laser." "The CO2 laser operating at a wavelength of 10,600 nm with energy outputs of 100 watts is effective at cutting and coagulation of SUPERFICIAL blood vessels." Joffe, Stephen N.; Schroder, Tom; Lasers in General Surgery, Year Book Medical Publishers, Inc., Laser Center of America, Cincinnati, OH, Pg. 125-130, 1987. 9. "We concluded that CO2 laser surgery for hemophiliacs has a confirmed place for modern laser technology." Santo-Dias, A.; "CO2 Laser Surgery in Hemophilia Treatment", Journal of Clinical Laser Medicine and Surgery, Pg. 297-301, Volume 10, No. 4, 1992. 10. "Because of the large amount of water in body tissue, this laser (CO2) will cause a vaporization of the tissue at the focal point and seal the small blood vessels and lymphatics. The laser creates an incision that leaves residual tissue undamaged." Kaplan, Isaac; "Twenty Years of CO2 Laser Surgery: A Review and Update", Journal of Clinical Laser Medicine and Surgery, Pg. 57-60, Volume 11, No. 2, 1993. 11. "Certain advantages of the use of the CO2 laser stand out: absence of hemorrhage and cellular vaporization which permit, due to a perfect visibility, appreciation at every moment of the quantity of tissue that needs to be removed." Dourov, Nicolas; Nammour, Samir; "Removal of Benign Tumors Using the CO2 Laser", Journal of Clinical Laser Medicine and Surgery, Pg. 109-113, Volume 10, No. 2, 1992.

12. "This action results in a fine hemostatic incision leaving the residual tissue relatively undamaged." "The treated areas heal rapidly because the skin appendages escape permanent damage." Kaplan, Isaac; "The CO2 Laser In Clinical Surgery: Past, Present, and Future", Journal of Clinical Laser Medicine and Surgery, Pg. 341-343, Volume 9, No. 5, 1991. 13. "Surgical laser technology has been available for nearly 30 years and is being used increasingly in many surgical disciplines including orthopedic surgery." Cahill, Sandy; Kopta, Joseph A.; Kosanke, Stanley D.; Rayan, Ghazi M.; Stanfield, Denver T.; "Effects of Rapid Pulsed CO2 Laser Beam on Cortical Bone In Vivo", Lasers in Surgery and Medicine, Pg. 615-620, Volume 12, No. 6, 1992. 14. "The lack of wound contraction, scarring, and good reepithelialization combined with precise tissue destruction makes CO2 laser surgery ideal for this procedure when compared with conventional techniques." Keng, S. B.; Loh, H. S.; "The Treatment of Epulis Fissuratum of the Oral Cavity by CO2 Laser Surgery", Journal of Clinical Laser Medicine and Surgery, Pg. 303-306, Volume 10, No. 4, 1992. 15. "The advantage of the CO2 laser technique was that it produced minimal thermal damage to the surrounding tissues." Fallouh, Hayel; Sultan, Raymond A.; "Combined CO2-Nd:YAG Radiation in Liver and Anorectal Diseases", Journal of Clinical Laser Medicine and Surgery, Pg. 255-263, Volume 10, No. 4, 1992.

FURTHER READING 1. Sherk, Henry H., Editor, Lasers in Orthopaedics, J.B. Lippincott Company, Philadelphia, PA, 1990. 2. Ballow, Edward B., D.P.M., Editor, Laser Surgery of the Foot, First Edition, International Society of Podiatric Laser Surgery, Doylestown, PA, 1988. 3. Joffe, Stephen N.; Schroder, Tom; Lasers in General Surgery, Year Book Medical Publishers, Inc., Laser Center of America, Cincinnati, OH, 1987. 4. "Lasers In Podiatry and Orthopedics", Nursing Clinics of North America, Vol. 25, No. 3, September 1990.

PHOTODYNAMIC THERAPY "PDT" MECHANISM OF OPERATION 1. Requires an injection, dissemination and systemic absorption of protoporphyrins 2. Malignant cells take up the protoporphyrin These can be visualized under UV light Patient must remain away from all light during this treatment session and have a photosensitivity up to six weeks post treatment 3. Laser radiation is applied at a specified frequency, usually red light area. and for a specified time - result is Joules to tissue 4. Wavelength depends on protoporphyrin 5. Results is a single oxygen produced which destroys malignant tissue selectively BIOSTIMULATION "BIOSTIM" 1. A few milliwatts hitting mitochondria stimulating thermal mechanism. 2. No heat is produced. 3. Mitochondrial chromophores. 4. This is FDA investigational. 5. Applied to wound healing, to nerve regeneration, and chronic pain--analgesic. 6. Elicits a systemic effects 7. 0 milliwatts, tunable dye, helium-neon, 12 joules per week for 30 weeks 8. Applied to rheumatoid arthritis, trigeminal neuralgia, osteoarthritis, sciatica, diabetic neuropathy. 9. Has 60 to 85% of pain relief 10. 5-hydroxyindolacetic acid, 5-HIAA produced Urinary HIAA output increase correlated with pain relief 11. Systemic effects: stimulation of human lymphocytes Decreased pain and inflammation of distant ion irradiated sites Increased urinary 5HIAA, product of serotonin metabolism 12. Dose: 50 milliwatts, tuneable dye or helium-neon laser, 12 joules per week for 30 weeks. 13. Proposed mechanism: absorption of light by photoreceptor or chromophore in the mitochondria activates the respiratory chain, resulting in a cellular response. 14. Primary process: a. Electron train excitation b. acceleration of electron transfer in redox pairs (activates and stimulates). c. Transfer of excitation energy from oxygen to single oxygen (oxidative effect inhibiting healing). d. Respiratory chain components are probably the primary photoacceptors. e. Flavins, cytochromes, cytochrome oxidase. f. Respiratory chain in a unitary dynamic system can be acted upon at various points causing change in the whole state of response. Summary: 1. Effects are dose dependent. Higher energies seem to be damaging. 2. Coherent light is preferred versus non-coherent. 3. Narrowed band monochromatic light preferred, i.e. helium-neon coherent and monochromatic light

4. Competing wavelengths cancel the effects, therefore coherent light is preferred. 5. Transcutaneous irradiation penetrates deeply enough to produce generalized effect in many cases. 6. 4 joules/cm2 penetrates approximately 1 cm. 7. Local radiation with systemic effects. i.e., 5-HIAA production from serotonin metabolism. 8. Depends upon the physiological status of cell before radiation. 9. The biostimulation effect is not always possible.

Chapter 38: Specific Radiological Pathology MRI Pathology

SPECIFIC RADIOLOGICAL STUDIES MRI Pathology 1. Posterior tibial tendon tear (grade 2): Photographs 1-4 Discussion: Photograph #1 is a T1 weighted image with a low signal around the posterior tibial tendon. The dark center is tendon, (clear arrow) which is not completely dark but has some areas of grey, which indicated an intrasubstance tear. The low signal around the tendon (dark arrow) indicates that there is fluid around the tendon. Photograph #2 is a T2 weighted image, which shows significant fluid around the posterior tibial tendon, indicating a Grade 2 tear. Photograph # 1

Photograph #2

Photograph #3 is a T1 weighted image (sagittal view) showing irregularity with in the tendon (lobulated dark area) with the white area below indicating fluid accumulation. Photograph #4 is a T2 weighted image (sagittal view) showing a white area of increased signal intensity behind the posterior tibial tendon consistent with a grade 2 tear Photograph #3

Photograph #4

2. Achilles tendon tear: Photograph 5 Discussion: A T1 weighted image (sagittal view) revealing a linear signal within the Achilles tendon of higher signal intensity, which is consistant with an intrasubstance tear and overall thickening about 4-6 cm above the insertion of the tendon Photograph #5

3. Achilles tendon rupture: Photograph 6 & 7 Discussion: Photograph #6 is a T1 weighted image (sagittal view) revealing a large signal of low intensity surrounding the Achilles tendon in Kager's triangle. Photograph #7 is a T2 weighted image (sagittal view) showing a signal of bright intensity (acute hemorrhage) with complete loss of continuity of the Achilles tendon Photograph #6

Photograph #7

4. Aneurysmal bone cyst: Photograph 8 & 9 Discussion: Photograph #8 is a T2 weighted image (axial view) through the calcaneus and tarsus. In the calcaneus there is a higher signal above and a lower signal below in each of the pockets. This is consistant with an aneurysmal bone cyst, which is multiloculated. The reason for the difference in signal intensity within the pockets, is the blood constituents settling to the bottom and serosanguinous materials settling to the top. Photograph #9 is a T1 weighted image (sagittal view) with a low homogenous signal from the calcaneus. Diagnosis can be made from the T2 image Photograph #8

Photograph #9

5. Tophaceous gout: Photograph 10 Discussion: Photograph # 10 is a T1 weighted image (sagittal view) with a low intensity signal visable over the dorsal aspect of the foot invading into the lesser tarsus. The T2 signal (not shown) has a brighter (higher) signal but not what fluid filled lesion would look like. This is consistent with tophaceous gout. Photograph #10

6. Giant cell tumor: Photograph 11 Discussion: Photograph #11 reveals a T1 weighted image (axial view) showing a low instensity signal mass inferior to the sesmoid and flexor apparatus. This is a giant cell tumor over the flexor hallucis longus Photograph #11

7. Avascular necrosis of tarsal navicular: Photograph 12 Discussion: Photograph #12 is a T1 weighted image (sagittal view) revealing a signal of low intensity throughout the navicular. This is consistent with a avascular necrosis Photograph #12

8. Osteochondritis dissecans: Photograph 13-15 Discussion: Photograph #13 is a T1 weighted (sagittal view) demonstrating a low signal lesion on the lateral talar dome. Photograph #14 is a T2 weighted image (sagittal view) demonstrating a high signal from the lateral talar dome. Photograph #15 is a T1 (coronal view) demonstrating a low signal intensity lesion of the anterior talar dome. This is consistent with osteochondritis dissecans Photograph #13

Photograph #14

Photograph #15

9. Osteogenic sarcoma: Photograph 16 & 17 Discussion: Photograph #16 is a proton density image (combination of a T1 and T2) demonstrating increased signal intensity with loss of normal fatty marrow signal. Also there is an increase in dark signal intensity of the posterior aspect of the tibia. Photograph #17 is a T1 weighted image through the tibia (sagittal view) showing increased signal intensity centrally. This lesion was proven by biopsy to be an osteogenic sarcoma

Photograph #17

10. Brodie's abcess/yeast infection: Photograph 18 & 19 Discussion: Photograph #18 is a T1 weighted image (sagittal view) demonstrating loss of fatty marrow signal in the tibia with a loculated-type lesion. Photograph #19 is a STIR image (a fat supression technique) demonstrating increased signal within the lobulated lesion, and increased signal intensity within the marrow of the distal tibia. This was consistent of a Brodie's abcess due to a yeast infection in a previously undiagnosed HIVpositive patient Photograph #18

Photograph #19

11. Diabetic osteolysis: Photograph 20 & 21 Discussion: Photograph #20 is a T1 weighted image (sagittal view) demonstrating loss of cortical margins of the first metatarsal head, with loss of signal intensity of the fatty marrow and destruction of the 1st metatarsal head. There is a plantar ulceration underneath the first metatarsal head. Photograph #21 is a STIR image revealing no increased signal within the meatarsal shaft which helps eliminate the diagnosis of osteomyelitis. This is consistent with diabetic osteolysis. Photograph #20

Photograph #21

References Abramson DI, Circulatory Problems in Podiatry, Karger, New York, 1985 ACFS, Complications in Foot Surgery, Williams & Wilkins, Baltimore, 1976 Advances in Ilizarov Apparatus Assembly, A. Bianchi Maiocchi (ED), Medicalplastic srl, Milan, Italy, 1994 Arrancia LJ, Rinaldi FT, Atlas of Rearfoot Surgery, Futura, New York, 1978 Balderston RA, Operative Techniques in Orthopedics: Foot and Ankle Procedures, Vol 2: Number 3, Saunders, Philadelphia, 1992 Bartlett JG, Pocketbook of Infectious Disease Therapy '91-'92, Williams & Wilkins, Baltimore, 1991 Berg D, The Resident's Quick Reference to Internal Medicine, Lippincot, Philadelphia, 1990 Clinics in Podiatry, Podopediatrics, Saunders, Philadelphia, December 1984 Clinics in Podiatric Medicine and Surgery, Plastic Surgery, Saunders, Philadelphia, April 1986 Clinics in Podiatric Medicine and Surgery, Pediatric Surgery of the Foot and Ankle, Saunders, Philadelphia, January 1987 Clinics in Podiatric Medicine and Surgery, Rheumatology, Saunders, Philadelphia, January 1988 Clinics in Podiatric Medicine and Surgery, Applied Biomechanics, Saunders, Philadelphia, July 1988 Clinics in Podiatric Medicine and Surgery, Nail Disorders, Saunders, Philadelphia, April 1989 Clinics in Podiatric Medicine and Surgery, Neurologic Disorders of the Lower Extremity I, Saunders, Philadelphia, October 1989 Clinics in Podiatric Medicine and Surgery, Neurologic Disorders Affecting the Lower Extremity II, Saunders, Philadelphia, January 1990 Clinics in Podiatric Medicine and Surgery, Heel Pain, Saunders, Philadelphia, April 1990 Clinics in Podiatric Medicine and Surgery, Infections in the Lower Extremity, Saunders, Philadelphia, July 1990 Clinics in Podiatric Medicine and Surgery, Wound Healing, Saunders, Philadelphia, October 1991 Clinics in Podiatric Medicine and Surgery, Peripheral Vascular Disease in the Lower Extremity, Saunders, Philadelphia, January 1992 Clinics in Podiatric Medicine and Surgery, Pharmacology, Saunders, Philadelphia, April 1992 Cole DR, DeLauro TM, Neoplasms of the Foot and Leg, Williams and Wilkins, Baltimore, 1990 DiNapoli DR, Reconstructive Surgery of the Foot and Leg, Update '90, Podiatric Institute, Tucker GA Draves DJ, Anatomy of the Lower Extremity, Williams & WIlkins, Baltimore, 1986 Fenstermacher K, Dysrhythmia Recognition and Management, Saunders, Philadelphia, 1989 Forrester DM, et. al., Imaging of the Foot and Ankle, Aspen, 1988 Jahass MH, Disorders of the Foot and Ankle, Saunders, Philadelphia, 1991 Jay RM, Current Therapy in Podiatric Surgery, BC Decker, Toronto, 1989 Joseph WS, Handbook of Lower Extremity Infections, Churchill Livingstone, N.Y., 1990 Keats TE, Lusted LB, Atlas of Roentgenographic Measurement, Year Book

Medical Publishers, Chicago, 1985 Kominsky SJ, Yearbook of Podiatric Medicine and Surgery 1992, Mosby, St. Louis, 1992 Marchino DE, Advanced Protocol for the Diagnosis and Treatment of Pedal Infections (Revised Edition), PICA Marcinko DE, Comprehensive Textbook of Hallux Abducto Valgus Reconstruction, Mosby, St. Louis, 1992 Marcinko DE, Medical and Surgical Therapeutics of the Foot and Ankle, Williams and Wilkins, Baltimore, 1992 McGlamry ED, Comprehensive Textbook of Foot Surgery (1st and 2nd edition), Williams ff Wilkins, Baltimore, 1987 McGlamry ED, Reconstructive Surgery of the Foot and Leg, Update '89, Podiatric Institute, Tucker GA Muller ME, Allgower M, Schneider R, Willenegger: Manual of Internal Fixation, 3rd ed, Springer Verlag, 1991, N.Y. Orthopedics Clinics, Bone Tumors: Evaluation and Treatment, Saunders, Philadelphia, 1989 Politz MJ, Clinical Laboratory Diagnosis, PMS vol 9, Futura, N.Y. 1977 Smith JW, Aston SJ, Grabb and Smith's Plastic Surgery, Little Brown, Boston, 1991 Root ML et. al., Biomechanical Examination of the Foot Volume 1, Clinical Biomechanics Corporation, Los Angeles, 1971 Samitz MH, Dana AS, Cutaneous Lesions of the Lower Extremities, Lippincott, Philadelphia, 1971 Sammarco, GJ, Foot and Ankle Manual, Lea & Febiger, Philadelphia, 1991 Sarrafian SH, Anatomy of the Foot and Ankle, Lippincott, Philadelphia, 1983 Seibel MO, Foot Function: A Programmed Text, Williams & Wilkins, Baltimore, 1988 Snow JC, Manual of Anesthesia, Little Brown, Boston, 1988 Vanore J, Osteosynthesis Techniques in the Foot and Ankle, P.P.M.A., 1989 Vender JS, Post Anesthesia Care, Saunders, Philadelphia, 1992 Weissman SD, Radiology of the Foot, Williams & Wilkins, Baltimore, 1989 Zang K: Traumatic Ankle Conditions, Futura, Mount Kisco, N.Y., 1976 Zier BG, Essentials of Internal Medicine in Clinical Podiatry, Saunders, Philadelphia, 1990

Hershey Board Certification Review Outline Study Guide

by

Jonathan M. Singer, D.P.M. Diplomate American Board of Podiatric Surgery Fellow American College of Foot and Ankle Surgeons Diplomate American Board of Podiatric Orthopedics & Primary Podiatric Medicine Fellow American College of Foot & Ankle Orthopedics & Medicine Edited by

James Lawton, D.P.M., Gene K. Potter, D.P.M., Ph.D., and Samuel L. Deitch, D.P.M. Contributors

Peter F. Kelly, D.P.M., Gene K. Potter, D.P.M., Ph.D., Steven J. Berlin, D.P.M., Steven Kravitz, D.P.M., Guido LaPorta, D.P.M., M.S., James Lawton, D.P.M., Arthur E. Helfand, D.P.M., Fredrick E. Youngblood, M.D., Douglas Glod, D.P.M., Christopher E. Attinger, M.D., Libby Cone, M.D., Edwin J. Juda, D.P.M., William H. Simon, D.P.M., John Walter, D.P.M. © 1998 Pennsylvania Podiatric Medical Association

Acknowledgements William Goldfarb D.P.M. and Nancy Sullivan, for supporting me and believing this book could be done James Lawton D.P.M., and Gene Potter, D.P.M. for their invaluable contributions in the general editing these review notes Jordon Fersel, M.D., for editing the chapters on Anesthesia, and Emergency Medicine, Deborah Wozniak, M.D., for editing the chapters on Perioperative Management, Fluid Management, and Postoperative Complications Warren Joseph, D.P.M., and Steven Maffei, D.P.M. for editing the chapter on Infectious Diseases Steven Kravitz, D.P.M., for editing the chapter on Biomechanics George Vito, D.P.M. for editing the chapter on Internal Fixation Peter F. Kelly, D.P.M. for writing the chapter on Lasers and Laser Physics Gene K. Potter, D.P.M., Ph.D. and Steven Berlin, D.P.M. for editing the chapters on Dermatology, Bone Tumors, and Soft Tissue Tumors Gene K. Potter, D.P.M., Ph.D., for proof reading, editing, and adding his phenomenal talent to this book Guido LaPorta, D.P.M., M.S. for writing the chapter on Ankle Arthroscopy

The Hershey Board Certification Review Outline Study Guide is prepared for distribution by the Hershey Surgical Seminars Committee Pennsylvania Podiatric Medical Association Guido La Porta, D.P.M., General Chairman

Author: Jonathan M. Singer, D.P.M. General Editor: James Lawton, D.P.M. Copy/Content Editor: Gene K. Potter, D.P.M., Ph.D. Cover Design: Marissa Singer Coordinator: Nancy Sullivan Published by the Pennsylvania Podiatric Medical Association ISBN # 0-9639030-04 Copyright © 1998

Pennsylvania Podiatric Medical Association 757 Poplar Church Road Camp Hill, Pennsylvania 17011 (800)-841-3668 All rights reserved This book is protected by copyright. No part of this book may be reproduced in any form or by any means, including photocopying, or utilized by any information storage or retrieval system without written permission from the copyright owner. Accurate indications, adverse reactions, and dose schedules for drugs are provided in this book, but It is possible that they may change. The reader is urged to review the package information data of the manufacturers of the medications mentioned. The author has made every effort to ensure the accuracy of the information herein. However, appropriate information sources should be consulted, especially for new or unfamiliar procedures. It is the responsibility of every practitioner to evaluate the appropriateness of a particular opinion in the context of actual clinical situations and with consideration to new developments. The author, editors, and publisher cannot be held responsible for any typographical or other errors found In this book. Printed in the United States of America.

Table of Contents Chapter 1: Emergency Medicine Cardiopulmonary Resuscitation: page 2-3 Advanced Life Support: page 3-4 Office Emergencies: page 5-7 Medical Emergencies (Cardiac Dysrhythmias): page 7-9 Summary of CPR: page 9 Other Medical Emergencies: page 9-12 Shock: page 12-13 Blood and Blood Products for Emergency Use: page 13-17 Chapter 2: Anesthesia Anesthesia Classifications: page 20 General Anesthesia: page 20-23 Intravenous Anesthesia: page 23 Local Anesthesia: page 23-26 Special Cases for Lowering the Maximum Allowable Dose: page 26 Pediatric Anesthesia: page 26-27 Lumbar Epidural and Caudal Anesthesia: page 27-28 Complications of Endotracheal Intubation: page 31 Nerve Injury During Anesthesia: page 31-32 Other Medical Compliccations From Anesthesia: page 32-34 Chapter 3: Perioperative Management The Healthy Patient: page 36 The Diabetic Patient: page 36-38 The Hypertensive Patient: page 38-39 The Patient on Steroid Therapy: page 39-40 The Asthmatic Patient: page 40-41 The Alcoholic Patient: page 41 The Patient on Anticoagulant Therapy: page 41-42 The Patient With Clotting Abnormalities: page 42 The Rheumatoid Patient: page 43 The Sickle Cell Patient: page 43-44 The Cardiac Patient: page 44-45 The Pulmonary Disease Patient: page 45 Perioperative Management of the Infant and Child: page 45-47 Mitral Valve Prolapse patient: page 47-48 The Gouty Arthritis Patient: page 48

Water and Electrolyte Imbalance: page 6566 Oliguria: page 66 Chest Pain: page 67 Postoperative Hypertension: page 67 Postoperative Infection: page 67-68 Anxiety and Pain Management: page 68-69 Nausea: page 69 Constipation: page 69 Shivering: page 69 DVT: page 69-70 Compartment Syndrome: page 70-73 Hemorrhage: page 72-73 Septic Syndrome: page 73 Thyroid Storm: page 73-74 Chapter 6: infectious Diseases Specific Diseases: page 76-81 Principles of Antiinfective Therapy: page 8184 Antibiotics: page 84-90 Drug Fever: page 90-91 Specific Antimicrobial Therapy: page 91-92 Surgical Considerations: page 92-93 Necrotizing Infections: page 93-94 Osteomyelitis: page 94-102 Septic Arthritis: page 102 Mycology: page 102-103 Viral Diseases: page 104 Rickettsial Diseases: page 104 Protozoan and Metazoan Infections: page 104-105 Chapter 7: Wound Healing Repair of Skin: page 108-111 Factors That Interfere With Wound Healing: page 111-113 Growth Factors in Wound Repair: page 113 Surgical Approaches: page 113-114 Wound Dressings: page 114 Suture Materials and Needles: page 115116 Tourniquets: page 116-118

Chapter 4: Preoperative Evaluation Screening Procedures: page 50-61 Summary of Perioperative Lab testing: page 61-62

Chapter 8: Plastic Surgery Skin Grafting: page 120-122 Local Cutaneous Flaps: page 122-124 Local Muscle and Cutaneous Flaps: Page 124 Fasciocutaneous Flaps: page 124-125 Microsurgery and Free Flaps: page 125-126 Diagrams of Skin Flaps: page 126-130

Chapter 5: Postoperative Care & Complications Fever: page 64-65 Altered Mental States: page 65

Chapter 9: Bone Healing Primary Bone Healing: page 132 Complications of Bone Healing: page 133135

Treatment of Nonunions: page 135 Fusion: page 135 Bone Grafting: page 135-137 Aseptic Necrosis Following 1st Metatarsal Osteotomy: page 138-139 Electrical Bone Stimulation: page 40 Cartilage Healing: page 140 Chapter 10: Burns and Frostbite Assessment and Treatment of Burns: page 142-145 Burn Deformities: page 145-146 Other Types of Burns: page 146 Frostbite: page 146-147 Chapter 11: Fluid Management and Replacement in the Surgical Patient Fluid Management: page 150-152 Complications of Total Parenteral Nutrition: page 152 Replacement Therapy: page 152-153 Blood Products and Indications for Use: page 153-156 Composition of IV Fluids: page156-157 Chapter 12: Bone Tumors Introduction: page 160 Staging Techniques: page 160-161 Surgical Staging System: page 161 Radiology of Bone Tumors: page 161-162 Bone Tumors: Page 163-168 Cystic Lesions of Bone: page 168-169 Other Tumors and Cancers: page 169-170 Bone Tumors: A Quick Reference Chart: page 170-171 Phases in Cancer Development: page 171 Benign vs. Malignant: page 172 Chapter 13: Dermatology The Skin: page 174 Dermatological Lesions: page 175-182 Chapter 14: The Arthropathies Causes of Joint Pain: A Summary: page 184 The Arthropathies: page 184-195 Lab Testing for the Arthropathies: page 195 Articular Disorders Affecting the Heel: page 195-196 Synovial Fluid Analysis: page 197 Charcot Foot: page 198-199 Chapter 15: Peripheral Vascular Disease Patient Evaluation: page 202-212 The Vascular Diseases: page 212-215 Chapter 16: Internal & External Fixation Objectives of Fixation Devices: page 218 Requirements of Implant Materials: page

218 Principles Affecting Internal Fixation: page 218 Internal Fixation Devices: page 219-229 AO Objectives: page 229 AO Principles: page 229-230 AO Technique: page 230-235 Jumping Screws: page 235-236 Other Techniques: page 236-238 Complications of Fixation Devices: page 238 External Fixation: page 239 Large Bone Fixation: page 239-252 Small Bone External Fixation: page 253254 Chapter 17: Nail Disorders & Surgery Nail Entities: page 256-260 Nail Anatomy: page 260 Surgical Nail Procedures: page 262-263 Chapter 18: Neurology Neurological Pathways: page 266 Presenting Features: page 266-270 Assessment of Clinical Problems: page 270278 Innervation of the Lower Extremity: page 278-281 Tarsal Tunnel Syndrome: page 282-284 Classification of Nerve Injuries: page 284285 Neuromuscular Causes of Cavus Foot: page 285 Types of Nerve Surgery: page 285-288 Chapter 19: Pediatrics Evaluation of the Pediatric Patient: page 290-293 Pedicatric Biomechanics-Normal Values: Newborn to Adult: page 293 Congential Deformities: page 293-302 Pediatric Radiology: page 302-304 Pediatric Gait Patterns: page 304-305 Intoe Gait: page 306-307 Pediatric Fractures: page 307-318 The Limp in Childhood: page 318-319 Juvenile Hallux Valgus: page 319-320 Biomechanical Examination of the Child: page 320-323 Corrective Casting Techniques in Infants: page 323-324 The Toe-Walking Child: page 324-326 Chapter 20: Drugs and Drug Interactions Introduction to Drug Interactions: page 328 Antibiotic Drug Interactions: page 328-329 Anticoagulant Drug Interactions: page 330 Antihypertensive Drug Interactions: page 330-331

Antipsychotic Drug Interactions: page 331 Cardiac Drug Interactions: page 331-332 Diuretic Drug Interactions: page 332 Non Steroidal Anti-Inflammatory Drug Interactions: page 332-333 Oral Contraceptive Drug Interactions: page 333 Mechanisms of Drug Interactions: page 333-335 Specific Drugs: page 335-344 Chapter 21: Surgery of the Congenital Foot Flatfoot Surgery (flexible): page 346-355 Subtalar Joint Blocking Procedures: (Arhroereises and Arthrodesis): page 355356 Flatfoot Surgery (rigid): Convex Pes Plano Valgus: page 356-358 Metatarsus Adductus Surgery: page 358362 Cavus Foot Surgery: page 362-367 Clubfoot Surgery: page 368-373 Chapter 22: Generalized Disease Conditions of Bone Soft Tissue Overgrowth: page 376 Abnormalities of Alignment: page 376-377 General Increased Bone Density: page 377 Osteopenia: page 377-378 Marrow Abnormalities: page 378379 The Dysplasias: page 379-380 Chapter 23: Radiology Standard Radiographic Techniques of the Foot and Ankle: page 382383 Specific Radiographic Studies: page 383-391 Anatomic Angles: page 391-396 Common Structural Measurements (Diagrams): page 396-402 Pediatric Radiology: page 402-406 The Osteochondritities: page 406-407 The Accessory Bones of the Foot: page 407 Chapter 24: Hallux Valgus & Related Disorders Goals of HAV Surgery: page 410 Anatomical Facts of the 1st MPJ: page 410-411 Predisposing Factors: page 412 Biomechanics: page 412-414 Etiology of HAV: page 414-415 Deformity Types: page 416-417 Radiological Measurements for HAV: page 417-418

Physical Examination: page 418-419 Preoperative Considerations: page 419 Arthroplasty Procedures: page 419 420 Capsule-Tendon Balancing Procedures: page 421-422 Implant Arthroplasty Procedures: page 422-426 Arthrodesing Procedures: page 426 429 Proximal Phalangeal Osteotomies: page 429-431 Distal Metatarsal Osteotomies: page 432-436 Proximal Metatarsal Osteotomies: page 436-438 Shaft Osteotomies: page 438-439 Combination Procedures: page 439 Other Procedures: page 439-440 Hallux Rigidus and Limitus: page 440-445 Hallux Varus: page 445-446 Hallux Hammertoe: page 446 Diff. Diagnosis of Pain In the Sesamoid Area: page 446 Complications of HAV Surgery: page 447 HAV Procedure Chart and Their Indications: page 448 Chapter 25: Trauma Medical Management and General Assessment of the Trauma Patient: page 450-451 Assessment of Lower Extremity Injury: page 451 General Evaluation and Treatment of Fractures: page 451-452 Calcaneal Fractures: page 452-460 Talar Fractures: page 460-463 Osteochondral Fractures: page 463 465 Navicular Fractures: page 466-470 Cuboid Fractures: page 470-472 Cuneiform Fractures: page 472 Fifth Metatarsal Base Fractures: page 472-474 Metatarsal Fractures: page 474-480 Ankle Fractures: page 480-493 Midtarsal Joint Dislocations: page 494 Tarsometatarsal Joint Dislocations/Fractures: page 494-498 Ankle Inversion Sprain: page 498 505 Deltoid Ligament Ruptures: page 506-507 Compartment Syndrome: page 507

508 Open Fracture Classification System and Tx: page 508-510 Soft Tissue Injuries: page 510-511 Crush, Gunshot, and Lawnmower Injuries: page 511-512 Puncture Wounds: page 512 Epiphyseal Plate Injuries: page 512-514 Digital Fractures and Dislocations: page 514-515 1st MPJ Trauma: page 516-517 Nail Bed Trauma: page 517-518 Toe Tip Injuries With Tissue Loss: page 518-519 Dog and Cat Bites: page 519 Chapter 26: Digital Deformities and Surgery Hammertoe Syndrome: page 522528 Mallet Toe Syndrome: page 528-529 Claw Toe Deformity: page 529 Overlapping 5th Toe: page 529-532 Hallux Hammertoe: page 532-533 Lesser Digital Arthrodesis: page 533 Hallux Interphalangeal Arthrodesis: page 533 Lesser Digital Arthrodesis: page 533534 Overlapping 2nd Toe: page 534 Syndactylization: page 534-535 Digital Implants: page 535-537 Floating Toe Syndrome: page 537 Blue Toe Syndrome: page 538-539 Polydactylism: page 539-541 Chapter 27: Muscle and Tendon Pathology Muscle Physiology: page 544-548 Principles of Tendon Repair: page 548-552 Tendon Lengthening and Tenotomy: page 552-554 Tendon Transfers: page 554-556 Tendon Grafts: page 556-557 Posterior Tibial Tendon Rupture: page 557-559 Posterior Tibial Tendon Dysfunction (Acquired Adult Flatfoot Syndrome): page 559-560 Peroneal Tendon Pathology: page 560-562 Achilles Tendon Rupture: page 562566 Lateral Ankle Stabilization Procedures: page 566-571 Postoperative Care and Training Following Tendon Transfer: page

571-572 Tenosynovitis: page 572 Chapter 28: Lesser Metatarsal Surgery Anatomy (Metatarsals 2-3-4): page 574-575 Differential Diagnosis of Metatarsalgia: page 575 Surgical Treatment of the IPK: page 575-578 Lesser Metatarsal Joint Replacement: page 578-579 Panmetatarsal Head Resection: page 579-581 Metatarsus Adductus: page 581-585 Freiberg's Disease: page 585-587 Tailor's Bunion: page 587-589 Splayfoot: page 589 Brachymetatarsia (Brachymetetopody): page 589-591 Skewfoot: page 591-592 Chapter 29: Ankle Conditions Differential Diagnosis of Chronic Ankle Pain: page 594 Tarsal Tunnel Syndrome: page 594597 Sinus Tarsi Syndrome: page 597599 Peroneal Subluxation: page 599600 Ankle Arthrodesis: page 600-602 Lateral Ankle Instability: page 603 Chronic Lateral Ankle Instability: page 604-607 Chronic Medial Ankle Instability: page 607 Ankle Equinus: page 607-611 Malunion and Nonunion of the Malleolei: page 611-614 Chapter 30: Heel Conditions Anatomy of the Heel: page 616-617 Radiological Evaluation of the Calcaneus: page 617-618 The Heel in Systemic Disease: page 618-621 Seronegative Arthritis and Heel Pain: page 621-622 Heel Spurs and Heel Spur Syndrome: page 622-623 Tumors of the Heel: page 623-626 Tarsal Coalitions: page 626-629 Sever's Disease: page 629-630 Causes of Heel Pain (a summary): page 630-631 Haglund's Deformity: page 631-632

Chapter 31: Amputations General Surgical Technique: page 634 Digital Amputations: page 634-635 MPJ Amputations: page 635 Transmetatarsal Amputations: page 635-636 Tarsometatarsal Amputations (Lisfranc's): page 637 Midfoot Amputations (Chopart's): page 638 Amputation of the Ankle (Syme's, Boyd, Pirogoff): page 638-639 Below Knee Amputation: page 639640 Chapter 32: Biomechanics Normal Values: page 641 Criteria of Normalcy in the Lower Extremity: page 642-643 Adult Biomechanical Examination: page 643-645 Common Structural Variations: page 646-648 Planes of Motion: page 648-649 Axes of Joint Motion: page 649-653 Angular and Axial Deformities in Children: page 654-656 Anatomy of Gait: Activity of Muscles: page 656-663 Observation of Gait: page 663-664 Subtalar Joint Measurements: page 664-666 Subtalar Joint Function: page 666667 Midtarsal Joint Function: page 667668 Chapter 33: Anatomy Neuroanatomy: page 670-676 Angiology: page 676-680 Myology: page 680-695 Arthrology: page 695-704 Chapter 34: Soft Tissue Tumors Soft Tissue Tumors: page 706-715 Chapter 35: Physical Medicine and Rehabilitation Physical Modalities and Diseases: page 718-720 Therapeutic Modalities and Procedures: page 720-730 Chapter 36: Arthroscopy Ankle Arthroscopy: page 731-740

Chapter 37: Laser Applications in Podiatric Surgery Laser and Laser Physics: page 741-751 Clinical Applications in Podiatric Surgery: page 751-775 Chapter 38: Specific Radiological Pathology MRI Pathology: page 777-800

Case Study #1 CC: 65 yr old female presents with an open sore on the bottom of her right foot. HPI: N: no pain L: corresponding to the area under the 1st metatarsal head D: x 3 weeks but probably longer O: gradual onset; started out as a blister A: none, except that it is starting to smell. (This is why her husband made her come in) T: clean it with hydrogen peroxide and apply Vasaline to it S: fever and nausea x 2 days. Pt arrived with a bandaid covering the area. Yellow drainage observed. PMH: 1. DM2 x 18 years. Last seen by MD 2 months ago. FBS at that time was 138 mg/dl. She was advised to check her blood sugar each morning using an accucheck machine, but does not do this regularly 2. HTN x 12 years. MD tells her that it is under control 3. Hyperlipidemia x 10 years PSH: 1. Fx ulna as a child 2. Hysterectomy, 20 years ago Allergies: 1. PCN She was told this as a child. She doesn’t know what happens if she takes this. Medications: 1. 40 units of NPH insulin q AM 2. HCTZ 3. Captopril 4. K-lor 5. Lipitor SH: 1. + Tobacco use – 1 ppd x 30 years 2. Denies EtOH and illicit drug use 3. Occupation: housewife FH: 2 children who are alive and well Father deceased from diabetic complications Mother alive and well with HTN

ROS: General: increased fatigue over the past 3 – 4 days Eyes: wears glasses Lungs: SOB upon exertion PV: leg cramps after walking 2 blocks Neuro: tingling and burning of the feet Physical Exam T = 101.5 P = 100 RR = 20 BP = 100/65 Accucheck = 280 Ht: 61 inches Wt: 185 lbs (84.1 kg) Derm/Integ: The right foot is substantially warmer than the left. The entire right foot is erythematous to the level of the ankle joint with increased intensity around the first and second rays. Deep ulceration 1.5 cm in diameter located under the 1st metatarsal head, right foot. The base is a mixture of granular and fibrotic tissue. Some dry yellow pus is apparent upon inspection of the wound. When the area proximal to the wound is squeezed, approximately 3cc of creamy yellow pus is expressed through the ulcer. With the use of a cotton tip applicator, the wound probes to the 1st MT head as well as laterally into the 1st interspace. Malodor is present but no specific smell can be distinguished. The borders are mildly hyperkeratotic. Vasc: DP and PT pulses are non palpable bilateral. Popliteal pulses are palpable bilateral. The entire right foot is edematous corresponding to the erythema. Neuro: Diminished protective sensation to the level of the ankle joint using SWMF. Achilles and patellar DTRs are 2/4 and symmetric. Muscle mass is WNL and muscle strength is 5/5. M/S: Plantarflexed 1st ray right greater than left. Dorsally contracted digits 2 – 5 bilateral. Slightly decreased medial arch bilateral.

Relevant Questions – Case Study #1 1. What are some tests that you may want to order & some consults to consider? - Order the standard 3 x-rays (AP, lateral and lateral oblique). You may also want to consider an axial sesamoidal view do to the location and way that this ulcer probes. There may be an infection in the sesamoids and this is a great way to see them unobsecured. This view may not be necessary, however. - Order labs: CBC with a differential, ESR, CRP, HbA1C, Chem 7, Albumin. CBC with diff: looking for a left shift. This means that there are more immature neutrophils (Bands) hanging out. ESR: This is a non-specific marker of inflammation. An ESR >70 is highly correlated with the presence of osteomyelitis. This is a measurement that can be followed to determine the effectiveness of treatment but BEWARE! ESR can lag behind clinical presentation. CRP: Used mainly as a marker of inflammation. Measuring and charting C-reactive protein values can prove useful in determining disease progress or the effectiveness of treatments. HbA1C: This is a marker of the long term glucose control in diabetic patients. Chem 7: There are several values that can be of interest in this panel. Potassium is important in heart function. Make sure that it isn’t going crazy. This is important if you are going to consider surgical intervention. BUN and creatinine are markers of kidney function. The nephrons of the kidney can be affected by the disease course of diabetes. These values can also be used to calculate any renal dosing of antibiotics. Anion gap can be calculated from several values in this panel Albumin: This is a marker of nutrition. Some clinicians use this as a measurement of whether or not a patient has the ability (base on a nutritional standpoint) to heal. - Gram stain, culture & sensitivity: If you are unsure of the infecting organism, this can be helpful. In this particular case, make sure that a deep culture is taken. It may be advantageous to consider a quantative culture as well. - Non-invasive Vascular studies: Doppler, ABI, TcPO2. Doppler: Audible exam of lower extremity arteries ABI: Ankle Brachial index. TcPO2: Transcutaneous oxygen pressure. All three of these tests, especially when their results are taken together, can provide insight into the vascular status of the patient and help determine at what level the patient can heal. - Pre-Op Testing As with all things this can be hospital or surgery center dependent. Some general tests may include the following: CXR: This patient is a smoker. Chest x-rays are always good in smokers. EKG: Takes a peak at the electrical activity of the heart and can help determine if any previous infarcts or other pathology exist. Acute MI are large killers of DM pts UA: Does she have a UTI?

Labs – Case Study #1 X-rays: No sign of osteomyelitis No soft tissue emphysema Edematous soft tissues around the entire right foot WBC HGB HCT PLT

15.38 (Lymph = 7.5%) (TLC = 1154) 11.13 HGB (11 – 16) 39.0 WBC ( 5 – 10) >------------------
Na 135 K 3.2 Cl 101 CO2 26 BUN 22 CR 2.9 Glucose 291

Na+ (135 – 145)| Cl – (98 – 109) | BUN (10 – 20) --------------------|--------------------|------------------< Glucose (70 – 120) K+ (3.5 – 5.5) | CO2 (20 – 30) | Cr (0.5 – 1.5)

Albumin 2.6 HbA1C 11.5 ESR: 92 UA: + protein Microbiology Gram stain: Many gram + cocci Few gram – rods Cultures: S. aureus E. coli B. fragilis Vascular Studies: Handheld Doppler reveals monophasic waveforms ABI:

L = 0.47 R = 0.31 (Should be greater than 0.45) TcPO2

L = 36.5 R = 20.7 (Should be greater than 30)

Relevant Questions – Case Study #1 1. If you were to write admit orders for this patient, what headings would you cover? Admit to service Diagnosis Condition Vitals Acronym: ADC VAN DILMAX Activity Nursing Diet Ins & Outs Labs Medications Ancillary X-rays 2. What are your radiographic findings for osteomyelitis? - soft tissue changes (swelling that obliterates the fat planes, possible soft tissue emphysema) - periosteal reaction - cortical destruction - sequestrum - involucrum 3. What is the lag time associated with x-rays findings of osteomyelitis? 10 – 14 days 4. What is a left shift? Neutrophils + bands > 80 Increase in the number of immature neutrophils present 5. What color denotes gram + organisms? Gram – organisms? (+) are pink (-) are purple 6. Name some gram + cocci Staphylococcus Enterococcus Streptococcus Micrococcus 7. Name some gram - rods S2P3HEK (S/P HEK) Escherichia Pseudomonas Hemophilus Klebsiella Serratia Salmonella Pasteurella Proteus

8. Name 5 anaerobes. Clostridium Bacteroides Peptostrepococcus Peptococcus Fusobacterium 9. Name 7 gas forming organisms BECKS+ Bacteroides Escherichia Clostridium Klebsiella Staph/Strep Serratia Fusobacterium Peptostrepococcus Peptococcus 10. Name some anti-pseudomonal drugs. FATZ – CIA Fortaz Aztreonam Ticracillin (Timetin) Pipercillin (Zosyn) Ciprofloxacin Imipenem Aminoglycosides 11. How do you calculate creatinine clearance? (140 – age) x weight (kg) (x 0.85 in women) 72 x serum Cr 12. What are some commonly used antibiotics that do not require renal dosing? Clindamycin, Erythromycin, Chloramphenicol, Cefoperazone 13. Name 4 common PCN combination drugs used in diabetic foot infections and their dosages Unacyn (Ampicillin/Sulbactam) 1.5, 3.0 g IV q6h Zosyn (Piperacillin/Tazobactam) 3.375 g q 4 – 6h; 4.5 g q4-6h for pseudomonas Timentin (Ticracillin/Clavualanate) 3.1 g q4 – 6h Augmentin (Amoxicillin/Clavualanate)500 – 879 PO BID or 250 – 500 PO TID 14. Estimate this patient’s blood glucose over the past 120 days. 15. At what HbA1C is a patient diagnosed with diabetes? 8.5% 16. What are some parameters used to evaluate a patient’s probability for healing? vascular (ABI > 0.45); nutrition (albumin > 3.0); immune status (TLC >1500)

17. What are the minimum levels of albumin and TLC required for healing? Albumin of 3.0 g/dl TLC of 1500 From: Dickhaut et al, JBJS 1984 18. What antibiotics are safe to use during pregnancy? Penicillins Cephalosporins Erythromycin 19. What antibiotics are not safe to use during pregnancy? Ticracillin Metronidazole Tetracycline 20. Which antibiotics are associated with ototoxicity? Aminoglycosides – irreversible Erythromycin – reversible with d/c of the drug Vancomycin – may or may not cause ototoxicity 21. Which class of antibiotics can cause a neuromuscular blockade and what do you give to reverse this? Aminoglycosides Give Calcium to reverse the blockade 22. Which antibiotics are most commonly associated with seizures? Penicillin Ampicillin Imipenem 23. Which antibiotics are associated with nephrotoxicity? Aminoglycosides Vancomycin Penicillins – interstitial nephritis Cephalosporins – intersititial nephritis 24. Which antibiotics are associated with hepatotoxicity? Tetracycline (may cause death in pregnant women) Erythromycin – reversible 25. What are possible antibiotics to treat C. diff associated diarrhea? Metronidazole: 500 mg PO q8h x 10 days Vancomycin: 125 mg PO q6h x 10 days 26. Which anaphylactoid response is unique to Vancomycin? Red man syndrome

27. Who studied the relationship between ABI and healing and what did he/them find? Wagner ABI > 0.45 28. What is the minimum TcPO2 needed for healing? Who said this? 30 mmHg Wyss, Harrington & Burgess, JBJS, 1988 29. What physical exam finding may lead to a decreased TcPO2? Edema due to cellulitis 30. Name several etiologies of peripheral neuropathies DANG THERAPIST Diabetics/drugs Alcoholic Nutritional Guillain-Barre Syndrome Toxic Hereditary Recurrent Amyloidosis Porphyria Infectious (syphilis, hansen’s dz) Systemic Tumor Meds 31. Three Diabetic Foot Classifications. Wagner (Foot & Ankle, 1981) 0: potential, preulcerations, no open lesions 1: superficial ulceration 2: deep ulceration penetrating to tendon, joint capsule of ligament 3: penetration to bone with presence of infection 4: gangrene of forefoot 5: gangrene of rearfoot University of Texas, JFAS 1996 This classification is based on wound depth and the presence or absence of ischemia and/or infection. The benefit of this classification system is that it has predictive value and can indicate treatment protocol. 0: pre- or post-ulcerative lesion that is completely epithelialized 1: superficial wound not involving tendon, capsule or bone 2: wound penetrating to tendon or capsule 3: wound penetrating to bone or joint

A: non-ischemic or clean wound B: infected wound C: ischemic wound D: infected and ischemic wound Meade & Mueller (Med Times, 1968) 1: dorsal foot phlegmon (non localizing, cellulitic, infectious process) 2: deep plantar space infection 3: mal perforans neuropathic foot ulcers (subclassed above) 32. Name 4 Different Insulin Preparations Ultra fast/ultrashort acting: -Lispro insulin -Aspart Short Acting -Regular insulin (crystalline zinc) SQ/IV -Semilente SQ Intermediate Acting -NPH (neutral protamine hagedorn) SQ -Lente Long Acting -Ultralente SQ -Protamine zinc Ultra Long Acting -Glargine

Rapid Intermediate Long Ultra long acting

Onset 10 – 30 minutes 1 – 4 hours 4 – 8 hours 4 hours

Peak 1 – 2 hours 6 – 12 hours 18 – 24 hours None

Duration 2 – 4 hours 18 – 24 hours 24 – 36 hours

33. Name some hypoglycemic drugs. Suflonureas -MOA: increased insulin secretion from the beat cells of the pancreas -1st generation: chlorpropamide -2nd generation: glipizide (glucotrol); glyburide (micronase) Biguanides -inhibits glyconeogenesis in the liver; increases peripheral insulin action -Metformin(glucophage) Alpha-Glucosidse Inhibitors -inhibit glucose uptake in the gut blunting the post prandial hyperglycemia -Acarbose (precose) Thiazolidinediones (TZDs) -antihyperglycemics that increase insulin sensitivity -Rosiglitazone -Troglitazone Other -Repaglinide: insulin secretagogue whose binding site differs from that of the suflonureas. Insulin release is rapid and brief. Very useful for post prandial hyperglycemia 34. What type of anti-hypertensive may cause hyperglycemia? Thiazide diuretics (HCTZ)

Elective Surgery and Pre-Operative Labs – The Chem 7 Sodium (Na): Normal 125 – 145 mEq/L Hypernaturemia: dehydration, sodium overload, diabetes insipidus or volume depletion (diarrhea, osmotic diuresis). Zebra: Cushing’s syndrome Hyopnaturemia: volume excess/edema, fluid retention (CHF), IV fluids, vomiting/diarrhea, renal failure (nephritic syndrome), heart failure, cirrhosis. Zebra: Addison’s disease Potassium (K): Normal 3.5 – 5.5 mEq/L Increases: dehydration, trauma (hemolysis), acidosis, renal disease, use of K sparing diuretics. Membrane potential will become closer to threshold
can lead to fibrillation and cardiac stand still Decreases: Vomitting/diarrhea, diuretics, excessive sweating, cellular shifts. Zebra: Cushing’s disease. Less excitable membranes can lead to bradycardia. Chloride (Cl-): Normal 89 – 109 mEq/L Strongly mirrors sodium. See above. Bicarbonate: Normal 23 – 32 mEq/L Why this is valuable: information as to overall perfusion and saturation of RBC. Significant alteration in either positive or negative directions is not desirable and may indicate the presence of an anemia or significant blood loss recently. BUN (Blood Urea Nitrogen): Normal 10 – 20% BUN is a produced by protein breakdown in liver and excretion by the kidney. Elevated BUN (azotemia) indicates possible crush injury, infection, excessive protein intake or an inability of kidneys to excrete BUN (renal dz, hypotension). Decreases: liver is unable to breakdown protein or malnutrition. Not as reliable as creatinine because BUN is dependent on age, gender, lean body mass and etc. Creatinine (Cr): Normal 0.7 – 1.4 Byproduct of creatine produced by the liver and kidneys and is used as an energy storehouse in skeletal muscle. Creatinine is completely filtered by the kidneys and is not reabsorbed or secreted, thus its an excellent measure of GFR (glomerular filtration rate). Elevated serum creatinine is most specific for renal dz, creatinine clearance, usually greater than 80 ml/min is the best way to assess renal function. It requires a 24 hr urine specimen, but it can be estimated using the equation: [(140 – age) x wt (kg) (0.85 for women)] / 72 x creatinine clearance Glucose: Normal 80 – 120 mg/dl Most offen used in diagnosing and managing diabetes. Diabetes can be diagnosed as a fasting blood sugar >126 mg/dl and 2 hour post prandial blood sugar over 200 mg/dl. Glucose can also be elevated by hyperthyroidism or from thiazide diuretics Glucose can be decreased in pancreatic neoplasms and Addison’s disease Hemoglobin A1C normal: 3 – 6% Can be 3 – 6% in non diabetics. In uncontrolled diabetics it can be as high as 10% (or higher). Good estimate for judging a patient’s long term control

Elective Surgery & Pre-Operative Labs – The CBC Can be done with or without a differential Agranulocytes: Lymphocytes, Monocytes Granulocytes: Neutrophils (PMN), Eosinophils, Baseophils WBC Normal 5000 – 10000 / mm Leukopenia (<4000/mm): drugs (most commonly); acute infection, vit B12 deficiency, SLE, RA. Leukocytosis (>12000/mm): infection, pregnancy, splenectomy, drugs (corticosteroids, lithium, epi, abx, sulfonamides) Neutrophils: Normal 40 – 75% Increases: bacterial infections Bands: immature neutrophils Segs: mature neutrophils Bands + Segs > 80
left shift has occurred Lymphocytes: Normal 15 – 45% Diverse group of cells Includes T cells and B cells Increase: usually a viral infection Eosinophils: Normal 1 – 6% Increase: allergic reactions, parasitic diseases Basophils: Normal 1 – 2% Source of histamine; contain heparin Increase in basophils is usually associated with an increase in Mast cells (basophils in tissue) Increase: myxedema, blood vessel injury Monocytes: Normal 1 – 10% Increase: protozoan infections, TB

Elective and Pre-Operative Labs – The H & H Most valuable in cases of malnutrition or suspected anemia. Hemoglobin (Hgb):

13 – 17 males 11 – 15 females Hemocrit (Hct): 39 – 51 3 x Hgb Mean corpuscular volume Hct/RBC 82 – 92 mm3 Microcytic MCV<80 Iron deficiency Blood loss Thalassemia

Normocytic MCV 80 – 100 Chronic dz Bone marrow Dz Hemolysis

Macrocytic MCV > 100 Folate def/Vit B12 def Liver dz Anticonvulsants

Microcytic anemias (Fe deficiency anemias) D/Dx pneumonic = TICS T – Thalassemias I – Iron Deficiency C – Chronic Inflammation (anemia) S – Sideroblastic anemia (check pt for Pb toxicity)

Normocytic anemias D/Dx pneumonic = NORMAL S(I)ZE N - Normal pregnancy (volume expands up to 30% plasma vol) O - Over hydration R - Renal (chronic renal disease => lower EPO production) M – Myelophistic: replacement of bone marrow w/ tumor A – Acute blood loss L – Liver disease S – Systemic Inflammation Z – Zero production E – Endocrine disorders e.g. hypothyroid disease

Macrocytic anemias D/Dx pneumonic = BIG FAT RED CELLS B – B12 deficiency I – Inherited problem G – G/I F – Folic Acid deficiency A – Alcoholism T – Thymine responsive R – Reticulocytes (larger than mature RBC), therefore inflate MCV E – Endocrine D – Dietary problems (lack of dietary folate, B12 etc.) C – Chemotherapeutic Rx E – Erythroleukemia L – Liver Disease L – Lesch- Nyan Syndrome (“zebra”) S – Splenectomy Hemolytic Anemias (Increased rate in destruction of RBC) D/Dx pneumonic = HEMATOLOG(I)ST H – Hemoglobinopathy (most common is sickle cell) E – Enzyme deficiency M – Medication (drug induced) A – Ab T – Trauma to RBC O – Ovalocytosis (Autosomal Dom disorder in pop w/ south east asia) L – Liver Disease O – Osmotic Fragility G – Glucose 6-P DH Deficiency S – Splenic destruction T – Transfusion related

Elective and Pre-Operative Labs – Coagulation Panel Bleeding Time: Normal 2 – 9 minutes Normal time is via a controlled forearm scratch. Increase: ASA and NSAIDs Platelet Count: Normal 150,000 – 450,000 Indication of cessation of bleeding following an operation. Below 25,000 may indicate spontaneous bleeding PT: Normal 11 – 16 sec Measures the extrinsic coagulation pathway Normal in Hemophilia A & B Increase in Vitamin K, impaired fat absorption, liver dz, warfarin (coumadin) PTT: Normal 25 – 35 sec Measures the intrinsic coagulation pathway Normal in thrombocytopenia, platelet dysfunction, von Willebrand’s dz Increased: Hemophilia A & B, prothrombin complex disorders, heparin Radiographic Analysis - always obtained for any patient undergoing osseous resection, penetrating wounds, ulcerations - several standard views (usually 3) - good quality -available at time of surgery Cultures - any open wound, especially in diabetic or immunocompromised patients - will help with individual tailoring of abx treatment Ancillary Tests - Women under the age of 50 – pregnancy or HCG test should be performed - Patients over the age of 40 – EKG to rule out arrhythmias - Over 50 with history of smoking – Chest X-ray

Case Study #2 HPI: 22 yr old female patient comes to the office seeking treatment for a three day history of left foot and ankle swelling, redness and warmth. Pt does not complain of pain and denies trauma or recent illness. PMH: Type I diabetes x 12 years with associated neuropathy Anorexia nervosa Chronic diarrhea Osteoporosis due to anorexia, chronic diarrhea and prolonged amenorrhea Hospitalization: several times for tx of DKA and exacerbation of her psychiatric problems PE:

Vitals: Ht 160 cm; Wt 52 kg; VSS, afebrile Integ: right foot and ankle is erythematous, warm, swollen; no open lesions Vasc: palpable pedal pulses Neuro: diminished perception of light touch in a stocking distribution M/S: normal muscle strength; no pain on palpation

Labs: ESR 130mm/hr WBC 8.7 with normal differential Hgb: 8.6 Hct: 29% Platelet count: 700,000/mm3 X-ray:

Diagnosis: Acute charcot arthropathy Treatment:

Posterior splint with compressive dressing x 3 days TCC applied once swelling subsided x 6 weeks Increased WB in short leg cast x 4 – 6 months Eventually went on to full WB in an AFO

Related Questions – Case Study #2 1. What are some differentials for this case study? Acute charcot Acute septic arthritis Osteomyelitis Avascular necrosis Cellulitis Pigmented villonodular synovitis DJD Psoriatic arthritis Gout Rheumatoid arthritis 2. What are the four factors necessary for charcot to develop? Peripheral neuropathy Hypervascularization Repetitive microtrauma Unrecognized injury 3. Eichenholtz’s three stages of Charcot are…. I – Acute, Developmental, Destructive, Dissolution – foot is inflamed, edematous and erythematous; radiographs demonstrate bone fragmentation (subchondral bone and articular cartilage) and debris formation; joint dislocation/subluxation may be present; typically lasts 6 – 8 weeks II – Coalescence – healing begins and inflammation subsides; radiographs show coalescence and resorption of bony fragments; larger fragments begin to fuse III – Remodeling, Resolution, Reconstructive, Quiescence – inflammation is resolved; return to normal radiographic density; reformation of the joint architecture. 4. What are the treatments associated with each stage? Stage I – resolution of edema with compression, elevation and rest; total immobilization of the limb by total contact casting, regular casting or pre-fabricated cast boot Stage II – progressive weight bearing in regular or total contact cast; as the disease progresses move from a cast to bracing such as a Charcot restraint orthotic walker (CROW), double upright metal AFO or other AFO with progressive weight bearing Stage III – long term AFO bracing; extra depth shoes or other types of accommodative foot wear ***Remember that you must use clinical judgment to decide when to progress to the next stage of treatment*** 5. What are the 6Ds of Charcot? Distension of joints Density increases Dislocation Debris production Disorganization Destruction 6. What disorder has the highest percentage of Charcot joints? Syringomyelia; up to 25% will have charcot joints 7. What percentage of diabetic patients will develop charcot joints? 1 in 680 From .13% to 25% This number depends on who is reporting it.

8. What are some disorders associated with Charcot? - Diabetes - Spina bifida - Tabes dorsalis (syphilis) - Meningomyelocele - Syringomyelia - Congenital insensitivity to pain - Chronic alcoholism - CMT - Hansen’s disease (leprosy) - Multiple sclerosis 9. Describe the two theories associated with the development of Charcot joints. Neurovascular (French) Theory
damage to the trophic nervous centers with an alteration in the sympathetic control of blood flow to bones and joints leads to persistent hyperemia and active bone resorption Neurotraumatic (German) Theory
An extreme progression of degenerative joint disease following loss of proprioception and protective pain sensation 10. How do you tell the difference between Charcot and osteomyelitis? - use of the MRI is becoming popular - definitive way: bone biopsy with microbiological diagnosis - use of the WBC labeled bone scan – osteomyelitis will be hot, charcot will not be hot - Plain radiographs: Charcot Osteomyelitis Bone destruction and fragmentation Bone destruction present Increased soft tissue density Increased soft tissue density Sclerosis may be present; osteoporosis may Early sclerosis with osteoporosis in later be present as diabetic osteolysis progression Progressive resorption is usually not Progressive resorption is present present Sequestrum formation may be mimicked Sequestrum formation occurs by fragmentation Subperiosteal new bone formation Subperiosteal new bone formation 11. What are the patterns of bone and joint involvement? Sanders & Frykberg. The Charcot foot, 1991. I – Forefoot Often atrophic and destructive findings mimicking osteomyelitis

Reported to occur 26 – 27%

II – Tarsometatarsal

15 – 43%

III – Talonavicular, CC, Navicularcuneiform IV – Ankle joint V – Calcaneus

Often with collapse of the midfoot, plantar ulceration often occurs at the apex of the deformity Characterized by dislocation of the navicular; can be solo or with other patterns Almost always results in severe deformity and instability. STJ can also be involved Insufficiency avulsion fx, least commonly reported

32%

3 – 10%

Brodsky J et al. Patterns of breakdown in the Charcot tarsus of diabetes and relation to treatment. Foot Ankle 5(12):353, 1986. Type 1 (Midfoot)

Type 2 (Hindfoot) Type 3A (Ankle)

Metatarsocuneiform & naviculocuneiform STJ, CC and TN jt Ankle joint

Type 3B (Calcaneus)

Tubercle of the calcaneus

Most common

~ 60%

Less common Serious long lasting changes Least common Secondary deformity and collapse of the distal portion of the foot

30 – 35% Associated with discrete trauma Associated with discrete trauma

Schon LC et al. Charcot Neuroarthropathy of the foot and ankle. Clinical orthopedics and related research. 349, 1998. Type I: Lis franc pattern Type II: Naviculocuneiform pattern Type III: Perinavicular pattern Type IV: Transverse tarsal pattern Subtypes A, B and C with increasing severity from A to C 12. During what stage(s) should surgical intervention be attempted? Well, like everything else in medicine recently, it depends on who you read. Eichenholtz: early stage I or late stage III Charcot joints pp 7 – 8. Springfield, IL 1996 Mann: early stage I (before development of osteopenia from local hyperemia) or late stage II when new bone formation is occurring Foot and Ankle Surgery, 1999. Johnson: operative treatment is usually carried out in Stage III after conservative care has been exhausted. An acute charcot fracture can be treated with ORIF in stage I if performed early before bone stock become insufficient for fracture. Johnson JE. Operative treatment of neuropathic arthropathy of the foot and ankle. JBJS 80A Nov 1998. Myerson: surgery is necessary in the acute phase of skin necrosis resulting from the pressure of a dislocated bone is imminent or other skin problems are likely to occur as a result of casting. Surgery is also indicated at this time for marked dislocation of the foot that is likely to cause problems with shoewear at a later date. Surgery can only be performed if bone stock is adequate, therefore, he rarely operates if more than 6 weeks after the beginning of the acute phase. In the setting of acute neuroarthropathy associated

with infection and surgery is indicated, Myserson uses an external fixator to stabilize the foot. Surgery should probably be reserved until Stage II or III. Foot and Ankle Disorders, 1999. Simon: First paper to demonstrate successful results in operative treatment in stage I Charcot. Authors operated on 14 patients in the acute phase of the disease with good anatomical reduction and good results. All patients had anatomic reduction, clinical union and stability without an increased risk of adverse outcome. Given this outcome along with decreased cost when compared to ulcer care, authors believe that early arthrodesis should be considered in patients with early stage I charcot. Simon SR et al. Arthrodesis as an early alternative to non-operative management of charcot arthropathy of the diabetic foot. JBJS 82A July 2000. 13. What is the natural history of Charcot arthropathy? - the foot goes numb - the bones become soft - the patient walks on the numb foot with soft bones - the soft bones fracture - the fractures heal with malposition of the fragments and deposition of fracture fragments in the adjacent joint capsule - the process repeats - the foot becomes shorter and wider and develops angular bony prominences - the foot becomes ulcerated and infected as the patient walks on the angular prominences - all hell breaks loose 14. What is the primary deforming force in many cases of Charcot? Ankle joint equinus 15. What is the history of Charcot in the literature? Musgrave 1703 – first to report neuropathic osteoarthropathy as an arthralgia secondary to venereal disease Jean Marie Charcot 1868 – French neurologist. Concisely describe the neuropathic component of the disease. Linked the condition to syphilis which was very common at the time. Jordan 1936 – Linked this condition to diabetes mellitus. Etiology of the Condition: Charcot 1868 – Deficient trophic centers in the spine Volkman, Virchow and the “German School” – neurotraumatic in nature. The neuropathic foot would fracture with exuberant bone formation. Eloesser (1917) – sectioned posterior nerve roots in cats and noted neurotrophic changes in 71% of the animals

Finsterbush & Friedman (1975) – repeated Eloesser’s experiment in rabbits but casted the rabbits hind legs. Different response noted in denervated and sensate rabbits. Concluded that trauma important but not primary factor. Edmonds et al (1985) – Increased blood flow was partially responsible for the osteopenia and ‘washing out of bone’ seen in Charcot. Neurovascular theory. 16. What are the relevant lab tests that can help lead to a diagnosis of charcot? WBC will be elevated with a left shift on the differential
acute osteomyelitis ESR is non specific
may not be helpful Tech 99 bone scans
may or may not be helpful Indium 111 bone scans
much more specific. If +
do bone biopsy to confirm osteomyelitis and r/o Charcot If -
dx is charcot until proven otherwise Certec scan
labeled white blood cells. May also be helpful Probe to bone If +
procede to bone biopsy If -
continue with other tests 17. What is the ‘gold standard’ for diagnosis? Bone biopsy Will histologically differentiate between osteo and charcot. 18 . What is a plan for the management of Acute Charcot? - Immobilization - Reduction of stress - Armstrong advocates the TCC (surprise, surprise) The reduced stride length and walking cadence will decrease the possibility of causing charcot in the other limb 19. What are the radiographic signs of Stage III Charcot ? trabecular bridging on serial radiographs

Hammer Digit Syndrome Three main categories of pathomechanical causes of hammer digits: - flexor stabilization - extensor substitution - flexor substitution What must happen in order for the rigid beam effect of the digits to occur? The muscles involved with gait must fire in the correct order. Breaks in the sequence lead to inability of the toes to purchase the ground. Flexible deformities
may be able to be managed with biomechanics; may not need surgery Rigid deformities
surgical correction probably necessary Flexor stabilization: - occurs in stance phase of gait - FDL gains mechanical advantage of the interossei - Can occur in flexible flatfoot, neuromuscular dz that leads to weakness of the interossei, spasticity of the FDL - Flexible flatfoot: quadratus plantae also looses mechanical advantage; FDL fires longer and sooner to help stabilize the floppy and abducted forefoot; oblique pull of FDL leads to adductovarus deformity of the 5th, 4th and possibly 3rd. SELDOM the 2nd. Contraction of these digits will be seen in mid to late stance phase of gait. Extensor substitution: - excessive dorsiflexion of digits during swing phase of gait and at heel strike - EDL has gained mechanical advantage over the lumbricales - causes: weak lumbricles, spastic EDL, pes cavus (especially flexible pes cavus), weak anterior group, contracture of the Achilles tendon, pain in the anterior part of the foot Surgical Correction: - Hibbs tenosuspension - detach the EDL at the MPJ - EDL attached to 3rd cuneiform - EDB transected and sewn to the EHL - may work to control HDS caused by extensor substitution - arthrodesis of the proximal interphalangeal joint - prox phalanx head resection with soft tissue release will lead to rapid recurrence - AFO or dropfoot leg brace Flexor substitution: - occurs when there is weakness of the triceps surae -FDL gains mechanical advantage as in flexor stabilization but b/c there is weakness in the Achilles tendon there is late stance phase supintaion rather than pronation

Flexor substitution: - arthrodesis of the PIPJ is often required - transfer the PT tendon and the PL tendon to the calcaneus - combination of the above Surgical Incisions for HDS surgery: - longitudinal - longitudinal oval - transverse - transverse oval - curvilinear - derotational ellipse for 5th digit Intraoperative Stepwise Approach - IP joint tenotomy/capsulotomy - resect the head of the proximal phalanx (post procedure)
reduces bony prominence and reduces the painful dorsal corns - release of the extensor sling and hood in longitudinal fashion parallel to the EDL and EDB tendons - Z plasty of the extensor tendons - capsulotomy of the MPJ joint - plantar release - flexor tendon transfer - proximal phalanx arthrodesis of the PIPJ

The Wondrous World of Hallux Abducto Valgus Goals of HAV Surgery 1. The establishment of a congruous 1st MPJ 2. The reduction of the abnormal osseous angles to normal parameters 3. Realignment of the sesamoid bones beneath the 1st metatarsal head – TSP <3 4. Restoration of weight bearing function of the 1st ray 5. Maintenance of the 1st MPJ pain free ROM 6. Repositioning of the hallux in rectus alignment 7. Decreasing ‘the bump’ 8. Control or correction of the factors which lead to the deformity Etiology of HAV 1. Primary
Pathobiomechanics a. Pronation is the root of all evil. We should know this by now. b. Hypermobile 1st ray c. Long 1st ray d. LLD e. Metatarsus primus elevatus (this is more a hallux limitus issue, however) 2. Secondary a. Trauma (like gun shots) b. Rheumatic: look at the RA x-rays, this is pretty obvious c. Neuromuscular: tendon/muscle imbalance d. Genetic or collagen disorders: Marfan’s or Down Syndrome e. Flat foot f. Gout g. Iatrogenic (i.e. tibial sesamoidectomy) Pathomechanics of HAV This is a progressive disorder characterized by 4 stages. The longer that it takes to progress from one stage to the next, the less severe the resulting deformity will be. The factors which affect the HAV deformity are: 1. walking surface 2. shoe gear 3. length of patient’s stride (increasing the propulsive phase) 4. STJ subluxation 5. MTJ subluxation 6. obesity 7. degree of calcaneal eversion 8. forefoot adduction 9. inflammation of the MPJ

Patho-Anatomy of HAV There are 4 articular facets within the synovial capsule: 1. metatarsal head 2. base of the proximal phalanx 3. tibial sesamoid 4. fibular sesamoid The 1st MPJ has 9 ligaments 1. 2 collateral ligaments 2. 2 metatarso-sesamoidal ligaments 3. 2 phalangeal-sesamoidal ligaments 4. Intersesamoidal ligament 5. Deep transverse metatarsal ligament 6. Capsule The 1st MPJ capsule incorporates 5 tendons: 1. FHB 2. Abductor hallucis 3. Adductor hallucis conjoined tendon 4. EHL 5. EHB
The FHL is the only tendon that does not have an attachment to the MPJ capsule
The weakest part of the MPJ capsule is dorsomedial.

Stage I

Stage II

Stage III Stage IV

Stages of HAV Lateral displacement of the proximal phalanx relative to the first metatarsal head Sagittal groove/sulcus where the corner of the proximal phalanx rubs into the metatarsal head Development of hallux abducto valgus deformity; the hallux abuts the 2nd toe 1st MPJ is fairly congruent Hallux abductus = abnormal IM = normal PASA = increased
more lateral deviation of the cartilage Increase in 1st IM angle Subluxed or dislocated hallux on the 1st metatarsal head

Axis Guides Guides (usually .062 K-wire) designed to change the direction of the osteotomy. So why do I care? - this allows correction in the 2 planes - these can change the direction of the osteotomy cut What would you like to do? Shorten the met Lengthen the met Plantarflex the met Dorsiflex the met

Direct the Axis Guide like this… Distal medial to proximal lateral Proximal medial to distal lateral No angulation from anterior to posterior Dorsal medial to plantar lateral No angulation from anterior to posterior Plantar medial to dorsal and lateral

Angle

Formed By:

Importance/Location of Deformity

Normal Value

Hallux Interphalangeus

- bisection of distal phalanx - bisection of proximal phalanx

IPJ of hallux Osseous deformity

0 – 10

DASA

- perpendicular to bisection of prox phalanx - cartilage prox phalanx base

Fixed deformity Prox phalanx
hallux abduction

7.5 (0 – 8) in some literature

PASA

- perpendicular to 1st met bisection - line connecting effective cartilage of 1st met head - prox phalanx shaft - 1st met head

Fixed deformity Trackbound joint Lateral deviation/ abduction of prox phalanx on 1st met head MPJ soft tissue deformity

7.5 (0 – 8) in some literature

IM Angle

- bisection 1st met - bisection 2nd met

1st ray fixed deformity

Metatarsus Adductus

- lesser tarsal axis - bisection 2nd met

Metatarsal Protrusion

- arc of 1st - arc of 2nd difference in mm - position of tibial seasmoid - bisection of 1st met

Increase in MA = increase in significance of other angles Large MA
HAV develops faster +
longer 1st met -
shorter 1st met

Hallux Abductus

Tibial Seasmoid

> 4 may indicate fib seasmoid removal or degenerating cristae

10 – 15

8 – 12 in rectus foot 8 – 10 in adducted foot <15

+/- 2 mm

1-3

Procedure Osseous Ex. Distal Akin Osseous Phalanx Ex. Proximal Akin Osseous at 1st met head Ex. Head wedgie procedure Capsule tendon balance – or – Osseous Depending on the other angles involved <14 – head 15 – 17 shaft >17 base Look at the IMt CBWO Chose carefully

Metatarsal Head Shapes Round – usually most prone to developing HAV, most reducible yet most the most unstable Square – more stable Square with a ridge – oblique or central ridge, helps prevent lateral deviation of hallux; compensatory hallux interphalangeus may be seen with this; more commonly associated with hallux rigidus or limitus; most stable Metatarsal Phalangeal Joint Positions Congruous – two articular surfaces are wholey articular and the joint space is equal Deviated – the lines representing the articular surfaces intersect outside the joint Subluxed – the lines representing the articular surfaces intersect inside the joint

1. 2. 3. 4.

Reading a Radiograph to Evaluate HAV Remove the hypertrophied eminence Bring 1st metatarsal head closer to the second metatarsal head – IM angle Obtain or maintain a congruous joint – PASA/DASA Straighten the toe – HA/HAI Capsulotomies A – Vertical B – U shaped C – H shaped D – T shaped E – L shaped A – Linear B – T shaped C – Inverted L E – Lenticular from dorsal view F – Oblique suture closure
corrects a frontal plane deformity G – Horizontal suture closure
corrects a transverse plane deformity C – Washington Monument type capsulotomy D – Suture to close the capsule E – Replace the capsular flap; aids in correction

Capsule Tendon Balancing Procedures Schede’s Exostectomy (1870s) - remove the bump

Lothrop’s Lateral Release (1873) - lateral release

Silver (Silver, David: The operative treatment of hallux valgus. JBJS 5:225, 1923) 1. curved medial incision 2. removal of bursal sac 3. resection of dorsomedial eminence 4. lateral capsulotomy with medial capsulorraphy designed to reinforce the medial collateral ligament and transpose dorsally the abductor hallucis tendon 5. lateral release McBride (McBride, Earl: A conservative operations for bunions. JBJS 10:735, 1928) 1. 5 cm incision from the toe web along the lateral border of EHL 2. resection of the dorsomedial eminence 3. lateral release consisting of lateral capsulotomy with fibular sesamoid excision 4. transfer of the adductor hallucis and lateral head of FHB to the dorsolateral aspect of the 1st met head
Adductor tendon transfer 1. dorsally through the capsule to reposition the sesamoids 2. into the 1st metatarsal neck to reduce the IM angle
transfer into the neck can be either dorsal to plantar or lateral to medial Hiss (Hiss, J: Hallux valgus, its cause and simplifies treatment, Am J Surg 11:51, 1931) 1. Resection of the dorsomedial eminence 2. lateral capsulotomy 3. transfer of abductor hallucis from plantar to medial to the 1st MPJ (abductor sutured into hole in the base of the proximal phalanx; acts as a ligament to strengthen the capsule medially) Stein (1938) 1. lateral release 2. resection of the medial eminence 3. Medial capsuloplasty to reposition to abductor hallucis more medially Joplin’s Sling (1950) 1. Modified McBride procedure by an adductor hallucis transfer through the metatarsal head to the medial side, instead of laterally on the head. 2. Very similar to the mini-tightropes being now used for juvenile HAV Component Procedures 1. adductor transfer 2. capsulorraphy 3. EHL tendon lengthening 4. EHB tenotomy

Phalangeal Osteotomies Proximal Akin (Akin, OF: The treatment of hallux valgus: a new operative approach and its results. Med Sentinel 33:678, 1925.) 1. Corrects for DASA 2. Osteotomy performed 5 – 10 mm from the MPJ 3. Proximal cut is parallel to the base of the proximal phalanx 4. Distal cut is perpendicular to the bisection of the proximal phalanx Distal Akin 1. Corrects for a large hallux interphalangeus angle 2. Performed 5 – 10 mm from the IPJ of the hallux 3. Distal cut is parallel to the surface of the head of the proximal phalanx 4. Proximal cut is perpendicular to the long axis of the shaft 5. Base medial; apex lateral 6. Fixation with 28-guage wire, single 0.045 K wire or 0.062 K wire with hinge intact, if broken, 2 crossed K wires Cylindrical Akin Type A – Corrects for long proximal phalanx Type B – Corrects for a long proximal phalanx and a high DASA and/or HI angle 1. Proximal cut 1 – 1.5 cm distal to the phalangeal base 2. Distal cut parallel to first cut or angulated to reduce abductus 3. Fixation with crossed K-wires (0.045 or 0.062) Oblique Akin 1. Indicated for and used to correct an increased hallux interphalangeus angle and an increased DASA 2. Leave the hinge intact
The following two procedures are named for where the apex is (proximal vs distal). The apex of the cut is always lateral. o Oblique Proximal  Base: medial and distal  Apex: lateral and proximal o Oblique Distal  Base: proximal and medial  Apex: distal and lateral

Shortening Sagittal Z 1. Good for a long proximal phalanx 2. Remove the darkened areas of the picture 3. Shortens the long hallux and reduces forces at the 1st met head
enhanced motion

Distal First Metatarsal Head Osteotomies Traditional Austin (Austin DW, Leventen EO: A New Osteotomy for hallux valgus: a horizontally directed “V” displacement osteotomy of the metatarsal head for hallux valgus and primus varus. Clinical Orthop. 157:105, 1981) 1. Resection of medial eminence 2. Osteotomy performed in the center of the metatarsal head with 60 degree angle between arms (plantar cut is made first)
Unicorrectional: normalizes IM angle
Bi correctional: normalized IM angle and PASA 4.Axis guides – utilize to lengthen, shorten, plantarflex or dorsiflex Youngswick – Austin Modification (Youngswick FD: Modifications of the Austin bunionectomy for treatment of metatarsus primus elevatus associated with hallux limitus. J Foot Surg 21:114, 1982) 1. Indicated for both hallux valgus and hallux limitus (early stages) 2. Resection of the medial eminence 3. Angle of the cut is 60 degrees 4. Plantar cut is the same as the Austin procedure. 5. Rectangular piece of bone is excised dorsally (Shortening the metatarsal head and decompressing the MPJ) Gerber-Massad (Bicorrectional) Modification to the Austin 1. Indicated for increased IM angle (mild) and increased PASA (mild) 2. Resection of the medial eminence 3. Plantar wing cut is the same and previously mentioned procedures 4. Dorsal wing is a medially based wedge of bone 5. Lateral movement decreases the IM angle 6. Closing the wedge rotates the head medially and decreases PASA

Kalish (Long Dorsal Arm) Modification to the Austin 1. Indicated for a larger IM angle 2. The cut is made at a 55 degree angle 3. Same plantar cut as previously mentioned procedures 4. Long dorsal arm that increases stability & allows for screw fixation 5. Reduce the larger IM angle (you are moving more bone) 6. Unable to swivel capital fragment to correct PASA Reverdin (Reverdin J: De la deviation en dehors du gros orteil et de son traitment chirugical. Tr Internat Med Congr 2:408, 1881) 1. Primarily used in conjuction with other procedures. 2. Indicated for an increased PASA and used by itself will only correct PASA.
Performed in metaphyseal bone
Vertical wedge cut in the distal portion of the metatarsal head
Distal cut (1st cut) is parallel to abnormal PASA
Proximal cut (2nd cut) is perpendicular to long axis of the 1st met
Lateral hinge should be preserved to increase stability Reverdin-Green (1977) 1. Indicated for an increased PASA 2. First cut is made parallel to the weight-bearing surface and exits the bone just proximal to the 1st MTH avoiding the articular surface 3. This preserves the articulation between the metatarsal heads and the sesamoids Reverdin-Green-Laird (1977) 1. Indicated for high PASA and high IM angle 2. Lateral cortex is cut, allowing lateral transposition of the capital fragment Reverdin-Todd (1978) 1. Corrects PASA & IM angle 2. Can be used to PF the metatarsal (for met primus elevatus) 3. Proximal ostetomy is angled either dorsal-distal to plantar-proximal (plantarflexing the capital fragment) or dorsal proximal to plantar distal (dorsiflexing the capital fragment) Peabody 1.Same as the Reverdin expect osteotomy is performed at the anatomical neck.

Hohmann 1. Indicated for high PASA, IM angle and sagittal plane displacement 2. Trapezoidal osteotomy (base orientated medially) at the level of the metatarsl neck. Through and through cut 3. Avoids sesamoidal irritation because this is a neck procedure.

Mitchell 1. Similar to the Hohmann. 2. Medial eminence resection 3. Lateral cortical strut left intact 4. No lateral release performed with this procedure. 5. Indications: Long first metatarsal (This procedure shortens the 1st met the most of any procedure)

Wilson 1. Oblique osteotomy oriented distal medial to proximal lateral (through and through) 2. Capital fragment is shifted proximally and laterally along the osteotomy 3. Capital fragment can also be translated dorsally or plantarly DRATO (Smith, 1971) 1. Derotational Angulated Tranpositional Osteotomy 2. Distal osteotomy – perpendicular to the long axis to the 1st metatarsal; through and through cut 3. Proximal osteotomy – angled proximal medial to distal lateral (PASA correction) 4. Dorsiflexes capital fragment to place the articular cartilage in a more functional position attempting to increase dorsiflexion at the 1st MPJ

Shaft Procedures for HAV Vogler Offset V 1. Apex of osteotomy at the metaphyseal-diaphyseal junction 2. Angle is 40 degrees 3. Longer dorsal arm allows for greater bone to bone contact 4. Length of dorsal wing determines how much swivel is possible 5. This is NOT the same procedure as a long arm Austin. Scarf or Z Osteotomy 1. Distal cut dorsal; proximal cut plantar
avoids the possibility of scoring the sesamoid apparatus; easier to fixate 2. Troughing effect: dorsal segment of the Z (cortical bone) wants to sink into the plantar segment when screws are tightened down.

Mau (1926) 1. The cut is distal dorsal to proximal plantar (‘the airplane is taking off to Maui’) 2. You can use the angle of the cut to swivel the bone and reduce the PASA

Ludloff (1918) 1. Cut medial to lateral through the bone from dorsal and proximal to plantar and distal 2. You can use the angle of the cut to swivel the bone and reduce the PASA

Proximal Osteotomies for HAV Crescentic (Weinstock) 1. Indicated for high IM angle, short metatarsal 2. ½ moon shaped osteotomy created approximately 1.5 cm distal to 1st met-cuneiform joint 3. When looking at the metatarsal from dorsal to plantar, the concave portion of the osteotomy faces distally 4. The distal segment can be dorsiflexed or plantarflexed 5. The distal segment can be rotated until desired correction is obtained Juvara (Oblique closing base wedge, 1919) 1. Long oblique osteotomy with a medial hinge 2. Originally described as a ‘double oblique section of the metatarsal’ performed at the junction of the middle and proximal thirds of the metatarsal shaft 3. Modifications
Oblique osteotomy from distal lateral to proximal medial
Proximal cortical apex is maintained
Fixation with one or two screws 4. Type A – Corrects the transverse plane Type B1 – Corrects the transverse and sagittal planes Type B2 – Corrects the transverse, sagittal planes & long or short met Type C1 – Sagittal correction only Type C2 – Sagittal and long/short met correction Loison – Balacescu (Loison M: Note sur le traitment chirurgical du hallux valgus, d’apres l’etude radiographique de la deformation, Bull Soc Chir 27:528, 1901.) (Balacescu J: Un caz de hallux valgus simetric, Rev Chir Orthop 7:128, 1903) 1. Originally described as being at a point just distal to the insertion of the peroneus longus tendon 2. Closing base wedge 1 cm from the met-cuneiform junction with medial cortex left intact Logroscino Double Osteotomy (Logroscino, D: IL trattemento chirugico dell’aluce valgo. Chir Organi 32:81, 1948) 1. Double osteotomy of the first metatarsal 2. Indicated for increased PASA (distal wedge) 3. Indicated for increased IM angle (proximal closing wedge) 4. For short first met: Reverdin and Trethowan 5. For long first met: Reverdin and Loison

Trethowan (Trewthowan J: Hallux valgus. In Choyce CC, ed: A System of Surgery, New York 1923, PB Hoeber) 1. Resection of the medial eminence 2. Use this resected bone for an opening base wedge (base of which is medial) of the 1st met base Opening Base Wedge

3:1 1. Capsule tendon balance procedure 2. Closing abductory base wedge 3. Proximal akin osteotomy Opening wedge of the medial cuneiform

Lapidus (Lapidus PW: Operative correction of metatarsus varus primus in hallux valgus, Surg Gynecol Obstet 58: 183, 1934) 1. Denuded cartilage of 1st met-cuneiform joint 2. Decorticated lateral aspect of the base of the 1st met and the adjacent surface of the 2nd metatarsal base 3. Packed bone chips obtained from the resected medial eminence 4. Indicated for very high IM angles, a medially orientated proximal edge of the medial cuneiform and a hypermobile first ray

Complications 1. Hallux varus A. Etiology 1. Staking the head 2. Negative IM angle 3. Aggressively biasing the capsule 4. Negative PASA 5. Fibular sesamoidectomy 6. Aggressive post-op bandaging B. Sequence of surgical correction 1. Scar revision 2. Dissection in planes 3. Capsuloplasty, V-Y or Z plasty or advancement (not simple linear capsulotomy) 4. Degloving the articulation 5. Adductor tendon reefing 6. Abductor tendon transfer to lateral side 7. EHL lengthening 8. If dislocated, tibial sesamoidectomy (if, at this point, both sesamoids have been removed do an IPJ arthrodesis) 9. Reverse Akin, Austin, Hohmann 10. Arthrodesis 2. Tibial sesamoid dislocation A. Etiology 1. Staking the head and removing the sagittal groove 2. Overtightening the medial capsule 3. A negative IM angle 3. Capsular defect 4. Staking the head – excessive bone removal on the medial 1st MT head, losing the plantar tibial sesamoid groove 5. Capital fragment on the floor (Christenson C: Intra operative contamination of the bone and cartilage during an Austin bunionectomy 31:285, 1992) A. Mix the following: 1 L normal saline, 1 ml Neosporin GU irrigant and 1:100,000 bacitracin B. Place fragment in this solution x 5 minutes C. Transfer to second basin with same solution x 5 minutes D. Transfer to third basin with same solution x 1 minute E. 1 gm Cefadyl IV @ 8, 16 and 24 hrs post op (1st generation cephalosporin) 6. Severing the EHL or the FHL 14. AVN 7. Infection 15. Nerve entrapment 8. Breaking the hinge 16. Sesamoiditis 9. Intra-articular osteotomy 17. Hallux limitus 10. Recurrence 18. Fixation failure 11. Delayed or non-union of the osteotomy site 12. 1st met shortening 13. 1st met elevatus

HAV Questions What are the goals of HAV surgery? 1. The establishment of a congruous 1st MPJ 2. The reduction of the abnormal osseous angles to normal parameters 3. Realignment of the sesamoid bones beneath the 1st metatarsal head – TSP <3 4. Restoration of weight bearing function of the 1st ray 5. Maintenance of the 1st MPJ pain free ROM 6. Repositioning of the hallux in rectus alignment 7. Decreasing ‘the bump’ 8. Control or correction of the factors which lead to the deformity Which of the above factors do the patients care most about? 1. Decreasing ‘the bump’ 2. Hallux in rectus alignment What are the etiologies of HAV? hypermobile 1st ray genetic disorders neuromuscular disorders rheumatic disorders tibial sesamoidectomy Which bones in the 1st met capsule have articular facets? Metatarsal head Proximal phalangeal base Tibial sesamoid Fibular sesamoid Name the ligaments in the 1st MPJ apparatus. 2 collateral ligaments 2 metatarsal-sesamoidal ligaments 2 phalangeal-sesamoidal ligament intersesamoidal ligament deep transverse metatarsal ligament capsule Name all of the tendons incorporated into the 1st MPJ. FDB Adductor hallucis Abductor hallucis EHL EHB Which hallucial tendon has no attachement to the 1st MPJ capsule? FHL

What is the weakest part of the 1st MPJ capsule? The dorsomedial aspect of the capsule What are these fibers called? Sharpey’s fibers Name the radiographic parameters that are used when evaluating a radiograph for HAV surgery and give the normal values. Met adducuts angle normal = 15 1st IM angle normal = 8 – 12 Hallux abductus normal < 15 PASA normal < 7.5 DASA normal < 7.5 HAI normal < 10 Met protrusion distance < 2 mm Tibial sesamoid position normal 1 – 3 What are the different shapes of the 1st metatarsal head and why are they important? Round – usually most prone to developing HAV, most reducible yet most the most unstable Square – more stable Square with a ridge – oblique or central ridge, helps prevent lateral deviation of hallux; compensatory hallux interphalangeus may be seen with this; more commonly associated with hallux rigidus or limitus; most stable What are the different metatarsal phalangeal joint positions? Congruous – two articular surfaces are wholey articular and the joint space is equal Deviated – the lines representing the articular surfaces intersect outside the joint Subluxed – the lines representing the articular surfaces intersect inside the joint What are axis guides and how do you orient them to get the desired effect? K-wire inserted primarily to define the apex and orientation of the osteotomy; most importantly serves to determine the direction of displacement for the capital fragment in all three body planes Distal Osteotomies Frontal plane: describes the lateral movement of the capital fragment in respect to the weight-bearing surface - from medial to lateral the K wire is directed dorsally, the capital fragment will shift dorsally - from medial to lateral the K wire is directed plantarly, the capital fragment will shift plantarly Transverse osteotomies: dictates lengthening or shortening of the metatarsal with lateral shifting - K-wire orientated parallel to the shaft of the 2nd metatarsal, with lateral displacement, the met will be shortened approximately the width of the saw blade - K-wire orientated distal medial to proximal lateral, shortens the met - K-wire orientated proximal medal to distal lateral, lengthens the met

Name the Medial capsulotomies. (VW HULT) Vertical H shaped U shaped L shaped T shaped Lenticular Washinton Monument Name the dorsal capsulotomies. (LiLT) Linear Inverted L shaped T shaped Describe the Washington Monument. (Not the one in Washington, the capsulotomy) Incision into the capsule medially Reflect the flap proximally Close the capsule Replace the capsule flap This aids in the correction of hallux valgus Name all of the Akin procedures & describe them to the best of your ability. Proximal Akin (Akin, OF: The treatment of hallux valgus: a new operative approach and its results. Med Sentinel 33:678, 1925.) Corrects for DASA Osteotomy performed 5 – 10 mm from the MPJ Proximal cut is parallel to the base of the proximal phalanx Distal cut is perpendicular to the bisection of the proximal phalanx Distal Akin Corrects for a large hallux interphalangeus angle Performed 5 – 10 mm from the IPJ of the hallux Distal cut is parallel to the surface of the head of the proximal phalanx Proximal cut is perpendicular to the long axis of the shaft Base medial; apex lateral Fixation with 28-guage wire, single 0.045 K wire or 0.062 K wire with hinge intact, if broken, 2 crossed K wires Cylindrical Akin Type A – Corrects for long proximal phalanx Type B – Corrects for a long proximal phalanx and a high DASA and/or HI angle Proximal cut 1 – 1.5 cm distal to the phalangeal base Distal cut parallel to first cut or angulated to reduce abductus Fixation with crossed K-wires (0.045 or 0.062) Oblique Akin Indicated for and used to correct an increased hallux interphalangeus angle and an increased DASA Leave the hinge intact


The following two procedures are named for where the apex is (proximal vs distal). The apex of the cut is always lateral. o Oblique Proximal  Base: medial and distal  Apex: lateral and proximal o Oblique Distal  Base: proximal and medial  Apex: distal and lateral Name all of the Reverdin modifications and describe the modification. Reverdin (Reverdin J: De la deviation en dehors du gros orteil et de son traitment chirugical. Tr Internat Med Congr 2:408, 1881) 1. Primarily used in conjunction with other procedures. 2. Indicated for an increased PASA and used by itself will only correct PASA.
Performed in metaphyseal bone
Vertical wedge cut in the distal portion of the metatarsal head
Distal cut (1st cut) is parallel to abnormal PASA
Proximal cut (2nd cut) is perpendicular to long axis of the 1st met
Lateral hinge should be preserved to increase stability Reverdin-Green (1977) – added plantar shelf 1. Indicated for an increased PASA Reverdin-Green-Laird (1977) – lateral cortex is cut, allowing for lateral transposition of the capital fragment Reverdin-Todd (1978) – Proximal osteotomy is angled either dorsal-distal to plantarproximal (plantarflexing the capital fragment) or dorsal proximal to plantar distal (dorsiflexing the capital fragment) 1. Corrects PASA & IM angle 2. Can be used to PF the metatarsal (for met primus elevatus) What does DRATO stand for? De-rotational angulated transpositional osteotomy Describe the orientation of the osteotomy for a Scarf Z and a reverse (inverted) Z osteotomy. For both of these osteotomies, the osteotomy is horizontally directed displacement Z cut that is performed at the diaphyseal junction level in an upper 2/3rd , lower 1/3rd manner. The distal apex is placed 1 cm proximal to the articular surface. The horizontal bone cut is approximately 2.5 – 3.0 cm in length and is angled 5 – 10 degrees in relation to the transverse plane in a plantar lateral direction. Scarf Z – Distal cut is dorsal, plantar cut is proximal. Both are angulated 70 – 80 degrees to the horizontal cut Reverse Z - Distal cut is plantar, proximal cut is dorsal. Both are angulated 70 – 80 degrees to the horizontal cut

Differentiate between a Mau and a Ludloff.

Mau – osteotomy oriented from plantar proximal to dorsal distal (Looking at this cut from the medial aspect of the foot, it looks like a plane is taking off to MAUI and flies over the toes before hitting the ocean) Ludloff – osteotomy oriented from dorsal proximal to plantar distal What are the Juvara subtypes and what do they correct? Type A – Corrects the transverse plane Type B1 – Corrects the transverse and sagittal planes Type B2 – Corrects the transverse, sagittal planes & long or short met Type C1 – Sagittal correction only Type C2 – Sagittal and long/short met correction Name as many bunion procedures as you can and categorize them according to osteotomy placement (i.e. head vs shaft vs base, etc) 1. Phalangeal Proximal Akin Distal Akin Transverse Akin Proximal Oblique Akin Distal Oblique Akin Cylindrical Akin Sagittal Shortening Z Keller 2. Capsule tendon balance Silver McBride Adductor tendon transfer 3. Head Schede Austin Traditional Youngswick Gerber – Massad (bicorrectional) Kalish (long dorsal arm) Logriscino (distal part) Reverdin Green Laird Todd 4. Neck - Mitchell - Hohman - Peabody - DRATO 5. Shaft Scarf

Off-set V Mau Ludlow 6. Base - Loison – Balacescu - Juvara - Cresecentic - Trethowan - Logriscino (proximal part) 7. 1 met/1 cuneiform - Lapidus Why might you want to dorsiflex the hallux when making the initial incisions of an Austin? Protects the articular cartilage of the 1st metatarsal head Describe the hinge axis principle. (Smith TF: The hinge concept in base wedge osteotomies. In Schlefman B (ed): Doctors Hospital Podiatry Institute Seminar Manual. Tucker, GA. 1983, 66 – 68) The function of an intact cortical hinge in a closing base wedge osteotomy acts as an axis of rotation. Traditional axis of the base wedge osteotomy was perpendicular to the metatarsal, subsequent lateral displacement of the metatarsal will result in sagittal plane dorsiflexion. If the osteotomy is made perpendicular to the weight bearing surface, then lateral displacement of the distal metatarsal will not dorsiflex or plantarflex the metatarsal head and should remain parallel to the weight bearing surface. What are the differences between a Silver and a McBride procedure? Silver, D: The operative treatment of hallux valgus. JBJS 5: 225, 1923 McBride E: A conservative operation for bunions. JBJS 10:735, 1928 McBride Silver Incision Lateral border of EHL Medial curved incision Capsule Dorsal to planter incision Y shaped incision Sesamoids Fibular sesamoidectomy No sesamoidectomy Tendon transfer Adductor tendon to lateral Adductor release st aspect of 1 met shaft What is the McBride test and what do the results indicate? From: McBride E. JBJS 1967. Patient is seated and toes are relaxed. Move the hallux towards the midline of the body. Can’t be brought into alignment with a little bit of overcorrection? There is capsular contraction. Surgically: remove fibular sesamoid, tenotomize the lateral capsule and transfer the conjoined tendon. Can be brought into alignment with a bit of overcorrection? Repeat the test standing. Can’t be brought into alignment? Capsule is not the deforming force, the adductor is. Surgically may be possible to just tenotomize the adductor tendon.

What are the mini frag, small frag and large frag set and what size screws do they contain? Mini frag set: 1.5, 2.0, 2.7 Small frag set: 3.5, 4.0 (partially threaded), 4.0 (fully threaded) Large frag set: 4.5, 4.5 (malleolar screw), 6.5 (partially threaded), 6.5 (fully threaded) What is a bunionectomy screw? A Herbert screw? A Reese screw? Bunionectomy screw: 4.0mm partially threaded cancellous thread diameter with a 2.7 screw head Herbert screw: a unique screw that has two threaded portions that are separated by a smooth portion centrally. The pitch difference in the threaded portions is the design mechanism that draws together two bone fragments and creates compression across an osteotomy or fracture. Ford T: The Herbert bone screw and its application in foot surgery. JFAS 33:346, 1994 Herbert TJ et al: Management of the fractured scaphoid using a new screw. JBJS 66B: 55 – 58, 1984) Reese screw: headless screw with clock-wise threads proximally and counter clock wise threads distally. Used for 1st IPJ fusions What material is the surgical screw driver handle made from? Pressed linen Name the modifications of the Austin bunionectomy. Youngswick – Austin Bicorrectional Austin Kalish Vogler Offset V What is meant by staking the head in a bunion surgery? Excessive bone removal on the medial 1st MT head which causes the loss of the tibial sesamoid groove Which structures attach to the fibular sesamoid? Lateral head of the FHB Lateral metatarso-sesamoidal ligament Lateral phalangeo-sesamoidal ligament Deep transverse metatarsal ligament Lateral conjoined tendon of the adductor hallucis Intersesamoidal ligament If you are planning to do a bunion procedure on a person with an already short 1st metatarsal, name as many procedures as you can that would take this into account and not shorten the metatarsal more. Bi-correctional Austin Scarf Z Juvara B2 and C2 Loison-Balacescu

Logriscino Trethowan Opening wedge of the met or the cuneiform

Describe the anatomy of the MPJ complex What are some common capsule tendon balance procedures? Silver (Silver, David: The operative treatment of hallux valgus. JBJS 5:225, 1923) 1. curved medial incision 2. removal of bursal sac 3. resection of dorsomedial eminence 4. lateral capsulotomy with medial capsulorraphy designed to reinforce the medial collateral ligament and transpose dorsally the abductor hallucis tendon 5. lateral release McBride (McBride, Earl: A conservative operations for bunions. JBJS 10:735, 1928) 1. 5 cm incision from the toe web along the lateral border of EHL 2. resection of the dorsomedial eminence 3. lateral release consisting of lateral capsulotomy with fibular sesamoid excision 4. transfer of the adductor hallucis and lateral head of FHB to the dorsolateral aspect of the 1st met head
Adductor tendon transfer 1. dorsally through the capsule to reposition the sesamoids 2. into the 1st metatarsal neck to reduce the IM angle
transfer into the neck can be either dorsal to plantar or lateral to medial Hiss (Hiss, J: Hallux valgus, its cause and simplifies treatment, Am J Surg 11:51, 1931) 1. Resection of the dorsomedial eminence 2. lateral capsulotomy 3. transfer of abductor hallucis from plantar to medial to the 1st MPJ (abductor sutured into hole in the base of the proximal phalanx; acts as a ligament to strengthen the capsule medially) Name three neck procedures. Peabody, Hohmann, Mitchell Name five base procedures. Loison – Balasecu Juvara Crescentic Trethowan Logriscino Starting at the rearfoot, explain in as much detail as possible Root’s theory on the formation of a bunion. Include all of the stages. (Root et al. Forefoot deformity caused by abnormal subtalar joint pronation. In Normal and Abnormal function of the foot. Clinical Biomechanics. Volume 2. Los Angeles. 1977 pg 349 – 462) List four broad categories of problems that can lead to HAV. NM conditions, arthritidies, trauma, biomechanical problems

What are the biomechanical relationships that can lead to hallux valgus? Compensated forefoot and rearfoot varus Pes valgus deformity Hypermobile 1st ray Excessive pronation resulting from ankle joint equinus Torsional deformity or rotational abnormalities of the LE Any condition that leads to abnormal subtalar joint pronation According to proper AO principles, explain the two screw placement for a CBWO of the 1st metatarsal. Proximal screw – anchor screw that is placed perpendicular to the metatarsal Distal screw – compression screw, placed perpendicular to the shaft of the metatarsal Why was the Herbert screw originally developed? Scaphoid fractures of the wrist How would you fixate an Austin bunionetomy? Original procedure fixation was not used and metatarsal head was allowed to ‘seek its own level’ Can use 1 screw, 2 screws, 2 K-wires, 1 screw and 1 K-wire, etc. Name complications of HAV surgery. 1. Hallux varus 2. Tibial sesamoid dislocation 3. Capsular defect 4. Staking the head – excessive bone removal on the medial 1st MT head, losing the plantar tibial sesamoid groove 5. Capital fragment on the floor (Christenson C: Intra operative contamination of the bone and cartilage during an Austin bunionectomy 31:285, 1992) 6. Severing the EHL or the FHL 7. Infection 8. Breaking the hinge 9. Intra-articular osteotomy 10. Recurrence 11. Delayed or non-union of the osteotomy site 12. 1st met shortening 13. 1st met elevatus 14. AVN 15. Nerve entrapment 16. Sesamoiditis 17. Hallux limitus 18. Fixation failure

Hallux Limitus and Rigidus Definition of Hallux Limitus: The proximal phalangeal base is plantarly subluxed upon the first metatarsal head. The hallux has limited dorsiflexion motion at the first MPJ during propulsion. There is a decrease in 1st MPJ ROM to < 20 degrees. Definition of Hallux Rigidus: Ankylosis of the first MPJ secondary to repetitive trauma during dorsiflexion. < 10 degrees of dorsiflexion Definition of Functional Hallux Limitus: Functional hallux limitus exists when the first MPJ DF ROM is reduced when the forefoot loads. Stage 1. Definition of Structural Hallux Limitus: Structural hallux limitus exists when first MPJ ROM is reduced with the forefoot loaded and unloaded. Etiology: Long first met or proximal phalanx Short first met MPE Trauma with DJD Hypermobile 1st ray Immobile 1st ray Neurogenic inflammation

Neuromuscular disease Gout Osteomyelitis/septic arthritis Charcot neuroarthropathy Neoplasms Septic arthritis Foreign bodies (implants)

Iatrogenic (i.e. Minimal invasive surgery, AVN, Joint immobilization, Poor dissection technique, Inadvertent metatarsal lengthening, failure to correct DF 1st ray previously, over aggressive capsulorraphy, osteotomy displacement, etc) Systemic arthridities (RA, PA, Gouty arthritis) Classification of Hallux limitus/rigidus Primary v Secondary 1. Primary a. Occurs in adolescent patients and is associated with a long first metatarsal b. Congenitally long first metatarsal 2. Secondary a. Occurs in older patients b. Usually caused by DJD, trauma, septic arthritis and systemic arthridities Structural v Functional 1. Structural a. DF of the hallux is decreased when the forefoot is loaded and unloaded 2. Functional a. DF of the hallux is decreased when the forefoot is loaded only

Pathobiomechanics - restricted first ray plantarflexion - first MPJ sagittal plane subluxation - bony adaptation - first MPJ DJD Clinical Findings – Symptoms 1. gradual onset of pain and limitation of 1st MPJ ROM 2. Pain localized to the dorsal aspect of the 1st MPJ 3. Pain with prolonged weightbearing or ambulation 4. Pain with shoe gear 5. Painful plantar IPJ callous 6. Lateral foot pain 7. Subungual hematoma Clinical Findings – Physical Exam 1. Dorsal or dorsomedial bump 2. Hallux is rectus 3. Tenderness with passive DF of hallux 4. Pain and crepitus first MPJ 5. Decreased painful ROM 6. Excessive IPJ dorsiflexion a. Associated with EHL spasm b. Ganglion cyst or adventious bursa associated with EHL tendon secondary to irritation from shoe gear c. Plantaremedial IPJ hyperkeratotic lesion 7. Check sesamoid mobility a. Load the 1st ray and palpate the sesamoids while mobilizing the first MPJ b. Arthrosed or fibrosed sesamoids prevent normal mobility and MPJ dorsiflexion 8. Antalgic, apropulsive gait with an early heel off

Radiographic findings 1. Non uniform joint space narrowing 1. Flattening of the first metatarsal head 2. Osteophytes on the met head and the proximal phalanx (i.e. dorsal flag or sailboat sign) 3. Subchondral sclerosis (eburnation) 4. Loose bodies within the joint space (joint mice) 5. MPE on the lateral view a. Proximal phalanx articulates with the plantar aspect of the 1st metatarsal head b. Bisection of the first met is superior to the talar bisection (Meary’s angle) 6. Positive 1st met protrusion distance

Stages and Classifications 1. Drago, Oloff and Jacobs a. Functional limitus b. Joint adaptation c. Joint deteriortation d. Ankylosis

2. Regnauld a. Development b. Established arthrosis c. Ankylosis

Non-Surgical Management  determine whether the deformity is functional or structural hallux limitus.  Functional responds better to orthotic control.  Shoe modifications o Rocker bottom o Metatarsal bar  NSAIDs  Orthoses o First ray cutout o Heel life o Kinetic wedge device  Periarticular v intra-articular steroid  ROM exercises  Manipulation and stretching  Physical Therapy Goals of Surgical Treatment 1. restore pain free ROM 2. re-establish joint space 3. remove osteophytic spurring and loose bodies 4. reduce osseous deformities like MPE or a long first metatarsal 5. attempt joint preservation o Must have 50% of the cartilage to do a joint preservation procedure 6. creation of slack in the flexor apparatus

Indications for joint preservation procedures 1. Need to reduce osseous deformities 2. Need to remove loose bodies 3. Being able to have enough viable cartilage to salvage the articulation (at least 50%)

Joint Preservation Procedures - Curettage and Drilling o .028 or .035 k-wires o Multiple drill holes to get to subchondral bone o Adjunctive procedure; not curative o Goal: promote the growth of fibrocartilage o Keep NWB for but do ROM - Cheilectomy o Remove dorsal bone spur on met head or phalangeal base o Adjunctive procedure not curative o Doesn’t give you more joint space or fix the osseous deformities - Bonney & Kessel o Use for a long proximal phalanx o Indicate for a plantar flexed hallux o Take a dorsal wedge of bone at proximal phalanx
close it o Does not address the MPE or redirect the cartilage on the 1st met head - Waterman o Metatarsal procedure o Take a dorsal wedge from the head of the met leaving the plantar hinge intact o Rotate the met head up
redirecting the cartilage o Does not address the MPE - Waterman – Hohmann o o o o o

-

Watermann – Green o o o o o

-

Do the Watermann procedure but break the plantar hinge Plantar flex the head of the metatarsal and fixate Shortens and decompresses the joint Re-direct the cartilage Addresses mild to moderate elevatus Similar to the bicorrectional Austin Dorsal cut: trapezoidal wedge that is wider medially Plantar cut: oblique, transverse osteotomy Angle = 45 degrees Shortens and plantarflexes the 1st met head

Regnauld o o

o o o

Enclavement procedure Base of the proximal phalanx is fashioned into a peg and then reinserted into the proximal phalanx (looks like a Mexican hat) Decompress the joint Good for long prox phalanx or short 1st met Shortens the proximal phalanx

-

-

-

-

Youngwick modification of the Austin bunionectomy o Use an Austin bunionectomy o Use parallel dorsal cuts & remove rectangle Sokoloff dorsal V o Create a V shaped osteotomy driving the drill from dorsal to plantar o Performed at the metatarsal neck o Good for MPE o Plantarflexes the first met head o Doesn’t decompress the joint or shorten the metatarsal Sagittal Logriscino o Waterman o Lamburnudi Lambrinudi o Proximal procedure o Take a wedge (either transverse or oblique cut) from the base of the 1st met o Gets rid of HUGE elevatus o Leave the dorsal cortex intact o Doesn’t redirect the cartilage

Joint Destructive Procedures - Keller o Resect 1/3rd of the base of the proximal phalanx o Problem: toe purchase o Good for old people or DM with ulceration under the base of the proximal phalanx; those who aren’t very active - Valenti o Take a V out o One cut in the metatarsal head that is directed proximal dorsal to distal plantar. This leaves the plantar one third of the cartilage intact. o One in the proximal phalanx base that is directed proximal plantar to dorsal distal o Immediate post-op complications: sesamoiditis o Doesn’t correct elevatus or reposition cartilage - Stone o Dorsal to plantar wedge resection of 1/4th of the metatarsal head - Mayo o Excision of 5 mm of the 1st metatarsal head including the articular surface - McKeever (MPJ funsion) o Remove remaining cartilage and fixate o Stress moves to the IPJ o Optimal positioning:  15-25 degrees DF; 10-15 degrees Abducted; no frontal plane deviation

-

Lapidus o See bunion procedures - Arthrosurface o Similar to a one sided joint implant o Looks like a giagantic thumb tak has been inserted into the first met head - Implant o Interpositional  Joint spacers  Good to use with keller procedures • Swanson flexible hinge • Sutter-Lawrence design • Sutter-LaPorte design • Hemi design o Total joint replacement  Implant properties: • Inert • Non-biodegradable • Durable • Non-irritating  Fabricated from: • Stainless steel • Silicone rubber • Cobalt chromium alloy • UHMW polyethelene  Semiconstrained • Only sagittal plane motion  Nonconstrained • Motion in more than one plane • Fabricated from: o Cobalt chromium o Titanium alloy o UHMW polyethylene Implant complications: - biomechanical failure - implant failure - soft tissue - bone failure - alignment failure ROM exercises are of the utmost importance and are the most important part of the post op course for HL/HR.

Ankle Fractures Oblique fracture: produced with combined loading of compression and torque. Usually a 45 degree fracture orientation. This is considered to be unstable and is usually fixed with ORIF Spiral fracture: this is always a type of torque fracture. It usually takes a 360 degree course with a vertical connecting segment between the two opposing sharp spikes of the fracture. This is also usually orientated at 45 degrees Comminuted fracture: this suggests the presence of two or more fracture planes and has at least three fragments. This is usually due to very high velocity loading, it is a high energy failure with load concentration over a small area of the bone. Eponyms for Fractures Percival Pott (1768): Described a fibular fracture 2 – 3 inches proximal to distal aspect fibula with a deltoid ligament fracture and an intact syndesmosis. Now: bimalleolar fracture Dupuytren (1819): Described a medial deltoid ligament tear or a medial malleolar fracture with a fibular fracture 2.5 inches proximal to most distal aspect of the fibula with diastasis always being present. Maisonneuve (1840): The New House fracture. Fracture of the proximal 1/3rd of the fibula. LeFort (1886): Described a vertical fracture of the fibula due to SAD type forces. Chaput – Tillaux (1872): In 1872 Tillaux described a medial deltoid injury or medial malleolar fracture, a fibular fracture 2 inches proximal to the ankle joint, AND an anterior lateral tibial tubercle fracture. In 1907, Chaput conducted laboratory studies of this fracture which is why the fracture of the anterior lateral tibial tubercle contains both names. Wagstaffe (1873): Distal fibular fracture due to avulsion of the anterior inferior tibialfibular ligament. An SER type injury. VonVolkman (1875): Originally described as an anterior lateral lip of the fibula fracture due to avulsion of the anterior tibial-fibular ligament and interosseous membrane due to PAB type forces. Now: posterior lateral tibial fracture Cotton (1915): Described a posterior malleolar fracture with a medial malleolar fracture and a fibular fracture just proximal to the joint level. Trimalleolar fracture.

Correlating Danis-Weber and Lauge-Hansen Danis—Weber

Lauge—Hansen Category SAD

Where to start the LH Clock Start lateral

SER

Start anterior and central

PAB

Start medial

PER

Start medial

A – fracture of fibula distal to the level of the ankle joint

B – fracture of the fibula originating at the level of the ankle joint

ALWAYS ask for a lateral film!!!!!

C – Fibular fracture originating proximal to the ankle joint mortise

Lauge—Hansen Type 1 – lateral ankle ligament injury – or – transverse fibular fracture distal to the level of the ankle joint 2 – near vertical fracture of the medial malleolus 1 – rupture of the anterior inferior tibial-fibular ligament 2 – fibular fracture with posterior spike 3 – rupture of the posterior tibial – fibular ligament 4 – fracture of the medial malleolus 1 – deltoid ligament rupture or medial malleolar fracture 2 – anterior tib-fib ligament rupture with posterior tibial fracture 3 – Danis Weber B fracture 1 – medial malleolar fracture or a deltoid ligament rupture 2 – anterior inferior tib-fib ligament rupture 3 – high fibular fracture 4 – posterior tib-fib ligament rupture or posterior malleolar fracture

Ankle Fracture Questions 1. What are the radiographic hallmark of each Lauge Hansen Injury? PER – high fibular fracture SER – spiral oblique fracture of the distal fibula PAB – short oblique fracture of the distal fibula SAD – short oblique fracture (near vertical) of the medial malleolus

2. What is the big difference between a SER type fracture and a PAB type fracture? SER has a posterior fibular spike while a PAB has a posterior tibial fracture 3. What fragment do you reduce first during ORIF of an ankle fracture? The fibular fracture 4. What do the two words of the Lague-Hansen classification system signify? The first word is the position of the foot at the time of injury. The second word is the direction of the deforming force or the direction the talus moves in the mortise. 5.What is the Danis-Weber classification system based on? The anatomic position of the fibular fracture in relationship to the tib-fib syndesmosis 6. You are called to see a patient in the ER. The ER nurse tells you in a stressed out near hysterical voice that this patient has a transverse fracture of the fibula and a near vertical fracture of the medial malleolus. What type of fracture is she describing? SER 2 or Danis Weber A 7. At what stage of the SER injury, would you see a Wagstaffe fracture? SER 1 8.When does a posterior malleolar fracture need to be fixated? If the fracture involves 25 – 30% of the articular surface 9. Apply Vassal’s principle as it applies to the ankle joint. When you reduce and fixate the fibular fracture to the appropriate length, the talus should fall back into the mortise. This doesn’t always work perfectly for the medial malleolus. 10. Who wrote the original article relating the displacement of the talus in the mortise and the affect of this displacement on the ankle joint congruity? What did this article conclude? Ramsey and Hamilton. JBJS. 1976. This article concluded that 1 mm of lateral displacement of the talus leads to a 42% reduction in contact area of the ankle joint. Meaning: reduce your freaking fibular fracture.However, when doing their cadaveric experiments, they removed all soft tissue from around the ankle joint and did not allow the talus to compensate for being displaced. More recent studies have indicated that the talus tends to move back into the mortise when compressed if allowed to do so.

11. What are the radiographic criteria for adequate reduction of displaced ankle fractures? - no widening of the medial clear space (<4mm) and symmetric joint space on mortise view - no displacement of malleoli on AP views - less than 2 mm of posterior displacement of lateral malleolus on lateral films - no angulations - fracture of less than 25 – 30% of the posterior malleolus 12. The key points for fixation are… - fibular fracture is the most important - restoration of fibular length takes precedent over repair of the inferior tibial-fibular syndesmosis - realign the ankle mortise - evaluation the talar done and tibial plafond - reapproximation of soft tissue supporting structures 13. Put the following in order according to priority - blood flow - reduction of marked dislocation or deformity - care of open wounds or other soft tissue injuries - precise anatomic reduction of bony structures - repair of damaged tendons and nerves - rehabilitation - prompt identification and treatment of any complications that may develop 14. What is the Cotton test and what does it tell you? - a way to evaluate the syndesmosis for rupture or injury - after fibular fixation, use a large bone hook to try to laterally distract the fibula from the tibia while observing the relationship of the two bones - if > 3 – 4 mm of lateral sift of the talus occurs, significant instability is present and a syndesmotic screw is recommended 15. When should you use a syndesmotic screw? - when there is a high fibular fracture or a positive Cotton test - more recent studies, however, suggest that if you have a fibular fracture 5.0 cm from the ankle joint and distal do not need to be fixated with a syndesmotic screw (Kennedy et al. J Orthop Trauma 14(5), 2000) 16. How do you insert a syndesmotic screw? - from the lateral fibula angulate the screw about 25% anteriorly and penetrate three cortices with the foot at 90 degrees to the leg. - Olerud (Arch Ortho Trauma Surg 104:299, 1985) demonstrated a 0.1 degree loss of dorsiflexion for every degree of plantarflexion that the ankle was in at the time of fixation of the syndesmosis 17. When is a syndesmotic screw removed? - No one agrees on this - Usually at 6 – 8 weeks post op or immediately before weight bearing - It can be left in for longer (12 – 14 weeks) for increased stability in syndesmotic ruptures - Or you can use a tightrope for syndesmosis fixation and you wouldn’t have to remove that at all 18. Which two classes of Lauge Hansen fractures will most commonly produce posterior malleolar fractures? SER and PER

19. What is the best way to assess for a posterior malleolar fracture? CT or a lateral film (x-ray) 20. When should a posterior malleolar fracture be fixated? > 25 – 30% of the joint surface is involved when ORIF is indicated 21. What are the names of two approaches to fixate a posterior malleolar fracture? - Anterior approach through the same incision used to fix the medial mall fractures - Posterolateral approach of Henry (1945). Incision between the peroneal and Achilles tendons; avoids damage to the sural nerve and avoids the NV bundle medially. The FHL muscle is used as a guide to the fragment 22. What is the posterior malleolus? A tubercle at the posterior border of the fibular notch on the lateral surface of the distal tibia 23. What is a triplane fracture and why does it occur? - Pediatric fracture that appears as a SH2 on the lateral (with the Thurston Holland sign) and a SH3 on the AP - Occurs in kids around 14 yrs of age where the medial aspect of the growth plate is closed and the lateral side remains open - Vertical fx of the epiphysis from the joint space to the physis that is orientated in the sagittal plane - This fracture changes directions when it reaches the physis and orientates itself in the transverse plane - It then changes direction again and continues into the metaphysic in the coronal plane and exits the bone posteriorly. 24. What should you do with a pediatric fracture? Order a CT to r/o a triplane fracture and to determine growth plate involvement 25. With which Saltar-Harris fracture pattern in a Juvenile Tillaux fracture associated? SH 3 26. How does a Danis-Weber B fracture displace? Posterior and superior 27. What is an antiglide plate? - This plate was developed because of the difficulty encountered with accurately reducing and securing the Danis-Weber B fibular fractures by traditional methods - This plate is put on the posterior side of the fibula - A 5 hole 1/3rd tubular plate is used with three holes above and two holes below the fracture - An interfragmentary screw can be used through one of the holes 28. Name some disadvantages of using a lateral fibular plate. - Frequent plate and screw irritation due to the superficial nature of this bone - Closure problems? Also due to superifical nature of the bone - Hard to fit the shape of the fibula due to the torque required - Possibility for penetration of the distal screws into the talofibular and tibiofibular articulations

29. What are the four principles of pilon fracture reduction? - reconstruction of the fibular fracture - reconstruction of the tibial articular surface - cancellous graft to fill the distal tibial metaphyseal defect - buttress plate application to the medial or anterior aspect of the tibia 30. Classifications for Pilon fractures a. Ruedi and Allgower Type I: Mild displacement and no comminution without major disruption of the ankle joint Type II: Moderate displacement and no comminution with significant dislocation of the ankle joint Type III: “Explosion fracture”; severe comminution and displacement of the distal tibial metaphysis; significant displacement and loss of cancellous bone b. Lauge Hansen, PDF Stage I – medial malleolar fracture Stage II – fracture of the anterior lip of the tibial plafond Stage III – fibular fx above the level of the syndesmosis Stage IV – transverse fracture of the distal part of the tibia at the same level as the proximal margin of the large tibial fracture c. Mueller (AO system) Type A – Extra articular Type B – Partially articular Type C – Completely articular All of the above can include: A: no comminution or impaction in the articular or metaphyseal surface B: impaction involving the supra-articular metaphysis C: comminution and impaction involving the articular surface with metaphyseal impaction 31. A pt presents to the ER and you are the resident on call. X-rays show a short oblique fracture of the fibula at the level of the syndesmosis. What else do you want to know about the x-rays and what do you tell your attending on the phone? X-rays: Fibular displacement Relationship of the talus to the tibia Medial clear space Posterior malleolus and syndesmosis involvement Tell your attending that you have bi mallelous fracture that needs ORIF

32. Radiographic evaluation of ankle fractures should include: - medial clear space < 4 mm on the mortise views with relatively symmetric joint space - talocrural angle 83 + 4 degrees - or – within 2 degrees of the contralateral side - talar tilt angle - Shenton’s line The continuous curve between the lateral talus and the recessed tip of the distal fibula - Syndesmotic width Less than 5 mm on the AP view

33. You have a 70 y.o. active female patient who sustains a Danis-Weber B type fracture that needs ORIF. Pt has a smoking history. What are you worried about? Quality of her bone – will it hold fixation? Healing potential 34. During her surgery, you attempt to apply a lateral plate and screws to fixate the fracture. After several attempts, it is deemed that the fixation will not help in her soft bone. What do you do? Insert an IM rod (Rush rod) from anterolateral at the distal end of the fibula and proceed proximally IM fixation is great in elderly patients; they can weight bear soon with this type of fixation. Pritchett (Ortho Review June 1993) showed 88% of pts treated with Rush rods had a good or fair functional result compared with 76% treated with the AO Method. FWB was possible 6 weeks earlier with Rush rods than with plates and screws. Study was done on pts over 65 y/o. 35. Muller classification of medial malleolar ankle fractures. Type A: avulsion of the tip Type B: avulsion at the level of the ankle joint Type C: oblique fracture Type D: vertical fracture 36. What are three ways to fixate the medial malleolus? a. single or double screw fixation b. K-wires c. Tension band wiring technique Johnson and Fallat JFAS, 1997, showed that cancellous screws (two) exhibited only 47.16% of the strength of tension band wiring at clinical failure. 37. What are some complications of ankle fractures? Delayed or non union NV injury Post traumatic arthritis Infection (particularly if open fracture) RSD 38. Using Lauge Hansen what is the most common ankle injury? SAD 39. Using Lauge Hansen, what is the most common ankle fracture? SER Pilon Fractures (As presented by Roy Sanders, MD, 9/21/2000 at Loyola University) Treatment: 1. Plate the fibula 2. External fixation; wait 10 – 21 days (edema resolution) 3. Fixate the tibia a. Metaphyseal plate (M-plate; Sanders & Bone) b. Spider plate c. Spring plate; spoon plate (6.5 cancellous screws) d. 1/3 tubular plate hammered flat Anatomic reduction: a congruous joint is the goal; the only way to achieve a congruous joint is to ORIF the injury Recommended text: Planning and Reduction Techniques in Traumatic Fractures

Calcaneal Fractures How often do intra-articular fractures occur? Approximately 75% are intra-articular What three factors determine the pattern of communition and location of the fracture lines? 1. position of the foot at impact 2. force at impact 3. bone quality Describe the Rowe classification. Ia: plantar tuberosity fracture Ib: sustentaculum tali fracture Ic: anterior process fracture IIa: fracture of the posterior aspect of the calcaneus not involving the Achilles tendon; ‘beak fracture’ IIb: avulsion fracture of the posterior aspect of the calcaneus III: fracture of the body without STJ involvement IV: fracture of the body with STJ involvement V: comminution of the body of the calcaneus Describe the Essex-Lopresti classification? - intra-articular fracture classification only - Tongue type fracture: primary fracture line runs superior to inferior and secondary fracture line exits from the posterior aspect of the calcaneus - Joint depression: primary fracture line runs superior to inferior with a second fracture line surrounding the STJ (posterior facet) On which imaging modality is the Sanders classification based and what slice is used? - CT imaging - Based on the widest section of the sustentaculum tali in 3 mm coronal slices Describe Sanders classification. - I: all non displaced articular fractures irrespective of the fracture lines - II: two part fracture of the posterior facet - III: three part fracture of the posterior facet with central joint depression - IV: four part articular fracture; often more pieces and highly comminuted How many stages are in the Sander’s classification (including subtypes)? Eight (I, IIA, IIB, IIC, IIIAB, IIIAC, IIIAB, IIIAC, IV) In the Sander’s line classification, is line A medial or lateral? Lateral The ecchymosis seen in calcaneal fractures is known as what? Mondour’s sign; this usually occurs plantarly but can also occur distal to both malleoli

Where are fracture blisters most commonly located in calcaneal fractures? The medial side because during the fracture there is predominantly shearing and stretching of the soft tissues on the medial side of the foot. What two important angles are associated with calcaneal fractures? 1. Bohler’s angle: normally 20 – 40 degrees; decreases with depression of the posterior STJ 2. Gissane’s angle: normally 120 – 140 degrees; will increase with the depression of the joint What plain film views would you order and what would you see on each? 1. Lateral foot: see joint depression; evaluate the two angles in the question above; check for loss of height of the posterior STJ 2. AP foot: to evaluate all other foot bones for additional fractures/pathology 3. Harris-Beath and/or Broden view: to evaluate the posterior facet of the STJ 4. Lateral oblique: anterior process of the calcaneus to check for CC joint involvement What is a Broden’s view and how is it taken? (Broden projection I) - a way to evaluate the posterior STJ on plain films - pt is supine with cassette under the foot; leg is internally rotated 30 – 40 degrees - x-ray beam is centered over the malleoli and four consecutive projections are made with the tube angled at 40, 30, 20 and 10 degrees toward the head of the patient What are the fragments usually seen in calcaneal fractures? 1. * Superomedial fragment (Constant or sustentacular fragment) 2. * Posterior facet fragment (superolateral, semilunar or comet fragment) 3. * Tuberosity fragment (main fragment) 4. Anterior process fragment 5. Anterior STJ fragment * The three important fragments that must be reduced What are the goals of ORIF with calcaneal fractures? 1. Restoration of length, width and height of the calcaneus 2. Anatomic reduction of all involved joint surfaces 3. Restitution of function by stable osteosynthesis without joint transfixition In July 2000 in the Journal of Orthopedic Trauma there was a report of using injectable bone cement for augmentation of ORIF of calcaneal fractures. The authors report using an injectable cement in the area of the neutral triangle under the posterior facet. This will allow for good resistance from compression that ORIF alone can’t give. At the end of their study, they were having patients fully weight bear at 3 weeks post op. This is about 10 weeks earlier than some authors report. This could potentially be a great tool for augmentation or internal fixation in these fractures. What are the four ways to treat calcaneal fractures? 1. non-operative 2. ORIF 3. Ex-fix 4. Primary STJ arthrodesis What else should be evaluated when dealing with calcaneal fractures? 1. proximal injuries (lower back, spine, neck and head) 2. bladder rupture

Which vertebrae are most commonly injured? 1. L1, L2 2. Wong (1966) found that 11% of males with calcaneal fractures also had vertebral compression fractures What is the ‘wrinkle test’? - A way to evaluate if the soft tissue swelling has reduced enough for surgical intervention - Dorsiflex and evert the foot and the skin on the lateral side of the foot will wrinkle What are the locations for the incisions of ORIF and the advantages of each? 1. Lateral extensile, Modified Ollier a. Easy visualization of posterior facet and calcaneocuboid joint b. Avoids neurovascular bundle 2. Medial a. Initially popularized by McReynolds b. Easy reduction of the sustentacular fragment 3. Seligson’s lateral extensile a. Described by Giouild (F&A, 1984) Some authors use both approaches so each fragment can be adequately visualized Many authors also use the lateral approach for which there are many variations. When should primary arthrodesis be done? In a highly comminuted intra articular fracture (i.e. Sander’s type IV) Name ten complications of treatment of calcaneal fractures. 1. Nerve damage 2. Post traumatic arthritis 3. RSD 4. Compartment syndrome 5. Nerve entrapment 6. Wound dehissance (with or without calcaneal osteomyelitis) 7. Malposition after fixation 8. Calcaneal malunion a. Classified by Stephens and Sanders b. Type I: large lateral exostosis with or without extremely lateral arthrosis of the STJ c. Type II: a lateral exostosis combined with major arthrosis across the width of the STJ d. Type III: a lateral exostosis, severe arthrosis of the STJ and malunion of the calcaneal body with the hindfoot in varus or valgus angulation 9. Peroneal tendonitis/subluxation 10. Heel pad pain a. Damage to the fatty plantar heel pad What is the most frequent post-op complication with ORIF of calcaneal fractures? Wound dehissance (cited numerous places in the literature) Note: There seems to be a large discrepancy in outcomes following treatment of intra-articular calcaneal fractures. This is seen between those injuries suffered while at work and those that are not. Since this injury frequently occurs in the working population, it is difficult not to include these subjects in studies. Recently, there have been reports alluding to this idea so hopefully in the future we will see studies on injuries that are not sustained at work.

Flexible Flatfoot Procedures Transverse plane dominant deformities: - Evans (bone insertion, lateral calcaneus) - CCJ distraction arthrodesis (similar to Evans but you fuse the CC joint) - Kidner (resection of the hypertrophic navicular and accessory bones and reattachment of the posterior tibial tendon to the navicular) Sagittal plane dominant deformities - Lowman (TNJ) - Hoke (NCJ) - Miller (NCJ, 1st MCJ) - Cotton (open PF wedge of the 1st cuneiform) - Lapidus (1st MCJ) - Young (Tib ant in keyhole of the navicular) - Cobb (hemisection of the tib ant to the PTT) - TAL Frontal plane deformities - Orthotics - Chambers (opening wedge inferior to posterior facet) - Baker (osteotomy inferior to STJ with graft) - Selakovich (opening wedge osteotomy of STJ) - Arthroeresis (MBA, Sta-peg, CSI) - Coleich (posterior oblique through and through osteotomy) - Lord (displaces the calcaneus anterior, inferior and medial) - Silver (lateral opening wedge) - Dwyer (medial closing wedge) - Koutsogiannis (posterior transpositional) Rigid Flatfoot 3. Tarsal coalition (see next page) 4. Congential Vertical Talus (treat with serial casting)

Pedal Coalitions Terminology Coalition – the union of things separate into single body or group True coalition – intra-articular fusion of two bones Bar or Bridge – extra articular fusion of two bones Etiology 1) Accessory Ossicles - Os Sustantaculi Proprium o Can be incorporated into the middle facet - Os Trigonum o Can be incorporated into the posterior facet 2) Failure Of Segmentation Of Primitive Mesenchyme - Autosomal Trait - Variable Penetrance Congenital vs. Acquired CONGENITAL - Mesenchymal Differentiation. ACQUIRED - Trauma - DJD can cause erosion of articular surface - Inflammatory rheumatoid conditions - Fractures - Fusion of accessory bones Classification by Development Complete Coalition - two bones joined by osseous union that limits all motion. Incomplete Coalition - two osseous projections united by intervening fibrous or cartilaginous tissue. Rudimentary Coalition - osseous projections from one or more involved bones which limits motion, without any tissue union between those segments. Histological Classification - SYNCHONDROSIS - Cartilaginous - SYNOSTOSIS - Osseous - SYNDESMOSIS – Fibrous Anatomical - Defined by osseous segments involved; best way to assess coalitions. Forefoot Coalitions • Interphalangeal • Intermetatarsal • Metatarsal – cuneiform • Navicular – cuneiform Midtarsal / Tarsal Coalitions • Calcaneo-navicular – common • Talonavicular – more common • Calcaneo-cuboid – relatively common

Subtalar Coalitions - Anterior facet - Middle facet - Posterior facet - Posterior process - Sustentaculum tali Navicular – cuboid - underreported Cuneiform – cuboid – fairly rare Talo – cuboid – very rare

Incidence • Males > Females • May be b/c males have traditionally been more active than women • Race: Equal • Bilateral in 50% of patients • Overall < 1% of total population *Jahss and Tachdjian • Fusion of middle/distal phalanx 5th digit most common pedal coalition (Approximately 50% of general population) • Tarsal coalition - talo-calcaneal - calcaneal navicular - talonavicular • 1-2% of the general population Ossification of Coalition • Talonavicular 3-5 years old • Calcaneal navicular 8- 12 years old • Talocalcaneal 12-16 years old - Age of ossification of coalition corresponds to the onset of symptoms Clinical Exam •Peroneal spasm – most common sign of involvement •Anterior/posterior tibial spasm •Pronation •Fixed rearfoot valgus •Very vague complaints of pain •Cavus deformity •Either cavus or planus feet Peroneal “Spastic Flatfoot” • Restricted Subtalar Motion • Rearfoot Valgus – occurs b/c they are trying to get the FF to the ground Differential Diagnosis •Rheumatoid arthritis •Trauma – needs to be R/O especially in kids •Acromegaly •Extra articular arthrodesis •Overcorrected clubfoot •Osteochondral defect •Infection •Neoplasm •Juvenile RA – very rare

•Pain •Local tenderness to palpation •Stiffness/decreased ROM

• • •

Forefoot Abduction “Taught Peroneal Tendons” Ext. Digitorum Brevis Spasm (severe cases

•CCPV •Peroneal muscle contracture • 2 TO Localized ISCHEMIA which can be caused by decreased padding in BK case •Neuromuscular disease

Coalition

Incidence

View

Associated Signs

Trivia/Other

Interphalangeal

Common

AP

May be synphalangism

Intermetatarsal

Not very common

AP Oblique

Diaphyseal fusions may be result of trauma

Metatarsal - cuneiform

AP Medial oblique (for medial column) Lateral oblique (for lateral column)

3rd metatarsal cuneiform coalition

Navicular – cuneiform

AP Oblique

Coalition may continue through the intercuneiform joints as well

Navicular – cuboid

Under reported

AP Lateral oblique

Calcaneocuboid

Relatively common

Lateral Lateral oblique

Can be bilateral in nature but can have unilateral symptoms

Talo-navicular

More common

AP Medial oblique

Putter Sign

On lateral, be sure to count your medial column bones

Calcaneonavicular

Common

Lateral oblique Lateral

Ant-eater Sign

Long snouted anterior process of calcaneus Ratty radiolucency and irregular sclerosis
fibrous union

S – shaped appearance of the calcaneus an navicular on lateral oblique

Anterior Facet

Lateral oblique Isherwood lateral oblique dorso-plantar

1. talar beaking 2. narrowing of the posterior TC joint space 3. rounding of the lateral talar process 4. middle STJ may not be visable 5. Halo effect

Middle Facet

Most common of the talocalcaneals

Harris and Beath

Posterior Facet

Harris and beath Broden medial oblique

Posterior Process Fusion

Lateral

1. talar beaking 2. narrowing of the posterior TC joint space 3. rounding of the lateral talar process 4. middle STJ may not be visable 5. Halo effect 6. Posterior and middle facets should be parallel 7. Middle facet is angulated in an inferior medial direction in a coalition 1. talar beaking 2. narrowing of the posterior TC joint space 3. rounding of the lateral talar process 4. middle STJ may not be visable 5. Halo effect

Flare Lack of differentiation of lateral process Os trigonum? (has a role)

Specialized Plain Film Studies • Harris & Beath: • identifies posterior/middle facets of STJ • Isherwood: • oblique lateral-anterior facet STJ • Broden: • medial oblique posterior STJ • Lateral oblique: • anterior facet • X-ray positioning: Podiatry Today, Sept. 1989 (Baron & Strugielski) Computed Tomography • Modality of choice for the assessment of coalitions • Planar analysis • Extent of coalition • Assess subtle cortical changes in surrounding osseous structures • Picture: bilateral coalitions • One side fibrous • One side bony Nuclear Imaging Technetium bones scans will assist in identification of “maturing coalitions” - see uptake on adjacent aspects of the involved bones - lack of uptake in region of “mature” coalition MR Imaging • Planar analysis • Identification of tissue matrix (may be better than a CT) • Loss of fluid signal intensity in area of coalition on T-2 weighted images

Associated Syndromes - Isolated fusions usually occur between bones of the same row (distal to proximal), those associated with other abnormalities occur across rows (medial to lateral). • Distal to proximal: isolated fusions • Medial to lateral: associated with other abnormalities - Cuneiform involvement points to possible associated syndrome. • Apert’s syndrome • Nievergelt-Pearlman syndrome

Apert’s Syndrome • Massive tarsal synostosis – • one big block of bones • Craniosynostosis – • born with normal mentation, • premature closure of the cranial bones
mental •

• • • • • •

deficiency. Midfacial hypoplasia – • mouse facies, • think mickey mouse
bones close early
decrease in size Broad distal phalanx of thumb and hallux Adaptive changes seen at the ankle joint Sagittal plane disorganization Same pt in the picture as in the radiographs Use palliative care Surgical intervention: less surgery = better

Nievergelt – Pearlman Syndrome • Synphalangism • Carpal fusion • Atypical clubfoot with massive tarsal fusions • Congenital dislocation of radial head • Conduction deafness • Three inner ear bones are fused
true conduction deafness • Ball and socket ankle joints • Gives the frontal plane motion at the ankle joint that the pt would have previously had at the STJ • Simple inversion may lead to dislocation • Lack normal flexor creases Treatment: - Immobilization - Supportive therapy - Orthotic therapy (pronated devices?) - NSAIDs - Surgical Intervention (resection v fusion)

Cavus Deformity Three guidelines should be followed: 1. All fixed deformities must be reduced 2. Proper muscle and tendon balance should be restored 3. Limit the likelihood of the recurrence of the deformity Bilateral Cavocarus Deformity: 1. Spinal cord tumor 2. CMT 3. Spina bifida 4. Diastematomyelia 5. CNS trauma 6. Poliomyelitis (uncommon) 7. Friedreich’s ataxia (uncommon) Unilateral Cavovarus Deformity: 1. spinal cord injury 2. poliomyelitis 3. deep posterior compartment syndrome 4. crush syndrome of the foot Classification Systems The classification systems for pes cavus are many, and often times confusing.   

 

Japas classified the deformity as: Anterior (local v. global), Anterior pes cavus is an increased plantarflexed attitude of the forefoot and is divided into four types, based upon the apex of the deformity. * Metatarsus cavus: at LisFranc’s LisFrancs palpable prominence * Lesser tarsus cavus: the entire lesser tarsal region Prominence in the lesser tarsal area * Forefoot cavus: at Chopart’s, with a distant prominence at the dorsal/lateral talar head * Combined anterior cavus: at 2 or more levels Posterior Combined

Ruch Classification Stage I: Deformity primarily restricted to the metatarsals, MPJ’s, or digits. Surgical management includes digital fusions, MPJ release, extensor tendon tenotomies, or flexor transfers. Stage II: Deformity primarily consists of a rigid PF first ray and RF varus. Surgical management included a DFWO, Dwyer, STATT, or Peroneal Stop. Stage III: A severe global RF and FF deformity of probable N/M etiology. Surgical management includes midtarsal osteotomies, triple arthrodesis, and tendon transfers.

 Other systems take into account combined sagittal / transverse plane or sagittal / frontal plane deformities, making the cavus foot even more perplexing.  Biggest question: IS IT NEUROMUSCULAR DZ?????

What are the goals of tendon transfers in patients with drop foot? 1. Pt should be able to clear the foot during gait 2. Muscle transferred should be in phase with paralytic muscle 3. Transferred tendon should be in line with the muscle and should not undergo angulation Bridle Procedure: done for anterolateral paralysis resulting in foot drop. The PL tendon and the TA tendon are anchored to the PTT which is transferred to the anterior side of the ankle. After injury to the common peroneal nerve, equinovarus develops because of the unopposed pull to the PT tendon: - Transfer of the PT tendon will restore DF to the foot and remove some of the deforming force of the tendon - Transfer is indicated to correct a foot drop with equinovarus deformity (transfer of the PT tendon through the interosseous membrane and insert it into the 3rd cuneiform) In paralysis of all lower leg muscles patients usually require some type of brace - It is possible to use the flaccid tendons to create a tenodesis for the foot and to minimize brace use (used for patients who want to be brace free) - Tenodesis of the extensor tendons and anchor them to the tibia; this will keep them in 10 degrees of dorsiflexion Paralysis of the tibial nerve usually results in a calcaneus deformity when the anterior leg muscles are preserved. - Over time with paralysis of the Achilles tendon and functioning dorsiflexors, the calcaneus will assume a vertical position as the intrinsic muscles of the foot continue to contract leading to a cavus deformity - There will be a marked increase in the pitch of the calcaneus, thickening of the plantar heel pad, dorsiflexion of the midfoot and slight flexion of the forefoot as a result of contraction of the plantar fascia. - Tendon transfer is difficult because no tendon has the strength to oppose the calf musculature - Arthrodesis (triple, tibiotalocalcaneal or pantalar) is usually performed

Surgical Options – Soft Tissue Procedures 1. Plantar fascia release a. Usually done with other bony procedures b. Steindler striping c. May need to release the long plantar ligament 2. Jones Tenosuspension a. Used for cock-up deformity of the hallux b. Usually seen in TA weakness c. EHL tendon is rerouted through a drill hole in the head of the 1st met d. IPJ fusion of the hallux is also done e. This procedure will DF the 1st met 3. Extensor shift procedure a. This is a modification of the Heyman procedure b. Done with Jones procedure c. EDL tendons are transected distally and tendons 1 & 2 are re-routed through a transverse drill hole in the shaft of the 3rd met; tendons 3 & 4 are re-routed through a transverse drill hole in the shaft of the 5th met 4. Hibbs tenosuspension a. Transfer of the EDL through a drill hole in the 3rd cuneiform

5. Girdlestone-Taylor transfer a. Transfer of the FDL tendons to the dorsal aspect of the digits b. Done for treatment of claw toes c. Usually done in conjunction with an arthroplasty 6. Heyman Procedure a. Transfer of all five long extensors to the respective metatarsal heads 7. Split Tibialis Anterior Tendon Transfer (STATT) a. Indicated for flexible cavus deformity b. The lateral half of the TA tendon is sectioned and anastamosed to the peroneus tertius near its insertion

8. Peroneal Anastamosis a. Transfer of PL to PB b. May be done in CMT when the PB function is diminished but the PL function is normal 9. Peroneus longus tendon transfer a. PL tendon is sectioned near the cuboid and the tendon is then re-routed down the EDL tendon sheath and inserted into the lesser tarsal area b. If split, the medial half is anastamosed to the TA tendon and lateral half is anastamosed to the peroneus tertius tendon near their insertions

10. Tibialis posterior tendon transfer a. TP tendon is sectioned at its insertion into the navicular b. The tendon is threaded through the interosseous membrane and down the EDL tendon sheath c. The tendon is then inserted into the lesser tarsal area

11. PL and TP tendon transfer to the calcaneus a. Both tendons are resected (PL near the cuboid and TP near insertion into navicular) and rerouted to reinforce the Achilled tendon or be inserted into a hole in the calcaneus b. Indicated for a weak Achilles tendon

Osseous Procedures 1. Metatarsal osteotomies a. Dorsally based wedge in the proximal metatarsal b. Usually just done to the 1st met c. Proximal cut is perpendicular to the long axis of the foot d. Distal cut is perpendicular to the long axis of the first met e. Proximal cut should be 1 cm distal to the metatarsocuneiform joint f. Usually done in conjuction with a plantar fascia release

2. Cole osteotomy a. Dorsally based closing wedge b. Proximal cut is made through the navicular and the cuboid c. Distal cut is made through the cuneiforms and the cuboid

3. Japas osteotomy a. V shaped osteotomy with the apex at the middle cuneiform and the medial border just proximal to the 1st MC joint and lateral border proximal to the cuboid 5th metatarsal joint b. The distal section is raised and the proximal portion is lowered

4. Jahss midfoot osteotomy a. Truncated tarsometatarsal wedge arthrodesis b. Dorsally based wedge osteotomy at the tarsometatarsal joints with arthrodesis

5. McElvenny-Caldwell Procedure a. Arthrodesis of the 1st MT – CN joint b. Procedure done after a serious of plaster casting with the heel in valgus and forefoot in supination

6. Dwyer calcaneal osteotomy a. Lateral based closing wedge b. Osteotomy is made 1 cm proximal to the posterior facet c. Fixation: canulated screws, staples

7. Dorsiflexory calcaneal osteotomy (Samilson) a. A cresentic, biplanar osteotomy of the posterior aspect of the calcaneus b. Section is rotated dorsally and out of varus c. May cause anterior impingement of the talus on the tibia and exacerbate anterior cavus

8. Triple arthrodesis a. Done for rigid deformities b. Siffert triple works well i. Moritising the navicular into the head of the talus ii. Depressing the navicular, cuboid and cuneiform while allowing the elevation of the metatarsal iii. Laterally closing wedge at the subtalar joint

Neurological Disorders/Pes Cavus Hereditary Peripheral Neuropathies Charcot Marie Tooth Disease - Inherited familial neuromuscular disease that affects peripheral nerves, causing slowing of sensory and motor nerve conduction - Progressive in nature - HMSN I: Classic CMT; usually beings in the 2nd decade of life - HMSN II: Clinical picture is similar although less pronounced. Manifests later in life. Usually causes bilateral symmetric neurogenic weakness and atrophy of the distal musculature of the lower extremity - Genetics: • Autosomal dominant (most common) • X-linked recessive • Autosomal recessive (least common) - Diagnosis: - Clinical • Claw toes: • Weak intrinsics and to a lesser degree EDL with normal long flexors lead to MPJ extension and IPJ flexion • EDL and EHL are recruited to DF the AJ which pull against the weaker intrinsics • Cavus: • Strong PL overpowers the weak TA causing plantarflexion of the first ray and a FF cavus • Strong TP overpowers the weak PB causing an adducted forefoot • There is then shortening and fibrosis of the short plantar muscles and contraction of the plantar fascia • RF varus: • Overpowering of the TP and the long flexors • May be a secondary deformity • May become rigid over time • Ankle instability: • Weak PB contributes • Varus heel puts ankle at risk • Foot drop: • Thin lower legs (chicken legs) • Stork leg deformity, inverted Champaign bottle appearance • Sensation loss may occur: vibratory and proprioception diminished • Pattern of muscular weakness: • Anterior group; peroneus brevis • Posterior muscles, PL retain normal strength • Marionette gait • Multiple lateral ankle sprains • Pes planovalgus is possible in a flexible deformity - Family history (genetic testing is now available) - Slow NCV

Treatment: - Non operative • Night splints • AFO • Orthotics • Extra depth shoes - Surgical • Multiple options depending on the deformity • Soft Tissue procedures: • Plantar fascia release • Peroneus longus to brevis transfer • TP transfer through the interosseous membrane • TAL • Jones procedure • Long extensory transfers (to cuboid, base of the 4th met) • Osseous Procedures • Metatarsal dorsal closing wedge osteotomies • Cole midfoot osteotomy • Triple arthrodesis: results seem to deteriorate with time • Dwyer calcaneal osteotomy Note: If an arthrodesis is performed, a tendon transfer to balance out the deformity should also be done. This is a progressive deformity and the fusion will deteriorate faster if a tendon transfer isn’t performed. Dejerine-Sottas Disease (Type III) - hypertrophic interstitial polyneuropathy - autosomal recessive - distal muscle weakness in the lower extremities - pes cavus and foot drop - progressive - similar to CMT - peripheral nerve enlargement and frequently palpable due to onion bulb formation Rouse-Levy Syndrome (CMT types V or VI) - similar to CMT - Clumsy gait, abnormal equilibrium, absent DTR, acquired cavus - Essential tremor in the hands that occurs during movement and is absent during rest Refsum’s Disease - progressive paresis of the distal aspects of the extremities - drop foot, pes cavus, decreased DTR, ataxia, night blindness - first symptom: night blindness - autosomal recessive - metabolic neuropathy caused by a disturbance of lipid metabolism which leads to an accumulation of phytanic acid - waxes and wanes

Friedrich’s Ataxia - pes cavus and drop foot deformity - more severe than CMT - by age 30 pts are incapacitated - degeneration of the post and caudal regions of spinal cord of unknown etiology - instability and ataxia due to cerebellar involvement - scoliosis and kyphoscoliosis are common - peroneal nerve weakness will occur followed by ulnar nerve weakness - glove and stocking distribution of decreased sensation - Trendelenburg gait or lurching due to weakness of gluteus medius Cerebrovascular Accidents - Condition is static and non-progressive - Surgical repair is very helpful - An UMN disease - Contractures of unopposed muscle groups is common - Foot deformities such as equinovarus, claw-toes, spastic equinus and drop foot - Bracing is part of treatment for joint imbalances - Pt are usually on anti-coagulant therapy Muscular Dystrophy - Group of disorders were muscle tissue dies or becomes dystrophic - Ankle equinus and equinovarus are common - Duchenne’s • The most severe • Sex linked disease that tends to affect males • Protein dystrophin is not produced • Pseudohypertrophy is seen as fatty deposits in the muscle; often seen in the calf • Goal of treatment: maintain ambulatory status of patient for as long as possible • Gower’s sign is seen - Becker’s • More benign • Abnormal dystrophin

Myelodysplasia Spina Bifida: - group of disorders that have a congenital manifestation of the spine - incomplete closure of the midline of the osseous, mesenchymal and ueral tissues - most often in the lumbar or sacral area - results in dynamic imbalance in the muscles of the lower extremity - progressive disorder - commonly a pes cavus develops but equinus, equinovarus and pes valgus are possible - many times these patients have a paralyzed bladder so catheterization is required during surgery

Spina Bifida Occulta: - isolated defect of the fusion of the posterior vertebral arch without disruption of the underlying neural tissue - many time asymptomatic - most common in posterior arches of L5 and S1 leading to a cavus foot - derm markers: - hairy tuft, dimple or teratoma (lipoma) of skin of lower back. These lesions may grow and compress cord - Etiology: genetic, environment, unknown - Hydrocephalus is common; shunts are used for treatment - Adhesions may cause symptoms as child grows: • The attachment of the spinal cord to the meningocele sac and the skin prevents normal cephalad migreation of the spinal cord with growth. This produces the so called tethered cord. Even after surgical release from the spinal cord, reattachement of the cord is likely during the healing process. As the child grows, the spinal cord is stretched, causing increasing neurological damage. - Sensory and proprioception abnormalities may be worse than motor abnormalities • The posterior aspect of the cord is exposed • Posterior section of the cord is responsible for sensory and proprioceptive function whereas the anterior part of the cord is involved in motor function Poliomyelitis - not very common today - viral infection of the anterior horn cells - paralysis of the muscles are involved; may be partial depending on the many cells or sequential portion of the cord is damaged - Tibialis anterior which is innervated by a short column of anterior horn cells is more vulnverable to complete paralysis - Paralysis is asymmetrical - Most common cause of posterior cavus (due to loss of Achilles tendon function) - Acute stage: • Fever, myositis, paralysis • Muscles are tender • Pt will contract and shorten the muscle to relieve pain and if held in that position then permanent contracture may remain - Subacute or convalescent stage: • Improvement of symptoms • Aggressive physical therapy should be initiated - Chronic Stage • Period of stability • Surgical intervention can be attempted • Non-progressive once in this stage

Cerebral Palsy - congenital neuromuscular disease caused by brain lesion - lesions may be formed before, during or after birth - common causes: • maldevelopment of the brain • cerebral anoxia during the prenatal period • trauma during birth • erythroblastosis secondary to Rh incompatability • neonatal encephalitis • prematurity - non progressive syndrome but muscle imbalances may progress over time - types • spastic (65%) • responds well to surgical repair of the deformities • muscles that cross more than one joint are often infected • the muscles of flexion, adduction and internal rotation tend to overpower those muscles of extension, abduction and external rotation • scissor gait is seen • TEV commonly develops • Other foot deformities such as talipes calcaneus, pes cavus, hallux valgus and hammer toe deformities • Athetoid (20%) • Other (15%)

Questions about Lis Franc Injuries How do you assess Lis Franc’s joint radiographically? AP: Medial border of the 2nd metatarsal base should be aligned with the medial border of the middle cuneiform 30 degree lateral oblique: Medial border of the 4th metatarsal base should be aligned with the medial border of the cuboid Lateral: Dorsal border of the 2nd metatarsal base should be aligned with the middle cuneiform base Desmond, FAI, 2006. Myerson, Foot & Ankle, 1986. What is the most common finding in a lis franc’s injury? Diastasis of the bases of the 1st and 2nd metatarsal What is the pathoneumonic finding for a Lis Franc’s injury? Fleck sign (90%) Desmond, FAI, 2006. Myerson, Foot & Ankle, 1986. How do you assess for calcaneal cuboid joint congruity?

Lateral oblique: No overlap with continuous trabecular patterns What classification systems exist for Lis Franc injuries? Quenu and Kuss (1909) ►Type A: Homolateral or total incongruity ►Type B: Isolateral or partial incongruity ►Type C: Divergent dislocation Hardcastle Classification (1982)

►Type A – Total incongruity in one plane (may be sagittal, coronal or combined) ►Type B – Partial incongruity: Displaced segment is in one plane which may be sagittal, coronal or combined. Medial displacement affects the first met either in isolation or combined with displacement of one or more of the second, third or fourth met. Lateral displacement affects one or more of the lateral four mets but the first met is not affected ►Type C – Divergent: partial or total incongruity. AP radiograph shows the first met displaced medially while any combination of the lateral metatarsals are displaced laterally. Sagittal and coronal plane displacement. Hardcastle PH, Reschauer R, Kutscha-Lissberg E, Schoffmann W. Injuries to the Tarsometatarsal Joint. JBJS. 1982, Vol 64-B, Jun(3):349-56

Myerson’s Modification (1986) ►Type A – Total incongruity st ►Type B1 – Partial incongruity 1 metatarsal ►Type B2 – Partial incongruity lesser metatarsals ►Type C1 – Divergent pattern, partial incongruity ►Type C2 – Divergent pattern, total incongruity ►B1, C1 and C2 also involve tarsal bones and the cuneiform joints Myerson MS, Fisher RT, Burgess AR, Kenzora JE. Fracture Dislocations of the Tarsometatarsal Joints: End Results Correlated with Pathology and Treatment. Foot Ankle. 1986, Vol 6; Apr(5):225-42

What other injuries are accociated with Lis Franc Fx/Dislocation? ►Nutcracker type fracture of the cuboid ►Chopart subluxation/dislocation ►Calcaneal fractures ►Proximal injuries ►Compartment syndrome ►Disrupted neurovascular supply ►Soft tissue envelope compromise What is the goal of reduction in displaced lis franc injuries? Anatomic alignment of the bases of the metatarsals with their respective tarsal bones. What are Charnley’s four steps to closed reduction? 1. Re-create/exaggerate the deformity 2. Distract the deformity 3. Reduce the deformity 4. Cast the body part What are principles to reduction that are specific to lis franc’s complex? ►Key to reduction: 2nd metatarsal ►Step 1: Medial column ►Step 2: Lis Franc ligament complex ►Step 3: Lateral rays From: Kelkikian. Operative Treatment of the Foot and Ankle. 1998.

If you take a lis franc injury to the OR, what are your fixation options? ►Closed reduction, cast immobilization ►PerQ fixation with K-wires only ►PerQ fixation with K-wires 4 – 5; ORIF of 1-3 PRN ►ORIF (no K-wires) with screws ►ORIF with plates ►External fixation ►Partial arthrodesis ►Full arthrodesis Outcome for this injury depends on…

►Injury ►Anatomic reduction ►Patient education ►Surgeon’s experience What are some of the major complications associated with this injury? DJD CRPS Compartment syndrome Cuboid syndrome Additional surgery/fusion Some good references for Lis Franc fracture/dislocations…. ► Aitken AP, Poulson D. Dislocations of the Tarsometatarsal Joint. JBJS. 1963, Vol 45-A; Mar(2):246-383 ► Chandran P, Puttaswamaiah R, Dhillon MS, Gill SS. Management of Complex Open Fracture Injuries of the Midfoot with External Fixation. JFAS. 2006, Vol 45; Sep/Oct (5):308-15 ► Chang T. Master Techniques in Podiatric Surgery: The Foot and Ankle. Lippincott, Williams and Wilkins, Philadelphia, PA. 2005:189-210 ► Desmond EA, Chou, LB. Current Concepts Review: Lisfranc Injuries. Foot and Ankle. 2006,Vol 26;Aug(8):653-60 ► Ebraheim NA, Haman SP, Lu J, Padanilam TG. Radiographic Evaluation of the Calcaneocuboid Joint: A Cadaveric study. FAI. 1999, Vol 20; Mar(3):178-81 ► English TA. Dislocations of the Metatarsal Bone and Adjacent Toe. JBJS. 1964, Vol 46-B; Nov(4):700-4 ► Gissane W. A Dangerous Type of Fracture of the Foot. JBJS. 1951, Vol 33-B; Nov(4): 535-8 ► Hardcastle PH, Reschauer R, Kutscha-Lissberg E, Schoffmann W. Injuries to the Tarsometatarsal Joint. JBJS. 1982, Vol 64-B, Jun(3):349-56 ► Kelkikian AS. Operative Treatment of the Foot and Ankle. The McGraw-Hill Companies. 1998:45579. ► Kuo RS, Tejwani NC, DiGiovanni CW, Holt KS, Benirschke SK, Hansen ST, Sangeorzan BJ. Outcome After Open Reduction and Internal Fixation of Lisfranc Joint Injuries. JBJS. 2000, Vol82A; Nov(11):1609-18 ► Lin SS, Bono CM, Treuting R, Shereff MJ. Limited Intertarsal Arthrodesis Using Bone Grafting and Pin Fixation. Foot Ankle. 2000, Vol 21; Sep(9):742-8 ► Ly TV, Coetzee JC. Treatment of Primarily Ligamentous Lisfranc Joint Injuries: Primary Arthrodesis Compared with Open Reduction and Internal Fixation, a Prospective Randomized Study. JBJS. 2006, Vol 88-A; March(3):514-20

► Mulier T, Reynders P, Dereymaeker G, Broos P. Severe Lisfranc Injuries: Primary Arthrodesis or ORIF? Foot and Ankle. 2002,Vol 23; Oct(10):902-5 ► Myerson MS, Fisher RT, Burgess AR, Kenzora JE. Fracture Dislocations of the Tarsometatarsal Joints: End Results Correlated with Pathology and Treatment. Foot Ankle. 1986, Vol 6; Apr(5):22542 ► Peicha G, Labovitz J, Seibert FJ. The Anatomy of the Joint as a Risk Factor for Lisfranc Dislocation and Fracture-Dislocation. An Anatomical and Radiological Case Control Study. JBJS. 2002, Vol 84B; Sep(7):981-5 ► Richter M, Wippermann B, Krettek C, Schratt HE, Hufner T, Thermann H. Fractures and Fracture Dislocations of the Midfoot: Occurance, Causes and Long-term Results. Foot Ankle. 2001, Vol 22; May(5):392-8 ► Saxena A. Bioabsorbable Screws for Reduction of Lisfranc’s Diastasis in Athletes. JFAS. 2005, Vol 44; Nov/Dec(6):445-9 ► Thompson MC, Mormino MA. Injury to the Tarsometatarsal Joint Complex. J Am Acad of Orthop Surg. 2003, Vol 11; Jul/Aug(4):260-7 ► Zgonis T, Roukis TS, Polyzois VD. Lisfranc Fracture-Dislocation: Current Treatment and New Surgical Approaches. Clin Podiatr Med Surg. 2006, Vol 23; Apr(2):303-22

Case Study CC: 22 y/o woman presents to our office c/o left ankle pain HPI: Hurt it at track practice 2 days ago; trainer iced the ankle and applied ACE wrap and told me to use crutches; was pushing off for a spring and it felt like someone kicked me in the back of the leg; stabbing pain; didn’t do my usual stretching and was late for practice. PMH: Severe pyelonepthritis diagnosed 1 month ago Meds: Ciprofloxacin 250 mg PO BID Allergies: none Family Hx: unremarkable Social Hx: student at the local university; scholarship track team – sprinter; denies EtOH, tobacco and drug use ROS: unremarkable Physical Exam: Integ: diffuse ecchymosis posterior calcaneus, left Vasc: palpable pedal pulses bilaterally; diffuse edema surrounding left ankle Neuro: intact bilaterally M/S: unable to do single leg toe raise on the left size. + Thompson test, left. + Knee flexion test Thompson-Doughtery Test Positive – patient prone, no plantarflexion while the calf is being squeezed Knee Flexion Test Patient asked to actively flex the knee to 90 degrees while lying prone and the foot on the affected side fails to neutral or dorsiflexion Differential Diagnosis Rupture of the Achilles tendon Partial rupture of gastrocnemius muscle Avulsion fracture of calcaneus (Rowe IIB) Radiographs: Increased soft tissue density and volume obliterating Kaeger’s triangle No fractures, dislocations or foreign bodies noted.

MR: T1: Disruption of signal within the tendon T2: Generalized increase in signal intensity with edema and hemorrhage at the site of the rupture with an area of high signal intensity Treatment for Partial Rupture 1. Jones compression dressing for 24 – 72 hours 2. BK cast in plantarflexion for 3 – 4 weeks 3. Another BK cast x 4 weeks with less plantarflexion Complete Rupture Operative Repair 1. Primary repair with suture/implant a. Ma and Griffith – percutaneous suture with non absorbabale suture on a straight needle b. Single suture Krakow c. Double suture Krakow

d. Modified Bunnell e. Double suture Bunnell

f. Double suture Kessler g. V-Y Graftoplasty

h. Turn down fascial graft i. Bosworth

Achilles Blood Supply 1.Muscle belly 2.Paratenon 3.Calcaneus Normal Achilles tendons do not rupture – 98% of the time a degenerative process preludes a rupture (i.e. fibrosis, peritendonitis or chronic tendonitis)

Anatomically – 3 distinct areas of concern: - myotendinous origin: 4 – 14% of ruptures - tendon: 72 – 73% of ruptures - osseous insertion – 14 – 24% of ruptures Watershed area – 2 – 6 cm proximal to the Achilles insertion; degenerates most rapidly here due to a physiological twist in the tendon, not blood supply Although…there may be some relation to blood supply because this area of the tendon is the least vascular MRI – Increases in intratendinous signal intensity should be regarded as abnormal Evaluate tendon - Signal response • Increase intratendonous signal on T1 (fibrosis) – not seen on T2 - Morphology • Increase thickness – fusiform/bulbous • Loss of concavity of the anterior portion of the tendon Pre-disposing factors to rupture - Collagen vascular diseases - Long term systemic steroid therapy - Local steroid injection - Flouroquinolones

Fifth Metatarsal Base Fracture Questions 1. What is the eponym associated with 5th MTB fractures? - Dancer’s fracture - Jones’ fracture 2. What are the two general types of the 5th MTB fractures? - avulsion fracture of variable sizes - Fracture of the metaphyseal – diaphyseal junction There is also the diaphyseal stress fracture that is sometimes included in this list, though it doesn’t occur in the base region. 3. What was Sir Robert Jones doing when he injured himself and subsequently described the fracture associated with his name? - 1902. Dancing around a tent pole at the military garden party in 1896. - He described a transverse fracture of the 5th metatarsal that did not heal quickly. 4. What is the suggested treatment for non-displaced avulsion fractures of the 5th MTB? - Heal sufficiently when immobilized in a cast or supported with elastic wrap. 3 – 4 weeks - Delayed and non-union are rare complications and in the event that satisfactory bony healing does not occur, most patients will remain asymptomatic because of fibrous tissue bridging across the defect. 5. Name three structures that insert into the 5th MTB from proximal to distal. - lateral cord of the plantar aponeurosis - peroneus brevis - peroneus tertius 6. Describe the Stewart Classification for 5th MTB fractures. Type I – Proximal metaphyseal – diaphyseal fracture (true Jones) Type II – Intra-articular avulsion fracture Type III – Extra-articular avulsion fracture Type IV – Intra-articular comminuted fracture Type V – Partial avulsion fracture of the epiphysis (located in a longitudinal direction); risks of Iselin’s AVN Where is a Jones fracture located? - at the metaphyseal-diaphyseal junction of the 5th MTB approximately 1.5 cm distal to the tuberosity - distal to the intermetatarsal ligament at the bases of the 4th and 5th metatarsals What are three ways that you can fixate a displaced avulsion fracture? - K-wires - Screws - Tension band wire

Case Study HPI: 45 y/o WF is seen at bedside at AM rounds. Pt complains that she feels lousy and had a difficult time sleeping last night. Pt is 2 days s/p triple arthrodesis of the right foot for severe acquired flatfoot. Pt denies F/V/CP/SOB and states that she feels cold and lousy. Allergies: PCN; codeine Meds: Clinda 600 mg q6h Atenolol 50 mg qd Glucotrol XL 5 mg qd ASA 325 mg every other day Premarin .625 mg qd Depomedrol injection every three months PMH: HTN, DM2 x 10 years SHX: Smokes 2ppd x 25 yrs. EtOH occasionally FHX: Mother deceased at 82 gunshot to the head; Father deceased at 74 from massive MI ROS: HEENT: occasional headaches; CV: dx with a heart murmur in 1998 PE: Vitals: Ht 62 inches; Wt 168 lbs; T 101.1; P: 92; R 24; BP 185/90 Integ: upon removal of the cast, medial and lateral incisions appear intact with some tension noted; suture intact; some periwound erythema and edema; right calf appears swollen compared to the left. Vasc: Non-palpable, right due to edema. Palpable pedal pulses, left. Neuro: decreased to SWM b/l M/S: pain to palpation of the right posterior calf What do you have to rule out at this point? And how do you rule it out? 1. Atelectasis – chest x-ray 2. UTI – UA with cultures 3. DVT – venous duplex doppler 4. Wound infection – clinical correlation 5. Drug fever What are the five causes of post – op fever and what is the time period in which they occur? Wind: 12 hours Water: 24 hours Walking: 12 – 48 hours Wound: 2 – 4 days Wonder Drug: anytime

Results: 1. Chest x-ray is negative; pt has been using the incentive spirometer once every hour for five minutes; pt does not complain of shortness of breath or chest pain 2. UA results are the following pH: 6.5 color: straw specific gravity: wnl WBC 2/field bacteria: 0 nitrities: negative Leukocyte esterase: negative 3. Duplex Doppler was positive for actute DVT in the posterior tibial vein of the right leg 4. No work up needed because no wound infection suspected. Normal post op changes to the peri-wound areas. Treatment: - Pt started on 15,000 u bolus of heparin IV - Pt given 1400 u heparin IV/hr - PTT was checked four hours after initiation of therapy and found to be 46 sec (normal = 25 – 35s) - Pt was given a bolus of 3000i IVP and 1452u/hr - PTT was checked again four hours after adjustment of therapy: 75 sec (you want the PTT to be 70 – 95here) - Pt was started on 10 mg of coumadin 24 h after initial diagnosis of DVT; pt was give 10 mg of coumadin the next day - PT was taken and INR was found to be 2.5 (you want it between 2 and 3) - Heparin was continued for five days after coumadin was started - Coumadin was continued for 3 months

Case Study HPI: 24 yr old WM presents to the ER c/o a thigh cast on his right leg. Pt had a haglund’s deformity removed 3 days prior. Pt states that the pain woke him up last night and has been present every since. Pt took two Tylenol #3 which didn’t help. PMH: unremarkable Medications: none Allergies: none SHx: denies tobacco, drugs; social EtOH ROS: unremarkable PE: Vitals: Ht 68 inches; Wt 215 lbs; VSS; afebrile Integ: R leg warm, slight erythema, diameter in center of calf is 3 cm > L calf; incision intact, no soi NV: intact MS: unremarkable A/P: R/O DVT Duplex Doppler was positive for DVT in the right calf Pt admitted to hospital and began anti-coagulant therapy

DVT Related Questions 1. What is virchow’s triad? - states of hypercoaguability - venous stasis - damage to the endothelial lining in the blood vessel 2. Pneumotic for risk factors of developing DVT. I AM CLOTTED Inactivity A Fib/Age MI Coaguable state Longevity of surgery Obesity Tobacco/tourniquet Tumor/trauma Estrogen (oral contraceptives) DVT hx 3. What are the common locations for DVT? - 20 % of calf emboli will become thigh emboli - 1/5th of PE come from the calf 4. How do you diagnose a DVT? Clinically: red, hot, swollen, painful calf - edema is the most reliable sign of DVT (compare suspected calf to the contralateral side) Homan’s test: DF foot elicits pain in the calf Pratt’s sign: compression of calf elicits pain Diagnostic Tests: 1.

2.

Non-invasive a. Duplex Doppler: lack of venous compression indicates DVT i. Can have color flow imaging to enhance sensitivity ii. Allows to determine direction of blood flow and the amount of reduction in lumen diameter iii. Good for symptomatic DVT iv. Grady-Bensmetal JBJS, 1994: duplex ultrasound has the positive predictive value of 7/9 v. Ciccone et al JBJS 1998: duplex ultrasound with color flow imaging is unreliable in detecting asymptomatic DVT post THR/TKR b. Impedence plethysmography Invasive a. Contrast venography i. Gold standard for detecting DVT ii. Not as reliable in detecting recurrent DVT iii. Has been known to cause PE during testing iv. New contrast media has decreased this risk

5. How do you diagnose a PE? Clinically: sudden onset of chest pain, dyspnea, hemoptysis, tachycardia Pt may be febrile, hypotensive and cyantic Diagnosis: 1. Blood gasses: PaO2 < 80 mmHg 2. Chest x-ray: 50% are normal; a normal or near normal chest x-ray in a dyspneic patient suggests PTE. Well – established abnormalities include focal oligemia (Westermark’s sign), a peripheral wedged shaped density above the diaphragm (Hampton’s hump) or an enlarged right descending pulmonary artery. 3. Ventilation – Perfusion Scan (V/Q Scan) a. A mismatch demonstrating an area of ventilation but no perfusion suggests PE b. Ventilation: inhalation of xenon 133 c. Perfusion: T99 labeled albumin d. V/Q mismatch: acute PE, previous PE, centrally located cancer, radiation therapy 4. Pulmonary angiography a. Definitive test b. Indicated if V/Q scan is inconclusive c. Diagnostic signs: intraluminal filling defect, abrupt vessel cutoff, loss of side branches 6. Prophylaxis a. Non-pharmacologic - compression stockings - intermittent compression pumps 1. increases levels of prostacyclin and fibrinolytic byproducts 2. prevents stasis due to increased venous return b. Heparin - 5000u SQ q2h pre-op - 5000u SQ q8-12h 7. Treatment a. Heparin IV - loading dose: 10,000 – 15,000u or 80u/kg - maintenance dose: start with 1,000 u/hr (18u/kg/hr) - adjust according to PTT (goal 57 – 90 seconds) - protamine sulfate reversed heparin - 1 mg protamine pre 100 u heparin - use with care in pts on NPH insulin - complications: hemorrhage, thrombocytopenia, ostoporosis with long term use b. Coumadin - start after heparin is therapeutic - commonly 2.5 mg qd - adjust according to PT (1 – 1.15 x normal/INR 2 – 3) PT normal = 11 – 13 INR normal 0.8 – 1.2 - vitamin K reversal

c. LMWH - Safer than regular heparin - no need to monitor PTT, easier dosing i. Lovenox Theraputic: 30 mg SQ BID Prophylatic: 1 mg/kg ii. Fragmin 2500 u SQ qd iii. Normiflo 5000 u – 10000 u SQ BID Compartment syndrome has been implicated with their use (McLaughlin et al JBJS 1998) d. Thrombolytic therapy - urokinase, streptokinase to dissolve clot - must be initiated within 24 – 48 hours e. Surgical therapy 1. venous interruption operation - Greenfield filter: placed in IVC below renal veins 2. Pulmonary embolectomy 8. Post-phlebetic syndrome (post thrombotic syndrome) - result of venous HTN due to recanalization of major thrombi which lead to patent but scarred/incompetent valves - occurs in 50 – 60% of patients with proximal DVT; 30% of patients with symptomatic calf DVT - blood can now flow from the deep to superficial veins which leads to persistent LE edema, stasis dermatitis may occur and breakdown of skin and ulceration develops 9. Pt has a DVT in his lower extremity. Clots are thrown and pt is found dead at home. Upon autopsy pt is found not to have died from a pulmonary embolism but from a massive CVA. How is this possible? Pt had an undiagnosed patent foramen ovale. This is called a paradoxical embolism. 10. What is usually the immediate cause of death from a PE? Right sided heart failure. Right ventricular dysfunction. Progressive right heart failure is the usual immediate cause of death from PTE. As pulmonary vascular resistance increases, right ventricular wall tension rises and perpetuates further right ventricular dilation and dysfunction. Consequently, the inter-ventricular septum bulges into and compresses an intrinsically normal left ventricle. Increased right ventricular wall tension also compresses the right coronary artery and may precipitate myocardial ischemia and right ventricular infarction. Underfilling of the left ventricle may lead to a fall in left ventricular output and systemic arterial pressure, thereby provoking myocardial ischemia due to compromised coronary artery perfusion. Eventually, circulatory collapse and death may ensue.

Case Study CC: Pain at the 1st MPJ HPI: 34 y/o healthy female s/p bunionectomy x 18 months presents to your office c/p pain, stiffness and swelling at the base of the left big toe joint. The symptoms began gradually approximately 6 months ago. Her condition has gradually worsened and now her big toe joint is almost as painful as it was pre-op. Symptoms are triggered predominately by weight-bearing. She has been treated with anti-inflammatory medication and rest by the physical that performed the surgery. This provides temporary relief of her symptoms. PMH: Seasonal allergies PSxH: Bunionectomy, left foot – 18 months ago Allergies: NKDA Meds: Claritin SH: Denies tobacco; EtOH and ilicits FH: All alive and well ROS: Non-contributory Physical Exam INT: warmth and erythema noted at the 1st MPJ VASC: palpable pedal pulses, edematous 1st MPJ NEURO: intact M/S: pain on palpation of the 1st MPJ, pain on passive and active ROM, decreased 1st MPJ ROM (approximately 15 degrees) List your differential diagnosis. You can list a million things but you MUST include: AVN and infection What would you like to order? X-rays Describe your radiographic findings. What is your diagnosis? AVN of the first metatarsal (Assman’s disease) Plan: What is your treatment plan?

Metatarsal head AVN Related Questions 1. List and describe the radiographic stages of AVN. Stage 1: Avascular Stage (several weeks to 3 months) - Relatively few clinical and radiographic changes • Soft tissue inflammation (increase in soft tissue density) • Thickened synovium (appears as capsulitis/synovitis) - The ossific nucleus of the epiphysis ceases to grown due to the interrupted blood supply • Smaller epiphysis on affected side • There is a relative increase in the density of the epiphysis which is illusional due to the adjacent osteopenia seen in the metaphysis • Joint space appears increased secondary to decreased size of the epiphysis • Articular cartilage is unaffected since it is nourished by synovial fluid - Minimal deformity - Mild arthralgia with associated edema, muscle atrophy and antalgic gait Stage 2: Revasculization Stage (1 – 4 years) - revascularization of the dead epiphysis, which further undermines its integrity due to significant vascular inbudding - there is a true increase in density of the epiphysis due to condensation and impaction, as the epiphysis collapses on itself - “head within head” appearance – the epiphysis appears very irregular due to deposition of new bone around existing dead bone - Subchondral fractures may occur during this extremely vulnerable stage, in which osteogenesis produces primary woven bone (soft bone) Stage 3: Remodelling Stage/Bony Healing - bony deposition predominates over bony resorption, replacing old necrotic bone - osseous structures still suseceptible to injury and deformity, but to a lesser degree than stage 2 - radiographic finding: return of the contour and outline of the epiphyseal center, which can only adequately be assessed when re-ossification is complete Stage 4: Residual Deformity - complete bony healing has occurred - epiphysis may be normal if sufficient treatment was rendered - resultant end stage deformity is assessed at this point How do you diagnose AVN? Sequential radiographs and clinical correlation If not evident on plain films, what other imaging modality can be used to detect AVN and how does it appear? MR imaging. Since most bone infarct occur in fatty tissue, MR imaging is very useful. Decreased signal intensity within medullary bone would be noticed in T1 and T2 weighted images. More sensitive and has better resolution than a bone scan.

How do you treat AVN? This is a self limiting process. We are trying to prevent residual deformity. Conservative Treatment: - NSAIDs - Orthotics - Analgesics - Protected/off weightbearing (casting, bracing, padding) Surgical Treatment: - arthrodesis According to the literature, what is the incidence of post-operative AVN following a distal 1st metatarsal osteotomy? - Lateral release of the fibular sesamoid, conjoined adductor tendon, deep transverse intermetatarsal ligament and joint capsule and excessive dissection, especially the periosteal tissues can compromise the blood supply to the first metatarsal head. - Wilkinson et al using MR imaging found a 50% incidence of AVN following Austin bunionectomy, with 10% of plain film in this study showing signs of AVN. - Wallace et al using a mailed survey to 45 podiatry surgeons, reported an incidence of only 0.11% in 13,000 head osteotomy bunionectomies. - Although AVN is a recognized complication of first metatarsal head osteotomy and may occur at a higher incidence than first recognized, clinical signs and symptoms are relatively rare. How do you reduce the incidence of AVN when performing a first metatarsal osteotomy? - rigid fixation - minimal dissection - minimal lateral release Name the true AVNs. - Renandier’s disease – tibial sesamoid - Trevor’s disease – fibular sesamoid - Freiberg’s disease – second metatarsal head - Kohler’s disease – navicular - Diaz/Mouchet disease – talus - Blount’s disease in adolescents – medial proximal tibial epiphysis - Legg Calve Perthes Disease – femoral head Name the AVNs that are NOT true. - Sever’s disease – calcaneus - Theimann’s disease – phalanges (hand and foot) - Islen’s disease – 5th MT base - Haglund’s disease – accessory navicular - Osgood Schlatter’s disease – tibial tuberosity - Blount’s disease in children – proximal medial tibial epiphysis

-

Scheurman’s disease – ring epiphysis of the vertebral body Calve’s disease – solitary vertebral body Buchman’s disease – iliac crest Van Neck’s disease – ischiopubic synchondrosis Mandle’s disease – greater trochanter of the femur Singling-Larson-Johannson disease – lower patella

Name the AVNs that may or may not be true AVNs. - Buschke’s disease – cuneiform(s) - Lewis/Liffert/Arkin – distal tibial epiphysis - Ritter’s disease – proximal fibula The AVNs by Bones in the foot. - Calcaneus – Sever’s disease - Talus – Diaz disease - Navicular – Kohler’s disease - Cuboid – Lance’s disease - Cuneiforms – Buschke’s disease - 1st MT Head – Assman’s disease - Tibial sesamoid disease – Renandier’s disease - Fibular sesamoid disease – Trevor’s disease - Lesser met heads – Frieberg’s disease - Phlanages – Theimann’s disease

Puncture Wounds Haverstock & Grossman. Puncture wounds of the foot. Clin Pod Med: Oct 1999 2 most important complications:

Soft tissue infection and Osteomyelitis (calcaneus is most common)

Most common puncture objects:

Nails Glass

Clinical Presentation - Patients usually present immediately due to pain and the inability to bear weight. - The puncture wound penetration site usually exhibits signs of acute injury: localized erythema and edema - If a patient delays in seeking medical care, infection may already be established in the wound. - When a foreign body is retained in the puncture wound, infection can manifest in 24 hours but may have a delayed presentation of 3 to 4 days Clinical Evaluation - Thorough history (time of injury, type of shoe, environment and a good description of the penetrating object. It is also important to find out if the patient has attempted to remove the object.) - Patient’s tetanus status must be ascertained and appropriately addressed (see tetanus prophylaxis) - Determining the location and depth of the wound is important - It must be determined if the wound was close to a joint, tendon, or any other NV structure (Patzakis, et al – Classification system) - Determining the depth of the puncture is essential because extension of the puncture wound to deeper structures may cause penetration of structures such as the intrinsic and extrinsic tendons, intermetatarsal bursae or joint capsules. These structures are less vascular and have a lower metabolic rate, allowing infectious organisms the opportunity to replicate and the infection to be established. Nerve damage should be evaluated by testing distal sensation. Tendons should be evaluated as well. - Inspect the borders of the wound. Jagged, irregular borders have an increased potential for infection due to decreased vascular perfusion of the apices. Radiographic Evaluation - Plain films should always be obtained to determine if any object has been retained or to see if any osseous structures have been involved. - A retained foreign body can be a nidus for infection - Can glass be seen on plain films? The size of the piece is the limiting factor - Plain film may be inadequate to show small pieces of glass, wood, plastic or material from socks and shoes - Xeroradiography, ultrasound, CT or MR may also be used. - CT is good to visualize wood in deep tissues - Ultrasound is good to detect non-radio-opaque bodies. May be useful when the puncture wound is near a vessel - Plain film, CT, MR, and radionuclide imaging also can be used to detect osteomyelitis Wound Microbiology - Most common gram positives responsible for soft tissue infections: • S aureus • S epidermidis • Streptococcus - Most common gram negatives responsible for soft tissue infections: • E coli

-

• Proteus • Klebsiella Pasteurella multocida in dog/cat bites Pseudomonas aeruginosa is the most common organism isolated in osteomyelitis following puncture wounds (especially in gym shoes). This is well documented. Patients without systemic illnesses usually have one pathologic organism Patients with systemic illnesses usually have more than one pathologic organism

Treatment - The goal of treating puncture wounds is to convert a contaminated or dirty wound into a clean wound. - Begin by cleansing the wound with sterile saline. If local anesthetic is needed, perform the block proximal to the wound. You do not want to spread the soft tissues around the wound. - The wound should be explored with a blunt sterile probe. Wounds extending beyond the deep fascia must be treated aggressively to present deep abscess formation and possible osteomyelitis. - Incision and drainage are required in all deep, contaminated or infected wounds. Once aggressive debridement is completed, the wound should then be irrigated, preferably with pressure irrigation. Deep wound cultures then are taken by removing deep tissue samples and sending them for culture and sensitivity. The wound should be packed open or closed over a drain to prevent hematoma or establishment of an anaerobic infection. Intraoperative radiographic techniques may be utilized, such as triangulation or a metal grid system. Antibiotics - Controversial issue - If the wound has not penetrated the plantar fascia and is clear of any foreign matter or necrotic tissues, then observation without antibiotics is sufficient - If the wound has penetrated deep through the plantar fascia, the likelihood of contamination may necessitate the use of prophylactic antibiotics - When puncture wound occurs in a shoe, the antibiotic must cover pseudomonas aeruginosa. • Recommend: • oral fluoroquinolones, such as cipro - Late puncture wounds with abscess formation or ascending cellulitis must be treated with IV antibiotics. • Recommend: • anti-pseudomonal penicillin class, such as ticracillin and pipercillin; • third generation cephalosporins, such as cefoperazone and ceftazidine; • aminoglycosides with clindamycin - Wound causing osteomyelitis must receive IV antibiotics x 6 weeks Wound Contamination Clean – No frank contamination. No break in aseptic technique. Most surgical wounds Clean – Contaminated – Minimal wound contamination owing to a minor break in technique Contaminated – Significant bacterial contamination. Most traumatic wounds. Dirty – Grossly contaminated with signs of frank infection.

Tetanus Prophylaxis Taken from Joseph, Warren S. Handbook of Lower Extremity Infections. 2nd edition. Chruchill Livington; St Louis, 2003. pg 87.

Hx of Tetanus Toxoid Admin Unknown or less than 3

More than 3

Clean, Minor Wound Toxoid Immunoglobulin Yes, and proceed with basic immunization

No

No, unless >10 yrs since last dose

No

Other Wounds Toxoid Immunoglobulin Yes, and proceed with basic immunization No, unless >5 years since last dose

Yes (250 U of human tetanus immunoglobulin) No

When determining what to give in regards to tetanus, there are three things to look at: 1. Immunization status 2. Timing of the patient’s last booster 3. Wound and wound treatment 4. Taken from: Brooks JW. Management of Pedal Puncture Wounds. JFAS 1994. 33(5):463 – 466.

Immunization Status Completed Completed in the previous 10 years Completed more than 10 years previously Completed more than 10 years previously

Booster Status

Wound

Tetanus

Within the last year None

None .5 ml toxoid (Td)

Within the previous 10 years

.5 ml Td

None within the previous 10 years

Minor wound Relatively clean Treated promptly and adequately Something other than minor wound Not clean Not treated promptly

Completed more than 10 years previously

No booster in the previous 5 years

No record or hx of immunization

No record of booster Minor wound Clean wound Treated promptly and adequately

No record or hx of immunization

No record of booster Wound not clean, not minor and not treated promptly or adequately

.5 ml Td

.5 ml Td 250 units tetanus immune globulin 500 units TIG if wound is clostridiaprone .5 ml Td 2nd injection 4 – 6 weeks later 3rd injection 6 – 12 months after second 250 units of TID (500 units TID if claustridium prone) w/above Td sequence

Hallux Varus Classification: 1. Congenital hallux varus (Tachdjian, 1982/1985) a. Primary: isolated deformity where a taught medial band of tissue extends from the medial side of the great toe to the base of the first metatarsal b. Secondary: associated with other congenital deformities: metatarsus varus and broadening and shortening of the first metatarsal. c. Tertiary: associated with developmental afflictions of the skeleton, i.e. diastrophic dwarfism 2. Acquired hallux varus a. Static: muscle balance undisturbed (i.e. met osteotomy) b. Dynamic: muscle imbalance (i.e. adductor transfer of the McBride type) Etiology 1. Excessive resection of medial eminence with disruption of the sagittal groove 2. Plantar lateral release 3. Excessive tightening of the medial capsular structures 4. Osseous over correction 5. Aggressive post operative bandaging or splinting 6. Excision of the fibular sesamoid 7. Muscle imbalance caused by previous HAV correction Relevant History: 1. HAV surgery Symptoms 1. Unable to wear conventional shoe gear 2. Pain present at medial aspect of hallux secondary to shoe pressure 3. Pain along the medial aspect of the arch secondary to muscle contracture 4. Pain at the first MPJ with or without shoe gear. Clinical Signs of Hallux Varus 1. Adducted position or varus rotation of the hallux 2. Contracture at the IPJ or involving the EHL or abductor hallucis tendon (cocked up hallux) 3. Pain on palpation of abductor hallucis 4. Pain and crepitus at the 1st ray 5. Hallux limitus or rigidus Radiographic Signs of Hallux Varus 1. Hallux abducted at 1st MPJ 2. Staked head of the 1st metatarsal with a peeking tibial sesamoid 3. Absent fibular sesamoid 4. Previous osteotomy of the 1st metatarsal 5. Reduced or negative IM angle 6. Negative PASA 7. Arthritic changes at the 1st MPJ and/or IPJ of hallux

Correction of Hallux Varus Conservative a. Adductovalgus strapping and splinting Surgical b. Soft tissue release i. Medial capsulotomy ii. Lateral capsulotomy c. Dynamic soft tissue procedure i. Abductor hallucis tendon transfer ii. Retransfer adductor hallucis tendon laterally d. Osseous procedures i. Correct abnormal IM angle or PASA (reverse Austin, etc.) e. Joint destructive procedures i. Arthroplasty (Keller) ii. Arthrodesis (McKeever) Stepwise Approach (Presby) Total soft tissue release at the 1st MPJ Medial capsulotomy Tibial sesamoidectomy (if 30 – 50% of sesamoid is peeking) Address abductor hallucis as a deforming force – transfer abductor hallucis to the plantar – lateral flexor apparatus and lateral base of the proximal phalanx Osseous correction a. Determine level of osseous deformity b. Revise the previous metatarsal osteotomy c. If the IM angle is negative, reverse the overcorrection with the appropriate osteotomy (Reverse Austin, reverse off-set V, reverse CBWO) Arthroplasty of the 1st MPJ for severe deformity and for non functional joint surfaces d. Keller e. Implant f. Keller with fusion of IPJ Arthrodesis of 1st MPJ g. McKeever h. Lapidus i. If both sesamoids are removed, fuse the IPJ of the hallux Systemic Repair of Hallux Varus (McGlamry) Complete soft tissue release Correction of structural deformity (IM angle) Tendon transfers Tibial sesamoidectomy Joint arthroplasty

Step-wise correction of Hallux Varus. 1. Skin incision – If the skin incision is contributing to the deformity, scar revision (e.g. Z-plasty) instead of reincision should be performed. 2. Soft tissue dissection will be more difficult and requires precise establishment of tissue planes. 3. Release all soft tissue from the joint – will help to determine of the deformity is positional, structural or both. 4. Release the medial capsule. V shaped capsulotomy is ideal for this. 5. Tenotomize the abductor hallucis tendon if it is contributing to the deformity. 6. Evaluate the IM angle and the PASA at this point. 7. Choose osseous procedure based on which procedure was performed before, length of the 1st metatarsal and the amount of correction needed. 8. If the tibial sesamoid is dislocated, relocation should be attempted. If this fails, remove the sesamoid and fuse the HIPJ. Taken from: Zahari & Girolamo. Hallux varus: a step-wise approach for correction. JFAS, 1991. 30(3):264 – 266.

Questions about Tarsal Tunnel Syndrome 1. What are the contents of the tarsal tunnel? - Tibialis posterior tendon - Posterior tibial artery - Posterior tibial nerve - Posterior tibial companion veins - Flexor digitorum longus - Flexor hallucis longus 2. Name some of the specific nerves that can be affected by tarsal tunnel syndrome. - Medial plantar nerve - Lateral plantar nerve - Nerve to the abductor digiti minimi (Baxter’s nerve) - 1st branch of the lateral plantar nerve 3. What are the attachments of the flexor retinaculum? - medial malleolus & medial surface of the calcaneus blending with plantar aponeurosis 4. Where does the bifurcation of the tibial nerve usually occur? - deep to the flexor retinaculum - a variety of branching patterns have been described; rarely does it branch proximal to the retinaculum 5. What are the borders in all directions as the tibial nerve courses under the flexor retinaculum? - superficially: the flexor retinaculum - deep: the medial side of the talus, sustentaculum tali, medial side of the calcaneus - superiorly: the deep aponeurotic fascia of the leg - inferiorly: the abductor hallucis muscle 6. Name ten etiologies of tarsal tunnel syndrome. - trauma (fracture, ruptured tendon) - varicosities (engorgement of the veins) - hypermobile flat foot - idiopathic tight tarsal canal - obesity - space occupying lesion - hypertrophic abductor hallucis muscles - RA - Diabetes - Post surgical fibrosis - Accessory FDL muscle

7. What two athletes have been cited as having a high incidence for tarsal tunnel syndrome? - long distance runners - jockeys: forced eversion against a flat foot while in stirrups 8. What are some conservative options for treatment? - Orthoses - NSAIDs - Injection with local anesthetic or corticosteroids - Ice - Physical therapy - Stretching exercises 9.What is anterior tarsal tunnel syndrome? - compression of the deep peroneal nerve within the fibro-osseous tunnel created by the inferior extensor retinaculum 10. What are the contents of the anterior tarsal tunnel? - deep peroneal nerve - dorsalis pedis artery and veins 11. Name some causes of anterior tarsal tunnel syndrome excluding those mentioned before. - tight laced shoe gear - osteophytes at the ankle or talonavicular joint - pt with cavus feet 12. Why is that the symptoms in a patient with anterior tarsal tunnel syndrome are accentuated during sleep? - foot drops into plantarflexion during sleep 13. Name the three types of nerve injury according to Seddon. a. Neuropraxia: physiological disruption rather than anatomic disruption. Often caused by compression and distortion of the myelin sheath and a transient loss of salutatory conduction. Some common causes are contusions, hematoma, unreduced fracture or dislocation pressure, iatrogenic. There is usually full recovery of nerve function. b. Axonotmesis: Anatomic disruption of the axon without disruption of the endoneurial tube. Axon undergoes Wallerian degeneration where the axonal material distal to the site of injury degenerated. Since the endoneurial tube is intact regeneration is possible. c. Neurotmesis: Anatomic disruption of the axon and the endoneurial tube and is usually irreversible 14. Name two iatrogenic causes of neuropraxia. - tourniquet - cast

15. Name the stages of Sunderland’s classification of nerve injury. - 1st degree: neuropraxia - 2nd degree: axonotmesis - 3rd degree: loss of axon and endoneurium with intact perineurium - 4th degree: 3rd degree plus loss of perineurium with intact epineurium - 5th degree: complete loss of entire nerve trunk 16. Name the two major types of nerve repair (neurorrhaphy) a. epineurial repair: suture the epineurium together - try to orientate the fascicles as closely as possible - advantages include technical ease, short OR time, minimal Rahimi (magnification) requirements b. fasicular (perineurium) repair: suture the perineurium together - this offers the potential for a better alignment of fascicles - disadvantages include the need for greater Rahimi requirements, longer surgical time, an increased potential for intraneural fibrosis

Chronic Lateral Ankle Instability Etiology Inversion injuries of ankle a. Most common soft tissue injury b. Athletes i. 16 – 21% of all athletic injuries ii. Basketball – 43% of injuries iii. Soccer – 31% of injuries iv. Running and jumping sports – 25% Proper diagnosis in the acute injury is critical c. Inadequate treatment = poor healing and chronic instability Anatomy Anterior talofibular ligament a. Intracapsular b. Origin: distal anterior fibula c. Insertion: body of the talus – anterior to articular facet Calcaneofibular ligament d. Extracapsular i. Confluent with peroneal tendon sheath e. Origin: anterior border of distal malleolus below the origin of the ATFL f. Insertion: lateral body of the calcaneus superior to peroneal tubercle Posterior talofibular ligament g. Intracapsular h. Origin: medial surface of lateral mallelous i. Insertion: broad, majority of posterior lip of talus Pathology of the Chronic Lateral Ankle Instability - Undiagnosed or untreated acute ankle sprains - Chronic ankle sprains - Leads to scarred or elongated ligamentous structures Diagnosis – Clinical Evaluation History a. Ankle ‘giving way’ b. Recurrent acute ankle sprains c. Restricted physical activity as a result of pain Physical Exam a. Positive anterior drawer test – ATFL b. Positive inversion stress test i. Sulcus between talus and lateral malleolus (sucking sign) c. Anterior and lateral aspect of the lateral malleolus ii. Tenderness iii. Chronic edema

Diagnosis – Radiographic Evaluation Routine radiographs a. AP, lateral and mortise Stress radiographs – Bilateral b. Talar tilt (inversion stress) i. Tests CFL ii. Normal up to 4 – 7 degrees iii. 5 degrees greater than contralateral side is pathological c. Anterior drawer i. Tests ATFL ii. Greater than 4 mm displacement is positive Classification of Lateral Ankle Sprains Anatomic System a. Grade I: ATF sprain b. Grade II: ATF and CF sprain c. Grade III: ATF, CF and PTF sprain AMA standard nomenclature system d. Grade 1: Ligament stretched e. Grade 2: Ligament partially torn f. Grade 3: Ligament completely torn Treatment Options Conservative a. Activity and shoe modification i. Lateral heel wedge, lowering heels, stiff soles b. Orthotics with lateral heel wedge c. Aircast, ankle corset, strapping d. Peroneal strengthening exercises e. Jones compression dressing f. RICE g. NSAIDs Surgical a. Success of conservative therapy b. Degree of ankle instability c. Activity level d. Compliance e. Surgical risk factors f. Primary repair or not primary repair i. Degree of ligament scarring and elongation ii. How old is the instability? g. Drill hole difficulty h. Tendon harvest length i. Single ligament repair vs double ligament repair j. Regional anatomy considerations iii. Intermediate dorsal cutaneous nerve iv. Sural nerve v. Small saphenous vein vi. Peroneal tendons

Surgical Goals: Restore proper geometric alignment of the ligaments Restore mechanical and functional stability to the lateral side Full ROM Surgical Management – Primary Repair of Ligaments - Brostrom – 1966 - Modified Brostrom – 1980 - Arthroscopic repair – 1985 (Lundeen) Surgical Management – Replacement of Ligaments - Nilsonne – 1932 - Elmslie – 1934 - Hambly – 1945 - Evans – 1953 - Winfield – 1953 - Watson-Jones – 1955 - Lee – 1957 - Christman and Snook – 1969 - Kelikian and Kelikian – 1985 - Split peroneus brevis lateral ankle stabilization Brostrom – 1966 - Imbrication of ATFL and CFL - Gold standard for procedure comparison - Reported satisfactory results in 85% of patients - Disadvantage: difficult to expose and suture torn ends due to scarring and elongation of the ligaments - Summary: anatomic reapproximation of the ATF and CF with possible ATF augmentation utilizing the lateral talocalcaneal ligament. ATF is not incised during the capsular incision. - Brostrom’s Logic for anatomic reconstruction: “previously used tenodesis operations are technically fairly complicated, that the healing time is long, that the normal anatomy is not fully restored, that increased stability is obtained at the price of diminished supination mobility , that they are unsuitable in children because of the risk of epiphyseal damage, and that in most cases they entail weakening of the peroneus muscles.” - Original article citation: Brostrom, Lennart. Sprained ankles VI. Surgical treatment of “chronic” ligament ruptures. Acta Chir Scand 132: 551-565, 1966. Modified Brostrom (Gould & Seligson) – 1980 - Imbrication of the inferior extensor retinaculum to reinforce repair - Suture whatever one can find - Reinforcing the ATF ligament repair with overlap of lateral talocalcaneal ligament plus inferior extensor retinaculum - 30 minute procedure - Small incision - Summary: Anatomic reconstruction/reapproximation of the lateral ankle ligaments with the use of the inferior extensor retinaculum for augmentation.

Modified Brostrom Procedure – 1994 o 1994, JFAS, Paden, Stone & McGarry from PSL Denver CO o Indications: Chronic lateral ankle instability o Summary: anatomic reconstruction of the ATF and CF (possibly) that differs from the original Brostrom in that 1) the ATF is incised during the capsular incision; 2) Mitek anchors are used and 3) lateral talocalcaneal ligament is not used for augmentation of the ATF. Arthroscopic Primary Repair - Intracapsular staple fixation to lateral aspect of talar dome - Standard lateral and medial portal with a third portal directly over AFTL for staple insertion - Subchondral bone denudation must be obtained for staple to hold Nilsonne – 1932 - Repair of ATF - Detach PB at musculotendinous junction - Suture in subperiosteal groove in lateral aspect of lateral malleolus - Does not recreate normal anatomical orientation of ATF Elmslie – 1934 - Repair of ATF and CF - Tensor fascia lata graft - Osseous canal in talar neck, lateral malleolus and lateral body of the calcaneus Hambly – 1945 - Repair of ATF and CF ligaments - Split PL - Suture to the lateral talar neck, pass through fibula anterior to posterior and fixated to CF ligament insertion Haig – 1950 - Summary: Used the bony attachment of the anterior inferior tibiofibular ligament to reinforce the ATF. Evans – 1953 - Summary: Peroneus brevis cut proximally and musculotendinous junction and passed through fibular drill hole from anterior-inferior to posterior-superior. Tendon sutured to the posterior fibular periosteum. Winfield – 1953 - Summary: Peroneus brevis tendon through osseous fibular tunnel, passed through calcaneal osseous tunnels and sutured to itself. Pouzet – 1954 - Summary: Peroneus longus tendon cut proximally, routed through the fibula from anterior to posterior and sutured back onto itself.

Watson – Jones – 1955 - Repairs ATF ligament - Detach PB at musculotedinous junction - Two holes in fibula in posterior superior direction - Trephine hole in the lateral talar neck - Route PB through superior fibular hole, talar trephine, inferior fibular hole - Suture tendon to itself Lee – 1957 - ATF ligament repair - Modification of Watson – Jones because of technical difficulty and need for excessive tendon length - One hole in fibula - Tendon is entered posteriorly to anteriorly and sutured to PB and PL tendons distally Storen – 1959 - Summary: Two stages. First stage utilized the medial 1/3rd of the tendo Achilles to pass posterior to anterior through the fibula and the talar neck from superior to inferior and sutured to the bifurcate ligament. Second stage cut the medial 1/3rd of the tendo Achilles at its attachment to the calcaneus and rerouted this proximally superficial to the peroneal tendons and into the calcaneal attachment of the CF ligament. Casting & Meunier – 1961 - Summary: Modification of the Lee. Peroneus brevis is rerouted in a more oblique fashion through the fibula (posterior inferior to anterior superior). Christman and Snook – 1969 - ATF and CF repair - Modification of the Elmslie - Split PB - Trephine hole in lateral talar neck, hole in fibula, trephine in lateral calcaneus - PB through talar neck, through fibula anterior to posterior through calcaneal trephine posterior to anterior - Remaining tendon directed anteriorly and sutured to PB Kelikian & Kelikian – 1985 - ATF and CF ligament - Plantaris tendon - Insertion intact - Drill hole from CF ligament towards the plantaris, fibula from anterior to posterior, trephine hole in lateral talar neck - Plantaris passed form posterior to anterior lateral calcaneus, through fibula posterior to anterior, through talar neck, through fibula anterior to posterior suture on itself. - 7 – 18% of population has absent plantaris

Split Peroneus Brevis Lateral Ankle Stabilization - ATF and CF ligament - Split PB at musculotedinous junction - Subperiosteal channel created in talar neck - Trephine hole anterior to posterior fibula and lateral calcaneal wall - Route tendon subperiosteally through talar neck, through fibular trephine anterior to posterior, through calcaneal trephine - Suture tendon to itself Common Procedures - Watson-Jones, Evans, Christman & Snook are the most widely used procedures and have a high rate of success - Disadvantages: • Do not place graft in anatomically correct position • Loss of eversion & plantarflexion due to use of peroneus brevis • Extensive surgical exposure Post – Op Care - 10 – 12 weeks of protection - NWB BK cast 4 – 6 weeks - WB BK cast 3 weeks - Physical therapy modalities and strengthening following cast removal Summary - Repair of ATF ligament only • Modified brostrom • Nilsonne • Evans • Watson Jones • Lee - Debate of only one vs two ligaments repair • ATF is the primary lateral stabilizer -

-

ATF and CF Repair • Brostrom • Elmslie • Hambly • Winfield • Christman and Snook • Kelikian and Kelikian • SPBLAS Full Tendon Graft • Nilsonne • Evans • Winfield • Watson-Jones • Lee • Kelikian & Kelikian

Ankle Fractures Oblique fracture: produced with combined loading of compression and torque. Usually a 45 degree fracture orientation. This is considered to be unstable and is usually fixed with ORIF Spiral fracture: this is always a type of torque fracture. It usually takes a 360 degree course with a vertical connecting segment between the two opposing sharp spikes of the fracture. This is also usually orientated at 45 degrees Comminuted fracture: this suggests the presence of two or more fracture planes and has at least three fragments. This is usually due to very high velocity loading, it is a high energy failure with load concentration over a small area of the bone. Eponyms for Fractures Percival Pott (1768): Described a fibular fracture 2 – 3 inches proximal to distal aspect fibula with a deltoid ligament fracture and an intact syndesmosis. Now: bimalleolar fracture Dupuytren (1819): Described a medial deltoid ligament tear or a medial malleolar fracture with a fibular fracture 2.5 inches proximal to most distal aspect of the fibula with diastasis always being present. Maisonneuve (1840): The New House fracture. Fracture of the proximal 1/3rd of the fibula. LeFort (1886): Described a vertical fracture of the fibula due to SAD type forces. Chaput – Tillaux (1872): In 1872 Tillaux described a medial deltoid injury or medial malleolar fracture, a fibular fracture 2 inches proximal to the ankle joint, AND an anterior lateral tibial tubercle fracture. In 1907, Chaput conducted laboratory studies of this fracture which is why the fracture of the anterior lateral tibial tubercle contains both names. Wagstaffe (1873): Distal fibular fracture due to avulsion of the anterior inferior tibialfibular ligament. An SER type injury. VonVolkman (1875): Originally described as an anterior lateral lip of the fibula fracture due to avulsion of the anterior tibial-fibular ligament and interosseous membrane due to PAB type forces. Now: posterior lateral tibial fracture Cotton (1915): Described a posterior malleolar fracture with a medial malleolar fracture and a fibular fracture just proximal to the joint level. Trimalleolar fracture.

Correlating Danis-Weber and Lauge-Hansen Danis—Weber

Lauge—Hansen Category SAD

Where to start the LH Clock Start lateral

SER

Start anterior and central

PAB

Start medial

PER

Start medial

A – fracture of fibula distal to the level of the ankle joint

B – fracture of the fibula originating at the level of the ankle joint

ALWAYS ask for a lateral film!!!!!

C – Fibular fracture originating proximal to the ankle joint mortise

Lauge—Hansen Type 1 – lateral ankle ligament injury – or – transverse fibular fracture distal to the level of the ankle joint 2 – near vertical fracture of the medial malleolus 1 – rupture of the anterior inferior tibial-fibular ligament 2 – fibular fracture with posterior spike 3 – rupture of the posterior tibial – fibular ligament 4 – fracture of the medial malleolus 1 – deltoid ligament rupture or medial malleolar fracture 2 – anterior tib-fib ligament rupture with posterior tibial fracture 3 – Danis Weber B fracture 1 – medial malleolar fracture or a deltoid ligament rupture 2 – anterior inferior tib-fib ligament rupture 3 – high fibular fracture 4 – posterior tib-fib ligament rupture or posterior malleolar fracture

Questions Related to Ankle Fractures 1. What is the big difference between a SER type fracture and a PAB type fracture? SER has a posterior fibular spike while a PAB has a posterior tibial fracture 2. What fragment do you reduce first during ORIF of an ankle fracture? The fibular fracture 3. How do you perform Cotton’s test and what does it signify? After fixating a fibular fracture, use a large bone hook to pull the fibula laterally. If everything moves, the test is negative. If only the fibula moves, the test is positive and indicates that the syndesmosis is torn or not intact. If this is the case, you would use a syndesmotic screw or a mini tightrope to fix this problem. 4. What do the two words of the Lague-Hansen classification system signify? The first word is the position of the foot at the time of injury. The second word is the direction of the deforming force or the direction the talus moves in the mortise. 5.What is the Danis-Weber classification system based on? The anatomic position of the fibular fracture in relationship to the tib-fib syndesmosis 6. You are called to see a patient in the ER. The ER nurse tells you in a stressed out near hysterical voice that this patient has a transverse fracture of the fibula and a near vertical fracture of the medial malleolus. What type of fracture is she describing? SER 2 or Danis Weber A 7. At what stage of the SER injury, would you see a Wagstaffe fracture? SER 1 8.When does a posterior malleolar fracture need to be fixated? If the fracture involves 25 – 30% of the articular surface 9. Apply Vassal’s principle as it applies to the ankle joint. When you reduce and fixate the fibular fracture to the appropriate length, the talus should fall back into the mortise. This doesn’t always work perfectly for the medial malleolus. 10. Who wrote the original article relating the displacement of the talus in the mortise and the affect of this displacement on the ankle joint congruity? What did this article conclude? Ramsey and Hamilton. JBJS. 1976. This article concluded that 1 mm of lateral displacement of the talus leads to a 42% reduction in contact area of the ankle joint. Meaning: reduce your freaking fibular fracture.However, when doing their cadaveric experiments, they removed all soft tissue from around the ankle joint and did not allow the talus to compensate for being displaced. More recent studies have indicated that the talus tends to move back into the mortise when compressed if allowed to do so.

AO Fixation Stress risers: areas of concentrated stress which can predispose the segment to fracture. This can be caused by screw holes, bone graft excision, entrance points of blood vessels, tumors or iatrogenic damage to the bone. AO Principles of Internal Fixation atraumatic operative technique accurate anatomic reduction rigid internal compression fixation early and pain free ROM Dynamic v Static Interfragmentary Compression Dynamic: achieved with the use of a tension band wire or tension band plate Static: generated by ‘pre load’ of lag screws or tubular plates that prevent separation of two surfaces as long as the functional load produced by limb performance is less than the preload generated by the screws or plates. The compression is constant in nature. This can also be accomplished by rigid external fixation. Interfragmentary compression usually requires multiple screws. Proximal anchor screw (perpendicular to the cortex of the bone) and the distal compression screw (perpendicular to the osteotomy site). Pauwels principle (tension band principle): an imposed load applied eccentrically is altered by application of a ‘band’ on the opposing side, canceling out bending and altering it into pure compression. This principle is dynamically created by functional limb loading. (ex putting a plate on the tension side of a fracture) Load screw technique: This technique is performed by using an offset (eccentric) drilled hole for the initial screws used to fixation the plate to the fracture fragments. The plate is aligned on the reduced fracture site, the thread hole is drilled at the far side of the plate hole or at the edge of the hole farthest from the fracture site. As the screw is inserted, the head of the screw will seat itself into the center of the hole in the plate by shifting the bone fragment in the direction of the fracture. This motion is countered by a similar shift from the opposite fragment, and as the two fragments are pushed toward each other, interfragmental compression is created. Only the initial two screws adjacent to the fracture line are used as load screws. This is the most common application of plate fixation used in the foot and ankle region. ½, 1/3, ¼, tubular plates have great tensile strength but do not resist against bending. Application of a pate plus interfragmentary compression with screw is a great way to created rigidity within the fracture area. Prebending the plate: This is used so the cortex opposite the plate does not gap. The offset holes are drilled before the plate is bent. The plate is bent slightly at its center. As the load screws are inserted, the bone fragments are drawn up against the undersurface of the plate, and the opposite

cortices come into contact before the surface of the fracture that is adjacent to the plate. As the load screws are tightened, the fragments are drawn closer together and the gap at the adjacent cortex decreases. As the gap reduces, the plate is bent back into a straightened position with even contact and pressure existing along the entire fracture surface. The load screw concept and the technique of prebending are fundamental principles from the creation of axial compression with plate fixation. Types of Plates Neutralization: Allowing the pathologic forces to be ‘transmitted’ through the implant (plate) rather than through the fracture interface, thus the plate takes the strain rather than the fracture (as in a neutralization plate for a fibular fracture.) This is a protection plate. The difference between a neutralization plate and a buttress plate is the way in which the plate is used. Buttressing: Used to ‘hold together’ a comminuted fracture. May times this is used in the metaphyseal area of long bones since they fail in a more random fashion than cortical bone. Dynamic compression plate: DCP incorporates the load screw technique with the added effect of geometrically designed slots within the body of the fixation plate. This plate is significantly thicker and stiffer than tension plates. DCP is suitable for a solitary fixation device for a transverse fracture. There are individual DCP for use with 4.5 mm, 3.5 mm and 2.7 mm cortical screws. The major problem with the DCP is an alteration in periosteal blood supply. This is due to contact of the undersurface of the plate for extended periods of time. Also, these plates are thick and may cause hardware irritation problems. Limited Contact Dynamic Compression Plates (LC-DCP): These plates have grooves on the underside of the plates so that the blood supply to the bone is not impaired. Lag screws: When the screw is placed across the failure plane so that its threads do not contact the near cortex side of the bone. Thus the threads of the screw will only purchase the far or distal cortex and pull the two surfaces together when the undersurface of the screw head contacts the proximal bone cortex. This is a principle and results from the use of the screw, not the design of the screw. Types of Internal Fixation K wires Monofilament wires Steinmann pins Intramedullary nails (rods) Screws Staples Plates

Herbert Bone Screw - headless screw that is threaded at both ends - proximal threads have a smaller pitch than the distal threads - this pitch difference provides compression between adjacent bony fragments - screw diameter is 4 mm - just need to tap the distal threads (proximal threads are self tapping) Reese Arthrodesis Screw: - design to provide greater compression across fusion site - clockwise (right handed) screw threads proximally and counterclockwise (left handed) threads distally Plate Sizes: semi tubular plate: fits 4.5 mm screws one third tubular plate: fits 3.5 mm & 4.0 mm one quarter tubular plate: fits 2.7 mm screw posterior anti-glide plate a. placed posteriorly on the fibula b. indicated for Danis-Weber type B fracture c. why? These fractures tend to displace posteriorly and superiorly d. the plate will resist the displacement and provide some compression External Fixation 7 Principles of Callus Distraction (some of these principles are relative to the particular anatomical correction) 1. Preservation of blood supply - atraumatic corticotomy 2. Rigid external fixation 3. Latency period before distraction - usually 7 – 14 days; allows 1st stage of bone healing to begin 4. Steady rate of distraction - about 1 mm / day 5. Ideal frequency of distraction - about .25 mm per turn (4 turns per day) 6. WB on limb during distraction 7. Post distraction healing time - for every 1 mm of lengthening you must rest for 1 week General Advantages • applicable to closed, open or limited open surgical techniques • device can be conformed to the shape of the leg and foot which will allow multifunctional correction • allows acute or gradual lengthening • can be adjusted post operatively • can be stable enough to permit early weight bearing General Disadvantages • Disliked by patients • Disliked by surgeons • Lengthy treatment time • Increase risk of infection compared to internal fixation (ex: pin tract infections) Largest role in foot & ankle surgery is with pilon fractures

Types of External Fixators Circular a. Ilizarov frame b. Taylor spatial frame i. Six color coordinated knobs ii. Radiographic parameters put into a computer iii. Knobs are turned to a certain number each day according to the computer calculations iv. New device Monolateral a. Orthofix b. Hidleburg c. Hoffman Hybrid a. Combination of the ilizarov and monolateral frames Functions of External Fixators 1. compression 2. distraction a. new bone that is formed is called the regenerate 3. angulation 4. translation 5. rotation Dynamimzation: process by where stress is gradually applied to the new bone that has formed so that the trabecular bone will remodel according to Wolf’s law making the regenerate strong and suitable for weight bearing without the device. This is initially done by loosening up the device gradually. If the is not done the regenerate will fracture very easily. Corticotomy (osteotomy) can be done differently • Osteotome (classic iliazarov method) • Pre-drilling and osteotome • Gigli saw method The Ilizarov method consists of passing numerous perpendicular wires through the bone at regular intervals and attaching them to the external rings and bars to stabilize the bone segment. This configuration makes it possible to move bone at a specific rate and frequency, while simultaneously providing rigid fixation of the adjacent bone for ambulation. The Ilizarov technique is called the callous distraction method (distraction histiogenesis). While rigid stabilization of two ends of a long bone is provided, the bone itself may be lengthened to correct a short extremity. Rapid healing takes place in the site from which the bone was stretched. This technique requires only a few small holes in the skin large enough for the passage of a small osteotome. This narrow, chisel-like tool is used with a mallet to cut circumferentially the cortex of the bone. Such a corticotomy leaves the marrow space intact. The low tensile strength of this portion of the bone allows it to be easily stretched. The blood supply to the segment is ‘transported’ 1 mm/day as the patient turns the screw on the device. As the cortex moves apart, rapid cortical healing takes place. The results in new bone formation at the donor site and in a longer extremity. The basis for 1 mm/day is so the neurovascular bundles aren’t acutely stretched and so the cortical bone can heal as distraction occurs.

Specific uses of external fixation in the lower extremity • non unions • trauma (pilon fractures, etc) • osteomyelitis (useful when large amounts of bone is resected) • lengthening (tibial, metatarsal) • arthrodesis (ankle, subtalar) - advantages: 1) longer lever arm than internal fixation; 2)post-op adjustability • correct malunions • severe deformities (clubfoot, etc) • joint preservation o re alignment of arthritic joints • supramalleolar osteotomy to realign the ankle joint o the anterolateral aspect of the ankle joint is the most loaded part and is usually where arthritis will begin o distraction of arthritis joints can decrease pain, though no studies have show that articular cartilage will regrow o CORA: center of rotation of angulation  Osteotomy at this point will lead to a full realignment of the foot & ankle

Bone Grafting in the Foot and Ankle Two basic types of bone grafts Cancellous • Used to fill smaller defects • Cancellous bone typically has superior osteogenic potential • Osteoinductive in nature; to some extent osteoconduction • Large amount of viable cells and proteins that increase the bone induction potential  Bone morphogenic protein (BMP) is present in bone matrix that acts as an inductor substance • Initially describe by Marshall Urist in the early 70s • Now is being produced through recombinant gene technology • They incorporate quicker than cortical graft • They are radiodense as they heal Cortical (structural) • generally used to fill large defects or where structural segments of the WB axis of the RF are missing (talus, calcaneus, tibia) • marked higher structural strength • osteoconductive in nature • can be obtained from the iliac crest, proximal tibia, distal tibia and fibula • after grafting, there is resportion of the graft during revascularization but some structural integrity usually remains during the process of bone graft incorporation to allow the graft to withstand the loads of weightbearing • since some osteoclastic resorption must precede osteogenesis, cortical graft will appear radiolucent • slower to incorporate compared to cancellous graft Osteoconductive: Osteo" means "bone". Osteoconduction refers to the ability of some materials to serve as a scaffold on which bone cells can attach, migrate (meaning move or "crawl"), and grow and divide. In this way, the bone healing response is "conducted" through the graft site, just as we say that electricity is conducted through a wire. Osteogenic cells generally work much better when they have a matrix or scaffold to attach to. Associated with the term creeping substitution. Osteoinductive: Induction of bone formation refers to the capacity of many normal chemicals in the body to stimulate primitive "stem cells" or immature bone cells to grow and mature, forming healthy bone tissue. Most, but not all of these signals are protein molecules called, as a group, "peptide growth factors" or "cytokines". Many of these growth factors are present in normal human bone. For this reason, methods have been developed to process human bone and prepare bone matrix which retains the normal growth factors, but limit, if not eliminate, the risk of transmitting diseases or viruses. "Allograft Bone" processed in this way is currently the only approved way in which surgeons can use an osteoinductive stimulus. Corticocancellous bone graft: combination of cortical and cancellous graft. This is the optimal graft to use in the foot and ankle. Tricortical graft taken from the iliac crest is an example of this. The choice of which bone graft to use depends on the biologic and mechanical properties of the graft required. Autograft: viable bone tissue taken from one area of the host and implanted into another

Allograft: non living bone graft from someone other than the host. - only functions as a substrate for osteoconduction - several types • frozen allograft • freeze dried allograft • demineralized or decalcified allograft • artificial allograft Techniques of Bone Grafting 1. onlay bone graft technique - uses large amount of autogenous cortical bone graft to bridge a non-union - graft is fixated with screws or wires - Phemister described an onlay graft which was not fixated - this technique is inferior to other because it doesn’t provide rigidity in the area 2. inlay bone graft technique - formation of a slot or window in which the bone graft is placed 3. sliding bone graft technique - create a graft from the shaft of a long bone - slide the graft across the non-union or arthrodesis site 4. papineau bone graft technique - originally described for treatment of chronic osteomyelitis and infected non-unions - involves three steps: 1. excision of necrotic bone 2. cancellous bone graft 3. skin coverage - this technique was designed for rapid revascularization Locations for autogenous bone graft Iliac crest: corticocancellous and cancellous bone can be harvested from this area Proximal tibia: excellent source for both cortical and cancellous bone; two locations are used: a) over the tibial tuberosity and b)over the anterior medial tibia Distal tibia: source of single cortical struts and cancellous bone; the amount of bone obtained from the area is limited Fibula: strictly used as a cortical strut; can be harvested as a vascular bone with the nutrient artery and vein intact Calcaneus: both cortical and cancellous bone can be obtained Other sites: navicular tuberosity, medial eminence of the 1st MT, phalangeal bone from arthroplastic procedures

Random Questions 1. Name as many classifications as you can for osteomyelitis as you can and explain them Waldvogel - hematogenous - contiguous focus - osteo secondary to PVD - chronic Cierny – Mader Anatomic Stage I: medullary II: superifical III: localized IV: diffuse

Physiologic Stage A: good systemic defense & local vascularity B: systemic & local compromise C: non candidate for surgery with tx increasing morbidity and mortality than non treatment

Buckholtz 7 surgical classifications for osteo I: wound induced II: mechanicogenic infection (implants) III: physeal osteo IV: ischemic limb disease V: combination (I – IV as acute osteo) VI: osteitis with septic arthritis VII: chronic osteo 2. What are the 5 D’s for the treatment of infection? Debridement Decompressions Drainage Dressings Drugs 3.What is the D-dimer assay used for? This is a new way to detect PE and more recently DVT. D-dimer is a fragment that is specific for the degradation of fibrin. (Barbe et al Am J Clin Path 1998) 4. Name 5 causes for bilateral edema. CHF Protein deficiency Prolonged standing Chronic venous valve insufficiency Myedema Drugs (corticosteroids, NSAIDs, BCP, Abx with increased sodium) Pregnancy

5. Name 5 causes for unilateral edema. Venous obstruction (DVT, post phlebotic syndrome) Lymphatic obstruction Infection Trauma Tumor Previous surgery Popliteal aneruysm Charcot AV fistula Milroy’s disease (swelling secondary to lymphatic obstruction) Filariasis Baker’s cyst Retroperitoneal fibrosis 6. Name the stages of wound healing. Inflammatory: PMN predominate Features – hemostasis, debridement, decontamination of the wound Day 3 – 4 Fibroblastic or Proliferative: macrophages predominate Features – collagen synthesis, neovascular formation, repithelialization Day 3 – 4 to day 14 – 21 Maturation or Remodelling: Features – remodeling and reorganization of collagen bundles; wound contraction, increase tensile strength Week 3 post injury to 1 yr post injury 7. What is Charnley’s description of closed reduction? Recreate the deformity Distract Reduce the deformity and realign Maintain correction with immobilization 8. What disease is the CREST syndrome associated with and what does it stand for? Associated with Scleroderma (systemic sclerosis); this syndrome occurs in the limited form of the disease C: calcinosis R: raynaud’s phemenon E: esophygeal dysmotility S: sclerodactyly T: telangectasia 9. What are the phases of bony healing? Inflammatory Reparative Remodelling

Secondary bone healing has been said to heal in six phases: Hematoma formation Hematoma organization Fibrocartilagenous callus Primary bone callus Primary bone callus resorption Remodelling (maturation) 10. Name the layers of skin. Stratum basale (germinativum) Stratum spinosum Stratus granulosum Stratus lucidum Stratus corneum 11. What clinical conditions occur in each stage of syphilis? Primary: chancre Secondary: skin lesions that resemble many other diseases (the Great Masquerader) Tertiary: tabes dorsalis, CNS effects, neuropathy 12. What is the Jarisch-Herxheimer reaction? This occurs when patients are being treated with antibiotics (Lyme disease). During the initial 24 hours of therapy, the patient becomes sicker with worsening of the symptoms. This is due to the massive destruction of the bacteria and the release of toxins into the blood as the bacteria dies. This can also occur in any treponemal infection (Syphillis) 13. Name 5 anaerobes. Clostridium Peptostrepococcus Fusobacterium

Bacteroides Peptococcus

14. If a pt is taking Rifampin and notice a red color in their urine, should they be worried? No, this is a normal side effect. Rifampin may turn body fluids red 15. Name 5 gas forming organisms. Bacteroides Clostridium Staph/Strep Fusobacterium Peptococcus

Escherichia Klebsiella Serratia Peptostrepococcus

16. Which side effect seen in aminoglycoside therapy is reversible? Kidney function

17. What are the peaks and troughs for gentamycin and vanco and what do they tell you? Gentamycin Trough – 2 Peak – 10 Vancomycin Trough – 10 Peak – 20 The peak gives information regarding the amount of the dosage The trough gives information regarding the timing of the dose (frequency) 18. Name all of the beta-lactamase penicillins and their dosages Augmentin (amoxicillin/clav) 250, 500, 875 mg PO (500 TID; 875 BID) 75 mg amoxicillin 125 mg clavulanic acid Timentin (ticracillin/clav) 3.1 g IV q6-8h 3 g ticracillin 100 mg clavulanic acid Unasyn (ampicillin/sulbactam) 1.5/3.0 g IV q6-8h 2:1 ratio Zosyn (pipercillin/tazobactam) 3.375 IV q6h –or—4.5 g IV q8h Pipercillin 3g Tazobactam 0.375g 19. Name some treatments for MRSA and VRE. MRSA: Vancomycin, Zyvox, Bactrim/Rifampin, Cipro/Rifampin, Minocycline VRE: Zyvox, Syndercid, Amp/Aminoglycoside 20. What is the characteristic color pattern in Raynaud’s phenomenon? White-blue-red 21. Explain the glucose tolerance test. Pt ingests 75 g of oral glucose. Blood sugar is tested at 0, .5, 1, 1.5 and 2 hours after ingesting. If the reading at 2 hrs and 1 other measurement is >200mg/dl then diabetes can be diagnosed. 22. Name 5 Disease modifying anti-Rheumatic drugs (DMARDS) Methotrexate Gold salts Penicilliamine Axathioprine Sulfasalazine Leflunonide 23. What is the hallmark of ankylosing spondylitis? Bilateral sacro-illitis (bamboo spine) 24. What is the half life of Tc-99, Gd and Indium? Tc 99 – 6 hours Gd – 79 hours Indium – 67 hours

25. What is the major distinction between Roussy-Levey Syndrome and CMT? Essential tremor expressed primarily in the hands (RLS) 26. What are the three stages of RSD? 1. Acute: hyperemic; lasts 1 – 3 months 2. Dystrophic: ischemic; lasts 3 – 6 months 3. Atrophic: 6 – 9 months 27. What are the three types of biopsy? - Shave: not commonly done - Incisional: usually a punch biopsy; done to remove a section of the lesion; pick the most aggressive appearing part of the lesion - Excisional: removal of the entire lesion 28. What are the four main types of malignant melanoma? - superficial spreading: the most common type - lentigo: most commonly seen in older men - acral lentiginous: see Hutchinson’s sign (color changes in the eponychium of subungual melanomas): most common in non-caucasians - nodular: the most malignant type 29. What are the three radiographic patterns of bone destruction? Geographic Moth eaten Permeative 30. Name types of periosteal reaction. Single layer Onion skin Codman’s triangle Velvet Sunburst Perpendicular (hair on end) 31. 5 D/Dx for chest pain. MI PE Angina Heartburn Pneumothorax Cardiac tamponade

Aortic dissection Aortic aneurysm Pericarditis Herpes Zoster Musculoskeletal pain

32. What is Felty’s syndrome? RA, splenomegaly, neutropenia

33. Which specific ascending pathway is responsible for vibratory, pressure, light touch and conscious proprioception? Dorsal column medial lemniscus 34. What is responsible for pain, temp, light touch and itch? Anterolateral spinothalamic tract

Social questions 1. What 5 adjectives would you use to describe yourself? 2. Tell me about yourself. 3. Why didn’t you choose a hard science major? Why ? 4. Why do you want to work here? 5. Why should we pick you over another applicant? 6. Are you married/single? 7. Do you have any questions? 8. Who is forcing you to become a podiatrist? 9. Why should we not take you for our program? 10. If we accepted you, how would you contribute? 11. Who do you respect most in podiatric medicine? 12. What do you know about me and my career? 13. What non-medical books have you read recently? Why those? What did you learn from it? 14. Would you sleep with anyone to get this residency? 15. There’s room for only 3 residents in this program…why should we pick you? 16. What are you worst attributes? 17. How do you feel about us reviewing your qualifications tonight over a drink? 18. Have you visited our program/facility before? Why or why not? 19. What do friends say behind your back? 20. How would your best friend describe you? 21. Who did you vote for President? Do you think that was a good decision? 22. What is your strongest quality? 23. What current movies describe your approach to life? 24. When you’re not studying, how do you relax? 25. What’s your GPA? Are you satisfied with that? 26. What do you like best about podiatric medicine? 27. What do you like least about podiatric medicine? 28. What is your favorite podiatric subject? Explain. 29. With which recreational drugs have you ever experimented? 30. What do women do better than men? 31. What do men do better than women? 32. What makes our program special compared to others? 33. How much time do you spend with your family? 34. If you weren’t a podiatrist, what other career path would you have pursued? 35. Do you prefer working alone or as part of a team? 36. What was your last complete medical check-up and what did they find? 37. What new skills have you developed over the past year? 38. What epitaph would you want inscribed on your tombstone? 39. What is your favorite TV program and why? 40. What mistakes have you made in your life that you really regret? 41. What major trends do you see in our specialty over the next 2-4 years? 42. What’s your idea of success? 43. What trade or professional journals do you subscribe to?

44. If you won the lotto, how would you spend it? 45. Everybody has a skeleton in their closet. What’s yours? 46. What’s the nicest thing you’ve ever done in your life? What’s the meanest? 47. What’s the most memorable moment in your life? 48. What’s one accomplishment are you especially proud of? 49. Are you smart? Would your fellow students agree? 50. What is the most important thing your parents/family taught you? 51. If you could change one thing about yourself, what would it be? 52. What makes you special? 53. Rate yourself on a scale of 1 – 10. 54. How would you describe your character? 55. Why should I consider you a strong candidate for this residency program? 56. What can you do for us that someone else can’t? 57. What will your strengths be as a resident? 58. What characteristics do you possess that will allow you to fit in at this program? 59. What characteristics do you think residents need to have to be successful at this program? 60. What do you want to be doing 5 years from now? 61. What are your most important long term objectives? 62. If you could change one thing about your personality what would it be? 63. Tell me about the one thing in your life of which you are proudest. 64. Tell me about the worst decision that you ever made. 65. Describe your work philosophy. 66. What does ‘success’ mean to you? 67. What does ‘failure’ mean to you? 68. With what extra-curricular activities were you involved? What made you choose these activities? 69. Which ones did you enjoy the most? Why? 70. Which ones did you enjoy the least? Why? 71. Which ones do you regret not choosing? Why? 72. Why did you choose podiatry? 73. Which courses did you like the most? 74. Which courses did you like the least? 75. What other professions did you consider? And why did you choose one and reject the others? 76. Where did you extern? 77. Tell us what you know about our hospital. 78. What did you learn from your externship here? 79. What have you learned at other externships? 80. Why did you pick those externships? 81. Why didn’t you visit this program? 82. Why are you applying to this program? 83. Are grades a good measure of ability? 84. What is your GPA? 85. What is your class rank? 86. Why didn’t you get better grades?

87. What is the most memorable accomplishment that you have had in your life? 88. What is the biggest failure that you have had in your life? What steps have you taken to make sure that this haven’t happen again? 89. What is your greatest weakness? 90. What would you say is the biggest problem that you have failed to overcome? 91. Tell me about the type of people that you have trouble getting along with. 92. What types of people have trouble getting along with you? 93. What other two programs do you think are equal to ours? 94. Are you an organized person? 95. Paint me a picture of your current desk. 96. Do you manage your time well? 97. How do you handle a challenge? 98. How do you go about making important decisions? 99. Do you work well under pressure? 100. Tell me about the last time pressure led you to indecision, a poor decision or a mistake. What would you have done differently? Have you found yourself in a similar situation since? What did you do? 101. Do you anticipate problems or just react well to them? 102. Are you a risk taker or do you prefer to play it safe? 103. Tell me about the last time you took a risk. Was it the right decision? What would you have done differently? 104. Do you plan on practicing with yourself or with others? 105. How you do get along with your superiors? 106. How do you generally handle conflict? 107. How do you behave when you have a conflict with a co-worker? 108. Tell me about the last time you lost your temper. 109. When was the last time you were upset? Why were you so upset? 110. How do you motivate people? 111. Tell me about the last time that you made a good decision. 112. Tell me about the last time that you failed to complete a project. 113. Tell me about the last time that you found a unique decision to a problem. 114. Tell me about the last time that you aimed too high. 115. Tell me about the last time that you aimed too low. 116. What do you do when you have trouble solving a problem? 117. What do you do when things are slow? 118. What do you do when things are hectic? 119. What do you do when you are burned out? 120. What do you do when you have multiple priorities? 121. What are the skills that you most need to acquire/develop? 122. What have your superiors criticized most about you? 123. How do you ‘stay in the loop’? 124. Have you received offers from other programs? If no, why not? If yes, are you willing to decline those offers to accept an offer from our program? 125. How do your classmates describe you? 126. The successful candidate for this residency program will be working with people who have been with this program for a long time, how will you mesh with them?

127. 128. 129. 130. 131. 132. 133. 134. 135. 136. 137. 138. 139. 140. 141. 142.

If you are unfairly criticized by an attending, what would you do? Would you like to be a residency director? Why or why not? What do you know about our residency program? What was the last paper that was published out of this program? What have you heard about this residency? What aspect of this residency excites you the least? What is the most important problem in podiatry today as you see it? Are you in good health? What do you do to stay in shape? Do you have any physical problems that will affect your ability to perform? How do you manage to balance your career and family? What turns you on in your off hours? What do you like to do when you are not at work? What is the last movie that you saw? What is the last CD that you bought? Aren’t you a little old to be a resident? Why did it take you so long to get interested in medicine?

THINGS I SHOULD KNOW Gram + Ancef (Staph/Strep/Bacilli) Gram – Gentamycin (Ecoli) Anaerobe Clindamycin

Vanco Supramax Flagyl

Two Abx to give for OM: Clinda and Cipro – two of the best bone penetrators + coverage for all bugs; then consult Infectious D. Augmentin (Amoxcillin + Clavulonic acid) Timentin (Ticaricillin + Clavulonic acid) Unasyn (Ampicillin + sublactam) Zosyn (Pipercillin + Tazobactam) Bactrim (Sulfamethoxazole + trimethoprim) in a 5:1 ratio Ancef 1G (Prophylaxis), Keflex 1G (Nail), Cefepime 4G (Serious/Pseudomonas – fruity smell) Clindamycin – Pseudomembranous colitis – Vanco PO or Flagyl PO MRSA Killers: Vanco/Bactrim/Linezolid/Clinda (if comm. Acquired)/Primaxin/Daptomycin/Tygacil Principles of AO fixation: Stable internal fixation, Anatomic reduction, early return to ADL, atraumatic technique >>> WHY? To prevent cast disease/disuse syndrome – arthritis, osteopenia Axis of evil forces at fixation site: bending, torsion, shear Primary bone healing is what we want, secondary = callus formation Mini frag set (1.5, 2.0, 2.7) Small (3.5, 4.0) Large (4.5,6.5) Bunion screw 4.0: No OD, 2.5UD, 2.7Countersink, 4.0Tap 1.5 screw UD1.1, 2.0 screw UD1.5, 2.7screw UD2.0 Capsacin – blocks substance P – for neuropathic patient who is having a lot of pain Toradol (IM/IV NSAID), Tramadol (abuser opioid like). Strength: Hydro then Oxy So: Morphine – Hydromorphone (dilaudid) – oxymorphone, then Hydrocodone (vicodin)- Oxycodone, then Darvocet (Propoxphene + acetaminophen) Vicodin (hydrocodone + acetominphen) Ester (PABA – allergies), Amide (Liver breakdown) Transfuse patient if <7/21or 6/18 FFP for DIC/Liver issues/Warfarin aka Coumadin INR: Surgery pt (1.0), Normal pt (0.8-1.2), DVT pt (2.0-3.0) – PT/Vit K/ F2,7,9,10 Intrinsic pathway – injury contact platelet and starts this pathway – PTT heparin (↑Antithrombin III) Extrinsic pathway – (more important) fibrin produced – PT – Coumadin aka warfarin Higher the INR = bleeder, Lower = clotter ↑INR – Coumadin, ASA, Abx (NSAID has no affect) ↓ INR – vitamin K, birth control, barbtituates (NSAID has no affect) D-dimer test: measures fibrin – to DX DVT

OZ

THINGS I SHOULD KNOW Lovenox, Fragmin – low molecular weight Heparin – prophylaxis for DVT Heparin for PTT – 5000U load, 1000U maintain – Protamine Sulfate to reverse Ibuprofen (proprionic a), ASA (salicylates), Indomethacin (indole), Celebrex (COX2inhib) Lidocaine 4mg/kg – 15cc (2%) or 30cc (1%) depending on %. Marcaine 2.5mg/kg – 35cc (0.5%) 70cc (0.25%) depending on % Lidocaine w/epi – 25cc or 50cc depending on % Marcaine w/epi – 45cc or 90cc depending on % 1cc has 10mg of Lidocaine/Marcaine Nausea/Vomit: Zofran (ondasetron), Dexamethasone, promethazine (antihistamine) Diarrhea: Codeine Constipation: MOM, Metamucil, Doculax, Docusate, colace, WALK PATIENT WALK! Vancomycin is renal toxic! Hence peaks/trough: draw 30 minutes before or after the 3rd admin dose Peak – Shouldn’t be 30+, Trough – Shouldn’t be more than 10+ + keep em hydrated with IV fluids GAS produces: BECKS Bacillus, Enterococc/Ecoli, Clostridium, Klebsiella, Staph/Strep Albumin should be 3.0 or your flap/sx won’t heal. Lab value lags 7 days – give ensure/protein powder Anion gap = (Na+K) – (Cl + bicarbonate) – if more than 15 = DKA High power (Dexamethasone, Betamethasone) Medium (Medrol dose pack) Low (Hydrocortisone) Decadron = dexamethasone DKA (Diabetic ketoacidosis) – extreme high glucose – no more insulin available: body switches to burning fat = ketone bodies. Symptoms: Kussmaul breathing, vomit, nausea, confusion, dehydration Diagnose via BMP (acetone in blood), ABG (= acidosis Allen test), UA (ketone bodies, glucose spill too) Treat via: IV FLUIDS + INSULIN + K + BICARBONATE

OZ

THINGS I SHOULD KNOW

Not shown are A and P perforating arteries! Rmr the the posterior ones are out of sync since the first one is actually the deep plantar!

OZ

THINGS I SHOULD KNOW

OZ

THINGS I SHOULD KNOW

OZ

Tibial nerve: LPN and MPN, and M calcaneal nerve Sural nerve: Lat. Dorsal cutaneous and L calcaneal nerve Note: malleolar fossa on fibula: Sup: inferior transverse ligament, Inf: PTFL Deltoid ligament: Superficial – tib-na, tib-calc, SUPERFICIAL POSTERIOR tib-talar Deep – DEEP POSTERIOR tib-talar, ANTERIOR tib-talar Spinal stenosis = pseduo claudication Monckenberg = calcifications w/o claudication = not occlusive! Fibromuscular dysplasia = SM in BV screwed = kidney HTN~! Trental - increase RBC flexibility + antiplatelet agg Pletal - antiplatelet agg TAO - thromboangiitis obliterans = inflammation of A and V! = smoker (Burgeurs disease) = 40 yo MALE Corkscrew arteries (collaterals) seen in beurger disease (TAO) Raynauds phenomenon - pain due to cold/stress pallor>cyanosis>rubor DIC disseminated intravasc coagulopathy: widespread activation of coag system = emboli + bleed treat w/ two things: infuse plates/plasma + IV heparin! TCPO2 >50mmHg = good

THINGS I SHOULD KNOW

OZ

Huge ulcers on the medial aspect of the leg - secondary to venous insuff > edema > skin looses nutrients = ulcer! KENDALL PUMP - pumps up - for venous insuff edema and elephantitis Homan's sign - DF foot = pain cuz of DVT IV HEPARIN - PTT - 5000units to load, 1000 per hour thereafter 4-6days REVERSE VIA protamine sulphate: half life is 1.5 hours Coumadin - VIT K factors: 7,9,10 - 10mg qd 6months REVERSE VIA vitK or FFP(faster reversal): half life is 20-60 hours (change dose as per INR) Streptokinase or Urokinase embolus: air/fat/shit = fracture thrombus: plaque Ischemia6Ps: polar, pulseless, pallor,paresthesia,poikliothermia Venous stasis ulcers: fibrin cuff - barrier to O2 diffusion GLYCOSYLATION of skin = loose flexibility Normal albumin = 3.5 / total protein = 7 Symes amputation = amputation at malleoli! AV fistula = thrill/bruit at auscultation Visatril - antiemetic + opioid booster Bone healing FIVE stages: (1 and 2) initial inflammation/hematoma = decreased o2 + acidity = promotes osteoprogenitors to differentiate (3) neovascularization (4) Clasts come in and remodel (5) remodel All American Procedure (Flatfoot/Severe PTTD): TAL, Medial displacement calc osteotomy, CCjoint lenghthening(Evans), FHL or FDL transfer to the PT PTTD = RF Valgus = TendoAchilles pulls more valgus onto it! Syndesmotic lig complex: ATFL, PTFL, Interosseous, inf transv tibfib = syndesmotic injury! Syndesmotic lig injury repair: debride the whole area, mitek to recreate ATFL, Syndesmotic screw thrown across tib and fib Spring ligament = calcaneo-navicular ligament Intramedulary rod/nailing - big ass rod in medulla

THINGS I SHOULD KNOW

Stevens–Johnson syndrome - autoimmune/hypersensitivity epidermis seperates from the dermis by Bactrim (Sulfamethoxazole and trimethoprim) Floroquin and/or steroid = collagen necrosis followed by repair = tendon rupture 3-wea (wetting, emulsifying, antiseptic) Keratoderma - horn like skin Grafts: Real: Autologous (self), Allogenic (same species - apli and derma), xenogenic (porcine) DERMAGRAFT: Dermis + fibroblasts APLIGRAF: Living skin/epidermis Synthetic: Collagen, hylauronic acid Allopurinol: Xanthine oxidase inhibitor (uric acid producer) Colchicine: raises pH, anti-inflamm properties, inhibit MT polymerization FHB: origon: M (from TP), L(3rd Cunei and Cuboid) Extensor Hallucis Capsularis/Peronues Digiti Minimi/ Woods muscle Third plantar common digital branch is where you get Mortons neuromas (often comm with Plantar common DB off LPN) CFL only ankle extracapsular ligament

I - Randomized dbl-blind controlled, systematic/meta analysis II - Cohort III - Case IV - animal research, expert opinion Macular- circumscribed, flat lesion Papular/nodular- circumscribed, solid elevation Vesicular/bullous- fluid-filled, elevated lesion Cystic- non-infected, deep-set collection surrounded by a wall of tissue Scales- thin flakes of dead epidermis Excoriations- scratch marks Erosions- essentially thick scratches that do not breach the dermis Ulcer- deep dermal defect that breaches the dermis or deeper Fissures- linear, deep epidermal cracks in the skin Pustule- elevated lesion containing pus, arising from infections of papule or bulla Abscess- deep collection of pus Arterial ulcers: lateral leg (or at trauma site – IPJ) – Lots of pain, no exhudate

OZ

THINGS I SHOULD KNOW

OZ

Venous ulcers: medial – little pain, lots of exhudate 1) ABI: 0.9-0.7 IC, 0.7-0.3 Rest pain, 0.3-0 Gangrene 2) Segmental pressures: no drop more than 20mmHg, plus all waveforms triphasic - These are taken at upper thigh, lower thigh, upper calf and ankle. 10-20-30 rule * The upper thigh pressure should be greater than 10mmHg greater than brachial pressure * Pressure differences of more than 20 mmHg for adjacent cuff sites on the same leg * Pressure differences of more than 30 mmHg over the entire leg. 3) Doppler – should be triphasic 4) Digital blood pressure – should be 70-110mmHg 5) PPG - Photoelectric plethysmography- light intensity of blood = norm is 50mmHg 6) TCPO2 – 0 = no movement 1 = trace movement 2 = movement with the aid of resistance 3 = movement against gravity 4 = movement against resistance supplied by the examiner 5 = normal strength Types of Neuropathy D - diabetic A - alcohol N - nutritional G - Guillan-Barre T - toxic H - hereditary R - recurrent A - amyloidosis P - porphyria I - infectious S - systemic T - tumor CRPS: pain is distal to the site of trauma to begin with but can spread proximally in later stages. Vasodilation can exhibit warm skin, dry skin, and hypohidrosis. Vasoconstriction can exhibit cyanosis, cool skin, edema of the part, and hyperhidrosis. Trophic changes involving the skin, muscles, bone and joints can occur in later stages. The examiner may see thin, atrophic skin, absent of hair and witness osteoporotic changes on x-ray. Neuromas (a misnomer) of the forefoot: Joplin’s - medial to the first metatarsal Hauser’s - the first intermetatarsal space Heuter’s - the second intermetatarsal space Morton’s - the third intermetatarsal space Islen’s - the fourth intermetatarsal space

THINGS I SHOULD KNOW

OZ

ASA1 – normal patient ASA2 – Systemic disease w/o manifestation (DM) ASA3 – Systemic disases w/ manifestation (DM w/ neuropathy) ASA4 –Systemic disease that is a threat to life (Renal failure) ASA5 – SuperObese Cannot survive w/o operation, emergency ASA6 – Brain dead, lets harvest organs Stages of anesthesia: I – Analgesia/Amnesia (pre, partial, total) II – Delirium (excitement etc) III – Surgical Anesthesia IV – Medullary paralysis Ester (pseudocholinesterase – Procaine), Amides (Lidocaine, Marcaine) Malignant hyperthermia Thought to be due to reduction in the reuptake of Ca by the sarcoplasmic reticulum necessary for the termination of muscle contraction Dantrolene 2.5 mg/kg IV initially – 175mg for 70kgmale Also do ice bath, bicarbonate, insulin Fracture: 1. Open vs. closed 2. Shape 3. Location 4. Intra-articular vs. extra-articular 5. Complete vs. incomplete 6. Displaced vs. non-displaced Gustillo and Anderson: I <1cm, clean, minor damage II >1cm, moderate damage III extensive damage and dirty (comminutated, crushed, skin missing, avulsion) a enough ST coverage to fracture site b not enough ST coverage c blood supply screwed! General Principles of Treatment of Open Fractures 1. 2. 3. 4. 5. 6. 7.

Tetanus history Thorough H&P with complete neurological, vascular and musculoskeletal exam Complete x-rays Antibiosis admitted in the ED with cultures Immediate debridement and irrigation All foreign bodies should be removed All marginal and macerated tissue should be debrided and re-debrided as necessary after 48-72 hours. 8. Types 1, 2 and 3A get delayed primary closure within 5-7 days

THINGS I SHOULD KNOW

OZ

9. Types 3B and 3C usually require skin flaps due to such a loss of tissue 10. External fixation for all type 3 and unstable type 2 fractures 11. Internal fixation should be used for articular and metaphyseal open fractures, preferably within 8 hours. Tetanus: Clean and minor wounds: Toxoid given only if last dose was given > 10 years ago. TIG not given All other wounds: Toxoid given if last dose given > 5 years ago TIG not given TIG is only given in patients (any age) when they have never received a tetanus shot (usually pediatric patients) Compartment syndrome: normal 5mmHg, exercise 150mmHg (returns to normal in 5 min), 30+ = with wick catheder Pre-op patients: CBC (for H/H) + EKG + CXR + HCG or UCG Insulin REDUCES potassium levels, Steroids RAISE Glucose levels. PRE-OP: DM PATIENT Early morning Sx is best. If not start D5W. Want glucose 150-200. Don’t take meds if <200. If 200+ take insulin. Minor procedure: can d/c oral meds for the day of surgery. For major procedures: ½ insulin dose on the morning of. Start D5W during case. And then give 1-2 units in surgery. If patient is taking more than 7.5mg of steroid per day – cannot d/c steroid! Give 100mg IV hydrocortisone pre op and then 100mg post op. Steroid: poor wound healing, infection. Heparin therapy: d/c day before sx Coumadin therapy: d/c 5-7 days before sx (20-60 hour half life!!) Heart attack? No surgery for another 6 months Gout patient for sx: give Colchicine 0.5mg TID for 5 days before, 5 days after Sx 5W’s: Wind (1 day post-op)- aspiration Water (2 days post-op)- UTI Wound (3 days post-op)- infection Walk (4 days post-op)- DVT

THINGS I SHOULD KNOW

OZ

Wonder (> 4 days)- drug reaction Screw is either: positional (ie holding the plate) OR is a lag screw (compressing – only if proximal threads don’t purchase – ie overdrill) Plate types: Static compression: normal compression Dynamic compression: static + physiological stress = more compression Neutralization plate: fracture first fixated via a lag-screw, then this plate is put on on top – to neutralize 3 evil forces: bending, torsion, shear Buttress plate: maintains length in case of big defect Note if the fracture length is TWICE that of the bone: use multiple lag screws! Tagaderm: to cover ulcer in OR PCA example: 4mg initial dose of Morphine. 1mg per 20 minute, with 10 minute lockout etc. D/C <8 breaths per min or systolic is <90mmHg Etomidate – Short term IV anesthetic for bedside ORIF Lidocaine is acidic (lower pKa) = burns, Marcaine is buffered MRI w/ contrast: used at: tendonopathy or fluid lesion Pre-Op: NPO + cardiac clearance + defib company rep in OR! Talus supplied by: PT (A of tarsal canal), DP (A of sinus tarsi), Perf peroneal: neck branches Lateral ankle ligaments: CFL, ATFL, PTFL, and Lateral Talo-Calc ligament Master knot of henry connects FHL and FDB to the navicular Sural nerve = medial sural cutaneous nerve + comm. Branch from lateral sural cutaneous nerve

THINGS I SHOULD KNOW

Nail and tip of toes are mostly by the plantar proper digital arteries Interossei: 4XDAB, 3XPAD Stopped at #10 on the first page

OZ

THINGS I SHOULD KNOW

OZ

DMC lecture Chronic wound definition: reduction in 50% area in 4 weeks (has not happened) >65N/m2 = ulcer since O2 tension is reduced TCPO2 30mmHg = good O2 – do it to determine amputation level MMPs – not good since they deactivate GF in wound Calciphylaxis is a syndrome of vascular calcification, thrombosis and skin necrosis (@ ESRD patient) Pyoderma gangrenosum – huge deep ulcers that are due to auto-immune diseases Dakin solution – bleach + water + baking soda Santyl – collegnase/self debrider Regranex – GF paste Apligraf – living epidermis (ALL GF) – after application don’t mess with it for one week Dermagraft: dermis + fibroblasts (MISSING SOME GF) Aquacell: absorbs exhudate + has silver in it Uncontrolled diabetic is >12Hb1Ac Residency Q: if start with a Wagner 3, and treat and it gets smaller: what is it now? Still a Wagner 3 Diabetic: Non-fasting > 200mg/dl Fasting > 126 Hb1Ac >6.5% (pre-diabetic 5.7 – 6.4) Glitazones – cause EDEMA Diabetic Drugs: Metformin – STANDARD DRUG – ↓ carb resportion + ↑ insulin sensitivity (WRONG) Glitazone - ↑ insulin sensiƟvity Acarbose - ↓ carb resporƟon Meglitinide - ↑ Bcells to secrete insuline Sulfonyureas -↑ Bcells to secrete insuline GLP analog – Glucagon like peptide – give sensation of being full Dpp4i inhibitor – DPP4 break down GLP First drug will lower Hb1ac by 1.5, second 0.7, third 0.5 Types of insulin: (short term) R, NPH, L, UL (long term) – Old method NEW: RAA or LAA rapid or Long acting analop LISPRO (Humalog) RAA – take with meals 5 units GLARGINE (Lantus) LAA – take at night time 20 units Sliding scale – controversial – basically see what patients glucose level is BEFORE meal and then give them units of insulin. However post-food glucose may be huge! Therefore trial and error method – give 5 units Lispro, see post-food glucose! If reached 900, try 10 units etc etc All surgery patients need to maintain 140-180 in the ICU. Note COPD patients take prednisone! = raise glucose and decrease insulin sensi! Therefore give em more insulin!

THINGS I SHOULD KNOW

OZ

D5W = 5% glucose = 50mg over 8 hours.

BUN and Creatinine Story BUN Blood urea nitrogen – filtered and REABSORBED Creatinine – only filtered Normal ratio 10-20:1 BUN:Creatinine ↑>20:1 Acute renal fail, GI bleed, old person (low muscle mass) – PRE-Renal problem (BUN resorb high) ↓<10:1 Liver disease – Renal damage (No resorb of BUN) Before Abx: kidney function, allergies, C+S, other abx Primaxin = imipenem + cilastatin (protect kidney via inhibiting enz that break down imipenem) = Gorillamycin since broadest spectrum SE: Seizures! PCN allergy: use CLINDA or CIPRO (cross sensitivity of PCN and CEF is 1-5%) Augmentin: 500 or 875mg, both have 125mg of Clauvulonic acid Timentin: raises Na levels!!! All Abx renal excreted: minus: Pipercillin aka ZOSYN Liver excreted: Clinda and Erythromycin 1st Gen Ancef(IV), Keflex(PO) 2nd Gen Ceclor 3rd Gen Rocephin 4th Gen Cefepime (aka Maxipime)

-G+ and G- (Peckss) -G+ and G- (Hen Peckss) -G+ and G- and Pseudomonas -G+ and G- and Pseudomonas

Hinflu, Neisseria, Proteus, Ecoli, Klebsiella, Shigella,Salmonella MRSE: Meth Resis Stap Epidermidis Vanco IV 1g q12 slow infuse(over 1 hour) or get red-neck syndrome (Red man syndrome = Rifampin) Tx Redman/neck with Benadryl Peak is high(lower dose), low(higher dose). Trough is high(increase interval), low(lower interval) Peak30/Trough10 Vanco SE: Ototox, Nephrotox, Redneck Aminoglycosides: Tobra/Gentamycin (G- Lover) 2mg/kg load, 4mg/kg maintain SE: IRREVERSIBLE OTOTOXCITIY Peak10/Trough2 Kidneyfuction: CC Creatinine clearance = (140)(weight in KG)/(72)(Creatinine) *0.85 if female Bactrim (Sulfamethaxole + Trimethoprim) – one tab PO BID – both kill folic acid production

THINGS I SHOULD KNOW

Bone penetration: Clinda + Flouroquinolones Bactrim contraindicated in DM patients with PO hypoglycemic Z pack aka Azithromycin – 250mg tab, 2 for first day, 1 each for 4 days Aztreonams: for pseudomonas – but super expensive Quinolones: Cipro/Levaquin – NOT FOR KIDS, Kills Cartilage! Diarrhea – Pseudo colitis (by Clostridium difficile) OR regular colitis (by S Aureus) TX with Vanco PO 125mg or Flagyl PO 500mg VRE – TX with Linezolid Pseudomonas KILLERS: Cefepime, Zosyn, Timentin, Cipro, Gentamycin MRSA KILLERS: IV – Vanco, Clinda, Linezolid, Primaxin, Bactrim, Rifampin PO – Clinda, Linezolid, Bactrim, Rifampin Topical - Bactroban Bactroban: isolated from Pseudomonas!!! Surgical prophylaxis: 2+hour surgery, implant, AIDS pt, Emergency/trauma, endocarditis ABx – change flora of GI
reduces Vit K absorption
increases INR Fever: mostly between 4pm and 8pm Augmentin for BITES Enterococcus: Augmentin! G+ and G- 1st choice: Keflex or Ancef, 2nd choice: Clinda or Cipro Anaerobe – 1st choice: Augmentin, 2nd choice: Clinda or Genta C. Perfingen (GAS): clinda or augmentin Xanthoma – Bactrim Lyme disease – Doxcyyline Necrotizing fasciitis – Primaxin Gas gangrene = deadly since: kidney fail + shock

28 bones in the foot, 35 joints, 107 ligaments, 19 muscles

OZ

THINGS I SHOULD KNOW

OZ

Remember the difference between Os Subtibiales and Os TibExternum Sharpey fibers: attach periosteum to bone Strongest lateral ankle ligament: Posterior Talo-fib Deepest medial ankle ligament: posterior-Tibio-talar Flexor retinaculum aka Laciniate ligament SERetinaculum aka Transverse Crural Ligament IERetinaculum aka Crural Cruciate ligament MPN – courses in 1st layer muscles: between ABD H and FDB LPN – courses between 1st and 2nd layer: between FDB and QP MEDIAL of foot – EHL – Deep peroneal nerve – Dorsalis Pedis artery – LATERAL of foot Pes Anseurinus – Semitendinous, Gracilis, Sartorius (longest muscle in body) DTML is deeper or dorsal to neuroma Circulation coming down from the heart: AA to common iliac to external iliac to femoral to popliteal - … NEVER LAFF at A FAD MPN: 1st lumbricle, ABD H, FDB, FHB MPA: FDB, ABD H, 1st dorsal interossei Remember the triangle:

Talus

Calcaneus Most symptomatic is CN Coalition

Navicular

3 causes for brachymetatarsia: Down syndrome, Polio, HEP B, Turners Hallux varus is post-fibular sesamoid removal Saggital groove is an articulation for the tibial sesamoid Skin graft healing stages: plasmatic (nutrient thru plasma), neovascular, reorganize, reinnevate Wound healing stages: inflamm, proliferative, remodel Bone graft stages: vascularization, blastic, osteoinduc, osteoconduc, remodel Complications of grafting: #1: seroma, #2: hematoma, #3: autoimm Primary bone heal: inflamm, osteoinduc, remodel Secondary bone heal: inflamm, osteoinduc, soft callus, hard callus, remodel Tailor’s bunion: IM 6 (9+ not good), Lateral deviation 8+ not good Haglunds: fowler phillip, PPP, total angle of Vega

THINGS I SHOULD KNOW

OZ

Von Recklinghausen aka Neurofibromatosis Kayexalate for hyperkalemia Hollow Mill: if you strip the head of a screw, use this – its drills out both screw and surrounding bone Charcot vs. OM: how to diagnose? Easy option: BIOPSY IT!! Difficult option: 3 phase bone scan with Indium 111 (more specific for OM) however very long half life! When to use Gadilinium for MRI? Neuroma (will be darkened) Fibroma (will light up – especially important pre-surg since want to know extent) Hemophiliac arthritis: Similar to PVNS – hemosiderin deposits in joints. GIANT CELL TUMOR: MOST LIKELY tumor or tendon sheath MRI: PT tendon is about 1.5-2X larger than the FDL tendon MRI: Peroneus Quartus = mass laterally! Inserts on Calc tubercule MRI: Accessory Soleus = mass posteriorly! MRI: no tendon sheaths for anterior tendons, TA, distal PT MRI: Fatty infiltrates in ABD H = Tarsal tunnel syndrome MRI: Fatty infiltrates in ABD digi quinti = Plantar fasciitis <> if not = baxter neuritis MRI: FHL tendon sheath communicates with Ankle joint DVT: compressible vs. non-compressible vein Compressible: No DVT Non-compressible: your probe is ON the DVT and the vein wont collapse! DVT: Augmentation: compress the foot and blood goes gushing by! Therefore no DVT! Iontophoresis: Therapeutic ultra sound w/steroid cream (supposed to make the steroid absorb deeper) Discoid meniscus: the lateral meniscus of the knee isn’t C shaped, and does taper, instead its thick (rare anamoly) ADA diet: low carb, AHA diet: low Na Vibrio Vulfincus: fresh water bacteria 4 grams is max does of Tylenol – therefore Vicodin(500/5): can only take 8 in a day! Integra: flowable wound matrix Promogran: collagen dressing (wet it first) Valium for muscle spasm – IE: TA lengthening!

THINGS I SHOULD KNOW

OZ

DVT: Least you can do is ASA 81mg Heparin SE: (within 5 days) HIT heparin induced thrombocytopenia! – basically heparin+platelet is thought of as a foreign body and is attacked by immune system = more and more thrombi! = MI or CVA Tx: Coumadin/discontinue heparin? ARGATROBAN: treatment of HIT Don’t forget: streptokinase: dissolves clot (nothing else dissolves clots!) Also TPA (tissue plasminogen activators – TP breaks down clots naturally) Coumadin/Warfarin SE: Warfarin necrosis – skin necrosis! BLACK. Associated with high loading dose, This is because Coumadin initially increases coagulation (paradoxical) – this is because Coumadin also kills protein C!!!!! Coumadin kills Vit k associated factors AND Protein C. (Rmr Protein C is also an anti-coagulator!) Pyoderma Grangrenosum: Auto-immune disease = deep ulcers w/ papules Necrotizing Fasciitis: C Perf, S Aureus, Vibrio Vulf LMA – Laryngeal mask airway – like General, except no intubation, more like a triangular mask over larynx Opiate strengths: Morphine then HYDRO then OXY Morphine > Hydromorphone (dilaudid) > Oxymorphone > Hydrocodone (vicodin)- Oxycodone> Darvocet (Propoxphene + acetaminophen) Vicodin (hydrocodone + acetominphen) Darvocet (Propoxphene + acetaminophen) Malalignment syndrome – keep it in mind, pelvis. Always look 2 joints above! Caffeine increases uptake of codeine Osteoporosis: Bisphospanates (Fosamax for example) Stops Clasts 1200 units of Ca, 2000 units of D Or can do Zoledronic acid IV injections = ONCE A YEAR! Qhs = Take nightly! ORIL – open reduce insert lock (IM aka INTRAMEDULARRY ROD) Voltaren – NSAID cream (PO is higher then normal) Sulindac 200mg PO BID – easy on the kidneys OTO-sil: silicone impression system for corns within interspaces. Verrucae plantaris: wart on plantar aspect Verrucae vulgaris: wart on dorsal aspect

THINGS I SHOULD KNOW

OZ

Onychomycosis: DDx may include: Lichen planus Monckenberg or plaques: BIG BV killed by DM Microangiopathy: Small BV killed by DM Plantar fasciosis: BAD BAD Plantar fasciitis Ultrasound thickness of P Fasciia: normal <3mm, >6mm is  Prolotherapy: inject with sugar water or PRP to instigate inflammation Liver enzymes: ALT – high also due to musc break down Creatinine Kinase – high due to MI (CK-MB more specific) Alk phosp – high due to biliary duct blockage Sporanox aka itraconazole – PO antifungal take 1 day 7 days daily, then 3 weeks off, then 7 days, then 3 weeks off, then 7 days Monsel’s solution – use for hemostasis in P+A Corti-sporin: ophthalmic solution used for P+A, I+D Reverse flow gradient: @ Monckenberg sclerosis Pressures: 100, 212, 104 = back flow! CHEST PAIN – MONA Morphine (reduce pain, reduce breaths per min) Oxygen (2L nasal canula) Nitroglycerin Slingual Aspirin Also get CXR(so its not a lung thing) and EKG and ABG (pulmonary gases, Allen test) Draw a MI Screen (troponin, CK-MB)

Poly-ol pathway and neuropathy: Hyperglycemia = ↑polyol pathway
↓NADPH
↓NO
vasocon
ischemia Hyperglycemia = ↑polyol pathway
↓NADPH = sorbitol accumulaƟon Hyperglycemia = ↑polyol pathway
↓NADPH
oxidative stress (as NADPH is needed in Gluthatione reductase) NOTE: NADPH used up in converting Glucose to Sorbitol

THINGS I SHOULD KNOW

OZ

↑ levels of homocysteine = KIDNEY, EYES, NEUROPATHY (retinopathy, glomerulopathy) B Vitamins lowers levels of homocysteine Cymbalta – neuropathy (ANTI-DEPRESSANT) Lyrica – neuropathy (pain kill) Metanx – Vitamin B6 B12 and folate Transfusion reaction: IGE mediated (Benadryl), Fever (Tylenol) – Stop if bronchospams Store blood = Citrate toxicity Give one unit over FOUR hours (this is for our patients, if emergency bleeding = give bolus/over one hour etc) 99% patients: 2 units over 8 hours – Do loop diuretic in between (so then can pee ins and outs) LASIX = FUROSEMIDE packedRBC raises hemoglobin by one 1%, hematocrit by 3% Types of transfusions: Whole blood – never given, give em what they need packedRBC – most common Albumin – increases volume only (wont help with healing) Platelet – to increase PT/PTT/INR for bleeder surgery FFP – for Coumadin Cryoprecipitate – (=fibrinogen) for VonWilder disease 10/30 is norm, transfure when <7/21 150-500K is normal platelet. 100K is minimum for Sx. <50 is = spontaneous bleed STJ: 42T 48F 16S Bohlers angle: top of anterior process to top of calc post facet to top of calc tuberosity Norm: 25-40 Gissane angle: (strut) ant and middle facet compared Norm: 120 – changes with calcaneal fractures Talo-calcaneal angle (on DP): 21 Talar declination angle: 21 Calc inclincation angle: 21 Note talar head is 15 degrees medial, and 25 degrees plantarflexed Cyma line: S shape line formed by CC and TN joints (supination moves it post, pron moves it anteriorly) Splay foot: increased IM angles for all (12+ for 1st and 2nd, 8+ between 4th and 5th)

THINGS I SHOULD KNOW

Toygar angle: usually achilles is 180 (its straight), when ruptured, it would be less

Surgical Dissection: Keller – base removed Mayo – head removed @ surgical neck - capsule Distal Akin – hallux interphalangeus Proximal Akin - DASA Oblique Akin – long PP Silver – bumpectomy + lateral release (Add H, FDB, DTML cut, lat capsulotomy, freeing fib sesamoid) Mcbride – Silver + fibular sesmoidectomy

Head Note True IM = Measured IM + (TAA -15) IM 12-14 head, 15-17 shaft, 18+ base

OZ

THINGS I SHOULD KNOW Austin – < Youngswick – < with extra dorsal cut Kalish – long dorsal arm Reverdin – thru n thru wedge Reverdin Green – w/shelf Reverdin Laird – thru n thru Reverdin Laird Todd – thru n thru and PF fragment Shaft Hohman – trapezoid Vogler – long dorsal arm Mau/Ludloff Base Juvara – thru n thru CWBO/OWBO Watermann – wedge taken out at head (base dorsal) Jacobi V – V looking DP Weil – straight cut into MT, slide head back Keck n Kelly – Wedge removed, base dorsal in calc

MT adductus procedures: Heyman Herdon Strong – cut off all tarsal-MT ligaments (except 5th-Cuboid) Bertman Gartland – cresenteric osteotomies of all MT

Flatfoot procedures: All American – Evans + TAL + Calc slide + FHL to TP ST procedures Young – TAL + TA re-rout thru nav Hoke – Nac-cunei fusion Arthroeresis “lift joint” MBA – SELF LOCKING – keeps the lateral process of talus off the sinus tarsi STA-PEG - AXIS ALTERING – eleveates the floor of the sinus tarsi Mushroom – IMPACT REDUCER – reduces impact Osteotomies Evans – Insert bone in CC joint Dwyer – remove wedge, base is medial Silver – insert wedge, into lateral Koutsugiannis – cresenteric Cavus procedures: ST procedures

OZ

THINGS I SHOULD KNOW Steindler stripping Jones tenosuspension STATT Peroneal stop – PL taken out via, suturing to PB, therefore more eversion Osteotomies Triple/STJ/AJ fusion Dwyer – opposite dwyer, wedge taken out, base medial Cole – wedge taken out at cuneis and cuboid, base is dorsal Japas – A V (looking DP) cut made and whole FF PFed

Hallux limitus: Jones Tenosuspension STATT

Lateral ankle stabilization: Brostrom: debride + tighten ligaments + Use IER to reinforce Watson-Jones – fibula and neck Evans - fibula Lee – Split PB thru fibula

Chrisman Snook split PB thru fib and calc

TAL Hoke – 3 small incisions 2 medial 1 lateral Baker tongue in groove – tongue is on the distal Frontal plane Z #1 Silverskoid Test: Limited DF @ both Limited DF @ knee extended

- GASTRO-SOLEAL tight: do Frontal plane Z - GASTROC tight: Baker tongue in groove

OATS procedure: for talar OCD – remove bone w/ cart from knee

OZ

THINGS I SHOULD KNOW

NON ABSORBABLE Ethilon - poly proplene Prolene - nylon

ABSORBABLE Vicryl - Lasts 4 weeks Monocryl - Lasts 2 weeks

RARE/Less commonly used PDS – absorbable – Lasts 6 months Chromic gut – absorbable – Lasts 3 months Dexon - absorbable Silk - nonabsorbable

OZ

THINGS I SHOULD KNOW

OZ

THINGS I SHOULD KNOW Classification systems: Danis Weber A = SAD B = SER, PAB C = PER, PDF Note: PDF = describes a Pilon Fx Wagstaffe: Fibula avulsed ant Tillaux-Chaput: tib ant Volksman: tib post Reudi + Allgower: Pilon fx – 1(no displacement) 2(intra-artic) 3(comminuted + intra-artic) AO for Pilon: extra/partial/complete intra-articular A no comm/no impact, B some, c both yes Sneppen: Talar body – 1(OCD) 2(body) 3(post tubercule) 4(lateral process) 5(crush) Essex-Loperesti: 1(tongue fx) 2(joint depression) Tongue fx: 2 fx lines, one goes D to P, other exits posteriorly Joint depression: same as above: plus line around STJ Johnson + Strom: I mild degen II attenuation III rupture IV rigid valgus Conti (MRI) I longitudinal tears II variable degen III diffuse swelling Note: Stewart: Mostly Jones (so type 1), Other most common is either 2 or 3 (cuz PB avulsion – 2Intra, 3Extra) JHASS = dorsal dislocation of PP and sesmoids (in all categories) 1 intersesm lig intact 2 not intact A(no fx), B(sesm fx) Rosenthal I(distal to PP), II(distal to lunula), III(PP) Drago, Olaff, Jacob I pain end ROM II adapt - flatten III deteriorate – osteophytes/sclerosis IV ankylosis

OZ

THINGS I SHOULD KNOW

OZ

Etiologies of Tailors Bunion: Incomplete development of DTML, malinsertion of add hallucis, FF splay, Congenital bowing of MT, abnormal STJ supination

Wound Care Products: All Silver products need to be removed before MRI Can change almost everything every 3 days MMPs – inactivated cuz sucked up into ie promogran Necrotic Wound Debrider: Accuzyme (papaine-urea) Panafil (Papaine-urea-chlorophill) Chloro for smell/swelling Santyl - debrider Antimicrobial dressing: Acticoat – Silver 100ppm for 3 days Actisorb – Charcoal and silver Aquacell – Aquacell Ag contains Silver Hydrofera Blue – Gentian Violet/Methylene Blue Compression dressings: Unna boot Pro-Fore (5 layers: contact layer, webril, bandage, elastic compression, Coban) Soft cast: Webril/Unna/Coban – Passive compression only (only when they walk) Non-Antimicrobial dressings: Iodosorb – beads with Iodine – bacteria and debris become trapped in it also – therefore wash wound then changing dressing with iodosorb application last time. 3x a week. Contra: allergy/hashimoto/goiter Prisma/Promogran – matrix/collagen Oasis – ECM Regranex – Platelet derived GF Xeroform – gauze + Vaseline + abx salt Grafts: Alloderm - collagen Dermagraft – dermis/fibroblast Apligraft – living epidermis Graft Jacket – human dermis

High K – CBIGKFAL – Calcium/Bicarb/Insuline/Glucose/K-axelate/Furosemide/Albuterol

THINGS I SHOULD KNOW

Normal Lab Ranges:

Admit after Sx: ADC VAANDIMAX Admit to s/p Diagnoses Condition Vitals Activity Allergies Nursing order Diet IV Meds Ancillary – PT/Vascular X-ray Same Day Sx: Admit to PACU s/p L 5th MT ORIF Please dispense Sx Shoe Non WB w/ crutches Elevate and Ice L LE D/C per anesthesia F/U with Dr. X on 2/3/21 Rx Percocet 5/325

OZ

THINGS I SHOULD KNOW

TBI = toe brachial index – more accurate than ABI for foot and calcified arteries. Normal value 0.7 Prevalone boot – decubitus heel ulcers Soft cast – webril, unna, coban Amitryptilyline – TCA for neuropathy Prominent calcaneal exostosis on the lateral aspect: peroneal tubercule Hba1c: 120mg/dl = 6, add 30 for each above Nickel allergy = allergy to stainless steel and/or titanium Titanium screw is weaker than stainless, however it is more elastic, and less scatter on MRI Titanium plates = best, since want some flexibility or it will break

Lesser MT: head procedure = may cut nutrient a. shaft procedure = no blood supply base procedure = too much correction Bunion re-surgery rate = 5% for Austin Bunion infection rate <1% Tight rope for bunion – biggest problem: 2nd MT stress Fx (since you have a hole in the 2nd head), will loosen up, will rupture = fiberwire We are born adductovarus
become adductovalgus MT adductus is NON-CONTRIBUTORY to HAV! Shaffer plate = arch support Ped devices: C = equal flanges = UCBL = Anti Splay A = M flange = Anti-Pron Whitman = cause pain at navic tuberosity at pronation Hollow Mill = Trephine Neural tube = cover both ends of the cut nerve to connect a cut nerve Bipolar cautery – no need to ground patient, spark only to the vessel Monopolar cautery – need to ground patient, whole local area sparked

OZ

THINGS I SHOULD KNOW

OZ

Double crush syndrome – same nerve damaged twice at two different spots – rmr neuropathic nerves are swelled up, hence tarsal tunnel + back injury + neuroma etc TRANSMALLEOLAR SCREWS: need to be removed in 12WEEKS (since motion between tibia and fibule) otherwise will break Neuropathy: (1) Demylinate via sorbitol (2) myelin production is down since need microvessels (3) Osmotic effect (hyperglycemia cuz nerve loves sugar – water comes/follows in) (4) oxidative stress Tyloma = HPK0 Thompson test – squeeze the calf for TA rupture Pratt test – squeeze the calf to test for DVT Hohman test – DF foot for DVT For ankle Fx: fix diastasis first and then the LM or MM fx ESR:

100+ Acute OM, <100 Chronic OM >60 Acute OM, 30-60 Chronic, 0-15 Normal

Sepsis if 2+ of the following are raised: Temp, PR, RR, WBC Vassal rule: Fixate the most unstable fx first (the others will take care of themselves) Vertical stress test: test for subluxable MTPJ – hold MT and PP and try to push up the proximal phalanx Plantar fasciitis is always on LEFT – since right arm and left leg are dominant and longer

Torsion: head n neck vs fem chondyles Version: head n neck vs frontal plane

Antetorsion - int Retrotorsion -ext Anteversion -ext Retroversion –int Note that physis in kids that are compressed, grow faster! In-toeing caused by (1) MT adductus (2) Femoral retroversion (3) Antetorsion (4) Int tib torsion (5) Int malleolar position

THINGS I SHOULD KNOW

Hip externally rotate 2.5degrees every 10 years. Constipation can cause low grade fever! Young – FHL to Navicular Fault at Nav-Cunei? Fuse it! Orthoses is to change GRF, not to correct deformity UCBL <6yo, Whitman 6-12yo SPRING LIGAMENT ALWAYS RIPS IN FLATFOOT TAL = reduces strength by 60% Bony union 6-8w, bone heals in 18months Wolf law: bone under stress will adapt Davis law: ST under stress will adapt Metaphyseal fx – ie 5th base – need WB to heal! Cast for 6 weeks (normal cast time 8w) Fx heal: adult – 8w, 12yo = adult, 6yo 4w, 2yo 2week! Physeal fx are at calcification zone OCD that is painful, and casting wont help: retrograde drilling Fragmin – low molecular weight heparin Abx not used on wounds, cuz caustic Abx beads = 90 days leach Abx beads taken out in 2 weeks (unless absorbable) Bone is NEGATIVELY charged – S.Aures sticks to it!!!! Ring sign: on X-ray for chronic OM Heat labile Abx = Clinda Charcot T1 Normal T2Increased

OM Decreased Increased

PMNA Poly-methyl-acrylate-beads Lateral process of the talus fracture = shepherd fx Medial process of the talus fracture = Cedell fx

Arthritis Normal Increased

OZ

THINGS I SHOULD KNOW

OZ

30 to 70 degree angle for arthroscopy (between camera and cutting tool) Remember that Sural nerve is formed by: M sural cutaneous (+ comm. Branch off L sural cutaneous) Distal syndesmotic tib-fib ligament: FOUR AITF, PITF, Interosseous, Transverse Tib-fib ligament Medial ankle ligament: FIVE Tib-Calc, Tib-Nav, Tib-Talus, Also: deep deltoid (deep tibio-calc) is deeper to tibio-calc (Sustentaculum Tali) AVN – Possible treatment options: Core decompression, Vascularized bone graft, non-vascularized bone graft, fusion (talo-calc, talo-tib, blair), talectomy. ALSO: percutaneous drilling w/Steinman pin Krischner wire diameter(1, 1.5, 2, 2.5, 3mm) STEINMAN PIN diameter(3, 3.5, 4, 4.5mm) Piezoelectric phenomenon: Negative Charge @ Compression = bone deposition (Thus Bone stim – apply cathode at where you want bone to be deposited!) Vanco and all other Abx cause Neutropenia: Daptomycin is the least causing of em all – good for OM Tx for Neutropenia is G-CSF True MTa = (Measured MT – 15) + IM Dermatome: Sciatic nerve: Ventral Rami of L4, L5, S1, S2, S3 Tibial: Ventral division of L4, L5, S1, S2, S3 Common Peroneal: Dorsal division of L4, L5, S1, S2

THINGS I SHOULD KNOW

Charcot vs. OM: Certec labeled Tech99 Lachman test = vertical push up test = for predislocation syndrome Reudi and Allgower (Pilon) I (no comm/no displacement) II (no comm/some disp) III(comminuted of joint and displacement) Neuropathy drugs: Metanx: Vit B12 supplements, Nuerontin: Gabapentin, Lyrica: Pre-Gaba, Cymbalta: depression 3:1 skin rule for incisions Creatinine increase: Kidney failed, BUN decreased: Liver failed Eccentric and Concentric drilling. DCP: only 2 holes nearest to fx are eccentric Hooks law – amount of strain = stress on bone Pauwels law – eccentric load = compression and tension on oppo sides. Charnley fx stability classification: (I: transverse most stable, II oblique most unstable, III short oblique <45 degrees medium stability) Coumadin dosages 2.5, 5, 7.5, 10 Close reduce: 3mg of Dilaudid, 3mg of Versed, 10mg of Zofran (Etomidate by ER doc) Bone healing stages: Primary infl, repair, remodel Secondary hematoma(1 week), soft callus(3m), hard callus(6m), remodel Skin graft healing stages: plasmatic (nutrient thru plasma), neovascular, reorganize, reinnevate Wound healing stages: inflamm, proliferative, remodel Bone graft stages: vascularization, blastic, osteoinduc, osteoconduc, remodel Codeine allergy: STUD: Toradol 10mg IV/IM, Ultram 100mg, Darvocet N-50/100 HDS proper technique: plasty PIPJ, hood release, tendon lengthen, capsulotomy, pp release, girdlestone/taylor and desis FF procedures: Young – TA rerouted thru Navicular Kidner – Rid of accessory navicular and reattach Porta Pedis: Roof QP, Floor ABD H STRESS-Sheilding: decresed stresses cause osteopenia since screw is bearing weight Lemont’s nerve: interm DC Baxter’s nerve: Nerve to the abdDM

OZ

THINGS I SHOULD KNOW

Thompson test – squeeze the calf for TA Pratt test – squeeze the calf to test for DVT Hohman test – DF foot for DVT A- Asymmetry, B-border, C-color, D-diameter, E-elevation Types: Superficial spreading (most common), acral lentigous (hutchingson sign), nodular True AVN’s: Koehlers, Friedburg, Assman, Diaz, Leg-Calve-Perthes AVN stages: Avasc, Revasc, bony healing, residual deformity X-ray finding on each: none, head within head and increase density, more bone deposited, residual CRPS stages: (1) Hyperemic – Pain+edema+hyperhydrosis (2) Dystrophy – more pain+brawny edema+spotty penia (3) Atrophic - less pain+diffuse penia+flexure contractures (volksman) Pagets: Osteolytic>combined>osteoblastic>Malignant degeneration(6%) Gout stages: Asymptomatic: elevating levels of uric a Acute: WOAH! Deposit = pain Intercritical: inbetween acute attachs Chronic tophaceous: 10 years+ Treat Charcot @ early stage 1 (right after dislocations/fractures) – cuz right after = osteopenia Or Stage 3: new bone laid down and no more inflammation Etiologies of HAV: Biomechanical (equinus, pronation, hypermobility, FF varus, DFFR, Hallux limitus) More Biomechanical (long 1st MT, MPE) Arthritic (psoriatic, gouty, rheumatoid) Others (Ehler-Danos, CMT, MS, CP) Shaft osteotomies: Mau/Ludloff, Lambrinudi(wedge taken out with apex prox-dorsal and base disalplantar –PF the head!), Kalish(shaft vogler) 3 fragments of Calcaneus: constant(S. Tali), Comet(post facet), main fragment(tuberosity) Reudi and Allgower – I (mild disp and comm) II (mod disp) III (severe disp and comm, AJ impacted) AO – I extra-artic, II partial, III complete intra-art 1/3 tubular plate for fibula, 3 screws each side of fx T-plate for tibia Hawkins % 12/42/91/91

OZ

THINGS I SHOULD KNOW

OZ

Posterior tubercule fx of talus – Watson Normal, enlarged, os trigonum, syn-chondrosis

Lateral – Hawkin Simple, comm, chip Sanders CT: Coronal Charnley = fracture stability Tillaux fragment @ Salter-Harris 3 Sedden: nerve neuropraxia, axontmesis, neurotmesis Eckert and Davis: Peroneal subluxation – retinaculum/fibrous tip/bone AVN stages: avasc, revasc, bony healing, residual French theory: neurovascular German: neurotrauma Avascular (0-3months) – ST swelling only/smaller epiphysis/illusional inc in density Revascular (1-3years) – very fragile!/increase in density as epiphysis collapses on itself head within head Remodel – bony deposition Residual – Raynauds phenomenon = Pallor, Cyanosis, Rubor Stratum basale, spinosum, granulosum, lucidum, corneum Shyphillis: primary: chancre, secondary: great masquredar/mimicks others, tertiary: tabes dorsalis/CNS Peak and trough is mg/L Malignant Melanoma – Superficial spreading (common), Acral lentigous, Lentigo, nodular(deadly) Bone destruction patterns: geographic, moth eaten, permeative

OZ

Interview Scenario List

Patient walks into ER with a DFU w/Puss, what do you do? 1. History and Physical • History o NLDOCAT o Ask about Systemic SOI – N/C/V/F o Local ulcer site SOI – Pus/Odour/swelling/erythema/pain o Ulcer history o ABx history o Tetanus status o NPO status o Meds and Allergies o PMH – Get DM history in detail o Others PSH, FH, SH, ROS • Physical o Vitals o Know how to work up non-palpable pulses 2. Start empiric ABx • Local SOI (augmentin), Cellulitis (Zosyn), Bone (Clinda/Cipro), Systemic (Vanco/Fortaz/Flagyl or Ancef/Gent/Clinda), Life threatening (Primaxin) 3. Order Labs • CBCwdiff/CMP/ESR/CRP/Albumin/a1C – know why for each 4. Order 3 views X-rays, possibly MRI if severe (need for Sx planning) 5. Depending on NPO status schedule OR time for I+D • Don’t forget things like consent/Fluid management/What drugs to DC/EKG/UCG/CXR • Cultures o Wound/ C+S o Bone • Ulcer = defect, hence cannot be closed, purpose is to clean it out. Then schedule follow up visits in office/wound clinic for wound healing.

Patient with Trauma presents to the ER, what do you do? Primary • ABCD • Tetanus • NPO • Is it polytrauma (Calc fx – get spinal and pelvic films) • NVS of your LE (for compartment syndrome etc) Secondary • History and Physical • X-rays/CT/MRI/Bone scans • Labs Surgery as appropriate o Open Fracture o Compartment syndrome o AJ o Pilon o Calc o LisFranc o Talus o MT fracture o Tendon o LawnMower o Sesamoid o GSW o Nec Fasciitis o FB

Open Fx: Primary and Secondary survey C+S Empiric Abx Debride in OR, Stabilize the fracture (temporary) Repeat debridement in 48-72hrs for G+A 3 Stabilize ORI (permanent) Abx start per C+S Delayed primary closure 5-7 days @ Type 1 and 2

Closed fracture
Check NV status
Perform local block
Close reduce (increase deform6ity, distract, decrease deformity)

Compartment Syndrome Remove all dressings/casts Dependence, hydrate, Nasal O2 Fasciotimize DPC (most important: pain, second most: Wick) GSW Velocity more important than mass High velocity (military >2000ft/s) – Radical debridement due to cavitation Low velocity (<2000 ft/s) Do primary and secondary survey (earlier in document) Fracture: consider it open, treat per G+A Otherwise debride, remove bullet if superficial or palpable Small wound closed, others left open with C+S and prophylactic Abx ST trauma Do primary and secondary survey I+D, Remove FB (if applicable) Control bleeding with Surgicel or Thrombin pad. Ensure H+H fro EBL Deep cultures always DPC (delayed primary closure) Lawn mower/nail/Rosenthal Do primary and secondary survey Treat per Rosenthal Rosenthal I (let it granulate or primary closure if <6hrs) II(V-Y or Z skin plasty) III (distal symes amp) If <25% subungual hematoma (trephinate it), if >25% nail avulsion + suture nail bed if its torn w/ abs suture Don’t forget to take xrays with any subungual hematoma. I know you know this though.

Puncture wounds/FB Do primary and secondary survey May triangulate FB position with THREE needles (one in each plane) Xeroradiograph is excellent for FB (wood) – now out of date I+D and removal Three things to ensure did not happen: OM, Cellulitis, Abscess DPC w/ packing + deep cultures + Empiric Abx Human/dog bite (Cats don’t bite, they are gentle creatures (unless pissed off))

Bugs looking for: E. corrodens/P. Multicoda/Rabies/Tetanus Augmentin 875 q12 (not the 500mg) Follow puncture guidelines: I+D, pack, DPC and Deep cultures *human bite also includes punching someone in the face, and their teeth opening skin on your fist

Burns and Frost bites Remove agent Cool w/ NS, Rewarm with 104 degree Saline Do primary and secondary survey Debridements everyday (depending on area involved) Escharectomy in burn patient (once eschar tissue is widespread) Blisters: do not pop, instead apply silvadene If amputation is required: allow skin to demarcate *Could not find article for prophylaxis (Presby says: NO! don’t want yeast/pseudomonas superinfection)

Calcaneus fracture Do primary and secondary survey Surgerize intra-articular fx only (75% of all) – can do traction initially Remember Essex-Loperesti technique for tongue type Schanz pin into tuberosity. Pull proximal for length, plantarward to DF the P. Facet, evert to take out of valgus Otherwise: always pin or screw comet fragment to constant fragment Pilon fracture Remember the four steps: restore fib length, reconstruct distal tibial articulation, graft tibia, restore medial aspect of tib Ankle fracture LM: place that inter-frag screw first (2.7mm) AP (pointing plantarly). Then throw a 1/3 neutralizing plate on the lateral side (6 hole, 3.5mm), ensure one hole is not screwed, do cottons test and screw in 4.5malleolar screw if need be MM: 2 crossed k-wires or 2 4.0 screws PM: usually not ORIF’d (unless greater than 25% articular involvement)

LisFranc fracture Remember to re-create the lisfranc ligament JHASS dislocation Don’t forget that type one needs to be OPEN reduced!

Patient walks into your office with: HAV HDS HL/HR

Cavus Flat ALWAYS TRY YOUR CONSERVATIVE CARE FIRST

ABPS 420

Examination Study Guide

American Board of Podiatric Surgery 445 Fillmore Street San Francisco, CA 94117-3404 (415) 553-7800 April 2009

ABPS 420 (April 2009)

Page 1

Table of Contents Page Introduction .................................................................................................................................. 2 How to Study for ABPS Examinations ........................................................................................ 3 Written Examinations .................................................................................................................. 4 General Information .................................................................................................................. 4 Format .......................................................................................................................................... 4 Subject Areas ............................................................................................................................ 4 Board Qualified and Recertification in Foot Surgery ............................................................... 5 Board Qualified and Recertification in Reconstructive Rearfoot/Ankle Surgery ..................... 5 Self-Assessment in Foot and Ankle Surgery ............................................................................ 6 Oral Examinations........................................................................................................................ 6 General Information .................................................................................................................. 6 Certification in Foot Surgery .................................................................................................... 8 Certification in Reconstructive Rearfoot/Ankle Surgery .......................................................... 8 Sample Written Questions ......................................................................................................... 10 Foot Surgery............................................................................................................................ 10 Reconstructive Rearfoot/Ankle Surgery ................................................................................. 25 Answer Key ............................................................................................................................ 30 Suggested Reading List .............................................................................................................. 31 Copyright 2009 ABPS Any unauthorized use, modification, reproduction, display, publication, performance, or distribution of this work without the prior written consent of the ABPS is prohibited and may violate the Copyright Act, 17 U.S.C. § 101 et seq. Such prohibited actions may result in legal action or the loss of privileges, benefits, qualifications, or certifications granted by the ABPS. U:\DOCS\ABPS Documents History\420\2009-ABPS420_09_v1.doc 4/29/09

Nondiscrimination policy. In accordance with applicable federal laws, the American Board of Podiatric Surgery does not discriminate in any of its policies, procedures, or practices on the basis of race, color, national origin, sex, sexual orientation, age, or disability. Americans with Disabilities Act. In compliance with the Americans With Disabilities Act, the American Board of Podiatric Surgery will make special provisions for individuals with disabilities if written request is made no later than thirty (30) days prior to the date(s) of the examination for which appropriate application has been made, fees paid, and credentialing completed.

ABPS 420 (April 2009)

Page 2

Introduction

While obtaining board certification is an important step in the career of every podiatric surgeon, board status is also important to hospitals and the general public. The profession of podiatric medicine has chosen to use the certification process and its examinations component to indicate that a board-certified podiatrist has demonstrated a level of knowledge appropriate to her/his specialty area. This Study Guide is provided to assist candidates in their preparation for the examinations of the American Board of Podiatric Surgery (ABPS). ABPS uses both written, oral, and Computer Based Patient Simulation (CBPS) examinations in its assessment of candidates' knowledge of podiatric surgery. While this guide is designed to represent the types of questions used in certification examinations, the examination content is subject to changes that reflect current technology and medical practice. The Examinations Committee, in consultation with the ABPS’ independent psychometric consultant, prepares the examinations. Scoring, interpretation of scores, and determination of passing scores are the responsibility of the Board of Directors. Candidates are tested in specific subject areas applicable to the practice of podiatric medicine and surgery and the perioperative care of the podiatric surgical patient. The written parts of the examinations use objectively scored (i.e., multiple-choice, true-false, etc.) questions to test declarative knowledge. The written examination may be adaptive or linear and will be administered by computer at testing centers throughout the United States. The oral examinations employ face-to-face interaction between the examiner and the candidate to test the candidate's ability to obtain and interpret clinical information, to reason logically, and to arrive at a diagnosis and treatment plan for each patient presentation. The CBPS examinations are computer-driven using an interactive screen to gather patient information, order tests and procedures, make a diagnoses and administer treatments. Before written, oral, and CBPS questions are incorporated into an examination, they are studied and field tested for efficacy. Each question is viewed statistically immediately after the examination. Some questions may be eliminated, or the number of acceptable responses broadened, if evidence of significant ambiguity is discovered.

ABPS 420 (April 2009)

Page 3

How to Study for ABPS Examinations 1. Read this Study Guide to learn as much as you can about the examination process. 2. Get maximum benefit from the sample written questions by answering them without looking at the answer key. Then score yourself and note any pattern showing a weakness in any particular subject area. 3. It is imperative that candidates sitting for the CBPS examinations access the practice questions sometime during the weeks prior to the actual examination. Studies have shown that candidates who do not practice the CBPS examination often do not have time to complete the actual CBPS examination. You must become familiar with the computer screens and how they function if you expect to efficiently move through the actual examinations. Candidates for the CBPS examination access the practice examination through their personal page on the ABPS web site using their user ID and passwords. Instructions for using the practice examinations are also found on the personal page. 4. Use references listed on the Suggested Reading List (beginning on page 31) to review the subject areas tested in ABPS examinations. 5. While ABPS does not endorse board certification review courses, candidates have reported that the review of subject areas and mock orals included in some review courses have been helpful in preparing for the examinations. Board review courses are advertised in national podiatric publications and are often associated with the colleges of podiatric medicine and state podiatric medical associations. 6.

Make time to prepare for the examinations. Cramming and intensive study may not be helpful. Candidates who prepare by carefully reviewing are sometimes less anxious at examination time and may perform better.

ABPS 420 (April 2009)

Page 4

Written Examinations: Board Qualified Foot Surgery Board Qualified Reconstructive Rearfoot/Ankle Surgery Recertification Foot Surgery Recertification Reconstructive Rearfoot/Ankle Surgery

General Information a. Format. The written examinations consist of objectively scored (i.e., multiple-choice, true-false, etc.) questions administered by computer. Adaptive testing uses a large pool of questions, the difficulty level of which was determined by the questions’ statistical performance in ABPS tests. In an adaptive test, the computer dynamically selects questions as the candidate takes the test and adjusts question selection based on the candidate’s demonstrated ability level. As each question is answered, the computer assesses the response and selects the next question based on whether the previous answer was right or wrong. Questions become progressively more or less difficult as the program assesses and establishes the test taker’s ability level. Each question has only one best answer. In this computer adaptive format, returning to previous questions for review and/or changing answers is not possible. It should be noted that in an adaptive test, each question is weighted according to its difficulty level and other statistical properties, and not by its position in the test. b. Subject Areas. The written examinations are based on the following subject areas applicable to the practice of podiatric medicine and surgery: Basic Science. Pathoanatomy. Pathomechanics. Pathophysiology. Diagnostic Evaluation/Medical Imaging. Surgical Principles. Surgical Procedures and Techniques. Procedural Perioperative Management. Surgically Relevant Medical Management. General medical. Anesthesia. Emergency Medicine. Lower extremity conservative. Complications.

ABPS 420 (April 2009)

NOTE:

Page 5

The following specific conditions may be tested under each response subject area:

Deformities. Infections. Neoplasm/tumors/masses. Other conditions. Acute trauma. c. Time considerations. Candidates with average reading skills should have ample time to complete each written examination session. Extra time has been factored in to allow most candidates to work steadily through the questions without running out of time. d. Scoring. Examination results are provided as a scale score. The score is determined by the difficulty level of the questions you are able to answer correctly. The examinations are not graded on a curve. All examinations will be administered at computer sites throughout the United States.. Except for the Reconstructive Rearfoot/Ankle Surgery Recertification Examination, all written examinations are adaptive. The Reconstructive Rearfoot/Ankle Surgery Recertification Examination is a linear examination. The Board of Directors sets passing scores. e. Review of Scores. Each examination is scored by computer, and failed examinations are automatically rechecked and re-scored. Therefore, once examination results are mailed to candidates, there is no further review of scores. f. Inclusion of Non-scored Questions. Some questions may be included in the ABPS examinations to improve the examination system and to provide data for investigations into the examination process. Such questions are not counted in determining your scores. Board Qualified and Recertification in Foot Surgery a. Content. The Foot Surgery examinations will test the diagnostic evaluation of conditions pertaining to the foot and ankle and intraoperative/perioperative management of both forefoot and non-reconstructive rearfoot procedures. b. Schedule. Both the Board Qualified and the Foot Surgery Recertification examinations will consist of 125 questions, given in one session of no more than three hours in length. Board Qualified and Recertification in Reconstructive Rearfoot/Ankle Surgery a. Content. The Reconstructive Rearfoot/Ankle examinations will test diagnostic, intraoperative, and perioperative management pertaining to reconstructive rearfoot and ankle procedures. b. Schedule. The Board Qualified examination will consist of 125 questions given in one session of no more than three hours. The Recertification examination in Reconstructive Rearfoot/Ankle Surgery will contain 100 questions, given in one session of no more than three hours.

ABPS 420 (April 2009)

Page 6

Self-Assessment in Foot and Ankle Surgery a. Content. The Foot and Ankle Surgery Self-Assessment examination will test diagnostic, intraoperative, and perioperative management pertaining to foot and ankle procedures. b. Schedule. The self-assessment examination in Foot and Ankle Surgery will consist of 100 questions. The examination is administered as a secured examination at compute test sites.

Oral and CBPS Examinations: Certification Foot Surgery Certification Reconstructive Rearfoot/Ankle Surgery The oral and CBPS examinations serve to evaluate the candidate's knowledge and skill in obtaining and interpreting clinical information as well as their ability to reason logically and to arrive at a diagnosis and a treatment plan for a specific patient presentation. General Information a.

Overall Process. Each candidate is assigned to a group with a unique schedule for the oral and CBPS examination sessions. Groups gather in a central meeting area until their schedule begins at which time they are escorted to the examination hallways in the hotel. Each oral examination session is held in a private room where the candidate and the oral examiner (selected by the Board of Directors) sit across from each other at a table. Candidates move between rooms until the group schedule is complete, and then return to the central meeting area. Every attempt is made to equalize waiting times for all groups. The CBPS questions are administered in larger groups with each candidate having access to a laptop computer.

b.

Oral Question Format. At the beginning of each question, the candidate receives a Candidate Information Sheet describing a clinical situation. Based on the described situation, the candidate must request additional information (such as patient history, physical examination, radiographs, laboratory reports, etc.) in a manner simulating a real patient encounter. The examiner will respond as a patient would and will only report, not interpret, any requested data. The examiner will not volunteer information, so the candidate must be thorough and specific when asking for all information needed to reach a diagnosis and treatment plan. The examiner scores each question by noting which predetermined essential areas are satisfactorily covered by the candidate.

ABPS 420 (April 2009)

Page 7

Example of an examiner/candidate interchange: Candidate: Examiner: Candidate: Examiner:

Is there a history of injury? Specifically? Is there history of injury to the foot or ankle? The patient says that he hurt his foot when he was very small.

c. Scoring. Examiners fill out scorecards for each candidate. Each oral question has predetermined essential areas that must be adequately covered to pass the question. A passing score is set by the Board of Directors based on psychometric evaluation of the examination. d. Review of Scores. The scorecards of failing candidates are automatically reviewed and rechecked for accuracy. Therefore, once examination results are mailed to candidates, there is no further review of scores. e. Challenge Examination. If a candidate feels that an oral examiner has been unfair, or that a personality conflict has interfered with the examination, the candidate may request a challenge examination by another examiner. The candidate must request the challenge immediately upon leaving the examiner's room. The Chairman of the Examinations Committee will determine whether a challenge examination is warranted. Specific instructions about this process will be given to candidates during the candidate orientation session prior to the examination. f.

CBPS Examination. A CBPS examination is “Candidate-Process Driven.” You will drive the examination by performing actions to collect and analyze information. You will select the necessary information for problem solving. For example, if you wanted to palpate a foot mass, you would select “palpate mass” in the “Physical Exam” section. If you wanted to aspirate the mass, you might select “aspirate needle” in the “Diagnostic Procedures” section. If you wanted to order a magnetic resonance image (MRI) on the foot, you would select the appropriate MRI in the “Imaging” section. Performing a surgical technique (procedure) on the mass is done in the “Treatment” section. Follow-up care is also selected, when appropriate, in the “Treatment” section. By practicing with the software and the simulated case examination, you will be become familiar with how to navigate through the simulation. You are to complete the CBPS as best you can by taking into account the relevant aspects of patient management, (case history, physical examination, imaging, labs, diagnostic procedures, diagnosis, treatment; and in some cases follow-up diagnoses and treatments). While collecting patient information, you must balance thoroughness with efficiency, as well as balancing quality versus quantity. You will need to pace yourself and be careful to not take too much time on any one point or decision as the CBPS is a timed examination. Field testing has demonstrated that users who have practiced the CBPS will have ample time to complete each case. As you collect information regarding your simulated case, keep in mind that relevancy holds the key to successful resolution of a clinical problem. For example if you are hesitant about whether a procedure is warranted, make the decision based on clinical indications. CBPS scoring is based on the relevancy of the processes or actions performed.

ABPS 420 (April 2009)

Page 8

Certification in Foot Surgery a. Schedule. There are six traditional (examiner/candidate) oral questions and six Computer Based Patient Simulation (CBPS) given in three sessions, over one and one-half days. b. Content. The questions will test the diagnostic evaluation of conditions pertaining to the foot and ankle, and intraoperative/perioperative management of both forefoot and nonreconstructive rearfoot procedures. c. Subject Areas. The Foot Surgery Certification Oral Examination (oral and CBPS) focuses on those deformities and conditions involving the forefoot and non-reconstructive rearfoot procedures. Questions may emphasize the following areas: Biomechanical/Acquired deformities. Congenital and/or pediatric deformities. Infections. Metabolic conditions and/or emergency medical management. Neoplastic (primary or metastatic) conditions. Traumatic conditions. Surgical or traumatic complications. d. Timing. Candidates receive six tradition oral questions divided between three sessions. Each question lasts 14 minutes. Candidates receive six CBPS questions divided between three sessions. Each question lasts 25 minutes. e. Passing Score. Each year a passing score is set by the Board of Directors based on psychometric evaluation of the examination. Certification in Reconstructive Rearfoot/Ankle Surgery a. Schedule. There are four traditional (examiner/candidate) oral questions and four Computer Based Patient Simulation (CBPS) questions given over one day. b. Content. The examination will involve diagnostic, intraoperative, and perioperative management pertaining to reconstructive rearfoot and ankle procedures.

ABPS 420 (April 2009)

Page 9

c. Subject Areas. The Reconstructive Rearfoot/Ankle Surgery Certification Examination (oral and CBPS) focuses on those deformities and conditions involving the rearfoot and ankle. Questions may emphasize the following subject areas: Common rearfoot/ankle trauma. Adult rearfoot/ankle deformities. Pediatric rearfoot/ankle trauma or deformities. Surgical or traumatic complications. Neoplasms or infections. d. Timing. Each oral question lasts for 20 minutes, while each CBPS lasts 25 minutes. e. Passing Score. Each year a passing score is set by the Board of Directors based on psychometric evaluation of the examination.

NOTE: Both the qualification examination and the certification examination in Reconstructive Rearfoot/Ankle Surgery must be passed for Certification in Reconstructive Rearfoot/Ankle Surgery. If a candidate sits for both the qualification and the certification examination and passes the qualification only, he/she is Board Qualified in Reconstructive Rearfoot/Ankle Surgery, provided the candidate has completed a PSR-24 or PSR-24+ or PM&S-36 residency (Board Qualified or Certification in Foot Surgery is a prerequisite for attaining Board Qualified status in Reconstructive Rearfoot/Ankle).

ABPS 420 (April 2009)

Page 10

SAMPLE FOOT SURGERY WRITTEN QUESTIONS Note: These questions are representative of the various formats used by the ABPS in its examinations. These questions are not meant to be representative of the scope or level of difficulty of any specific examination. Answers found on page30. 1. A patient presents with painful hallux abductovalgus deformity. There is pain-free range of motion of the first metatarsophalangeal joint (MPJ). Radiographs reveal: hallux abductus angle: intermetatarsal angle: proximal articular set angle: distal articular set angle: metatarsus adductus angle:

35 degrees 15 degrees 22 degrees 4 degrees 8 degrees

What is the most appropriate procedure? A. B. C. D.

closing wedge with McBride. proximal Akin with McBride. closing base wedge with Reverdin-Green. Austin with proximal Akin.

2. Following removal of the proximal phalanx of the fifth digit, what is an appropriate surgical procedure for prevention of fifth digit flailing? A. B. C. D.

syndactylism of the fourth digit to the fifth digit. arthrodesis of the distal interphalangeal joint. shortening of the flexor tendons. flexor tendon transfer.

3. A patient presents with an acute dorsal dislocation of the third metatarsophalangeal articulation. Radiographs show no fractures and closed reduction is performed under local anesthetic. What is the proper sequence of maneuvers to reduce the dislocated digit? A. B. C. D.

longitudinal traction and plantarflexion of the digit. plantarflexion and then longitudinal traction of the digit. dorsiflexion, longitudinal traction, and plantarflexion of the digit. longitudinal traction, dorsiflexion, and plantarflexion of the digit.

4. A patient with a history of true penicillin allergy is scheduled for a total joint implant. Antibiotic prophylaxis would best be served with which of the following medications? A. B. C.

piperacillin (Pipracil). cephalothin (Keflin). ciprofloxacin (Cipro).

ABPS 420 (April 2009)

D.

Page 11

vancomycin (Vancocin).

5. A 60-year-old male suddenly begins complaining of a "crushing" sensation in his chest. The episode lasts very briefly then subsides. It begins again and is more intense. What should you administer to this patient? A. B. C. D.

nitroglycerin (Nitrogard) 0.5 mg. diazepam (Valium) 5 mg. ephedrine (Racephedrine) 25 mg. morphine sulfate 15 mg.

6. Radiographs taken of a 25-year-old male with a painful bunion indicate the following: interphalangeal abductus angle: hallux abductus angle: distal articular set angle: proximal articular set angle: metatarsus primus adductus angle: deviated first metatarsophalangeal joint

18 degrees 30 degrees 6 degrees 7 degrees 14 degrees

Based upon this information, what is the procedure of choice? A. B. C. D.

proximal Akin with Austin. proximal Akin. distal Akin with Austin. distal Akin with Reverdin.

7. What procedure should be performed on a patient with a 25 degree metatarsus primus adductus angle and a severe first ray hypermobility? A. B. C. D.

Lapidus. lateral closing wedge osteotomy. crescentic osteotomy. Logroscino.

8. A 32-year-old woman has a history of a slowly enlarging, subcutaneous, multinodular, painless mass beneath the flexor surface of the great toe. There is radiographic evidence of marginal bone erosion. What is the most likely diagnosis? A. B. C. D.

glomus tumor. enchondroma. giant cell tumor of the tendon sheath. ganglion.

9. What would a dorsoplantar radiograph of the foot with a plantarflexed first ray taken in the angle and base of gait show the position of the hallucal sesamoids to be? A. B. C. D.

medial to the metatarsal head. proximal to the metatarsal head. distal to the metatarsal head. lateral to the metatarsal head.

ABPS 420 (April 2009)

Page 12

10. A patient presents with an inversion ankle sprain. Stress inversion radiographs reveal a 15 degree difference between the symptomatic and asymptomatic ankle. A peroneal tenogram reveals contrast media within the ankle joint and extravasation anterior, lateral, and distal to the lateral malleolus. These findings are consistent with rupture of the: A. B. C. D.

anterior talofibular ligament. anterior talofibular and calcaneofibular ligaments. anterior talofibular ligament and peroneal tendons. anterior talofibular, calcaneofibular, and posterior talofibular ligaments.

11. A 65-year-old female diabetic on insulin therapy arrives at the surgeon’s office. While waiting she begins to feel faint and loses consciousness. What would be the treatment of choice? A. B. C. D.

administer phenytoin (Dilantin) 200 mg. intramuscularly (I.M.). administer epinephrine 0.5 cc. intramuscularly (I.M.). protect patient from injury and observe. administer 25 cc. of 50 percent dextrose in water intravenously (I.V.)

12. A 25-year-old female has unremitting numbness in the lesser digits. The pain becomes more severe while walking and is difficult to relieve. Over the past several months, the pain has been sharp with radiating sensation in the arch. What is the most likely diagnosis? A. B. C. D.

neuroma of the third intermetatarsal nerve. sciatica. diabetes mellitus. compression of the posterior tibial nerve.

13. What is an alternate approach to hallux limitus that does not require a joint destructive procedure? (note negative format) A. B. C. D.

dorsiflexory osteotomy of the proximal phalanx. Jones tenosuspension. lengthening of extensor hallucis longus. dorsiflexory osteotomy of first metatarsal base.

14. A plantar fibroma is removed. Two months later the wound has healed, but the three medial digits begin to hyperextend at the metatarsophalangeal joints (MPJ). A possible cause would be the severance of which of the following nerves or muscles? A. B. C. D.

medial plantar nerve. quadratus plantae. saphenous nerve. flexor digiti minimi.

ABPS 420 (April 2009)

Page 13

15. A 30-year-old male complains of a painful right ankle after sustaining a forced plantarflexion injury. Plantarflexion of the foot and dorsiflexion of the hallux greatly exacerbate the symptoms. What is the most probable diagnosis? A. B. C. D.

flexor digitorum longus tendinitis. fracture of the sustentaculum tali. fracture of the posterior lip of the tibia. fracture of the posterior tubercle of the talus.

16. Three weeks following excision of a neuroma in the third intermetatarsal space, the third digit drifts into an adducted position. The most probable cause would be severance of which of the following anatomical features? A. B. C. D.

second lumbrical muscle. third dorsal-interossei tendon. second plantar interossei muscle. lateral capsule of the third metatarsophalangeal joint.

17. In using a Z-plasty to correct a skin contracture, what should the surgeon do? A. B. C. D.

keep the Z as small as possible. make the central incision of the Z parallel to the contracted skin. place the Z perpendicular to Langer's lines of tension. make the wings of the Z angled 25 degrees from the central incision.

18. A 36-year-old female has a history of recurrent masses in the medial longitudinal arch of the right foot. What is the most likely primary lesion of the foot causing metastasis to the lung? A. B. C. D.

melanoma. rhabdomyosarcoma. fibrosarcoma. neurofibromatosis.

19. A 15-year-old female sustained an injury resulting in a Salter-Harris type V epiphyseal fracture of the first metatarsal base. What should initial treatment include? A. B. C. D.

cast immobilization. open reduction and ASIF fixation. soft cast and wooden shoe. no treatment is necessary.

20. Which of the following procedures is not an appropriate treatment of a dog bite on the foot which occurred eight hours ago? (note negative format) A. B. C. D.

debridement of wound and primary closure. pulsed lavage irrigation of wound. saline web-to-dry daily dressing changes. OR debridement.

ABPS 420 (April 2009)

Page 14

21. Keratoses beneath the second metatarsal head are frequently observed in association with hallux valgus deformities. What is the most common cause of these keratoses? A. B. C. D.

hypermobility of the first ray. short second metatarsal bone. long first metatarsal bone. rigid plantarflexed first ray.

22. A patient has a history of hypertension which is controlled by furosemide (Lasix) 40 mg. (q.d.). What is the most frequent electrolyte disturbance observed in this type of patient? A. B. C. D.

hypokalemia. hyponatremia. hyperkalemia. hypernatremia.

23. Which benign soft-tissue lesion may be invasive into bone? A. B. C. D.

synovioma. histiocytoma. villonodular synovitis. neurilemmoma.

24. What is the condition that must be present before attempting an extensor suspension (Jones) procedure of the first metatarsal? A. B. C. D.

contracted hallux. flexible plantarflexed first metatarsal. forefoot supinatus that is reducible by manual pressure. adequate interphalangeal joint motion.

25. A 25-year-old female sustained an inversion ankle sprain 24 hours ago. The area is severely edematous and ecchymotic. Diagnostic tests reveal rupture of the lateral collateral ligaments. What should the treatment consist of at this time? A. B. C. D. E.

compression dressing for 24-to-48 hours. open ligament repair. posterior splint and warm compresses for 24-to-48 hours. tape strapping with high top athletic shoe for 24-to-48 hours. short-leg walking cast.

26. To derotate an adductovarus fifth digit, how is the lenticular incision made? A. B. C. D.

distal medial to proximal lateral. distal lateral to proximal medial. lateral to medial. medial to lateral.

ABPS 420 (April 2009)

Page 15

27. A 40-year-old female presents with a ganglion at the base of the first metatarsal medially. After surgical excision of the ganglion, the patient complains of anesthesia along the medial aspect of the foot, up to the first metatarsal head. Which peripheral nerve was involved? A. B. C. D.

medial plantar. lateral plantar. saphenous. common peroneal.

28. What coalition does the Harris-Beath view (axial view of the calcaneus) best demonstrate? A. B. C. D.

talonavicular coalition. calcaneonavicular coalition. talocalcaneal coalition. calcaneocuboid coalition.

29. When performing a Lapidus procedure for hallux abductovalgus, what structure should be avoided when exposing the first metatarsocuneiform articulation? A. B. C. D.

deep perforating artery. flexor hallucis longus tendon. deep peroneal nerve. anterior tibial tendon.

30. A 41-year-old female has a unilateral flatfoot of six-months duration. The patient relates a history of multiple cortisone injections by another doctor for "os tibial externum." What is the most likely cause of this patient's condition? A. B. C. D.

dorsal tear of the plantar fascia. subtalar degenerative arthritis. rupture of the peroneus brevis tendon. rupture of the posterior tibial tendon.

31. A 60-year-old male develops an anaphylactic reaction secondary to a drug injection. Epinephrine (Adrenalin) 0.5 cc. is injected intramuscularly (I.M.) immediately. What is the purpose of administering this drug in this situation? A. B. C. D.

slow the rate of absorption of the offending drug. strengthen myocardial contractions. combat cardiac arrhythmias. dilate the bronchioles.

32. What is most often the cause of anterior process fractures of the calcaneus? A. B. C. D.

inversion with the foot plantarflexed. eversion with the foot plantarflexed. inversion with the foot dorsiflexed. eversion with the foot dorsiflexed.

ABPS 420 (April 2009)

Page 16

33. When is electrical stimulation of the bone best indicated? A. B. C. D.

synovial pseudoarthrosis. hypertrophic nonunion. fibrous nonunion. fibrous malunion.

34. Three months after resecting a ganglion from the dorsum of the midfoot, a patient presents complaining of persistent numbness along the adjacent sides of the second and third digits. The most likely diagnosis is iatrogenic severance of which nerve? A. B. C. D.

saphenous. deep peroneal. lateral dorsal cutaneous. medial dorsal cutaneous.

35. What procedure most effectively transfers the action of the flexor digitorum longus to the metatarsophalangeal joint (MPJ) of the lesser digit? A. B. C. D.

arthroplasty of proximal interphalangeal joint. arthrodesis of proximal and distal interphalangeal joints. flexor lengthening. extensor tenotomy.

36. What is the major reason for countersinking? A. B. C. D.

reduce screw prominence. disperse compression force of screw head evenly. allow for shorter screw utilization. provide proper angulation of screw.

37. In the early stages of superficial spreading malignant melanoma, which of the following conditions is not present? (note negative format) A. B. C. D.

change in size. pain and bleeding. variation in color. irregular borders.

38. On a peripheral blood smear stained with hematoxylin and eosin, the presence of "rosettes" (clusters of polynuclear leukocytes surrounding an extracellular hematoxylin body) most likely indicates which of the following systemic disorders? A. B. C. D.

rheumatoid arthritis. lupus erythematosus. hematogenous infection. thrombocytopenic purpura.

ABPS 420 (April 2009)

Page 17

39. Shortly after general anesthesia, a patient is nauseous and treatment is required. Which of the following would be the most appropriate treatment? A. B. C. D.

diazepam (Valium) 10 mg. intramuscularly (I.M.). prochlorperazine (Compazine) 10 mg. intramuscularly (I.M.). fentanyl (Sublimaze) 0.05 mg. intramuscularly (I.M.). meprobamate (Meprospan) 100 mg. intramuscularly (I.M.).

40. A patient presents with a brachymetatarsia on the fourth metatarsal right foot. What is the limiting factor when considering the maximum length that may be added to the metatarsal? A. B. C. D.

tendon length. nerve length. adjacent metatarsal length. vascular length.

41. The dynamic compression plate is most suitable as a solitary fixation device for which of the following fractures? A. B. C. D.

oblique. spiral. transverse. compression.

42. Why should burning of bone with a power saw be avoided? A. B. C. D.

it decreases phagocytosis at operative site. it causes an increased zone of resorption at the osteotomy site. it results in necrotic bone in which white blood cells fail to migrate. additional inflammation causes a decrease in phosphate and displacement of calcium in bone matrix.

43. A 30-year-old female complains of a painful, six-month-old lesion on the bottom of her foot. Examination shows a hyperkeratotic lesion beneath the third metatarsal head without a central nucleated core. The third digit is contracted at the proximal interphalangeal joint and is nonreducible. The metatarsal parabola is normal. What is the procedure of choice? A. B. C. D.

flexor tendon transfer. flexor tenotomy of the third digit. arthrodesis fusion of the third digit. resection of the third metatarsal head.

44. A patient presents eight weeks after sustaining a fracture through the neck of the talus. What finding is a prognostic indicator that the vascular supply is intact? A. B. C. D.

resorption of subchondral bone of talar dome. increased density of the talar body. increased trabecular pattern across fracture. absence of degenerative arthritis.

ABPS 420 (April 2009)

Page 18

45. Which procedure for hallux abductovalgus has the least effect on growth centers in a young child? (note negative format) A. B. C. D.

Austin. opening abductory wedge. Lapidus. closing abductory wedge.

46. Which complication is not associated with the Keller bunionectomy? (note negative format) A. B. C. D.

loss of hallux purchase. diminished propulsion of digit. stress fracture of second metatarsal. tibial sesamoiditis.

47. In a Steindler stripping, which group of muscles is sectioned? A. B. C. D.

flexor digitorum brevis, abductor digiti quinti, abductor hallucis. flexor digitorum brevis, adductor hallucis, abductor hallucis. abductor hallucis, adductor hallucis, quadratus plantae. quadratus plantae, abductor digiti quinti, flexor digitorum brevis.

48. Twenty-one hours after an Austin bunionectomy under general anesthesia, the patient develops a temperature of 102 degrees Fahrenheit. What is the most likely cause? A. B. C. D.

pulmonary atelectasis. postoperative wound infection. superficial thrombophlebitis. constipation.

49. The preoperative complete blood count (CBC) on a 45-year-old male reveals the following: platelets: leukocytes: hemoglobin:

1.0 million 10,000 low

What is the most likely cause of these abnormal values? A. B. C. D.

myelofibrosis. polycythemia vera. thrombocythemia. leukemia.

50. Bence-Jones proteinuria is most commonly associated with which of the following diseases? A. B. C. D.

lymphoma. systemic lupus erythematosus. scleroderma. multiple myeloma.

ABPS 420 (April 2009)

Page 19

51. What is the local anesthetic that should be used on a patient with cirrhosis of the liver? A. B. C. D.

lidocaine (Xylocaine). mepivacaine (Carbocaine). procaine (Novocain). bupivacaine (Marcaine).

52. The most severe nerve injury is complete disruption of the axon, Schwann cell, and endoneurial tubes with varying disruption of the perineurium and epineurium. What is the term used to designate this condition? A. B. C. D.

neuropraxia. axonotmesis. neurotmesis. neuritis.

53. The most probable etiology of heloma molle of the fourth interdigital space is pressure between which of the following structures? A. B. C. D.

head of the fifth proximal phalanx and the base of the fourth proximal phalanx. head of the fourth proximal phalanx and the base of the fifth proximal phalanx. head of the fourth metatarsal and the base of the fifth proximal phalanx. head of the fifth metatarsal and the base of the fourth proximal phalanx.

54. For the traditional Austin procedure to be modified to produce both shortening and plantarflexion of the capital fragment, how must the osteotomy be angulated? A. B. C. D.

proximal-medial dorsal and distal-lateral plantar. distal-medial dorsal and proximal-lateral plantar. dorsal proximal-lateral and plantar-medial distal. medial plantar and dorsal lateral.

55. Which of the following results is seen in simple chronic anemia? A. B. C. D.

hemoglobin and hematocrit increase. hemoglobin and hematocrit decrease. hemoglobin decreases and hematocrit increases. hemoglobin increases and hematocrit decreases.

56. A 50-year-old nondiabetic male cigarette smoker presents with one block right calf claudication. Bilateral femoral pulses are palpable with no bruits. The left pedal pulse is present, but the right popliteal and pedal pulses are absent. What is the most likely level of arterial occlusion? A. B. C. D.

abdominal aorta. right common iliac artery. right popliteal artery. right superficial femoral artery.

ABPS 420 (April 2009)

Page 20

57. In performing a McBride bunionectomy under local anesthesia, which of the following nerves should not be anesthetized? (note negative format) A. B. C. D.

saphenous. deep peroneal. medial dorsal cutaneous. intermediate dorsal cutaneous.

58. Charcot joints are not commonly associated with which disease? (note negative format) A. B. C. D.

syringomyelia. gout. diabetes mellitus. alcoholism.

59. A 43-year-old male with Addison's disease of 20 years duration is on a maintenance dose of 30 mg. hydrocortisone per day. Prior to surgery, how should this patient be treated? A. B. C. D.

be supplemented with additional hydrocortisone. discontinue hydrocortisone. be supplemented with thyroxin. maintain his daily hydrocortisone dosage.

60. A two-and-one-half-year-old has been under treatment for the past year for a unilateral metatarsus adductus. The most recent treatment included a series of eight weekly casts with manipulation. Radiographs now show a metatarsus adductus angle of 25 degrees. What is the indicated treatment? A. B. C. D.

additional casting and manipulation. tarsometatarsal and intermetatarsal base releases and casting. Denis-Browne night splints. metatarsal base osteotomies with casting for six-to-eight weeks.

61. A 45-year-old male sustains a crushing-type injury to the left foot. Radiographs are negative for fracture and dislocation. Which of the following tests is the most helpful in determining skin flap viability? A. B. C. D.

fluorescein dye study. disital plethysmography. segmental pressure gradients. indium scan.

62. Which radiographic finding is most important in evaluating placement of an osteotomy for correction of hallux valgus? A. B. C. D.

tibial sesamoid position. hallux abductus angle. first intermetatarsal angle. first metatarsal protrusion distance.

ABPS 420 (April 2009)

Page 21

63. Surgical excision of the hallucal sesamoids would most directly result in what condition? A. B. C. D.

hallux limitus. lack of propulsive stability of the hallux. inability of the first ray to dorsiflex. inability of the forefoot to evert.

64. A man is coughing and wheezing from a foreign body lodged in his airway. What should be done? A. B. C. D. E.

give him four back blows. give him four back blows and four manual thrusts. give him water. attempt to dislodge the foreign body by sweeping your fingers through his mouth. encourage him to continue coughing.

65. Which malignant melanoma is most commonly misdiagnosed as a pyogenic granuloma? A. B. C. D.

superficial spreading. nodular. lentigo malignant. acral lentiginous.

66. A 35-year-old male presents with a hallux abductovalgus deformity of the left foot. Radiographs reveal the following: intermetatarsal angle: proximal articular set angle: distal articular set angle: hallux abductus angle: metatarsal adductus angle: metatarsal protrusion: medial exostosis is present

13 degrees 12 degrees 8 degrees 20 degrees 27 degrees +1 mm.

Which statement is true regarding findings of the intermetatarsal angle? A. B. C. D.

less important because of the hallux abductus angle. less important because of the metatarsus adductus angle. more important because of the hallux abductus angle. more important because of the metatarsus adductus angle.

67. A 31-year-old female presents with a complaint of pain of the dorsal distal aspect of the hallux. Radiographs reveal a radiolucent area at the distal phalanx with surrounding sclerosis. There is no sign of infection, no sinus tract, and no edema. What is the clinical diagnosis? A. B. C. D. E.

subungual exostosis. enchondroma. osteoid osteoma. osteochondroma. aneurysmal bone cyst.

ABPS 420 (April 2009)

Page 22

68. Excision of a second intermetatarsal neuroma results in an abducted third digit. Damage to which intrinsic muscles would produce this deformity? A. B. C. D.

first plantar interossei. third dorsal interossei. second lumbrical. flexor digitorum brevis.

ABPS 420 (April 2009)

Page 23

The following are examples of VISUAL questions. 69. The radiograph shown below is consistent with which type of Charcot diabetic osteoarthropathy? A. B. C. D.

developmental atrophic. developmental hypertrophic. coalescence atrophic. coalescence hypertrophic.

70. Shown below is a radiograph of a 14-year-old male who fell six feet and presented to the emergency department two hours after the injury. Which of the following diagnostic tests is the most important to order? A. B. C. D.

axial radiograph of the foot. computed tomography (CT) scan of the foot. magnetic resonance imaging (MRI) of the foot. spine radiograph.

ABPS 420 (April 2009)

71. The radiograph shown below was taken 29 days postoperatively. Which treatment is appropriate? A. B. C. D.

a minimum of 13 additional days of fixation is required. the pin can be removed as clinical healing is noted. the pin must remain in place since a nonunion is developing. re-evaluate the patient’s condition in one week.

Page 24

ABPS 420 (April 2009)

Page 25

SAMPLE RECONSTRUCTIVE REARFOOT/ANKLE WRITTEN QUESTIONS Answers found on page 30.

72. A 20-year-old male sustains his first ankle injury which is diagnosed as a rupture of the lateral collateral ligaments of the ankle. What is the most appropriate treatment plan? A. B. C. D.

splinting and functional rehabilitation elastic-type ankle support for six weeks. open repair of lateral ligaments. short-leg nonweightbearing cast for eight-to-ten weeks.

73. A 27-year-old man develops a deep wound infection three weeks following open reduction and internal fixation of a pilon ankle fracture with interfragmental screws and a medial buttress plate. The wound is debrided and the patient is placed on intravenous (I.V.) antibiotics. What should be done with the hardware? A. B. C. D.

removed regardless of the degree of fracture healing. removed and an external fixator applied. left in place until fracture union is obtained, unless loosening occurs. removed only if exposed.

74. Why is the trephine technique to fuse the posterior facet during a triple arthrodesis contraindicated in a cavus foot? (note negative format) A. B. C. D.

varus deformity in rearfoot cannot be corrected. cavus deformity creates too much stress through posterior facet. calcaneal and talar posterior facets are oblique to each other. it is too difficult technically to perform a trephine technique in a cavus foot type.

75. What is a contraindication to performing a Young tenosuspension flatfoot procedure? (note negative format) A. B. C. D.

talonavicular fault. patient age 12. rigid deformity. dorsiflexed first metatarsal.

76. How is chronic peroneus longus rupture resulting in a dorsiflexed and inverted foot best treated? A. B. C. D.

lateral transfer of anterior tibial tendon to cuneiforms. transfer of anterior tibial tendon to plantar aspect of foot. Young tenosuspension. Kidner procedure.

ABPS 420 (April 2009)

Page 26

77. The advancement of the Achilles tendon more anteriorly toward the posterior aspect of the subtalar joint on the dorsum of the calcaneus is useful in treating which of the following conditions? A. B. C. D.

spastic equinus. spastic heel varus. talipes calcaneus deformity. peroneal spastic flatfoot.

78. Axial load forces creating instability in diaphyseal fibular and tibial fracture surfaces may be dissipated by the use of which of the following mechanisms? A. B. C. D.

buttress plate. neutralization plate. tension band cerclage wiring. double compression plate.

79. In a patient with Charcot-Marie-Tooth disease (peroneal muscular atrophy) and weak anterior group muscles, which of the following tendons should be transferred to improve foot function? A. B. C. D.

posterior tibial. flexor digitorum longus. anterior tibial. flexor hallucis longus.

80. What is the most appropriate fixation technique for a small, displaced avulsion fracture of the lateral malleolus? A. B. C. D.

tension band. single lag screw. single lag screw and a one-third tubular plate. dynamic compression plate.

81. What is the muscle that is most commonly transferred through the interosseous membrane to function as a dorsiflexor of the foot? A. B. C. D.

posterior tibial. anterior tibial. peroneus longus. flexor digitorum longus.

82. A 21- year- old female presents with pain and swelling to the right ankle. The patient states that last week she jumped from a high fence on to uneven ground, twisted her foot and fell forward. Assuming that the foot was inverted and then forced into dorsiflexion, this type of trauma would suggest what type of frequently missed fracture? A. B. C. D.

lateral process of the talus. avulsion of the medial malleolus. oblique proximal fibula. sustentaculum tali of the calcaneus.

ABPS 420 (April 2009)

Page 27

83. In performing a pantalar arthrodesis, which materials would be least effective in compression fixation of the ankle and subtalar joint? (note negative format) A. B. C. D.

external fixator. intramedullary nail. large cancellous screws crossing both joints. crossed Steinman pins.

84. A 30-year-old male, who had a resection of a calcaneonavicular bar at age 11, exhibits fixed valgus deformity of his foot. Radiographs demonstrate the recurrence of a calcaneonavicular coalition with subtalar joint degeneration and talar beaking. What is the appropriate surgical treatment? A. B. C. D.

resection of coalition with interposition of extensor digitorum brevis muscle. subtalar joint arthrodesis. resection of coalition with subtalar arthroereisis. triple arthrodesis.

85. For a severe rigid and painful talipes equinovarus in an adult, what primary surgical approach is contraindicated? (note negative format) A. B. C. D.

soft-tissue release and tendon transfer. talectomy and foot-to-leg arthrodesis. tarsal osteotomies. triple arthrodesis.

86. In performing a posteromedial release for a congenital clubfoot deformity, what is the most important joint to release to prevent recurrence of the deformity? A. B. C. D.

ankle. subtalar. talonavicular. calcaneocuboid.

87. In a six-month-old child, aggressive casting for the equinus component of a clubfoot deformity may result in which of the following conditions? A. B. C. D.

dislocation of the ankle. subluxation of the midtarsal joint. compression of the subtalar joint. rupture of posterior talotibial ligament.

88. What condition is a contraindication in performing a lateral subtalar arthroereisis? (note negative format) A. B. C. D.

15 degrees of calcaneal valgus. plantarflexed talus. significant internal femoral torsion. weakness of the posterior tibial muscle.

ABPS 420 (April 2009)

Page 28

89. What is the ankle fusion technique that is indicated in a child to preserve the potential for growth of the distal tibial and fibular physis? A. B. C. D.

Blair fusion. transfibular fusion. distraction-compression fusion. Charnley compression fusion.

90. What is the first step in the open reduction and internal fixation of an ankle pilon fracture? A. B. C. D.

bone grafting of the metaphyseal defect. fixation of the fibular fracture. fixation of the medial malleolar fracture. restoration of the articular surface of the distal tibia.

91. Hypertrophy of synovial villi with impingement between capsule and joint surfaces and resultant thickening of the tissue may lead to which of the following pathological intra-articular structures encountered in ankle arthroscopy? A. B. C. D.

chondral lesions grade I-IV. osteochondral lesions. meniscoid bodies. impingement exostosis.

92. Which phrase best describes the physeal fracture of Tillaux? A. B. C. D. E.

occurs more frequently in adolescents than in children. represents a supination-external rotation mechanism. represents a Salter-Harris type III injury. all of the above. A and B only.

93. For a one-year-old patient with calcaneal valgus, what is an acceptable treatment plan? A. B. C. D. E.

manipulation only. manipulation with serial casting. soft-tissue release. arthroereisis. triple arthrodesis at skeletal maturity.

94. In the treatment of the equinovarus foot as described by Ponsetti, what is the last stage to be corrected by casting? A. B. C. D.

varus component. forefoot adductus component. supination at the subtalar joint component. equinus deformity.

ABPS 420 (April 2009)

Page 29

95. What is the primary indication for the Evans calcaneal osteotomy with insertion of a bone graft? A. B. C. D.

congenital vertical talus. residual talipes equinovarus. transverse plane flatfoot deformity. tarsal coalition.

96. A 16-year-old male with peroneal spastic flatfoot has 8 degrees tibia varum. What is the proper position of the calcaneus to the tibia for triple arthrodesis? A. B. C. D.

0 degrees. 2 degrees inverted. 6 degrees everted. 10 degrees everted.

97. A 52-year-old female presents with a unilateral dropfoot condition. Following electromyelography, nerve conduction studies and full neurological work-up the etiology remains obscure. Physical examination notes loss of the anterior tibial and long extensors, and weakness of the posterior tibial, peroneal, and triceps. A flaccid pes valgus dropfoot gait is noted. What is the most appropriate method of treatment? A. B. C. D.

subtalar fusion. triple arthrodesis. ankle fusion. pantalar fusion.

98. Which of the following techniques is not appropriate fixation for a Salter-Harris type III fracture of the distal tibial physis? (note negative format) A. B. C. D.

two smooth Kirschner wires through the fragment, across the physis, and into the metaphysis. one cancellous screw through the fragment and into the epiphysis. tension band wiring using two Kirschner wires through the fragment, across the physis, and into the metaphysis. one cancellous screw and one Kirschner wire through the fragment and into the epiphysis.

99. Which radiographic sign is not consistent with congenital convex pes planovalgus? (note negative format) A. B. C. D.

talus parallel with the longitudinal axis of the tibia. dorsiflexion of the calcaneus. navicular dorsal to the talus. talocalcaneal angle greater than 40 degrees on the anteroposterior view.

100.What is an indication for primary fusion of the subtalar joint following a calcaneal fracture? A. B. C. D.

concomitant peroneal injury. widening of the calcaneal body. large osseous defect. severe comminution.

ABPS 420 (April 2009)

Page 30

Answers for Sample Written Questions

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26.

C A C D A C A C C B D D A A D B B C A A A A C B A A

27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52.

C C A D D A B D B B B B B D C B C A A D A A C D C C

53. 54. 55. 56. 57. 58. 59. 60. 61. 62. 63. 64. 65. 66. 67. 68. 69. 70. 71. 72. 73. 74. 75. 76. 77. 78.

A B B D D B A A A C B E B D B A D D B A C A C A A B

79. 80. 81. 82. 83. 84. 85. 86. 87. 88. 89. 90. 91. 92. 93. 94. 95. 96. 97. 98. 99. 100.

A A A A D D A C B C C B C D B D C D D C B D

ABPS 420 (April 2009)

Page 31

SUGGESTED READING

The following references are a sampling of books from which readings may be helpful in preparation for ABPS written and oral examinations. The list is suggested only, and may not be exhaustive for any particular examination. Abramson, C. (ed.): Infectious Diseases of the Lower Extremities. Philadelphia, Williams & Wilkins, 1991. * Adelaar, R.S.: Disorders of the Great Toe. Rosemont, IL, AAOS, 1997. Adelaar, R.S.: Complex Foot and Ankle Trauma. Philadelphia, Lippincott, 1999. Alexander, I.: The Foot: Examination, Diagnosis and Conservative Care, 2nd ed. New York, Churchill Livingstone, 1996. Andreoli, T.E. (ed.): Cecil Essentials of Medicine, 5th ed. Philadelphia, Saunders, 2000. Baxter, D.E.: Foot and Ankle in Sport. St. Louis, Mosby, 1995. Berquist, T.H. (ed.): Radiology of the Foot and Ankle, 2nd ed.

New York, Raven Press, 2000.

Birrer, R.B.: Common Foot Problems in Primary Care, 2nd ed.. St. Louis, Mosby, 1998. Bouysset, M. (ed.): Bone and Joint Disorders of the Foot and Ankle: a Rheumatological Approach. New York, SpringerVerlag, 1998. Butterworth, R.: Color Atlas and Text of Forefoot Surgery. St. Louis, Mosby, 1992. Cailliet, R.: Foot and Ankle Pain, 3rd ed. Philadelphia, Davis, 1997. Canale, S.T.: Campbell’s Operative Orthopaedics, 9th ed. St. Louis, Mosby, 1997. Carrel, J.M. (ed.): Complications in Foot and Ankle Surgery, 3rd ed. Baltimore, Williams & Wilkins, 1992. * Cole, D.R. and DeLauro, T.M. (ed.): Neoplasms of the Foot and Leg. Baltimore, Williams & Wilkins, 1990. * Condon, R. (ed.): Manual of Surgical Therapeutics, 9th ed. Boston, Little-Brown Co., 1996. Coughlin, M.J. (ed.): Surgery of the Foot and Ankle, 7th ed. St. Louis, Mosby, 1999. Coussons, T.R. (ed.): Manual of Medical Care of the Surgical Patient, 4th ed. Boston, Little-Brown Co., 1990. * Crim, J.: Imaging of the Foot and Ankle. Philadelphia, Lippincott, 1996. Deutsch, A.L. (ed.): MRI of the Foot and Ankle. New York, Raven Press, 1992. DeValentine, S.J. (ed.): Foot and Ankle Disorders in Children. New York, Churchill Livingstone, 1991. * Dockery, G.L.: Color Atlas of Foot and Ankle Dermatology. Philadelphia, Lippincott, 1999. Dockery, G.L.: Cutaneous Disorders of the Lower Extremity. Philadelphia, Saunders, 1997.

* Out of print Compiled: September 2000

ABPS 420 (April 2009)

Page 32

Downey, M.S. and Malay, D.S.: Manual of Digital Surgery of the Foot. New York, Churchill Livingstone, 1991. * Draves, D.J.: Anatomy of the Lower Extremity. Baltimore, Williams & Wilkins, 1986. * Drennan, J.C. (ed.): The Child's Foot and Ankle. New York, Raven Press, 1992. Falanga, V.: Leg & Foot Ulcers: a Clinician’s Guide. St. Louis, Mosby, 1995. * Ferkel, R.D.: Arthroscopic Surgery: the Foot and Ankle. Philadelphia, Lippincott, 1996. Forrester, D.M., et al.: Imaging of the Foot and Ankle. Rockville, Aspen Publ., 1988. * Frykberg, R.G. (ed.): The High Risk Foot in Diabetes Mellitus. New York, Churchill Livingstone, 1991. * Gerbert, J. (ed.): Textbook of Bunion Surgery, 2nd ed. Mt. Kisco, NY, Futura Publ. Co., 1991. * Gilman, A.G.: Goodman and Gilman's Pharmacological Basis of Therapeutics, 9th ed. New York, Macmillan and Co., 1996. Goldman, D. (ed.): Perioperative Medicine: Medical Care of the Surgical Patient, 2nd ed. New York, McGraw-Hill, 1994. Gould, J.S. (ed.): Operative Foot Surgery. Philadelphia, Saunders, 1994. Greenfield, G.: Radiology of Bone Diseases, 5th ed. Philadelphia, Lippincott, 1990. Guhl, J.F. (ed.): Foot and Ankle Arthroscopy, 2nd ed. . Thorofare, NJ, Slack Inc, 1993. * Hansen, S.: Functional Reconstruction of the Foot and Ankle. Philadelphia, Lippincott, 2000. Harkless, L.B.: Foot and Ankle Secrets. Philadelphia, Hanley & Belfus, 1997. Harkless, L.B. and Krych, S.M. (eds.): Handbook of Common Foot Problems. New York, Churchill Livingstone, 1990. * Heim, U.: Internal Fixation of Small Fractures. New York, Springer-Verlag, 1988. Helal, B. (ed.): Surgery of Disorders of the Foot and Ankle. Philadelphia, Lippincott, 1996. Hetherington, V.J. (ed.): Hallux Valgus and Forefoot Surgery. New York, Churchill Livingstone, 1994. * Holmes, G.B. (ed.): Surgical Approaches to the Foot and Ankle. New York, McGraw-Hill, 1994. Jahss, M.H.: Disorders of the Foot and Ankle, 3 Vols., 2nd ed. Philadelphia, Saunders, 1991. Jay, R.M. (ed.): Current Therapy in Podiatric Surgery. Philadelphia, B.C. Decker, Inc., 1989. * Jay, R.M. (ed.): Pediatric Foot and Ankle Surgery. Philadelphia, Saunders, 1999. Johnson, K.A. (ed.): Foot and Ankle. New York, Raven Press, 1994. Johnson, K.A.: Surgery of the Foot and Ankle. New York, Raven Press, 1989. Joseph, W. S.: Handbook of Lower Extremity Infections. New York, Churchill Livingstone, 1990. Kang, H.S. and Resnick, D.: MRI of the Extremities: An Anatomic Atlas. Philadelphia, Saunders, 1990. * Out of print Compiled: September 2000

ABPS 420 (April 2009)

Page 33

Katzung, B.G.: Basic and Clinical Pharmacology, 7th ed. Stamford, CT, Appleton & Lange, 1998. Kelikian, H.: Disorders of the Ankle. Philadelphia, Saunders, 1985. * Kelikian, A.S. (ed.): Operative Treatment of the Foot and Ankle. Stamford, CT.: Appleton & Lange, 1999. Klenerman, L.: Foot and Its Disorders, 3rd ed. Oxford, Blackwell, 1991. Kominsky, S.J. (ed.): Advances in Podiatric Medicine & Surgery. St. Louis, Mosby, 1995-96. 3 Volumes * Kominsky, S.J. (ed.): Medical and Surgical Management of the Diabetic Foot. St. Louis, Mosby, 1994. Kozak, G.P. (ed.): Management of Diabetic Foot Problems, 2nd ed. Philadelphia, Saunders, 1995. * Lankhorst, G.J. (ed.): Management of Ankle Injuries. Kirtland, WA, Hogrefe & Huber Publ., 1991. * Levy, L.A. and Hetherington, V.J. (eds.): Principles and Practice of Podiatric Medicine. New York, Churchill Livingstone, 1989. * Longnecker, D.E., et al. (eds.): Dripps’ Introduction to Anesthesia, 9th ed. Philadelphia, Saunders, 1997. Luces, J.R. (ed.): Color Atlas of Foot Disorders. Mt. Kisco, NY, Futura Publ. Co., 1990. * Lundeen, R.O.: Manual of Ankle and Foot Arthroscopy. New York, Churchill Livingstone, 1992. * Lutter, L.D.: Atlas of Adult Foot and Ankle Surgery. St. Louis, Mosby, 1997. Mandel, S. (ed.): Handbook of Lower Extremity Neurology. New York, Churchill Livingstone, 2000. Marcinko, D.E. (ed.): Comprehensive Textbook of Hallux Abducto Valgus Reconstruction. St. Louis, Mosby, 1992. * Marcinko, D.E.: Infection of the Foot: Diagnosis, Management and Prevention. St. Louis, Mosby, 1998. Marcinko, D.E. (ed.): Medical and Surgical Therapeutics of the Foot and Ankle. Baltimore, Williams & Wilkins, 1992. * Masquelet, A.C. (ed.): Atlas of Surgical Exposures of the Lower Extremity. Philadelphia, Lippincott, 1993. Mayer, D.D., et al.: Foot and Ankle: a Sectional Imaging Atlas. Philadelphia, Saunders, 1993. McDermott, J.E.: The Diabetic Foot. Rosemont, IL, AAOS, 1995. McGlamry, E.D. (ed.): Comprehensive Textbook of Foot Surgery. 2 Vols., 2nd ed. Baltimore, Williams & Wilkins, 1992. McMinn, R.M.H.: Color Atlas of Foot and Ankle Anatomy, 2nd ed. St. Louis, Mosby, 1996. Merriman, L. (ed.): Assessment of the Lower Limb. New York, Churchill Livingstone, 1995. Mizel, M.S.: Orthopedic Knowledge Update: Foot and Ankle, 2nd ed. Rosemont, IL, AAOS, 1998. Morrissy, R.T. (ed.): Lovell and Winter's Pediatric Orthopedics, 2 vols., 4th ed. Philadelphia, Lippincott, 1996. Muller, M.E. (ed.): Manual of Internal Fixation, Techniques Recommended by the AO-ASIF Group, 3rd ed. New York, Springer-Verlag, 1991. * * Out of print Compiled: September 2000

ABPS 420 (April 2009)

Page 34

Myerson, M. (ed.): Current Therapy in Foot and Ankle Surgery. St. Louis, Mosby, 1993. * Myerson, M.S. (ed.): Foot and Ankle Disorders. Philadelphia, Saunders. 2000 Negus, D.: Leg Ulcers: A Practical Approach to Management, 2nd ed. Newton, MA., Butterworth, 1995. Oestreich, A.E.: How to Measure Angles from Foot Radiographs. New York, Springer-Verlag, 1990. * Oloff, L.M. (ed.): Musculoskeletal Disorders of the Lower Extremity. Philadelphia, Saunders, 1994. Omer, G.E. (ed.): Management of Peripheral Nerve Problems, 2nd ed. Philadelphia, Saunders, 1994. Ouriel, K.: Lower Extremity Vascular Disease. Philadelphia, Saunders, 1995. Peacock, E.E., Jr.: Wound Repair, 3rd ed. Philadelphia, Saunders, 1984. * Pfeffer, G.B. and Frey, C.C. (eds.): Current Practice in Foot and Ankle Surgery. New York, McGraw-Hill. Volume 1: 1993 *, Volume 2: 1994. Ranawat, C.S. (ed.): Disorders of the Heel, Rearfoot, and Ankle. New York, Churchill Livingstone, 1999. Resnick, D.: Bone and Joint Imaging, 2nd ed. Philadelphia, Saunders, 1996. Robbins, J.M.: Primary Podiatric Medicine. Philadelphia, Saunders, 1994. Root, N.L.: Normal and Abnormal Function of the Foot. Los Angeles, Clinical Biomechanics Corp., 1977. Salter, R.: Textbook of Disorders and Injuries of the Musculoskeletal System, 3rd ed. Baltimore, Williams & Wilkins, 1998. Sammarco, G.J. (ed.): Foot and Ankle Manual, 2nd ed. Philadelphia, Lea & Febiger, 1998. Sammarco, G.J. (ed.): Rehabilitation of the Foot and Ankle. St. Louis, Mosby, 1995. Sarrafian, S.K.: Anatomy of the Foot and Ankle, 2nd ed. Philadelphia, Lippincott, 1993. * Schwartz, S. (ed.): Principles of Surgery, 7th ed. New York, McGraw-Hill, 1999. Scurran, B.L. (ed.): Foot and Ankle Trauma, 2nd ed. New York, Churchill Livingstone, 1995. Shereff, M.J.: Atlas of Foot and Ankle Surgery. Philadelphia, Saunders, 1993. Sherk, H.H. (ed.): Lasers in Orthopaedics. Philadelphia, Lippincott, 1990. * Simons, G.W. (ed.): Clubfoot: the Present and a View of the Future. New York, Springer-Verlag, 1994. * Stiehl, J.B. (ed.): Inman's Joints of the Ankle. Baltimore, Williams & Wilkins, 1991. * Tachdjian, M.O.: Atlas of Pediatric Orthopedic Surgery. Philadelphia, Saunders, 1994. Tachdjian, M.O.: Clinical Pediatric Orthopedics. Stamford, CT, Appleton & Lange, 1997. Tierney, L.M. (ed.): Current Medical Diagnosis and Treatment, 40th ed. Norwalk, Appleton & Lange, 2001.

* Out of print Compiled: September 2000

ABPS 420 (April 2009)

Tollafield, D.R. (ed.): Clinical Skills in Treating the Foot. New York, Churchill Livingstone, 1997. Valmassy, R. L. (ed.): Clinical Biomechanics of the Lower Extremities. St. Louis, Mosby, 1995. Witkowski, J.: Color Atlas of Cutaneous Disorders of the Lower Extremities. New York, Igaku-Shoin, 1993. * Weinstein, S.L. (ed.): Turek's Orthopedics, 2 vols., 5th ed. Philadelphia, Lippincott, 1994. Williams, P.L. (ed.): Gray's Anatomy, 38th ed.. New York, Churchill Livingstone, 1995. Wulker, N. An Atlas of Foot and Ankle Surgery. St. Louis, Mosby, 1998. Yao, J.S.T.: Ischemic Extremity: Advances in Treatment. Norwalk, Appleton-Lange, 1995. Young, J.R. (ed.): Peripheral Vascular Diseases, 2nd ed. St. Louis, Mosby, 1996. Zier, B.G. (ed.): Essentials of Internal Medicine in Clinical Podiatry. Philadelphia, Saunders, 1990. *

* Out of print Compiled: September 2000

Page 35

NATIONAL BOARD OF PODIATRIC MEDICAL EXAMINERS PART II Clinical Science Examination

PRACTICE TEST 1

The Part II Practice Tests are representative of the content covered in the Part II Examination. They include question formats found in the actual examination. They also include questions of varying difficulty. A candidate’s performance on a Practice Test does not guarantee similar performance on the actual examination.

Copyright © 2008 by the National Board of Podiatric Medical Examiners. All rights reserved.

3

Practice Test 1

CLINICAL SCIENCE EXAMINATION PRACTICE TEST 1 60 questions

Directions for questions 1-56: These questions are followed by four suggested answers. Select the one answer that is best in each case. NOTE: Throughout this test, the term “medial oblique foot” refers to a nonweightbearing medial oblique position in which the film is flat on the orthoposer, the medial side of the foot is closest to the film and the sole forms a 45° angulation with the film, and the central beam is 90° to the film (the tubehead is angulated 0°). The converse is true for the term “lateral oblique.”

1. A 6-month-old child exhibits a limitation of hip abduction and an increase in thigh folds on the left side. The most likely diagnosis is (A) (B) (C) (D)

cerebral palsy transient synovitis of the left hip a congenitally dislocated left hip a fracture of the left femur

2. In a podiatric physician’s office, the best method to prevent HIV infection and/or hepatitis B infection is to use (A) (B) (C) (D)

an eyewash station thorough handwashing appropriate handling and disposal of sharps appropriate handling and disposal of waste

3. Following fifth-toe surgery, a patient reports that the toe is unstable and feels “floppy.” X-rays reveal loss of bone mass including the distal two-thirds of the proximal phalanx and most of the middle phalanx. A flail toe condition is diagnosed. The best procedure for this patient would be (A) (B) (C) (D)

a distal Syme's amputation amputation of the metatarsophalangeal joint removal of the base of the proximal phalanx surgical syndactylization of the fourth and fifth toes

4. Which of the following is the most appropriate antibiotic therapy for pseudomembranous colitis? (A) (B) (C) (D)

Vancomycin Gentamicin Ciprofloxacin Ticarcillin

5. Vertical talus presents with which of the following x-ray changes? (A) (B) (C) (D)

Dorsiflexed talus Dislocated navicular Increased first metatarsal declination angle High calcaneal inclination angle

6. Which of the following is a true statement about a fracture of the styloid process of the fifth metatarsal? (A) It is also known as a Jones fracture. (B) The mechanism of injury usually involves a strong force applied by the fibularis (peroneus) brevis. (C) It needs to be treated surgically due to an increased likelihood of nonunion. (D) Treatment may include immobilization, with the foot in an inverted position. 7. The most important factor for the treatment of a navicular stress fracture involves early (A) (B) (C) (D)

short leg casting internal fixation nonweightbearing use of electrical stimulation

Practice Test 1

8. Which of the following is a radiographic hallmark of dominant sagittal plane pronatory compensation? (A) (B) (C) (D)

Navicular bulge Increased cuboid abduction angle Decreased calcaneal inclination angle Decreased talar declination angle

9. A 4-year-old girl who has asthma presents with a persistent, pruritic, vesiculating, erythematous eruption of both feet. Which of the following is the most likely diagnosis? (A) (B) (C) (D)

Psoriasis Herpes simplex virus infection Atopic dermatitis Lichen planus

10. All of the following conditions contribute to hallux varus deformity EXCEPT (A) (B) (C) (D)

a negative intermetatarsal angle excision of the fibular sesamoid aggressive medial capsulorrhaphy lengthening of the extensor tendon

11. The scope of practice of podiatric medicine is primarily determined by (A) (B) (C) (D)

act of Congress state law the American Podiatric Medical Association the U.S. Department of Health and Human Services

12. Which of the following is the most sensitive blood test for neuromuscular disorders? (A) (B) (C) (D)

Creatine phosphokinase Lactate dehydrogenase Alkaline phosphatase Acid phosphatase

13. Proprioception and vibratory sensations are mediated by which of the following pathways? (A) (B) (C) (D)

Posterior column Corticospinal tract Extrapyramidal tract Lateral spinothalamic tract

4

14. Which of the following impressions from an MRI would be most consistent with a diagnosis of osteomyelitis of the first metatarsal? (A) A decreased signal intensity in a T1-weighted image (B) An increased signal intensity in a T2-weighted image (C) A decreased signal intensity in a T2-weighted image (D) A signal void in a T1-weighted image 15. The most common mechanism of ankle fracture is (A) (B) (C) (D)

supination adduction supination external rotation pronation external rotation pronation abduction

16. A 62-year-old obese patient has been hospitalized for the treatment of an infected foot ulcer. The patient is placed on subcutaneous heparin for prophylaxis against deep vein thrombosis. Which of the following laboratory findings would indicate effective heparin management? (A) Prothrombin time (PT) = 14.0 sec (B) Partial thromboplastin time (PTT) = 60.0 sec (C) Bleeding time = 5 min (D) Platelet count = 150,000/cu mm 17. A patient complains of pain in the posterior aspect of the ankle with palpation. Pain is particularly aggravated by dorsiflexion and plantarflexion of the hallux. Which of the following would be the best radiographic view to confirm the diagnosis? (A) (B) (C) (D)

An anteroposterior view of the affected ankle A medial oblique view of the foot A lateral view of the foot and ankle A Harris-Beath (calcaneal axial) view

5

18. In the application of a short leg cast, the main advantage of plaster of Paris over synthetic materials is that plaster of Paris is more (A) (B) (C) (D)

durable moldable porous radiolucent

19. Which of the following is an appropriate cleansing agent for a surgeon who is allergic to iodine? (A) (B) (C) (D)

Acetic acid Hexachlorophene Dakin’s solution Povidone-iodine

20. A doctor may NOT refuse to treat a prospective patient because the patient (A) (B) (C) (D)

has AIDS is unable to pay the doctor appears to be under the influence of drugs has been a plaintiff in previous malpractice suits

Practice Test 1

21. An individual with bronchial asthma triggered by an allergic reaction is likely to have elevated (A) (B) (C) (D)

monocytes in the WBC differential lymphocytes in the WBC differential eosinophils in the WBC differential sodium in the serum chemistry

22. Which of the following is a true statement about rigid forefoot valgus? (A) It is the cause of medial ankle sprains. (B) It is compensated for by subtalar joint supination. (C) It is confirmed by a positive anterior drawer sign. (D) It can be identified on a weightbearing x-ray if the talocalcaneal angle is increased.

Practice Test 1

6

23.

Initial treatment of the condition shown in this radiograph would most appropriately include (A) (B) (C) (D)

resection of the spur and plantar fasciotomy transcutaneous nerve stimulation nonweightbearing casting for 2 weeks mechanical support of the plantar fascia

____________________________________________________________________________________________

24. Blood pressure may drop when spinal anesthesia is used because (A) the patient is recumbent (B) sympathectomy may cause vasodilatation (C) motor blockade affects the vasoconstrictor muscles (D) sensory blockade obviates the need for higher pressure 25. Which of the following casting techniques allows the best visualization of the neutral subtalar joint position and the forefoot-to-rearfoot relationship? (A) (B) (C) (D)

Prone suspension Supine modified Langer Biofoam partial weightbearing BioVac inshoe vacuum

26. In a medical malpractice action, the plaintiff must prove that the podiatric physician did not meet the standard of care, which is defined as (A) that care necessary to correct the patient’s problem so the patient is cured (B) the care a reasonable podiatric physician would provide under the same or similar circumstances (C) the care a compassionate podiatric physician would provide under the same or similar circumstances (D) the best care that could be provided by any podiatric physician under the same or similar circumstances

7

27. Arrhythmia may occur from the toxic effects of which of the following medications? (A) (B) (C) (D)

Hydrochlorothiazide Nifedipine Digitalis Quinine

28. Balancing the heel of a positive cast used to fabricate a functional orthotic in an inverted position effectively decreases (A) (B) (C) (D)

supination around the subtalar joint axis supination around the midtarsal joint axis pronation around the subtalar joint axis dorsiflexion around the first metatarsophalangeal joint axis

29. The laying down of new bone surrounding an area of infection is referred to as (A) (B) (C) (D)

a cloaca an involucrum a sequestrum emphysema

30. Wound dehiscence may result from all of the following EXCEPT (A) (B) (C) (D)

infection hematoma sutures that are too tight everted wound margins

Practice Test 1

31. A 12-year-old patient who is being evaluated for hip pain of several weeks’ duration has other complaints that are more acute. The patient complains of headache and fever, some photophobia, and “just not feeling well.” These symptoms began yesterday and appear to be getting worse. The podiatric physician notices that the patient moves slowly and carefully and that the neck is painful and somewhat stiff. Temperature is 103°F. There is no sign of head trauma, and the pupils are equal and reactive. The lungs and heart are normal. There is no skin rash. The left hip is slightly tender over the trochanter but has full range of motion. The patient appears neurologically intact. Which of the following is the most likely diagnosis for these acute symptoms? (A) (B) (C) (D)

Osteomyelitis Lyme disease Meningitis Viral upper respiratory infection

32. A lateral weightbearing roentgenogram of a flexible flatfoot will demonstrate (A) a well-visualized sinus tarsi (B) a plantarflexed attitude of the talus (C) an increased angle of declination of the metatarsals (D) a decrease in the talocalcaneal angle

Practice Test 1

33. Which of the following intravenous medications is indicated for nausea? (A) (B) (C) (D)

Midazolam Meperidine Phenobarbital Promethazine

34. Ultrasound therapy is an appropriate treatment for which of the following? (A) (B) (C) (D)

Arterial insufficiency Enthesopathy Thrombophlebitis A stress fracture

35. Which of the following would be an appropriate cast for a patient who has undergone repair for an Achilles tendon rupture? (A) A long leg cast with the ankle plantarflexed 20º (B) A long leg cast with the foot 90º to the leg (C) A short leg cast with the ankle plantarflexed 20º (D) A short leg cast with the foot 90º to the leg 36. The primary function of neutrophils in the body’s defense is to (A) assist lymphocytes in response to anaphylaxis (B) phagocytize and destroy microorganisms (C) initiate the IgE immunologic response (D) release histamine 37. Which of the following phases of wound healing is characterized by the release of vasoactive amines and initial vasoconstriction? (A) (B) (C) (D)

Proliferative Inflammatory Maturation Fibroblastic

8

38. A town has a population of 500,000 in a particular year. During that year there are 500 live births and 500 deaths, 100 of which are of children under 1 year of age. What is the infant mortality rate? (A) 1/1,000 (B) 5/1,000 (C) 200/1,000 (D) 500/1,000 39. Which of the following bone tumors is malignant? (A) (B) (C) (D)

Chondroma Giant cell tumor Ewing’s sarcoma Osteoid osteoma

40. A 65-year-old woman has undergone an emergency incision and drainage of a plantar ulcer associated with ascending cellulitis. She has a history of insulin-dependent diabetes, hypertension, and chronic venous insufficiency. On the third postoperative day, the patient complains of severe substernal chest pain radiating to the back. Which of the following is the LEAST likely cause of the pain? (A) (B) (C) (D)

Costal chondritis Pulmonary embolism Myocardial infarction Dissecting aortic aneurysm

41. After administration of a general anesthesia, a podiatric physician injects 8 cubic centimeters of 2% lidocaine in Mayo fashion into a 42-year-old patient in order to perform a modified McBride procedure. During the prep and drape, the patient experiences increased temperature, arrhythmias, and muscle rigidity. The patient is most likely experiencing (A) (B) (C) (D)

anaphylaxis malignant hyperthermia a hypertensive crisis a myocardial infarction

9

42. Performing an inversion stress test with the ankle in a neutral position is useful in the detection of injury to which of the following ligaments? (A) (B) (C) (D)

Calcaneofibular Posterior talofibular Anterior talofibular Anterior inferior tibiofibular

43. Which of the following nail changes is characteristic of lichen planus? (A) (B) (C) (D)

Pitting Pterygium Thickening Oil drop staining

44. If all other factors remain unchanged, a blacker radiograph can be produced by (A) (B) (C) (D)

increasing the source-to-image distance increasing the mA decreasing the kVp decreasing the exposure time

45. An increase in the thickness of the calcaneal fat pad is a cardinal sign of which of the following conditions? (A) (B) (C) (D)

Hyperparathyroidism Cushing’s syndrome Acromegaly Hypervitaminosis A

Practice Test 1

46. Fever that occurs during the first postoperative day after a general anesthetic has been administered is most likely the result of which of the following? (A) (B) (C) (D)

Atelectasis Infection Malignant hyperthermia Urinary tract infection

47. Tibial varum should be measured with the rearfoot (A) (B) (C) (D)

parallel with the leg perpendicular to the ground in the neutral calcaneal stance position in the relaxed calcaneal stance position

48. Which of the following tendons is exposed during neuroma surgery performed on the third interspace through a dorsal approach? (A) (B) (C) (D)

Plantar interosseous to the third toe Flexor digitorum brevis to the third toe Lumbrical to the fourth toe Dorsal interosseous to the fourth toe

Practice Test 1

10

49.

Which type of image is depicted in this slide? (A) MRI T1 (B) MRI T2 (C) CT scan (D) Bone scan ____________________________________________________________________________________________

50. A 65-year-old patient presents for a bunionectomy. The patient has been healthy and takes no medications. A reasonable intervention to prevent pulmonary emboli postoperatively would be (A) (B) (C) (D)

elastic stockings warfarin subcutaneous heparin an inferior vena cava filter

51. All of the following are appropriate drugs for the treatment of rheumatoid arthritis EXCEPT (A) (B) (C) (D)

penicillamine prednisone pentoxifylline piroxicam

52. After surgery for a dislocated hammer toe, the digit is still slightly dorsiflexed at the metatarsophalangeal joint, despite the fact that a complete sequential reduction was performed. At the time of surgery, the podiatric physician should have done which of the following? (A) Performed a flexor tendon lengthening procedure. (B) Performed an extensor tendon lengthening procedure. (C) Stabilized the digit to the base of the proximal phalanx with a Kirschner wire. (D) Stabilized the digit to the base of the proximal phalanx and across the metatarsophalangeal joint with a Kirschner wire.

11

56. Peroneal muscular atrophy is best known as

53. Lidocaine can be used to (A) (B) (C) (D)

Practice Test 1

(A) (B) (C) (D)

increase cardiac contractility control premature ventricular contractions control atrial flutter control atrial fibrillation

Questions 54-55 refer to the following case.

57. Which of the following are mandates of state departments of health? Select the two that apply.

A 67-year-old woman presents with complaints of a tender, progressively flattening arch on the left foot. She has no pain in the right foot, and modifying her shoe gear to softer, more “comfortable” styles has not helped alleviate her symptoms. Her symptoms began approximately 6 weeks ago when she heard a popping sound in her foot. 54. Which of the following is the most likely diagnosis? (A) (B) (C) (D)

(A) (B) (C) (D)

(A) (B) (C) (D)

Manage educational services Manage environmental services Set public health policies and standards Collect, analyze, and disseminate health information (E) Set drug dispensing standards

58. Which of the following accessory bones are sesamoid bones? Select the two that apply. (A) (B) (C) (D) (E)

A Lisfranc’s fracture dislocation A form of arthritis A stress fracture of the fifth metatarsal A ruptured tibialis posterior tendon

55. Which of the following diagnostic modalities would be best for confirming the diagnosis? An MRI scan of both feet A CT scan of both feet Multiple x-ray views An arthritis panel to include SMAC-12, ANA, ESR, C-reactive protein, RA, and LE prep

Charcot-Marie-Tooth disease Refsum’s disease Dejerine-Sottas disease Guillain-Barré syndrome

Os peroneum Os trigonum Os supra naviculare Accessory navicular type I Accessory navicular type II

59. Which of the following are potential signs of early sepsis in the elderly? Select the three that apply. (A) (B) (C) (D) (E)

Agitation Respiratory acidosis Respiratory rate of 24 Polyuria Nocturnal disorientation (“sundowning”)

____________________________________________________________________________________________ 60. List the following steps in a McBride bunionectomy in the order in which they are performed (from first to last). (A) (B) (C) (D) (E)

Section of the deep transverse intermetatarsal ligament Release of the conjoined adductor tendon Medial capsulotomy Removal of the fibular sesamoid Exostectomy

END OF PRACTICE TEST 1

1. 2. 3. 4. 5.

_____ _____ _____ _____ _____

NATIONAL BOARD OF PODIATRIC MEDICAL EXAMINERS PART II Clinical Science Examination

PRACTICE TEST 2

The Part II Practice Tests are representative of the content covered in the Part II Examination. They include question formats found in the actual examination. They also include questions of varying difficulty. A candidate’s performance on a Practice Test does not guarantee similar performance on the actual examination.

Copyright © 2008 by the National Board of Podiatric Medical Examiners. All rights reserved

Practice Test 2

15

CLINICAL SCIENCE EXAMINATION PRACTICE TEST 2 60 questions

Directions for questions 1-56: These questions are followed by four suggested answers. Select the one answer that is best in each case. NOTE: Throughout this test, the term “medial oblique foot” refers to a nonweightbearing medial oblique position in which the film is flat on the orthoposer, the medial side of the foot is closest to the film and the sole forms a 45° angulation with the film, and the central beam is 90° to the film (the tubehead is angulated 0°). The converse is true for the term “lateral oblique.”

1. Generalized osteopenia is a characteristic feature of (A) (B) (C) (D)

osteomyelitis osteosarcoma osteoporosis osteoarthritis

2. Which of the following anesthetics is normally administered intravenously? (A) (B) (C) (D)

Thiopental Enflurane Halothane Nitrous oxide

3. A 19-year-old male patient presents with an itchy and burning rash on the bottom of his foot. Physical examination reveals patchy scaling on an erythematous base. The lesions are dry and extend to the sides of the foot in a moccasin distribution. Which of the following would be an appropriate presumptive diagnosis? (A) (B) (C) (D)

Psoriasis Tinea pedis Lichen planus Pityriasis rubra pilaris

4. Which of the following is the single most important preventable risk factor for peripheral vascular disease? (A) (B) (C) (D)

Stress High fat diet Cigarette smoking Alcohol abuse

5. All of the following conditions may cause pes planus EXCEPT (A) (B) (C) (D)

vertical talus gastrocnemius equinus posterior tibial tendon rupture Charcot-Marie-Tooth disease

6. The film/cassette is placed vertically in the orthoposer for which of the following views? (A) (B) (C) (D)

Weightbearing lateral Weightbearing dorsoplantar Weightbearing calcaneal axial Nonweightbearing medial oblique

7. Which of the following tests is used in the management of patients on warfarin? (A) (B) (C) (D)

Erythrocyte sedimentation rate (ESR) Partial thromboplastin time (PTT) Prothrombin time (PT) Rumpel-Leede test

8. When implant surgery is performed, the most appropriate antibiotic prophylaxis is provided by which of the following? (A) (B) (C) (D)

First-generation cephalosporins Third-generation cephalosporins Aminoglycosides Quinoline

Practice Test 2

9. Which of the following would be most useful in the treatment of a patient with ankle fusion secondary to trauma? (A) (B) (C) (D)

A stiff sole shoe A rocker-bottom shoe A shoe with a Thomas heel A lateral heel flare

10. A 28-year-old female patient presents with pain in the left forefoot that began after a long hike on a mountainous trail. There is no history of trauma. Physical examination reveals nontender range of motion of the metatarsophalangeal joints. Deep palpation of the intermetatarsal spaces does not reproduce the patient’s symptoms; however, palpation along the second metatarsal is painful. Which of the following is the most likely diagnosis? (A) Intermetatarsal space neuroma in continuity (B) Capsulitis of the second metatarsophalangeal joint (C) Stress fracture of the second metatarsal (D) Degenerative joint disease of the second metatarsophalangeal joint 11. The radiographic weightbearing lateral view of the foot requires (A) placing the film flat on the orthoposer (B) placing the lateral side of the foot against the film (C) directing the central beam at the ankle (D) angling the tubehead 90° from vertical 12. Which of the following findings is most commonly observed in the first phase of neuropathic arthropathy (Charcot’s joint)? (A) (B) (C) (D)

Ankylosis Cyanosis Pain Erythema

16

13. Ankle stress radiographs of an isolated rupture of the calcaneofibular ligament will reveal a (A) positive anterior drawer sign and negative talar tilt (B) positive anterior drawer sign and positive talar tilt (C) negative anterior drawer sign and negative talar tilt (D) negative anterior drawer sign and positive talar tilt 14. A 38-year-old patient with diabetes mellitus is in the preoperative holding area and surgery has been delayed for 2 hours. One-half of the patient’s prescribed AM NPH insulin dose was administered at 7:00 AM. It is now 9:30 AM and the patient suddenly becomes disoriented and begins to perspire profusely. Which of the following actions would be most appropriate? (A) Obtain an electrocardiogram (EKG). (B) Perform a finger-stick blood glucose evaluation. (C) Administer the remaining half of the patient’s prescribed AM NPH insulin. (D) Administer midazolam 2 mg to the patient. 15. All of the following are radiographic features of closed-kinetic-chain subtalar joint pronation EXCEPT an (A) (B) (C) (D)

increased metatarsus adductus angle increased talar declination angle increased talocalcaneal angle anterior break in the cyma line

16. A podiatric physician who submits a report of child abuse will be (A) liable if no abuse in fact occurred (B) liable if the report was true but made with malice (C) immune from liability if there was reasonable cause to suspect abuse (D) immune from liability only if the podiatric physician personally examined the child

Practice Test 2

17

17. Which of the following antibiotic combinations, given orally, would offer the best overall coverage for gram-positive, gram-negative, and anaerobic infections? (A) Penicillin and ofloxacin (B) Erythromycin and trimethoprim/sulfamethoxazole (C) Clindamycin and ciprofloxacin (D) Metronidazole and oxacillin Questions 18-19 refer to the following case. A 12-year-old patient presents with pain on the lateral side of the right ankle when standing. The subtalar joint is restricted in motion, and pain is elicited on palpation of the fibular (peroneal) tendons. 18. A lateral x-ray would most probably demonstrate (A) (B) (C) (D)

a large os trigonum a posteriorly broken cyma line an increased calcaneal inclination dorsal talar head and neck beaking

19. If the medial oblique view of the foot is negative, which of the following views will probably be positive? (A) Harris-Beath (calcaneal axial) (B) Anteroposterior (C) Sesamoidal axial (D) Mortise ankle ___________________________________________ 20. Dual, curvilinear soft tissue calcifications that are parallel to one another and somewhat serpiginous in appearance are radiographic features of (A) (B) (C) (D)

phleboliths atherosclerosis Mönckeberg’s arteriosclerosis tumoral calcinosis

21. Which of the following statements is true concerning therapeutic ultrasound? (A) It is best used without a coupling agent. (B) It will dissolve intratendinous calcifications. (C) It can be used to diagnose acute and chronic tendon ruptures. (D) Sonic energy increases the temperature in deep tissues. 22. Decreased metatarsal bone girth is seen in which of the following? (A) (B) (C) (D)

Osteogenesis imperfecta Thyroid acropachy Acromegaly Paget’s disease

23. The most common cell types seen in cases of immediate hypersensitivity are (A) (B) (C) (D)

lymphocytes and monocytes neutrophils and eosinophils mast cells and basophils band cells

24. Which of the following local anesthetics has the shortest duration of action? (A) (B) (C) (D)

Tetracaine Lidocaine Bupivacaine Etidocaine

Practice Test 2

25.

The radiograph shown is most characteristic of (A) (B) (C) (D)

osteoarthritis gouty arthritis psoriatic arthritis rheumatoid arthritis

18

Practice Test 2

19

26. Which of the following is the first step in basic life support (BLS)? (A) (B) (C) (D)

Ventilation Airway restoration Restoration of circulation Assessment for unresponsiveness

27. A 42-year-old patient underwent second interspace neuroma surgery 2 years ago. The patient now complains that the second toe is deviated medially. Damage to which of the following muscles during surgery would result in this finding? (A) (B) (C) (D)

First plantar interossei Second dorsal interossei Third dorsal interossei Lumbricales

28. Which of the following is a CONTRAINDICATION to the resection of a calcaneonavicular coalition? (A) (B) (C) (D)

Peroneal spasm Talar beaking A completely ossified bar Degenerative disease of the subtalar joint

29. An apparently nervous 25-year-old female patient demonstrates lid lag during examination, along with a fine tremor of her outstretched hands. Her skin is warm, moist, and smooth. Her nervousness is most likely the result of which of the following? (A) (B) (C) (D)

Addison’s disease Cushing’s syndrome Pheochromocytoma Hyperthyroidism

30. The proliferative phase of wound healing is characterized by (A) (B) (C) (D)

neutrophilic infiltrates remodeling and scar tissue formation epithelialization and connective tissue repair inflammation and decreased tensile strength

31. Stabilization of toes at the metatarsophalangeal joint during midstance is aided by which of the following muscles? (A) (B) (C) (D)

Gastrocnemius Quadratus plantae Tibialis posterior Extensor digitorum longus

32. Running in a shoe with a sole that is too rigid across the metatarsophalangeal joints increases a person’s risk of developing (A) (B) (C) (D)

piriformis syndrome posterior tibial tendinitis fibularis (peroneus) longus tendinitis anterior tibial shin splints

33. The hinge axis concept is useful when planning which of the following procedures? (A) (B) (C) (D)

A hallux interphalangeal joint arthrodesis A subtalar joint arthroereisis A metatarsal basilar osteotomy A Kidner procedure

34. Intravenous barbiturates can produce all of the following EXCEPT (A) (B) (C) (D)

hypnosis unconsciousness with increased doses myocardial excitation with increased doses interference with the sensitivity of the medullary respiratory center to carbon dioxide

35. Capitation is generally part of which of the following health care delivery systems? (A) (B) (C) (D)

PPO IPA HMO Fee-for-service

36. From a plantar approach, the common digital nerve divides into two proper digital nerves which, in relation to the deep transverse metatarsal ligament, are (A) (B) (C) (D)

superficial superior proximal deep

Practice Test 2

37. A 64-year-old male patient complains of a cold left foot and cramping pain in his left calf and buttock when walking. He also states that he is impotent. Examination reveals a weak femoral pulse on the left side and nonpalpable pulses at the popliteal and pedal arteries. It is most likely that an occlusion has occurred in which of the following arteries? (A) (B) (C) (D)

Deep femoral Superficial femoral Common femoral Common iliac

38. A 21-year-old basketball player sustained a complete rupture of the Achilles tendon. It is now 5 days after the injury and the patient has been immobilized in a posterior splint. The most appropriate treatment at this time is (A) a primary anastomosis with an augmentation graft if necessary (B) resection of the fibrous plug and an augmentation graft of the defect (C) a long leg cast for 4 weeks followed by a short leg cast for 4 weeks (D) a short leg cast for 6 weeks followed by aggressive physical therapy 39. Radiographs of a college basketball player who presents with a foot injury reveal a minimally displaced fracture of the proximal shaft of the fifth metatarsal. Treatment should consist of which of the following? (A) (B) (C) (D)

Tape and immobilization A nonweightbearing cast An Ace bandage and ambulation as tolerated An Unna’s boot and partial weightbearing with crutches

40. All of the following are clinical signs of anabolic steroid use in young athletes EXCEPT (A) (B) (C) (D)

alopecia hypertension osteoporosis temporary sterility

20

41. Which type of exercise should be recommended to minimize muscle atrophy in a patient with a short leg cast? (A) (B) (C) (D)

Concentric Isotonic Isokinetic Isometric

42. When a dressing is applied after a flexor to extensor tendon transfer for stabilization, it is most important to (A) allow the toe to seek its own level (B) apply povidone-iodine to prevent infection (C) plantarflex the proximal phalanx at the metatarsophalangeal joint (D) dorsiflex the proximal phalanx at the metatarsophalangeal joint 43. Which of the following therapies is recommended for initial treatment of an acute asthmatic attack? (A) (B) (C) (D)

Intravenous theophylline Inhaled glucocorticoids Inhaled beta-adrenergic agonists Intramuscular antihistamines

44. A podiatric physician suspects that a patient may be abusing the hydrocodone prescribed for the patient’s foot surgery. All of the following signs and symptoms would indicate hydrocodone abuse EXCEPT (A) (B) (C) (D)

miosis diarrhea drowsiness pruritus of the nose

45. Which of the following is true about the talocalcaneal angle? (A) (B) (C) (D)

It is 8°-10° in the normal foot. It is increased in a flatfoot deformity. It is increased in a supinated foot deformity. It is decreased in a pronated foot deformity.

Practice Test 2

21

46. In civil court, the performance of a procedure on a patient without the patient’s informed consent could be considered (A) (B) (C) (D)

assault malpractice abuse battery

47. Which of the following gait patterns is most commonly seen in cases of lower motor neuron pathology? (A) (B) (C) (D)

Steppage Circumduction Festinating Ataxic

48. A 30-year-old male patient with a history of seizures since childhood has a seizure during a routine office visit for a wound check. The podiatric physician should immediately (A) (B) (C) (D)

insert a bite block turn the patient on his side administer phenytoin, 500 mg, IV administer diazepam, 10 mg, IV

49. Which of the following is a typical radiographic finding in cases of osteochondroma? (A) Epiphyseal location (B) Moth-eaten appearance (C) Osseous protuberance that grows toward the joint (D) Osseous protuberance with the cortex continuous with the parent bone 50. In podiatric radiology, the standard anode-film distance usually falls within a range of (A) (B) (C) (D)

12-17 inches 18-23 inches 24-30 inches 31-36 inches

51. Which of the following is the best treatment for a dermatofibroma on the anterior ankle? (A) Fulguration or laser ablation (B) Salicylic acid treatments with debridement (C) Surgical excision and pathological examination (D) Wide excision, pathological examination, and probable chemotherapy 52. The doctor-patient privilege may be waived (A) by the patient only (B) by the doctor only (C) only if both the patient and the doctor agree to waive it (D) only with the consent of a judge 53. How often should a patient’s vital signs be monitored following general inhalation anesthesia? (A) (B) (C) (D)

Every 15 minutes until stable Every hour Twice a day Every nursing shift

54. The risk of which of the following is increased most for patients who undergo hip and knee-joint replacement procedures? (A) (B) (C) (D)

Pneumonia Atelectasis Pulmonary embolism Myocardial infarction

55. A patient’s blood laboratory results reveal elevated levels of creatine phosphokinase, aldolase, and alanine transaminase. Which of the following is the most likely diagnosis? (A) (B) (C) (D)

Muscular dystrophy Rheumatoid arthritis Aneurysmal bone cyst Cerebral palsy

Practice Test 2

22 58. Which of the following radiographic angles in a dorsoplantar view are most indicative of talipes equinovarus? Select the three that apply.

56. If a person falls from a height, causing the lateral process of the talus to drive into the calcaneus over the neutral triangle, the most likely calcaneal fracture would be (A) (B) (C) (D)

(A) (B) (C) (D) (E)

a beak fracture a sustentaculum fracture a joint depression fracture an avulsion fracture

59. Typical presentations of multiple myeloma include which of the following? Choose the three that apply.

57. In a T1-weighted MRI of the foot, which of the following lesions will have the lowest signal intensity? Select the three that apply. (A) (B) (C) (D) (E)

Talo-first metatarsal angle of 10° Talo-first metatarsal angle of 5° Kite’s angle (talocalcaneal angle) of 5° Kite’s angle (talocalcaneal angle) of 25° Bohler’s angle of 30°

(A) (B) (C) (D) (E)

Ganglion cyst Unicameral bone cyst Adamantinoma Interosseous lipoma Hemangioma

Bone pain Renal failure Hypocalcemia Normocytic anemia Multiple areas of uptake on a bone scan

___________________________________________________________________________________________ 60. List the order in which the components of the talipes equinovarus deformity should be corrected during casting treatment (from first to last). (A) (B) (C) (D)

Adduction component Inversion component Equinus component Internal torsional component at the tibia

1. 2. 3. 4.

_____ _____ _____ _____

END OF PRACTICE TEST 2

NATIONAL BOARD OF PODIATRIC MEDICAL EXAMINERS PART II Clinical Science Examination

PRACTICE TEST 3

The Part II Practice Tests are representative of the content covered in the Part II Examination. They include question formats found in the actual examination. They also include questions of varying difficulty. A candidate’s performance on a Practice Test does not guarantee similar performance on the actual examination.

Copyright © 2008 by the National Board of Podiatric Medical Examiners. All rights reserved.

Practice Test 3

25 CLINICAL SCIENCE EXAMINATION PRACTICE TEST 3 60 questions

Directions for questions 1-55: These questions are followed by four suggested answers. Select the one answer that is best in each case. NOTE: Throughout this test, the term “medial oblique foot” refers to a nonweightbearing medial oblique position in which the film is flat on the orthoposer, the medial side of the foot is closest to the film and the sole forms a 45° angulation with the film, and the central beam is 90° to the film (the tubehead is angulated 0°). The converse is true for the term “lateral oblique.”

1. Diazepam is used in the anesthetic setting to reduce (A) (B) (C) (D)

cardiac depression respiratory tract secretions postoperative pain anxiety

2. Which of the following classes of drugs is used to treat osteoporosis? (A) (B) (C) (D)

Calcium channel blockers Bisphosphonates Antiestrogens Steroids

3. Radiographically, the inversion ankle stress view is most useful in evaluating which of the following conditions? (A) (B) (C) (D)

Achilles tendon rupture Lateral ligament rupture Osteoarthritis Osteochondral defect

4. Which of the following is the phase of gait during which the body’s center of mass is directly over the metatarsophalangeal joints and the sesamoids are most compressed? (A) (B) (C) (D)

Just after heel contact Midstance Just before heel lift Swing

5. When should a podiatric physician prescribe ambulation and range-of-motion exercises for a postoperative patient with a history of deep vein thrombosis? (A) Before symptoms develop, for prevention (B) After symptoms develop but before a definitive diagnosis is made (C) After a definitive diagnosis is made (D) Three days after a venous thrombus has been identified 6. Which of the following conditions has a strong (short) T1 signal on MRI? (A) (B) (C) (D)

Lipoma Osteomyelitis Hemangioma Ganglionic cyst

7. In football players, the most common mechanism of metatarsophalangeal dislocation is (A) (B) (C) (D)

hyperdorsiflexion hyperplantarflexion hyperadduction hyperabduction

8. The main concern during surgery following an inadvertent scrape or needle stick is (A) (B) (C) (D)

hepatitis A infection hepatitis B infection a positive TB test a gram-positive infection

Practice Test 3

9. A 60-year-old male patient is scheduled for a neurectomy in a podiatric physician’s office. On preoperative examination his blood pressure is 160/115 mm Hg on three consecutive readings. In this situation, the podiatric physician should do which of the following? (A) Cancel the surgery. (B) Administer calcium channel blockers and proceed with the surgery 15 minutes later. (C) Change the procedure to an in-hospital setting for the next day. (D) Proceed with the surgery as planned. 10. A patient presents with interdigital lesions that fluoresce coral pink under a Wood’s light. The drug of choice for treatment is (A) (B) (C) (D)

tetracycline erythromycin ciprofloxacin terbinafine

11. A 26-year-old patient presents to the emergency department with a puncture wound of the right foot, sustained while working in a construction zone. Emergency department records confirm a similar injury 1 year ago, at which time the patient was given a tetanus immunization. Which of the following is a true statement about tetanus prophylaxis at this time? (A) No additional tetanus immunization is necessary. (B) The patient will require half of the normal dose of tetanus toxoid. (C) The patient will require tetanus immunoglobulin only. (D) The patient will require tetanus immunoglobulin and tetanus toxoid. 12. All of the following are risk factors for the development of deep vein thrombophlebitis EXCEPT (A) (B) (C) (D)

obesity varicose veins use of local anesthetics smoking

26

13. In closed-chain kinetics, internal rotation of the leg results in (A) (B) (C) (D)

locking of the midtarsal joint effective weightbearing of the first ray pronation of the subtalar joint abduction of the talus

14. Twelve hours postoperatively, a patient with a cast complains of severe pain, bluish discoloration of the digits, numbness, and throbbing. Which of the following would be the most appropriate treatment? (A) (B) (C) (D)

Apply heat. Apply ice and elevate. Apply a bivalve cast. Administer intramuscular meperidine.

15. The establishment of the doctor-patient relationship requires a (A) written contract between doctor and patient that must be witnessed or notarized (B) written contract that must be signed by both doctor and patient (C) written or oral contract that must be acknowledged by both doctor and patient (D) written, oral, or implied contract between doctor and patient 16. Which of the following conditions would benefit most from immobilization alone? (A) (B) (C) (D)

Atrophic nonunion Hypertrophic nonunion Infected nonunion Pseudoarthrosis

17. Patients with rheumatoid arthritis frequently have a subluxation of (A) (B) (C) (D)

the subtalar joint the lumbar spine C1 and C2 T2 and T3

Practice Test 3

27

18. Aggressive dissection of the first interspace at the time of a fibular sesamoid release is most likely to damage the intrinsic muscle belly of which of the following muscles? (A) (B) (C) (D)

Quadratus plantae Abductor hallucis First dorsal interosseous First plantar interosseous

19. In the oral treatment of onychomycosis, which of the following drugs is fungicidal at low concentrations? (A) (B) (C) (D)

Griseofulvin Terbinafine Fluconazole Itraconazole

20. In a Lisfranc’s fracture of the midfoot, the most common displacement seen is (A) (B) (C) (D)

dorsal and lateral dorsal and medial plantar and lateral plantar and medial

21. After the primary repair of a ruptured anterior tibial tendon, the most appropriate casting technique would be a (A) (B) (C) (D)

short leg cast with the ankle neutral short leg cast with the ankle plantarflexed long leg cast with the ankle plantarflexed long leg cast with the ankle neutral

22. OSHA regulations require that an employer do which of the following? (A) Provide hepatitis B vaccinations for all employees. (B) Post OSHA regulations in a highly visible area for all employees. (C) Require that all employees receive CPR certification. (D) Establish a contractual agreement with an OSHA-approved management program.

23. In order to classify a neuromuscular disorder as cerebral palsy, there must be (A) (B) (C) (D)

cranial trauma a brain tumor a nonprogressive lesion paralysis of the lower extremity

24. On lateral weightbearing radiographs, markedly increased density is noted in the area of the subtalar joint and sustentaculum tali. Osteophytosis is noted at the level of the talar neck. The differential diagnosis should include all of the following EXCEPT (A) (B) (C) (D)

osteoarthritis tarsal coalition compression fracture of the subtalar joint osteomyelitis

25. The inflammatory phase of wound healing normally lasts approximately (A) (B) (C) (D)

24 hours 3-5 days 14 days 6 weeks

26. In the normal development of the foot, the center of ossification appears last in the (A) (B) (C) (D)

talus calcaneus lateral cuneiform navicular

27. When surgical scars are planned, it is important to remember that skin tension lines appear in which direction relative to the direction of muscle movement? (A) (B) (C) (D)

Oblique Parallel Tangential Perpendicular

Practice Test 3

28. The initial treatment of choice for reflex sympathetic dystrophy in the lower extremity is (A) (B) (C) (D)

surgical sympathectomy the administration of vasoconstrictors immobilization of the affected extremity physical therapy of the affected extremity

29. Which of the following instruments has strong, heavily constructed opposing jaws, each of which is scooped out like the tip of a curette? (A) (B) (C) (D)

A gouge A malleable retractor A rongeur forceps A double-action bone cutting forceps

30. Transcutaneous electrical nerve stimulation (TENS) is used for (A) (B) (C) (D)

neuromuscular reeducation edema reduction pain relief biofeedback to overcome postinjury muscle inhibition

28

31. A 58-year-old female patient has a septic ankle joint that requires irrigation. She has a negative cardiac history and takes no medications. The patient has had fevers to 103.2°F and blood cultures are positive for Staphylococcus aureus. Which of the following anesthesia options would be CONTRAINDICATED in this patient? (A) (B) (C) (D)

Spinal anesthesia Sciatic block anesthesia General endotracheal anesthesia Laryngeal mask anesthesia

32. A patient presents with a second toe that is dislocated in the sagittal plane. One year ago, the proximal phalangeal base of the toe was removed. The most likely cause of the dislocation is loss of attachment of the (A) first lumbrical and the first and second dorsal interossei (B) first lumbrical and the first and second plantar interossei (C) first and second lumbricals and the first dorsal interosseous (D) first and second lumbricals and the first plantar interosseous

29

Practice Test 3

33.

Which of the following organisms would most likely produce the finding displayed in the radiograph? (A) (B) (C) (D)

Staphylococcus aureus Pseudomonas aeruginosa Streptococcus pyogenes Clostridium perfringens

Practice Test 3

34. Below the knee, osteoid osteomas are most commonly found in the (A) (B) (C) (D)

calcaneus tibia metatarsal navicular

35. Which of the following findings is most suggestive of child abuse? (A) (B) (C) (D)

Limping gait Multiple leg bruises A spiral fracture of the humerus Fractures in different stages of healing

36. A 30-year-old patient presents with bilateral ankle pain. A systems review is positive for shortness of breath and a dry cough. Physical examination reveals multiple tender erythematous subcutaneous nodules on both legs. The probable etiology of the ankle pain is (A) (B) (C) (D)

sarcoidosis psoriatic arthritis enteropathic arthritis rheumatoid arthritis

37. All of the following are considered seronegative spondyloarthropathies EXCEPT (A) (B) (C) (D)

psoriatic arthritis ankylosing spondylitis erythromelalgia Reiter’s syndrome

38. An intra-articular epiphyseal fracture extending through the physis and epiphysis would be classified as which type of Salter-Harris fracture? (A) (B) (C) (D)

Type I Type II Type III Type IV

30

Questions 39-40 refer to the following case. A 47-year-old patient has pain in the right ankle of several weeks’ duration. The patient remembers no inciting event but says the pain worsens with increased activity. The right foot appears more pronated than the left foot on weightbearing; on attempts to rise to the toes, the patient has considerable pain and the rearfoot does not invert. Pain is found on palpation just proximal to the navicular tuberosity. 39. Which of the following is the most likely diagnosis? (A) (B) (C) (D)

Popliteal rupture Talonavicular bar Calcaneal stress fracture Tibialis posterior tendinitis

40. Which of the following examination techniques would be most appropriate? (A) Side-to-side compression of the calcaneus (B) Supination of the subtalar joint against resistance (C) A calf squeeze (D) A Coleman block test

31

41. Rheumatic heart disease is characterized by (A) (B) (C) (D)

mitral valve damage tricuspid valve damage holosystolic murmur a history of Staphylococcus aureus infection

42. Which of the following sets of parameters will result in the lowest radiation dose to the patient? (A) (B) (C) (D)

15 mA, 10/60 sec, 69 kVp 15 mA, 10/60 sec, 60 kVp 15 mA, 5/60 sec, 69 kVp 30 mA, 5/60 sec, 60 kVp

43. Absorbable pins are an appropriate method of fixation for which of the following procedures? (A) (B) (C) (D)

Proximal metatarsal osteotomy Austin bunionectomy Base wedge osteotomy Metatarsophalangeal joint fusion

44. A 53-year-old female patient presents with a 1-year history of an unsightly painless “bump” on the dorsum of the right foot. She has worked outdoors in sandals all of her adult life. The lesion is 1 centimeter in diameter. It has an elevated, “rolled” translucent border and a central umbilication with a central crust that bleeds on debridement. Which of the following would be an appropriate presumptive diagnosis? (A) (B) (C) (D)

Red ant bite Verruca vulgaris Basal cell carcinoma Molluscum contagiosum

45. A nerve block procedure may NOT be successful in the presence of infection for which of the following reasons? (A) Local anesthetics are bases and may be neutralized by the acidic environment of an infection. (B) Local anesthetics may be degraded by the increased amounts of pseudocholinesterase. (C) Local anesthetics may be degraded by the bacteria. (D) Edema and inflammation may prevent the anesthetic from crossing the nerve’s lipid barrier.

Practice Test 3

46. Which of the following immune reactions best describes allergic contact dermatitis? (A) (B) (C) (D)

Immune-complex formation Hapten-mediated cytotoxicity IgE-mediated allergic reaction Delayed cutaneous hypersensitivity

47. A 20-year-old male patient with hemophilia presents for podiatric treatment of a paronychia. He is currently under treatment by his physician and requires routine transfusion and Factor VIII administration. Which of the following would provide the most pertinent information? (A) (B) (C) (D)

Platelet count Reticulocyte count Prothrombin time (PT) Partial thromboplastin time (PTT)

48. If a patient presents with the classic symptoms of a stress fracture, but the radiographs are initially normal, the next special imaging study to order would be (A) (B) (C) (D)

ultrasound xeroradiography bone scintigraphy angiography

49. Which of the following is the most common bone lesion? (A) (B) (C) (D)

An aneurysmal bone cyst An enchondroma An osteochondroma An osteoblastoma

50. A competitive collegiate basketball player presents with a 1-week history of lateral midfoot pain and swelling. Radiographs reveal a nondisplaced transverse fracture at the proximal metaphyseal-diaphyseal junction of the fifth metatarsal. No intramedullary sclerosis is present at the fracture site. The most appropriate treatment would be (A) (B) (C) (D)

a posterior splint a bone stimulator with partial weightbearing fracture shoe immobilization for 6-8 weeks open reduction and internal fixation with an intramedullary screw

Practice Test 3

51. Which of the following is considered a violation of sterile technique? (A) (B) (C) (D)

Double-gloving Hands above the head Hands below the waist Switching positions back-to-back

52. A 45-year-old construction worker sustains a severe crush injury to the right foot, and on admission to the emergency department is noted to be hypotensive. The paramedics report that the patient lost approximately 1,000 cubic centimeters of blood during transit to the hospital. Packed red cell transfusions are instituted. Approximately 4 hours later, the patient is in shock with severe back pain, flushing, and fever. Which of the following is a likely diagnosis? (A) (B) (C) (D)

Sepsis Pulmonary edema Myocardial infarction Major hemolytic reaction

53. Following repair of an Achilles tendon rupture, which type of cast should be applied? (A) A short leg cast with the foot in a neutral position (B) A short leg cast with the foot in an equinus position (C) A long leg cast with the foot in a neutral position (D) A long leg cast with the foot in an equinus position 54. The number of electromagnetic waves that pass a given point per unit of time is referred to as the (A) (B) (C) (D)

wavelength wave frequency photon length speed of propagation

55. In the United States, the largest percentage of the health dollar is utilized in which of the following age categories? (A) (B) (C) (D)

0-1 year 2-8 years 19-64 years 65 years and older

32

56. A T1 image on an MRI scan is described by which of the following parameters? Select the two that apply. (A) (B) (C) (D) (E)

TE of 25 msec TE of 125 msec TE of 1000 msec TR of 25 msec TR of 500 msec

57. Which of the following complications are commonly caused by sickle cell disease? Select the three that apply. (A) (B) (C) (D) (E)

Osteoporosis Early puberty Chronic hematuria Aseptic necrosis of the hips Chronic osteomyelitis caused by Salmonella

58. A patient with a unilateral flatfoot deformity presents with pain centered over the medial navicular. Radiographic studies of the involved foot demonstrate the presence of a small rounded ossicle-like structure adjacent to the medial navicular. Which of the following are likely conclusions? Select the three that apply. (A) (B) (C) (D)

This is an os tibiale externum type I. This is an os tibiale externum type II. This is an avulsed fracture fragment. This has nothing to do with the symptomatology. (E) Contralateral studies may make MR evaluation unnecessary.

33

59. Which of the following statements regarding normal first ray function and anatomy are true? Select the three that apply. (A) The first ray axis has a supinatory-pronatory nature. (B) The first ray consists of the first metatarsal and proximal phalanx. (C) Inversion and adduction motions are coupled with dorsiflexion of the first ray. (D) The first ray axis orientation runs from posteromedial and dorsal to anterolateral and plantar. (E) The fibularis (peroneus) longus stabilizes the first ray against the lesser tarsus and ground in midstance.

Practice Test 3

60. Informed consent may be legally obtained from which of the following? Select the three that apply. (A) (B) (C) (D) (E)

A geriatric patient A legal guardian A 19-year-old patient An intoxicated patient A minor patient

END OF PRACTICE TEST 3

35

Practice Test 1

PRACTICE TEST 1 ANSWER KEYS AND RATIONALES

Sequence: Key 1 C In congenital hip dislocation, the femoral head is usually posterior and superior to the acetabulum, resulting in shortening of the limb with an increase in thigh folds and limited hip abduction on the affected side. Sequence: Key 2 C Even though actual transmission is rare, because sharps injuries are so commonly associated with occupational transmission of HIV and HBV, sharps management is the best method to prevent infection. Sequence: Key 3 D Surgical syndactylization of the fourth and fifth toes provides stability and a predictable position for a flail fifth digit. Sequence: Key 4 A Vancomycin is most appropriate in this case because it produces a rapid response to treat the disorder. Sequence: Key 5 B Congenital vertical talus presents as the talus fixed in a vertical position with hypoplasia of the talar neck and head. The navicular is dislocated and articulates with the dorsal aspect of the talar neck. The tibionavicular and dorsal talonavicular ligaments are contracted preventing reduction of the navicular. Sequence: Key 6 B The fibularis (peroneus) brevis tendon inserts on the styloid process of the fifth metatarsal and can cause fracture of the process with excessive traction applied to the bone by the tendon.

Sequence: Key 7 C Uncomplicated navicular stress fractures will usually heal with strict nonweightbearing for 6 to 8 weeks; surgical treatment is usually not recommended unless the navicular is unstable. Sequence: Key 8 C The greater the angle formed between the axis and the plane of motion, the more motion is available in that plane. As the calcaneal inclination angle decreases, the sagittal plane compensation becomes more significant. Sequence: Key 9 C The presence of asthma along with these symptoms makes atopic dermatitis the most likely etiology. Sequence: Key 10 D Lengthening of the extensor tendon will affect sagittal plane positioning but will not affect transverse plane (hallux varus) deformities. Sequence: Key 11 B The extent to which a podiatric physician can practice is determined by the state legislature in a set of laws called the State Practice Act. Sequence: Key 12 A Creatine phosphokinase is an enzyme found in heart, brain, and skeletal muscle tissue. It is used to detect muscle disorders in serum blood testing. Sequence: Key 13 A The posterior columns of the spinal cord carry the sensory nerve fibers for position, vibration, and proprioception.

Practice Test 1

36

Key Sequence: 14 B MRI T2-weighted images of osteomyelitis have an increased signal intensity.

Sequence: Key 21 C Allergic or atopic diseases are some of the most common causes of eosinophilia.

Sequence: Key 15 B The most common mechanism of a fractured ankle is supination external rotation. At the time of injury the foot is in a supinated position and an external rotatory force is applied.

Sequence: Key 22 B Rigid forefoot valgus that cannot be compensated for by forefoot inversion and first ray dorsiflexion will require supination of the subtalar joint.

Sequence: Key 16 B The typical normal PTT range is 28-30 sec. Effective prophylaxis against deep vein thrombosis is typically considered to require a 1.5-fold to 2.5-fold elevation in the PTT.

Sequence: Key 23 D A heel spur or plantar fasciitis is shown on the radiograph. Plantar fasciitis is a biomechanical condition caused by overuse and is best treated mechanically. Mechanical support initially includes shoe modification, stretching, and taping and later includes orthotics to support the plantar fascia.

Sequence: Key 17 C A lateral radiograph is the most appropriate view to evaluate the posterior aspect of the ankle. The posterior process of the talus is clearly visualized on a lateral view of the foot and ankle.

Sequence: Key 24 B Hypotension during spinal anesthesia is the result of arterial and venous dilation.

Sequence: Key 18 B The primary advantage of plaster of Paris compared to synthetic materials is that it is more moldable. This is particularly important for pediatric orthopedic conditions which often require close contouring and molding of the cast to the extremity in order to maintain proper alignment and accurate positioning. Sequence: Key 19 B Hexachlorophene does not contain iodine and is sufficient for surgical preparation. Sequence: Key 20 A Patients with AIDS have been found to be protected by the Americans with Disabilities Act. It is illegal to discriminate against these patients by refusing to treat them or referring them to others based on their HIV status.

Sequence: Key 25 A With the prone suspension technique, the forefoot-torearfoot relationship can be visualized from behind, allowing the subtalar joint to be manipulated through its range of motion to help determine the joint’s neutral position. Sequence: Key 26 B The definition of standard of care is the level of practice of the average, prudent provider in any given community. Sequence: Key 27 C Digitalis poisoning can cause a variety of arrhythmias.

37

Key Sequence: 28 C Since calcaneal inversion (frontal plane motion) is a component of subtalar joint supination, placing the heel in an inverted position also puts the subtalar joint in a supinated position, thus limiting subtalar joint pronation. Sequence: Key 29 B An involucrum is new bone formed beneath an elevated periosteum surrounding necrotic bone in osteomyelitis. Sequence: Key 30 D Generalized causes of wound dehiscence include infection, hematoma, injury to the wound, and incorrect suturing technique. Sequence: Key 31 C The symptoms of acute meningitis include fever, headache, and a stiff neck. Sequence: Key 32 B A lateral roentgenogram of a flatfoot pronated in stance will reveal talar plantarflexion. Sequence: Key 33 D Promethazine is a drug used prophylactically against postoperative nausea and vomiting. Sequence: Key 34 B Ultrasound therapy is used to treat enthesopathy, which is inflammation at the site of attachment of muscle tendons and ligaments to bones or joint capsules. Ultrasound therapy reduces tightness and spasms, decreases inflammation, and assists in healing.

Practice Test 1

Sequence: Key 35 A A long leg cast with the ankle plantarflexed 20º will immobilize the medial and lateral heads of the gastrocnemius muscle across the knee and also reduce the tension of the Achilles tendon distally. Sequence: Key 36 B Neutrophils evolve from stem cells with the specialized ability to move toward and completely engulf bacteria and fungi. They are capable of producing a number of different granules containing potent chemicals, which results in the destruction of the engulfed organisms. Sequence: Key 37 B During the inflammatory phase of wound healing collagen exposed during wound formation activates the clotting cascade. After injury to tissue occurs the cell membranes, damaged from wound formation, release thromboxane A2 and prostaglandin 2-alpha, potent vasoconstrictors. This helps to limit hemorrhage. After a short period, capillary vasodilatation occurs secondary to local histamine release. Sequence: Key 38 C Infant mortality rate in a population is defined as the number of deaths of children under the age of 1 during a year divided by the number of live births that year. The rate is expressed per 1,000 live births. Sequence: Key 39 C By definition, Ewing’s sarcoma is a malignant bone tumor. Sequence: Key 40 A Costal chondritis will not usually be localized to the substernal area. It will normally present as moderate, generalized chest pain.

Practice Test 1

Key Sequence: 41 B Malignant hyperthermia is a potentially life-threatening though rare disorder characterized by extremely high fever, muscle rigidity, cardiac arrhythmias, and acidosis. It may be precipitated by inhaled anesthetics, both depolarizing and nondepolarizing, neuromuscular blocking agents and by other means including stress. Sequence: Key 42 A The calcaneofibular ligament is specifically stressed when the ankle is in a neutral position and inversion force is applied against the foot relative to the tibia. Sequence: Key 43 B Pterygium is frequently seen when nails are affected by lichen planus due to involvement of the nail matrix. Sequence: Key 44 B When a radiograph is taken, current is measured in milliamperes (mA). Increasing the current increases the number of electrons emitted, which in turn increases the intensity of the rays produced, thus resulting in a blacker radiograph. Sequence: Key 45 C Enlargement of the hands and feet is an early feature of acromegaly. Sequence: Key 46 A Of the options presented, the most likely cause of a fever that occurs during the first postoperative day is atelectasis. Sequence: Key 47 C To properly assess tibial varum, which is the inward angulation of the distal third of the shaft toward the midline in the frontal plane, the rearfoot should be in the neutral calcaneal stance position.

38

Sequence: Key 48 C Of the options listed, the only tendon encountered in the third interspace is the lumbrical to the fourth toe. Sequence: Key 49 C CT scans use special x-ray equipment to produce multiple images of the inside of the body. A computer is used to join the images together to produce cross-sectional views of the area of interest. The image in this question was taken at the level of the foot. Sequence: Key 50 A In the absence of any hypercoagulable state or significant risk factors, the mechanical compression provided by elastic stockings is usually sufficient to prevent blood clot formation postoperatively. Sequence: Key 51 C Pentoxifylline is used for the treatment of arterial insufficiency. Sequence: Key 52 D A complete sequential reduction will reduce the deformity, but the position must be maintained with temporary fixation to prevent redislocation. Sequence: Key 53 B Lidocaine helps suppress ectopic ventricular rhythms by depressing automaticity which decreases the slope of phase IV depolarization. Sequence: Key 54 D A rupture of the posterior tibial tendon is followed by symptoms which often include pain, swelling, a flattening of the arch, and an inward rolling of the ankle. Generally these symptoms do not improve with conservative treatment such as shoe modification.

39

Key Sequence: 55 A An MRI scan is the imaging study of choice to confirm the diagnosis. An MRI scan can reveal a complete or incomplete rupture of the tibialis posterior tendon. Sequence: Key 56 A Charcot-Marie-Tooth disease is also known as peroneal muscle atrophy. As the disease progresses, symmetrical muscular atrophy and weakness are apparent in peroneal muscles and toe extensors. Sequence: Key 57 CD Health departments pursue a legislative policy agenda promoting health. They also design and implement a health care delivery system.

Practice Test 1

Sequence: Key 58 AD Accessory bones are bones that are not regularly present. A sesamoid is a type of accessory bone that is embedded within a tendon or joint capsule. On x-ray, this type of variant anatomy may be mistaken for pathology. Sequence: Key 59 ACE Urinary incontinence and dehydration are often early signs of sepsis in elderly patients. Polyuria is rare. Because of the increased respiration rate, respiratory alkalosis is a risk. Sequence: Key 60 The order is: C E A B D The McBride procedure is an important historical procedure for hallux valgus correction in which the sequence of steps is medial capsulotomy, exostectomy, section of the deep transverse intermetatarsal ligament, release of the conjoined adductor tendon, and removal of the fibular sesamoid.

Practice Test 2

40 PRACTICE TEST 2 ANSWER KEYS AND RATIONALES

Sequence: Key 1 C Generalized osteopenia on a radiograph is a characteristic feature of osteoporosis; however, it cannot be used as the only diagnostic criterion for the condition. Sequence: Key 2 A Thiopental is an intravenous sedative-hypnotic that is used as an induction agent. Sequence: Key 3 B Tinea pedis most often appears as dryness and scaling in a moccasin distribution. Sequence: Key 4 C The use of tobacco is the most prevalent and preventable risk factor involved in lower extremity ischemia and disease. Sequence: Key 5 D Charcot-Marie-Tooth disease specifically increases the spasticity of the fibularis (peroneus) longus muscle, resulting in the supination of the entire foot around the subtalar joint, producing a pes cavus appearance of the foot. Sequence: Key 6 A In a weightbearing lateral view, the film is placed vertically in the orthoposer with the medial aspect of the foot and ankle against the plate. Sequence: Key 7 C PT measures blood clotting ability and is increased with the use of warfarin.

Sequence: Key 8 A First-generation cephalosporins are most effective against Staphylococcus aureus, the most common cause of postoperative infection. Sequence: Key 9 B A rocker-bottom shoe acts as a dynamic lever to decrease the need for required ankle motion in the sagittal plane during the gait cycle, allowing the patient to ambulate with a more normal gait. Sequence: Key 10 C Stress fracture of the metatarsal can occur after excessive cyclic loading of the bone, such as after prolonged, strenuous weightbearing activity. Sequence: Key 11 D When a lateral radiograph is taken, the patient stands with the medial side of the foot placed against the film and the tubehead angled 90 degrees from vertical. Sequence: Key 12 D Swelling and erythema are seen in the initial phase of Charcot arthropathy. Sequence: Key 13 D An isolated rupture of the calcaneofibular ligament will allow the talus to invert relative to the tibia due to lateral instability but will not allow anterior displacement of the talus to the tibia if the anterior talofibular ligament is intact.

41

Key Sequence: 14 B Blood glucose levels should be measured preoperatively and postoperatively. The need for additional measurements is determined by the duration and magnitude of surgery and the stability of the diabetes. Signs of hypoglycemia include tachycardia, hypertension, and diaphoresis. Sequence: Key 15 A An increased metatarsus adductus angle is associated with the podopediatric condition of metatarsus adductus. It involves medial displacement of the metatarsals and is not a feature of subtalar joint pronation. Sequence: Key 16 C Child abuse legislation in most states provides for immunity from prosecution arising from reporting suspected child abuse in good faith. Sequence: Key 17 C Clindamycin is used for anaerobic infections. Ciprofloxacin is primarily used to treat gram-negative infections but also provides gram-positive coverage. Sequence: Key 18 D X-ray findings in tarsal coalition include dorsal talar head and neck beaking. Pain is a common symptom. Limitations of subtalar motion and valgus deformity vary in severity. Sequence: Key 19 A The Harris-Beath (calcaneal axial) view can allow visualization of the middle facet of the talocalcaneal joint. The joint space is obliterated in the case of osseous coalition. If there is fibrocartilaginous coalition, the joint space appears narrow and subchondral sclerosis may be present.

Practice Test 2

Sequence: Key 20 C Mönckeberg’s arteriosclerosis occurs in peripheral arteries of the lower limbs as calcification of the tunica media. The radiographic appearance has been called “rail tracking” and described as a pipe stem pattern. Sequence: Key 21 D In therapeutic ultrasound, high frequency sound waves are absorbed primarily by connective tissue, such as tendons and ligaments, heating the tissue, increasing blood flow, and reducing chronic inflammation. Sequence: Key 22 A Osteogenesis imperfecta is a genetic disease that results in weakness of the bones secondary to a malfunction of the body’s production of collagen. Pedal manifestations include decreased metatarsal girth. Sequence: Key 23 C Immediate hypersensitivity is the result of antigen binding to IgE, which is attached to circulating tissue mast cells and basophils. Sequence: Key 24 B Lidocaine is commonly used for peripheral nerve blocks and has a usual duration of 1-3 hours. Sequence: Key 25 A Common radiographic findings of osteoarthritis include subchondral sclerosis, asymmetric joint space narrowing, and marginal osteophyte formation. Sequence: Key 26 D The American Heart Association Basic Life Support Guidelines establish the assessment for unresponsiveness as the initial action to be performed.

Practice Test 2

Key Sequence: 27 B It is critical to understand the surgical anatomy of the second interspace in order to avoid potential complications. Severing of the second dorsal interossei will cause the second toe to deviate medially. Sequence: Key 28 D Degenerative disease of the subtalar joint with a calcaneonavicular coalition requires arthrodesis, not resection of the coalition. Sequence: Key 29 D Clinical features of hyperthyroidism include warm moist skin, lid lag, and fine tremors. Sequence: Key 30 C The second phase of wound healing is the proliferative phase, which is characterized by epithelialization, angiogenesis, granulation tissue formation, and collagen deposition. Sequence: Key 31 B Stabilization of the toes in midstance is assisted by the plantar intrinsic musculature, which includes the quadratus plantae. Sequence: Key 32 D A shoe that does not flex at the metatarsophalangeal joints has the effect of increasing the lever arm of ground reactive force at the ankle. The longer the lever arm of ground reactive force, the greater the tension on the Achilles tendon in plantarflexing the ankle. This results in overuse of the tibialis anterior muscle as it attempts to counteract the resistance of the Achilles tendon, causing inflammation where the muscle of the tibialis anterior attaches to the anterior aspect of the tibia. Sequence: Key 33 C Maintaining the hinge axis for a metatarsal basilar osteotomy is critical to provide another point of stabilization.

42

Sequence: Key 34 C The cardiovascular effects of barbiturates include a decrease in blood pressure and a compensatory increase in heart rate. Sequence: Key 35 C Capitation is a fixed periodic HMO payment calculated to cover the expected cost of providing services to patients over a period of time. Sequence: Key 36 A When an excision is performed through a plantar approach, the two proper digital nerves that are divisions of the common digital nerve are found superficial to the deep transverse metatarsal ligament. Sequence: Key 37 D Symptoms of iliac artery occlusion include weak femoral pulses, sexual dysfunction, and buttock claudication. Sequence: Key 38 A Young healthy athletes have a high rate of success with surgical repair of an Achilles tendon rupture. Sequence: Key 39 B The patient is at risk for delayed union or nonunion of the fracture due to instability and limited blood supply in the region of the fracture. Nonweightbearing is a necessary part of the conservative post-injury treatment to allow for complete healing in a timely manner. Sequence: Key 40 C Anabolic steroids are FDA-approved for use to relieve the bone pain associated with osteoporosis. They do not cause osteoporosis in young athletes.

43

Key Sequence: 41 D Muscle atrophy due to disuse is a major concern when a patient is in a cast. Isometric exercises, a form of resistance training where the muscle contracts but does not change length while exerting a force, allows muscles to be exercised while the limb is immobilized. Sequence: Key 42 C A flexor to extensor tendon transfer for stabilization requires healing with the proximal phalanx plantarflexed at the metatarsophalangeal joint to ease tension on the tenodesis. Sequence: Key 43 C Inhaled beta-adrenergic agonists provide immediate relief of asthma symptoms by causing direct dilation of the constricted air passages. Sequence: Key 44 B Opioid agonists cause constipation. Sequence: Key 45 B The talocalcaneal angle is important in the evaluation of a flatfoot deformity. When the talocalcaneal angle is markedly increased, heel valgus is said to be present, which indicates a more significant deformity. Sequence: Key 46 D Under civil law, the performance of a procedure without consent is an offense referred to as battery. Sequence: Key 47 A Lower motor neuron lesions cause weakening of muscles and paralysis which leads to a steppage gait. Sequence: Key 48 B The greatest immediate risk to this patient is aspiration of vomit, which is minimized when the patient is turned on his side. Vomiting is not uncommon in patients experiencing seizures.

Practice Test 2

Sequence: Key 49 D A key radiographic feature that defines an osteochondroma is the continuity of the cortex of the lesion with the cortex of the involved bone. Sequence: Key 50 C The standard distance between the film and anode when a podiatric foot x-ray is performed is 24-30 inches. Sequence: Key 51 C Dermatofibromas are common benign tumors but some pigmented basal cell carcinomas and even some melanomas can present with a similar appearance, so excision with pathological examination is often indicated. Sequence: Key 52 A In many states, the doctor can invoke a legal privilege on the patient’s behalf when asked to disclose or divulge information about the patient. This privilege belongs to the patient, not the doctor, so only the patient may waive it, usually by written consent. Sequence: Key 53 A After a general anesthetic is administered, a minimal level of monitoring must be provided in the postanesthesia care unit. Vital signs including blood pressure, heart rate, breathing rate, airway patency, and level of consciousness should be monitored every 15 minutes. Sequence: Key 54 C The risk of deep vein thrombosis associated with total hip arthroplasty ranges from 20% to 80%; for total knee replacement the risk is approximately 50%. Patients who undergo these procedures are at increased risk for the development of pulmonary embolism.

Practice Test 2

Key Sequence: 55 A All three tests when elevated suggest myopathy or a neuromuscular disease such as muscular dystrophy. Sequence: Key 56 C The mechanism of injury produces an intra-articular fracture of the calcaneus, creating a posterior facet fragment that is impacted or “depressed” into the calcaneal body. Sequence: Key 57 ABC Tissues consisting primarily of water have the lowest signals on T1-weighted images. Sequence: Key 58 ABC In talipes equinovarus, the increase in the talo-first metatarsal angle from the normal range of 0° to -20° is due to the adductus of the forefoot, while the decrease in the talocalcaneal angle from the normal range of 20° to 50° reflects the inversion (varus) of the heel.

44

Sequence: Key 59 ABD Lytic lesions are frequently seen on bone scans as “cold” areas. Hypercalcemia is frequently seen due to increased bone destruction and release of calcium into the circulation. Sequence: Key 60 The order is: A B D C To reduce a talipes equinovarus deformity accurately, the casting treatment should correct the components in the following order: adduction, inversion, internal torsion at the tibia, and equinus.

45

Practice Test 3

PRACTICE TEST 3 ANSWER KEYS AND RATIONALES

Sequence: Key 1 D In the anesthetic setting, diazepam is used as a preoperative medication and adjuvant drug partly because of its anxiolytic properties. Sequence: Key 2 B Bisphosphonates are a class of compounds that slow bone resorption and are used to treat osteoporosis. Sequence: Key 3 B The inversion ankle stress view or “talar tilt” test is most useful for evaluating injury to the lateral ankle ligaments. Sequence: Key 4 C The metatarsophalangeal joints and sesamoids are regions that receive maximal ground reactive force at the very end of the midstance phase of gait, just before heel lift. Sequence: Key 5 A Deep vein thrombosis is a serious medical complication that needs to be addressed preventively, prior to formation. Sequence: Key 6 A A fat-containing lesion like a lipoma has a short T1 signal and a long T2 signal.

Sequence: Key 7 A Extreme dorsiflexion of the metatarsophalangeal joint causes the metatarsal head to rupture the plantar joint capsule with dorsal and proximal displacement of the digit. The injury is common among football players due to the combination of artificial playing surfaces which require the use of more flexible shoegear and the frequency with which the player is positioned with the toes fixed on the playing surface and the heel raised. Sequence: Key 8 B The hepatitis B virus (HBV) is a blood borne pathogen that causes serious viral disease and targets the liver. It can cause chronic infection, cirrhosis, and death. HBV is the longest known occupational pathogen, and infection is largely preventable through vaccination. Sequence: Key 9 A Patients with poorly controlled hypertension may be at an increased risk for intraoperative or postoperative myocardial infarct or stroke. A traditional recommendation has been to delay surgery if the diastolic blood pressure is greater than 110 mm Hg. Sequence: Key 10 B Erythromycin is the drug of choice for treatment of erythrasma which fluoresces coral pink under a Wood’s light. Sequence: Key 11 A Tetanus toxoid immunization booster administration is recommended every 10 years by the CDC.

Practice Test 3

Key Sequence: 12 C The use of local anesthetics is not a risk factor for deep vein thrombophlebitis. Sequence: Key 13 C In closed-chain subtalar joint pronation, the talus adducts and plantarflexes, and the leg internally rotates. Sequence: Key 14 C The application of a bivalve cast will provide immediate relief of the patient’s symptoms and restore blood flow. Sequence: Key 15 D The establishment of a doctor-patient relationship requires an individual to voluntarily seek a doctor’s care and expect that the communication be held in confidence. The relationship can be defined in writing but can also be oral or implied. Sequence: Key 16 B Hypertrophic nonunion results from excessive motion, so eliminating movement will allow complete bone healing. Sequence: Key 17 C Clinical features of rheumatoid arthritis include tendon and ligament erosion which in the cervical spine leads to instability between the C1 and C2 vertebrae. Sequence: Key 18 C The only muscle belly present in the first interspace is the first dorsal interosseous. Sequence: Key 19 B Terbinafine is fungicidal rather than fungistatic at the minimum therapeutic dose.

46

Sequence: Key 20 A Displacement after a Lisfranc’s fracture most commonly occurs in a dorsal and lateral direction. The dorsal ligaments are intrinsically weak and more likely to rupture than the plantar ligaments. Lateral deviation occurs due to rupture of Lisfranc’s ligament. Sequence: Key 21 A A short leg cast with the ankle neutral will provide zero tension and ideal positioning for healing of a repaired anterior tibial tendon. Sequence: Key 22 B OSHA regulations state that it is “mandatory to post” regulations in a location all employees routinely visit. Sequence: Key 23 C Cerebral palsy is defined as a nonprogressive lesion in the brain that alters motor control, leading to disorders of movement and posture. Sequence: Key 24 D Markedly increased density is not a radiographic feature of osteomyelitis; therefore, it can be excluded from the differential diagnosis. Sequence: Key 25 B The inflammatory phase of wound healing lasts approximately 3-5 days. Blood fills the wound, epithelial cells mobilize, and venules are more permeable. Sequence: Key 26 D A long leg cast immobilizes both knee and ankle joints, reducing strain on the gastrocnemius-soleus complex and Achilles tendon. Casting the foot in an equinus position reduces the risk that the tendon will heal in an elongated, weakened position.

47

Practice Test 3

Key Sequence: 27 D Flexion-extension creases in the skin form tension lines perpendicular to the direction of muscle pull over joints.

Key Sequence: 35 D Whenever a child presents with multiple fractures at various stages of healing, child abuse should be at the top of the differential diagnosis.

Sequence: Key 28 D Physical therapy is the best initial treatment for reflex sympathetic dystrophy because inactivity can exacerbate the disease and perpetuate the pain cycle.

Sequence: Key 36 A Erythema nodosum and subcutaneous nodule formation are common in the latter stages of sarcoidosis. The presence of shortness of breath and nonproductive cough are also manifestations of sarcoidosis.

Sequence: Key 29 C A rongeur forceps has strong, heavily constructed opposing jaws, each of which is scooped out like the tip of a curette. Sequence: Key 30 C TENS is a relatively safe, noninvasive method of pain management. Sequence: Key 31 A A spinal anesthetic is not recommended for a patient with sepsis due to the increased risk for meningitis. Sequence: Key 32 A The first lumbrical and the first and second dorsal interossei all insert in the base of the proximal phalanx of the second digit. Sequence: Key 33 D Soft tissue “emphysema” or gas on a radiograph is most commonly associated with Clostridium perfringens. Sequence: Key 34 B Half of all osteoid osteomas are seen in the tibia and femur, making the tibia the most likely location below the knee.

Sequence: Key 37 C Erythromelalgia is a neuropathic pain syndrome, not a seronegative spondyloarthropathy. Sequence: Key 38 C A Salter-Harris type III injury occurs through the physis and the epiphysis. The fracture passes through the hypertrophic layer of the physis and extends to split the epiphysis, inevitably damaging the reproductive layer of the physis. Sequence: Key 39 D The tibialis posterior muscle acts as a supinator of the subtalar joint, counterbalancing the effects of the fibularis (peroneus) brevis muscle, which acts as a pronator. Posterior tibial tendinitis will result in weakness of the muscle, causing a more pronated appearing foot, as well as discomfort at the tendon’s insertion on the navicular tuberosity. Sequence: Key 40 B Since the tibialis posterior muscle is a supinator of the subtalar joint, having the muscle contract against resistance should demonstrate both pain and weakness associated with tendon dysfunction. Sequence: Key 41 A A common complication of rheumatic fever is thickening and stenosis of the mitral valve.

Practice Test 3

48

Key Sequence: 42 C The least time of radiation exposure while minimizing the current (mA) takes precedence over the kVp when trying to minimize radiation dose to the patient.

Sequence: Key 49 C Osteochondroma is an overgrowth of cartilage and bone. It is the most common benign bone tumor accounting for 20-50 percent of benign bone tumors and 10-15 percent of all bone tumors.

Sequence: Key 43 B Absorbable pins provide stability for inherently stable osteotomies, such as the commonly performed Austin bunionectomy.

Sequence: Key 50 D In a competitive athlete, this type of fracture should be treated aggressively due to the increased incidence of delayed union or nonunion associated with this injury.

Sequence: Key 44 C The presence of asymptomatic central ulceration, which may be dry and crusted, is highly suggestive of basal cell carcinoma. This is frequently associated with sun exposure.

Sequence: Key 51 C Hands below the waist is considered a violation of sterile technique.

Sequence: Key 45 A Acidosis from local infection retards the diffusion of local anesthetics because of increased ionization.

Sequence: Key 52 D These symptoms occurring during this time frame after transfusion are most likely the result of acute hemolysis resulting from a reaction to the transfusion.

Sequence: Key 46 D Contact dermatitis is a T cell mediated phenomenon wherein the T cells are sensitized with exposure to a specific antigen, then activated by subsequent re-exposure to the antigen. Sequence: Key 47 D PTT is elevated when an inadequate level of Factor VIII is present. Sequence: Key 48 C Scintigraphy records on film the distribution of radioactivity in tissue following the use of radioactive tracer substances. When a stress fracture is strongly suspected and the initial radiographs are normal, the next study to order would be a triple phase nuclear medicine bone scan.

Sequence: Key 53 D The ossification center of the navicular bone appears at approximately 3 years of age and is the last center of ossification to appear in the foot. Sequence: Key 54 B Wave frequency is simply defined as the number of electromagnetic waves that pass a given point per unit of time. Sequence: Key 55 D Health costs for those age 65 and older are more than three times higher than for younger age groups.

49

Key Sequence: 56 AE In clinical practice the TE is always shorter than the TR and usually it is lower than 30 msec. The TR is usually lower than 500 msec. TE and TR scan parameters can help determine if the image is T1-weighted or T2-weighted. Sequence: Key 57 CDE Sickle cell disease complications are due to vascular effects caused by the altered red blood cell shape and function. Osteoporosis and delayed puberty are primarily endocrine effects and are not commonly seen in sickle cell disease. Sequence: Key 58 ADE In this case, the os tibiale externum is a normal finding. A smooth rounded appearance categorizes this ossicle as type I and disassociates it from the flatfoot deformity. When there is doubt about normal anatomical x-ray findings, contralateral studies can eliminate the need for MRI.

Practice Test 3

Sequence: Key 59 CDE The first ray axis runs through all three planes of motion from a posteromedial and dorsal direction to an anterolateral and plantar direction. As a result, when the first ray dorsiflexes, it also inverts and adducts. The fibularis (peroneus) longus stabilizes the first ray in midstance. Sequence: Key 60 ABC Consent is regulated by laws that vary from state to state but generally define competent adults eligible to make health care decisions.

NATIONAL BOARD OF PODIATRIC MEDICAL EXAMINERS PART II Clinical Science Examination

PRACTICE TEST 1

The Part II Practice Tests are representative of the content covered in the Part II Examination. They include question formats found in the actual examination. They also include questions of varying difficulty. A candidate’s performance on a Practice Test does not guarantee similar performance on the actual examination.

Copyright © 2005 by the National Board of Podiatric Medical Examiners. All rights reserved.

Practice Test 1

-3CLINICAL SCIENCE EXAMINATION PRACTICE TEST 1 60 questions

Directions: Each of the questions or incomplete statements below is followed by four suggested answers or completions. Select the one that is best in each case. NOTE: Throughout this test, the term “medial oblique foot” refers to a non-weight-bearing medial oblique position in which the film is flat on the orthoposer, the medial side of the foot is closest to the film and the sole forms a 45° angulation with the film, and the central beam is 90° to the film (the tubehead is angulated 0°). The converse is true for the term “lateral oblique.”

1. Venous stasis ulcers of the lower extremities usually respond best to which of the following types of treatment? (A) (B) (C) (D)

Oral antibiotics Topical antibiotics Arterial revascularization Compressive contact dressings

2. Hemoglobin A1c is most useful in the evaluation of which of the following conditions? (A) (B) (C) (D)

Diabetes mellitus Diabetes insipidus Adrenal cortical hyperplasia Hyperparathyroidism

3. The most common location for an Achilles tendon rupture is (A) (B) (C) (D)

the myotendinous juncture the posterior aspect of the calcaneus 2 to 6 cm proximal to its insertion 8 to 10 cm proximal to its insertion

4. A stratum granulosum is found in which of the following anatomical locations? (A) (B) (C) (D)

Plantar skin Hair Nail bed Oral mucosa

5. Which of the following imaging modalities results in no ionizing radiation exposure to the patient? (A) (B) (C) (D)

CT scan MRI Xeroradiography Technetium bone scan

6. One week after the application of a short leg fiberglass cast, a patient complains of pain and burning in her right foot. Homans’ sign is positive. Her past medical history is unremarkable with the exception of a 15-year history of cigarette smoking (1 pack per day) and oral contraceptive use. The cast is removed and the leg is noted to be hot, red, and indurated with superficial venous engorgement. Which of the following is the most appropriate preliminary diagnosis? (A) (B) (C) (D)

Phlebothrombosis Deep vein thrombosis Superficial thrombophlebitis Thromboangiitis obliterans

7. A hemi-implant is used with the Keller procedure primarily to (A) establish intrinsic muscular stability (B) reestablish the function of the flexor hallucis brevis (C) reestablish normal range of motion (D) act as a spacer following bone removal

GO ON TO THE NEXT PAGE.

Practice Test 1

8. Twenty minutes into a procedure, a patient develops laryngoedema, loses consciousness, and becomes cyanotic. Which of the following is the most likely diagnosis? (A) (B) (C) (D)

Vasovagal attack Anaphylaxis Insulin-induced hypoglycemia Myocardial infarction

9. The most common adverse reaction to intravenous sedation with morphine is (A) (B) (C) (D)

hypertension anaphylaxis respiratory depression renal failure

10. The running gait cycle differs from the walking gait cycle in that the runner (A) (B) (C) (D)

supinates rather than pronates at heel contact pronates during the propulsive phase of gait does not have a double support phase of gait does not have a float phase of gait

11. If a skin incision is made directly over a tendon, there is an increased risk of (A) (B) (C) (D)

adhesion infection synovitis skin slough

-4-

12. A 10-year-old girl is brought to a hospital emergency department. She is seen by a podiatric physician for treatment of a large abscess on the dorsum of the foot, where she was bitten by an insect 3 days ago. Physical examination reveals a temperature of 103°F with a grade IV/VI holosystolic murmur radiating all over the chest wall. In this situation, it would be most appropriate for the podiatric physician to do which of the following? (A) Request a cardiac consultation and take no further action until the consultation (B) Order an echocardiogram and take no further action until the results are reviewed (C) Take prophylactic measures for endocarditis and proceed with surgery (D) Admit the patient to the hospital, begin intravenous antibiotics, and wait for a stat. cardiac consultation before taking further action 13. Podiatric services that are eligible for payment under Medicare are determined by which of the following? (A) The state insurance commission (B) The state podiatric medical association (C) The Centers for Medicare & Medicaid Services (D) The American Podiatric Medical Association 14. Which of the following is true with respect to magnetic resonance imaging of the Achilles tendon? (A) The normal diameter generally does not exceed 5 mm. (B) Close to the calcaneal insertion, the anterior aspect is convex in the axial view. (C) The signal intensity is normally isointense with muscle on a T2-weighted image. (D) A high intratendinous signal intensity on a heavily water-weighted image is suggestive of an acute rupture or injury.

GO ON TO THE NEXT PAGE.

Practice Test 1

-5-

15. Secondary radiographic findings of a subtalar joint coalition include all of the following EXCEPT (A) (B) (C) (D)

talar beaking loss of sinus tarsi increased calcaneal inclination angle blunting of the lateral process of the talus

16. In a 75-year-old patient with bowel incontinence and an infected heel decubitus ulcer, which of the following is the most likely pathogen? (A) (B) (C) (D)

Escherichia coli Bacteroides fragilis Neisseria gonorrhoeae Pseudomonas aeruginosa

17. The four elements of the tort of medical malpractice are (A) (B) (C) (D)

duty, breach, causation, abandonment duty, breach, causation, damages duty, consent, causation, damages duty, standard, relationship, damages

18. A wet-to-dry dressing for an infected wound is used primarily to (A) cover the wound in order to prevent further contamination (B) apply antibacterial solutions to the wound (C) mechanically debride the wound (D) keep the wound moist 19. In an anteroposterior radiographic view, a talonavicular articulation of less than 70 percent is a sign of (A) (B) (C) (D)

pronation supination metatarsus adductus skew foot

20. A 12-year-old patient presents with arch pain. Gait evaluation reveals hyperpronation throughout the stance phase of gait. Resting calcaneal stance position is 2 degrees valgus. Radiographic evaluation reveals an anterior break in the cyma line and an increased Kite's angle. This patient most likely has (A) (B) (C) (D)

a flexible flatfoot a clubfoot deformity a cavovarus foot an equinovarus foot

21. The primary goal of implant surgery of the first metatarsophalangeal joint is to (A) (B) (C) (D)

eliminate joint pain improve joint motion increase the stability of the first ray preserve the plantar intrinsic musculature

22. A 2-year-old child presents with symptoms of jaundice, chronic anemia, and episodes of abdominal, back, and limb pain. The child's symptoms seem to be precipitated by dehydration. Physical examination reveals swelling of the hands and feet. Treatment consists of fluid maintenance and the administration of analgesics. This case description is characteristic of (A) (B) (C) (D)

juvenile diabetes juvenile arthritis sickle cell anemia collagen disease

23. Which of the following provides the best compression and alignment for an Austin bunionectomy? (A) (B) (C) (D)

Cerclage wire Threaded Kirschner wire Cancellous screws Orthosorb pins

24. A complication of halothane anesthesia is (A) (B) (C) (D)

bronchospasm hepatic necrosis peripheral vasoconstriction hypertension

GO ON TO THE NEXT PAGE.

Practice Test 1

25. The female athlete triad is composed of (A) eating disorders, stress fractures, and infections (B) eating disorders, amenorrhea, and osteoporosis (C) amenorrhea, stress fractures, and infections (D) osteoporosis, stress fractures, and increased incidence of endometrial cancer

-6-

29. The inflammatory arthritis associated with hemophilia most commonly affects which of the following joints? (A) (B) (C) (D)

Shoulder Hip Knee Metatarsophalangeal

30. The Thompson test is useful in the detection of 26. A 5-year-old boy presents with a slight equinus deformity. His parents state that he has had a tight gastrocnemius-soleus complex ever since he was an infant. He appears to be a healthy, well-nourished, and well-developed child. Duchenne type muscular dystrophy is suspected. All of the following tests would provide useful information relative to this diagnosis EXCEPT (A) a muscle biopsy (B) a muscle strength evaluation (C) a genetic screening for a sex-linked recessive disorder (D) an acetylcholine receptor (AChR) antibody test 27. A runner presents with a history of posteromedial shin splints due to overuse of the deep posterior muscles of the leg as a compensation for a structurally long limb on the involved side. Evaluation of the patient's shoe wear pattern on the involved side would reveal (A) excessive lateral forefoot outsole wear (B) heel counter tipping medially in a valgus position (C) compression of the lateral rearfoot midsole (D) abnormal wear of the uppers in the region of the fifth digit due to lateral crowding 28. In a nursing home population of 200, 12 people are diagnosed with onychomycosis in one year. In the first 4 months of the next year, 5 more people are diagnosed with onychomycosis. What is the incidence rate for the second year? (A) (B) (C) (D)

5/17 12/17 5/200 17/200

(A) (B) (C) (D)

an Achilles tendon rupture a calcaneofibular ligament sprain an anterior talofibular ligament sprain a bucket handle tear of the medial meniscus

31. A 52-year-old man experienced pain in his left arm, chest, and jaw for 5 minutes. He took nitroglycerin sublingually with no relief. He is taken to the emergency department where it is determined that he has had an acute myocardial infarction. Which of the following is a life-threatening dysrhythmia he will most likely experience during the first hour following the myocardial infarction? (A) (B) (C) (D)

Atrial flutter Atrial fibrillation Ventricular flutter Ventricular fibrillation

32. The nutrient artery of the first metatarsal enters the midshaft (A) (B) (C) (D)

medially laterally dorsally plantarly

33. An asymptomatic, fragmented, irregular, sclerotic, calcaneal apophysis in an 8 year old is most indicative of (A) (B) (C) (D)

Köhler's disease calcaneal apophysitis a nonunion fracture a normal anatomic variant

GO ON TO THE NEXT PAGE.

Practice Test 1

-7-

34. Somatization disorder is a neurotic illness characterized by all of the following EXCEPT (A) weakness and paralysis of muscle groups (B) dramatic, emotional presentation of complaints (C) multiple, vague complaints referable to any part of the body (D) dissatisfaction with care from one physician to the next 35. A patient with a long-standing varicose ulcer over the medial malleolus is at higher risk for the development of which of the following within the ulcer? (A) (B) (C) (D)

Melanoma Hemangioma Basal cell carcinoma Squamous cell carcinoma

36. Which of the following cells normally develops into a macrophage when it infiltrates tissue? (A) (B) (C) (D)

Monocyte Mast cell Lymphocyte Basophil

37. Yellow discoloration of radiographic film is most likely due to inadequate (A) (B) (C) (D)

development fixation mAs kVp

38. A 56-year-old woman is seen for pain involving her right ankle. The patient reports no specific traumatic incident. Recently she has noticed mildto-moderate pain across her midfoot and her ankle with increased activity. Physical examination reveals pain and swelling along the medial ankle. On the single heel rise test, she is unable to invert the right hindfoot. On weight bearing, the right forefoot is abducted on the rearfoot and the arch appears to flatten significantly more on the right foot than on the left. Which of the following therapies would NOT be appropriate? (A) (B) (C) (D)

Steroid injection Walking brace/boot Prescription foot orthosis Nonsteroidal anti-inflammatory drugs (NSAIDs)

39. Neuromuscular causes of cavus foot include all of the following EXCEPT (A) (B) (C) (D)

cerebral palsy myelomeningocele muscular dystrophy Charcot-Marie-Tooth disease

40. The presence of Bence Jones proteins in the urine is diagnostic of (A) (B) (C) (D)

amyloidosis multiple myeloma monoclonal gammopathy Waldenström's macroglobulinemia

41. Which of the following is a periosteal elevator? (A) (B) (C) (D)

Sayre Hohmann Weitlaner Seeburger

GO ON TO THE NEXT PAGE.

Practice Test 1

42. A 23-year-old man is seen in the emergency department for a diagnosed right ankle fracture/dislocation. Vascular evaluation reveals an absence of all pulses below the knee. Closed reduction is not successful. The patient has just eaten a large meal. Assuming a thigh tourniquet will be used, what is the most appropriate type of anesthesia for this patient? (A) (B) (C) (D)

Spinal Local infiltration General (inhalation anesthesia) Intravenous sedation

43. The minimal acceptable treatment for a diastasis of the ankle joint would include which of the following? (A) (B) (C) (D)

Low Dye strapping with a crossover J A reinforced Unna's boot and a surgical shoe Internal fixation Immobilization with a short leg cast

44. In radiology, the Harris-Beath (calcaneal axial) projections are indicated to determine the presence of a talocalcaneal coalition that involves which of the following anatomic locations? (A) (B) (C) (D)

Anterior facet only Posterior facet only Anterior and middle facets Middle and posterior facets

45. Which of the following is normally associated with Paget's disease? (A) (B) (C) (D)

Increased osteoblast activity only Increased osteoblast and osteoclast activity Decreased serum alkaline phosphatase levels A male-to-female ratio of occurrence of 4:1

-8-

46. Which of the following fractures has the best prognosis? (A) (B) (C) (D)

Rowe type Ia Rowe type IV Rowe joint depression Essex-Lopresti joint depression

47. A 6 year old presents with a painful ankle injury of 3 days’ duration. There is swelling and pain on direct palpation of the lateral malleolus. X-rays are unremarkable. Which of the following would be the treatment of choice? (A) (B) (C) (D)

A short leg cast An Ace bandage Ligamentous repair Activity, as tolerated

48. Which of the following statements about Lyme disease is true? (A) The disease is transmitted via feline to human contact. (B) The diagnostic test of choice is the erythrocyte sedimentation rate (ESR). (C) The drug of choice is metronidazole. (D) The most commonly associated dermatologic lesion is erythema chronicum migrans. 49. A runner who twisted her ankle 6 months ago still has ankle pain and an occasional sensation of the ankle giving way and locking. She has no apparent swelling or pain on range of motion. The most likely diagnosis is (A) (B) (C) (D)

sinus tarsi syndrome osteochondral talar dome fracture synovitis of the fibular (peroneal) tendons fracture of the os trigonum

GO ON TO THE NEXT PAGE.

Practice Test 1

-9-

50. Pyoderma gangrenosum is most often found in individuals with which of the following diseases? (A) (B) (C) (D)

Ulcerative colitis Sarcoidosis Lupus erythematosus Psoriasis

51. Which of the following ligaments is most commonly damaged in an inversion sprain of the ankle? (A) (B) (C) (D)

Anterior talofibular Posterior talofibular Calcaneofibular Deltoid

52. Radiographic findings indicative of Freiberg's infraction are initial joint-space (A) widening followed by a long-term increase in subchondral bone density (B) widening with no long-term effect on subchondral bone density (C) narrowing followed by a long-term increase in subchondral bone density (D) narrowing with no long-term effect on subchondral bone density 53. Multiple sclerosis is characterized by all of the following signs and symptoms EXCEPT (A) (B) (C) (D)

55. Which of the following tumors is associated with night pain that is relieved by salicylates? (A) (B) (C) (D)

Osteoblastoma Chondroblastoma Osteoid osteoma Chondromyxoid fibroma

56. A podiatric physician can best minimize drug interactions by (A) (B) (C) (D)

limiting the number of prescription refills performing an adequate physical examination taking a thorough medical history ordering appropriate laboratory tests

57. Which of the following is an inhibitor of prostaglandins? (A) (B) (C) (D)

Aspirin Warfarin Insulin Heparin

58. Which of the following is the most common postoperative infective organism in podiatric surgery? (A) (B) (C) (D)

Streptococcus Pseudomonas Staphylococcus Clostridium

ataxia impaired vision bladder dysfunction fibular (peroneal) muscular atrophy

54. A custom molded shoe is the primary choice for treatment of which of the following? (A) (B) (C) (D)

Multiple sclerosis Metatarsal stress fracture Advanced Charcot foot deformity Severe osteoarthritis of the tarsus and lesser tarsus

GO ON TO THE NEXT PAGE.

-10-

Practice Test 1

The next 2 questions refer to the following case. A male patient presents with an induration, pain, and bluish discoloration over the second interspace area of the left foot. The pain and size of the lesion have been increasing over the last month. X-rays show a calcification of portions of the lesion. There is no history of trauma and the skin texture is normal.

59. Which of the following is the most likely diagnosis? (A) (B) (C) (D)

Neuroma Fibroma Glomus tumor Cavernous hemangioma

60. The correct treatment would be (A) (B) (C) (D)

surgical excision of the lesion steroid injection of the lesion padding of the lesion ultrasound and whirlpool

END OF PRACTICE TEST 1

NATIONAL BOARD OF PODIATRIC MEDICAL EXAMINERS PART II Clinical Science Examination

PRACTICE TEST 2

The Part II Practice Tests are representative of the content covered in the Part II Examination. They include question formats found in the actual examination. They also include questions of varying difficulty. A candidate’s performance on a Practice Test does not guarantee similar performance on the actual examination.

Copyright © 2005 by the National Board of Podiatric Medical Examiners. All rights reserved

-12-

Practice Test 2

CLINICAL SCIENCE EXAMINATION PRACTICE TEST 2 60 questions Directions: Each of the questions or incomplete statements below is followed by four suggested answers or completions. Select the one that is best in each case. NOTE: Throughout this test, the term “medial oblique foot” refers to a non-weight-bearing medial oblique position in which the film is flat on the orthoposer, the medial side of the foot is closest to the film and the sole forms a 45° angulation with the film, and the central beam is 90° to the film (the tubehead is angulated 0°). The converse is true for the term “lateral oblique.”

1. Which of the following diagnostic tests is appropriate for a patient with suspected herpes simplex on the foot? (A) (B) (C) (D)

Gram’s stain Tzanck smear Ova and parasite smear Dermatophyte test medium (DTM)

2. Which of the following is associated with an increased incidence of osteosarcoma? (A) (B) (C) (D)

Paget's disease Ankylosing spondylitis Rheumatoid arthritis Osteomalacia

3. The best modality to confirm an osseous subtalar joint coalition is (A) (B) (C) (D)

a bone scan a CT scan an MRI tomography

4. A 68-year-old woman undergoes a complex reconstructive rearfoot surgical procedure with general anesthesia without complication. Within 48 hours the patient develops dyspnea, tachypnea, and a temperature of 101.5°F. Which of the following is the most likely diagnosis? (A) (B) (C) (D)

5. Which of the following agents is associated with drug-induced systemic lupus erythematosus? (A) (B) (C) (D)

Procainamide Lidocaine Bupivacaine Etidocaine

6. In a histologic section of normal skin of the dorsal foot, melanocytes are located (A) (B) (C) (D)

in the cornified layer in the subcutaneous fat deep in the reticular dermis in the basal cell layer of the epidermis

7. A 23-year-old runner presents with anterior leg pain that has been present for 3 weeks and is greatest when running on hills. Pain is elicited on palpation of the anterior aspect of the lower leg, lateral to the anterior crest of the tibia. The most likely diagnosis is (A) (B) (C) (D)

peroneal tendinitis anterior shin splints iliotibial band syndrome anterior tibial compartment syndrome

Septicemia Pulmonary emboli Deep vein thrombosis Acute appendicitis

GO ON TO THE NEXT PAGE.

Practice Test 2

-13-

8. Which of the following is a chronic inflammatory disease characterized by proliferative synovitis with subsequent bony erosion and destruction of the articular cartilage? (A) (B) (C) (D)

Gouty arthritis Osteoarthritis Rheumatoid arthritis Psoriatic arthritis

9. A 45-year-old overweight patient with a pes planus deformity reports “aching” pain at the tuberosity of the navicular that has progressed over the past 3 months. Radiographs show an enlarged navicular medially without fracture. The patient wears poorly supported shoes to work at a department store. The podiatric physician’s next step should be (A) foot and ankle strapping, a nonsteroidal antiinflammatory drug (NSAID), and a discussion about shoes (B) a short leg non-weight-bearing cast for 6 weeks (C) an Unna's boot for 4 weeks with ice and elevation (D) a technetium-99m 3-phase bone scan 10. A patient manifests a serpiginous eruption on the dorsal aspect of the foot that is successfully treated with topical thiabendazole. Which of the following is the most likely diagnosis? (A) (B) (C) (D)

Tuberculosis verrucosa cutis Erythema nodosum leprosum Cutaneous larva migrans Erosio interdigitalis blastomycetica

11. Which of the following is true of Sever’s disease? (A) (B) (C) (D)

It rarely affects females. It is a self-limiting disease. Ecchymosis and edema are pathognomonic. X-rays reveal a crescent sign in the Achilles tendon.

12. The Bunnell technique is used for (A) (B) (C) (D)

tenorrhaphy arthrodesis capsulodesis capsulorrhaphy

13. Differential diagnosis of Kaposi's sarcoma includes (A) (B) (C) (D)

stasis dermatitis hypertrophic lichen planus malignant melanoma dyshidrotic eczema

14. Which of the following bone lesions is characterized by dense bone surrounding a lytic central nidus? (A) (B) (C) (D)

Giant cell tumor Aneurysmal bone cyst Osteoid osteoma Osteosarcoma

15. In a patient with bacterial endocarditis who has no known allergies, the most appropriate prophylactic drug is (A) (B) (C) (D)

tetracycline gentamicin erythromycin amoxicillin

16. Semi-weight-bearing impression foam foot castings are most appropriate for which of the following? (A) (B) (C) (D)

Rigid foot with fixed deformity Flexible flatfoot deformity Flexible cavus foot deformity Hypermobile first ray deformity

17. When a soft-tissue lesion on the foot is excised, the standard length-to-width ratio for the incision is (A) (B) (C) (D)

2:1 3:1 3:2 5:2

18. Which of the following is a muscle that directly prevents the longitudinal arch from collapsing? (A) (B) (C) (D)

Abductor hallucis Plantar aponeurosis Fibularis (peroneus) longus Posterior tibial

GO ON TO THE NEXT PAGE.

Practice Test 2

-14-

19. Following lesser digital arthroplasty, the digit should be splinted in which of the following positions?

(A) (B) (C) (D)

Metatarsophalangeal Joint Dorsiflexed Dorsiflexed Slightly Plantarflexed Slightly Plantarflexed

Proximal Interphalangeal Joint Straight Plantarflexed Straight Plantarflexed

20. Which of the following is (are) most sensitive to radiation? (A) (B) (C) (D)

Spermatogonia Neutrophils Neurons Skin

21. On a lateral radiograph, a decreased calcaneal inclination angle with an increased talar declination angle would indicate (A) (B) (C) (D)

supination of the foot pronation of the foot talipes equinovarus metatarsus adductus

22. Radiographic subject contrast is best controlled by the manipulation of (A) (B) (C) (D)

kVp mAs source-to-image distance developer temperature

23. Which of the following Salter-Harris fractures has the best prognosis? (A) (B) (C) (D)

I II III IV

Distal Interphalangeal Joint Straight Straight Straight Plantarflexed

25. In addition to gloves, OSHA-designated personal protective equipment includes (A) (B) (C) (D)

gowns and eye protection steam sterilizers and masks self-sheathing needles and gowns sharps containers and eye protection

26. A patient with a painful limb, who will be using a single cane, should be instructed to use the cane (A) with the elbow fully extended (B) in a manner to shift weight away from the cane (C) on the side opposite the painful/injured side (D) angled away from the body about 40 degrees 27. Serial casting is likely to be successful in the treatment of all of the following EXCEPT (A) (B) (C) (D)

metatarsus adductus calcaneovalgus windswept deformity congenital vertical talus

28. Which of the following tendons is found plantar to the deep transverse metatarsal ligament? (A) (B) (C) (D)

Lumbrical tendon Abductor tendon Plantar interosseous tendon Dorsal interosseous tendon

24. The fifth toe can clearly be seen in all of the following standard radiographic views EXCEPT the (A) (B) (C) (D)

lateral lateral oblique medial oblique dorsoplantar

GO ON TO THE NEXT PAGE.

-15-

29. A podiatric physician is examining a 57-year-old patient who has a 21-year history of poorly controlled diabetes mellitus. A neurosensory examination reveals a loss of proprioception. Further examination of the patient would most likely reveal a (A) symmetric absence of deep tendon reflexes (B) loss of protective sensation with 10-gram monofilament (C) loss of sharp-dull discrimination (D) plantar reflex with a bilateral flexion response 30. An individual can functionally increase limb length by (A) (B) (C) (D)

dorsiflexing the ankle joint supinating the subtalar joint supinating the longitudinal midtarsal joint pronating the oblique midtarsal joint

31. All of the following radiographic signs are associated with excessive pronation EXCEPT (A) (B) (C) (D)

obliteration of the sinus tarsi anterior displacement of the talus a talocalcaneal angle of 10° a metatarsus primus adductus angle of 20°

32. Which of the following general anesthetics is most likely to sensitize the myocardium to catecholamines? (A) (B) (C) (D)

Enflurane Isoflurane Halothane Nitrous oxide

33. A Young procedure performed on the tibialis anterior is best described as (A) (B) (C) (D)

tendon transfer tendon translocation tendon lengthening tenolysis

Practice Test 2

34. The formation of Heberden’s nodes at distal interphalangeal joints is associated with (A) (B) (C) (D)

osteoarthritis rheumatoid arthritis systemic lupus erythematosus ankylosing spondylitis

35. Which of the following local anesthetics is NOT recommended for use in children under 12 years of age? (A) (B) (C) (D)

Lidocaine Mepivacaine Bupivacaine Procaine

36. A patient presents with a single, nonpruritic vesicle on the dorsum of the third toe. There is no history of trauma and the patient has not made any change in shoe gear. Inspection reveals an umbilicated vesicle. The most likely diagnosis is (A) (B) (C) (D)

verruca plana acute contact dermatitis molluscum contagiosum bullous diabeticorum

37. Which of the following is most characteristic of venous stasis ulcerations? (A) (B) (C) (D)

A punched-out border A gray mucoid base A red, granulating base Pain

38. The most prominent physical finding of right-sided congestive heart failure is (A) (B) (C) (D)

S3 gallop rapid breathing moist rales in the lungs lower extremity dependent edema

39. In a flexor tendon transfer for hammer toe correction, the flexor tendon is inserted into the (A) (B) (C) (D)

plantar aspect of the distal phalanx plantar aspect of the middle phalanx dorsal aspect of the proximal phalanx dorsal aspect of the middle phalanx

GO ON TO THE NEXT PAGE.

Practice Test 2

40. Which of the following statements applies to a podiatric physician who suspects that an elderly patient has been abused? (A) The podiatric physician should report the suspicion only if he or she is convinced beyond a reasonable doubt that abuse has occurred. (B) The podiatric physician should report the suspicion as a matter of moral but not legal obligation. (C) The podiatric physician may be criminally liable for failure to report the suspicion. (D) The podiatric physician may not report the suspicion because of the doctor-patient privilege. 41. An orthopedic shoe with a steel shank from heel to toe and a rocker bar would be appropriate for treating (A) (B) (C) (D)

drop foot spastic flatfoot flexible hammer toes an arthritic ankle and subtalar joint

42. Which of the following is a true statement about healing by first intention? (A) It implies suppuration or necrosis. (B) It involves excessive formation of granulation tissue. (C) It profoundly diminishes the strength of the surgical wound. (D) It is demonstrated in the closure of an uncomplicated skin incision. 43. A patient is experiencing anterior leg pain. On examination of muscle strength, the anterior compartment muscles are graded 3/5. Which of the following nerves is most likely responsible for this finding? (A) (B) (C) (D)

Tibial Saphenous Deep fibular (peroneal) Superficial fibular (peroneal)

-16-

44. In a lateral osteochondral talar dome fracture, the most common mechanism of injury is (A) (B) (C) (D)

inversion, plantarflexion inversion, dorsiflexion eversion, plantarflexion eversion, dorsiflexion

45. Which of the following is associated with normochromic, normocytic anemia? (A) (B) (C) (D)

Iron deficiency Hemolysis Folate deficiency Lead poisoning

46. A patient with 3º forefoot valgus was casted for functional orthoses, but the negative cast reflected 10º of forefoot valgus. This most likely occurred because the clinician (A) supinated the long axis of the midtarsal joint (B) dorsiflexed the fourth and fifth metatarsophalangeal joints (C) pronated the subtalar joint when locking the midtarsal joint (D) did not check to make sure the patient was not contracting the anterior tibial muscle 47. A 35-year-old patient fell from the roof of a house and sustained a fracture of the talus. X-rays reveal fracture of the talar neck and dislocation of the talar body from the ankle mortise and subtalar joint. Which of the following describes this type of fracture and the most likely complication associated with it? (A) Berndt-Harty stage II fracture with a severe risk of osteochondritis (B) Stewart type III fracture with a slight risk of avascular necrosis (C) Hawkins type III fracture with a high risk of avascular necrosis (D) Sanders fracture (Tongue type) with a risk of degenerative arthritis

GO ON TO THE NEXT PAGE.

-17-

48. Which of the following conditions may cause delayed relaxation of Achilles tendon reflexes? (A) (B) (C) (D)

Diabetes Porphyria Alcoholism Hypothyroidism

49. A 33-year-old woman presents with heat intolerance headaches and excessive sweating of 2 months’ duration. She has a visible hand tremor and her handwriting is uneven. She jogs 5 miles a day, 5 times a week. Over the past 2 months her tolerance for exercise and her running times have decreased. Physical examination reveals a thin, well-developed and anxious woman. The patient's blood pressure is 130/50 mm Hg and her pulse is 120. Ocular inspection reveals lid retraction and stare. She also presents with proximal muscle weakness. Examination of the neck reveals diffuse enlargement of the thyroid and audible bruit. There is no history of drug intake. Which of the following is the most likely diagnosis? (A) (B) (C) (D)

Subacute thyroiditis Exogenous thyroid hormone Graves’ disease Multinodular goiter

50. Emergency treatment of an acute myocardial infarction includes all of the following EXCEPT (A) (B) (C) (D)

thrombolysis heparin warfarin angioplasty

Practice Test 2

51. Thrombophlebitis of the small veins frequently occurs with intravenous administration of (A) (B) (C) (D)

diazepam propofol droperidol fentanyl

52. Which of the following is the correct ventilationto-chest-compression ratio in one-rescuer CPR? (A) (B) (C) (D)

2 ventilations : 3 chest compressions 2 ventilations : 15 chest compressions 4 ventilations : 8 chest compressions 8 ventilations : 15 chest compressions

53. Generalized subperiosteal bone resorption is characteristic of (A) (B) (C) (D)

osteomalacia hyperparathyroidism osteoporosis osteosarcoma

54. Unusual infections such as Mycobacterium avium-intracellulare are commonly seen in association with (A) (B) (C) (D)

HIV pelvic inflammatory disease sarcoidosis cystic fibrosis

55. In a prospective epidemiologic study of a disease, the cohort originally selected consists of persons (A) (B) (C) (D)

with the disease without the disease with a family history of the disease without a family history of the disease

GO ON TO THE NEXT PAGE.

Practice Test 2

-18-

56. Which of the following is NOT a characteristic of plantar fasciitis? (A) Post-static dyskinesia (B) A tight gastrocnemius-soleus complex (C) Pain at the medial plantar aspect of the calcaneus (D) Occurrence in boys between the ages of 4 and 7 years 57. The patellar reflex is largely mediated by which of the following nerve roots? (A) (B) (C) (D)

L1-L2 L3-L4 L5-S1 S2-S3

58. Which of the following medications is most likely to contribute to the formation of a deep vein thrombosis? (A) (B) (C) (D)

Multivitamins with zinc Oral contraceptives Enteric-coated aspirin Dipyridamole

The next 2 questions refer to the following information. A 40-year-old African-American man presents with an injury to his right foot sustained 5 days ago when a heavy sheet of glass fell onto the top of his foot. An examination reveals a laceration over the first metatarsophalangeal joint with erythema, edema, and drainage. A loss of active dorsiflexion of the first metatarsophalangeal joint is noted, indicating that some tendon damage may have occurred. The patient has not had past tetanus immunization.

59. Conservative treatment fails and surgery is performed. Three days postoperatively, the patient presents with pain. Physical examination reveals severe localized edema, erythema, serosanguineous drainage, induration, and pain on palpation. The most likely diagnosis is (A) (B) (C) (D)

hematoma causalgia Freiberg's infraction normal postoperative course

60. Preoperative laboratory tests should include which of the following? (A) (B) (C) (D)

Uric acid Sickle cell trait Hemoglobin A and hemoglobin C Erythrocyte sedimentation rate (ESR)

END OF PRACTICE TEST 2

NATIONAL BOARD OF PODIATRIC MEDICAL EXAMINERS PART II Clinical Science Examination

PRACTICE TEST 3

The Part II Practice Tests are representative of the content covered in the Part II Examination. They include question formats found in the actual examination. They also include questions of varying difficulty. A candidate’s performance on a Practice Test does not guarantee similar performance on the actual examination.

Copyright © 2005 by the National Board of Podiatric Medical Examiners. All rights reserved.

Practice Test 3

-20CLINICAL SCIENCE EXAMINATION PRACTICE TEST 3 60 questions

Directions: Each of the questions or incomplete statements below is followed by four suggested answers or completions. Select the one that is best in each case. NOTE: Throughout this test, the term “medial oblique foot” refers to a non-weight-bearing medial oblique position in which the film is flat on the orthoposer, the medial side of the foot is closest to the film and the sole forms a 45° angulation with the film, and the central beam is 90° to the film (the tubehead is angulated 0°). The converse is true for the term “lateral oblique.”

1. Deep vein thrombosis is diagnosed in a hospitalized, 3-day postoperative patient. The initial treatment of choice is (A) (B) (C) (D)

oral warfarin intravenous heparin compression wraps local heat and elevation

2. Metatarsus adductus is evaluated radiographically by utilizing which two axes? (A) (B) (C) (D)

Navicular and first metatarsal Calcaneal and second metatarsal Second metatarsal and long axis of the talus Second metatarsal and lesser tarsal

3. When griseofulvin is prescribed, it is important to perform which of the following tests in addition to a complete blood cell count (CBC)? (A) (B) (C) (D)

Culture and sensitivity KOH or fungal culture Wood's light examination Gram's stain

4. Which of the following is a postoperative nonadherent dressing utilized in immediate wound care? (A) (B) (C) (D)

Adaptic dressing Kerlix fluff dressing Kling roller bandage dressing Sterile 4" x 4" gauze dressing

5. The Hardcastle classification system was developed for classifying (A) (B) (C) (D)

subtalar joint dislocations Lisfranc's joint dislocations metatarsophalangeal joint dislocations extra-articular fractures of the os calcis

6. When a short leg cast is applied, which superficial nerve needs to be protected in the area of the fibular neck? (A) (B) (C) (D)

Sural Saphenous Femoral Common fibular (peroneal)

7. In the normal development of the foot, the center of ossification appears last in the (A) (B) (C) (D)

talus calcaneus lateral cuneiform navicular

8. Which of the following types of padding would be best for an arthritic hammer toe? (A) (B) (C) (D)

A metatarsal pad A crest pad A Morton's pad A heel-lift pad

GO ON TO THE NEXT PAGE.

-21-

9. True acquired clubbing of the fingernails is associated with which of the following diseases? (A) (B) (C) (D)

Lung cancer Osteoarthritis Rheumatoid arthritis Ulcerative colitis

10. Chemical exposure in the podiatric laboratory is controlled by the (A) (B) (C) (D)

Public Health Service National Institutes of Health Drug Enforcement Agency Occupational Safety and Health Administration

11. Adverse reactions associated with nonsteroidal anti-inflammatory drugs (NSAIDs) include all of the following EXCEPT (A) (B) (C) (D)

nausea interstitial nephritis respiratory depression peptic ulcer disease

12. A 45-year-old man presents with a history of pain in the medial aspect of the right ankle and foot for the past 6 months. The pain has become progressively worse and causes the patient to limp at the end of the workday. The pain is sharp at times; otherwise it is a throbbing, aching pain. Examination findings are pain on palpation posterior and proximal to the medial malleolus and also at the tuberosity of the navicular and stance heel valgus with a collapse of the longitudinal arch. The remaining examination is unremarkable. To form a treatment plan, it would be most helpful for the podiatric physician to review the results of (A) (B) (C) (D)

an MRI a CT scan a soft tissue ultrasound an EMG/NCV study

Practice Test 3

13. An avulsion fracture of the anterior process of the calcaneus is associated with which of the following ligaments? (A) (B) (C) (D)

Spring Bifurcate Long plantar Interosseous talocalcaneal

14. Which of the following radiographic findings is most consistent with chronic tophaceous gout? (A) (B) (C) (D)

Osteopenia Osteophytosis Early joint destruction Large bony erosions

15. Which of the following types of Salter-Harris epiphyseal injuries do NOT involve a fracture through the metaphysis? (A) (B) (C) (D)

I and II I and III II and III III and IV

16. In the 18- to 30-year-old age group, the most common infective organism in septic arthritis is (A) (B) (C) (D)

Staphylococcus epidermidis Staphylococcus aureus Haemophilus influenzae Neisseria gonorrhea

17. Which of the following blood tests measures the coagulation time via the intrinsic pathway? (A) (B) (C) (D)

Bleeding time Sedimentation rate Prothrombin time (PT)/INR Partial thromboplastin time (PTT)

18. A Charcot joint is caused by (A) (B) (C) (D)

motor neuropathy sensory neuropathy vascular insufficiency dystrophic ulceration

GO ON TO THE NEXT PAGE.

Practice Test 3

19. The Hoffman-Clayton procedure is most commonly indicated for which of the following conditions? (A) (B) (C) (D)

Pes cavus Hallux valgus Hammer toe Rheumatoid arthritis

20. Which of the following is the usual mechanism of injury in football turf-toe injuries to the first metatarsophalangeal joint complex? (A) (B) (C) (D)

Hyperextension with compression Hyperflexion with tension Hyperflexion with shear Axial load on the sesamoid complex

21. A 35-year-old patient with rheumatoid arthritis has a severe hallux valgus deformity with a dislocated first metatarsophalangeal joint. She takes ibuprofen, prednisone, and methotrexate for the arthritis and has a severe penicillin allergy. Her bunion-last, extra-depth shoes no longer relieve her symptoms and she requests surgical intervention. The podiatric physician decides to perform a first metatarsophalangeal joint fusion under general anesthesia using internal fixation. In addition to a complete blood cell count (CBC) and a urinalysis, preoperative studies should include (A) (B) (C) (D)

a thyroid profile cervical radiographs patch testing for other antibiotic allergies muscle biopsy to evaluate her potential for malignant hyperthermia with general anesthesia

22. Which of the following is a true statement about gout? (A) Acute septic joint disease mimics gout. (B) Blood uric acid levels above 7 mg/dL are pathognomonic of gout. (C) Early acute gout is best treated by uricosuric agents. (D) Salicylates are administered to potentiate the effects of uricosuric agents.

-22-

23. Pulmonary embolism is most definitively diagnosed by (A) (B) (C) (D)

pulmonary angiography ventilation perfusion scans chest x-ray studies arterial blood gas studies

24. A 68-year-old man reports coldness and numbness of both feet for the past 6 months and leg pain with increased activity that is relieved with rest. Physical examination shows absent DP and PT pulses. Subpapillary venous filling time is more than 8 seconds in all digits. The skin of both feet is cool to the touch, shiny, and pale, and there is a lack of digital hair growth. Doppler and plethysmography show minimal blood flow to both feet and lower legs. The likely diagnosis is (A) (B) (C) (D)

arterial embolism arteriosclerosis obliterans dissecting aortic aneurysm Raynaud's phenomenon

25. Which of the following findings should be expected in a 14-year-old patient with congenital soleus equinus? (A) Limited dorsiflexion of the ankle with the knee flexed and extended (B) Limited dorsiflexion of the ankle with the knee extended but not flexed (C) Normal dorsiflexion of the ankle with the knee flexed but not extended (D) Normal dorsiflexion of the ankle with the knee extended but not flexed 26. A 50-year-old patient presents with a tender mass on the lateral forefoot. A radiograph reveals an expansile “soap bubble” lesion in the fifth metatarsal. The most likely diagnosis is (A) (B) (C) (D)

giant cell tumor osteochondroma Ewing’s sarcoma unicameral bone cyst

GO ON TO THE NEXT PAGE.

-23-

27. When a dorsal wedge osteotomy is performed at the base of the third metatarsal, which interosseous muscle belly is first seen between the second and third metatarsals? (A) (B) (C) (D)

Second dorsal Third dorsal Second plantar Third plantar

28. An abnormal “Q” angle is most commonly associated with (A) (B) (C) (D)

anterior cruciate tears posterior cruciate tears bucket handle meniscus tears patellar malalignment

29. A 40-year-old woman complains of a painful hammered hallux of the right foot. Examination shows a rigid hammering of the interphalangeal joint of the right hallux with an associated flexible plantarflexed first ray. Which of the following is the most appropriate operation for this patient? (A) Jones tenosuspension with interphalangeal fusion (B) Arthroplasty of the interphalangeal joint (C) Dorsiflexory wedge osteotomy of the first metatarsal with interphalangeal fusion (D) First metatarsophalangeal joint fusion

Practice Test 3

32. Postanesthesia headache is most likely to occur after which of the following types of anesthesia? (A) (B) (C) (D)

33. A 30-year-old patient is scheduled to have major rearfoot reconstruction. The patient has a history of asthma and is currently on an albuterol nebulizer and has taken prednisone, 7.5 milligrams, daily for the past 2 years. Prior to surgery, the podiatric physician should do which of the following? (A) Begin aspirin therapy 24 hours prior to surgery. (B) Begin antibiotic prophylaxis to prevent endocarditis. (C) Increase the prednisone dose to at least 20 milligrams per day. (D) Stop the prednisone 2 days prior to surgery to aid in wound healing. 34. Which of the following steps should be followed when an individual is using an automated external defibrillator? (A) (B) (C) (D)

30. Penicillin dose adjustment must be considered when (A) (B) (C) (D)

renal excretion is impaired hepatic excretion is impaired hepatic metabolism is impaired oral absorption is increased

31. An increased risk of deep vein thrombosis is associated with (A) (B) (C) (D)

diabetes mellitus iron deficiency anemia polycythemia vera rheumatoid arthritis

Spinal Local Epidural Subarachnoid

Wipe the patient's chest dry with alcohol. Remove any medication patch prior to use. Place the pads over implantable devices. Delay use until after hypothermia, if present, is treated.

35. Chest compressions in infant cardiopulmonary resuscitation should be (A) (B) (C) (D)

0.5-1.0 inch 1.0-1.5 inches 1.5-2.0 inches 2.0-2.5 inches

36. Which of the following skin lesions is derived from a distinctive cell line of melanized cells? (A) (B) (C) (D)

Dermal nevus Junctional nevus Compound nevus Blue nevus

GO ON TO THE NEXT PAGE.

Practice Test 3

37. Which of the following is NOT a side effect of glucocorticoids? (A) (B) (C) (D)

Psychosis Edema Hypokalemia Chronic active hepatitis

38. A 60-year-old resident of a skilled nursing facility suffers from osteomyelitis of her calcaneus. Her past medical history includes stroke syndrome, inability to swallow, and chronic nasogastric tube feeding. She undergoes a 2-hour procedure. Two days later the patient is noted to have fever with shortness of breath and production of fetid sputum. The most likely diagnosis is (A) (B) (C) (D)

acute bronchitis atelectasis aspiration pneumonia pulmonary embolism

39. Hand-foot-and-mouth disease is a mild infectious disease of childhood caused by a (A) (B) (C) (D)

staphylococcus bacteria streptococcus bacteria herpesvirus coxsackievirus

40. In normal radiographic anatomy, the lateral (third) cuneiform bone is LEAST visible with which of the following standard pedal studies? (A) (B) (C) (D)

Anteroposterior foot Lateral foot Medial oblique foot Lateral oblique foot

41. Bone healing with rigid internal fixation is known as (A) (B) (C) (D)

secondary bone healing periosteal bone healing primary bone healing cartilage phase healing

-24-

42. A 42-year-old patient is seen by a podiatric physician 48 hours after an ankle sprain. Examination reveals moderate to severe edema and moderate ecchymosis. Which of the following would be the best course of treatment? (A) (B) (C) (D)

Primary repair Lateral ankle stabilization A short leg weight-bearing cast A Jones compression dressing, non-weightbearing

43. In order to attain better x-ray penetration of the tarsal bones and avoid an increase in the overall film density the (A) kilovoltage and the mAs both must be increased (B) kilovoltage must be increased and the mAs must be decreased (C) kilovoltage must be decreased and the mAs must be increased (D) kilovoltage and the mAs both must be decreased 44. Two measurements used for the evaluation of Haglund’s deformity are the (A) parallel pitch lines and Böhler’s angle (B) parallel pitch lines and the Fowler-Philip angle (C) Fowler-Philip angle and Böhler’s angle (D) angle of Gissane and Böhler’s angle 45. Which of the following materials would be LEAST appropriate for extrinsic posting of functional orthotics? (A) (B) (C) (D)

Acrylic Crepe Cork Leather

46. The ability of a test to give a negative finding when the person screened is truly free of the condition is called the test’s (A) (B) (C) (D)

validity sensitivity specificity variation

GO ON TO THE NEXT PAGE.

-25-

47. Fog on a developed radiographic film most likely indicates (A) (B) (C) (D)

a light leak excessive fixing low developer temperature weak developing solution

48. Statutes of limitations are determined by (A) (B) (C) (D)

state laws state podiatry associations the Department of Justice the American Podiatric Medical Association

49. Which of the following is an appropriate treatment for a Salter-Harris type V fracture? (A) (B) (C) (D)

An Ace bandage A functional orthosis Casting immobilization Open reduction internal fixation

50. A 25-year-old runner presents with achy soreness poorly localized to the lateral border of the foot and complains of something “going out of” and “popping into” place. This condition has been present for several months with periods of exacerbation and remission. The area is not warm or swollen and the patient has never noticed edema or redness. Palpation localizes tenderness to the calcaneocuboid joint. The most likely diagnosis is (A) (B) (C) (D)

plantar fasciitis a midtarsal stress fracture cuboid subluxation syndrome peroneal tendinitis

Practice Test 3

51. A patient presents with a chief complaint of interdigital itching and maceration. Physical examination reveals fissuring and maceration of the third and fourth web spaces bilaterally. A KOH preparation is performed and reveals multiple budding pseudohyphae. The most likely diagnosis is infection caused by (A) (B) (C) (D)

Candida albicans Trichophyton rubrum Trichophyton mentagrophytes Corynebacterium minutissimum

52. Which of the following dysplasias is characterized by multiple bone islands in periarticular areas? (A) (B) (C) (D)

Osteopetrosis Osteogenesis imperfecta Osteopoikilosis Melorheostosis

53. Common precipitating triggers of asthma include all of the following EXCEPT (A) (B) (C) (D)

smoke exercise dust mites topical cortisone

54. In long bones, primary ossification occurs at which of the following sites? (A) (B) (C) (D)

Metaphysis Diaphysis Epiphysis Metaphyseal-diaphyseal junction

GO ON TO THE NEXT PAGE.

Practice Test 3

-26-

55. A patient who presents with an adducted, toe-walking, scissor-type gait most likely has (A) (B) (C) (D)

A patient with a documented penicillin allergy inadvertently receives an intravenous infusion of cefazolin. The patient complains of shortness of breath and develops a rash and pruritus.

cerebral palsy muscular dystrophy multiple sclerosis amyotrophic lateral sclerosis

56. A patient presents with a hemoglobin A1c of 8.0 and a fasting blood glucose level of 210 mg/dL. Clinical examination strongly indicates that sensory polyneuropathy is present. A symptom of this would be (A) (B) (C) (D)

Babinski’s reflex a positive Thompson test diminished deep tendon reflexes an inability to feel a 10-gram SemmesWeinstein monofilament

57. Standards for quality of care by health systems are developed by the (A) (B) (C) (D)

The next 2 questions refer to the following case.

National Institutes of Health Centers for Medicare & Medicaid Services National Committee for Quality Assurance Joint Commission on Accreditation of Healthcare Organizations

59. Which of the following medications is indicated as the first line of therapy? (A) (B) (C) (D)

Epinephrine Sodium bicarbonate Verapamil Nifedipine

60. As part of the workup a complete blood cell count (CBC) is obtained. Which of the following cell types are most likely to be elevated? (A) (B) (C) (D)

Monocytes Lymphocytes Eosinophils Basophils

58. The most common side effect of fentanyl, sufentanil, and thiopental is (A) (B) (C) (D)

tachycardia hypokalemia respiratory depression hyperglycemia

END OF PRACTICE TEST 3

-27-

Practice Test 1

PRACTICE TEST 1 ANSWER KEYS AND RATIONALES

Sequence: Key 1 D Stasis ulcers are caused by blood pooling in the legs secondary to venous distention and a failure of the venous valves to maintain an upward flow of venous blood against gravity. Compression dressings are an effective way to compensate for this lack of proper venous function. Sequence: Key 2 A Hemoglobin A1c is an end product produced when hemoglobin glycosylates due to hyperglycemia. Assessment of hemoglobin A1c provides useful information related to a patient’s regulation of blood glucose during the previous 3 months. Sequence: Key 3 C Approximately 2 to 6 cm proximal to its insertion, the Achilles tendon has an area of decreased blood flow, making this region more vulnerable to strain and rupture. Sequence: Key 4 A The stratum lucidum is one of the five layers of the normal plantar skin epidermis. The stratum granulosum lies just above the mucosal layer of the epidermis. Sequence: Key 5 B MRI uses nonionizing radio frequency pulses that are absorbed and then emitted by tissue lying inside a magnetic field. Sequence: Key 6 B The patient has several risk factors for deep vein thrombosis (DVT), i.e., smoking, immobilization, and oral contraceptive use. The description of the leg as “hot, red, and indurated” is most consistent with DVT. Homan’s sign is a diagnostic sign, although unspecific for DVT.

Sequence: Key 7 D Removal of the proximal phalangeal base of the hallux may result in shortening and postoperative contracture of the hallux. Maintaining this space with a hemi-implant may reduce this complication. Sequence: Key 8 B Stridor, laryngospasm, wheezing, angioedema, hives, possible hypotension, and circulatory collapse are symptoms of anaphylaxis. A lack of oxygen due to bronchospasm is the primary cause of death. Sequence: Key 9 C Morphine causes depression of ventilation. Sequence: Key 10 C Stance phase is shortened as running speed increases, which decreases the time in stance and results in the elimination of the brief time when both feet are in stance at the same time. Sequence: Key 11 A Fibrous scar tissue often causes adhesions between a tendon and its sheath and the overlying skin. Sequence: Key 12 D Although the intensity of the murmur does not indicate the severity of a valve defect, a patient with cardiac murmur should be medically cleared by an M.D. or D.O. prior to undergoing any invasive treatment such as surgical intervention. In this case, there is the potential for incision and drainage.

Practice Test 1 Sequence: Key 13 C The Centers for Medicare & Medicaid Services (CMS) is the government agency responsible for determining the fees and services that are eligible for payment for Medicare and Medicaid recipients. Federal law to provide that direction defines this agency. Sequence: Key 14 D On MRI, a rupture or an injury appears as an area of increased signal in the tendon. Sequence: Key 15 C Subtalar joint coalition is most often associated with pes planus and peroneal spasm, with available motion seen usually in the pronatory direction. All of these findings are associated with a decreased calcaneal inclination angle. Sequence: Key 16 A Escherichia coli is transmitted from fecal material and isolated from stool cultures. In a patient with bowel incontinence, the ulcer is most likely infected from the patient’s fecal material. Sequence: Key 17 B A tort is an act of wrongdoing, which is civil in nature rather than criminal. It is a wrong independent of contract or criminality. Health care providers have a duty to do what is right and reasonable. The elements of the tort of malpractice address situations in which there is a breach of duty that causes or results in harm. Sequence: Key 18 C When a wet-to-dry dressing is removed, superficial necrotic tissue is also removed from the wound. Sequence: Key 19 A The talus adducts and plantarflexes in closed chain pronation, and actually decreases the amount of articulation of the talus and navicular.

-28Sequence: Key 20 A The clinical and radiographic features described in this question are associated with an excessively pronated foot, such as flexible flatfoot. Sequence: Key 21 A The implant functions as a spacer between the proximal phalanx and the first metatarsal after the painful joint has been resected. Sequence: Key 22 C Sickle cell anemia manifests itself in infancy. Clinical manifestations include all the symptoms described in the question. Management is largely symptomatic and supportive. Sequence: Key 23 C A partially threaded screw is used to create interfragmental compression by the lag principle. This technique is commonly used to provide the best compression and alignment for an Austin bunionectomy. Sequence: Key 24 B In genetically susceptible patients, an oxidative trifluoroacetyl metabolite of halothane may evoke the production of neoantigens directed against hepatocytes. Sequence: Key 25 B The female athlete triad, which affects women and girls in many sports, is defined by the following symptoms: disordered eating (bulimia or anorexia), amenorrhea, and osteoporosis. Sequence: Key 26 D Acetylcholine is found in the autonomic nervous system, which is not involved in the development of muscular dystrophy.

-29Key Sequence: 27 B Compensation for a structurally long limb produces excessive pronation of the foot on the involved side. The wear pattern of the shoe on the involved foot would, therefore, be greatest on the medial side. Sequence: Key 28 C Incidence is the number of new cases of a specific disease occurring during a given period in a specified population. In this question there are 200 nursing homes residents. In one year, there were 12 patients who presented with onychomycosis. During the next year, there were 5 new cases diagnosed. The incidence rate for the second year is 5/200, representing only new cases. Sequence: Key 29 C Hemarthrosis from hemophilia occurs in up to twothirds of patients and is heralded by pain, warmth, and stiffness. The knee, elbow, and ankle are the joints most frequently affected. Sequence: Key 30 A The Thompson test is performed by squeezing the calf muscle of a patient lying in the prone position, and observing for plantarflexion of the foot. Absence of foot plantarflexion is indicative of disruption of the Achilles tendon. Sequence: Key 31 D Ventricular fibrillation is a life-threatening dysrhythmia that occurs in the early phases of a myocardial infarction.

Practice Test 1 Sequence: Key 34 A Weakness and paralysis of muscle groups are not characteristic of somatization disorder. Sequence: Key 35 D Many types of chronic skin irritations and longstanding ulcers, such as venous stasis ulcers, can undergo malignant transformations, the vast majority of which result in well-differentiated squamous cell carcinoma. Sequence: Key 36 A A monocyte is a large phagocytic cell that transforms into a macrophage once it enters tissues. Sequence: Key 37 B Flaws in the fixation process are the most common cause of yellow discoloration of radiographic film. Sequence: Key 38 A The systematic evaluation and examination findings are indicative of posterior tibial tendinitis. The tendon is intact due to the inversion noted with the heel rise test. Excessive calcaneal eversion with progressively increasing forefoot abduction is a hallmark of posterior tibial tendinitis. Injection of a steroid near or within a tendon increases the risk of iatrogenic rupture. Injected corticosteroids (and even oral steroids) have been well documented to predispose a tendon to rupture because they weaken collagen cross-linking.

Sequence: Key 32 B The nutrient artery of the first metatarsal enters the midshaft on the lateral aspect.

Sequence: Key 39 C In muscular dystrophy, contractures of the gastrocnemius muscles appear early and result in tightening of the heel cords, which causes the patient to have an equinus deformity and walk on the toes.

Sequence: Key 33 D The apophysis of the calcaneus can develop normally from multiple ossification centers with the adjoining metaphysis appearing sclerotic, irregular, or even serrated.

Sequence: Key 40 B Bence Jones proteins in the urine are diagnostic of multiple myeloma (a malignancy of plasma cells). These proteins are produced by plasma cells and are considered the first tumor marker.

Practice Test 1

-30-

Sequence: Key 41 A Of the choices listed, only the Sayre is a periosteal elevator.

Sequence: Key 48 D The dermatologic lesion most commonly associated with Lyme disease is erythema chronicum migrans.

Sequence: Key 42 A Open reduction and internal fixation are now indicated for the patient. Spinal anesthesia would provide anesthesia at the appropriate level for lower extremity surgery with a thigh tourniquet. Also, with spinal anesthesia there is no risk that the food recently eaten by the patient will be aspirated.

Sequence: Key 49 B The anatomic location of the patient’s symptoms narrows the diagnosis to an intra-articular injury of the ankle joint.

Sequence: Key 43 D Latent ankle diastasis requires no reduction and is treated by cast immobilization. Distal syndesmotic ligamentous injuries without fractures or gross widening of the ankle mortise are treated nonoperatively with a short leg cast, followed by physical therapy. Sequence: Key 44 D The orientation of this view is 45 degrees from the long axis of the foot. This orientation most closely parallels the plane of the posterior and middle calcaneal facets, thus visualizing the joint space. Sequence: Key 45 B Osteoblast and osteoclast activity both increase in Paget’s disease. Sequence: Key 46 A Rowe classifications I through III describe extraarticular calcaneal fractures, which comprise about 25 percent of calcaneal fractures and have the best prognosis. Sequence: Key 47 A Since there is no visible fracture on x-ray, an epiphyseal fracture of the lateral malleolus is likely. A short leg cast for 3 weeks would be the treatment of choice.

Sequence: Key 50 A Pyoderma gangrenosum is thought to be an autoimmune disease and can be caused by many systemic diseases, although the exact etiology is unknown. It is associated with inflammatory bowel diseases such as ulcerative colitis and Crohn’s disease. Sequence: Key 51 A Most inversion ankle sprain injuries occur when the foot is plantarflexed and inverted at the ankle joint, which results in instability. The anterior talofibular ligament is the first ligament of the lateral ankle area to be maximally stretched and torn with this type of injury. Sequence: Key 52 A Freiberg’s infraction is a true osteonecrosis of the second metatarsal head, with the inflammation causing the initial joint space widening. The resultant osteoarthritis causes the subchondral sclerosis commonly seen. Sequence: Key 53 D Patients with multiple sclerosis do not usually have signs and symptoms affecting the lower motor neurons. Lower extremity reflexes are generally hyperactive.

-31Key Sequence: 54 C Charcot neuroarthropathy is a progressive deterioration of a joint characterized by peripheral neuropathy. The goal of treatment is to maintain a stable foot in order to decrease the tendency of the foot to subluxate or dislocate without support. A custom molded shoe will help maintain the foot in a stable position and help protect the extremity from repetitive microtrauma and skin breakdown. Sequence: Key 55 C Osteoid osteoma is classically described as associated with pain at night, relieved by the use of salicylates. Sequence: Key 56 C A thorough medical history is the only method listed that covers the identification of all of the prescription and over-the-counter medications a patient has taken or is taking.

Practice Test 1 Sequence: Key 57 A Aspirin inhibits prostaglandins. Sequence: Key 58 C Coagulase-positive Staphylococcus aureus has consistently been the most common infecting organism in postoperative infections. This also applies to foot and ankle surgery. Closely following this is the less but increasingly virulent organism coagulase-negative Staphylococcus epidermidis. Sequence: Key 59 D Pain and the rapid increase in size without trauma make cavernous hemangioma the most likely diagnosis. Sequence: Key 60 A An aggressive lesion is best treated with surgical curettage and packing.

Practice Test 2

-32PRACTICE TEST 2 ANSWER KEYS AND RATIONALES

Sequence: Key 1 B Herpes simplex is diagnosed with a Tzanck smear in which fluid from an intact vesicle is smeared on a glass slide, dried, and stained with Giemsa’s stain. Sequence: Key 2 A The most serious complication of Paget’s disease is sarcomatous degeneration. Osteosarcomas are most common but fibrosarcomas and chondrosarcomas can also be seen. Sequence: Key 3 B A CT scan is definitive in the diagnosis of osseous subtalar joint coalition, particularly in terms of preoperative planning. Sequence: Key 4 B Pulmonary emboli are usually released from deep venous structures of the lower extremity. They lodge in pulmonary vasculature, which causes a decrease in oxygen levels and an increase in pulmonary blood pressure. The result is air hunger, tachypnea, and dyspnea. Sequence: Key 5 A Patients who take procainamide for prolonged periods often develop anticardiolipin antibodies as well as anti-DNA and anti-histone antibodies. Druginduced systemic lupus erythematosus is rare and usually subsides once the medication is discontinued. Sequence: Key 6 D Melanocytes are contained in the stratum germinativum, also known as the basal layer of the epidermis.

Sequence: Key 7 B The anatomic location of the patient’s pain narrows the diagnosis to the anterior muscle compartment. Shin splints are a common injury in runners and are most symptomatic when a person is running on hills. Overpronation is often the etiology. Sequence: Key 8 C Rheumatoid arthritis is characterized by synovial inflammation. Joint destruction in rheumatoid arthritis targets articular cartilage, ligaments, tendons, and bone. Sequence: Key 9 A Conservative therapy that consists of rest, antiinflammatory medication, and shoe modification is the first step in the treatment of a painful pes planus deformity. Sequence: Key 10 C Cutaneous larva migrans is a disorder caused by nematode larvae, is serpiginous in appearance, and responds to treatment with thiabendazole. Sequence: Key 11 B Sever’s disease is limited to the posterior aspect of the heel and resolves by the time the apophysis fuses with the body of the calcaneus. Sequence: Key 12 A The Bunnell suturing technique is an effective and commonly used end-to-end technique for the repair of tendon ruptures. Sequence: Key 13 C Malignant melanoma would produce the type of pigmented skin changes that could mimic Kaposi’s sarcoma.

-33Key Sequence: 14 C Osteoid osteoma is a small benign osteoblastic tumor. It initially appears as a sclerotic bone island with a central lucent defect. Sequence: Key 15 D Prophylaxis against Staphylococcus aureus and Staphylococcus epidermidis consists of amoxicillin 3 gm orally 1 hour before the procedure and 1.5 gm orally 6 hours later. Sequence: Key 16 A The goal of the semi-weight-bearing technique is to capture an accurate impression of the size and shape of the foot. The cast produced via this technique is most appropriate for an accommodative orthosis. Sequence: Key 17 B Generally, excisional biopsies for skin lesions are performed in the shape of an ellipse with pointed ends. The long axis of the ellipse should be roughly three times its central and greatest width to prevent buckling of the skin. Sequence: Key 18 D The posterior tibial muscle, an inverter of the foot, is the only muscle listed that is powerful enough to support the arch and counteract the effect of fibularis (peroneus) brevis, an everter of the foot. One of the main characteristics of posterior tibial dysfunction is loss of the arch. Sequence: Key 19 C The positions listed in the answer slightly overcorrect for the preoperative hammer toe deformity and are the positions most likely to prevent recurrence. Sequence: Key 20 A This sensitivity refers to the significant genetic effect radiation has on the chromosomes in germ cells.

Practice Test 2 Key Sequence: 21 B In pronation, the talus is positioned more distally and plantarly, which increases the talar declination angle. The calcaneus is lowered and everted, which decreases the calcaneal inclination angle. Sequence: Key 22 A Manipulation of the kVp will affect radiographic subject contrast. A lower kVp will increase the contrast; a higher kVp will decrease the contrast. Sequence: Key 23 A A Salter-Harris type I fracture is simply a fracture of the growth plate without joint involvement. Sequence: Key 24 A In the lateral view, the fifth toe is juxtaposed against the other four toes and the metatarsal heads; therefore, it is not clearly visible. Sequence: Key 25 A In addition to gloves, OSHA-designated personal protection includes gowns and eye protection, which provide protection especially from blood splatter. Sequence: Key 26 C The cane is held on the stronger side of the body and the weight is shifted away from the weaker/painful limb. Sequence: Key 27 D Congenital vertical talus is a complex deformity involving bone, tendon, capsule, and soft tissue abnormality. It has a similar appearance at birth to talipes calcaneovalgus, but there is lack of motion at the subtalar joint and ankle joint within 6 months after birth, a negative calcaneal inclination angle, and complete dislocation of the talonavicular joint. It cannot be reduced with serial casting. Sequence: Key 28 A The lumbrical tendon is located plantar to the deep transverse metatarsal ligament.

Practice Test 2

Sequence: Key 29 B A patient with a loss of proprioception will also have a loss of protective sensation, which is best detected with a 10-gram monofilament. Sequence: Key 30 B In closed kinetic chain supination of the subtalar joint, the talus and tibia externally rotate, the calcaneus inverts, and the longitudinal arch of the foot is elevated, all of which result in a functionally longer limb. Sequence: Key 31 C The normal value for the talocalcaneal angle is 20 to 40 degrees. The talocalcaneal angle becomes smaller with supination, so a value of 10 degrees would be indicative of supination, not excessive pronation. Sequence: Key 32 C With the exception of halothane, all volatile anesthetics contain an ether linkage. Volatile anesthetics with an ether linkage are less likely than halothane to produce cardiac dysrhythmias in the presence of exogenous epinephrine injection. Sequence: Key 33 B The tibialis anterior tendon remains attached at its insertion and is simply routed through a groove created in the navicular. Since its insertion has not changed, it is a translocation. Sequence: Key 34 A People with osteoarthritis frequently have bony enlargement of the distal interphalangeal joints, referred to as Heberden’s nodes. Sequence: Key 35 C Bupivacaine is not recommended for use in children under 12 years of age. It is long acting, and longacting local anesthetics carry an increased risk of cardiac and CNS toxicity.

-34Sequence: Key 36 C Molluscum contagiosum is a viral infection of the skin characterized by the appearance of a few to numerous small, pearly, umbilicated papular epithelial lesions that contain numerous inclusion bodies known as molluscum bodies. Sequence: Key 37 C Practically all venous stasis ulcers exhibit a red, granulating base. Sequence: Key 38 D Lower extremity dependent edema is a sign of rightsided congestive heart failure. Sequence: Key 39 C Surgically changing the insertion of the flexor digitorum longus tendon from the base of the distal phalanx to the dorsal aspect of the proximal phalanx will correct the proximal interphalangeal joint contracture of the hammer toe by pulling the proximal phalanx into a more congruous position with the middle phalanx. Sequence: Key 40 C The failure to report a suspicion of patient abuse may potentially result in harm or death. In such cases, the practitioner may be criminally liable. Sequence: Key 41 D Rocker sole modification is used for any type of pathologic or pathomechanical condition that limits normal movement of the ankle, metatarsal, or metatarsophalangeal joint. A rocker sole is a dynamic lever that assists with the normal movement of the lower extremity during gait and prevents flexing of the sole of the shoe during all phases of gait. Sequence: Key 42 D Routine primary suturing is categorized as healing by first intention.

-35-

Practice Test 2

Key Sequence: 43 C Motor innervation to the anterior compartment muscles of the lower leg is supplied by the deep fibular (peroneal) nerve.

Sequence: Key 50 C Warfarin is an oral anticoagulant and therefore has no effect on established thrombi, nor does it reverse ischemic tissue damage.

Sequence: Key 44 B During ankle joint dorsiflexion, the anterior and widest portion of the talar dome is wedged in the ankle mortise. With inversion, the lateral border of the talar dome is compressed against the lateral malleolus.

Sequence: Key 51 A Diazepam is insoluble in water and contains propylene glycol, a tissue irritant that causes pain on injection and venous irritation.

Sequence: Key 45 B Hemolytic anemia is normochromic and normocytic. Sequence: Key 46 C A pronated subtalar joint would result in pronation of the midtarsal joint, and forefoot valgus would increase. Sequence: Key 47 C The Hawkins classification of talar neck fractures is universally accepted as a way of defining the different fracture patterns of this injury. The severity of the injury and the associated risk of avascular necrosis of the talus increases in a stepwise fashion from type I to type IV. The severity of the injury is directly correlated with anatomic disruption of blood supply to the talus. Sequence: Key 48 D In hypothyroidism, the relaxation of Achilles tendon reflexes is delayed. This is sometimes referred to as hypothyroid neuropathy. Sequence: Key 49 C The patient’s presentation is fairly classic for Graves’ disease. The audible bruit described is generally found only in Graves’ disease. The classic triad in this common disorder is hyperthyroidism with goiter, ophthalmopathy, and dermopathy.

Sequence: Key 52 B The correct ventilation-to-chest-compression ratio in one-rescuer CPR is 2 ventilations for every 15 chest compressions. Sequence: Key 53 B Hyperparathyroidism, which can affect bone in many ways, appears on radiographs as osteopenia. Excess parathyroid hormone results in an increase in bone metabolism, which may appear as microfractures, bone cysts, brown tumors, and pathologic fractures. Sequence: Key 54 A Mycobacterium avium-intracellulare is one of the most common bacterial infections in people with HIV. One study demonstrated the presence of these bacteria in 43 percent of people within 2 years of an HIV diagnosis. This is a disseminated infection that thrives in the presence of a weakened immune system and low CD4+ counts. Sequence: Key 55 B A cohort represents a designated group of individuals who are followed or traced over a period of time. Epidemiology is the study of how a disease presents itself or occurs within a population. Prospective studies examine patients rather than a review of the records. To study a disease and how it presents from one point in time forward, one looks at those who are free of the disease.

Practice Test 2 Sequence: Key 56 D Heel pain in boys 4 to 7 years old is more likely to be caused by irritation of the growth plate of the calcaneus. Sequence: Key 57 B The patellar reflex tests the femoral nerve, which innervates the quadriceps tendon. The nerve is made up of spinal roots L2, L3, and L4. Sequence: Key 58 B The use of oral contraceptives puts a woman at risk to develop deep vein thrombosis.

-36Sequence: Key 59 A Severe localized edema, erythema, serosanguineous drainage, induration, and pain on palpation 3 days postoperatively all indicate that a vessel was damaged, causing a hematoma. Sequence: Key 60 B Sickle cell crisis is a medical emergency in AfricanAmerican patients, and the risks associated with this condition can be minimized by using a sickle cell trait screening test.

-37-

Practice Test 3

PRACTICE TEST 3 ANSWER KEYS AND RATIONALES

Sequence: Key 1 B The initial treatment of choice for deep vein thrombosis is intravenous heparin. Sequence: Key 2 D Measurement of the angle formed by the bisection of the second metatarsal and the line perpendicular to the lesser tarsus bisection gives the metatarsus adductus angle. Sequence: Key 3 B A KOH preparation and/or fungal culture should be done to ensure that a fungal infection exists before griseofulvin is prescribed due to the risk of side effects. Sequence: Key 4 A Adaptic dressing is the only nonadherent dressing listed. Sequence: Key 5 B The Hardcastle classification is universally recognized as a diagnostic and therapeutic system specific only to Lisfranc’s joint dislocation injuries. Sequence: Key 6 D The common fibular (peroneal) nerve winds around the neck of the fibula as it travels distally, lying superficial to the bone and deep to the skin, distal to the knee. If the proximal edge of a short leg cast is not properly padded, it can put pressure on the nerve and damage it. Sequence: Key 7 D The ossification center of the navicular bone appears at approximately 3 years of age and is the last center of ossification to appear in the foot.

Sequence: Key 8 B The crest pad is used when one or several digits of a patient’s foot are in moderate contracture and are becoming irritated at the distal end of the digit. Its purpose is to mechanically dorsiflex and extend the affected digits. It creates an upward thrust and places weight bearing on the padded plantar aspect of the toes, alleviating painful lesions. Sequence: Key 9 A The clubbing seen in lung cancer and certain other pulmonary diseases is generally considered to be a secondary effect of hypoxemia-induced local vasodilatation and is thus an acquired deformity. Sequence: Key 10 D The Occupational Safety and Health Administration is the government agency responsible for chemical exposures. Sequence: Key 11 C Nonsteroidal anti-inflammatory drugs do not cause respiratory depression. Sequence: Key 12 A MRI will assess the ligaments and tendons as well as the integrity of the associated osseous structures of the foot. Sequence: Key 13 B The bifurcate ligament, which originates on the anterior process of the calcaneus and attaches to the navicular and cuboid, is associated with this type of fracture.

Practice Test 3 Sequence: Key 14 D Radiographic evaluation of chronic tophaceous gout usually reveals large bony erosions, which are caused by pressure necrosis of bone adjacent to a periarticular accumulation of monosodium urate crystals. Sequence: Key 15 B The Salter-Harris classification of epiphyseal injury defines fracture pattern on the basis of which zone or zones of the epiphysis in a long bone are disrupted. By definition, the fracture pattern of type I and type III injuries does not extend into or through the metaphysis of a long bone. Sequence: Key 16 D Neisseria gonorrhea is the infective organism that most commonly causes septic arthritis in young adults. Commonly polyarticular in onset, it is often associated with skin lesions. Sequence: Key 17 D Partial thromboplastin time (PTT) evaluates the intrinsic coagulation system. It is commonly used to monitor heparin therapy. Sequence: Key 18 B Charcot joint is caused by impairment of deep pain sensation or proprioception, which affects the joint’s normal protective reflexes. It commonly occurs in patients with diabetes in joints formed by the tarsal bones. Sequence: Key 19 D The severe debilitating effects of rheumatoid arthritis commonly require complete excision of the lesser metatarsophalangeal joints, a technique known as the Hoffman-Clayton procedure.

-38Sequence: Key 20 A A plantar capsular-ligamentous sprain of the first metatarsophalangeal joint occurs when the hallux is hyperextended and compressed at the metatarsophalangeal joint. This can be caused by the friction of artificial surfaces resulting in fixation of the hallux, which causes hyperextension and jamming of the joint on the already dorsiflexed hallux. Sequence: Key 21 B Atlantoaxial subluxation is present in 40% of patients with rheumatoid arthritis, and marked flexion of the neck during anesthesia may cause severe neurological interruption. The anesthesiologist should be consulted preoperatively for evaluation, and flexion-extension lateral cervical neck radiographs should be obtained for patients at risk. Sequence: Key 22 A Acute septic joint disease produces a red, hot, swollen, and painful joint, which mimics the symptoms of gout. Sequence: Key 23 A The gold standard for the diagnosis of pulmonary embolism is the pulmonary angiogram. Sequence: Key 24 B Arteriosclerosis obliterans refers to the occluded peripheral arterial system hallmarked by the examination findings listed in this question. Sequence: Key 25 A The soleus muscle does not cross the knee joint. Limited ankle joint dorsiflexion with the knee flexed is due to soleus equinus, since the influence of the gastrocnemius and plantaris muscles has been eliminated.

-39Key Sequence: 26 A Giant cell tumors are benign lesions, usually solitary and locally aggressive. They classically appear with a radiolucent center and denser periphery. They are eccentric and expansile, with a border that is well defined but not sclerotic, and have a “soap bubble” appearance. Sequence: Key 27 A When a dorsal incision for a dorsal wedge osteotomy is performed at the base of the third metatarsal, the second dorsal interosseous muscle belly is seen first between the second and third metatarsals. Sequence: Key 28 D The Q angle is formed in the frontal plane by two line segments: one segment from the tibial tubercle to the middle of the patella, and one segment from the middle of the patella to the anterior superior iliac spine (ASIS). Patellofemoral tracking problems and anterior knee pain are associated with an increased Q angle. Sequence: Key 29 A Extensor hallucis longus transfer to the first metatarsal head will elevate the plantarflexed first ray, and fusion of the hallux interphalangeal joint will prevent a hallux hammer toe. Sequence: Key 30 A Penicillin excretion occurs mainly by glomerular filtration. If renal excretion is impaired, the dose must be adjusted to accommodate the decreased renal function. Sequence: Key 31 C The combination of intravascular hyperviscosity due to a high red cell mass and a high platelet count with functionally abnormal platelets puts patients with polycythemia vera at high risk for stroke, myocardial infarction, and venous thromboembolism.

Practice Test 3 Sequence: Key 32 A The headache associated with a spinal anesthetic is believed to result from the loss of cerebrospinal fluid through the meningeal needle hole, which results in decreased buoyant support for the brain. The headache is characteristically mild or absent when the patient is supine, but head elevation results in fronto-occipital headache. In the upright position, the brain sags in the cranial vault, putting traction on the pain-sensitive structures. Sequence: Key 33 C Long-term steroid usage suppresses the hypothalamic-pituitary axis (HPA) and increases the risk for hypotensive shock. Preoperative supplementation with high-dose steroids will help avert this complication. Sequence: Key 34 B If an automated external defibrillator is to be used on a patient who has a medication patch, the patch should be removed prior to use of the defibrillator. Small burns to the skin may result if a defibrillator pad is placed on a medication patch. Sequence: Key 35 A In infant cardiopulmonary resuscitation, the chest compressions should be 0.5-1.0 inch. Sequence: Key 36 D Blue nevi arise from dendritic melanocytes. This benign nevus is believed to form from nerves and not from the basal layer of the epidermis. Sequence: Key 37 D Glucocorticoids (steroids) do not cause hepatitis. Sequence: Key 38 C Swallowing difficulty, prior stroke, chronic nasogastric tube feeding, and fetid sputum 2 days postoperatively are all clues of an infection in the lung.

Practice Test 3 Sequence: Key 39 D Hand-foot-and-mouth disease has a viral etiology and is caused by a coxsackievirus. Sequence: Key 40 B In the standard lateral view, the third metatarsalcuneiform joint is usually not visible. Sequence: Key 41 C The two basic requirements for primary bone healing are an intact vascular supply to the bone and stable rigid fixation of the fracture fragments. Sequence: Key 42 D Treatment of acute ankle injury is generally conservative and consists of rest, ice, compression, and elevation. A modified Jones compression dressing to control edema and immobilize the extremity for 24 to 73 hours is recommended. Sequence: Key 43 B Increasing the kilovoltage increases the penetrating power of the x-rays emitted from the x-ray tube, with more photons reaching the x-ray film through the target tissue. This increases the exposure of the film and thus increases radiographic density. To keep the radiographic density constant, it is, therefore, necessary to reduce the mAs, which controls the total number of x-rays produced at the x-ray tube. Sequence: Key 44 B In Haglund’s deformity, an increase in the FowlerPhilip angle of more than 75 degrees can be seen on a lateral radiograph. Positive parallel pitch lines or excessive bone on the calcaneus are also present. These measurements are used to evaluate the extent of the deformity and to plan surgical correction. Sequence: Key 45 D Leather is not a good material for extrinsic posting of a functional orthotic due to its tendency to wear and compress with weight bearing.

-40Sequence: Key 46 C The specificity of a test is the degree to which it accurately provides a negative result for persons who are free of the disease. Sequence: Key 47 A Light leakage is the most common cause of fogging on developed radiographic film. Sequence: Key 48 A Statues of limitations are a segment of an individual state’s rights and are, therefore, determined by state law. Sequence: Key 49 C Salter and Harris described the type V injury as an uncommon injury secondary to a crushing force to the physis through the epiphysis. There is no visible fracture and no displacement. It is recommended that this injury be treated by placing the patient in a nonweight-bearing cast for 3 to 4 weeks, followed by range-of-motion exercises to prevent premature fusion secondary to immobilization. Sequence: Key 50 C The calcaneocuboid joint is prone to abduction in runners with pronation. This can then progress to subluxation, unless it is controlled with an orthotic device. Sequence: Key 51 A Candida albicans is a yeast that will reveal pseudohyphae on a KOH preparation. Sequence: Key 52 C Osteopoikilosis is a sclerosing bone disorder characterized by numerous, small, symmetrical bone islands prominent in metaphyseal areas. Sequence: Key 53 D Topical cortisone is an anti-inflammatory agent applied to the skin to treat various dermatologic conditions and is not known to induce asthma.

-41-

Practice Test 3

Key Sequence: 54 B Each long bone usually has separate centers of ossification: the shaft (diaphysis) and each end (epiphysis). The first (primary) center to ossify is always the diaphysis.

Sequence: Key 58 C Fentanyl, sufentanil, and thiopental cause depression of ventilation. They also cause cardiovascular depression and bradycardia, slowed gastric emptying, and antidiuretic hormone release.

Sequence: Key 55 A An adducted, toe-walking, scissor-type gait is most often associated with the spastic disorder of cerebral palsy.

Sequence: Key 59 A Epinephrine is the drug of choice for shock, angioedema, airway obstruction, bronchospasm, and urticaria in severe anaphylactic reactions. Its action is via adrenergic effect.

Sequence: Key 56 D The 5.07 (10-gram) monofilament is used to screen for protective sensation loss in patients with diabetes. Sequence: Key 57 C The National Committee for Quality Assurance sets the standards for patient care.

Sequence: Key 60 C Mild to moderate eosinophilia is associated with drug allergy. When drug-induced eosinophilia is suspected, termination of the offending agent generally terminates the problem.

Admission orders (ADC VANDILMAX) ● Admit ● Diagnosis ● Condition ● Vitals ● Ambulatory ● Nursing orders ● Diet ● Ins/outs ● Labs ● Medications ● Ancillary ● Xray Post op Notes (SAPPPAHEMICCC) ● Surgeon ● Assistants ● Pre-op dx ● Post-op dx ● Procedure ● Anesthesia ● Hemostasis ● EBL (estimated blood loss) ● Materials ● Injectables ● Culture ● Condition ● Complications

(SAPPPAHEMIPC) Surgeon Assistants Pre-op diagnosis Post-op diagnosis Procedure Anesthesia Hemostasis EBL Materials Injectables Pathology Complications

Diuretics [“Aces For Bilal’s Ethnic Spirit And Try Hard Insight”] ● Proximal Tubule: ○ Acetazolamide ● Loop ○ Furosemide ○ Bumetamide ○ Ethacrynic Acid ● K+ sparing (Collecting Duct) ○ Spironolactone ○ Amiloride ○ Triamterene ● Thiazides (Distal Convoluted Tubule) ○ Hydrochlorothiazide ○ Indapamide Triple Arthrodesis (order of fusion according to Coughlin and Mann) 1. STJ 2. TNJ 3. CCJ Pes Cavus -

-

-

Anterior Cavus
Metatarsal (Lis francs)
Lesser Tarsal (middle of lesser tarsal bones)
Forefoot (Choparts)
Combined Rearfoot Cavus Pseudoequinus
In the rigid form of anterior pes cavus, compensatory dorsiflexion cannot be absorbed by the forefoot. Therefore, the entire foot must dorsiflex at the ankle to allow the heel to contact the ground Radiographic Angles st
Meary’s – 1 MT and talar neck st
Hibb’s – 1 MT and calcaneus

-

-

-


Calcaneal inclination angle
Talar declination angle
TC angle (Lateral and AP-Kite’s)
CYMA line Coleman Block Test
To determine if the deformity is flexible or rigid.
Lateral foot except heel and medial forefoot in on 2inch wooden block. st
If heel moves from varus to neutral  deformity is due to PF 1 ray
If heel stays in varus  deformity is rigid If flexible, do ST correction
Steindler stripping (release PF, abd hallucis, FDB, abd digiti minimi, long plantar ligament)
STATT st st
Jones tenosuspension (EHL through 1 MT head: removes windlass mech.. no PF of 1 MT) If rigid, do osseous correction
Cole
Japas
Dwyer (CBWO base lateral)
Reverse Koutsogiannis (lateral calcaneal slide)

Hallux Limitus - Drago, Oloff, and Jacobs o I – functional HL o II – Joint adaptation o III – Joint deterioration o IV – Hallux Rigidus (ankylosis) - Etiologies o Trauma** st o Short 1 MT st o Long 1 MT o MPE o Arthritic (DJD) st o Hypermobile 1 ray st o Round or square 1 MT head - Seiberg index (evaluation of MPE on lateral xray) nd st o The perpendicular distance from the dorsum of the 2 MT to the dorsum of the 1 MT shaft is st st measured at the 1 MT neck and 1.5 cm from the 1 MT base. o The proximal measurement is subtracted from the distal measurement to give the Seiberg index. o A positive number indicates an elevated first metatarsal. o On average, the distal measurement is about 8mm in elevatas - Treatment o Joint preserving
Cheilectomy
Watermann-Green – PF and shortens… note: can also translate capitol frag laterally for IMA 1. Cheilectomy (dorsal and medial prominences) rd 2. Plantar arm (plantar 2/3 of MT) 3. Distal dorsal arm parallel to articular surface (PASA) st 4. Proximal dorsal arm (perpendicular to shaft of 1 MT)
Watermann nd
Youngswick (Austin with 2 dorsal arm) – PF and shortens
Lambrinudi
Valenti
Hohmann o Joint destructive
Keller
Mayo
Stone
Implants (total and hemi)
Mc Keever
Lapidus DDX List: Posterior heel pain

Achilles tendon rupture Achilles tendonitis or –osis (insertional or non-insertional) Fracture a. Avulsion fracture of superior posterior calcaneus (Rowe 2) b. Shepard’s fracture c. Cedell’s fracture d. Calcaneal fracture 4. Stress fracture of calcaneus (pathologic or insufficiency fx) 5. Bursitis (retrocalcaneal or subcutaneous calcaneal bursa) 6. Haglund’s deformity (pump bump) 7. Calcaneal apophysitis 8. Osteomyelitis 9. Bone tumor a. ABC b. UBC c. Intraosseous lipoma d. Enostosis Dorsal foot pain (proximal) 1. Anterior process of calcaneus fracture (Rowe 1c) 2. Sinus tarsi syndrome (compensation from pes planus?) 3. Stress fracture (any proximal dorsal bones) 4. Fracture 5. Tendonitis or tendon rupture 6. Arthritis 7. Gout 8. Charcot 9. Osteomyelitis 10. AVN 11. Bone tumor 12. CRPS 13. Neuropraxia 14. Ganglion cyst Dorsal foot pain (distal) 1. Predislocation syndrome 2. Stress fracture (any distal dorsal bones) 3. Fracture 4. AVN 5. Tendonitis or tendon rupture 6. Arthritis 7. Gout 8. Charcot 9. Neuroma 10. Neuropraxia 11. Ganglion cyst 12. Mucoid cyst (if in toes) 13. Osteomyelitis 14. Bone tumor a. Enchondroma b. Osteochondroma or chondrosarcoma Plantar foot pain 1. Tarsal tunnel syndrome 2. Plantar fasciitis 3. Baxter’s neuritis 4. Stress fracture 5. Fracture a. Calcaneal tuberosity fracture (Rowe 1a) b. Sesamoid fracture 6. Tendonitis or tendon rupture 7. Neuropraxia 8. Plantar’s wart 9. Plantar fibroma 10. Neuroma 1. 2. 3.

11. Bone tumor a. UBC b. ABC c. Intraosseous lipoma d. Enostosis Medial foot pain 1. PTTD 2. Tendon rupture or tendonitis a. TA b. TP 3. Medial ligamentous sprain (deltoid) 4. Sustentaculum tali fx (Rowe 1b) 5. Avulsion of navicular tuberosity 6. Stress fracture 7. Tarsal tunnel syndrome 8. Neuropraxia 9. Bone tumor Lateral foot pain 1. Tendon rupture or tendonitis a. PB b. PL 2. Lateral ligamentous sprain (CFL, ATFL, PTFL) 3. Neuropraxia (sural nerve lateral dorsal cutaneous nerve) 4. Stress fracture 5. Fracture a. Nutcracker fracture 6. AVN th 7. Avulsion fracture of tuberosity of 5 MT (Stewart) 8. Avulsion fracture of lateral malleolus 9. Peroneal tendon dislocation (Ekert and Davis) a. SER rupture th 10. Iselin’s disease (apophysitis of 5 MT base) 11. Tarsal Coalition 12. Bone tumor Aside: ● 3 main principles of ORIF for ankle fractures ○ Restore length of fibula ○ Fix ankle mortise ○ Fix syndesmosis ● 4 main principles of ORIF for pilon fractures ○ Restore fibular length ○ Fix ankle mortise ○ Fill in cancellous defects ○ Support tibia with plate ● 4 main principles of ORIF for calcaneal fractures ○ Fix height of calcaneus ○ Fix width of calcaneus ○ Take heel out of varus ○ Articular reduction Journal Articles ● Subtalar Fusion After Displaced Intra-Articular Calcaneal Fractures: Does Initial Operative Treatment Matter? ○ JBJS 2009: Craig S. Radnay, Michael P. Clare and Roy W. Sanders ○ 2 patient groups: conservative non-ORIF vs. non-conservative ORIF after intraarticular calcaneal fracture. ○ Both groups got post traumatic arthritis and underwent STJ fusion ○ Better functional outcomes and fewer wound complications in patients who originally underwent ORIF
This is due to the fact that ORIF restored calcaneal shape, height, and alignment which facilitated fusion. ● Screw Fixation Compared with Suture-Button Fixation of Isolated Lisfranc Ligament Injury ○ JBJS 2009. Panchbhavi

Suture-button fixation can provide stability similar to that provided by screw fixation in cadaver specimens after isolated transection of the Lisfranc ligament. ○ Fixation with a suture button may be an acceptable alternative to screw fixation in the treatment of isolated Lisfranc ligament injuries, avoiding subsequent surgery to remove the hardware prior to weightbearing. Cast-Saw Burns: Evaluation of Skin, Cast, and Blade Temperatures Generated During Cast Removal ○ JBJS 2008. Shuler ○ The highest skin temperatures were recorded for fiberglass casts with two layers of padding. The lowest skin temperatures were recorded for plaster casts with four layers of padding. Four layers of cast padding compared with two layers significantly reduced skin temperatures for both plaster and fiberglass casts. Fractures of the Lower end of the Tibia into the Ankle Joint ○ Ruedi and Allgower 1969 ○ 4 main principles of ORIF in Pilon Fractures:
Restore length of fibula ● Incision: longitudinal parallel to posterior edge of fibula
Reconstruct articular surface of tibial plafond ● Incision: anterior tibia curving to medial malleolus
Fill in cancellous defects using bone graft
Support medial tibia with plate to prevent varus ● T- plate allows 2 cancellous screws to be inserted into lower articular fragments ○ Classification of Pilon Fractures (Ruedi and Allgower)
Type 1 – minimal displacement
Type 2 – significant displacement. Not comminuted
Type 3 – comminuted, displaced, and impacted Ankle Fractures ○ Clinics in Podiatric Medicine and Surgery 2006. Mandi et al ○ Always check NV status!! If not intact… maybe think compartment syndrome ○ If vascular compromise exists, it most commonly is caused by severe malalignment or dislocation of ankle
Emergent reduction should be performed. ○ 3 views always: AP, mortise (15deg internally rotated), lateral ○ On mortise view, assess: think lateral displacement of the talus
If medial gutter space is >4mm ● Accd to Ramsay and Hamilton… 1mm displacement = 42% loss of tib-talar contact area
The tibia-fibula overlap should be at least 10 mm. ● <10mm overlap would lead the observer to expect syndesmotic rupture. ○ If >25-30% of articular surface is involved in posterior malleolus fracture fixate ○ Protocol
Check NV status
Perform local block
Close reduce (increase deform6ity, distract, decrease deformity)
If need to go to OR: ● Debride devitalized tissue ● Aggressive irrigation ● Empiric antibiotics … cephs and aminoglycosides ○ If too swollen…
Jones compression with posterior splint
Elevation and ice
2-3 days is usually sufficient to decrease edema. Look for skin wrinkles to return!!! ○ Fibula usually shortens in ankle fractures causing lateral displacement of the talus 1mm lateral displacement = 42% loss of tibiotalar contact ankle joint instability!! ○ Fibula Fixation
Bone reduction forceps to hold alignment
Interfrag screw (4.0 partially threaded) rd
1/3 tubular plate bent to contour the fibula ● SER: Posterolateral surface of fibula to prevent proximal gliding (anti-glide) ● PAB: dynamic compression plate used as buttress
3.5 screws (6-8 cortices purchased proximal to the fracture line and 4-6 distal) into plate ● 3-4 screws proximal ● 2-3 screw distal (note this cannot always be done due to location of fracture so in this case you insert what you can) ○

●

●

●

Syndesmosis Fixation
Cotton test (aka Hook test) can be used to evaluate syndesmosis after fibular fixation
Repair is recommended if talus shifts laterally 3-4mm
Approach laterally
1-2 screws 1.5 – 3.0cm proximal to tibial plafond ● AO recommends use of a fully threaded screw (3-4 cortices) ○ In this paper: 3.5 corticol screws with 4 cortices purchased ○ Some use 4.0 cancellous screws with 3 cortices purchased
Allows earlier weight bearing ● Tightrope, partially threaded screws, or bioabsorbable screws can also be used ○ Tightrope allows the earliest return to weight bearing and no need for removal
Angle screws posterolateral to anteromedial (15 degrees) to account for the fact fibula is a little posterior to tibia
Make sure foot is in maximal dorsiflexion during repair! ● Fibula moves ~2mm laterally with ankle dorsiflexion ● You lose 0.1 degrees of DF for every degree of PF of the ankle at time of syndesmosis repair
Remove syndesmotic screw after signs of radiographic healing ● Reports from 2-4 months before removal ● Beware of full weight bearing… may cause screw breakage ○ Medial malleolar fixation
Muller classification ● Type A – Avulsion fx distal to ankle mortise ● Type B – Avulsion fx at the level of the ankle mortise ● Type C – Oblique fx of the medial malleolus ● Type D – Vertical fx of medial malleolus (ie. SAD)
1 or 2 screws (lag fashion) for compression ○ Posterior malleolar fixation
Most often associated with SER and PER fractures
If >25-35% of joint surface is involved, posterior frag should be reduced and fixated
Usually anterior incision (through same incision used for medial malleolar reduction) ● Posteromedial and posterolateral approaches have also been used.
1 or 2 cannulated screws aided by fluoroscopy ○ Post-op
SLC with strict NWB 4-6 weeks
ROM exercises begin at 2 weeks (sagittal plane) ○ Complications
Post-traumatic osteoarthritis
Delayed union, malunion, non-union (rare)
Hardware irritation Management of the Diabetic Charcot Foot ○ Diabetes/Metabolism Research and Reviews, 2000. Robert Frykberg ○ Sanders and Frykberg anatomic classification of Charcot neuroarthropathy ■Pattern I - IPJs, phalanges, MTPJs, metatarsals ■Pattern II - Tarsometatarsal joints ■Pattern III - NC, TN and CC joints ■Pattern IV - Ankle joint ■Pattern V - Calcaneus ○ Effective conservative management of Charcot neuroarthropathy is dependent on its presentation pattern. Once the patient exits the acute phase, management is directed at prolonged or permanent bracing for ambulation. ■Pattern I-III - Custom full-length inserts + extra depth shoes; severe midfoot deformities: fabrication of custom shoes to accommodate the misshapen foot ○

●

■Pattern IV – Mild: high-top custom-molded shoe with a full-length orthotic device; moderate: solid

○

AFO + therapeutic shoe; severe: patellar tendon bearing brace in custom shoe ■Pattern V – Immobilization via casting for minimally displaced fractures (NWB until radiographic evidence of union, 8 weeks) The goal of treatment: to achieve stable plantigrade foot with intact skin

AUTHOR(S): ASTION, DONNA J., M.D.†; DELAND, JONATHAN T., M.D.‡; OTIS, JAMES C., PH.D.‡; KENNEALLY, SHARON, B.S.‡, NEW YORK, N.Y. Investigation performed at The Hospital for Special Surgery, New York City J Bone Joint Surg [Am] 1997; 79-A; 241-6 ABSTRACT: Arthrodesis of the subtalar joint, triple arthrodesis (involving the subtalar, talonavicular, and calcaneocuboid joints), double arthrodesis (involving the talonavicular and calcaneocuboid joints), arthrodesis of the talonavicular joint, and arthrodesis of the calcaneocuboid joint were simulated in a cadaver model, and the range of motion of each joint not involved in the simulated arthrodesis was measured with a three-dimensional magnetic space tracking system. The excursion of the posterior tibial tendon was also measured under all of these conditions. We found that any combination of simulated arthrodeses that included the talonavicular joint severely limited the motion of the remaining joints to about 2 degrees and limited the excursion of the posterior tibial tendon to 25 per cent of the preoperative value. Simulated arthrodesis of the calcaneocuboid joint had little effect on the range of motion of the subtalar joint, and it reduced the range of motion of the talonavicular joint to a mean of 67 per cent of the preoperative value; a mean of 73 per cent of the excursion of the posterior tibial tendon was retained. After simulated arthrodesis of the subtalar joint, a mean of 26 per cent of the motion of the talonavicular joint, 56 per cent of the motion of the calcaneocuboid joint, and 46 per cent of the excursion of the posterior tibial tendon was retained. The talonavicular joint is the key joint of the triple joint complex. The talonavicular joint had the greatest range of motion, and simulated arthrodesis of this joint essentially eliminated motion of the other joints of the complex. CLINICAL RELEVANCE: Arthrodesis of any of the joints of the so-called triple joint complex (the subtalar, talonavicular, and calcaneocuboid joints) limits the motion of the remaining, unfused joints. However, clinical estimates of these limitations are imprecise and motion of the individual joints cannot be specifically measured clinically. It is important to be able to measure the limitation of motion of each joint after arthrodesis of the other joints in order to understand the clinical implication of the arthrodesis. Also, it is necessary to ascertain the effect of limiting the motion of

these joints on the excursion of the posterior tibial tendon in order to determine when it is appropriate to reconstruct the tendon concomitantly with these arthrodeses. Motion of the so-called triple joint complex (the subtalar, talonavicular, and calcaneocuboid joints) is necessary for the foot to accommodate variations in ground surface and rotation from the lower extremity. Although gross differences in the amount of motion of the triple joint complex remaining after different arthrodeses has been recognized in vivo and in vitro (2-4,9), the amount of motion remaining has not been measured accurately, to our knowledge. While it is difficult to measure this motion precisely in the clinical setting, Mann and Baumgarten estimated clinically that about 50 per cent of the motion of the transverse tarsal joint remained after arthrodesis of the subtalar joint. They therefore advocated the use of isolated arthrodesis of the subtalar joint rather than triple arthrodesis, when possible, to leave the foot as flexible as possible. Fogel et al. found that isolated arthrodesis of the talonavicular joint provided satisfactory results but clinically limited subtalar motion compared with that of the contralateral foot. With use of a standard manual goniometer and reference pins in the tibia, calcaneus, and second metatarsal, Gellman et al. measured the motion of the foot and the ankle in vitro after various combinations of simulated arthrodeses of the ankle and tarsal joints. Those authors did not include arthrodesis of the talonavicular or calcaneocuboid joints, or both, or measure the motion of individual joints. Unlike motion of the major joints of the lower extremity, motion of the joints of the foot cannot be measured accurately with an external goniometer. It is possible, however, to measure the change in position of individual bones of the foot in threedimensional space with a three-dimensional magnetic space tracking system; the range of motion of the joints can then be calculated. This system has been used in the past to study the mechanics of the wrist(7, 8) . Most pronation and supination of the foot occurs in the triple joint complex. The posterior tibial muscle and the peroneal muscles are the principal muscles acting on these joints. Arthrodesis of any one of the joints of the triple joint complex affects the excursion of the posterior tibial tendon. The purpose of the present study was to quantify, in vitro, the effect of simulated arthrodesis of selected joints of the triple joint complex on both the range of motion of the remaining, unfused joint or joints and the excursion of the posterior tibial tendon. We believe that these in vitro data will help a practitioner to determine when to perform a transfer of the flexor digitorum longus tendon to replace the function of a ruptured or otherwise non-functional posterior tibial tendon concomitantly with arthrodesis. Materials and Methods Ten fresh-frozen cadaveric foot specimens, amputated at the middle of the tibia, were used in this

Downloaded from www.ejbjs.org on October 23, 2006

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

JBJA Journal of Bone and Joint Surgery American 1996 - 1998 February 1997, Volume 79-A, Number 2 241 Motion of the Hindfoot after Simulated Arthrodesis* Article

muscles acting on the triple joint complex. In preliminary testing, a pull on the peroneus longus tendon did not cause greater motion in the triple joint complex than a pull on the peroneus brevis tendon did. Stainless-steel wires were sutured to the posterior tibial and peroneus brevis tendons proximal to the malleoli. The sutures were attached to gauges that measured linear displacement through wire cables threaded through pulleys. Use of the pulleys allowed a direct line of pull on each tendon and allowed the excursion of these tendons to be measured as the foot was moved (Fig. 1). As neither the peroneus brevis tendon nor the posterior tibial tendon inserts into the calcaneus, testing of the initial specimens was performed with a load placed on the calcaneus to stabilize it against the talus and to prevent it from acting as a free body. Subsequent testing showed no difference in joint motion or tendon excursion with or without a load on the calcaneus. However, for consistency, all of the specimens were tested with the calcaneus loaded. For the purpose of this study, the motion produced in the triple joint complex by placement of a load on the peroneus brevis tendon is defined as pronation and the motion produced by placement of a load on the posterior tibial tendon is defined as supination. To achieve the pronated position of the foot, a thirtysix-newton load was placed on the peroneus brevis tendon and an eleven-newton load was placed on the posterior tibial tendon (Fig. 1). The loads were exchanged to achieve the supinated position of the foot. These loads were chosen because preliminary testing had demonstrated that greater loads did not produce noticeable additional motion of the joints under investigation. After each simulated arthrodesis, the linear displacement reading for the excursion of the posterior tibial tendon and the three-dimensional position of the bones were recorded for each of three supination trials and three pronation trials. The simulated conditions included no arthrodesis, arthrodesis of the subtalar joint, triple arthrodesis (involving the subtalar, talonavicular, and calcaneocuboid joints), double arthrodesis (involving the talonavicular and calcaneocuboid joints), arthrodesis of the talonavicular joint, and arthrodesis of the calcaneocuboid joint. The order of the simulated arthrodeses was maintained to minimize the number of times that hardware was placed into the bones to be fixed together, thereby allowing more rigid stabilization of the bones. During the experiment, the foot was held in a neutral plantigrade position while each joint was fixed. The subtalar joint was fixed with the heel in the neutral position, as fixing of this joint in varus results in more restricted motion of the talonavicular and calcaneocuboid joints(11). To simulate an arthrodesis, a combination of at least two screws or threaded pins, with a firm hold in bone, were placed across the joint to be fixed. No cartilage was removed from the joints. From the data collected, the range of motion of the subtalar, talonavicular, and calcaneocuboid joints and the excursion of the posterior tibial tendon were

Downloaded from www.ejbjs.org on October 23, 2006

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

study. All of the specimens had a grossly normal posterior tibial tendon and had no radiographic evidence of osteoarthrosis. The exact ages of the donors were not known, but all feet were from adults and all growth plates were closed. The soft tissue about the ankle and the malleoli was left intact, and the more proximal soft tissue was cleared from the tibia and the fibula. The ankle was fixed in a neutral position with three large screws. Elimination of motion of the ankle was necessary to isolate motion of the triple joint complex and to allow reliable and reproducible measurement of the tendon excursion. The three-dimensional locations of the talus, calcaneus, navicular, and cuboid were monitored with a magnetic space tracking system (Fastrak; Polhemus Navigational Sciences Division, Colchester, Vermont). This system consists of a source that generates a magnetic field and four sensors, the positions of which are detected within the magnetic field. The accuracy of the system is dependent both on the amount of metal in the field and on the distance between the sensor and the source(10). Metal objects of a certain composition, size, and shape can be used in the space tracking system without causing interference. The metal components (screws, wires, and threaded pins) used during this experiment were placed in various locations about the source to verify that they did not create any detectable distortion. The manufacturer determined the accuracy of the tracking system (0.8 millimeter along each of the three translational axes and 0.15 degree about each of the three rotational axes) with the sensor thirty inches (76.2 centimeters) from the source. The present study was conducted with the sensor no more than twelve inches (30.5 centimeters) from the source. The accuracy with the shorter distance was determined, before the study was conducted, to be 0.1 millimeter along each translational axis and 0.1 degree about each rotational axis. The magnetic source of the space tracking system was fixed to the test frame, and the sensors were attached to each of the four bones (Fig. 1). The position of the sensor in each bone was selected so that the sensors did not come into contact with each other throughout the range of motion of the foot. To attach the sensors rigidly to each bone, each sensor was mounted on a small Plexiglas plate that was connected to two 3.0-millimeter carbon vinyl ester pins. The pins were press-fit into two undersized holes in the bone six millimeters apart. Two pins were used with each sensor to prevent rotation at the pin-bone interface. The specimens were placed plantar side up in the testing apparatus, which stabilized the tibia and allowed unrestricted motion of the foot (Fig. 1). Placement of the foot plantar side up also simplified the use of weights and wires for the application of loads. Tendon pulls were used to move the foot through a reproducible range of motion without imposing an artificial axis of motion. The tendons of the posterior tibial and peroneus brevis muscles were selected because they are antagonists and the principal

Statistical Analysis Statistical analysis was performed with each foot acting as its own control. Analysis of variance with pair-wise comparisons with Bonferroni corrections were applied to account for multiple measurements. A level of significance of p ≤ 0.05 was used. If 3 degrees of motion or more occurred at the site of a simulated arthrodesis, data from that arthrodesis as well as data from subsequent conditions that included the inadequately fixed site, were excluded. For example, if excessive motion was present after the simulated subtalar arthrodesis, this condition as well as the simulated triple arthrodesis were excluded for that foot. However, if excessive motion occurred after simulated arthrodesis of the calcaneocuboid joint (the last condition simulated), the measurements of the previous simulations were not excluded. Results Before the simulated arthrodeses, the talonavicular joint had the greatest range of motion (36.7 ± 13 degrees [mean and standard deviation]), followed by the subtalar joint (20.4 ± 8 degrees) and the calcaneocuboid joint (14.4 ± 6 degrees), in all ten feet. Simulated arthrodesis of the talonavicular joint and simulated double arthrodesis significantly limited the range of motion of the subtalar joint, in the nine feet for which it was recorded, to a mean of 8 and 9 per cent, respectively, of the subtalar motion before the simulated arthrodeses (p < 0.0001 for both) (Fig. 2). Simulated arthrodesis of the subtalar joint resulted in a significant decrease in the range of motion of the talonavicular joint (p < 0.0001) and the calcaneocuboid joint (p = 0.005), in the nine feet for which it was recorded, to a mean of 26 per cent (Fig. 3) and 56 per cent (Fig. 4), respectively, of the range of motion before the simulated arthrodeses. Simulated arthrodesis of the calcaneocuboid joint had little effect on the range of motion of either the talonavicular joint, which retained a mean of 67 per cent of the motion that it had had before the simulated arthrodeses (Fig. 3), or the subtalar joint, which retained a mean of 92 per cent of its motion (Fig. 2), in the five feet for which these data were recorded. The mean excursion of the posterior tibial tendon in the ten feet was 17 ± 5 millimeters (range, ten to twenty-seven millimeters) before the simulated arthrodeses. In the five feet for which it was recorded, a mean of 73 per cent of the excursion was maintained after simulated arthrodesis of the calcaneocuboid joint (Fig. 5). With the number of specimens in this study, we could not show a significant difference between the tendon excursion before the simulated arthrodesis of the calcaneocuboid joint and that after it. However, the excursion of the posterior tibial tendon was significantly decreased, compared with before the simulated arthrodeses, after all of the simulated arthrodeses that involved the talonavicular joint

(arthrodesis of the talonavicular joint, double arthrodesis, and triple arthrodesis) (p < 0.0001 for all). Simulated arthrodesis of the subtalar joint and simulated arthrodesis of the talonavicular joint decreased the tendon excursion, in the nine feet for which it was recorded, to a mean of 46 and 25 per cent, respectively, of the excursion before the simulated arthrodeses. After simulated double arthrodesis (in the nine feet for which it was recorded) and after simulated triple arthrodesis (in the eight feet for which it was recorded), the remaining excursion was a mean of 25 per cent of that before the simulated arthrodeses (Fig. 5). Discussion There have been several clinical studies involving patients who had various arthrodeses of the triple joint complex. Lapidus reported on a patient who had arthrodesis of the subtalar joint in one foot and arthrodesis of the talonavicular joint in the other. He reported that the foot that had had arthrodesis of the subtalar joint had better compensatory motion compared with the foot that had had arthrodesis of the talonavicular joint; however, the amount of motion remaining was not quantified in either foot. Mann and Baumgarten retrospectively evaluated eleven feet that had had isolated arthrodesis of the subtalar joint. With use of the contralateral side for comparison, they estimated that about 50 per cent of the transverse tarsal (talonavicular and calcaneocuboid) motion had been maintained. Hall and Pennal clinically estimated that 25 to 50 per cent of transverse tarsal motion remained after arthrodesis of the subtalar joint. In the present study, a mean of 26 per cent of the motion of the talonavicular joint and 56 per cent of the motion of the calcaneocuboid joint remained after simulated arthrodesis of the subtalar joint. Fogel et al., in their follow-up study of patients who had had arthrodesis of the talonavicular joint, noted that subtalar as well as transverse tarsal motion was severely limited. This clinical result is in accordance with our in vitro finding that the subtalar and calcaneocuboid joints retained 3 degrees of motion or less after simulated arthrodesis of the talonavicular joint. Our in vitro measurements are consistent with the in vivo estimates of motion retained by the transverse tarsal joint after arthrodesis of the subtalar joint and by the subtalar joint after arthrodesis of the talonavicular joint. The mean range of motion of the subtalar joint (20.4 degrees) before the simulated arthrodeses in the present study was within the 18-to-24-degree range determined by Inman in two cadaveric studies(11). The results of the present study, however, cannot be compared with those reported by Gellman et al. because those authors determined the motion remaining in the foot as a whole after various simulated arthrodeses. Also, Gellman et al. moved the foot manually in a predetermined direction, whereas we used tendon pulls with constant loads to move the feet. With our experimental model, we were able to quantify several important clinical observations. The degree to which simulated arthrodesis of a joint of the

Downloaded from www.ejbjs.org on October 23, 2006

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

calculated for each condition from full supination to full pronation of the foot.

joint (a mean of 25 per cent remained after arthrodesis of the talonavicular joint, after double arthrodesis, and after triple arthrodesis). These data suggest that excursion of the posterior tibial tendon is most related to mobility of the talonavicular joint and that any arthrodesis that preserves mobility of the talonavicular joint, such as arthrodesis of the calcaneocuboid or subtalar joint, also preserves excursion of the posterior tibial tendon. It follows that transfer of the flexor digitorum longus tendon to the navicular tuberosity, to restore the function of a ruptured or otherwise non-functional posterior tibial tendon, will also maintain its excursion if the talonavicular joint remains mobile. Therefore, this tendon transfer can be performed to restore the function of the posterior tibial tendon in conjunction with arthrodesis of the calcaneocuboid joint or, possibly, arthrodesis of the subtalar joint, both of which preserve motion of the talonavicular joint. In summary, this cadaveric study demonstrated that motion of the talonavicular joint is the key to motion of the triple joint complex. Any simulated arthrodesis that includes fixation of the talonavicular joint essentially eliminates the motion of the other joints in the complex and severely limits excursion of the posterior tibial tendon. After simulated arthrodesis of the subtalar joint, some motion of the talonavicular and calcaneocuboid joints is retained, as is a mean of 46 per cent of the excursion of the posterior tibial tendon. Simulated arthrodesis of the calcaneocuboid joint preserves a good deal of the motion of the talonavicular joint, most of the motion of the subtalar joint, and most of the excursion of the posterior tibial tendon. These results are consistent with clinical observations that the amount of motion remaining in these joints influences the patient's postoperative function. References: (1-11)

1.

2.

3.

4.

5.

Deland, J. T.; Otis, J. C.; Lee, K.-T.; and Kenneally, S. M.: Lateral column lengthening with calcaneocuboid fusion: range of motion in the triple joint complex. Foot and Ankle 1995; 16:729-733. Fogel, G. R.; Katoh, Y.; Rand, J. A.; and Chao, E. Y. S.: Talonavicular arthrodesis for isolated arthrosis. 9.5-year results and gait analysis. Foot and Ankle 1982; 3:105-113. Gellman, H.; Lenihan, M.; Halikis, N.; Botte, M. J.; Giordani, M.; and Perry, J.: Selective tarsal arthrodesis: an in vitro analysis of the effect on foot motion. Foot and Ankle 1987; 8:127-133. Hall, M. C.; and Pennal, G. F.: Primary subtalar arthrodesis in the treatment of severe fractures of the calcaneum. J. Bone and Joint Surg. 1960; 42-B(2):336-343. Hintermann, B.; Nigg, B. M.; and Sommer, C.: Foot movement and tendon excursion: an in vitro study. Foot and Ankle 1994; 15:386395.

Downloaded from www.ejbjs.org on October 23, 2006

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

triple joint complex affects motion of the remaining joints is associated with the amount of motion that the joint had before the arthrodesis. The calcaneocuboid joint had the least motion before the simulated arthrodeses, and the simulated arthrodesis of this joint had the least effect on the motion of the other joints. Conversely, the talonavicular joint had the most motion before the simulated arthrodeses and the simulated arthrodesis of this joint restricted motion more than the simulated arthrodesis of any of the remaining joints did. Simulated arthrodeses that included fixation of the talonavicular joint (arthrodesis of the talonavicular joint or double arthrodesis) eliminated nearly all motion of the remaining joint or joints. After either simulated arthrodesis of the talonavicular joint or simulated double arthrodesis, the motion of the subtalar joint was limited to about 2 degrees (about 9 per cent of the motion of the subtalar joint before the simulated arthrodeses), which was the same as the motion of the subtalar joint after simulated arthrodesis of the subtalar joint. After simulated arthrodesis of the subtalar joint, 26 per cent of the motion of the talonavicular joint (about 9 degrees) remained and 56 per cent of the motion of the calcaneocuboid joint (about 7 degrees) remained. Simulated arthrodesis of the calcaneocuboid joint affected the motion of the remaining joints the least. We previously demonstrated that most of the motion of the subtalar and talonavicular joints was retained after simulated arthrodesis of the calcaneocuboid joint with a bone block (lengthening of the lateral column)(1). The mean excursion of the posterior tibial tendon before the simulated arthrodeses in the present study is consistent with that determined by Hintermann et al. In their study, the excursion of all of the extrinsic muscles of the plantigrade foot were determined in various degrees of plantar flexion and dorsiflexion with varying degrees of inversion and eversion. Those authors demonstrated that the excursion of the posterior tibial tendon was less affected by flexion of the ankle from -20 to 30 degrees (mean, 4.4 millimeters of excursion; range, 1.8 to 9.3 millimeters of excursion) than by inversion and eversion of the foot. With 0 degrees of plantar flexion, they found the mean excursion of the posterior tibial tendon to be 16.3 millimeters (range, 6.8 to 22.3 millimeters) from inversion to eversion. In the present study, the mean excursion of the posterior tibial tendon before the arthrodeses was 17 ± 5 millimeters (range, ten to twenty-seven millimeters) with the ankle fixed in neutral. As far as we know, the effect of various arthrodeses on excursion of the posterior tibial tendon has not been studied previously. In the present study, the amount of excursion remaining after a particular simulated arthrodesis was associated with the amount of motion remaining in the triple joint complex. A mean of 73 per cent of the excursion of the posterior tibial tendon was retained after simulated arthrodesis of the calcaneocuboid joint, whereas a mean of 46 per cent was retained after simulated arthrodesis of the subtalar joint. Excursion was most restricted by simulated arthrodeses that included the talonavicular

7.

8.

9.

10. 11.

Lapidus, P. W.: Subtalar joint, its anatomy and mechanics. Bull. Hosp. Joint Dis. 1955; 16:179-195. Logan, S. E.; Groszewski, P.; Krieg, J. C.; and Vannier, M.: Upper extremity kinematics assessment using four coupled six degree of freedom sensors. Biomed. Sci. Instrum. 1988; 24:75-81. Logan, S. E.; Vannier, M. W.; Bresina, S. J.; and Weeks, P. M.: Wrist kinematic analysis using a 6 degree of freedom digitizer. In Proceedings of the Seventh Annual Conference of the IEEE Engineering in Medicine and Biology Society, pp. 13-16. Piscataway, New Jersey, IEEE Service Center, 1985. Mann, R. A.; and Baumgarten, M.: Subtalar fusion for isolated subtalar disorders. Preliminary report. Clin. Orthop. 1988; 226:260-265. Polhemus Navigational Sciences Division: Personal communication, 1992. Sangeorzan, B. J.: Subtalar joint: morphology and functional anatomy. In Inman's Joints of the Ankle, edited by J. B. Stiehl. Ed. 2, p. 31. Baltimore, Williams and Wilkins, 1991. Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

6.

Downloaded from www.ejbjs.org on October 23, 2006

Fig. 2 Graph of the mean range of motion (ROM) (and standard deviation) of the subtalar joint before the simulated arthrodeses (black bars) and after simulated arthrodeses (gray bars) of the talonavicular (TN) joint, the calcaneocuboid (CC) joint, and both joints (double arthrodesis). The numbers below the bars are the number of feet included for each simulated arthrodesis.

Fig. 3 Graph of the mean range of motion (ROM) (and standard deviation) of the talonavicular joint before the simulated arthrodeses (black bars) and after simulated arthrodeses (gray bars) of the subtalar (ST) joint and the calcaneocuboid (CC) joint. The numbers below the bars are the number of feet included for each simulated arthrodesis.

Downloaded from www.ejbjs.org on October 23, 2006

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

Fig. 1 Illustration of the foot in the apparatus used to test the range of motion of the subtalar, talonavicular, and calcaneocuboid joints as well as excursion of the posterior tibial tendon.

Fig. 5 Graph of the mean excursion (and standard deviation) of the posterior tibial tendon before the simulated arthrodeses (black bars) and after simulated arthrodesis (gray bars) of the subtalar (ST) joint, triple arthrodesis, double arthrodesis, arthrodesis of the talonavicular (TN) joint, and arthrodesis of the calcaneocuboid (CC) joint. The numbers below the bars are the number of feet included for each simulated arthrodesis.

Downloaded from www.ejbjs.org on October 23, 2006

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

Fig. 4 Graph of the mean range of motion (ROM) (and standard deviation) of the calcaneocuboid joint before the simulated arthrodeses (black bars) and after simulated arthrodeses (gray bars) of the subtalar (ST) joint and the talonavicular (TN) joint. The numbers below the bars are the number of feet included for each simulated arthrodesis.

CLINCIAL PRACTICE GUIDELINE

Diagnosis and Treatment of First Metatarsophalangeal Joint Disorders. Section 1: Hallux Valgus Clinical Practice Guideline First Metatarsophalangeal Joint Disorders Panel: John V. Vanore, DPM,1 Jeffrey C. Christensen, DPM,2 Steven R. Kravitz, DPM,3 John M. Schuberth, DPM,4 James L. Thomas, DPM,5 Lowell Scott Weil, DPM,6 Howard J. Zlotoff, DPM,7 and Susan D. Couture8

T his clinical practice guideline (CPG) is based upon consensus of current clinical practice and review of the clinical literature. The guideline was developed by the Clinical Practice Guideline First Metatarsophalangeal (MTP) Joint Disorders Panel of the American College of Foot and Ankle Surgeons. The guideline and references annotate each node of the corresponding pathways. 1 Chair, Gadsden, AL; 2 Everett, WA; 3 Richboro, PA; 4 San Francisco, CA; 5 Board Liaison, Birmingham, AL; 6 Des Plaines, IL; 7 Camp Hill, PA; and 8 Park Ridge, IL. Address correspondence to: John V. Vanore, DPM, Gadsden Foot Clinic, 306 South 4th St, Gadsden, AL 35901; e-mail: [email protected] Copyright © 2003 by the American College of Foot and Ankle Surgeons 1067-2516/03/4203-0002$30.00/0 doi:10.1053/jfas.2003.50036

Diagnosis and Treatment of First MTP Joint Disorders (Pathway 1)

Pathology of the first MTP joint encompasses a variety of disorders from acquired orthopedic deformities and traumatic injuries to overuse problems and systemic disorders. These clinical problems typically involve the first MTP joint and are encountered daily by the foot and ankle surgeon. This document will review current practice guidelines for the diagnosis and treatment of: hallux valgus (Pathway 2), hallux rigidus (Pathway 3), hallux varus (Pathway 4), sesamoid disorders (Pathway 5), trauma (Pathway 6), and other disorders of the first MTP joint (Pathway 7).

PATHWAY 1

112

THE JOURNAL OF FOOT & ANKLE SURGERY

PATHWAY 2

Hallux Valgus (Pathway 2) Hallux valgus deformity is one of the most common foot problems seen today by foot and ankle specialists. Hallux valgus is a deformity at the first MTP joint with abduction and valgus rotation of the great toe combined with a medially prominent first metatarsal head. A complete spectrum of pathology and symptoms is seen with this condition. A vast array of surgical procedures has been described for the symptomatic patient. The treatment may be more challenging than one may initially expect, because the deformity may range from benign and asymptomatic to severe and disabling.

may also occur with a lesser degree of transverse plane deformity with limitation of joint movement and degenerative changes. This is referred to as hallux valgus rigidus.

Associated Findings (Node 3) Hallux valgus can present with numerous associated findings (8) that are part of a syndrome of forefoot derangement and may include: ●

Significant History (Node 1) ●

Patients presenting with this deformity often have a significant family history of bunion deformity (1,2). The deformity may be noted in adolescence, although it is more prevalent in women older than 30 years (2– 6). Symptoms may occur early or they may not manifest until later in life. Pain is generally associated with irritation at the medial subcutaneous bunion, although even significant deformities may be asymptomatic. The condition may be aggravated by short or tight footwear, particularly with regard to women’s shoe gear. Hallux valgus is considered to be a progressive condition and patients present with varied degrees of deformity from mild enlargement of the metatarsal head to severe dislocation of the first MTP joint.

●

●

●

Significant Findings (Node 2) Hallux valgus is readily apparent with clinical inspection of the patient. Significant findings may include a subcutaneous bony prominence or medial bump. The great toe is abducted or deviated laterally, often with a degree of axial or valgus rotation (7,8). Shoe irritation may result in a painful medial bursitis with inflammation surrounding the first MTP joint or neuritis of the adjacent medial dorsal cutaneous nerve (6). Patients note widening of the forefoot; this contributes to difficulty wearing shoes comfortably. First MTP joint range of motion should occur completely within the sagittal plane, but with hallux valgus, the motion may be in an oblique manner with abduction and eversion during dorsiflexion (9 –11). Adaptation occurs at the metatarsal articular surface with lateral deviation, and joint motion may become track-bound laterally (12–14). An assessment of the patient standing and limited gait analysis is undertaken. First ray hypermobility secondary to rear-foot pronation is generally considered responsible for elevation of the intermetatarsal (IM) angle (15–19) Hallux valgus 114

THE JOURNAL OF FOOT & ANKLE SURGERY

●

Hammertoe deformity of the second toe—Lateral deviation of the great toe may cause instability of the second toe and the second MTP joint. The second toe may overlap (dislocation syndrome) or under lap the hallux, or the toes may abut each other. Interdigital lesions are not uncommon. Plantar callus—Hyperkeratotic lesions may vary from a diffuse callus subsecond, -third, and -fourth metatarsal heads to a localized or nucleated lesion usually under the second metatarsal head. Formation of these lesions is believed to be caused by abnormal metatarsal pressures during gait (20,21). Central metatarsalgia—Generally, bunion formation is associated with first ray insufficiency, leading to lateral weight transfer and symptoms that may include metatarsalgia or a localized capsulitis of the second MTP joint (22–25). Pronated foot type—Pronation may be responsible for the weak foot characteristics, leading to forefoot deformities such as bunions and hammertoes (10,11). Ankle equinus—Ankle or gastrosoleus equinus is defined clinically as a limitation of ankle dorsiflexion. Ankle equinus is a detrimental force leading to pronation of the foot and development of foot deformities (26). Ingrown toenail—Ingrown toenails may occur on either nail border and are caused by the valgus and abducted position of the great toe or from abutment with the second toe (11).

Radiographic Findings (Node 4) Radiographic evaluation should include assessment of general radiographic parameters and angular relationships of the osseous segments involved in this deformity (2,5,13, 27–29). These parameters allow assessment of the severity of deformity and provide a basis for surgical procedural selection (Node 9). Radiographs should be weightbearing views of the feet and taken with the patient standing in the angle and base of gait (30). ●

Medial prominence of the first metatarsal head—The

●

●

●

with increases in the IM angle. The relationship of the tibial sesamoid to the first metatarsal bisection is determined (7,35). Axial rotation of the hallux—Valgus rotation of the great toe occurs with advanced hallux valgus deformity. This is a qualitative determination and is assessed by the symmetry of the proximal phalanx on the dorsoplantar radiograph (13). Hallux abductus interphalangeus angle—This angle is defined by the longitudinal bisections of the hallucal proximal and distal phalanges. Normal values are considered less than 10° (28). Degenerative joint disease—With long-standing or severe hallux valgus, degenerative joint disease may develop.

Initial Treatment Options (Node 5)

FIGURE 1 The HA angle is formed by the angle between the longitudinal axis of the hallux and first metatarsal; it is a reliable indicator of the severity of a bunion or a hallux valgus deformity.

●

●

●

●

●

medial prominence may be caused by the increased IM angle and/or hypertrophy of the medial epicondyle. The metatarsal head may square off or present with erosions (2,7,31). Joint space—The joint space may be normal or show narrowing with or without degenerative changes. Endstage deformities may show dislocation of the joint (13). Hallux abductus (HA) angle—This angle is defined by the longitudinal bisections of the hallucal proximal phalanx and the first metatarsal, and is measured on the dorsoplantar radiograph (Fig. 1). Values greater than 20° are often pathologic and correlate with severity of deformity (32). Proximal articular set angle—Lateral adaptation of the distal first metatarsal articular surface occurs with longstanding HA, and this can be assessed radiographically. This angular value is described by a perpendicular line drawn to the longitudinal bisection of the first metatarsal at a point intersecting a line drawn to the functional articular surface of the metatarsal head. This has also been described as the distal metatarsal articular angle. Normal values are 0° to 8°, but interobserver variability exists and the value may not correlate with intraoperative observations (29,33). IM angle—The IM angle, formed by the longitudinal bisections of the first and second metatarsals, increases with severity of deformity (Fig. 2). Abnormal values are greater than 10°. Metatarsus adductus may alter the significance of this measurement (5,34). Lateral displacement of the sesamoids—Displacement of the sesamoids occurs with hallux valgus and correlates

When symptoms begin to interfere with a patient’s lifestyle, initial treatment (eg, wider, lower-heeled shoes; bunion pads; ice; and over-the-counter analgesics) is often self-directed. Patients who are unresponsive to the initial treatment or unable to fulfill the self-directed regimen should be directed to a podiatric foot and ankle surgeon for evaluation. Nonsurgical care involves patient education, including a discussion of the natural history of the disorder, evaluation of footwear, and prior treatment. Prescription anti-inflammatory nonsteroidal drugs may be indicated for symptomatic arthralgias or bursitis. Nonsurgical alternatives include shoe modifications, with pocketing of the medial shoe contour or wider causal shoes. Although there is no scientific

FIGURE 2 The IM angle is formed by the longitudinal axis of the first and second metatarsals, respectively; this angle is also generally elevated in more severe deformities.

VOLUME 42, NUMBER 3, MAY/JUNE 2003

115

TABLE 1

Relative corrective ability of hallux valgus procedures

Surgical Procedure

Capsule tendon balance Green-Reverdin Hohmann Chevron Long arm V SCARF CAWO (intact hinge) Crescentic Proximal chevron Lapidus Keller MTP arthrodesis

IM

⫹ ⫹ ⫹⫹ ⫹⫹ ⫹⫹⫹ ⫹⫹⫹ ⫹⫹⫹⫹ ⫹⫹⫹⫹ ⫹⫹⫹ ⫹⫹⫹⫹ ⫹⫹ ⫹⫹⫹

Type of Correction Able to Be Achieved Sagittal Plane Deformity

Linear Metatarsal Deformity

E E ⫹ ⫹ ⫹ ⫹⫹ ⫹ ⫹ ⫹ ⫹⫹⫹⫹ E E

E E ⫹⫹ ⫹⫹ ⫹⫹ ⫹⫹⫹ ⫹ ⫹ ⫹ ⫹⫹⫹⫹ E ⫹⫹⫹

PASA

E ⫹⫹⫹⫹ ⫹⫹⫹⫹ ⫹⫹⫹⫹ ⫹⫹ ⫹⫹ E E E E E E

Frontal Plane Deformity

Postoperative Care

⫹a E ⫹⫹ E E E E E E ⫹ ⫹⫹a ⫹⫹⫹a

WB WB PWB WB PWB/WB WB NWB PWB/NWB PWB/NWB NWB WB PWB

NOTE. E, no corrective value/no effect; ⫹ to ⫹⫹⫹⫹, relative value scale indicative of potential to correct type of deformity. Abbreviations: CAWO, closing abductory wedge osteotomy; NWB, nonweightbearing; PASA, proximal articular set angle; PWB, partial weightbearing; WB, weightbearing. a Frontal plane correction at first MTP joint.

evidence to support the efficacy of orthotic devices in the treatment of hallux valgus, symptomatic relief may be realized by some patients (36,37). Surgical recommendations might be considered on the initial evaluation of hallux valgus deformity. Because hallux valgus is a progressive disorder and is often evaluated in the second or third stage, surgical consideration can be undertaken early in the course of treatment. Clinical Response (Nodes 6, 7, and 8) When nonsurgical care is rendered, the clinical response is assessed (Node 6). If the patient is doing well, initial treatment may be continued (Node 7). If there has been little or no improvement or if initial improvement deteriorates, surgical treatment is appropriate. If a primary care physician performed the initial evaluation and treatment, referral to a podiatric foot and ankle surgeon is indicated (Node 8). Assessment of Deformity and Arthrosis (Node 9) Hallux valgus deformity may be classified into stages 1, 2, and 3 (Nodes 10, 11, and 12). These stages are based on the progression and degree of deformity of HA and the IM angle. In each stage, surgical intervention includes a capsuletendon balancing procedure (which may include medial exostectomy), a lateral release, and a medial capsulorrhaphy. 116

THE JOURNAL OF FOOT & ANKLE SURGERY

Surgical Treatment: Stage 1 (Node 10) Stage 1 hallux valgus deformity is defined as an IM angle ⬍12° and an HA angle ⬍25°. Although the appearance of the deformity may not be significant, there is often deviation of the joint and medial enlargement of the first metatarsal head. Typically, soft tissue tendon balance (38 – 45) and exostectomy with/without a distal osteotomy are performed to correct the deformity (46 –77). If hallux abductus interphalangeus is present, a phalangeal osteotomy may be indicated (28,78 –91) (Table 1; Figs. 3 and 4). Surgical Treatment: Stage 2 (Node 11) Stage 2 deformities are more significant and have an IM angle ⱕ16° with an HA angle of ⱖ25°. The joint congruency must be evaluated. Capsule-tendon balancing is performed with or without osteotomy of the first metatarsal and/or proximal phalanx (92–99). When hypermobility of the first ray is encountered or is in the presence of severe deformity, a metatarsal cuneiform arthrodesis may be considered (17,25,34,100 –106). If hallux abductus interphalangeus is present, a phalangeal osteotomy may be indicated (Table 1; Figs. 5 and 6). Surgical Treatment: Stage 3 (Node 12) Stage 3 deformities are considered severe and generally more disabling. These deformities have an IM angle that is

FIGURE 3 Distal metatarsal osteotomy is a common procedural alternative and may be performed with a variety of techniques including the Austin or chevron osteotomy. (A) Preoperative anteroposterior (AP) radiograph, (B) postoperative radiograph.

FIGURE 4 Phalangeal osteotomy has been performed as variations of the Akin osteotomy. (A) Preoperative and (B) postoperative oblique Akin with Kirschner wire fixation.

VOLUME 42, NUMBER 3, MAY/JUNE 2003

117

FIGURE 5 Proximal first metatarsal osteotomy is selected for cases of significant elevation of the first intermetarsal angle. (A) Preoperative AP radiograph and (B) postoperative AP radiograph.

FIGURE 6 The Lapidus or first metatarsal cuneiform joint fusion is useful in cases of hallux valgus with large IM angles or first ray hypermobility. (A) Preoperative AP radiograph and (B) postoperative AP radiograph.

118

THE JOURNAL OF FOOT & ANKLE SURGERY

FIGURE 7 The Keller bunionectomy with resection of the proximal phalangeal base still is a useful procedure for hallux valgus deformities. (A) Preoperative and (B) postoperative AP views.

FIGURE 8 First MTP joint fusion is not only a useful salvage technique for recurrent (A) preoperative, (B) postoperative, or arthritic deformities but also useful as a primary procedure for the correction of hallux valgus.

VOLUME 42, NUMBER 3, MAY/JUNE 2003

119

FIGURE 9 Reconstruction of the rheumatoid forefoot may be described as a forefoot arthroplasty combining (A) resection arthroplasty (Keller), (B) first MTP joint implant, or (C) first MTP joint fusion with lesser metatarsal procedures.

usually ⬎16° and an HA angle ⱖ35°. The MTP joint may be deviated or subluxed. Severe deformities often present with associated findings (Node 3) in addition to hallux valgus. Deformities in this stage may be corrected through capsule-tendon balancing with an osteotomy of the first metatarsal and/or proximal phalanx. Double osteotomy of the first metatarsal provides an additional option (56,107–113). Determination of location of the osteotomy is influenced by the degree of deformity and/or the presence of associated degenerative arthritis. Metatarsal cuneiform arthrodesis may also be considered. If hallux abductus interphalangeus is present, a phalangeal osteotomy may be indicated. In certain situations, first MTP joint resection arthroplasty (114 –120), with or without a joint implant (121–132), or arthrodesis (133–139) may be performed, as in the case of patients with rheumatoid arthritis or degenerative joint disease or in patients requiring revision surgery (123–125,140 –157) (Table 1; Figs. 7–9). In summary, hallux valgus deformity is an inherited, progressive deformity often associated with certain foot types, with symptoms aggravated by shoe wear. Although conservative measures may be used initially to reduce the symptomatology associated with this deformity, surgical repair is often necessary to correct the hallux valgus and its associated deformities. 120

THE JOURNAL OF FOOT & ANKLE SURGERY

References 1. Coughlin MJ, Roger A. Mann Award. Juvenile hallux valgus: etiology and treatment. Foot Ankle Int 16:682– 697, 1995. 2. Hardy R, Clapham JCR. Observations on hallux valgus. J Bone Joint Surg 33B:376 –391, 1951. 3. Gould N, Schneider W, Ashikaga T. Epidemiological survey of foot problems in the continental United States: 1978-1979. Foot Ankle 1:8 –10, 1980. 4. Kilmartin TE, Barrington RL, Wallace WA. Metatarsus primus varus. A statistical study. J Bone Joint Surg 73B:937–940, 1991. 5. Piggott H. The natural history of hallux valgus in adolescence and early adult life. J Bone Joint Surg 42B:749 –760, 1960. 6. Rosen JS, Grady JF. Neuritic bunion syndrome. J Am Podiatr Med Assoc 76:641– 644, 1986. 7. Haines RW, McDougall A. The anatomy of hallux valgus. J Bone Joint Surg 36B:272–293, 1954. 8. Kelikian H. Hallux Valgus, Allied Deformities of the Forefoot and Metatarsalgia. WB Saunders, Philadelphia, 1965. 9. Eustace S, Byrne JO, Beausang O, Codd M, Stack J, Stephens MM. Hallux valgus, first metatarsal pronation and collapse of the medial longitudinal arch—a radiological correlation. Skeletal Radiol 23: 191–194, 1994. 10. Shaw AH. The biomechanics of hallux valgus in pronated feet. J Am Podiatry Assoc 64:193–201, 1974. 11. Root ML, Orien WP, Weed H. Forefoot deformity caused by abnormal subtalar joint pronation. In Normal and Abnormal Function of the Foot, pp 349 – 462, Clinical Biomechanics, Los Angeles, 1977. 12. Coughlin MJ. Hallux valgus in men: effect of the distal metatarsal articular angle on hallux valgus correction. Foot Ankle Int 18:463– 470, 1997.

13. Laporta G, Melillo T, Olinsky D. X-ray evaluation of hallux abducto valgus deformity. J Am Podiatry Assoc 64:544 –566, 1974. 14. Evans RD, Lile LN. Proximal articular set angle. Radiographic versus intraoperative measurement. J Am Podiatr Med Assoc 90:199 –202, 2000. 15. Prieskorn DW, Mann RA, Fritz G. Radiographic assessment of the second metatarsal: measure of first ray hypermobility. Foot Ankle Int 17:331–333, 1996. 16. Rush SM, Christensen JC, Johnson CH. Biomechanics of the first ray. Part II: metatarsus primus varus as a cause of hypermobility. A three-dimensional kinematic analysis in a cadaver model. J Foot Ankle Surg 39:68 –77, 2000. 17. Faber FW, Kleinrensink GJ, Verhoog MW, Vijn AH, Snijders CJ, Mulder PG, Verhaar JA. Mobility of the first tarsometatarsal joint in relation to hallux valgus deformity: anatomical and biomechanical aspects. Foot Ankle Int 20:651– 656, 1999. 18. Carl A, Ross S, Evanski P, Waugh T. Hypermobility in hallux valgus. Foot Ankle 8:264 –270, 1988. 19. Inman VT. Hallux valgus: a review of etiologic factors. Orthop Clin North Am 5:59 – 66, 1974. 20. Gibbs RC, Boxer MC. Abnormal biomechanics of feet and their cause of hyperkeratoses. J Am Acad Dermatol 6:1061–1069, 1982. 21. Eulry F. Static metatarsalgia. Rev Prat 47:37– 42, 1997. 22. Viladot A. Metatarsalgia due to biomechanical alterations of the forefoot. Orthop Clin North Am 4:165–178, 1973. 23. Roy KJ. Force, pressure, and motion measurements in the foot: current concepts. Clin Podiatr Med Surg 5:491–508, 1988. 24. Raymakers R, Waugh W. The treatment of metatarsalgia with hallux valgus. J Bone Joint Surg 53B:684 – 687, 1971. 25. Hansen ST. Hallux valgus surgery. Morton and Lapidus were right! Clin Podiatr Med Surg 13:347–354, 1996. 26. Yu GV, Johng B, Freireich R. Surgical management of metatarsus adductus deformity. Clin Podiatr Med Surg 4:207–232, 1987. 27. Palladino SJ. Preoperative evaluation of the bunion patient: etiology, biomechanics, clinical and radiographic assessment. In Textbook of Bunion Surgery, pp 1– 87, edited by J Gerbert, Futura Publishing, Mount Kisco, NY, 1991. 28. Sorto LA, Balding MG, Weil LS, Smith SD. Hallux abductus interphalangeus: etiology, x-ray evaluation and treatment. J Am Podiatry Assoc 66:384 –396, 1976. 29. Whitney AK. Radiographic Charting Tecnhique, PCPM Press, Philadelphia, 1978. 30. Spinner SM, Lipsman S, Spector F. Radiographic criteria in the assessment of hallux abductus deformities. J Foot Surg 23:25–30, 1984. 31. Mann RA, Coughlin MJ. Hallux valgus— etiology, anatomy, treatment and surgical considerations. Clin Orthop 157:31– 41, 1981. 32. Root ML, Orien WP, Weed JH. Motion of the joints of the foot. In Normal and Abnormal Function of the Foot, pp 1– 63, edited by Orien WP, Root ML, Weed JH, Clinical Biomechanics, Los Angeles, 1977. 33. Amarnek DL, Mollica A, Jacobs AM, Oloff LM. A statistical analysis on the reliability of the proximal articular set angle. J Foot Surg 25:39 – 43, 1986. 34. Lapidus PW. Operative correction of the metatarsus varus primus in hallux valgus. Surg Gynecol Obstet 58:183–191, 1934. 35. Judge MS, LaPointe S, Yu GV, Shook JE, Taylor RP. The effect of hallux abducto valgus surgery on the sesamoid apparatus position. J Am Podiatr Med Assoc 89:551–559, 1999. 36. Kilmartin TE, Barrington RL, Wallace WA. A controlled prospective trial of a foot orthosis for juvenile hallux valgus. J Bone Joint Surg 76B:210 –214, 1994. 37. Moraros J, Hodge W. Orthotic survey. Preliminary results. J Am Podiatr Med Assoc 83:139 –148, 1993.

38. McBride ED. The conservative operation for “bunions.” End results and refinements of technique. J Am Med Assoc 105:1164 –1168., 1935. 39. McBride ED. The McBride bunion hallux valgus operation. J Bone Joint Surg 49A:1675–1683, 1967. 40. McGlamry ED, Feldman MH. A treatise on the McBride procedure. A review of the McBride publications on hallus valgus correction with observations on rationale of the original procedure and the current modifications. J Am Podiatry Assoc 61:161–173, 1971. 41. Pfeffinger LL. The modified McBride procedure. Orthopedics 13: 979 –984, 1990. 42. Lawton J, Evans R. Modified McBride bunionectomy. J Am Podiatry Assoc 65:670 – 688, 1975. 43. Kempe SA, Singer RH. The modified McBride bunionectomy utilizing the adductor tendon transfer. J Foot Surg 24:24 –29, 1985. 44. Schwitalle M, Karbowski A, Eckardt A. Hallux valgus in young patients: comparison of soft-tissue realignment and metatarsal osteotomy. Eur J Pediatr Surg 8:42– 46, 1998. 45. Mann RA, Pfeffinger L. Hallux valgus repair. DuVries modified McBride procedure. Clin Orthop 272:213–218, 1991 46. Shapiro F, Heller L. The Mitchell distal metatarsal osteotomy in the treatment of hallux valgus. Clin Orthop 107:225–231, 1975. 47. Dovey H. The treatment of hallux valgus by distal osteotomy of the first metatarsal. Acta Orthop Scand 40:402– 408, 1969. 48. Funk FJ, Wells RE. Bunionectomy—with distal osteotomy. Clin Orthop 85:71–74, 1972. 49. Grill F, Hetherington V, Steinbock G, Altenhuber J. Experiences with the chevron (V-)osteotomy on adolescent hallux valgus. Arch Orthop Trauma Surg 106:47–51, 1986. 50. Hyytinen T, Lantto E, Kallio P, Salo S, Kaukonen JP. Modified distal metatarsal osteotomy for hallux valgus. Ann Chir Gynaecol 84:81– 84, 1995. 51. Johnson JB, Smith SD. Preliminary report on derotational, angulational, transpositional osteotomy: a new approach to hallux abducto valgus surgery. J Am Podiatry Assoc 64:667– 675, 1974. 52. Auerbach AM. Review of distal metatarsal osteotomies for hallux valgus in the young. Clin Orthop 70:148 –151, 1970. 53. Austin DW, Leventen EO. A new osteotomy for hallux valgus: a horizontally directed “V” displacement osteotomy of the metatarsal head for hallux valgus and primus varus. Clin Orthop 157:25–30, 1981. 54. Chou LB, Mann RA, Casillas MM. Biplanar chevron osteotomy. Foot Ankle Int 19:579 –584, 1998. 55. Christensen PH, Hansen TB. Hallux valgus correction using a modified Hohmann technique. Foot Ankle Int 16:177–180, 1995. 56. Coughlin MJ, Carlson RE. Treatment of hallux valgus with an increased distal metatarsal articular angle: evaluation of double and triple first ray osteotomies. Foot Ankle Int 20:762–770, 1999. 57. Mitchell CL, Fleming JL, Allen R, Glenney C, Sanford, GA. Osteotomy-bunionectomy for hallux valgus. J Bone Joint Surg 40A:41– 60, 1958. 58. Peabody CW. Surgical cure of hallux valgus. J Bone Joint Surg 13:273–282, 1931. 59. Warrick JP, Edelman R. The Hohmann bunionectomy utilizing A-O screw fixation: a preliminary report. J Foot Surg 23:268 –274, 1984. 60. Wilson JN. Oblique displacement osteotomy for hallux valgus. J Bone Joint Surg 45B:552–555, 1963. 61. Laird PO, Silvers SH, Somdahl J. Two Reverdin-Laird osteotomy modifications for correction of hallux abducto valgus. J Am Podiatr Med Assoc 78:403– 405, 1988. 62. Beck EL. Modified Reverdin technique for hallux abducto valgus (with increased proximal articular set angle of the first metatarsophalangeal joint). J Am Podiatry Assoc 64:657– 666, 1974. 63. Kalish SR, Spector JE. The Kalish osteotomy. A review and retro-

VOLUME 42, NUMBER 3, MAY/JUNE 2003

121

64. 65. 66. 67.

68. 69. 70.

71.

72.

73. 74. 75.

76.

77.

78. 79. 80. 81. 82. 83. 84. 85.

86. 87. 88.

89. 90.

122

spective analysis of 265 cases. J Am Podiatr Med Assoc 84:237–242, 1994. Barker AE. An operation for hallux valgus. Lancet 1:655, 1884. Hohmann G. Der hallux valgus und die uebrigen Zehenverkruemmungen. Ergeb Chir Orthop 18:308 –348, 1925. Hohmann G. Fuss und Bein, pp 145–192, JF Bergmann, Munich, 1951. Pollack RA, Bellacosa RA, Higgins KR, Sharp BE, McCloskey TF. Critical evaluation of the short “Z” bunionectomy. J Foot Surg 28:158 –161, 1989. Quinn MR, DiStazio JJ, Kruljac SJ. Herbert bone screw fixation of the Austin bunionectomy. J Foot Surg 26:516 –519, 1987. Reverdin J. Anatomie et ope´ ration de l’hallux valgus. Internat Med Congr 2:408 – 412, 1881. Reverdin J. De la de´ viation en dehors du gros orteil (hallux valgus, vulg. “oignon,” “bunions,” “Ballen”) et de son traitement chirurgical. Tr Internat Med Congr 2:408 – 412, 1881. Bass SJ, Gastwirth CM, Green R, Weinstock RE. A modification of the Austin bunionectomy. (The tongue and groove osteotomy bunionectomy). J Am Podiatry Assoc 69:608 – 615, 1979. Boc SF, D’Angelantonio A, Grant S. The triplane Austin bunionectomy: a review and retrospective analysis. J Foot Surg 30:375–382, 1991. Wu KK. Modified Mitchell’s bunionectomy (Wu’s bunionectomy). Orthopedics 20:253–257, 1997. Keogh P, Jaishanker JS, O’Connell RJ, White M. The modified Wilson osteotomy for hallux valgus. Clin Orthop 255:263–267, 1990. Winston L, Wilson RC. A modification of the Hohmann procedure for surgical correction of hallux abducto valgus. J Am Podiatry Assoc 72:11–14, 1982. Vega MR, Jackson-Smith JL. A variable first metatarsal distal “L” osteotomy with adductor tendon transfer. J Foot Ankle Surg 34:384 – 388, 1995. Miller S, Croce WA. The Austin procedure for surgical correction of hallux abducto valgus deformity. J Am Podiatry Assoc 69:110 –118, 1979. Barouk LS. Osteotomies of the great toe. J Foot Surg 31:388 –399, 1992. Boberg JS, Menn JJ, Brown WL. The distal akin osteotomy: a new approach. J Foot Surg 30:431436, 1991. Bordelon RL. Technique and use of Akin osteotomy. Contemp Orthop 23:38 – 41, 1991. Frey C, Jahss M, Kummer FJ. The Akin procedure: an analysis of results. Foot Ankle 12:1– 6, 1991. Donahue WE. The proximal phalangeal osteotomy. A technically advanced approach. Clin Podiatry 2:449 – 455, 1985. Gerbert J, Melillo T. A modified Akin procedure for the correction of hallux valgus. J Am Podiatry Assoc 61:132–136, 1971. Gohil P, Cavolo DJ. A simplified preoperative evaluation for Akin osteotomy. J Am Podiatry Assoc 72:44 – 45, 1982. Green AH, Bosta SD. Akin osteotomy of the hallux proximal phalanx utilizing Richards mini staple fixation. J Foot Surg 25:386 –389, 1986. Kinnard P, Cantin S. The Akin procedure in hallux valgus. Can J Surg 34:491– 493, 1991. Levitsky DR. Percutaneous osteoclasp fixation of Akin osteotomy: an alternative fixation technique. J Foot Surg 20:163–166, 1981. Levitsky DR, DiGilio J, Kander R, Rubin B. Rigid compression screw fixation of first proximal phalanx osteotomy for hallux abducto valgus. J Foot Surg 21:65– 69, 1982. Schwartz NH, Iannuzzi PJ, Thurber NB. Derotational akin osteotomy. J Foot Surg 25:479 – 483, 1986. Akin OF. The treatment of hallux valgus—an operative procedure and its results. Med Sentinel 33:678 – 679, 1925.

THE JOURNAL OF FOOT & ANKLE SURGERY

91. Meyer HR, Muller G. Regnauld procedure for hallux valgus. Foot Ankle 10:299 –302, 1990. 92. Lynch FR. Applications of the opening wedge cuneiform osteotomy in the surgical repair of juvenile hallux abducto valgus. J Foot Ankle Surg 34:103–123, 1995. 93. Ludloff K. Die besetigung des hallux valgus durch die schraege planto-dorsale osteotomie des metatarus 1. Arch Klin Chir 110:364 – 387, 1918. 94. Weil LS. Scarf osteotomy for correction of hallux valgus. Historical perspective, surgical technique, and results. Foot Ankle Clin 5:559 – 580, 2000. 95. Gudas CJ. Compression screw fixation in proximal first metatarsal osteotomies for metatarsus primus varus: initial observations. J Foot Surg 18:10 –15, 1979. 96. Schuberth JM, Reilly CH, Gudas CJ. The closing wedge osteotomy: a critical analysis of first metatarsal elevation. J Am Podiatry Assoc 74:13–24, 1984. 97. Mau C, Lauber HT. Die operative Behalung des hallux valgus (Nachuntersuchungen). Dtsch Ztschr Chir 197:361–377, 1926. 98. Amarnek DL, Juda EJ, Oloff LM, Jacobs AM. Opening base wedge osteotomy of the first metatarsal utilizing rigid external fixation. J Foot Surg 25:321–326, 1986. 99. Zettl R, Trnka HJ, Easley M, Salzer M, Ritschl, P. Moderate to severe hallux valgus deformity: correction with proximal crescentic osteotomy and distal soft-tissue release. Arch Orthop Trauma Surg 120: 397– 402, 2000. 100. Lapidus PW. Dorsal bunion: its mechanics and operative correction. J Bone Joint Surg 22:627– 637, 1940. 101. Lapidus PW. The author’s bunion operation from 1931 to 1959. Clin Orthop 16:119 –135, 1960. 102. Rutherford RL. The Lapidus procedure for primus metatarsus adductus. J Am Podiatry Assoc 64:581–584, 1974. 103. Catanzariti AR, Mendicino RW, Lee MS, Gallina MR. The modified Lapidus arthrodesis: a retrospective analysis. J Foot Ankle Surg 38:322–332, 1999. 104. Frankel JP. The misuse of the Lapidus procedure. J Foot Ankle Surg 36:71–72, 1997. 105. Grace D, Delmonte R, Catanzariti AR, Hofbauer M. Modified Lapidus arthrodesis for adolescent hallux abducto valgus. J Foot Ankle Surg 38:8 –13, 1999. 106. Sangeorzan BJ, Hansen ST. Modified Lapidus procedure for hallux valgus. Foot Ankle 9:262–266, 1989. 107. Lidge RT. Hallux valgus—surgical correction by three-in-one technique. In Foot Science, pp 188 –210, edited by JE Bateman, WB Saunders, Philadephia, 1976. 108. Evins RJ. Alternate method of reducing metatarsus primus adductus angle. J Foot Surg 16:9 –11, 1977. 109. Mitchell LA, Baxter DE. A Chevron-Akin double osteotomy for correction of hallux valgus. Foot Ankle 12:7–14, 1991. 110. Osterwalder A, Maestretti G. Metatarsus primus double osteotomy, a logical and non-disabling surgical technique for treatment of hallux valgus. Helv Chir Acta 60:245–248, 1993. 111. Peterson HA, Newman SR. Adolescent bunion deformity treated with double osteotomy and longitudinal pin fixation of the first ray. J Pediatr Orthop 13:80 – 84, 1993. 112. Tollison ME, Baxter DE. Combination chevron plus Akin osteotomy for hallux valgus: should age be a limiting factor? Foot Ankle Int 18:477– 481, 1997. 113. Wattling WO, Cox KL. Double osteotomies for structural correction of hallux abducto valgus. J Foot Surg 15:61– 64, 1976. 114. Ganley JV, Lynch FR, Darrigan RD. Keller bunionectomy with fascia and tendon graft. J Am Podiatr Med Assoc 76:602– 610, 1986. 115. McGlamry ED, Kitting RW, Butlin WE. Keller bunionectomy and

116. 117. 118.

119. 120. 121.

122.

123.

124.

125. 126. 127.

128. 129.

130.

131. 132. 133.

134.

135. 136. 137.

hallux valgus correction. An appraisal and current modifications sixty-six years later. J Am Podiatry Assoc 60:161–167, 1970. Keller WL. Further observations of the surgical treatment of hallux valgus and bunions. N Y Med J 95:696 – 698, 1912. Keller WL. The surgical treatment of bunions and hallux valgus. N Y Med J 80:741–742, 1904. Rix RR. Modified Mayo operation for hallux valgus and bunion—a comparison with the Keller procedure. J Bone Joint Surg 50A:1368 – 1378, 1968. Vitek M, Steinbock G. Value of cerclage fibreux for the KellerBrandes procedure. Arch Orthop Trauma Surg 108:104 –106, 1989. Cosentino GL. The Cosentino modification for tendon interpositional arthroplasty. J Foot Ankle Surg 34:501–508, 1995. LaPorta GA, Pilla P, Richter KP. Keller implant procedure: a report of 536 procedures using a Silastic intramedullary stemmed implant. J Am Podiatry Assoc 66:126 –147, 1976. Kalish SR, McGlamry ED. The modified Keller hallux valgus repair utilizing Silastic implants with some comments on implants in general. J Am Podiatry Assoc 64:761–773, 1974. Cracchiolo A, Weltmer JB, Lian G, Dalseth T, Dorey F. Arthroplasty of the first metatarsophalangeal joint with a double-stem silicone implant. Results in patients who have degenerative joint disease failure of previous operations, or rheumatoid arthritis. J Bone Joint Surg 74A:552–563, 1992. Vanore JV. Implants. In McGlamry’s Comprehensive Textbook of Foot and Ankle Surgery, pp 373– 417, edited by SJ Miller, Lippincott, Williams & Wilkins, Philadelphia, 2001. Vanore J, O’Keefe RG, Pikscher I. Current status of first metatarsophalangeal joint implants. Foot Ankle Q 8:121–134, 1995. Swanson AB. Implant arthroplasty for the great toe. Clin Orthop 85:75– 81, 1972. Swanson AB. Implant arthroplasty in disabilities of the great toe. In The American Academy of Orthopaedic Surgeons Instructional Course Lectures, CV Mosby, St Louis, 1972. Albin RL, Weil LS. Flexible implant arthroplasty of the great toe: an evaluation. J Am Podiatry Assoc 64:967–975, 1974. Arenson DJ. The angled great toe implant (Swanson design/Weil modification) in the surgical reconstruction of the first metatarsophalangeal joint. Clin Podiatry 1:89 –102, 1984. Weil LS, Pollak RA, Goller WL. Total first joint replacement in hallux valgus and hallux rigidus. Long-term results in 484 cases. Clin Podiatry 1:103–129, 1984. Vanore JV, Lawrence BR, Weil LS, Zang K. First MPJ implant symposium. Foot Ankle Q 8:1995, 1995. Zlotoff H. Swanson flexible hinge toe implant. A preliminary report. J Am Podiatry Assoc 73:347–355, 1983. McKeever DC. Arthrodesis of the first metatarsophalangeal joint for hallux valgus, hallux rigidus and metatarsus primus varus. J Bone Joint Surg 34A:129 –134, 1952. Harrison MHM, Harvey FJ. Arthrodesis of the first metatarsophalangeal joint for hallux valgus and rigidus. J Bone Joint Surg 45A: 471480, 1963. Bourdillon JF. Metatarsophalangeal fusion for hallux valgus. Can Med Assoc J 121:1351, 1979. von Salis-Soglio G, Thomas W. Arthrodesis of the metatarsophalangeal joint of the great toe. Arch Orthop Trauma Surg 95:7–12, 1979. Vanore JV. First metatarsophalangeal joint arthrodesis. In Musculo-

138. 139. 140.

141. 142.

143. 144. 145.

146. 147.

148.

149.

150.

151.

152.

153.

154.

155. 156.

157.

skeletal Disorders of the Lower Extremities, pp 545–558, edited by LM Oloff, WB Saunders, Philadelphia, 1994. Kampner SL. Total joint replacement in bunion surgery. Orthopedics 1:275–284, 1978. Kampner SL. Total joint prosthetic arthroplasty of the great toe: a 12-year experience. Foot Ankle 4:249 –261, 1984. Andre S, Champetier de Ribes B, Sauzieres P, Tomeno B. Swanson silastic implant arthroplasty in pathology of the metatarsophalangeal joint of the great toe. Rev Chir Orthop Reparatrice Appar Mot 71:95–100, 1985. Baskwill D, Kanat IO. Surgical considerations in hallux abducto valgus with rheumatoid arthritis. J Foot Surg 26:429 – 433, 1987. Beauchamp CG, Kirby T, Rudge SR, Worthington BS, Nelson, J. Fusion of the first metatarsophalangeal joint in forefoot arthroplasty. Clin Orthop 190:249 –253, 1984. Benson GM, Johnson EW. Management of the foot in rheumatoid arthritis. Orthop Clin North Am 2:733–744, 1971. Brattstrom H, Brattstrom M. Resection of the metatarsophalangeal joints in rheumatoid arthritis. Acta Orthop Scand 41:213–224, 1970. Budiman-Mak E, Roach KE, Stuck R, Spencer F, Polizos T, Conrad KJ. Radiographic measurement of hallux valgus in the rheumatoid arthritic foot. J Rheumatol 21:623– 626, 1994. Clayton ML. Surgery in the forefoot in rheumatoid arthritis. Clin Orthop 16:136 –140, 1960. Cracchiolo A, Swanson A, Swanson GD. The arthritic great toe metatarsophalangeal joint: a review of flexible silicone implant arthroplasty from two medical centers. Clin Orthop 157:64 – 69, 1981. Groulier P, Curvale G, Piclet-Legre B, Kelberine F. Arthrodesis of the first metatarsophalangeal joint. Rev Chir Orthop Reparatrice Appar Mot 80:436 – 444, 1994. Laird L. Silastic joint arthroplasty of the great toe. A review of 228 implants using the double-stemmed implant. Clin Orthop 255:268 – 272, 1990. Mann RA, Thompson FM. Arthrodesis of the first metatarsophalangeal joint for hallux valgus in rheumatoid arthritis. J Bone Joint Surg 66:687– 692, 1984. Mann RA, Thompson FM. Arthrodesis of the first metatarsophalangeal joint for hallux valgus in rheumatoid arthritis. 1984. Foot Ankle Int 18:65– 67, 1997. Moeckel BH, Sculco TP, Alexiades MM, Dossick PH, Inglis AE, Ranawat CS. The double-stemmed silicone-rubber implant for rheumatoid arthritis of the first metatarsophalangeal joint. J Bone Joint Surg 74A:564 –570, 1992. Pfeiffer WH, Cracchiolo A, Grace DL, Dorey FJ, Van Dyke E. Double-stem silicone implant arthroplasty of all metatarsophalangeal joints in patients with rheumatoid arthritis. Semin Arthroplasty 3:16 – 24, 1992. Swanson AB, Lumsden RM, Swanson GD. Silicone implant arthroplasty of the great toe. A review of single stem and flexible hinge implants. Clin Orthop 142:30 – 43, 1979. Trnka HJ. Arthrodesis procedures for salvage of the hallux metatarsophalangeal joint. Foot Ankle Clin 5:673– 686, 2000. Vanore JV, Pikscher I. Forefoot arthroplasty. In Musculoskeletal Disorders of the Lower Extremities, pp 496 –515, edited by LM Oloff, WB Saunders, Philadelphia, 1994. Merkle PF, Sculco TP. Prosthetic replacement of the first metatarsophalangeal joint. Foot Ankle 9:267–271, 1989.

VOLUME 42, NUMBER 3, MAY/JUNE 2003

123

This is an enhanced PDF from The Journal of Bone and Joint Surgery The PDF of the article you requested follows this cover page.

Hallux Rigidus. Grading and Long-Term Results of Operative Treatment Michael J. Coughlin and Paul S. Shurnas J Bone Joint Surg Am. 2003;85:2072-2088.

This information is current as of September 5, 2008 Letters to The Editor are available at http://www.ejbjs.org/cgi/content/full/85/11/2072#responses Reprints and Permissions

Click here to order reprints or request permission to use material from this article, or locate the article citation on jbjs.org and click on the [Reprints and Permissions] link.

Publisher Information

The Journal of Bone and Joint Surgery 20 Pickering Street, Needham, MA 02492-3157 www.jbjs.org

 COPYRIGHT © 2003

BY

THE JOURNAL

OF

BONE

AND JOINT

SURGERY, INCORPORATED

Hallux Rigidus GRADING

AND

LONG-TERM RESULTS

OF

OPERATIVE TREATMENT

BY MICHAEL J. COUGHLIN, MD, AND PAUL S. SHURNAS, MD Investigation performed at St. Alphonsus Regional Medical Center, Boise, Idaho

Background: There have been few long-term studies documenting the outcome of surgical treatment of hallux rigidus. The purposes of this report were to evaluate the long-term results of the operative treatment of hallux rigidus over a nineteen-year period in one surgeon’s practice and to assess a clinical grading system for use in the treatment of hallux rigidus. Methods: All patients in whom degenerative hallux rigidus had been treated with cheilectomy or metatarsophalangeal joint arthrodesis between 1981 and 1999 and who were alive at the time of this review were identified and invited to return for a follow-up evaluation. At this follow-up evaluation, the hallux rigidus was graded with a new fivegrade clinical and radiographic system. Outcomes were assessed by comparison of preoperative and postoperative pain and AOFAS (American Orthopaedic Foot and Ankle Society) scores and ranges of motion. These outcomes were then correlated with the preoperative grade and the radiographic appearance at the time of follow-up. Results: One hundred and ten of 114 patients with a diagnosis of hallux rigidus returned for the final evaluation. Eighty patients (ninety-three feet) had undergone a cheilectomy, and thirty patients (thirty-four feet) had had an arthrodesis. The mean duration of follow-up was 9.6 years after the cheilectomies and 6.7 years after the arthrodeses. There was significant improvement in dorsiflexion and total motion following the cheilectomies (p = 0.0001) and significant improvement in postoperative pain and AOFAS scores in both treatment groups (p = 0.0001). A good or excellent outcome based on patient self-assessment, the pain score, and the AOFAS score did not correlate with the radiographic appearance of the joint at the time of final follow-up. Dorsiflexion stress radiographs demonstrated correction of the elevation of the first ray to nearly zero. There was no association between hallux rigidus and hypermobility of the first ray, functional hallux limitus, or metatarsus primus elevatus.

Conclusions: Ninety-seven percent (107) of the 110 patients had a good or excellent subjective result, and 92% (eighty-six) of the ninety-three cheilectomy procedures were successful in terms of pain relief and function. Cheilectomy was used with predictable success to treat Grade-1 and 2 and selected Grade-3 cases. Patients with Grade-4 hallux rigidus or Grade-3 hallux rigidus with <50% of the metatarsal head cartilage remaining at the time of surgery should be treated with arthrodesis. Level of Evidence: Therapeutic study, Level IV (case series [no, or historical, control group]). See Instructions to Authors for a complete description of levels of evidence.

H

allux rigidus is a term used to describe symptoms commonly associated with degenerative arthritis of the first metatarsophalangeal joint. Surgical treatment of protracted symptomatic hallux rigidus includes cheilectomy1-13, excisional arthroplasty14-20, interposition arthroplasty13,21-25, phalangeal osteotomy26-30, first metatarsal osteotomy16,31-40, implant arthroplasty16,41-47, and arthrodesis14,48-68. Cheilectomy has been recommended in a number of reports1-4,6-8,11-13,69; however, in many of the studies, the duration of follow-up was less than one year2,3,12,69 or some or all of the patients were not examined at the time of final follow-up12,69. In some studies, a substantial number of patients were lost to final follow-up11,13; in others, cheilectomy was combined with phalangeal osteotomy13,27,29, metatarsal osteotomy34 , or inter-

position arthroplasty23. Some authors reported a technique consisting solely of the removal of the osteophytes in line with the dorsal metatarsal cortex2,6,8-10,12,16,21,23,27,29,48, and several of them recommended cheilectomy as a treatment for early disease only2,6,8,12. Although Nilsonne21 and Bonney and Macnab70 found cheilectomy to be unsuccessful, others have reported successful results with cheilectomy for all levels of disease3,7,11 and have recommended a more aggressive resection of the metatarsal head. Radiographic signs of deterioration of the metatarsophalangeal joint over time have been reported after cheilectomy1,4,7,8, but continued good clinical function despite the worsening radiographic appearance has been noted in these studies. Arthrodesis of the first metatarsophalangeal joint has

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

HAL LUX RIG IDUS

TABLE I Clinical-Radiographic System for Grading Hallux Rigidus Grade

Dorsiflexion

Radiographic Findings*

Clinical Findings

0

40° to 60° and/or 10% to 20% loss compared with normal side

Normal

No pain; only stiffness and loss of motion on examination

1

30° to 40° and/or 20% to 50% loss compared with normal side

Dorsal osteophyte is main finding, minimal joint-space narrowing, minimal periarticular sclerosis, minimal flattening of metatarsal head

Mild or occasional pain and stiffness, pain at extremes of dorsiflexion and/or plantar flexion on examination

2

10° to 30° and/or 50% to 75% loss compared with normal side

Dorsal, lateral, and possibly medial osteophytes giving flattened appearance to metatarsal head, no more than 1/4 of dorsal joint space involved on lateral radiograph, mild-to-moderate joint-space narrowing and sclerosis, sesamoids not usually involved

Moderate-to-severe pain and stiffness that may be constant; pain occurs just before maximum dorsiflexion and maximum plantar flexion on examination

3

≤10° and/or 75% to 100% loss compared with normal side. There is notable loss of metatarsophalangeal plantar flexion as well (often ≤10° of plantar flexion)

Same as in Grade 2 but with substantial narrowing, possibly periarticular cystic changes, more than 1/4 of dorsal joint space involved on lateral radiograph, sesamoids enlarged and/or cystic and/or irregular

Nearly constant pain and substantial stiffness at extremes of range of motion but not at mid-range

4

Same as in Grade 3

Same as in Grade 3

Same criteria as Grade 3 BUT there is definite pain at mid-range of passive motion

*Weight-bearing and anteroposterior and lateral radiographs are used.

been evaluated as a treatment for hallux rigidus by several authors48-68. However, in many series, the duration of followup was less than one year50,51,55-57, multiple surgeons were involved52,56,61, or more than one technique was performed53,56. Some studies included patients with other diagnoses such as rheumatoid arthritis or hallux valgus49,52,55,57,58,67, and others provided inadequate information on the patients or the method of evaluation48,51,53,56,58,59,65-67 or patients were not evaluated at the time of final follow-up66. We found only two reports50,68 that dealt exclusively with the treatment of hallux rigidus, and both included patients with less than one year of follow-up. On the basis of their individual beliefs about the etiology of hallux rigidus, authors have proposed several grading systems with either three1,2,12,22,71-73 or four stages35,41,50,71,74 determined according to radiographic criteria only12,71 or a combination of clinical and radiographic criteria1,2,17,22,41,50,72,73. Several of these grading systems add modifications to an existing scheme2,4,6,8,11,69, while in others the grades or treatment recommendations are based on poorly studied concepts such as metatarsus primus elevatus41,50,71 or functional hallux limitus17,41,50. All of these variations make comparisons between studies difficult. The purpose of the present study was to evaluate the predictability of a clinical-radiographic grading scale for choosing a surgical procedure, and to examine the long-term results of cheilectomies and arthrodeses performed by one surgeon.

Materials and Methods ne hundred and forty consecutive patients were treated, by the senior author (M.J.C.), with either a cheilectomy or an arthrodesis of the first metatarsophalangeal joint as surgical treatment for a symptomatic hallux rigidus deformity between November 1981 and November 1999. Twenty-one patients were excluded from the present study because of a diagnosis of gout, rheumatoid arthritis, systemic lupus erythematosis, poliomyelitis, or previous pyarthrosis, and five other patients died during the study period. Of the 114 remaining patients with a diagnosis of hallux rigidus, four were unavailable or had moved away; 110 (96%) returned for a final followup evaluation. Of these 110 patients (127 feet), eighty (ninety-three feet) were treated with cheilectomy and thirty (thirty-four feet) were treated with arthrodesis. Thirteen patients had bilateral cheilectomy, and four patients had bilateral arthrodesis. No patient underwent a cheilectomy on one side and an arthrodesis on the contralateral side. Sixty-nine (63%) of the 110 patients were female. The average age at the onset of symptoms was forty-three years (range, thirteen to seventy years), and the average age at surgery was fifty years (range, sixteen to seventysix years).

O

Grading At the time of final follow-up, the patients were evaluated with a five-level clinical-radiographic grading system (Table I and

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

HAL LUX RIG IDUS

Fig. 1-B

Figs. 1-A and 1-B Radiographs demonstrating Grade-1 hallux rigidus. Fig. 1-A The anteroposterior radiograph demonstrates a small lateral marginal osteophyte (arrow) but a well-preserved joint space. Fig. 1-B The lateral radiograph demonstrates a small dorsal spur (arrow). Fig. 1-A

Fig. 2-B

Figs. 2-A and 2-B Radiographs demonstrating Grade-2 hallux rigidus. Fig. 2-A The anteroposterior radiograph demonstrates a substantial lateral marginal osteophyte, mild flattening of the metatarsal head, mild joint-space narrowing, and sclerosis. Fig. 2-B The lateral radiograph demonstrates narrowing of less than one-fourth of the joint space (primarily dorsally) and a more prominent dorsal spur. Fig. 2-A

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

Figs. 1-A through 4-B) that incorporates many features of all of the classification systems used by previous authors1,2,12,22,72,74 but is not based on hypothetical concepts or notions17,41,50,71. All range-of-motion measurements used in the system refer to passive motion. Pain at mid-range of passive motion refers to pain that is elicited not only at the extremes of passive dorsiflexion and plantar flexion of the metatarsophalangeal joint but also in between. Loose bodies or osteochondral defects can occur with any grade. Their presence does not affect the assigned grade. There is intentional overlap of the ranges of motion of the different grades as range of motion is only one of the three general factors determining the eventually assigned grade of hallux rigidus. Range-of-motion, clinical, and radiographic examinations are utilized to determine the individual grade. Preoperative Findings The indication for surgery was intractable pain isolated to the first metatarsophalangeal joint that was refractory to shoe modifications, use of rigid shoe inserts, nonsteroidal antiinflammatory medications, and modification of activities. Symptoms referable to the great toe and foot were compiled from a chart review. The operative reports were also evaluated to record the estimated percentage of the cartilage surface of the metatarsal head that remained, which had been ob-

HAL LUX RIG IDUS

served and routinely recorded at the time of surgery. A cheilectomy was always recommended for Grade-1 and Grade-2 hallux rigidus, whereas a cheilectomy or an arthrodesis was recommended for Grade-3 hallux rigidus. An arthrodesis was recommended when radiographs demonstrated end-stage arthrosis and the clinical examination demonstrated a painful range of motion. When an arthrodesis was performed, such patients were typically found to have <50% of the cartilage surface remaining on inspection at surgery. Determining the best type of treatment was the most difficult for patients with similar radiographic findings who had minimal pain during the range of motion except at maximum plantar flexion and dorsiflexion. If it was acceptable to them, such patients gave consent for both arthrodesis and cheilectomy, and the surgeon chose the procedure at the time of the operation on the basis of the amount of cartilage surface that remained. Although an arthrodesis was always recommended to patients with endstage arthritis, which we later characterized as Grade-4 hallux rigidus, eight of these patients refused the arthrodesis and underwent cheilectomy instead. Early in the study, the magnitude of preoperative pain was quantified as none, mild, moderate, severe, or quite severe; later, a visual analog scale was used by the patients to quantify the level of pain numerically. In order to compare the preoperative and postoperative pain scores in the treatment

Fig. 3-B

Figs. 3-A and 3-B Radiographs demonstrating Grade-3 hallux rigidus. Fig. 3-A The anteroposterior radiograph demonstrates substantial joint-space narrowing and sesamoid irregularity. Fig. 3-B The lateral radiograph demonstrates narrowing of more than one-fourth of the joint space and a prominent dorsal spur. Fig. 3-A

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

HAL LUX RIG IDUS

Fig. 4-B

Figs. 4-A and 4-B Radiographs demonstrating Grade-4 hallux rigidus. Both the anteroposterior (Fig. 4-A) and the lateral (Fig. 4-B) radiographs demonstrate more advanced degenerative changes than the radiographs showing the Grade-3 disease. (Grades 3 and 4 may look identical radiographically and must be distinguished clinically.) Fig. 4-A

groups (cheilectomy and arthrodesis) on the basis of the 10point visual analog score that was eventually used, a number was assigned retrospectively to the preoperative pain described by the patients seen early in the study. None was quantified as 0; mild, as 3; moderate, as 6; severe, as 9; and quite severe, as 10. Preoperatively, twenty-one patients had moderate pain and the remainder had severe or quite severe pain. Although the AOFAS (American Orthopaedic Foot and Ankle Society) hallux metatarsophalangeal scale75 was not available until 1994, the chart information and radiographs allowed us to also calculate a preoperative AOFAS score retrospectively for each patient. Follow-up Evaluation The mean duration of follow-up was 9.6 years (range, 2.3 to 20.3 years) after the cheilectomies and 6.7 years (range, 2.1 to 12.2 years) after the arthrodeses. At the time of follow-up, patients were assessed with a standardized questionnaire and examination. Patients were asked to characterize their postoperative pain as none, mild, moderate, severe, or quite severe and also to rate it on a 10-point visual analog scale in which 0 indicated no pain and 10 indicated the most severe pain. Patients were also asked to localize the pain, if they had any, and to specify their main symptom (pain, stiffness, cosmetic appearance, locking, or a gait problem). In addition, patients were questioned about their clinical history, including use of orthotics, age at

the onset of the symptoms, and duration of pain or other symptoms. Patients were asked to rate their satisfaction with the result of the surgery according to a previously published scale76. In that scale, a result is considered excellent if the patient has no problems related to the foot, is very satisfied, has mild or no pain, walks with mild or no difficulty, and would have the surgery again under similar circumstances. A result is considered good if the patient has a few problems, is satisfied, has mild pain, walks with no or mild difficulty, and would have the surgery again under similar circumstances. A fair result means that the patient has moderate pain, some difficulty with walking, and reservations about the success of the surgery. A poor result indicates that the patient has continued pain, has little or no improvement in walking, and regrets having had the surgery. More specific questions regarding shoe wear were asked to determine whether the patient could wear fashionable shoes (a 2-in [5-cm] or higher heel) postoperatively, felt pressure from constricting shoes, or had any other difficulty with shoe wear. Patients were asked to characterize their shoe-wear restrictions (preoperatively and postoperatively) as none (could wear fashionable shoes), could wear comfortable shoes only, or required modified custom shoes or orthotic devices. Patients were asked if they could walk on tiptoe and the time to maximal comfort and recovery from the surgery. They were asked to characterize any activity restrictions (preoperatively and postoperatively) as none (no restriction of sports

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

or recreational activity), mild (not enough to interfere with everyday activity but some limitation of sports or recreational activity), moderate (limitation of daily and recreational or sports activity), or severe (major limitation of any activity). The physical examination included inspection and palpation of the foot with attention to posture, sensation, motion, motor function, strength, and appearance. Both feet of all patients were examined. Stance and gait were assessed with attention to the position of the foot when the patient walked. Passive motion of the metatarsophalangeal and interphalangeal joints of the great toe was measured with a goniometer, with the plantar aspect of the foot considered to be neutral. These joints were then assessed for stability in the sagittal plane. Pain that occurred in the mid-range, between maximum plantar and dorsiflexion, of a passive range of motion of the hallux metatarsophalangeal joint was noted. The plantar aspect of the foot was assessed for callosities or areas of tenderness. Motor strength of the hallux was quantitated on a 5-point scale in which 1 indicated no strength; 2, active movement with gravity eliminated; 3, active movement against gravity only, without resistance; 4, active movement against gravity with some resistance; and 5, active movement against gravity with full resistance. An AOFAS hallux metatarsophalangeal score75 was de-

HAL LUX RIG IDUS

termined for all patients at the time of final follow-up. This is a 100-point scale composed of separate sections for pain (40 points), function (45 points), and alignment (15 points). In the scale for pain, 40 points is given for no pain; 30 points, for mild, occasional pain; 20 points, for moderate, daily pain; and 0 points, for severe, constant pain. Function is graded on the basis of activity (10 points for no limitation, 7 points for limitation of recreational activity but not daily or job-related activities, 4 points for limitation of daily and recreational activities, and 0 points for severe limitation of daily and recreational activities), shoe wear (10 points for the ability to wear fashionable and regular shoes with no insert, 5 points for the ability to wear only comfortable shoes or the need for an insert, and 0 points for the need to wear modified shoes or a brace), motion (dorsiflexion plus plantar flexion) of the metatarsophalangeal joint (10 points for ≥75°, 5 points for 30° to 74°, and 0 points for <30°), motion (plantar flexion) of the interphalangeal joint (5 points for no restriction and 0 points for <10°), stability (in all directions) of the metatarsophalangeal joint (5 points for stable and 0 points for unstable), and callus related to the metatarsophalangeal and interphalangeal joints (5 points for no or an asymptomatic callus and 0 points for a symptomatic callus). In the alignment section of the scale, 15 points is given for a well-aligned

Fig. 5-B

Radiographs demonstrating the technique for measuring the joint width. On the preoperative and postoperative radiographs, three points were placed along the corresponding articular surfaces of the base of the proximal phalanx and the distal part of the metatarsal. On the anteroposterior radiograph (Fig. 5-A), these points were placed at the medial, central, and lateral aspects of the joint surFig. 5-A

faces. On the lateral radiograph (Fig. 5-B), these points were placed at the dorsal, middle, and plantar aspects of the joint surface. On a line connecting each pair of corresponding points, the joint width was measured in millimeters. The six scores were added and then divided by six, to provide an average width for each joint.

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

Fig. 6

Diagram demonstrating measurement of metatarsus primus elevatus and the first metatarsal declination angle on weight-bearing lateral radiographs. To measure metatarsus primus elevatus, a line is drawn along the distal dorsal metaphyseal cortex of the first and second metatarsals. A perpendicular line is drawn between the two cortical

HAL LUX RIG IDUS

lateral radiograph was made for all feet3. This is a weightbearing lateral radiograph made with manual dorsiflexion stress applied by grasping the proximal phalanx and passively extending the metatarsophalangeal joint (Figs. 7-A and 7-B). The dorsiflexion measured on the weight-bearing stress radiograph was compared with the dorsiflexion measured with a goniometer without weight-bearing, and any discrepancy was recorded in order to measure the magnitude of functional hallux limitus81-83. In addition, metatarsus primus elevatus was measured on the stress radiograph and compared with the metatarsus primus elevatus on the non-stress standard weight-bearing lateral radiograph to evaluate the extent to which the metatarsus primus elevatus was a secondary change.

lines, and the distance between the two lines is measured in millimeters. To measure the first metatarsal declination angle, the lateral longitudinal axis of the first metatarsal is drawn with use of middiaphyseal reference points. A second line estimating the plantar surface of the foot is drawn, intersecting reference points on the plantar aspect of the calcaneus and the medial sesamoid. The intersection of these two lines forms the first metatarsal declination angle (angle A).

hallux; 8 points, for fair alignment with some deformity but no symptoms; and 0 points, for symptomatic malalignment. With use of this scale, 90 points is the highest score attainable after an arthrodesis. Radiographic Evaluation Standardized preoperative weight-bearing radiographs77 were reviewed and compared with standardized postoperative weightbearing radiographs made at the time of the final follow-up. The width of the metatarsophalangeal joint was determined by a summation method based on six separate measurements (Figs. 5-A and 5-B). Recurrence of the dorsal osteophyte was assessed on the lateral radiograph by drawing a line along the dorsal cortex of the metatarsal and measuring any osteophyte above that line in millimeters. Interphalangeal joint arthritis was graded on the anteroposterior radiograph with use of a previously described method78. With this method, Grade 1 indicates no degenerative changes; Grade 2, mild changes with <1 mm of chondrolysis; Grade 3, moderate changes with 1 to 2 mm of chondrolysis; and Grade 4, severe changes with malalignment, cysts, and/or joint destruction. Periarticular sclerosis at the metatarsophalangeal joint was recorded as 0 (no sclerosis), +1 (mild), +2 (moderate), or +3 (severe), as seen on the preoperative and postoperative anteroposterior radiographs of the patients treated with cheilectomy. Elevation of the first ray (metatarsus primus elevatus) was measured on the weight-bearing lateral radiograph79. The difference between the dorsal cortices of the first and second metatarsals measured at the head-neck junction was recorded in millimeters. A normal value is ≤8 mm79. The first metatarsal declination angle was measured as well79. Normal values are reported to range from 19° to 25°80 (Fig. 6). A dorsiflexion stress

Fig. 7-A

Figs. 7-A and 7-B Metatarsus primus elevatus and dorsiflexion stress test. Fig. 7-A A postoperative standing lateral radiograph demonstrating 9 mm of metatarsus primus elevatus.

Fig. 7-B

A standing lateral radiograph of the same foot with application of dorsiflexion stress, demonstrating an absence of metatarsus primus elevatus.

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

Surgical Techniques A cheilectomy is performed with use of regional anesthesia and with an Esmark bandage (Medline Industries, Mundelein, Illinois) employed as a tourniquet1,3,7. A 3-cm dorsal longitudinal incision is centered over the metatarsophalangeal joint and is deepened through the capsule on the medial aspect of the extensor hallucis longus tendon. The capsule is preserved for later repair. Hypertrophic synovial tissue and loose bodies are fully débrided from the joint, and the percentage of viable cartilage remaining on the metatarsal head is estimated. The proximal phalanx is plantar flexed, exposing the metatarsal head. An osteotome is used to remove the dorsal, medial, and lateral osteophytes along with 25% to 33% of the metatarsal head dorsally. Usually, all or almost all of the cartilagedeficient surface of the metatarsal head is resected. At least 70° of dorsiflexion should be achieved intraoperatively. The osteophytes are then removed from the dorsal aspect of the base of the proximal phalanx, and the joint is lavaged. Bone wax is applied to the dorsal region of the metatarsal head. The capsule is repaired beneath the extensor hallucis longus tendon with interrupted absorbable sutures, and the skin is approximated in a routine fashion. A gauze-and-tape compression dressing is applied at the conclusion of the surgery and is changed every ten days. Passive range-of-motion exercises are begun within ten days after surgery, and aggressive stretching is allowed as pain and swelling subside. Walking is permitted following surgery with the patient wearing a stiff-soled postoperative shoe and bearing weight as tolerated. Arthrodesis of the first metatarsophalangeal joint is performed with use of regional anesthesia and with use of an Es-

HAL LUX RIG IDUS

mark bandage as a tourniquet1,52,76,84. A dorsal longitudinal incision, 4 to 5 cm long, is centered over the metatarsophalangeal joint and is deepened through the capsule on the medial aspect of the extensor hallucis longus tendon. The capsule is preserved for later repair. The joint is débrided, and osteophytes and loose bodies are removed. The proximal phalanx is plantar flexed, a 0.62-mm Kirschner wire is proximally centered on the first metatarsal articular surface and driven in, and an appropriately sized cannulated cylindrical reamer is used to create a cylinder-shaped metatarsal. A concave cannulated metatarsal reamer (small joint reamer; Howmedica, Rutherford, New Jersey) is then utilized to create a convex cancellous metatarsal surface. The Kirschner wire is removed, and attention is then directed to the proximal phalanx. A Kirschner wire is centered on the articular surface of the base of the proximal phalanx and is driven distally to prepare for cannulated reaming. Convex phalangeal reamers are used to create a concentric matching surface on the phalangeal base to match the metatarsal head. The hallux is placed in neutral rotation, 15° of valgus, and 20° of dorsiflexion in reference to the axis of the first metatarsal. It is stabilized with a six-hole Vitallium mini-compression plate and a lag screw. A gentle dorsal bend in the plate allows better conformity to the dorsal osseous surfaces to achieve approximately 20° of dorsiflexion. Closure is identical to that used for a cheilectomy. A gauze-and-tape compression dressing is applied at the conclusion of the surgery and is changed every ten days for eight to twelve weeks, until there is radiographic evidence of a successful fusion. The foot is placed in a stiff-soled postoperative shoe after surgery, and weight-bearing on the heel and the lateral aspect of the involved foot is permitted. The first ray is

TABLE II Preoperative and Postoperative Symptoms and Functional Factors in Patients Treated with Cheilectomy or Arthrodesis* Postop. Symptom or Functional Factor

Preop. (N = 110)

Cheilectomy (N = 80)

Arthrodesis (N = 30)

Stiffness

109

10 (13%)

14 (47%)

24

Pain

110

46 (58%)

9 (30%)

55

Locking

20

0

0

0

Dissatisfaction with cosmetic appearance

60

0

0

0

Eversion gait

Total (N = 110)

108

10 (13%)

2 (7%)

12

Able to rise up on toes

11

66 (83%)

15 (50%)

81

Pain at metatarsophalangeal joint (main symptom)

55

46 (58%)

9 (30%)

55

Painful dorsal bump (main symptom)

55

0

0

0

Insert or orthotic

20

9

9

18

Able to wear fashionable shoes

50

56

21

77

Able to wear comfortable shoes

110

80

30

110

Discomfort from shoe pressure

110

10

3

13

*The values are given as the number of patients.

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

HAL LUX RIG IDUS

TABLE III Preoperative and Postoperative Clinical Scores and Findings on Examination for Patients Treated with Cheilectomy or Arthrodesis Score or Finding on Examination

Cheilectomy Preop.

Pain score on visual analog scale* (points)

8 (6-10)

Arthrodesis Postop.

Preop.

Postop.

1.5 (0-8)

8.7 (6-10)

0.4 (0-5)

Total Series (Postop.)

AOFAS score* (points)

45 (24-70)

90 (67-100)

38 (24-60)

89 (72-90)

Subjective patient selfassessment score (no.)

All fair or poor

58 excellent, 19 good, 3 fair, 0 poor

All fair or poor

26 excellent, 4 good, 0 fair or poor

MTP dorsiflexion*† (deg)

14.5 (0-45)

39 (10-65)

7 (−15-10)

0

Dorsiflexion improved 24.5°

MTP total motion*† (deg)

39.2 (5-80)

63.7 (15-110)

22.1 (5-30)

0

Total motion improved 24.5°

Callus† (no. of patients/ location)

5/2nd MTP, plantar

5/IP joint, plantar

4/2nd MTP, plantar

4/IP joint, plantar

9/IP joint, plantar and medial

*The values are given as the mean with the range in parentheses. †MTP = metatarsophalangeal joint and IP = interphalangeal joint.

unweighted in this fashion until there is radiographic evidence of a fusion. Statistical Analysis Descriptive and comparative statistical analysis was performed with use of InStat software (GraphPad Software, San Diego, California). Standard chi-square analysis was performed on continuous variables. Pearson and binary correlation coefficients were used to evaluate the noncontinuous data, and positive coefficients (r values) closer to one indicate strong correlation while values closer to zero indicate weak or no correlation. Differences were considered to be significant when the p value was ≤0.05. Results ighty patients (ninety-three feet) treated with a cheilectomy and thirty patients (thirty-four feet) treated with an arthrodesis were evaluated at the final examination. At the time of follow-up, at a mean of 9.6 years postoperatively, seven (8%) of the ninety-three cheilectomies had failed. At the time of follow-up, at a mean of 6.7 years postoperatively, thirty-two (94%) of the thirty-four arthrodeses had successfully fused. There were sixteen associated surgical procedures, including four repairs to treat a hammertoe deformity of the second toe, nine repairs to treat capsular instability of the second metatarsophalangeal joint, and three Akin phalangeal osteotomies performed for severe hallux valgus interphalangeus at the time of metatarsophalangeal joint arthrodesis.

E

Historical Data (Table II) The most common primary preoperative symptoms were metatarsophalangeal joint pain (fifty-five patients) and a painful dorsal bump (fifty-five patients). These symptoms decreased postoperatively in both treatment groups. Interestingly, the same number of patients listed their primary symptom as metatarsophalangeal joint pain both preoperatively and post-

operatively. However, there was a significant reduction (p = 0.0001) in the postoperative pain score indicated on the visual analog scale. Postoperatively, patients no longer complained of a dorsal bump or pressure from the shoe, but they continued to have metatarsophalangeal joint pain. The time to maximum postoperative improvement averaged 2.4 months (range, one to 4.5 months) after the cheilectomies and 2.8 months (range, 1.5 to four months) after the arthrodeses. Clinical Scores (Table III) One hundred and seven (97%) of the 110 patients had an excellent or good self-assessment (subjective) score at the time of follow-up, whereas all patients had a fair or poor score preoperatively (as estimated retrospectively). A good or excellent outcome based on the patient self-assessment score, visual analog score for pain, and AOFAS score did not correlate with the radiographic appearance of the joint (loss of joint space) at the time of final follow-up (r = 0.08, p = 0.34). At the time of final follow-up, the mean AOFAS score was significantly improved in both the group treated with cheilectomy (p = 0.0001, difference in the means = 45.7, 95% confidence interval = 43.3 to 48.1) and the group treated with arthrodesis (p = 0.045, difference in the means = 50.4, 95% confidence interval = 46.5 and 54.4). The cheilectomy group had a significantly higher preoperative mean AOFAS score than did the arthrodesis group (45 compared with 38 points, p = 0.025, difference in the means = 6.6, 95% confidence interval = 1.8 and 9.1), but there was no difference in the mean postoperative AOFAS scores (89 compared with 90 points, p = 0.3). However, the maximum possible AOFAS score in the arthrodesis group was 90 points, as 10 points are unavailable because of loss of motion. When the patients treated with cheilectomy were grouped according to the grade of the hallux rigidus, a significant difference in both preoperative and postoperative AOFAS score was found among the subgroups (r = 0.3, p = 0.02). Also, a

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

HAL LUX RIG IDUS

TABLE IV Mean Range of Motion and Follow-up Scores for Patients Treated with Cheilectomy Postop. Pain Score on Visual Analog Scale (points)

Grade

Preop.

Postop.

Change

Preop.

Postop.

Change

Postop. AOFAS score (points)

1

33.3

56.7

23.4

53.3

76.7

23.4

95.7

1.1

2

21.1

46.4

25.3

38.9

62.1

23.2

92.9

1.5

3

9.5

34.5

25

21.5

44.7

23.2

89.8

1.7

4*

5.8

−5.8

12.5

−12.5

88.9

0.4

Dorsiflexion (deg)

Total Motion (deg)

*Five of nine Grade-4 feet underwent arthrodesis and had a mean loss of motion.

TABLE V Mean Radiographic Values for Patients Treated with Cheilectomy or Arthrodesis Cheilectomy* Radiographic Parameter Metatarsus primus elevatus (mm)

Arthrodesis*

Preop.

Postop.

Preop.

Postop.

5.3 (0-10)

6.1 (0-15)

5.6 (0-12)

1.8 (0-10)

First metatarsal declination angle (deg)

20.4 (15-27)

21.1 (12-30)

23.4 (19-30)

Hallux valgus angle (deg)

12.2 (0-20)

12.6 (0-24)

12.2 (0-20)

11.7 (5-19)

1st-2nd intermetatarsal angle (deg)

7.3 (2-24)

7.7 (2-15)

8.1 (4-14)

8.1 (4-13)

Joint width (mm)

1.6 (0.3-2.7)

1.2 (0-3)

0.9 (0.5-1.6)

0.01 (0-0.5)

Periarticular sclerosis

1.8 (0-3)

2.2 (0-3)

2.6 (2-3)

Fused

Interphalangeal joint width (mm)

1.1 (1-2)

1.1 (1-2)

1.1 (1-2)

20 (15-26)

1.2 (1-2)

*The values are given as the mean with the range in parentheses for the feet.

correlation was found between increasing grade and lower preoperative AOFAS scores (r = 0.4, p = 0.01). Results of Clinical Examination (Table IV) The total range of motion of the metatarsophalangeal joint at the time of final follow-up after the cheilectomies averaged 64°: the average dorsiflexion of the metatarsophalangeal joint improved from 14.5° preoperatively to 38.4° postoperatively (p = 0.0001, difference in the means = 23.8°, 95% confidence interval = 20.9° to 26.6°). Postoperatively, no significant difference was noted between passive dorsiflexion and dorsiflexion with stress at either the metatarsophalangeal or the interphalangeal joint of the hallux (p = 0.4, difference in the means = 1.2°). Dorsiflexion of the interphalangeal joint averaged 8° in both treatment groups at the time of final followup. Motor strength was graded as 5/5 (normal) in all subjects. All first metatarsophalangeal joints were stable on manual examination following cheilectomy. Three patients had a Tinel sign over the dorsal-medial aspect of the metatarsophalangeal joint preoperatively, but no patient had a sensory disturbance postoperatively. Radiographic Data (Table V) Comparison of the extent of arthritic changes in the interphalangeal joint between the preoperative and postoperative ra-

diographs demonstrated no progression of arthritis in either treatment group. There was significant progression of periarticular sclerosis of the metatarsophalangeal joint (p = 0.0001, difference in the means = 0.5, r = 0.84, 95% confidence interval = 0.3 to 0.6) and of loss of the metatarsophalangeal joint width (p = 0.0001, difference in the means = 0.4 mm, r = 0.8, 95% confidence interval = 0.25 and 0.46) in the cheilectomy group. Twenty-one metatarsophalangeal joints were noted to have a loose body on preoperative radiographs and confirmatory findings at the time of surgery, but no loose bodies were noted on final follow-up radiographs. The average size of the recurrent dorsal osteophytes was 0.72 mm (range, 0 to 3 mm) after the cheilectomies and 0 mm after the arthrodeses. Grading of the Hallux Rigidus (Table VI) In the cheilectomy group, the mean clinical-radiographic grade of the hallux rigidus was 2.50 (range, 1 to 4) preoperatively compared with 2.59 (range, 1 to 4) postoperatively (p = 0.1). Nine patients had an increase of one grade at the time of final follow-up. In the cheilectomy group, patients with a lower grade preoperatively had a better AOFAS score both preoperatively and postoperatively. No patient had an increase in the grade after an arthrodesis, and no patient in the series had an increase of more than one grade. Following

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

HAL LUX RIG IDUS

TABLE VI Preoperative and Postoperative Clinical-Radiographic Grades for Patients Treated with Cheilectomy or Arthrodesis* Grade 1

Grade 2

Grade 3

Grade 4

Before cheilectomy

6 (8%)

32 (40%)

34 (43%)

8 (10%)

After cheilectomy

4 (5%)

31 (39%)

33 (41%)

12 (15%)

10 (33%)

20 (67%)

Before arthrodesis *The values are given as the number of patients with the percentage in parentheses.

the cheilectomies, the patients with Grade-1 hallux rigidus had a mean AOFAS score of 95.7 points and a mean pain score on the visual analog scale of 1.1 points, and all four feet were subjectively rated as excellent. Patients with Grade 2 had a mean AOFAS score of 92.9 points and a mean pain score on the visual analog scale of 1.5 points; of the thirty-eight feet, thirty-five were rated as excellent and three were rated as good. Patients with a Grade-3 rating had a mean postoperative AOFAS score of 89.8 points and a mean pain score on the visual analog scale of 1.7 points; of the thirty-four feet, twenty-nine were rated as excellent and five were rated as good. Integrity of the Articular Surface at the Time of Surgery As estimated by inspection of the metatarsophalangeal joint at the time of surgery, an average of 17% (range, 0% to 40%) of the articular surface of the metatarsal head remained in the arthrodesis group and an average of 60% (range, 55% to 90%) remained in the cheilectomy group. There was a correlation between an estimation of <50% of the metatarsal head cartilage remaining and failure of cheilectomy (p = 0.002, r = 0.4). Also, an estimation of >50% of the metatarsal head cartilage remaining in a patient undergoing a cheilectomy correlated with a long-term AOFAS score of >80 points and a good or excellent subjective score (p = 0.01, r = 0.4) at the time of final follow-up. Metatarsus Primus Elevatus (Table VII) There was good correlation between the first metatarsal declination angle and metatarsus primus elevatus in both treat-

ment groups (r = 0.6, p = 0.01). Preoperatively, 120 (94%) of the 127 feet had <8 mm of elevation, which was within the range of normal. The mean preoperative and postoperative measurements of elevatus were 5.3 mm and 6.1 mm in the cheilectomy group. There was a correlation between the postoperative grade and the amount of elevatus (r = 0.44, p = 0.02). Moreover, the elevatus reduced to a mean of 1.2 mm on dorsiflexion stress examination in the cheilectomy group at the time of final follow-up. This value was significantly different from the measurements of elevatus on weight-bearing lateral radiographs both preoperatively (p = 0.001, difference in the means = 3.9 mm, 95% confidence interval = 1.6 to 5.2 mm) and postoperatively (p = 0.001, difference in the means = 4.5 mm, 95% confidence interval = 1.3 to 5.1 mm). Both before and following cheilectomy, an increased value for elevatus was associated with a higher grade of hallux rigidus (p = 0.04, r = 0.44). In addition, elevatus decreased postoperatively in patients with Grade-1 or 2 hallux rigidus but it increased in those with Grade-3 or 4. The mean preoperative elevatus in the arthrodesis group was 5.6 mm, and this was significantly reduced postoperatively to 1.7 mm (p = 0.009, difference in the means = 3.9 mm, 95% confidence interval = 2.7 to 4.9 mm). Complications Five of the eighty patients in the cheilectomy group and two of the thirty in the arthrodesis group required oral antibiotics for the treatment of mild postoperative cellulitis. There were no deep wound infections. No patient in either group had tenodesis or scarring of the extensor hallucis longus, concerns

TABLE VII Metatarsus Primus Elevatus, According to Grade of Hallux Rigidus, in the Patients Treated with Cheilectomy or Arthrodesis Metatarsus Primus Elevatus (mm) Grade 1

Grade 2

Grade 3

Before cheilectomy*

2.6 (0-8)

5.2 (0-8)

5.2 (0-10)

6 (5-10)

After cheilectomy*

2.5 (0-5)

4.7 (0-8)

8 (0-15)

8.4 (5-10)

0.086

0.0001

P value

Grade 4

0.0001

0.0001

Before arthrodesis*

5.3 (0-10)

6.2 (0-12)

After arthrodesis*

1.1 (0-5)

1.5 (0-6)

*The values are given as the mean with the range in parentheses.

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

HAL LUX RIG IDUS

about the cosmetic appearance of the foot, neuritis, or a hypertrophic dorsal scar. Seven failed cheilectomies in six patients resulted in seven additional surgical procedures. There were two outcomes that were unexpected on the basis of the grades assigned with our rating system during the study period. These two outcomes consisted of rapid chondrolysis (within one year after the surgery), and both patients had a metatarsophalangeal joint arthrodesis (at seven and eight years following the cheilectomy). The other four patients (five feet) in which the cheilectomy failed had originally been advised to have an arthrodesis for the treatment of Grade-4 disease; a metatarsophalangeal joint arthrodesis was eventually performed in these four patients. The other four patients with Grade-4 changes (who did not have additional surgery after the initial cheilectomy) had a mean long-term AOFAS score of 74 points (range, 67 to 80 points); three rated the result as fair and one rated it as good after a mean duration of follow-up of 7.4 years (range, 2.5 to 8.4 years). Thus, of the nine feet with Grade-4 changes for which arthrodesis was recommended but cheilectomy was performed at the patient’s request, five had failure of the procedure and later underwent arthrodesis (at a mean 6.9 years after the cheilectomy) as initially recommended. The other four had inferior subjective results (three fair and one good) at the time of follow-up but had radiographic signs of deterioration of the joint space and a mean pain score of 4.7 points on the visual analog scale. Two plates were removed because of pain following a successful fusion. Two of the thirty-four feet that had undergone arthrodesis had a painless fibrous union, and the AOFAS score was 90 points for both of these feet at the time of follow-up.

metatarsophalangeal joint pain (mean pain score, 4.4 points). However, the cheilectomy unexpectedly failed in two of thirtyfour patients with Grade-3 hallux rigidus. Both had radiographic evidence of chondrolysis within one year after the surgery, with progressive pain, and subsequently underwent arthrodesis of the metatarsophalangeal joint at seven and eight years following the cheilectomy. To improve the accuracy and predictability for Grade-3 hallux rigidus, the percentage of metatarsal head cartilage remaining, as estimated with direct surgical inspection, should be considered, as <50% of the cartilage remaining correlated with failure. The indications for cheilectomy described in the literature have varied greatly. While some authors have recommended cheilectomy for early disease only2,12, others have used the procedure to treat both early and moderate disease4,5; still others have used it for all levels of disease3,7,11,69. The results of this study support the use of cheilectomy for all levels of disease except Grade 4. As a result of all of the different grading systems (or a lack of grading) and differences in the technique of cheilectomy, it is difficult to compare the results of different studies. However, rates of satisfaction after cheilectomy have been favorable, ranging from 72% to 90%2-4,11-13,69. We favor a uniform grading system to allow comparisons between studies and to distinguish between a Grade-3 and a Grade-4 metatarsophalangeal joint. Of interest was a significant progression in objective evidence of periarticular sclerosis as well as loss of joint space width in our patients who had undergone cheilectomy; however, there was no correlation between loss of joint width and the AOFAS score, pain score, or patient self-assessment.

Discussion Grading System he grading system used in this study had been modified on the basis of the findings of Easley et al.1 in order to add Grade 4 for advanced hallux rigidus. A grade-0 stage was also added to include asymptomatic patients with early loss of metatarsophalangeal joint motion. The initial grading system was a clinical-radiographic scheme described by one of us (M.J.C.)73. The classification system shown in Table I and Figures 1-A through 4-B incorporates many of the best elements of prior grading systems1,12,22,72 and requires both subjective and objective examination and radiographic data to determine the grade. When applied retrospectively, the system appeared to be reliable as it correctly predicted a successful outcome in 108 of 110 patients. Moreover, it accurately predicted a fair or poor outcome in patients with Grade-4 hallux rigidus treated with cheilectomy. Its key utility was in the distinction between Grade-3 and Grade-4 hallux rigidus. Cheilectomy uniformly failed in patients with Grade-4 hallux rigidus, as predicted; five of the nine feet in which Grade-4 hallux rigidus was treated with cheilectomy subsequently had an arthrodesis, and two of the four remaining patients had moderate to severe

Recurrence and Chondrolysis Easley et al.1 reported that dorsal osteophytes recurred in twenty-one of sixty-eight feet following cheilectomy, although the authors did not specify how the recurrence was quantified. Several authors have noted that the metatarsophalangeal joint deteriorates radiographically following cheilectomy1,4,7,11. Others have reported that cheilectomy hastens deterioration of the joint2, and still others have reported that deterioration is uncommon3. Smith et al.85 reported on the natural history of hallux rigidus treated nonoperatively and observed that the metatarsophalangeal joint deteriorated radiographically and clinically with time (in sixteen of twentyfour feet). The results of our study support the finding of those authors that a metatarsophalangeal joint with hallux rigidus naturally deteriorates if followed for a long enough period of time. Cheilectomy does not appear to alter the natural progression of the disease process, but it enables a patient to be more comfortable during the course of degeneration.

T

Metatarsophalangeal Joint Motion Improved metatarsophalangeal joint motion following cheilectomy has been emphasized in several studies1,2,6,11. Dorsiflexion has reportedly been improved by 28° to 50°, depending on

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

the individual study and the specific surgical technique used for the cheilectomy1,3,7,13. Authors using the technique described by Mann et al.3 have reported 20° to 30° improvements in dorsiflexion and total range of motion1,3,4,7,11,13, whereas those using a minimal resection technique have reported about 50% less improvement in dorsiflexion2,6,12. Several authors have reported diminishing improvements in motion with increases in the grade of the disease2,6,12, whereas others1, including us, have found fairly uniform improvement in motion even in patients with more advanced disease. We reported an increase in mean dorsiflexion from 14.5° preoperatively to 38.4° postoperatively and an increase in mean total motion from 39.2° to 64°. This improvement occurred consistently across all grades, and it corresponds very closely with the findings reported by several authors1,3,7,11,13, confirming the reliability of our cheilectomy technique. Thus, it appears that minimal resection techniques are not as versatile, especially for more advanced grades of disease2,6,8,12. With our more aggressive resection technique, the indications can be extended to include more advanced disease without compromising the result or creating an unstable joint3,7,13,69. Pain Relief Pain relief has been reported consistently following cheilectomy1,3,7,69, but some authors have noted less pain relief with

HAL LUX RIG IDUS

higher grades of disease2,12,13. A cheilectomy alters the joint in some fashion, providing pain relief even in the presence of more advanced disease. However, there is a point (Grade-4 disease) at which reliable results are more difficult to obtain. We support the notion of Easley et al.1 that a clinical finding of pain at the mid-range of motion (Grade 4) is a harbinger of a poor result following cheilectomy and that it is critical to recognize this finding especially in the presence of advanced radiographic changes. However, as noted by others7,69, radiographic findings alone do not correlate with the final clinical result, and we believe that purely radiographic grading systems should be discarded. Arthrodesis There is little information on the performance of arthrodesis solely for the treatment of hallux rigidus52,53,57,58. Fitzgerald53 reported that arthritis developed in the interphalangeal joint when the metatarsophalangeal joint had been fused in <15° of valgus. One of us (M.J.C.)78 previously reported that arthritis was more common in interphalangeal joints when the metatarsophalangeal joint had been fused in <22° of dorsiflexion. Other studies have shown progression of interphalangeal joint arthritis after metatarsophalangeal joint arthrodesis78,86,87. However, these studies included a large number of patients with rheumatoid arthritis. In the current study, which dealt only with hallux rigidus, we noted no progression of degener-

Fig. 8-A

Figs. 8-A and 8-B Radiographs of a foot with a long-term good result of cheilectomy. Fig. 8-A Preoperative anteroposterior radiograph showing a foot with Grade-3 hallux rigidus. Fig. 8-B Anteroposterior radiograph made eighteen years following cheilectomy; the foot still has Grade-3 hallux rigidus.

Fig. 8-B

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

Fig. 9-A

HAL LUX RIG IDUS

Fig. 9-B

Figs. 9-A and 9-B Failure of cheilectomy. Fig. 9-A The preoperative anteroposterior radiograph shows a foot with symptomatic hallux rigidus. Fig. 9-B Two years following cheilectomy, painful arthrosis developed.

ative changes in the interphalangeal joint following cheilectomy or arthrodesis. Complications Arthrodesis resulted in a 94% fusion rate, and neither of the fibrous unions was painful. Two patients underwent hardware removal because of pain. There were no failures of hardware or other complications. Although Easley et al.1 suggested that a medial approach is preferable for cheilectomy because of the risk of tenodesis or scarring of the extensor hallucis longus tendon, because of cosmetic concerns, and to avoid creating a hypertrophic dorsal scar, we found no evidence of these complications in any patient. Metatarsus Primus Elevatus The concept of metatarsus primus elevatus as a cause of hallux rigidus has been endorsed in several reports2,8,23,28,30,34,36,37,41,50,70,81,82,88,89, whereas radiographic evidence to the contrary79,80,90 has also been reported. Functional hallux limitus (reduction of dorsiflexion of the first metatarsophalangeal joint with loading of the foot compared with passive dorsiflexion with non-weightbearing) has also been proposed as a cause of hallux rigidus81-83. Attempts to quantitate the magnitude of elevatus have been

Fig. 9-C

Radiograph made following arthrodesis of the metatarsophalangeal joint.

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

made with use of two different measurements, the first metatarsal declination angle80 and the difference in elevation between the dorsal cortices of the first and second metatarsals as seen on a weight-bearing lateral radiograph79,90. Normal elevatus is considered to be ≤8 mm, and the normal first metatarsal declination angle has been reported to be between 19° and 25°79,90. The mean preoperative elevatus was 5.5 mm in our patients, well within the limits of normal. Moreover, the mean first metatarsal declination angle was within normal limits both preoperatively and postoperatively in our patients. Metatarsus primus elevatus is rarely a structural problem that needs to be corrected by an osteotomy, as has been recommended by others32,34,36-39,74. In our series, it consistently decreased after cheilectomy in patients with lower grades of disease. We noted that these patients had the least amount of elevatus. Elevatus corrected to nearly zero with the dorsiflexion stress test (with any grade of hallux rigidus). While the elevatus decreased with passive dorsiflexion stress, we found no difference between first metatarsophalangeal joint motion with the dorsiflexion stress test and passive metatarsophalangeal joint motion. These findings call into question the concept of functional hallux limitus that has been reported in the literature81-83. However, we hypothesized that functional hallux limitus may represent the residual elevatus that we occasionally noted on the dorsiflexion stress radiographs of patients with more advanced disease. This study demonstrates that a simple procedure such as cheilectomy tends to reduce elevation of the first ray as the joint functions more normally. We believe that when the joint has deteriorated clinically to the point where elevation of the first ray is pronounced, it is an indication for metatarsophalangeal arthrodesis because first-ray elevation significantly diminished after arthrodesis in our series. Our study had the longest mean duration of follow-up after both cheilectomy and arthrodesis for the treatment of hallux rigidus. Ninety-six percent of the patients followed for

HAL LUX RIG IDUS

an average of 9.6 years after cheilectomy and 100% of those followed for an average 6.7 years after arthrodesis had a good or excellent subjective result. Pain scores in both groups were significantly reduced compared with the preoperative scores, and AOFAS scores were significantly improved. The clinical-radiographic grading system used in this study appears to be reliable. We believe that cheilectomy can be used with success for Grades 1, 2, and 3 hallux rigidus (Figs. 8-A and 8-B), but patients with Grade 4 or with <50% of the cartilage surface of the metatarsal head remaining at the time of surgery should be treated with arthrodesis (Figs. 9-A, 9-B, and 9-C). For patients who desire preservation of motion and are willing to accept less than total pain relief, cheilectomy provides a high proportion of good and excellent long-term results. However, arthrodesis should be considered for patients who clearly have pain in the mid-range of motion on examination. A high proportion of these patients can be expected to have a good or excellent long-term result after arthrodesis performed with the technique described in this study.
NOTE: The authors thank Mary Sampson, MS, for assistance with the statistical analysis.

Michael J. Coughlin, MD 901 North Curtis Road, Suite 503, Boise, ID 83706. E-mail address: [email protected] Paul S. Shurnas, MD Regional Orthopaedic Health Care, No. 3 Medical Plaza, Mountain Home, AR 72653 The authors did not receive grants or outside funding in support of their research or preparation of this manuscript. They did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.

References 1. Easley ME, Davis WH, Anderson RB. Intermediate to long-term follow-up of medial-approach dorsal cheilectomy for hallux rigidus. Foot Ankle Int. 1999; 20:147-52. 2. Geldwert JJ, Rock GD, McGrath MP, Mancuso JE. Cheilectomy: still a useful technique for grade I and grade II hallux limitus/rigidus. J Foot Surg. 1992; 31:154-9. 3. Mann RA, Coughlin MJ, DuVries HL. Hallux rigidus: a review of the literature and a method of treatment. Clin Orthop. 1979;142:57-63. 4. Mulier T, Steenwerckx A, Thienpont E, Sioen W, Hoore KD, Peeraer L, Dereymaeker G. Results after cheilectomy in athletes with hallux rigidus. Foot Ankle Int. 1999;20:232-7.

9. Feldman RS, Hutter J, Lapow L, Pour B. Cheilectomy and hallux rigidus. J Foot Surg. 1983;22:170-4. 10. Gould N. Hallux rigidus: cheilotomy or implant? Foot Ankle. 1981;1: 315-20. 11. Feltham GT, Hanks SE, Marcus RE. Age-based outcomes of cheilectomy for the treatment of hallux rigidus. Foot Ankle Int. 2001;22:192-7. 12. Hattrup SJ, Johnson KA. Subjective results of hallux rigidus following treatment with cheilectomy. Clin Orthop. 1988;226:182-91. 13. Lau JT, Daniels TR. Outcomes following cheilectomy and interpositional arthroplasty in hallux rigidus. Foot Ankle Int. 2001;22:462-70.

5. Shereff MJ, Baumhauer JF. Hallux rigidus and osteoarthritis of the first metatarsophalangeal joint. J Bone Joint Surg Am. 1998;80:898-908.

14. Giannestras NJ. Hallux rigidus. In: Foot disorders: medical and surgical management. 2nd ed. Philadelphia: Lea and Febiger; 1973. p 400-2.

6. Mackay DC, Blyth M, Rymaszewski LA. The role of cheilectomy in the treatment of hallux rigidus. J Foot Ankle Surg. 1997;36:337-40.

15. Kurtz DH, Harrill JC, Kaczander BI, Solomon MG. The Valenti procedure for hallux limitus: a long-term follow-up and analysis. J Foot Ankle Surg. 1999; 38:123-30.

7. Mann RA, Clanton TO. Hallux rigidus: treatment by cheilectomy. J Bone Joint Surg Am. 1988;70:400-6. 8. Pontell D, Gudas CJ. Retrospective analysis of surgical treatment of hallux rigidus/limitus: clinical and radiographic follow-up of hinged, silastic implant arthroplasty and cheilectomy. J Foot Surg. 1988;27:503-10.

16. Chang TJ. Stepwise approach to hallux limitus. A surgical perspective. Clin Podiatr Med Surg. 1996;13:449-59. 17. Saxena A. The Valenti procedure for hallux limitus/rigidus. J Foot Ankle Surg. 1995;34:485-8.

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

18. Cleveland M, Winant EM. An end-result study of the Keller operation. J Bone Joint Surg Am. 1950;32:163-75. 19. Grady JF, Axe TM. The modified Valenti procedure for the treatment of hallux limitus. J Foot Ankle Surg. 1994;33:365-7. 20. Jordan HH, Brodsky AE. Keller operation for hallux valgus and hallux rigidus. An end result study. Arch Surg. 1951;62:586-96.

HAL LUX RIG IDUS

DH, Cestari VA. The use of a grommet bone liner for flexible hinge implant arthroplasty of the great toe. Foot Ankle. 1991;12:149-55. 47. Townley C, Taranow W. A metallic hemiarthroplasty resurfacing prosthesis for the hallux metatarsophalangeal joint. Foot Ankle Int. 1994;15: 575-80. 48. Bingold AC, Collins DH. Hallux rigidus. J Bone Joint Surg Br. 1950;32:214-22.

21. Nilsonne H. Hallux rigidus and its treatment. Acta Orthop Scand. 1930;1: 295-302.

49. Smith NR. Hallux valgus and rigidus treated by arthrodesis of the metatarsophalangeal joint. Br Med J. 1952;2:1385-7.

22. Barca F. Tendon arthroplasty of the first metatarsophalangeal joint and hallux rigidus: preliminary communication. Foot Ankle Int. 1997;18:222-8.

50. Lombardi CM, Silhanek AD, Connolly FG, Dennis LN, Keslonsky AJ. First metatarsophalangeal arthrodesis for treatment of hallux rigidus: a retrospective study. J Foot Ankle Surg. 2001;40:137-43.

23. Cosentino GL. The Cosentino modification for tendon interpositional arthroplasty. J Foot Ankle Surg. 1995;34:501-8. 24. Hamilton WG, O’Malley MJ, Thompson FM, Kovatis PE. Capsular interposition arthroplasty for severe hallux rigidus. Foot Ankle Int. 1997;18: 68-70.

51. Chana GS, Andrew TA, Cotterill CP. A simple method of arthrodesis of the first metatarsophalangeal joint. J Bone Joint Surg Br. 1984;66:703-5. 52. Coughlin MJ, Abdo RV. Arthrodesis of the first metatarsophalangeal joint with Vitallium plate fixation. Foot Ankle Int. 1994;15:18-28.

25. Ganley JV, Lynch FR, Darrigan RD. Keller bunionectomy with fascia and tendon graft. J Am Podiatr Med Assoc. 1986;76:602-10.

53. Fitzgerald JAW. A review of long-term results of arthrodesis of the first metatarsophalangeal joint. J Bone Joint Surg Br. 1969;51:488-93.

26. Moberg E. A simple operation for hallux rigidus. Clin Orthop. 1979;142: 55-6.

54. Fitzgerald JA, Wilkinson JM. Arthrodesis of the metatarsophalangeal joint of the great toe. Clin Orthop. 1981;157:70-7.

27. Thomas PJ, Smith RW. Proximal phalanx osteotomy for the surgical treatment of hallux rigidus. Foot Ankle Int. 1999;20:3-12.

55. Gimple K, Amspacher JC, Kopta JA. Metatarsophalangeal joint fusion of the great toe. Orthopedics. 1978;1:462-7.

28. Kessell L, Bonney G. Hallux rigidus in the adolescent. J Bone Joint Surg Br. 1958;40:668-73.

56. Harrison MH, Harvey FJ. Arthrodesis of the first metatarsophalangeal joint for hallux valgus and rigidus. J Bone Joint Surg Am. 1963;45:471-80.

29. Blyth MJ, Mackay DC, Kinninmonth AW. Dorsal wedge osteotomy in the treatment of hallux rigidus. J Foot Ankle Surg. 1998;37:8-10.

57. Johansson JE, Barrington TW. Cone arthrodesis of the first metatarsophalangeal joint. Foot Ankle. 1984;4:244-8.

30. Citron N, Neil M. Dorsal wedge osteotomy of the proximal phalanx for hallux rigidus. Long-term results. J Bone Joint Surg Br. 1987;69:835-7.

58. Marin GA. Arthrodesis of the metatarsophalangeal joint of the big toe for hallux valgus and hallux rigidus. A new method. Int Surg. 1968;50:175-80.

31. Davies-Colley M. Contraction of the metatarso-phalangeal joint of the great toe. Br Med J. 1887;1:728.

59. McKeever DC. Arthrodesis of the first metatarsophalangeal joint for hallux valgus, hallux rigidus, and metatarsus primus varus. J Bone Joint Surg Am. 1952;34:129-34.

32. Youngswick FD. Modifications of the Austin bunionectomy for treatment of metatarsus primus elevatus associated with hallux limitus. J Foot Surg. 1982;21:114-6. 33. Southgate JJ, Urry SR. Hallux rigidus: the long-term results of dorsal wedge osteotomy and arthrodesis in adults. J Foot Ankle Surg. 1997;36: 136-40. 34. Cavolo DJ, Cavallaro DC, Arrington LE. The Watermann osteotomy for hallux limitus. J Am Podiatry Assoc. 1979;69:52-7. 35. Viegas GV. Reconstruction of hallux limitus deformity using a first metatarsal sagittal-Z osteotomy. J Foot Ankle Surg. 1998;37:204-11. 36. Lundeen RO, Rose JM. Sliding oblique osteotomy for the treatment of hallux abducto valgus associated with functional hallux limitus. J Foot Ankle Surg. 2000;39:161-7. 37. Ronconi P, Monachino P, Baleanu PM, Favilli G. Distal oblique osteotomy of the first metatarsal for the correction of hallux limitus and rigidus deformity. J Foot Ankle Surg. 2000;39:154-60. 38. Davies GF. Plantarflexory base wedge osteotomy in the treatment of functional and structural metatarsus primus elevatus. Clin Podiatr Med Surg. 1989;6:93-102. 39. Feldman KA. The Green-Watermann procedure: geometric analysis and preoperative radiographic template technique. J Foot Surg. 1992;31: 182-5. 40. Kissel CG, Mistretta RP, Unroe BJ. Cheilectomy, chondroplasty, and sagittal “Z” osteotomy: a preliminary report on the alternative joint preservation approach to hallux limitus. J Foot Ankle Surg. 1995;34:312-8. 41. Drago JJ, Oloff L, Jacobs AM. A comprehensive review of hallux limitus. J Foot Surg. 1984;23:213-20.

60. Moynihan FJ. Arthrodesis of the metatarso-phalangeal joint of the great toe. J Bone Joint Surg Br. 1967;49:544-51. 61. Riggs SA Jr, Johnson EW Jr. McKeever arthrodesis for the painful hallux. Foot Ankle. 1983;3:248-53. 62. von Salis-Soglio G, Thomas W. Arthrodesis of the metatarsophalangeal joint of the great toe. Arch Orthop Trauma Surg. 1979;95:7-12. 63. Thompson FR, McElvenny RT. Arthrodesis of the first metatarsophalangeal joint. J Bone Joint Surg Am. 1940;22:555-8. 64. Tupman S. Arthrodesis of the first metatarsophalangeal joint. J Bone Joint Surg Br. 1958;40:826. 65. Turan I, Lindgren U. Compression-screw arthrodesis of the first metatarsophalangeal joint of the foot. Clin Orthop. 1987;221:292-5. 66. Wilkinson J. Cone arthrodesis of the first metatarsophalangeal joint. Acta Orthop Scand. 1978;49:627-30. 67. Wilson JN. Cone arthrodesis of the first metatarso-phalangeal joint. J Bone Joint Surg Br. 1967;49:98-101. 68. Wilson CL. A method of fusion of the metatarsophalangeal joint of the great toe. J Bone Joint Surg Am. 1958;40:384-5. 69. Keogh P, Nagaria J, Stephens M. Cheilectomy for hallux rigidus. Ir J Med Sci. 1992;161:681-3. 70. Bonney G, Macnab I. Hallux valgus and hallux rigidus. A critical survey of operative results. J Bone Joint Surg Br. 1952;34:366-85. 71. Hanft JR, Mason ET, Landsman AS, Kashuk KB. A new radiographic classification for hallux limitus. J Foot Ankle Surg. 1993;32:397-404.

42. Albin RK, Weil LS. Flexible implant arthroplasty of the great toe: an evaluation. J Am Podiatry Assoc. 1974;64:967-75.

72. Regnauld B. Disorders of the great toe. In: Elson R, editor. The foot: pathology, aetiology, semiology, clinical investigation and therapy. New York: Springer; 1986. p 269-81, 344-9.

43. Blair MP, Brown LA. Hallux limitus/rigidus deformity: a new great toe implant. J Foot Ankle Surg. 1993;32:257-62.

73. Coughlin M. Arthritides. In: Coughlin MJ, Mann RA, editors. Surgery of the foot and ankle. 7th ed, vol 1. St. Louis: Mosby; 1999. p 605-50.

44. Hanft JR, Merrill T, Marcinko DE, Mendicino R, Gerbert J, Vanore JV. Grand rounds: first metatarsophalangeal joint replacement. J Foot Ankle Surg. 1996; 35:78-85.

74. Selner AJ, Bogdan R, Selner MD, Brunch EK, Mathews RL, Riley J. Tricorrectional osteotomy for the correction of late-stage hallux limitus/rigidus. J Am Podiatr Med Assoc. 1997;87:414-24.

45. LaPorta GA, Pilla P Jr, Richter KP. Keller implant procedure: a report of 536 procedures using a Silastic intramedullary stemmed implant. J Am Podiatry Assoc. 1976;66:126-47.

75. Kitaoka HB, Alexander IJ, Adelaar RS, Nunley JA, Myerson MS, Sanders M. Clinical rating systems for the ankle-hindfoot, midfoot, hallux, and lesser toes. Foot Ankle Int. 1994;15:349-53.

46. Swanson AB, de Groot Swanson G, Maupin BK, Shi SM, Peters JG, Alander

76. Coughlin MJ. Arthrodesis of the first metatarsophalangeal joint with mini-

 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 85-A · N U M B E R 11 · N O VE M B E R 2003

fragment plate fixation. Orthopedics. 1990;13:1037-44. 77. Smith RW, Reynolds JC, Stewart MJ. Hallux valgus assessment: report of research committee of American Orthopaedic Foot and Ankle Society. Foot Ankle. 1984;5:92-103. 78. Coughlin MJ. Rheumatoid forefoot reconstruction. A long-term follow-up study. J Bone Joint Surg Am. 2000;82:322-41. 79. Horton GA, Park YW, Myerson MS. Role of metatarsus primus elevatus in the pathogenesis of hallux rigidus. Foot Ankle Int. 1999;20:777-80. 80. Bryant A, Tinley P, Singer K. A comparison of radiographic measurements in normal, hallux valgus, and hallux limitus feet. J Foot Ankle Surg. 2000;39:39-43. 81. Dananberg HJ. Gait style as an etiology to chronic postural pain. Part I. Functional hallux limitus. J Am Podiatr Med Assoc. 1993;83:433-41. 82. Dananberg HJ. Gait style as an etiology to chronic postural pain. Part II. Postural compensatory process. J Am Podiatr Med Assoc. 1993;83:615-24. 83. DiNapoli D. Gait analysis based on first MTPJ function: the functional hallux

HAL LUX RIG IDUS

limitus concept. In: Reconstructive surgery of the foot and leg update ’93. Tucker, GA: The Podiatry Institute; 1993. p 27-32. 84. Coughlin MJ. Arthrodesis of the first metatarsophalangeal joint. Orthop Rev. 1990;19:177-86. 85. Smith RW, Katchis SD, Ayson LC. Outcomes in hallux rigidus patients treated nonoperatively: a long-term follow-up study. Foot Ankle Int. 2000; 21:906-13. 86. Mann RA, Thompson FM. Arthrodesis of the first metatarsophalangeal joint for hallux valgus in rheumatoid arthritis. J Bone Joint Surg Am. 1984;66:687-92. 87. Mann RA, Schakel ME 2nd. Surgical correction of rheumatoid forefoot deformities. Foot Ankle Int. 1995;16:1-6. 88. Jack EA. The aetiology of hallux rigidus. Br J Surg. 1940;27:492-7. 89. Lambrinudi C. Metatarsus primus elevatus. Proc R Soc Med. 1938;31:1273. 90. Meyer JO, Nishon LR, Weiss L, Docks G. Metatarsus primus elevatus and the etiology of hallux rigidus. J Foot Surg. 1987;26:237-41.

OSTEOTOMY

OF

CALCANEUM

THE

F. C. DWYER, Since

cavus upon

the

publication

in older patients. the late results In children on whether little more deformity

my

earlier

gradual

LIVERPOOL,

paper

the condition than a high progresses

(Dwyer

1955)

of the calcaneum, extended to embrace

is idiopathic arch is well

to embrace

of

Todd

CAVUS

ENGLAND

describing

the

treatment

many more patients have the more severe deformities

the

plantar

or neurological in origin. controlled by a metatarsal

the

following

fascia

characteristics

; 3) clawing

of

the

development of a varus deformity of the heel It should be appreciated that, contrary to some

by

PES

of

pes

been operated encountered

Over five years have now elapsed since the first operation was performed, and indicate that the procedure is sound. pes cavus develops at any time after the age ofthree, the age ofonset depending

2) contracture

out

of

in children by osteotomy and the procedure has been

FOR

(1935),

uncomplicated

pes

contracture cavus;

of the

equinus

is

calcaneal

confined

: 1) dropping

toes

and

of the

callosity

the

is not forefoot,

the

; 4)

and

a usual and

forefoot;

formation

and forefoot. text-book descriptions

tendon to

In the earlier stages what is bar, but in many cases the the

as pointed

accompaniment

of

heel

is usually

(1932),

Todd

well

developed. Operations and for

such

others well

for

the

established

Whatever the

the

becomes calcaneal

the

inner

of

the

plantar

Secondly,

the

80

cavus

cavus

walks

Steindler on

an

1).

two

years

of the

active much

heel

invertor

the

heel, 2).

In

consequence

of

its

the

outer

border

(1921),

Lambrinudi

whole,

proved

after

that,

it is certain

(Fig. on

the

(Fig.

twelve,

adduction

becomes of

aged

etiology, With

fascia

by have,

in adolescents

underlying

border child

described pes

in a patient

worse. tendon

on

of

deformity

Pes

rapidly

as those relief

force

with

the

onset

foot,

of varus,

deforming since

its

thus THE

pull is

deformity

appear.

First

is concentrated thick

pulled

increasing JOURNAL

the

influences to the

forefoot

(1935)

especially

operation.

is transmitted the

of the

a Steindler

three and,

disappointing,

medial

portion

towards the

OF

largely

BONE

varus AND

the

heel.

deformity. JOINT

SURGERY

OSTEOTOMY

heel

in

bearing fails to stretch and contracture results.

Finally,

with

the

that

the

I have

described

these

deforming

heel

into

bearing

to

THE

OPERATION

the

plantar

dropping of the of the calcaneum a

curved

turned

incision

cleared.

and

from

the

longus, This cortex,

tapers

which

complete Pressing

the

against

the

obtain

closure

base

is

below

the

as be

pull

of

to

the up

the

flap of

the

calcaneal

is invariably

eight

to

peroneus (Fig.

the to

3).

ensure gap.

dorsiflexion tendon

due

FIG. 2 With inversion of the heel, weight bearing and the pull of the calcaneal tendon become deforming forces, allowing the plantar fascia to contract with resultant approximation of heel and forefoot.

medial

resulting into

The are

removed

a guide broken

of

forefoot

whole

its

down

must

closure

obvious

tendon

width,

just

is used

the

is exposed. of the bone

in

calcaneum which

wedge

the

with

millimetres

81

divided

the

the

muscle surfaces

A wedge,

twelve

CAVUS

The outer aspect exposed through

until

peroneus longus upper and lower

PES

weight

is

reduce

forefoot. is then

forwards

shifting

fascia

to

FOR

weight

allowing

correction.

subcutaneously

CALCANEUM

at overcoming by

and

THE

plantar fascia The operation

aims

produce

First

varus,

influences

valgus

OF

to

leaving

brings

the

a small

bony

surfaces

piece

of

the

together apex

behind.

nicely. (It

Failure is important

FIG. 3 Technique of operation. A wedge is removed from the lateral aspect of the calcaneum. The osteotomy is made just below the peroneus longus tendon and the posterior tabcalcaneal joint. The medial cortex must be cracked to allow the distal fragment to close easily.

41 B,

VOL.

F

NO.

1,

FEBRUARY

1959

to

82

F. C. DWYER

4

FIG.

Case

l-Pes

cavus

with

early

varus

deformity

complicating

FIG.

Case

1-Three

years

after

operation.

poliomyeitis

in a boy

of five.

5

Foot

virtually

normal THE

JOURNAL

and

toes OF

straight. BONE

AND

JOINT

SURGERY

OSTEOTOMY

OF THE

CALCANEUM

this

stage

CAVUS

83

2-The

to

same

be

is in a neutral

sure

foot

that

or even

a year

the

after

varus

slightly

removal

of a lateral

deformity

valgus

tendons

and

8

FIG.

Case

heel

PES

FIG. 7 of foot in a boy of six, three years after accidental division of both peroneal a year after transplantation of tibialis anterior to base of fourth metatarsal.

Case 2-Deformity

at

FOR

has

wedge

been

from

properly

the calcaneum.

corrected

and

that

the

position.) DISCUSSION

An

early

effect

of the

operation

is that

walking

and

shoe

wear

are

remarkably

improved.

With the varus deformity of the heel corrected, the forefoot gradually follows and the whole foot becomes plantigrade. With certain exceptions that will be mentioned later, relapse is rare and steady improvement takes place provided that the heel has been fully corrected (Figs. 4 to 12). first

The

principle

seen

eight

of the already

underlying

months

tibialis anterior well established, 7).

on the

progressive

VOL.

41 B,

NO.

1,

type

irreparable

of

correction

division

was

of both

to the base of the fourth metatarsal failed to halt the progress of the

age of six (Fig. ground,

this

after

Osteotomy

FEBRUARY

of

the

improvement 1959

calcaneum

took

was

place

well

peroneal

in

tendons.

weight

and,

bearing

a boy

of

three,

Transplantation

two years later, deformity, which

performed,

with

illustrated

with

(Fig.

when varus was was severe at the the

heel

8).

squarely

F. C. DWYER

84

FIG.

Case

3-Recurrent

cavo-varus

Case upon,

3-The same and correction

patient four years after wedge of the clawing has been brought

9

deformity in a boy aged twelve, two years after operation. (Same patient as in Figure 1.)

Failure

to correct

fully

the

varus

Since it was first performed times in forty-one children

three

improvement, clawing

not of the

passage

of

cavus.

In

fasciotomy in

a

for to that

time

that

alone

is indicated.

cases

was an

one

it seems

it

has

not

obtained

may

in some

important encounters

cause such

shoe

striking.

this

wear,

early been

necessary the

instances because recurrence.

first be

to

repeat

was

but

in cases well

real

of

THE

for

muscular

JOURNAL

in

heel,

BONE

pes

a plantar

complete

because The

reason

imbalance

seems

and

bifida

a patient OF

and by the

established

recurrence.

poliomyelitis

illustrated

forefoot

fulfilled

of the

either

of

tendency,

of the

varus

operation

of recurrence

so well

operation no

to recurrence

been undertaken sixtyIn all the patients the

been

other

because

lead

incidence

dropping

has and

the or

primary

it is particularly This

only

high

has now years.

in the

any

arch

operation the

also

inevitably

the

promise

perform

a high

will

operation to sixteen

early

to

with

heel

explains

but

The

unnecessary

at

of the

9), and

in May 1952 this aged from three and

been

presenting

recurrence be

in gait

has

patients few

correction

only

toes,

osteotomy of the calcaneum. The toes were not operated about simply by weight bearing after correction of the heel.

deformity

(Fig.

of a Steindler

10

FIG.

or progress ofthe initial deformity after the older types of operation.

the performance

of AND

spina seven, JOINT

with SURGERY

OSTEOTOMY

OF THE

CALCANEUM

FIG.

Case

4-Severe

deformity

years

marked varus later, a second there was overcome

of the heel osteotomy

Recurrence

after

initial

height

VOL.

Three

heels

the

original

wedge

41 B,

heel the

into and

in one

after at the

operation

because

there

1,

FEBRUARY

1959

with with

multiple

spina

filleting

bifida

operation improving at an

the

who

the varus

was

some

established

arch

the

interval

can

bony

tibialis

suffered

had

arthrodesis

but, even

two after

of

years that,

anterior

infection

to of the

of a sequestrum. not come properly

deformity

which

was corrected

the effect

by

of increasing

deformity. varying

varus

and

was obtained recurred and,

by transplanting

of the calcaneum,

time

repeated

with

sinus cleared up after removal and it was rather small and did

side

same

was

operation

patient

the original

the inner

together

Good correction because varus had

A persistent of the heel

had been too narrow. in older children, with well flattening of the longitudinal

NO.

12

of the heel the toes.

poliomyelitis. necessary

85

CAVUS

II

which was dealt of the evertors.

also

years

wedge

of the

In six

Even

after was

occurred

a bone

appreciable

of the varus

after the operation. then still some varus

to the ground. the

correction

further recurrence, the relative weakness

calcaneum There was inserting

after

PES

of feet in a girl of sixteen.

II.

Case 4-Two

FOR

from

deformity,

probably

deformity

be demonstrated

six to eighteen

of

some

the

time

months because

forefoot,

after

the quite

correction

86 of

F. C. DWYER

the heel

and and

(Figs.

not expect overcomes allows greater

12).

The

degree

to see so much change the important problem

contracture

is present

in the cavus of excessive

it must

the cavus deformity. In adults with a high

toes,

good

from

the heel

forefoot

correction

can

site

to correct

price

to pay

arch,

seen

in Figure

12 is better

element. Nevertheless wear of the outer sides

preservation

be

first

varus

by

and

longer

with

gross

the

fascia

correction is the

heel

means.

appreciated,

than

by a separate

of the

same

the plantar

up to full

It must deal

be dealt

obtained

inversion,

a good

for

be

be brought region.

takes

fixed

can

then

tarso-metatarsal this

of correction

than

average,

which takes place depends on the age at the time of operation In boys, with rather stronger bones than in girls, one does correction of the of the shoes, and

the toes to straighten out if they are malleable. The subjective than the objective because the feet are properly balanced. In patients with pes cavus one seldom encounters real contracture

lfsuch of

1 1 and

the extent offalling ofthe arch on the strength of the bones.

of mid-tarsal-subtalar

with

before

forefoot

and

lateral

is divided.

however, case

and

The to

tendon. correction

clawing

wedge

dropped

of the

is removed

and

an appropriate that

is much

of the calcaneal

operation,

A large

by taking

improvement

heel also

distorted

wedge

from

achieve

sound

fusion

wedge.

This

a mid-tarsal

the at

is a small

movement.

SUMMARY

1 . A new surgical in a subcutaneous

approach division

to the treatment of the contracted

of pes cavus plantar

is suggested. fascia and

The operation correction of

the

consists varus

deformity of the heel by removing a wedge from its lateral aspect. It is submitted that, by approaching the deformity from behind and overcoming the varus of the heel, the foot is rendered plantigrade and that thereafter weight bearing exerts a corrective influence which results in progressive improvement of the deformity. The operation is essentially a prophylactic one and 2.

and, for the while active Even

best results, it should growth is still taking

in patients

than this simple in older patients,

over

the

operation. inversion

age

be performed place.

of fourteen,

improvement

In the presence of fixed is corrected by removing

the cavus advantage movement

by taking a dorsal wedge from of producing good correction at the mid-tarsal-subtalar joint.

corrective plantigrade

treatment, but foot produces

before

there

is gross

is obtained

deformity a lateral

structural

by doing

of the forefoot, wedge from the

deformity nothing

more

as encountered calcaneum and

the tarso-metatarsal region. This has the double of deformity, while at the same time preserving Fixed clawing of the toes will require appropriate

if the toes are malleable gradual correction.

the

simple

effect

of weight

bearing

on

the

REFERENCES DwYER,

F.

orthopCdique, Traumatologie, HALLGRLMSSON,

C.

(1955):

A

New

Approach

to

the

Treatment

of

Pes

Cavus.

Sixi#{232}me Congr#{232}s de

Chirurgie

Berne, 30 ao#{252}t-3septembre 1954. Soci#{233}t#{233} Internationale de Chirurgie Orthop#{233}dique et de p. 551. Bruxelles: Imprimerie Lielens. 5. (1939): Pes Cavus, seine Behandlung und einige Bemerkungen #{252}ber seine Atiobogie. Acta

Orthopaedica

Scandinavica, 10, 73. C. (1932): Use and Abuse of Toes. Post-Graduate Medical Journal, 8, 459. STEINDLER, A. (1921): The Treatment of Pes Cavus (Hollow Claw Foot). Archives of Surgery, 2, 325. TODD, A. H. (1935): The Treatment of Pes Cavus. Proceedings of the Royal Society of Medicine (Section Orthopaedics), 28, 117. LAMBRINUDI,

THE

JOURNAL

OF

BONE

AND

JOINT

SURGERY

of

DEFORMITY

CALCANEO-VALGUS DILLWYN

EVANS,

CARDIFF,

WALES

A discussion of the essential deformity in calcaneo-valgus feet develops a theme originally put forward in 1961 on the relapsed club foot (Evans 1961). Whereas in the normal foot the medial and lateral columns are about equal in length, in talipes equino-varus the lateral column is longer and in calcaneo-valgus shorter than the medial column. The suggestion is that in the treatment of both deformities the length of the columns be made equal. A method is described of treating calcaneo-valgus deformity by inserting cortical bone grafts taken from the tibia to elongate the anterior end of the calcaneus.

The

material

made in the put forward 1961). correct

in this

In that article I described club foot in the older

concept

that

one

element

relative

overgrowth

of

and

I suggested

that

necessary deliberately bone from the lateral cuboid amount resulted

Figure

article

arises

out

of

joint. It of bone

an operation child. It was

in the the in

deformity

lateral the

older

child

270

foot

of

the

it

might

is

foot, be

to equalise the columns by excising column at the level of the calcaneowas important because removal

in under-correction

of

the

to

excise of too

the correct little bone

deformity,

whereas

foot

showing joint. deformity

been

of too

much

bone

produced

a short

foot with a convex medial border. The features of such a case are shown in Figures

could on the

of club

column

removal

a theme (Evans

which based

1-A radiograph of the original relapsed club 2-After wedge resection of the calcaneo-cuboid over-corrected. The clinical effect is a rigid valgus talo-navicular relationship has

Figure

a mistake

treatment of club foot and develops in a previous article in this Journal

restored

suggested

that

if this

shape

had

been

sive shortening of the lateral column, to improve the shape by lengthening by the insertion of a bone graft. arthrodesis

was

cuboid bones with cortical The illuminating

prised taken

result was because

assumptions

the medial Too much of the foot.

therefore

were bone

: first,

displacement

bone

gratifying it seemed that

of the navicular removed and 3-After lengthening

shape THE

produced

the

and

the

by exces-

calcaneus gap

and the to justify

varus

valgus

it should be possible the lateral column The calcaneo-cuboid

apart and the from the tibia.

has been

Figure

and the clinical

undone,

rigid

radiological 1 to 3. Logic

valgus

was

and plugged

experience was two theoretical are

opposite

bone on the head of the talus. talo-navicular dislocation is the calcaneus. The normal

of the foot is satisfactory. JOURNAL

OF

BONE

AND

JOINT

SURGERY

CALCANEO-VALGUS

271

DEFORMITY

Fio. 8 The operation. position. This

Figure instrument,

4-The

of the instrument. VOL.

57-B,

No.

3, AUGUST

Fio.

incision. Figure 5-The which has proved invaluable,

1975

Figure

8-Three

exposure. is described

grafts

Figure in the

in position.

6-The text.

Figure

calcaneus has Figure 7-Insertion

9-The

wound

9

divided and the “spreader” is in of the first graft between the blades is usually closed easily. been

272

D.

deformities two

; and,

in terms

second,

of tarsal

that

the

structure

difference

lay in the

between relative

the

lengths

of the two columns of the foot. A long lateral column was associated with varus deformity of the tarsus, including a varus heel and possibly also equinus, whereas a short

lateral

column

was

of the tarsus, including calcaneus deformity.

associated

with

a valgus

heel

valgus and

If these assumptions are sound it should to improve other calcaneo-valgus deformities ing the lateral border ofthe foot; but at what it be lengthened

?

Experience

.a

had

shown

deformity

possibly

also

be possible by lengthenlevel should that

the

only

EVANS

point at shortened because

which the lateral in club foot was of the

need

to pull

column could be at the calcaneo-cuboid the

navicular

bone

effectively joint, laterally

relation to the talus. It was obviously desirable, however, to preserve the calcaneo-cuboid joint, and it seemed reasonable to think that if the calcaneus itself in

could be lengthened near its anterior end this might have the effect of pushing the navicular bone medially and so straightening the foot. It was reasonable, therefore, to do an osteotomy of the anterior end of the calcaneus about 1 .5 centimetres and in a plane parallel

behind the calcaneo-cuboid with that joint. The two

joint parts

of

12

A boy, born in November 1949, developed anterior poliomyelitis at the age of I 5 months which caused a calcaneo-valgus deformity of the left foot. This deformity, which was passively correctable, was treated by talo-navicular arthrodesis in the hope that this would hold the foot in the corrected position. It failed to do so. In July 1959, when he was 10, the left calcaneus was elongated. It was found that this corrected the deformity but only after the talo-navicular arthrodesis had been undone to free the midtarsal joint. Figures 10 and I 1 show the clinical appearance before and after the operation and Figures 12 and 13 show the radiographs before and after the lengthening

of the calcaneus. THE

JOURNAL

OF

BONE

AND

JOINT

SURGERY

CALCANEO-VALGUS

the

calcaneus

lateral

could

column, The

first

case

a calcaneo-valgus -in a foot that

was

the

be forced gap

chosen

could for

apart

to lengthen

be plugged

this

that what practice. pushed

had As

was

the

valgus

foot,

bone. that

part

deviation

A boy

sustained valgus

secondary

a cut over and planus

the inner deformity

appearance VOL

57-B,

No.

3, AUGUST

before 1975

and types

of

An incision parallel ing the The

it seemed of valgus

and after operation,

indications

describe

the

and

contra-

operation.

anterior joint

caneus

is then

of

peroneal

the

elongated

and Figures

but the practical valgus deformity. in Figures 4 to 9.

is made over thelateralsurface

with, sural

cuboid

age of 6 which was

OPERATION

The operation is constant in principle details vary with the aetiology of the The constant factors are shown

varus more

side of the left foot at the ofthe foot. The calcaneus

discussing

I shall

THE

in theory of the

heel took up a more at the ankle became

clinical result was encouraging to apply the operation to other

before

of

restricted. it was apparent as this was happening that if the calcaneus were lengthened enough the equinovarus deformity of club foot would be produced. The justifiable

but

indications,

poliomyelitis arthrodesis-

been anticipated the anterior

forward,

the forefoot disappeared, the position and passive extension

the

with

operation

deformity resulting from had been selected for triple

and it was found came about in calcaneus

then

and

273

DEFORMITY

divided at the

andjust nerve half

of the bone

is identified. divided

through

the tendon of 15 years.

16 and 17 the corresponding

is exposed The

tubercle

age

ofthe

calcaneus

above, the peroneal tendons, avoidlest it become involved in the scar.

by

and

anterior its narrow

an

of tibialis

osteotome,

end

the calcaneoof the part the

cal-

in front line

of

posterior. He developed 14 and 15 show the clinical radiographs. Figures

a

274

D.

division

being

behind

the

parallel

the calcaneus and a graft inserted

with

and

calcaneo-cuboid

about

joint.

the

blades

of the

CLINICAL

1 .5 centimetres

The

cut

are then prised apart by means of cortical bone taken from

between

EVANS

surfaces

The

of a spreader the tibia is

spreader

the

calcaneus

to be prised

or holding,

graft

apart

but

to be inserted

to maintain

they

also

before

allow

operation

was

first

found to be ofvalue in valgus deformity

done

radiograph

the

that

the instrument

of

the

talus

the

foot

points

in the

girl born in 1949 developed anterior poliomyelitis at the age of in 1956. She was first seen in 1961 and found to have 25 centimetres of shortening in the left leg, weakness throughout the limb, valgus pronation

of the

left

foot

and

1959

and

much

weakness

standing

in a medial

A

and

in

it has

been

as an alternative to triple arthrodesis from four causes-over-corrected

talipes equino-varus, calcaneo-valgus following poliomyelitis, rigid flat foot, and gross idiopathic calcaneo-valgus. These deformities all show a radiological feature which indicates a need for the operation ; an antero-posterior

separation of the two pieces of the calcaneus. The spreader* that I use (Fig. 6) was designed for this purpose by Mr Q. S. Otto, now of Johannesburg; its blades are so arranged that they not only enable the cut surfaces of first,

MATERIAL

of

of tibialis

position

direction

and

shows that

the

7

anterior

and posterior muscles. The extensors of the toes were strong and there was “dropping” of the forepart of the foot. In May 1961 the calcaneus was elongated. This produced an equinus deformity (despite

the

fact

that

extension

was

possible

to

10 degrees

above

the right angle before the operation) and the calcaneal tendon was therefore elongated. The long extensor tendon of the great toe was transferred into the neck of the first metatarsal bone to improve the “dropping”

of the

forefoot.

operation, is withdrawn. Inspection of the reveal that the forepart of the foot that

the

heel

the ankle:has and further graft

has

moved

into

varus

become less free. grafts are inserted

to ensure

remain apart. the same side.

that

the

two

foot has

cut

at this become

and

The above

that

Figure

and Figure

stage will adducted,

extension

of

spreader is removed and below the first

surfaces

of the calcaneus

All grafts are obtained from the tibia of The wound is then closed and the foot

immobilised comfortably in plaster in a position of slight equino-varus. The plaster is retained for about four months to allow consolidation of the new calcaneus, but weight-bearing is needed

when

is allowed

at four

the

is removed.

plaster

weeks.

No

after-care

1 8 shows the 19 afterwards.

Obtainable

from

Messrs

before

navicular bone is displaced laterally head of the talus-that is, the reverse of club

in relation to the of the deformity

foot.

The operation operations

were

twenty-five

for

infancy

(Figs.

eighteen

for

has been done over-corrected

for

deformities

(Figs. 10 to 13 and traumatic division

resulting

18 and 19), two of the tendon

14 to idiopathic

on fifty-six feet. Four talipes equino-varus,

17),

nine

valgus

from

Downs

of the Surgical THE

ankle

and

for

rigid

(Figs.

that

poliomyelitis

for deformity following of tibialis posterior in flat

20 to 29)

one case of Marfan’s syndrome (Figs. been found (Figs. 18 to 25) that the extension

*

appearance

foot,

30 to 33). It has operation restricts

it reduces

the

range

Ltd. JOURNAL

OF

BONE

AND

and

including

JOINT

SURGERY

of

CALCANEO-VALGUS

A boy abductus operation

VOL.

presented type and

57-B,

No.

at the and the the range

age of 15 because of pain in the calves of both legs after activity. His feet were found to be calcaneal lengthening was done on both feet. Figures 20 and 21 show the clinical appearance of movement before and after this is shown in Figures 22 and 23, from which it is seen that there of dorsifiexion. Figures 24 and 25 are the radiographs before and after operation.

3, AUGUST

1975

275

DEFORMITY

of the plano-valgusbefore has

been

and

after

restriction

276

D.

side-to-side

movements

sive eversion. been

damage

scar

and

the

An

to the sural

sensory

foot and

nerve,

impairment

by eliminating unnecessary,

which

exceserror

produces

along

the

lateral

has

18 and and

poliomyelitis

ideal

age

for

but

the

operation

19)-The

twelve

if the done

from years,

severity of the deformity early in life, or if the

operation

may

of eight and twelve. with severe deformity

have

correction

13 and eight

be done

earlier

necessary. If is very severe,

between

may attempt,

the

ages

not be possible but it should

to obtain full correction or three years later.

Experience of

is between this

to be repeated

I._.

10 to

can

makes deformity

Full correction at the first

A child of 12 had idiopathic were restricted. The parents calcaneal lengthening and

(Figs.

be possible done two

a painful border

foot.

Calcaneo-valgus

the

in the

occasional,

EVANS

correct

has

valgus

shown

deformity

it is not

operation

possible

aetiology.

to over-

On the contrary,

adequate correction may be difficult because sufficient separation of the divided parts of the calcaneus may not be possible without dividing all the soft tissues on the lateral side of the foot, including the peroneal tendons. When the

this

has been

limiting

Rigid flat adolescence it tends

done,

difficulty

in skin

closure

becomes

factor. foot-These ; the foot to

resist

cases is rigid

correction

tend and, ; the

to present in early as in paralytic cases, soft

tissues

have

to

be

1-._. 29

__

calcaneo-valgus were concerned the radiograph

that

ofthis

at a second

feet, with

no symptoms but the muscles were weak and the movements of inversion and eversion about the shape of the feet. Figures 26 and 27 show the clinical appearance before and after before operation is shown in Figure 28 and another, taken ten years afterwards, in Figure 29. THE

JOURNAL

OF

BONE

AND

JOINT

SURGERY

CALCANEO-VALGUS

divided and over-correction tion has succeeded in feet bar

has

improved pain

been

present.

but

and

Severe

the

is not in which

The most

a subjective

feeling

idiopathic

shape

gratifying

valgus

of the

foot

features

of freedom (Figs. 20 to

within 33)-Here

relief the

of foot. it is

between simple mild valgus which and severe valgus which is clearly

abnormal.

is necessary

only

when

is severe and the foot is obviously abnormal, valgus of the heel and of the forefoot and bulging cular

medial in

border;

relation

to

lateral the

head

deformity

with marked with a convex

displacement

of

of

will

the

talus

present until to know that

is slightly

are

necessary to distinguish is a variant of normal, Correction

in radiographs

possible. The operaa calcaneo-navicular

the be

naviseen

277

DEFORMITY

too

easy

taken

to produce

group the calcaneus necessary to produce not bedivided

standing.

about the age over-correction

and

an

Such

cases

do not

equinovarus

deformity.

57-B,

No.

3, AUGUST

1975

In

this

should be lengthened only as far as is a normal shape ; the soft tissues must the peroneal

tendons

must

not be injured.

Conditions in which the operation is confra-indicatedThe operation is inappropriate for neurological disorders including spasticity in children and spina bifida. Overcorrection is too prevalent spina bifida the calcaneus and

the

grafts

tend

to sink

in spastic is too soft into

the

disorders, and to allow correction

in

bone.

A boy, born in February 1957, presented in June 1961. He had Marfan’s syndrome, with long feet, plano-valgus in shape, and There was also valgus deviation and pronation at the midtarsal joints with a valgus deformity of the heels on weight-bearing. the talus was prominent on the medial side ofeach foot. The left calcaneus was elongated in June 1961 and the right calcaneus The wound on the right foot failed to heal by first intention and a skin-graft was necessary. Figures 30 and 31 show the clinical and Figures 32 and 33 the radiographs, also before and after calcaneal lengthening. VOL.

usually

of eight, and it is important is possible and that it is all

hypermobile. The head of in June 1962. appearance,

278

D.

EVANS

DISCUSSION The operation has means of averting theoretical

proved triple

to be of practical arthrodesis but

implications

which

are

of some

cause it throws some light on the nature of some deformities of the tarsus. Three drawn

from Firstly,

valgus

opposites.

Some

a short

calcaneal

not

necessarily

article suggest may produce without structures

such

tendon

so ; the

produced

reduce

to

opposite

and

because

of this

experiences

may

said

because experience the calcaneal tendon

equinus.

This,

this

or to the calf possible that

: one produced structures, and

by deformity be

in

of tarsal relationships on the operating table

of equinus of the calf

primarily

belief,

recorded

of course,

by

of the some

is true

but

tarsus,

that

has shown in a baby’s

not and

true lost

at an early and plastic.

in the older child when much of their plasticity.

fact that it is possible the equinus deformity) I wish to thank Miss Orthopaedic Hospital

secretarial

it

is

that tranfoot will

it is true

age when the tarsal It is demonstrably

the bones have ossified This, combined with the

and Mr C. contribution

M.

the

medial

be a more

as the cavo-varus

foot

(1959).

by Dwyer

more likely of deformity abnormality

column

the shape of the It plays no part

treated

so well

doubtful primary

if the factor

complex

has

described

and

lateral column in producing

back body

its structure-the from this study

equino-varus

and

(twenty-five

Walker of the Departments to this article and Miss L.

M.

and

(two (nine

by old cases), cases),

idiopathic calcaneo-valgus value in spastic disorders to over-correct of spina bifida too

the of

It appears foot is the

calcaneo-valgus.

cases),

tendon of tibialis posterior flat foot in young people

soft

it has to take the foundation

has been successful in over-corrected (four cases), calcaneo-valgus caused

by poliomyelitis

tendency in cases

to feel that arthrohold it there, only so (Figs. 10 to 13);

into valgus when and this is because

operation equino-varus

disabling is of no

of the foot a deformity;

lateral column-is unsound. that the lateral column of the

to structural

talipes

so effectively

to a good shape until by equalising the to twist a weakened,

paralytic foot into a good shape and desis of the talo-navicular joint should to find in practice that it does not do

The

enormous

But whatever its origin, once developed-and it is betrayed of the talus and navicular

bones--the foot cannot be restored the inequality has been eliminated columns. It is possible, sometimes,

key

an

foot, even if it is not the in some deformities, such

is it a secondary, or adaptive, consequence initiated by other factors such as congenital or the forces of muscle imbalance acting on

a plastic growing skeleton. this factor of inequality has radiologically by relationship

only

to produce a club foot (including simply by over-lengthening the

B. Wales for their

of

the foot falls weight of the

under certain conditions ; these are, first, that the tarsal deformity is corrected by other means such as by manipulation or by division of other tight structures, and second, that the operation is done bones are still cartilaginous

length

It is also is in fact the

in a club however,

that equinus may appeared to be.

Thirdly, the lateral column is the foundation of the skeletal structure of the foot. It is the base on which the foot stands. It does not vary much in shape but it varies in length, and the length of this column relative to

calcaneo-valgus

being done to the ankle 18 to 25). It is therefore

as in club foot. Against this it

unacceptable section of

the

but I have found of the evidence,

many that this is produced of the calf muscles. This,

there may be two kinds primarily by contracture another

that

talus, most

that rearrangement immediate equinus

anything (Figs.

calcaneus suggests subject than it has

influence on only factor.

in regard to an equinus deformity, it has that it is a deformity at the ankle produced

it is accepted by foot by contracture is

be-

and calcaneo-

believe

and experimental, points opposite of equino-varus.

Secondly, assumed

been by

the

interest,

and structure conclusions are

of equino-varus

of club foot is congenital vertical little to support this view, and theoretical as being

as a has

the

this study. the deformities

are

value it also

injury

in painful and in

(eighteen (in which

to the rigid severe

cases). there

It is a

and so produce equino-varus) in which the bones of the foot

or are

yielding.

of Radiology and Clinical Photography Thomas, Miss M. A. Angove and Miss

at the Prince H. R. Taylor

of Wales for their

help. REFERENCES

Dwyer, Evans,

F. C. (1959) D.

(1961)

Osteotomy

Relapsed

of the club

foot.

calcaneum

Journal

for

ofBone

pes

cavus.

andJoint

Journal Surgery,

ofBone 43-B,

and Joint

Surgery,

41-B,

80-86.

722-733.

THE

JOURNAL

OF

BONE

AND

JOINT

SURGERY

INJURIES

TO

THE

INCIDENCE,

CLASSIFICATION

P. H. HARDCASTLE,

From

TARSOMETATARSAL

R. RESCHAUER,

the Department

AND

TREATMENT

E. KUTSCHA-LISSBERG,

ofAccident

Surgery,

JOINT

W. SCHOFFMANN

Landeskrankenhaus,

Graz,

Austria

Injuries to the tarsometatarsal (Lisfranc) joint are not common, and the results of treatment are often unsatisfactory. Since no individual is likely to see many such injuries, we decided to make a retrospective study of patients from five different centres. In this way 119 patients with injuries of the Lisfranc joint have been collected. This paper classifies these injuries and describes their incidence, mechanism of production, methods of treatment, results and complications. Sixty-nine of the patients attended for review: 35 of these had been treated by closed methods, 27 had had an open reduction and seven patients had had no treatment. On the basis ofour study we suggest that these injuries should be classified according to the type of injury rather than the nature of the deforming force and that their treatment be based upon this classification. It seems that, whatever the severity of the initial injury, prognosis depends on accurate reduction and its maintenance. The tarsometatarsal joint, at which the bases of the five metatarsals articulate with the three cuneiforms and the cuboid, was named after Lisfranc a French surgeon serving in the Napoleonic Army, who described amputation through that joint (Cassebaum 1963). Dislocation and fracture-dislocation are both rare and are said to occur at the rate of one person per 55 000 per year (Aitken and Poulson 1963 ; English 1964). They result from direct or indirect forces (Rainaut, Cedard and d’Hour 1966) acting on or through the Lisfrancjoint. Although the anatomy and the various mechanisms of the injury have been well described (Gissane 1951; Aitken and Poulson 1963; Jeffreys 1963; Wiley 1971; Bonnel and Barth#{233}l#{233}my 1976), there is considerable difference of opinion regarding classification and treatment (BOhler 1958; Granberry and Lipscomb 1962; Wilppula 1973 ; Engelhardt and Ganz 1 975). The purpose of this present study was to try to clarify both. .

.

.

TYPE

QO’3

A

TOTAL

.

tAT

P. H. Hardcastle, MD, Hollywood Orthopaedic E. Kutscha-Lissberg, Unfailabteilung

A.O.

FRCS

Ed, FRACS,

R. Reschauer, MD, Dozent W. Schoffmann, MD Landeskrankenhaus, Auenbruggerplatz,

©

1982

VOL.

British

64-B.

Editorial

No. 3, 1982

Senior

Service, Sir Charles MD, Dozent Krankenhaus, A-2620,

Society

Graz ofBone

and

Orthopaedic

Gairdner

8036, Joint

tAT.

MED

TYPE

B

Li

INCONGRUITY

PARTIAL

Medal

dislocation

Lateral

dislocation

J

%“IIil

TYPE C DIVERGENT

“UM’

Total

Partial

displacement

Fig Classification

of

Lisfranc

injuries

displacement

I (modified

from

Qu#{233}nu and

KOss

1909).

Registrar

Hospital,

Neunkirchen,

MED

#{231}\

CLASSIFICATION Previous classifications have been based on the mechanisms ofinjury (Francesconi 1925; Jeffreys 1963; Wilson 1972; Bonnel and Barth#{233}l#{233}my 1976). These mechanisms are complex and varied. Direct forces may crush the metatarsals displacing them plantarwards, with secondary medial or lateral displacement, depending on the nature of the applied force. With indirect rotational

C

INCONGRUITY

Nedlands,

Perth,

Western

Australia.

Austria.

Austria. Surgery

030l-620X/82/3065-0349

$2.00

349

350

P. H. HARDCASTLE,

R. RESCHAUER,

E. KUTSCHA-LISSBERG,

forces the foot must be in plantarfiexion for dislocation to occur (Wiley 197 1 The dorsal aspect of the Lisfranc joint is unable to resist tensile forces of any magnitude, in contrast to the much stronger soft-tissue support on the plantar aspect. Forces applied to the plantarfiexed foot may be angular or rotational; since they are applied at a point distant from the joint they are collectively called indirect forces.

W.

SCHOFFMANN

affects one or more of the lateral first metatarsal is not affected.

).

Type

four metatarsals

but the

There may be partial On an anteroposterior radiograph is seen to be displaced medially, of the lateral four metatarsals laterally. Sagittal displacement with the coronal displacement.

C.

or total the first while any may be occurs in

Divergent.

incongruity. metatarsal combination displaced conjunction

Number of patients 42

35

40

. .

I

20

10

2

I I

Ml-4

No

fracture

Fracture

of the of one

44

2

M2-5

M2

toot

or more

Fracture of cuneitorms. talus and or caicaneus

II

3

I

M3-5

M4-5

MS

2

2

42

(1-2

M : metatarsal C: cuneiform

metatarsals cuboid.

navicular

Fig. Concomitant

injuries

involving

the

2 foot

Such classifications give information regarding the nature of the deforming force but their value is limited since they do not provide information which would influence treatment. Our study shows that treatment and prognosis depend not so much on the direction of the causal force as upon whether there is incongruity (partial or total) of the tarsometatarsal joint. The classification described by Qu#{233}nuand K#{252}ss (1909) has the virtue of being simple to apply. It divides the injuries into three groups (homolateral, isolated and divergent) but does not include every variety of displacement. Their classification forms the basis for the one we now present (Fig. 1), upon which treatment can be based. Type A Total. There is incongruity of the entire tarsometatarsaljoint. Displacement is in one plane which may be sagittal, coronal or combined. Type B : Partia!. There is incongruity of part of the joint. Again the displaced segment is in one plane which may be sagittal, coronal or combined. Partial injuries are of two kinds whose treatment and prognosis differ : medial displacement affects the first metatarsal either in isolation or combined with displacement of one or more of the second, third or fourth metatarsals ; lateral displacement

in 1 19 cases

For

this

of the

Accident

Salzburg,

injury.

MATERIAL AND METHODS study the notes and radiographs

retrospective

injuries

the

of Lisfranc

tarsometatarsal

joint

Departments

at Graz,

were

reviewed.

There

documentation and radiographs; between 18 months and I 2 years injuries each

was

approximately

year. There

were injuries

accidents,

10 occurred

twisting

injury

tarsal

dislocated assess

that

in those

plantar

patients

or

who

were

have

shown

were

not available. The

by using

skeletal

fixation

was

reduction

was

achieved.

In

care

was

and

used

at

all

the where

the

THE

there

five

primary

JOURNAL

was

object

tarsometa-

of the

same

foot.

that

were

and centres general

clinically closed

an

associated

a

it possible

in

Percutaneous

congruent was

to the

many

radiographs,

under

reduction when

a height,

was

accurately. Bonnel

traffic

from

bones.

upon

oblique

of 39 years.

segments

of other

(B#{246}hler 1958).

if

parts

different

operated

upon,

treatment

14 cases

considered

were

population

age

a fall

in other

by manipulation

performed

in

and

adequate

48 to road

In addition

(B#{246}hler 1958;

traction

a mean

fractures

operated

of the

accidents,

displacement

either

1978

Linz

with

60 000

with

of the

who

dorsal not

per

fractures

of concomitant patients

patients

with

and

Vienna.

16 involved

incidence

initial

reduction

person

accident.

often

the

displacement

Treatment. closed

were

1 19

to industrial

at sport

both

and

Only

.

there

2 shows

Kiagenfurt,

33 women

due

1965

of these, 69 attended for review, after the injury. The incidence of these

or a household

injury,

Figure

and

were

of patients

between

were

one

86 men

Forty-five

treated

to

of

which

could

Barth#{233}l#{233}my 1976) was

to attempt

anaesthesia,

or

Kirschner

wire

unstable.

Open

reduction

was

not

open

wound

its

of treatment.

OF BONE

AND

the

JOINT

SURGERY

INJURIES Table

I. Treatment

and

TO THE

TARSOMETATARSAL

weeks

results

after

worn few

Results

for

injury. three

wore

the

Assessment. Type of injury A.

Treatment

Total

Closed Operative

Good

Fair

9 6

I 3

reduction

Poor

residual

‘Good”

Partial Medial

Lateral

C.

Closed Operative

Divergent

Closed Operative

4

-

reduction

2

3

-

4

reduction

10 4

We

stand

patient results.

above-knee

with

amputation

has

was

liked

then

surgical

fitted

and

shoes,

but

as good,

gait,

deformity

that

symptoms

fair

or

poor

and

were

trivial

on

the

basis

radiological or

of

features.

tip-toe, showed pain

of the and

a at

on

normal most

gait,

absent,

the

patient

to walk,

radiographic

standing

shape,

of degeneration.

and

slight

“Poor” inability

deformity,

implied to stand

evidence

and

degeneration.

difficulty

good

ability

no

minimal

activity,

reasonably

evidence

affected

had

of

on

moderate

a

“Fair” on

tip-toe,

to

moderate

a

marked

pain

tip-toe,

limp,

to

severe

degeneration.

I

been

results

on

foot

deformity,

-

I

not

a

which

Obviously

-

these The these

graded

which

radiographic

-

I

shoe

patients

function,

moderate

limp,

2

-

-

or surgical

Most

supports.

implied

could

3

14

reduction

support

months.

-

implied Closed Operative

An arch

to six

pain,

radiograph B.

351

JOINT

included

in

the end

features, relationship

not

all patients

so an overall between

were

in the

assessment our

same

was

classification,

group

used. the

Table

treatment

for every

one

of

I summarises used

and

the

result.

RESULTS Of

the

I 19 patients,

43 required weeks after The whether

subsequent

anteriorly,

was

was

knee

walking

used,

progressive

applied

cast

Fig. difficult

to define

VOL.

64-B.

or open

was

and

3 and 8-

was

by closed the

4

any

applied.

was

3. 1982

Kirschner

most

methods.

successful

in 69;

allowed wires

whether

instances weeks

fixation prevented

were

removed

displacement

and 9 and

lateral 10-Three

lateral

views

open

a below-

had

been

by other six

to eight

A: Total (22 patients). There were 15 good, four fair and three poor results in this group. In one case where reduction was held in a plastercast without any Kirschner wires, redisplacement occurred (Figs 3 to 10). In eight patients closed reduction was held with percutaneous Kirschner wires, and all obtained good results. Open reduction was performed in 12 patients ; three had fair

Type

8

lateral displacement found at operation. 5 and 6-Redisplacement is evident demonstrating the ideal positioning of the two Kirschner after injury milddegenerative changes are seen in the entire

is plantar

radiographs years

same,

cast,

later

unless

Fig. the

the

internal

7 and

2 to 12

A plaster

Two

Where was

-Anteroposterior

Anteroposterior Figures

No.

in

leg elevated.

weight-bearing

The

and

reduction

management and

plaster

Figures

7

closed

open reduction (which, in 16 cases was performed injury); and seven patients were left untreated.

reduction

injuries.

primary

of Type

or dorsal.

A with

Figures

With only these views it is on the films in plaster. Figures wires with Type A injuries. Lisfranc joint.

352

P. H.

HARDCASTLE,

R. RESCHAUER,

and three had poor results. One patient with a fair result had redisplaced after closed reduction and plaster; open reduction was not performed until three months after injury. A second patient with a fair result had a total medial and dorsal displacement with open fractures of the cuboid bone; his postoperative course was complicated by sepsis. The third patient with a fair result had dorsolateral displacement with fractures of the second, third and fourth metatarsals which were reduced, but only a single Kirschner wire was used for stabilisation; at review he had a cavus deformity with associated pain in the Lisfranc joint and a limp. Two of the poor results in this group were in patients who required early amputation of the forefoot for ischaemia. The third patient with a poor result had a total dislocation medially, with associated fractures of the navicular and medial cuneiform. Redislocation occurred in plaster following the initial closed reduction and a second reduction was performed two weeks later; although this was anatomically accurate and was held with percutaneous Kirschner wires, he developed severe degenerative changes. Comment. In this type of injury, forefoot ischaemia and

E. KUTSCHA-LISSBERG,

W.

SCHOFFMANN

redisplacement

after closed reduction without fixation causes of unsatisfactory results. Type B: Partial (43 patients). There were 30 good, 1 1 fair and two poor results. There was little difference between those treated by closed and those treated by open methods ; nor did the direction of displacement (plantar or dorsal) affect the results. When the first metatarsal was openly reduced two patients had a good result and three fair. Two patients with fair results were men aged 48 in whom delayed open reduction and Kirschner wire fixation had been performed two and eight weeks respectively after the injury (Figs 1 1 to 16 ; 17 to 22) ; both soon redisplaced with consequent pain, mild deformity and severe osteoarthritis. The other patient had open reduction and stabilisation with a single Kirschner wire as a primary procedure ; however, at follow-up redisplacement was evident. Two patients with fair results had had a closed reduction held with a single percutaneous Kirschner wire; at follow-up there was clinical evidence of deformity, though when redislocation occurred is unknown. The two poor results, when only a single metatarsal was displaced (Type B lateral injuries), were treated by are the main

Figures I 1 and I 2-Type B. There the first three metatarsals. The cuneiforms was due to interposition Note the large articular fragment

Figures anteroposterior held with

13

and

14-Open

is medial displacement involving diastasis between the first two of the tibialis anterior tendon. from the first metatarsal (L).

reduction

was

and lateral radiographs show Kirschner wires. Figures 15 and result is fair, with mild degenerative

THE

JOURNAL

OF BONE

necessary

and

the

satisfactory alignment 16-At five years the changes.

AND

JOINT

SURGERY

INJURIES

TO THE

TARSOMETATARSAL

closed reduction and plaster. At review dorsal angulation was apparent at the fracture site and was associated with metatarsalgia. Comment. Redisplacement in the lateral group resulted from failure to use Kirschner wire stabilisers. Displace-

353

JOINT

ment, with or without fracture of the first metatarsal, is an unstable injury and redisplacement occurred unless more than one stabilising wire was used (Figs 23 to 27). Type C: Divergent (three patients). Only three patients with this rare injury were reviewed. One had a good

Fig.

19

Fig.

20

Figures 17 and 18 Type B. This patient had medial and plantar displacement of the first metatarsal. Note the concomitant fractures of the metatarsal shafts. Figures 19 and 20- Open reduction was necessary because of inadequate closed reduction, and was stabilised with Kirschner wires. Figures 21 and 22-Anteroposterior and lateral radiographs four years later show mild degenerative changes localised

to

the

metatarsocuneiform

fractures

of the

joint,

metatarsal

with

malunion

of

the

shafts.

I,

Fig.

23

Fig.

24

Fig.

I

Fig.

25

Fig.

26

27

Figures 23 and 24-Type B showing dislocation of the lateral three metatarsals. The second metatarsal has not been displaced although this was an indirect rotational injury. Figures 25 and 26-Position of the percutaneous Kirschner wires following adequate reduction by closed methods. Figure 27-Lateral photograph of the same foot showing the deformity which may result ifdorsal displacement recurs.

VOL.

64-B.

No. 3. 1982

354

P. H. HARDCASTLE,

R. RESCHAUER,

E. KUTSCHA-LISSBERG,

W.

SCHOFFMANN

Figures 28 and 29-Type C. This injury There is medial displacement of the displacement of the second and third. reduction was necessary. Good alignment internal fixation. Figures 32 and 33-Four the foot is good and degenerative

Fig.

34

Figure 34-Type C. Direct joints are also seen. Figure months later a “fair” result

Fig.

35

Fig.

was due to an indirect force. first metatarsal and lateral Figures 30 and 31 Open was obtained and held by years later the alignment of changes only mild.

36

Fig.

injury (open). The first metatarsal was carried in by the patient. Concomitant injuries to the 35-After open reduction with osteosynthesis; a delayed split-skin graft was performed. Figures has been achieved with revascularisation of the first metatarsal. The deformity of the four lateral from inadequate reduction and stabilisation at the time of operation.

THE

JOURNAL

OF BONE

37

metatarsophalangeal 36 and 37Eighteen metatarsals resulted

AND

JOINT

SURGERY

INJURIES

TO

THE

TARSOMETATARSAL

the initial closed reduction was inadequate and open reduction was performed two weeks after injury, when the swelling had subsided (Figs 28 to 33). The patient with a fair result (Figs 34 to 37) had a severe open crushing injury with complete devascularisation of the first metatarsal, which the patient brought into hospital; open reduction, reimplantation and osteosynthesis with a small AO plate was performed. His postoperative course was uncomplicated but he developed a painful valgus deformity of the hallux. His final outcome is unknown as he was seen only a few weeks after an operation to correct the hallux valgus. The third patient had a poor result. Closed reduction failed, but, at operation, there was marked comminution involving the Lisfranc joint and an adequate reduction was not obtained, so this injury was treated without fixation. result

;

DISCUSSION Since the time of Lisfranc, the causes of injury to the tarsometatarsal joint have changed ; road accidents and industrial injuries are now the commonest. The most common segmental displacement in our series was one involving only the first metatarsal and resulting from a direct crushing force or an indirect pronation force acting on a fixed forefoot in equinus. This contrasts with previous reports where either dorsolateral displacement of all five metatarsals (Aitken and Poulson 1963; Cassebaum 1963 ; Wilson 1972), or of the four lateral metatarsals (Wilppula 1973) were the commonest injuries. Radiographs

in three

planes

(anteroposterior,

lateral

JOINT

355

redisplacement was diagnosed nine days after the initial closed reduction, was successfully treated by a further closed reduction and percutaneous wires. In these five cases, redisplacement had occurred before the patients had been allowed to take weight. A further five patients with clinical and radiological evidence of redisplacement were seen, but it was not possible to ascertain when this had occurred. When Kirschner wires had been used to stabilise the reduction, redisplacement occurred only in Type B medial injuries where the first metatarsal was displaced (at least three cases) and in Type C injuries (two cases); in all these, only a single wire had been used to stabilise the medial segment. Kirschner wires are undoubtedly valuable as stabilisers. In their absence redisplacement may follow when, as the swelling diminishes, the plaster becomes loose. The strong plantar muscles and tendons bowstring across the tarsometatarsaljoint and, on contraction, shorten the plantar aspect of the foot, leading to displacement if the dorsal ligaments have been torn. This bowstring effect is less marked in the more lateral injuries where the curvature of the Lisfranc joint is less. In those injuries with plantar displacement the peroneus longus tendon acts as a deforming force, depressing the medial side of the tarsometatarsal joint and elevating the lateral side. Osteoarthritis is an almost inevitable sequel of tarsometatarsal displacements because of damage to the articular surface at the time of injury (Jeffreys 1963). It is usually confined to the displaced segment and may be associated with the formation ofan exostosis, particularly on the dorsum of the foot. Moderate to severe degenerative changes in the Lisfranc joint occurred in approximately 30 per cent of our patients.

and 30-degree oblique) are essential in order to diagnose the initial displacement and also to assess whether reduction is sufficiently accurate. Unhappily, in many of Treatment our cases oblique views had not been taken. It is also With regard to treatment, we feel that, whenever there is important to include the entire foot and ankle, otherwise displacement, closed reduction should be attempted. It is concomitant injuries may be missed. best achieved by longitudinal traction in the line of the Our study defined three patterns of displacement foot and must be checked radiographically. Providing and our classification is based on that ofQu#{233}nuand K#{252}ss reduction is adequate it should be stabilised with (1909). This has, however, been expanded to include percutaneous wires. With Type A injuries (total inconplantar and medial displacement injuries, and dislocagruity) one Kirschner wire is placed from the first tions where four metatarsals are involved. This modified metatarsal to the medial cuneiform bone, and a second classification is simple to apply and gives information placed laterally from the fifth metatarsal to the cuboid. regarding prognosis and treatment. Of the Type B injuries (partial displacements) those of the lateral segment need only a single Kirschner wire. Complications But if the first metatarsal is displaced, the injury is The complications which accounted for most of the inherently unstable and two wires are needed. With Type unsatisfactory results were vascular impairment, redisC injuries(divergent displacements)one or two Kirschner placement, skin complications (necrosis or cicatrisation wires are used to stabilise the medial fragment, with if transverse or plantar incisions were used), and another single wire for the lateral displacement. osteoarthritis. It is clear from the results in our series that when an At follow-up we were often unable to diagnose early adequate reduction can be achieved by closed methods, redisplacement (within six weeks) because radiographs open reduction, as advocated by some authors (Gissane were not available. In four of the 27 patients reviewed 1951 ; Jeffreys 1963; Engelhardt and Ganz 1975), is not who required open reduction the operation became necessary. Early closed reduction is unlikely to succeed necessary because of redisplacement after the initial where there is soft-tissue interposition, marked commiclosed reduction and plaster. A further case, in which VOL.

64-B,

No.

3, 1982

356

P. H. HARDCASTLE,

nution, the

or a large

medial

articular

and

fragment.

intermediate

RESCHAUER,

R.

Diastasis

cuneiform

E. KUTSCHA-LISSBERG,

In several cases good results followed open reduction up to six weeks after injury. However, the two patients treated by open reduction and fixation after this period had only fair results. It is probably better not to attempt reduction after six weeks.

between

bones

suggests

interposition of the tibialis anterior tendon. In such cases and, indeed, whenever closed reduction is inadequate, open reduction should be performed as soon as possible and certainly within six weeks of the injury. The absolute indication for open reduction is vascular insufficiency that does not improve after closed reduction. We suggest the technique advocated by Gissane 1 95 1 ), where both dorsalis pedis and posterior tibial arteries are explored. In the two cases of forefoot ischaemia in our series, open reduction was performed but the posterior tibial artery was not explored and gangrene developed. For open reduction in the absence of ischaemia, the longitudinal incisions advocated by Aitken and Poulson

Primary

give

adequate

exposure.

The

first

incision

a single

contracture,

incisions, may

which

do not

lead

to necrosis

necessary

to obtain

The authors Australia,

may

occur.

follow

transverse

A single

because

or plantar

midline

excessive

incision

skin

also

retraction

is

access.

would like to thank Professor for his assistance in preparing

Sydney Nade, this paper.

Professor

is advocated

by Granberry

and

Kirschner

wire

was

used,

and

we

therefore

recommend using two wires. With regard to after-care, previous reports recommend non-weight-bearing for a period of at least six weeks after injury. We found, however, that taking weight as soon as the swelling subsided (approximately two weeks) did not seem to affect the final outcome, provided the foot was protected in a plaster cast and reduction stabilised by internal fixation.

is

between the first and second metatarsals, and the second (if a second is needed) is made more laterally over the tarsometatarsal joint. With these incisions skin necrosis and

arthrodesis

Lipscomb (1962) and by Bonnel and Barth#{233}l#{233}my (1976). We have had no experience with this procedure but it is possible that it may have a place in those injuries where there is considerable comminution and where maintenance of reduction by internal fixation is difficult. Niederecker (1956) recommended arthrodesis of the metatarsocuneiform joint as a standard procedure in all dislocations involving the first metatarsal. Certainly in our series redisplacement sometimes occurred when only

(

(1963)

W. SCHOFFMANN

ofOrthopaedic

Surgery,

Queen

Elizabeth

Medical

Centre.

Nedlands,

Western

REFERENCES Aitken

AP,

Poulson

D. Dislocation

B#{246}hlerL. Dislocations Grune and Stratton,

of the

tarsometatarsaljoint.

in Lisfranc’s joint. l958;3:213&-7.

In : Wallner

J Bone A and

Bonnel

F, Barth#{234}l#{234}my M. Traumatismes de l’articulation et classification biomecanique. J Chir (Paris) 1976;

Cassebaum

WH.

Engelhardt

P, Ganz

English

TA.

Francesconi

Gissane

Lisfranc

fracture-dislocations.

R. Die

Dislocations

of the

F. Sopra

un caso

W. A dangerous

C/in

Luxationsfrakturen

type

des

metatarsal

bone

di lussazione

of the

Granberry WM, Lipscomb PR. Dislocation Jeifreys TE. Lisfranc’s fracture-dislocation Joint Surg [Br] I963 :45-B: 546-51. Niederecker

K. Operative

Behandlung

foot.

der

Wilson

E. Tarsometatarsal DW.

Injuries

: entroses

Orthop

l963;30:

1 16-28.

Lisfranc

Gelenkes.

adjacent

toe.

Chir

Organi

J Bone

Moe

Joint

Surg

Acta joints.

Orthop

J Bone

Joint

Scand Surg

45-A

o/fracture.s,

luxations,

[Br]

: 246-60.

treatment

praxis

Surg

fractures

der

haden

1964:46-B

5th

English

edition.

New

: #{233}tudede 39 observations

badt’nr.s

rei/ze

1975

York:

personnelle

9 : 896--8.

:700-4.

1925;9:589-604. [Br]

1951 :33-B:

Surg study

535-8.

Gvneco/ Obstet of tarso-metatarsal

Dtsch

Ges

m#{233}tatarsotarsiennes)

tarsometatarsiennes. injuries. J Bone

1963 The

graves,

Joint

Verh

(luxations

[Am]

Orthopadische

J Bone

MittlefussknochenbrOche. du metatarse

fracture-dislocation.

of the tarso-metatarsal

Surg

translators.

of the tarsometatarsaljoints. : a clinical and experimental

Rainaut JJ, Cedard D, d’Hour JP. Les luxations Wiley ii. The mechanism of tarso-metatarsaljoint Wilppula

Joint 0,

de Lisfranc 1 1 1 : 573-92.

di Lisfranc.

of fracture

Qu#{234}nuE, KBss G. #{201}tudesur les luxations 39: 281-336, 720-91, 1093-134.

and

Russe

Orthop

1962

;

114: 467-9. dislocations

1956:44:

du diastasis

and

fracture-dislocations.

J Bone

358-63.

entre

le I

et le 2e metatarsien.

Ret

Chir

I 909:

Rev Chir Orthop 1966:52:449-62. Joint Surg [Br] 1971 :53-B :474-82. 1973:44:335-45. [Br]

1972

54-B

: 677-86.

THE

JOURNAL

OF BONE

AND

JOINT

SURGERY

ORIGINAL RESEARCH

Effects of Isolated Weber B Fibular Fractures on the Tibiotalar Contact Area John Harris, DPM,1 and Lawrence Fallat, DPM, FACFAS2 Fractures of the lateral malleolus can occur without rupture of the deltoid ligament or fracture of the medial malleolus. Controversy exists regarding the necessity of surgery on supination-external rotation stage II ankle fractures. Theoretically, as long as the medial structures are intact, the talus cannot displace enough to cause degenerative arthritis of the ankle joint. The purpose of this study was to measure changes in contact area between the tibial plafond and the talar dome with serial displacement of the distal fibula in both a lateral and a superolateral direction. Twelve cadaver lower extremities were used. Distal fibular fractures were replicated by creating an osteotomy. Displacement was accomplished with a customized apparatus that displaced and held the distal fibula in a malaligned position. Tibiotalar contact area was measured with pressure sensitive film at the following intervals of fibular displacement: 0 mm, laterally 2 mm and 4 mm, and then posteriorly and superiorly 2 mm and 4 mm. A servohydraulic testing apparatus was used to apply the same physiologic load to all limbs while measuring contact area. Key independent variables included the direction and amount of displacement of the distal fibula. Mean tibiotalar contact area decreased from baseline (no displacement) 361.1 mm2 (SD ⫾ 49.0) to 162.2 mm2 (SD ⫾ 81.3) and 82.6 mm2 (SD ⫾ 30.6) for 2 mm and 4 mm lateral displacement of the distal fibula respectively. With posterior/superior displacement of 2 mm and 4 mm mean tibiotalar contact decreased to 219.3 mm2 (SD ⫾ 56.7) and 109.2 mm2 (SD ⫾ 39.0), respectively. Statistical significance was found ( P ⬍ .001) when comparing normal ankle alignment with displaced fractures at all levels of displacement. ( The Journal of Foot & Ankle Surgery 43(1):3–9, 2004) Key words: SER II fractures, tibiotalar contact area, Weber B fractures, ankle fracture

S upination-external rotation (SER) injuries of the ankle comprise 40% to 55% of malleolar fractures (1). Approximately 85% of fractures of the lateral malleolus occur without substantial injury to the medial side of the ankle joint (2, 3). There has been an extensive debate over whether or not surgical correction is needed for LaugeHansen SER stage II ankle fractures (1, 4 –16). Many of these studies focus on the need for anatomic reduction of the From the Department of Podiatric Surgery, Oakwood Healthcare System, Dearborn, MI. 1 Submitted During Second-Year Surgical Residency, Oakwood Healthcare System. 2 Diplomate, American Board of Podiatric Surgery; Director, Podiatric Surgery Residency, Oakwood Healthcare System. Address correspondence to: Lawrence Fallat, DPM, FACFAS, Director, Podiatric Surgical Residency, Oakwood Healthcare System, 20555 Ecorse Rd, Taylor, MI 48180. E-mail: [email protected] Copyright © 2004 by the American College of Foot and Ankle Surgeons 1067-2516/04/4301-0002$30.00/0 doi:10.1053/j.jfas.2003.11.008

distal fibula. Ramsey and Hamilton (8) concluded that lateral displacement of the talus can be significant enough to alter tibiotalar joint dynamics in isolated fibular fractures and an intact deltoid ligament, thereby supporting the need for surgical repair. Curtis et al (17) also found a decrease in tibiotalar contact area with shortening and external rotation of the fibula with an intact deltoid ligament. There are several reports that have shown that the tibiotalar contact area decreases only when the deltoid ligament is severed (1, 7, 18). Michelson et al (18) reported that tibiotalar contact area does not significantly change with lateral displacement of the fibula without sectioning the deltoid ligament. Moody et al (1), while investigating SER IV ankle fractures without medial malleolar fractures, found that tibiotalar contact area decreases with lateral shift of the talus. Thordarson et al (7) found increased tibiotalar contact pressures with shortening, lateral displacement, and external rotation of the distal fibula after sectioning the deltoid ligament.

VOLUME 43, NUMBER 1, JANUARY/FEBRUARY 2004

3

On the other hand, there have been challenges to the concept that ankle joint dynamics are altered after a distal fibular fracture, with or without lateral displacement of the talus (3, 10, 18 –29). These and other authors credit the deltoid ligament for maintaining the position of the talus when the fibula is fractured (18, 25–27, 29, 30). Some of these studies show no significant change in contact pressures with lateral displacement of the fibula (10, 20, 21, 23, 24). The fundamental basis for examining tibiotalar contact area is that, as the total contact area decreases, stress per area increases (31). This contact area helps determine effects on ankle joint dynamics. Additional researchers have investigated the contact area and pressures of the normal ankle joint, which can serve as a baseline for comparison to the pathologic or fractured ankle (32, 33). Given the discrepancies regarding tibiotalar contact characteristics after fracture of the fibula (8, 10, 17, 18, 20, 21, 24), this study examines tibiotalar contact area with lateral and posterosuperior displacement of the distal fibula while the deltoid ligament remains intact.

Materials and Methods Six paired fresh-frozen, above-knee cadaveric lower extremities were obtained for the study. The 12 specimens were thawed by placing them in a refrigerator at 4°C for 2 days. After the specimens were thawed, they were kept in ice water for the duration of the study. Average age of the specimens was 72 years (range, 48 to 91 years; 4 women and 2 men). Exclusion criteria included radiographic and gross evidence of arthritis and/or previous trauma. All skin and soft tissue were removed from the anterior and lateral ankle of each limb with the exception of tendons and ligaments. The anterior joint capsule was dissected from its attachments on the anterior surface of the tibia, the superior surface of the talus, and the medial and lateral malleoli. The deltoid ligament and the anterior talofibular ligament were kept intact. A small window of skin and subcutaneous tissue was also removed from the lateral malleolus, leaving a 9 ⫻ 5 cm rectangular void that was centered over the lateral malleolus. The superior extensor retinaculum was separated from its attachment to the anterior aspect of the lateral malleolus and the anterior tibiofibular ligament was severed sharply as in a supination external rotation injury (4). The peroneal tendons, superior peroneal retinaculum, calcaneofibular ligament, and posterior talofibular ligament were all kept intact. An osteotomy was performed in the proximal tibia perpendicular to the long axis of the tibia and 1.5 to 2 cm distal to the articular surface. Through the window made over the lateral malleolus, an osteotomy was created in the distal fibula to replicate and oblique SER stage II fibular fractures. 4

THE JOURNAL OF FOOT & ANKLE SURGERY

FIGURE 1

Apparatus in place on cadaveric limb.

A saggital saw and a 2108-110 blade (Stryker, Kalamazoo, MI) were used to create the simulated fracture. Osteotomies were directed from anterior-distal, beginning at the level of the ankle joint, to posterior-proximal. An apparatus was designed and built to precisely displace and to hold the distal fibula in a malaligned position. The distal tibia was firmly fixated to the device with 4 brass 5/16⬙ screws (Fig. 1). A 5/64⬙ Steinmann pin was inserted through the distal fibula from anterior to posterior, while either end of the pin was tightly fastened to the apparatus (Fig. 1). Two machined tracks in the apparatus ensured displacement in the proper plane. Millimeter markings on the tracks confirmed the amount of displacement along that track. Controlled variables were the direction and the amount of displacement of the distal fibula. Tibiotalar contact area was recorded sequentially at the 0-mm, 2-mm, and 4-mm intervals of lateral fibular displacement. Contact area was also determined at 2 mm and 4 mm of posterior/superior fibular displacement. The right specimen was tested first followed by the left for each trial. Tibiotalar contact area was measured with ultra–superlow Fuji (Fuji Photo Film Co, Tokyo, Japan) (0.5 MPa to 6.0 MPa) pressure-sensitive film. Because this study examined contact area only, there was no need to use film that measured higher pressures. The film was shaped in a manner to maximize contact between tibia and talus (1, 7, 10, 19, 32, 33). The film was then covered with 2 layers of thin, clear packing tape to keep cadaveric fluid from corrupting the film. The thickness of the film and tape together, measured with digital calipers, was approximately 0.27 mm. The film was inserted into the ankle anteriorly between extensor hallucis longus and extensor digitorum longus. While the limb was being loaded, the film was held in place posteriorly by the posterior ankle joint capsule, medially and laterally by folding into the medial and lateral gutters of

TABLE 1 Mean tibiotalar contact area (mm2) by degree and direction of displacement Positions of Fibular Displacement

Mean

SD

Baseline (0 mm) 2 mm posterior/superior 4 mm posterior/superior 2 mm lateral 4 mm lateral

361.1 219.3 109.2 162.2 82.6

49.0 56.7a 38.9a 81.3a 30.6a

a

FIGURE 2

Statistically significant change from baseline.

tibia was held in the crosshead with three 1 ⫻ 1 ⫻ 5 inch aluminum blocks cemented to the crosshead plate (Fig. 3). The crosshead on the tensiometer was lowered into position at a manually controlled rate, not exceeding 5 mm/ min, until a static force of 686 N was observed. The load was manually decreased back to 0 at the same rate. The limb was removed and the film was retrieved and immediately photographed and stored for future measurement. The photographs were taken with the film placed in a grid, with the camera centered directly over the grid. Each pressure film was photographed on a separate piece of numbered paper. A separate log was kept of each limb, along with amount and direction of displacement correlating to the numbered pressure film. This insured no bias when measuring surface area on each film. This exact technique was used for each limb with each fibular displacement. All testing was performed by the same individual (J.H.). Data were analyzed by using 2 repeated-measures analysis of variance (posterosuperior and lateral displacement) by using SPSS (SPSS, Chicago, IL). All post-hoc comparisons used a Bonferroni correction for inflated error rate

Saw bone model showing film insertion.

Results

FIGURE 3

Apparatus on limb, with limb in the Instron tensiometer.

the ankle, and anteriorly by the hemostat used to place the film into the joint (Fig. 2). The limb was then loaded with an Instron model 5866 servohydraulic tensiometer (Instron, Canton, MA) with the ankle in neutral position and the limb perpendicular to the supporting surface to minimize slippage. Proximally, the

Descriptive statistics for contact area by type and degree of displacement are presented in Table 1 and Fig 4. The overall change in mean contact area for posterosuperior displacement was significant (P ⬍ .001). Post hoc comparison of mean contact area change from baseline to 2-mm posterosuperior displacement (361 ⫾ 49 vs. 219.3 ⫾ 56.7) was highly significant (P ⬍ .001) as was 4-mm displacement (P ⬍ .001) (361 ⫾ 49 vs. 109.2 ⫾ 38.9). The change in contact area from 2-mm to 4-mm posterosuperior displacement was also significant (P ⬍ .001). A similar pattern was found for lateral displacement by using the same data analytical strategy. Lateral displacement of the distal fibula on tibiotalar contact area showed an overall decrease (P ⬍ .001). Post hoc comparisons of contact area change from baseline for lateral displacement at 2 mm (P ⬍ .001) (361 ⫾ 49 vs. 162.2 ⫾ 81.3) and 4 mm (P ⬍ .001) (361 ⫾ 49 vs. 82.6 ⫾ 30.6), respectively. The change from 2-mm to 4-mm lateral displacement was also significant (P ⬍ .001).

VOLUME 43, NUMBER 1, JANUARY/FEBRUARY 2004

5

FIGURE 4

Mean surface area (mm2).

Discussion Baseline contact area between all limbs was similar and was comparable to other studies of tibiotalar contact area without pathology (1, 32). Lateral displacement of the fibula resulted in a slightly greater decrease in contact area than did posterosuperior displacement. Our data indicate that lateral displacement of only 2 mm results in a 55% decrease in contact area and lateral displacement to 4 mm results in a 77% decrease (Fig. 5). Two millimeters of posterosuperior displacement yields a 39% decrease in contact area, and, at 4 mm, shows a 70% decrease. A nearly linear relationship exists between increasing fibular displacement and decreasing amount of tibiotalar contact area (Fig. 4). These findings support prior studies that show a decrease in tibiotalar contact area with SER II ankle fractures (8, 17). This study clearly shows that tibiotalar contact area decreases with simulated SER II ankle fractures despite intact superficial and deep fibers of the deltoid ligament and all other medial structures. A recent study reported that axial loading stabilizes the ankle joint and prevents lateral displacement of the talus, thereby maintaining tibiotalar contact area (23). In contrast, this study shows physiologic axial 6

THE JOURNAL OF FOOT & ANKLE SURGERY

loading of the ankle joint allows for decreased tibiotalar contact area when the lateral bony support is absent. This decrease in contact area gives an increase in force per unit area (31). Generation of high-stress concentrations can damage not only articular cartilage but also osseous components of the distal tibia, diminish function through loss of congruence, and may be considered a decisive factor in the pathogenesis of osteoarthritis (34, 35). Changes in joint alignment may lead to degenerative changes and ankle pain (36, 37). Indeed, several clinical investigators have shown radiographic signs of ankle osteoarthritis in ankle malunions with greater than 1 or 2 mm of lateral talar shift (12, 15, 38 – 40). Others have stated that the major indication for open reduction with internal fixation of fibula fractures is lateral shift of the talus of 2 mm or greater (12–16). Our results support the notion that open reduction with internal fixation be preformed on SER II ankle fractures with 2 mm or more of lateral and/or posterior and superior displacement of the fibula. This investigation differs from previous studies in several key areas. In our study, tissue dissection was minimal and only involved the lateral and anterior ankle. All ligaments and tendons that would be intact after a SER II ankle fracture were kept intact to

FIGURE 5

Percent of tibiotalar contact area lost.

maintain the structural integrity of the limb. Other studies reviewed removed all soft tissue with the exception of ligaments from their cadaveric specimens (7, 10, 17–24, 31, 33, 41). Effects on tibiotalar contact area of simultaneous displacement posteriorly and superiorly of the fibula have not been studied. In contrast, other studies (7, 10, 17, 24) examined just shortening of the fibula, without posterior displacement as this study did. The displacement of the fibula in 2 planes, as in this study, verses 1 affords a possible difference in results between this study and others (7, 10, 24). Lateral displacement alone had an increased loss of tibiotalar contact area compared with the posterior and superior displacement without lateral displacement. Perhaps with lateral displacement of the fibula, the eventual restraining mechanism of displacement of the talus becomes the deltoid ligament. There are no osseous structures that physically block lateral displacement of the talus. With pure superior displacement only, there may still be some residual impairment of lateral talar shift. Also, the apparatus that was designed and built for this investigation held the distal fibula in a malaligned position, allowing for axial loading of the limb without artificially inducing the talus to displace. Artificially inducing the talus to move laterally is quite often considered a shortcoming of other studies (1, 8). The apparatus used in this study came

into contact with the cadaveric specimen only on the tibia and the fibula. This apparatus held the distal fibula in a fixed space, in relation to the rest of the limb, during axial loading in an attempt to replicate actual conditions as close as possible. This most likely resulted in a more realistic stressor. There are several limitations in this study. First, the sample size of 12 specimens was relatively small. Nevertheless, our findings were highly statistically significant. There is an inherent degree of imprecision when dealing with cadavers and fitting of pressure film in the joint; therefore, some variability is unavoidable. Regardless, we feel this study was accurate enough to indicate that displacement of the lateral malleolus both laterally and posterosuperiorly results in significant loss of ankle joint contact area with the deltoid ligament intact. Second, true spiral oblique fractures are unable to be replicated with a saw. As such, the difference between the experimentally induced and the clinical fracture configurations cannot be determined. Last, we tried to minimize slippage by ensuring that the limb was perpendicular to the supporting surface. However, limb migration in increments not visible to the naked eye could have occurred and modified the results. Future areas of research may involve measuring the actual stresses such as shear stresses within the pathologic

VOLUME 43, NUMBER 1, JANUARY/FEBRUARY 2004

7

ankle joint. Instability may result in shear stresses that may be more damaging to cartilage than elevated contact stresses (19). There are also discrepancies in the literature as to which side of the joint should be examined (42).

15.

16.

Summary Findings of this study show that lateral and posterosuperior displacement of the lateral malleolus significantly affect ankle joint dynamics and allow for decrease in tibiotalar contact area. This may have in important role in the management of SER II ankle fractures.

17.

18. 19. 20.

Acknowledgment The authors thank Steven Schwartz, PhD, for help with statistical analysis and Kurt Miller and Larry Maciag from Axel Products (Ann Arbor, MI) for help with design and testing of the apparatus.

21.

22.

23.

References 1. Moody ML, Koeneman J, Hettinger E, Karpman RR. The effects of fibular and talar displacement on joint contact areas about the ankle. Orthop Rev 21:741–744, 1992. 2. Michelson JD, Helgemo SL. Kinematics of the axially loaded ankle. Foot Ankle Int 16:577–782, 1995. 3. Harper MC. The short oblique fracture of the distal fibula without medial injury: an assessment of displacement. Foot Ankle Int 16:181– 186, 1995. 4. Lauge-Hanson N. Fractures of the ankle. II. Combined experimentalsurgical and expalimental-roentgenologic investigation. Arch Surg 60: 957–985, 1950. 5. Kleiger B. The treatment of oblique fractures of the fibula. J Bone Joint Surg 43A:969 –979, 1961. 6. Magnusson R, On the late results in non-operative cases of malleolar fractures. I. Fractures by external rotation. Acta Chir Scand 90(Suppl 84):11–116, 1944. 7. Thordarson DB, Motamed S, Hedman T, Ebramzadeh E, Bakshian S. The effect of fibular malreductionon contact pressures in an ankle fracture malunion model. J Bone Joint Surg 79A:1809 –1815, 1997. 8. Ramsey P, Hamilton W. Changes in tibiotalar area of contact caused by lateral talar shift. J Bone Joint Surg 58A:356 –357, 1976. 9. Maynou C, Lesage P, Mestdagh H, Butruille Y. Is surgical treatment of deltoid ligament necessary in ankle fractures? Rev Chir Orthop Reparatrice Appar Mot 83:652– 657, 1997. 10. Yoshimine F. Effects of fibular malunion on contact area and stress distribution at the ankle with six simulated loading conditions. Nippon Seikeigeka Gakkai Zasshi 69:460 – 469, 1995. 11. DeSouza LJ, Gustilo RB, Meyer TJ. Results of operative treatment of displaced external rotation-abduction fractures of the ankle. J Bone Joint Surg 67A:1066 –1073, 1985. 12. Joy G, Patzakis MJ, Harvey JP Jr. Precise evaluation of the reduction of severe ankle fractures. Technique and correlation with end results. J Bone Joint Surg 56A:979 –993, 1974. 13. Cedell CA. Is closed treatment of ankle fractures advisable? Acta Orthop Scand 56:101–102, 1985. 14. Mast JW, Teipner WA. A reproducible approach to the internal fixa-

8

THE JOURNAL OF FOOT & ANKLE SURGERY

24.

25. 26.

27. 28.

29.

30. 31. 32.

33.

34.

35.

36.

tion of adult ankle fractures: rational, technique, and early results. Orthop Clin North Am 11:661– 679, 1980. Pettrone FA, Gail M, Pee D, Fitzpatrick T, Van Herpe LB. Quantitative criteria for prediction of the results after displaced fracture of the ankle. J Bone Joint Surg 65A:667– 677, 1983. Phillips WA, Schwartz HS, Keller CS, Woodward HR, Rudd WS, Spiegel PG, Laros GS. A prospective, randomized study of the management of severe ankle fractures. J Bone Joint Surg 67A:67– 78, 1985. Curtis MJ, Michelson JD, Urquhart MW, Byank RP, Jinnah RH. Tibiotalar contact and fibular malunion in ankle fractures. Acta Orthop Scand 63:326 –329, 1992. Michelson JD, Clarke HJ, Jinnah RH. The effect of loading on tibiotalar alignment in cadaver ankles. Foot Ankle Int 10:280 –284, 1990. Vrahas M, Fu F, Veenis B. Intraarticular contact stresses with simulated ankle malunions. J Orthop Trauma 8:159 –166, 1994. Clarke HJ, Michelson JD, Cox QG, Jinnah RH. Tibiotalar stability in bimalleolar ankle fractures: a dynamic in vitro contact area study. Foot Ankle Int 11:222–227, 1991. Kimizuka M, Kurosawa H, Fukubayashi T. Load-bearing pattern of the ankle joint. Contact area and pressure distribution. Arch Orthop Trauma Surg 96:45– 49, 1980. Yablon IG, Heller FG, Shouse L. The key role of the lateral malleolus in displaced fractures of the ankle. J Bone Joint Surg 59A:169 –173, 1977. Sasse M, Nigg BM, Stefanyshyn DJ. Tibiotalar motion— effect of fibular displacement and deltoid ligament transaction: in vitro study. Foot Ankle Int 20:733–737, 1999. Zindrick MR, Knight GW, Gogan WJ, Patwardhan AG, Vanderby R, Hoyt JS. The effect of fibular shortening and rotation on the biomechanics of the talocrural joint during various stages of stance phase. Orthop Trans 8:259 –260, 1984. Pankovich AM. Fractures of the fibula proximal to the distal tibiofibular syndesmosis. J Bone Joint Surg 60A:221–229, 1978. Pankovich AM, Shivaram MS. Anatomical basis of variability in injuries of the medial malleolus and the deltoid ligament. Acta Ortho Scand 50:225–236, 1979. McCullough CJ, Burge PD. Rotatory stability of the load-bearing ankle. An experimental study. J Bone Joint Surg 62B:460 – 464, 1980. Yde J, Kristensen KD. Ankle fractures: supination-eversion fractures stage II primary and late results of operative and non-operative treatment. Acta Orthop Scand 51:695–701, 1980. Burns WC, Prakash K, Adelaar R, Beaudion A, Krause W. Tibiotalar joint dynamics: indications for the syndesmotic screw, a cadaver study. Foot Ankle Int 14:153–158, 1993. Michelson JD. Current concepts review fractures about the ankle. J Bone Joint Surg 77A:142–152, 1995. Gere JM, Timoshenko SP Axially loaded members, chapter 2. In Mechanics of Materials, 3rd ed, PWS Publishing, Boston, 1990. Driscoll HL, Christensen JC, Tencer AF. Contact characteristics of the ankle joint. Part 1: the normal joint. J Am Podiatr Med Assoc 84:491– 498, 1994. Hartford JM, Gorezyea JT, McNamara JL, Mayor MB. Tibiotalar contact area contribution of posterior malleolus and deltoid ligament. Clin Ortho Rel Res 320:182–187, 1995. Lieberman DE, Devlin MJ, Pearson OM. Articular area responses to mechanical loading: effects of exercise, age, and skeletal location. Am J Phys Anthropol 116:266 –277, 2001. Glaser C, Putz R. Functional anatomy of articular cartilage under compressive loading: quantitative aspects of global, local and zonal reactions of the collagenous network with respect to the surface integrity. Osteoarthritis Cartilage 10:83–99, 2002. Trias A. Effect of persistent pressure on the articular cartilage: an experimental study. J Bone Joint Surg 43B:376 –386, 1961.

37. Wagner KS, Tarr RR, Resnick C, Sarmiento A. The effect of simulated tibial deformities on the ankle joint during gait cycle. Foot Ankle 5:131–141, 1984. 38. Hughes JL, Weber H, Willenegger H, Kaner EH. Evaluation of ankle fractures: non-operative and operative treatment. Clin Orthop 138: 111–119, 1979. 39. Wilson FC, Skilbren LA. Long-term results of displaced bimalleolar fractures. J Bone Joint Surg 48A:1065–1078, 1966.

40. Brunnel HN, Charnley AD. The treatment of displaced fractures at the ankle by rigid internal fixation and early joint movement. J Bone Joint Surg 47B:634 – 660, 1965. 41. Kura H, Kitaoka HB, Luo ZP, An KN. Measurement of surface contact area of the ankle joint. Clin Biomech 13:365–370, 1998. 42. Michelson JD, Checcone M, Kuhn T, Varner K. Intra-articular load distribution in the human ankle joint during motion. Foot Ankle Int 22:226 –233, 2001.

VOLUME 43, NUMBER 1, JANUARY/FEBRUARY 2004

9

Tibialis Posterior Tendon Dysfunction KENNETHA. JOHNSON,M.D., AND DAVIDE. STROM,M.D.

casions, have only an aching along the medial aspect of the ankle that is exacerbated by physical activity and has probably modified his or her activities to be less strenuous. Although it may be difficult for patients to localize the discomfort, with specific questioning they will point along the course of the TPT from a few centimeters proximal to the tip of the medial malleolus to its major attachment at the undersurface of the navicular. The onset of pain will have been gradual, and only infrequently can an inciting episode be recalled. Occasionally, a young athlete will remember a twisting episode with subsequent persistent pain. On examination, the points of maximal tenderness will be detected along the tendon from just before it passes around the medial malleolus to its navicular insertion. When localized, the site of tenderness corresponds well to areas of TPT pathologic changes. Swelling is best appreciated by viewing the standing patient from a posterior vantage. Fullness of the region just inferior to the medial malleolus is evident when compared with the unaffected foot. The alignment of the hindfoot-forefoot will still be normal at this stage. In the authors' experience, manual testing for weakness has been essentially useless. It has been suggested2that testing the TPT with the hindfoot in eversion and the forefoot in abduction with toe flexors relaxed will eliminate the synergistic action of the tibialis anterior and flexor digitorum longus, thus allowing determination of the strength of the TPT. However, because the TPT power is so strong, and probably because of substitution

Dysfunction of the tibialis posterior tendon evolves through a series of stages. The pain symptoms, clinical signs, and roentgenographic changes for each of these stages are characteristic. This staging system permits clarificationand individualization of dysfunction, expected pathologic changes, and surgical treatment. The importance of the tibialis posterior tendon in normal hindfoot function and its treatment when injured are now being properly appreciated.

Afflictions of the tibialis posterior tendon (TPT) are now being recognized and treated ',I2 with increased frequency and It is important to be aware of this problem and its stages of presentation in order to make a proper diagnosis. This article reviews the evolving concepts of presentation and formulates a plan of rational care. DIAGNOSTIC AND RADIOGRAPHIC CONSIDERATIONS The stages of TPT dysfunction are quite distinct (Table 1). Each stage will be discussed with regard to pain symptoms, physical findings, and roentgenographic changes. STAGE1-TENDON LENGTHNORMAL Many TPT problems remain unrecognized because pain symptoms are only mild to moderate. The patient may, on multiple ocDr. Johnson is Consultant in Orthopedics, Mayo Clinic Scottsdale, Scottsdale, Arizona, and Professor of Orthopedic Surgery, Mayo Medical School, Rochester, Minnesota. Dr. Strom is a Fellow in Foot Surgery, Mayo Clinic Scottsdale, Scottsdale, Arizona. Reprint requests to Kenneth A. Johnson, M.D., Mayo Clinic Scottsdale, 13400 East Shea Blvd., Scottsdale, AZ 85259.

196

Number 239 February, 1989

Tibialis Posterior Tendon Dysfunction

197

TABLE 1. Changes Associated With Various Stages of TPT Dysfunction Stage 2

Stage 1

Stage 3

TPT condition

Peritendinitis andfor tendon degeneration

Elongation

Elongation

Hind foot

Mobile, normal alignment

Mobile, valgus position

Fixed, valgus position

Pain

Medial: focal, mild to moderate

Medial: along TPT, moderate

Medial: possibly lateral, moderate

Single-heel-risetest

Mild weakness

Marked weakness

Marked weakness

“Too-many-toes’’ sign with forefoot abduction

Normal

Positive

Positive

Pathology

Synovial proliferation, degeneration

Marked degeneration

Marked degeneration

Treatment

Conservative, 3 months; surgical, 3 months with synovectomy, tendon debridement, rest

Transfer FDL* for TPT

Subtalar arthrodesis

* Flexor digitorurn longus.

by the other extrinsic muscle-tendon units in spite of efforts to negate them, this method of testing has not been accurate when correlated with surgical findings. The single-heel-rise test is very good for testing TPT strength. The patient is asked to rise up on the ball of the foot while the other foot is held off the ground (the patient may use a door or wall for balance). The normal sequence for a single-heel rise is as follows. First, the TPT is activated, which inverts and locks the hindfoot, thus providing a rigid structure. Next, the gastrosoleus muscle group pulls up the calcaneus and the heel rise is completed. With elongation of the TPT, however, the initial heel inversion is weak and the patient either rises up incompletely without locking the heel or does not get up on the ball of the foot at all (Figs. 1A and 1 B). In the Stage 1 condition, the patient usually will be able to get up on the ball of the affected foot and will be able to tell that it is more painful and somewhat weaker than the other side. At this early stage, there will not be

much in the way of secondary deformity, and overall forefoot-hindfoot alignment will be unaffected. On routine standing roentgenograms the changes will be minimal. If the diagnosis is in question, magnetic resonance imaging (MRI) may demonstrate if tendon degeneration is present. STAGE 2-TENDON ELONGATED, HINDFOOTMOBILE From Stage 1 to Stage 2 the change in symptoms evolves over several months to years. During Stage 1, when pain is mild to moderate, patients have often seen a physician but were not given a specific diagnosis. Often these patients have been told to live with the discomfort. In Stage 2, the pain increases in seventy and distribution, is present even after cessation of weight bearing, and is significantly troublesome. The patient has already applied for a handicapped parking sticker and actively wants relief. Pain is located along the TPT for a greater length. The

198

Johnson and Strom

ClinicalOrthopaedics and Related Research

FIGS.1A AND 1B. The single-heel-rise test. (A) Normal. The TPT inverts the hindfoot and the patient rises on the forefoot. (B) Abnormal. Ability to rise on the forefoot is decreased or absent. Instead, the patient just rolls to the outside ofthe foot. (By permission of Mayo Foundation.) tendon has been disrupted, and secondary changes are developing. Swelling with tenderness is still present inferior to the medial malleolus when viewed posteriorly. The single-heel-rise test becomes even more abnormal because the tendon is weakened. Another helpful diagnostic sign is that of “too many toes,” i.e., seeing more toes than normal from this view (Fig. 2). In this test, the patient is asked to assume a comfortable knee-leg alignment toward a wall. From

FIG.2. “Too many toes.” This patient had right TPT dysfunction. Four toes show on the right with forefoot abduction, but only two toes show on the normal left foot. (From Johnson.* By permission of J. B. Lippincott.)

a direct posterior midline vantage, the examiner counts the number of toes on each foot that are visible laterally. As the heel goes into increased resting eversion and the forefoot goes into abduction, too many toes are seen on the affected side. The number of extra toes seen is a recordable measurement of the degree of deformity and is surprisingly reproducible. Changes on routine standing roentgenograms now become evident. To understand these changes, it is useful to think of the foot as consisting of only two pieces (Figs. 3A3C). One piece, the talus, is fixed in the ankle mortise. It can move only in flexion-extension, not in a varus-valgus plane. The second piece of the foot is everything else, i.e., the calcaneus, cuboid, navicular, and bones distalward move as a unit with motion being in a varus-valgus plane through the subtalar joint. With elongation ofthe TPT, the second piece rotates from beneath the talus laterally to produce a hindfoot in valgus and a forefoot in abduction. When the head of the talus is left unsupported, the talus flexes. The changes on routine roentgenograms are then predictable. On the anteroposterior (AP) view, the forefoot will be abducted in relation to the hindfoot. Also, the navicular will have subluxed off the head of the talus and

Number 239

Tibialis Posterior Tendon Dysfunction

February, 1989

199

A Frontal View

B

A

I

II A

C

I

Superior Vlew

i ! B

I

FIGS. 3A-3C. Two-piece concept of foot. (A) Talus is held in the ankle mortise while the calcaneus rotates laterally because of loss of TPT function. (B) The second piece (calcaneus, cuboid, navicular, and bones distalward) moves to produce forefoot abduction. (C) As the sustentaculum tali of the calcaneus moves from beneath the talus, the talus rotates into a plantar-flexed position.

Lateral Vlew

the angle between the long axes of the talus and the calcaneus will be increased. In a lateral view, there will be sagging at the talusnavicular joint and divergence of the long axis of the talus from the long axis of the calcaneus, If the diagnosis is in question, MRI' can show a tendon discontinuity as well as a proximal balling-up ofthe tendon (Fig. 4). At first, it might be thought that a tenogram would be

helpf~l.~.In the authors' experience, however, this is not the case. Either the diagnosis is so evident that it is not necessary or in cases of difficult diagnosis the tenogram is equivocal. STAGE 3-TENDON ELONGATED, AND STIFF HINDFOOT DEFORMED The pain may transfer to the lateral aspect of the hindfoot and be located over the sinus

200

Johnson and Strorn

FIG.4. MRI shows the balled-up tendon (arrow) just behind the medial malleolus. (From Alexander ef al.’ By permission of the American Orthopaedic Foot and Ankle Society.) tarsi because the tendon is now completely disrupted and intrinsically less painful. This has allowed the hindfoot to go into eversion. As this occurs, the bone projection from the inferior surface of the talus at the anterior

Clinical Orthopaedics and Related Research

margin of the posterior facet will impinge on the superior aspect of the calcaneus in the sinus tarsi. Pressing on the sinus tarsi will reproduce the patient’s pain symptoms. In Stage 3, the pain also may be more suggestive of degenerative arthritis, exhibiting an activity-related sharp pain that is present long after the activity ceases. Deformity is the most prevalent change. When viewed posteriorly, the fullness beneath the medial malleolus may not be so evident, but the hindfoot eversion and forefoot abduction are significant. The single-heel-rise test will demonstrate the absence of locking hindfoot inversion along with a diminished ability to rise on the ball of the foot. Also, too many toes will be seen. At this stage, the foot appears severely flat (Fig. 5). The hindfoot valgus and forefoot abduction will be seen on standing AP and lateral roentgenograms, much the same as in Stage 2 but more marked. Secondary degenerative changes with joint narrowing and osteophyte formation may also appear in the subtalar, talonavicular, and calcaneocuboid joints. If that anterior margin of the posterior facet projecting inferiorly off the talus is impinging on the superior aspect of the calcaneus, sclerosis will appear in the midsuperior calcaneus at the site of impingement. This bony condensation is called the “sinus tarsi impingement sign.” If a technetium scan is done, the delayed views will show uptake at the site of sinus tarsi impingement as well as at sites of secondary degenerative arthritis. PATHOLOGIC AND TREATMENT CONSIDERATIONS With an understanding of the diagnostic signs and symptoms along with roentgenographic abnormalities as presented above, the pathologic changes can be anticipated and a treatment program offered.

FIG.5 . Acquired pes planus as a late result of TPT rupture. (From Johnson.*By permission of J. B. Lippincott.)

STAGE1-TENDON LENGTHNORMAL At this stage, the length of the tendon appears normal. This early presentation, how-

Number 239 February, 1989

ever, is the most varied and hardest to describe and explain. In some instances, there is almost a pure peritendinitis. That is, when the TPT retinaculum is opened, much clear amber synovial fluid will escape.I3 The tendon itself will look and feel essentially normal, but a luxuriant synovial proliferation will be present within the tendon sheath. In other cases, there will be minimal synovial fluid and synovial thickening; however, in this case the tendon, in a location just distal to the medial malleolus, will be firm and have an off-white color (Fig. 6A). There may be some longitudinal split tears within the tendon substance, and it may be enlarged in a bulbous configuration to almost twice the normal tendon width.” This would be a pure tendon degeneration. Combinations of peritendinitis and degeneration may also be seen. Still, the tendon length appears normal. It is unclear whether the different presentations represent different causes, e.g., peritendinitis from systemic inflammatory disease or degeneration from acute traumatic interstitial tears. The current treatment in this situation (Fig. 6B) is to open the sheath from the TPT musculotendinous junction all the way to its insertion, leaving only a 1-cm pulley just posterior to the medial malleolus.18 Synovectomy is performed and the tendon is debrided. If the tendon is enlarged to more than 1.5 times its normal size, a wedge is removed from the substance to debulk the tendon and the gap is sutured closed.” Small flap tears are debrided and larger tears are sutured. As the wound is closed, some betamethasone is left around the tendon. A short-leg walking cast is then applied and worn for three weeks. This treatment method seems to be successful in stopping the inflammation and tendon degeneration that would otherwise proceed to Stage 2 changes. In a few cases, excising or reattaching the tendon was not ~atisfactory.~ It is important that the patient with Stage 1 physical findings does not progress to Stage 2 or 3 with conservative care. For three to six

Tibialis Posterior Tendon Dysfunction

201

months, trials of antiinflammatory agents, rest, arch supports, and perhaps medial shoe wedges or orthotics may be appropriate. Because steroid injection has been implicated in tendon ~ e a k e n i n gits , ~use is not suggested. If improvement does not occur, then the surgical treatment just outlined should be used to break the inflammation cycle. This applies also to patients with rheumatoid arthritis in whom loss of TPT function and subsequent deformity can be as disabling as some large joint involvement. STAGE 2-TENDON ELONGATED, HINDFOOTMOBILE In this situation, the tendon may show marked degeneration over several centimeters. The tendon is enlarged and has multiple longitudinal tears with secondary adhesions to the tendon sheath. It will be a varied yellowish white-brown color and firm in consistency. Proximal to the directly involved region, the tendon will have a peculiar white, fish-flesh appearance if the tear is old and tension has not been transmitted through the tendon for some time. In other situations, there will be a single complete transverse tear of the tendon with rounding off of the tendon ends. The tendon that remains will then have the off-white, fish-flesh appearance. When the TPT has been elongated, the flexor digitorum longus (FDL) is transferred to substitute for the TPT.4,6,8*’2 This transfer entails detaching the FDL distally and reinserting it into the undersurface of the navicular through a drill hole (Figs. 7A-8G). The distal portion of the FDL does not need to be tenodesed to the adjacent flexor hallucis longus tendon. The intrinsic toe flexors are So good in the foot that leaving the distal stump alone will cause no functional loss in lesser toe function later. Avoiding this tenodesis also allows a greater length of FDL to be used for transfer. Should the FDL be left in its own sheath or rerouted through the flexor hallucis longus

202

Johnson and Strom

Clincal Onhopaedlcs and Related Research

FIGS.6A AND 6B. Medial view of right foot. (A) TPT is exposed, leaving a pulley just posterior to the medial malleolus. The off-white discoloration of the tendon just distal to the medial malleolus is seen. (B) At completion of the surgical procedure, the tendon sheath has been released and synovectomy is completed.

Number 239 February, 1989

sheath? It does not make sense to reroute a healthy tendon through a diseased tendon sheath. The FDL tendon is probably strong enough for substitution. The anatomic crosssectional area of the FDL is only about onethird that of the TPT,I5 but it seems to be holding up well clinically. Perhaps it hypertrophies. The FDL should be pulled as tight as reasonably possible. With the ankle in equinus and the forefoot in varus, the tendon is pulled quite taut and sutured distally. (There is no anatomic rationale for this but it seems to work.) A proximal attachment of the TPT muscle should not necessarily be made to the FDL. If, when the proximal stump of the TPT is pulled, the muscle seems to be nonyielding and fibrotic, the proximal attachment is not done because the muscle is nonfunctional. A soft-tissue static transfer is also usually unnecessary. Although some authors6 have advocated reefing the talonavicular capsule and the calcaneonavicular (spring) ligament, this has not been done as a part of the repair procedure. Suturing of the FDL to the undersurface of the talonavicular region may accomplish this to some degree. Static transfers alone, historically, have not been successful in maintaining the arch of the foot. A negative exploration for a suspected TPT dysfunction has become more and more infrequent. Usually what is found at operation is more extensive than suspected clinically. It is necessary to carry the surgical dissection all the way to the TPT insertion where the tearing and elongation may be located. The results of transfer of the FDL for the elongated TPT have been quite Initially, resuturing or reattachment of the elongated tendon was recommended but the results were not satisfactory. Because the FDL seems to be so expendable, liberal use of this transfer seems reasonable. There are two signs that will indicate a complete disruption of the TPT before the whole tendon is visualized. The first is the white sign. If, when the sheath of the TPT is

Tibialis Posterior Tendon Dysfunction

203

- -TlBlALlS P0STERK)R - - FLEXOR DlGlTORUM LONGUS - - FLEXOR HALLUCIS LONGUS

-1IBIALIS

POSTERIOR

- FLEXOR DlGlTORUM LONGUS

B

FIGS.7A AND 7B. Diagrams showing (A) the discontinuity in the TPT and the position of adjacent tendons and (B) the transfer of the FDL to substitute for the TPT. (By permission of Mayo Foundation.) opened several centimeters proximal to the medial malleolus, the tendon appears white compared to the adjacent FDL, the tendon will be completely disrupted distally. The second is the resident sign and is only possible when practicing in a training program with residents. If, upon entering the operating room one hears the resident muttering “Tom, Dick, and Harry,” followed by the statement that the patient does not have a TPT, then the tendon is torn. The reason is that the tendon has changed color and is scarred closely behind the tibia and has not yet been correctly identified.

204

Johnson and Strom

ClinlcalOrthopaedics and Related Research

FIGS.8A-8G. Transfer of FDL to substitute for TPT. (A) Medial view of left foot, showing incision and TPT apparent just beneath the flexor retinaculum proximally. (B) Fish-flesh discoloration of TPT in contrast to normal FDL just beneath it. (C) FDL tendon is uncovered and retracted prior to transection distally. (D) Zigzag suture is placed in the end of the FDL tendon. (E) Drill hole is made from superior to inferior through navicular tuberosity. (F) Tendon of the FDL is drawn through the drill hole and sutured to the surrounding soft tissues. (G) Transfer of the FDL is completed. Distally, the transferred tendon runs beneath the TPT and is sutured to it. Proximally, tenodesis of the TPT to the FDL was not done because of the fibrotic changes within the tibialis posterior musculotendinous structure.

Number 239 February. 1989

Tibialis Posterior Tendon Dysfunction

STAGE 3-TENDON

ELONGATED,

HINDFOOTDEFORMED AND STIFF

The tendon changes are much the same as in Stage 2. The static supports of the foot also have been damaged, and fixed flatfoot has developed. A dynamic tendon transfer against a fixed deformity is not reasonable. Instead, a realignment followed by an arthrodesis is done. Controversy rages as to whether subtalar arthrodesis,16 talonavicular arthrodesis,I6 talonavicular with calcaneocuboid arthrodesis,” or triple arthrodesis should be done. In fact, it probably does not make much difference. Arthrodesing any one of the hindfoot joints will effectively block hindfoot motion. It is important that the method ofarthrodesis not malalign the adjacent joints. The authors’ personal preference is for an isolated subtalar arthrodesis in most cases. Based on the two-piece concept of the foot (Fig. 3), the talus and everything else distally, with the subtalar arthrodesis being the everything else, is repositioned beneath the talus. The subtalar arthrodesis should not disrupt t t e relative positions at the talonavicular and calcaneocuboidjoints. For the subtalar arthrodesis, a morcellated bone graft from the anterior iliac crest is inserted into the subtalar joint with temporary fixation by a Steinmann pin across the neck of the talus into the calcaneus. An arthrodesis with ten weeks of cast immobilization and then gradual recuperation may seem a bit drastic. But the FDL tendon transfer requires six weeks of casting followed by an even longer period of recuperation. If there is any question as to which of the two should be done, based on the degree and rigidity of hindfoot change, the authors select the arthrodesis. DISCUSSION The tibialis posterior muscle-tendon unit is a prime stabilizer of the hindfoot. By virtue of its position posterior to the axis of the ankle joint and medial to the subtalar axis, it provides plantar flexion at the ankle and in-

205

version of the hindfoot. The tendon excursion is short and the muscle is powerful. Thus, elongation of the tendon will decrease its function significantly. The recent concepts of the TPT difficulties have evolved through the efforts of multiple authors. Two particularly important contributions were the paper by Kettelkamp and Alexander’ clearly describing the problem, and that by Goldner et aL6 suggesting tendon transfers. Since then, the experience and variations of others have been added. It is interesting to speculate that perhaps the most efficacious pain relief aspect of the tendon transfer procedures is really the release of the TPT sheath. Earlierlo.’491* it was reported that release of the sheath of the TPT alone was satisfactory. Still, it is reasonable to add the strength of the FDL to substitute for the TPT and to avoid progression of the flatfoot deformity. When this information is presented at a meeting someone will inevitably say that he or she has been in practice for 20 years and has never seen a case of TPT dysfunction. Then, a few weeks later, this same doctor surprisingly finds his or her first case. These patients are out there and can be helped. There is probably also a Stage 4 TPT dysfunction. This is when the hindfoot has become fixed in eversion, over a number of years, to produce a valgus tilt of the talus within the ankle mortise and lateral tibiotalar degeneration. This pattern may be seen without prior history of trauma. For these patients, an arthrodesis from the tibia to the calcaneus can be done. With awareness of the TPT problem, such an extensive reconstructive procedure could have been avoided. REFERENCES 1. Alexander, 1. J., Johnson, K. A., and Berquist, T. H.:

Magnetic resonance imaging in the diagnosis of disruption of the posterior tibia1 tendon. Foot Ankle 8: 144,1987. 2. Citron, N.: Injury of the tibialis posterior tendon: A cause of acquired valgus foot in childhood. Injury 16:610, 1985. 3 . Ford, L. T., and DeBender, J.: Tendon rupture after local steroid injection. South. Med. J . 72:827, 1979.

206

-

Clinical Orlhopaedics and Related Research

Johnson and Strorn

4. Funk, D. A., Cass, J. R., and Johnson, K. A.: Acquired adult flat foot secondary to posterior tibialtendon pathology. J. Bone Joint Surg. 68A:95, 1986. 5. Gilula, L. A., Oloff, L., Caputi, R., Destouet, J. M., Jacobs, A,, and Solomon, M. A.: Ankle tenography: A key to unexplained symptomatology. Radiology 151:581, 1984. 6. Goldner, J. L., Keats, P. K., Bassett, F. H. 111, and Clippinger, F. W.: Progressive talipes equinovalgus due to trauma or degeneration of the posterior tibial tendon and medial plantar ligaments. Orthop. Clin. North Am. 939, 1974. 7. Jahss, M. H.: Spontaneous rupture ofthe tibialis posterior tendon: Clinical findings, tenographic studies, and a new technique of repair. Foot Ankle 3:158, 1982. 8. Johnson, K. A.: Tibialis posterior tendon rupture. Clin. Orthop. 177:140, 1983. 9. Kettelkamp, D. B., and Alexander, H. H.: Spontaneous rupture of the posterior tibial tendon. J. Bone Joint Surg. 5 lA:759, 1969. 10. Key, J. A,: Partial rupture ofthe tendon of the poste-

II. 12. 13. 14. 15.

16. 17. 18.

nor tibial muscle. J. Bone Joint Surg. 35A:1006. 1953. Leach, R. E., DeIorio, E., and Harney, R. A,: Pathologic hindfoot conditions in the athlete. Clin. Orthop. 177:I 16, 1983. Mann, R. A., and Thompson, F. M.: Rupture of the posterior tibial tendon causing flat foot. J. Bone Joint Surg. 67A:556, 1985. Mueller, T. J.: Ruptures and lacerations of the tibialis posterior tendon. J. Am. Podiatr. Med. Assoc. 74: 109, 1984. Nonis, S. H., and Mankin, H. J.: Chronic tenosynovitis of the posterior tibial tendon with new bone formation. J. Bone Joint Surg. 60B:523, 1978. Sutherland, D. H.: An electromyographic study of the plantar flexors of the ankle in normal walking on the level. J. Bone Joint Surg. 48A:66, 1966. Thomas, W. H.: Personal communication, 1986. Trevino, S., Gould, N., and Korson, R.: Surgical treatment of stenosing tenosynovitis at the ankle. Foot Ankle2:37, 1981. Williams, R.: Chronic non-specific tendovaginitis of tibialis posterior. J. Bone Joint Surg. 45B542, 1963.

This is an enhanced PDF from The Journal of Bone and Joint Surgery The PDF of the article you requested follows this cover page.

Treatment of Acute Achilles Tendon Ruptures. A Meta-Analysis of Randomized, Controlled Trials Riaz J.K. Khan, Dan Fick, Angus Keogh, John Crawford, Tim Brammar and Martyn Parker J Bone Joint Surg Am. 2005;87:2202-2210. doi:10.2106/JBJS.D.03049

This information is current as of June 10, 2007 Supplementary material

Commentary and Perspective, data tables, additional images, video clips and/or translated abstracts are available for this article. This information can be accessed at http://www.ejbjs.org/cgi/content/full/87/10/2202/DC1 Letters to The Editor are available at http://www.ejbjs.org/cgi/content/full/87/10/2202#responses

Subject Collections

Articles on similar topics can be found in the following collections Adult Trauma (574 articles) Foot/Ankle (161 articles) Ankle (82 articles) Soft Tissue Trauma (213 articles)

Reprints and Permissions

Click here to order reprints or request permission to use material from this article, or locate the article citation on jbjs.org and click on the [Reprints and Permissions] link.

Publisher Information

The Journal of Bone and Joint Surgery 20 Pickering Street, Needham, MA 02492-3157 www.jbjs.org

2202 COPYRIGHT © 2005

BY

THE JOURNAL

OF

BONE

AND JOINT

SURGERY, INCORPORATED

Treatment of Acute Achilles Tendon Ruptures A META-ANALYSIS

OF

RANDOMIZED, CONTROLLED TRIALS

BY RIAZ J.K. KHAN, FRCS(TR&ORTH), DAN FICK, MBBS, ANGUS KEOGH, MBBS, JOHN CRAWFORD, FRCS(TR&ORTH), TIM BRAMMAR, FRCS(TR&ORTH), AND MARTYN PARKER, MD Investigation performed at Perth Orthopaedic Institute, Department of Surgery and Pathology, University of Western Australia, Perth, Australia

Background: There is a lack of consensus regarding the best option for the treatment of acute Achilles tendon rupture. Treatment can be broadly classified as operative (open or percutaneous) or nonoperative (casting or functional bracing). Postoperative splinting can be performed with a rigid cast (proximal or distal to the knee) or a more mobile functional brace. The aim of this meta-analysis was to identify and summarize the evidence from randomized, controlled trials on the effectiveness of different interventions for the treatment of acute Achilles tendon ruptures. Methods: We searched multiple databases (including EMBASE, CINAHL, and MEDLINE) as well as reference lists of articles and contacted authors. Keywords included Achilles tendon, rupture, and tendon injuries. Three reviewers extracted data and independently assessed trial quality with use of a ten-item scale. Results: Twelve trials involving 800 patients were included. There was a variable level of methodological rigor and reporting of outcomes. Open operative treatment was associated with a lower risk of rerupture compared with nonoperative treatment (relative risk, 0.27; 95% confidence interval, 0.11 to 0.64). However, it was associated with a higher risk of other complications, including infection, adhesions, and disturbed skin sensibility (relative risk, 10.60; 95% confidence interval, 4.82 to 23.28). Percutaneous repair was associated with a lower complication rate compared with open operative repair (relative risk, 2.84; 95% confidence interval, 1.06 to 7.62). Patients who had been managed with a functional brace postoperatively (allowing for early mobilization) had a lower complication rate compared with those who had been managed with a cast (relative risk, 1.88; 95% confidence interval, 1.27 to 2.76). Because of the small number of patients involved, no definitive conclusions could be made regarding different nonoperative treatment regimens. Conclusions: Open operative treatment of acute Achilles tendon ruptures significantly reduces the risk of rerupture compared with nonoperative treatment, but operative treatment is associated with a significantly higher risk of other complications. Operative risks may be reduced by performing surgery percutaneously. Postoperative splinting with use of a functional brace reduces the overall complication rate. Level of Evidence: Therapeutic Level I. See Instructions to Authors for a complete description of levels of evidence.

T

he Achilles tendon, which is formed by the merging of the tendons of the gastrocnemius and soleus, is the thickest and strongest tendon in the human body. Acute ruptures occur most commonly in men in the third and fourth decades of life who participate in sports intermittently, and the left side is ruptured more commonly than is the right side1. The mechanisms of injury include sudden forced plantar flexion of the foot, unexpected dorsiflexion of the foot, and violent dorsiflexion of a plantar flexed foot2. The prevalence is approximately 18 per 100,000 per year (in Finland) and is thought to be rising3. It is generally accepted that ruptures occur in previously abnormal tendons2,4. A number of etiological theories have been proposed, including the adverse influence of oral and

topical corticosteroids5,6, fluoroquinolone antibiotics (e.g., ciprofloxacin)7, exercise-induced hyperthermia8, and mechanical abnormalities of the foot9. Treatment of acute Achilles tendon ruptures can be broadly classified as operative (open or percutaneous) or nonoperative (cast immobilization or functional bracing). Generally, open operative treatment has been used for athletes and young, fit patients; percutaneous operative treatment has been used for those who do not wish to have an open repair (e.g., for cosmetic reasons); and nonoperative treatment has been used for the elderly10-13. Previous reviews have examined the relative advantages of operative and nonoperative treatment14-17. However, to our knowledge, there has not been a systematic review of different

2203 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 87-A · N U M B E R 10 · O C T O B E R 2005

methods of nonoperative treatment, operative treatment, and postoperative splinting. The aim of the present meta-analysis was to identify and summarize the evidence from randomized, controlled trials on the effectiveness of all treatment interventions for acute Achilles tendon ruptures. Materials and Methods ll randomized, controlled trials comparing operative and nonoperative methods for the treatment of acute Achilles tendon ruptures were considered for inclusion. Quasi-randomized trials (for example, those involving allocation by alternation or the date of birth) and trials in which the treatment allocation was inadequately concealed were also considered. We searched the Cochrane Musculoskeletal Injuries Group specialized register, reference lists of articles, and proceedings of relevant conferences, and we contacted authors when additional clarification was required. This register is compiled from multiple databases and includes the results of regular searches of the Cochrane Central Register of Controlled Trials in the Cochrane Library, MEDLINE (which combines subject-specific terms with the optimal trial search strategy18), EMBASE, CINAHL,

A

Fig. 1

System used for the scoring of methodology.

TRE A T M E N T O F A C U T E A C H I L L E S TE N D O N R U P T U RE S

and manual search results. In MEDLINE (OVID-WEB), the following subject-specific search was combined with all three levels of the optimal trial search strategy18: Achilles Tendon, (achill#s or tendoachill#s).tw., or/1-2, Rupture/, rupture$.tw., or/4-5, and/3,6, Tendon Injuries/, and/3,8, or/7,9. Articles in all languages were considered for inclusion and were translated when necessary. We excluded retrospective studies, studies with insufficient reporting of primary outcomes, studies with inadequate methods of randomization, and unique randomized, controlled trials (where pooling of data was not possible, making them unsuitable for meta-analysis). Participants included adults with acute ruptures of the Achilles tendon. Patients with delayed presentation (more than three weeks after the injury) and rerupture were excluded. The types of interventions included operative repair (open and percutaneous) and nonoperative treatment (cast immobilization and functional bracing). The primary outcomes were complications of treatment and rerupture. Other outcomes, such as the level of sporting activity, patient satisfaction, and the length of hospital stay, were omitted because they lack quantity and uniformity to support rigorous meta-analysis.

2204 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 87-A · N U M B E R 10 · O C T O B E R 2005

TRE A T M E N T O F A C U T E A C H I L L E S TE N D O N R U P T U RE S

Fig. 2

Flowchart depicting the method by which the twelve randomized, controlled studies were chosen.

Trials were independently assessed for inclusion by four reviewers (R.J.K.K., D.F., A.K., and T.B.). Data on the outcomes listed above were extracted by three reviewers (R.J.K.K., D.F., and T.B.). Differences were resolved by discussion. Ten aspects of methodology were used to assign a maximum score of 12 to each study, similar to the scale described by Detsky et al.19 (Fig. 1). In addition, the risk of pre-allocation disclosure of assignment was rated as A, B, or C according to the Cochrane Reviewers’ Handbook20. For each study, relative risks and 95% confidence intervals were calculated for dichotomous outcomes, and weighted mean differences and 95% confidence intervals were calculated for continuous outcomes. The results of individually randomized trials were pooled whenever possible with use of the fixedeffects model of Mantel-Haenszel. Heterogeneity between comparable studies was tested with the use of a standard chisquare test. The random-effects model of DerSimonian and Laird was used when there was statistical or graphical evidence of heterogeneity. Results hirty-six articles were identified with use of our search strategy; of these, twenty-four were excluded from the meta-analysis (Fig. 2). Details on the twelve randomized, controlled trials that were included in the review are documented in the Appendix. A total of 800 patients were involved. Four studies, involving 356 patients, compared open operative treatment with nonoperative treatment21-24. Five studies, involving 273 patients, compared postoperative splinting in a cast alone (i.e., rigid) with splinting in a cast followed by a functional brace (i.e.,

T

semi-mobile)25-29. Two studies, involving ninety-four patients, compared percutaneous repair with open operative repair24,30. Two studies, involving ninety patients, compared different nonoperative treatment regimens31,32. The group of thirteen patients managed with open operative treatment as described by Schroeder et al.24 were analyzed in two sections of the present review, which accounts for the discrepancy in the overall number of patients and studies involved. The methodological quality scores of the included studies are detailed in Table I. Low scores indicate poor methodology. TABLE I Methodological Quality Scores Scores for Ten Items

Total Score (Maximum, 12)

Cetti et al.21

1110110010

6

Cetti et al.25

1110010011

6

3110100111

9

0110110011

6

0100010101

4

0110111010

6

3110110111

10

2110110010

7

0010010011

4

3110010010

7

Saleh et al.

1100110011

6

Schroeder et al.24

1100100000

3

Study

Kangas et al.

29

Kerkhoffs et al.26 Lim et al.

30

Maffulli et al.28 Moller et al.

22

Mortensen et al.27 Nistor

23

Petersen et al.32 31

2205 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 87-A · N U M B E R 10 · O C T O B E R 2005

TRE A T M E N T O F A C U T E A C H I L L E S TE N D O N R U P T U RE S

Fig. 3

Illustration indicating the prevalence of rerupture associated with open operative and nonoperative treatment. The values are given as the number of patients with a rerupture (n)/number of patients in the group (N), with a summation of the totals and the relative risk (RR) and 95% confidence intervals (95% CI).

Fig. 4

Illustration indicating the prevalence of complications other than rerupture associated with open operative and nonoperative treatment. The values are given as the number of patients with a complication (n)/number of patients in the group (N), with a summation of the totals and the relative risk (RR) and 95% confidence intervals (95% CI).

Open Operative Treatment Compared with Nonoperative Treatment21-24 The rate of rerupture is summarized in Figure 3. One study22 revealed a significant difference between the operative group and the nonoperative group with regard to the rate of rerupture (one of fifty-nine compared with eleven of fifty-three; p = 0.0013). Of the three remaining studies, one showed no difference between operative and nonoperative treatment21, one included no reruptures24, and one did not involve statistical analysis23. Results gave a pooled rate of 3.5% (six of 173) in the operatively treated group and of 12.6% (twenty-three of 183)

in the nonoperatively treated group (relative risk, 0.27; 95% confidence interval, 0.11 to 0.64). The mean duration of followup used for the calculation of rerupture rates ranged from eight to thirty months. Nistor23 and Moller et al.22 reported more adhesions, disturbed sensibility, and deep or superficial wound infection in the operative group. No statistical analysis was performed. Cetti et al.21 reported a significant increase in the rates of delayed wound-healing, adhesions, and disturbed sensibility in the operative group (p = 0.004). The pooled rate of reported complications (other than rerupture) was 34.1% (fifty-nine of 173) in

Fig. 5

Illustration indicating the prevalence of wound infection associated with open operative and nonoperative treatment. The values are given as the number of patients with a wound infection (n)/number of patients in the group (N), with a summation of the totals and the relative risk (RR) and 95% confidence intervals (95% CI).

2206 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 87-A · N U M B E R 10 · O C T O B E R 2005

TRE A T M E N T O F A C U T E A C H I L L E S TE N D O N R U P T U RE S

Fig. 6

Illustration indicating the prevalence of rerupture associated with open surgery and percutaneous surgery. The values are given as the number of patients with a rerupture (n)/number of patients in the group (N), with a summation of the totals and the relative risk (RR) and 95% confidence intervals (95% CI).

the operative group and 2.7% (five of 183) in the nonoperative group (relative risk, 10.60; 95% confidence interval, 4.82 to 23.28). Similar analysis demonstrated an overall rate of wound infection of 4.0% (seven of 173) in the operative group; there were no infections in the nonoperative group (relative risk, 4.89; 95% confidence interval, 1.09 to 21.91). These results are summarized in Figures 4 and 5. Open Compared with Percutaneous Operative Repair24,30 Schroeder et al.24 reported no reruptures, whereas Lim et al.30 found no significant difference between the groups with regard to the rate of rerupture. The pooled rate of rerupture was 4.3% (two of forty-six) in the open group and 2.1% (one of forty-eight) in the percutaneous group (relative risk, 2.00;

95% confidence interval, 0.19 to 21.00). The mean duration of follow-up used for the calculation of the rerupture rates ranged from six to eight months. These results are summarized in Figure 6. The pooled rate of reported complications (excluding rerupture) was 26.1% (twelve of forty-six) in the open group and 8.3% (four of forty-eight) in the percutaneous group (relative risk, 2.84; 95% confidence interval, 1.06 to 7.62). Lim et al. reported a significantly higher rate of wound infection in the open group as compared with the percutaneous group (p = 0.01)30. The pooled rate of infection was 19.6% (nine of fortysix) in the open group and 0% (zero of forty-eight) in the percutaneous group (relative risk, 10.52; 95% confidence interval, 1.37 to 80.52). The results of these analyses are summarized in Figures 7 and 8.

Fig. 7

Illustration indicating the prevalence of complications other than rerupture associated with open surgery and percutaneous surgery. The values are given as the number of patients with a complication (n)/number of patients in the group (N), with a summation of the totals and the relative risk (RR) and 95% confidence intervals (95% CI).

Fig. 8

Illustration indicating the prevalence of wound infection associated with open surgery and percutaneous surgery. The values are given as the number of patients with an infection (n)/number of patients in the group (N), with a summation of the totals and the relative risk (RR) and 95% confidence intervals (95% CI).

2207 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 87-A · N U M B E R 10 · O C T O B E R 2005

TRE A T M E N T O F A C U T E A C H I L L E S TE N D O N R U P T U RE S

Fig. 9

Illustration indicating the prevalence of rerupture associated with postoperative splinting with casting alone and casting followed by functional bracing. The values are given as the number of patients with a rerupture (n)/number of patients in the group (N), with a summation of the totals and the relative risk (RR) and 95% confidence intervals (95% CI).

Postoperative Splinting: Cast Immobilization Alone Compared with Cast Immobilization Followed by Functional Bracing25-29 Rerupture rates are summarized in Figure 9. No individual study demonstrated a significant difference between the groups. The pooled rate of rerupture was 5.0% (seven of 140) in the cast immobilization group and 2.3% (three of 133) in the functional bracing group (relative risk, 2.04; 95% confidence interval, 0.59 to 7.06). The mean duration of follow-up used for the calculation of the rerupture rates ranged from five months to 6.7 years. Complications were more common in the cast-only group; specifically, the cast-only group had higher rates of adhesions (18.6% compared with 9.7%), disturbed sensibility (8.6% compared with 3.8%), keloid or hypertrophic scarring (5% compared with 3%), and infection (3.5% compared with 3%). The pooled rate of reported complications (other than rerupture) was 35.7% (fifty of 140) in the cast immobilization group and 19.5% (twenty-six of 133) in the functional bracing group (relative risk, 1.88; 95% confidence interval, 1.27 to 2.76). The results are summarized in Figure 10. Nonoperative Treatment: Casting Immobilization Compared with Functional Bracing31,32 Pooled data revealed a rerupture rate of 2.4% (one of forty-one) in the functional bracing group and of 12.2% (six of forty-nine) in the casting group (relative risk, 3.59; 95% confidence inter-

val, 0.59 to 21.76). The mean duration of follow-up used for the calculation of the rerupture rates was twelve months for both studies. The results are summarized in Figure 11. Discussion welve prospective randomized studies involving the treatment of acute Achilles tendon rupture fulfilled the inclusion criteria for this meta-analysis. Quality assessment scores were calculated for each study in order to assess the level of methodological rigor. They were not used as a criterion for exclusion or to weight the pooled data. However, the findings of studies with higher methodological quality should naturally be considered to be of greater importance. The scores indicate a variable level of methodological rigor, particularly with regard to the method of randomization and concealment of allocation. The quality of the primary study used for pooled analysis influences the results of a meta-analysis33. The inclusion of poorly randomized trials can lead to over-reporting of treatment effect, and thus all recommendations should be critically appraised. Recommendations have been made on the basis of analysis of pooled data extracted from what were believed to be the most rigorously conducted studies. The rate of rerupture was consistently higher among nonoperatively treated patients as compared with operatively treated patients. The most methodologically sound study22 provided the most favorable rerupture rate with operative interven-

T

Fig. 10

Illustration indicating the prevalence of complications other than rerupture associated with postoperative splinting with casting alone and casting followed by functional bracing. The values are given as the number of patients with a complication (n)/number of patients in the group (N), with a summation of the totals and the relative risk (RR) and 95% confidence intervals (95% CI).

2208 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 87-A · N U M B E R 10 · O C T O B E R 2005

TRE A T M E N T O F A C U T E A C H I L L E S TE N D O N R U P T U RE S

Fig. 11

Illustration indicating the prevalence of rerupture associated with nonoperative treatment (casting alone and casting followed by functional bracing). The values are given as the number of patients with a rerupture (n)/number of patients in the group (N), with a summation of the totals and the relative risk (RR) and 95% confidence intervals (95% CI).

tion, suggesting that there is a legitimate advantage associated with surgery. However, there was a consistent finding of increased rates of complications (other than rerupture) in the operatively treated group, with all studies demonstrating similar rates. In summary, nonoperatively treated patients have a more than three times higher risk of rerupture but have a minimal risk of other complications resulting from treatment. One-third of operatively treated patients have a complication. A meta-analysis by Bhandari et al.15 comparing open operative treatment with nonoperative treatment of acute Achilles tendon ruptures did not provide a strong recommendation for surgery. The authors suggested that patients who are reluctant to undergo an operation may choose nonoperative treatment. Their meta-analysis included six studies, three of which were omitted from the present meta-analysis because of inadequate reporting of results34, discontinuation of treatment in the control group because of a high recurrence rate and no allocation concealment (personal communication with the author)35, and inadequate randomization36. We included an extra study24 that did fulfill our strict inclusion criteria. Nevertheless, the results reported by Bhandari et al.15 are similar to ours; specifically, the rerupture rate was 3.1% for operatively treated patients and 13% for nonoperatively treated patients (p = 0.005) and the infection rate was higher among operatively treated patients (4.7% compared with 0%; relative risk, 4.6; p = 0.03). Lo et al.14 compiled two prospective trials and seventeen case series for their comparison of operative and nonoperative treatment. The studies by Moller et al.22 and Schroeder et al.24 were not included in that analysis. Lo et al. found it difficult to recommend one treatment over the other on the basis of the combined complication rates14. They suggested that patients with poor healing potential should be managed nonoperatively and that active patients should be offered both operative and nonoperative treatment. In other reviews, Lynch16 and Wong et al.17 included sixteen studies and 125 studies, respectively. Both groups of investigators included nonrandomized trials in their analysis. The studies concurred in their recommendation for surgical intervention combined with early functional mobilization for the treatment of acute Achilles tendon ruptures; nonoperative management with early functional mobilization may be an acceptable alternative for patients who are reluctant to undergo a surgical procedure.

Using a technique of analysis not previously applied to rupture of the Achilles tendon, Kocher et al.37 performed an expected-value decision analysis of operative and nonoperative management. Expected-value decision analysis involves allocating utility scores to outcomes and allows quantitative analysis of decision-making. A decision tree was constructed, and prospective patients progressed through the various alternatives. Article selection for the generation of outcome probabilities followed the criteria of Lo et al.14. With use of this technique, operative treatment was found to be the optimal strategy. However, the authors stressed that the decisionmaking process should be shared between doctor and patient. In our analysis of studies comparing open and percutaneous repair, we noted a tendency for a lower overall rate of complications (particularly infection) in the percutaneously treated group. However, this finding is based on pooled data from a small number of patients, and there is some discrepancy between studies with regard to the rate of infection in the open treatment group. In a previous review of prospective and retrospective studies regarding operative and nonoperative treatment, Wong et al.17 reported a lower rate of wound complications in patients undergoing percutaneous repair. However, they also noted that patients in the percutaneous group had relatively high rates of complications (notably sural nerve injury), particularly when the procedure was combined with early active mobilization. One of the most important aspects of the present review is that pertaining to postoperative splintage. This subject has not been previously evaluated with use of meta-analysis. The functional bracing group had a significantly lower rate of complications (p = 0.001), particularly with regard to adhesion formation. The early mobilization group also tended to have a lower rerupture rate. Conclusions made on the basis of the pooled data must be interpreted with caution because of the variety of regimens used. Limited conclusions can be drawn from the two studies comparing nonoperative treatment in a cast and functional bracing because of the small numbers involved (ninety patients), differences in regimens, and minimal reporting of outcomes31,32. It is interesting to note, however, that the pooled rate of rerupture in the functional bracing group (2.4%) was lower than that for patients managed with operative treatment (3.5%). Indeed, it was almost equivalent to that seen for patients managed with

2209 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 87-A · N U M B E R 10 · O C T O B E R 2005

immobilization in a functional brace after open repair (2.3%). This apparent discrepancy may be explained by the small numbers of patients managed nonoperatively. In conclusion, open operative treatment of acute Achilles tendon ruptures significantly reduces the risk of rerupture compared with nonoperative treatment but has the drawback of a significantly higher risk of other complications, including wound infection. Complications may be reduced by performing surgery percutaneously. Postoperative splinting in a cast followed by a functional brace rather than a cast alone reduces the overall complication rate. Additional rigorously conducted prospective randomized trials with larger sample sizes, full reporting of outcomes, and blinding of assessors are required. Increased transparency is needed if the same cohort of patients is reported on in different studies, and avoidance of multiple publications is strongly recommended. Appendix A table presenting the characteristics of the included studies is available with the electronic versions of this article, on our web site at jbjs.org (go to the article citation and click on “Supplementary Material”) and on our quarterly CDROM (call our subscription department, at 781-449-9780, to order the CD-ROM). 

TRE A T M E N T O F A C U T E A C H I L L E S TE N D O N R U P T U RE S

Riaz J.K. Khan, FRCS(Tr&Orth) Department of Orthopaedics, Norfolk and Norwich University Hospital, Colney Lane, Norwich, Norfolk, NR4 7UY, United Kingdom. E-mail address: [email protected] Dan Fick, MBBS Angus Keogh, MBBS Department of Surgery and Pathology, University of Western Australia, Perth, WA 6009, Australia John Crawford, FRCS(Tr&Orth) Tim Brammar, FRCS(Tr&Orth) Addenbrooke’s Hospital, Cambridge, CB2 2QQ, United Kingdom Martyn Parker, MD Peterborough District Hospital, Peterborough, PE3 6DA, United Kingdom The authors did not receive grants or outside funding in support of their research or preparation of this manuscript. They did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.

doi:10.2106/JBJS.D.03049

References 1. Hattrup SJ, Johnson KA. A review of ruptures of the Achilles tendon. Foot Ankle. 1985;6:34-8.

16. Lynch RM. Achilles tendon rupture: surgical versus non-surgical treatment. Accid Emerg Nurs. 2004;12:149-58.

2. Arner O, Lindholm A. Subcutaneous rupture of the Achilles tendon: a study of 92 cases. Acta Chir Scand. 1959;116:1-51.

17. Wong J, Barrass V, Maffulli N. Quantitative review of operative and nonoperative management of achilles tendon ruptures. Am J Sports Med. 2002;30:565-75.

3. Leppilahti J, Puranen J, Orava S. Incidence of Achilles tendon rupture. Acta Orthop Scand. 1996;67:277-9.

18. Alderson P, Green S, Higgins JPT, editors. MEDLINE highly sensitive search strategy for SilverPlatter-MEDLINE, OVID-MEDLINE, and PubMed. Cochrane reviewers’ handbook 4.2.1; Appendix 5B. In: The Cochrane library, Issue 1. Chichester, UK: John Wiley and Sons; 2004.

4. Tallon C, Maffulli N, Ewen SW. Ruptured Achilles tendons are significantly more degenerated than tendinopathic tendons. Med Sci Sports Exerc. 2001; 33:1983-90. 5. Mahler F, Fritschy D. Partial and complete ruptures of the Achilles tendon and local corticosteroid injections. Br J Sports Med. 1992;26:7-14. 6. Newnham DM, Douglas JG, Legge JS, Friend JA. Achilles tendon rupture: an underrated complication of corticosteroid treatment. Thorax. 1991;46:853-4. 7. Royer RJ, Pierfitte C, Netter P. Features of tendon disorders with fluoroquinolones. Therapie. 1994;49:75-6. 8. Wilson AM, Goodship AE. Exercise-induced hyperthermia as a possible mechanism for tendon degeneration. J Biomech. 1994;27:899-905.

19. Detsky AS, Naylor CD, O’Rourke K, McGeer AJ, L’Abbe KA. Incorporating variations in the quality of individual randomized trials into meta-analysis. J Clin Epidemiol. 1992;45:255-65. 20. Alderson P, Green S, Higgins JPT, editors. Assessment of study quality. Cochrane reviewers’ handbook 4.2.1; Section 6. In: The Cochrane library, Issue 1. Chichester, UK: John Wiley and Sons; 2004. 21. Cetti R, Christensen SE, Ejsted R, Jensen NM, Jorgensen U. Operative versus nonoperative treatment of Achilles tendon rupture. A prospective randomized study and review of the literature. Am J Sports Med. 1993;21:791-9.

9. Clement DB, Taunton JE, Smart GW. Achilles tendinitis and peritendinitis: etiology and treatment. Am J Sports Med. 1984;12:179-84.

22. Moller M, Movin T, Granhed H, Lind K, Faxen E, Karlsson J. Acute rupture of tendon Achillis. A prospective randomised study of comparison between surgical and non-surgical treatment. J Bone Joint Surg Br. 2001;83:843-8.

10. Bossley CJ. Rupture of the Achilles tendon. J Bone Joint Surg Am. 2000; 82:1804.

23. Nistor L. Surgical and non-surgical treatment of Achilles tendon rupture. A prospective randomized study. J Bone Joint Surg Am. 1981;63:394-9.

11. Maffulli N. Rupture of the Achilles tendon. J Bone Joint Surg Am. 1999; 81:1019-36.

24. Schroeder D, Lehmann M, Steinbrueck K. Treatment of acute achilles tendon ruptures: open vs. percutaneous repair vs. conservative treatment. A prospective randomized study. Orthop Trans. 1997;21:1228.

12. Martinelli B. Rupture of the Achilles tendon. J Bone Joint Surg Am. 2000; 82:1804. 13. Raisbeck CC. Rupture of the Achilles tendon. J Bone Joint Surg Am. 2000; 82:1804-5. 14. Lo IK, Kirkley A, Nonweiler B, Kumbhare DA. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a quantitative review. Clin J Sport Med. 1997;7:207-11. 15. Bhandari M, Guyatt GH, Siddiqui F, Morrow F, Busse J, Leighton RK, Sprague S, Schemitsch EH. Treatment of acute Achilles tendon ruptures: a systematic overview and metaanalysis. Clin Orthop Relat Res. 2002;400:190-200.

25. Cetti R, Henriksen LO, Jacobsen KS. A new treatment of ruptured Achilles tendons. A prospective randomized study. Clin Orthop Relat Res. 1994;308:155-65. 26. Kerkhoffs GM, Struijs PA, Raaymakers EL, Marti RK. Functional treatment after surgical repair of acute Achilles tendon rupture: wrap vs walking cast. Arch Orthop Trauma Surg. 2002;122:102-5. 27. Mortensen NH, Skov O, Jensen PE. Early motion of the ankle after operative treatment of a rupture of the Achilles tendon. A prospective, randomized clinical and radiographic study. J Bone Joint Surg Am. 1999;81:983-90. 28. Maffulli N, Tallon C, Wong J, Lim KP, Bleakney R. Early weightbearing and an-

2210 THE JOUR NAL OF BONE & JOINT SURGER Y · JBJS.ORG VO L U M E 87-A · N U M B E R 10 · O C T O B E R 2005

kle mobilization after open repair of acute midsubstance tears of the achilles tendon. Am J Sports Med. 2003;31:692-700. 29. Kangas J, Pajala A, Siira P, Hamalainen M, Leppilahti J. Early functional treatment versus early immobilization in tension of the musculotendinous unit after Achilles rupture repair: a prospective, randomized, clinical study. J Trauma. 2003;54:1171-81. 30. Lim J, Dalal R, Waseem M. Percutaneous vs. open repair of the ruptured Achilles tendon—a prospective randomized controlled study. Foot Ankle Int. 2001;22:559-68. 31. Saleh M, Marshall PD, Senior R, MacFarlane A. The Sheffield splint for controlled early mobilisation after rupture of the calcaneal tendon. A prospective, randomised comparison with plaster treatment. J Bone Joint Surg Br. 1992; 74:206-9. 32. Petersen OF, Nielsen MB, Jensen KH, Solgaard S. [Randomized comparison of CAM walker and light-weight plaster cast in the treatment of first-time Achilles tendon rupture]. Ugeskr Laeger. 2002;164:3852-5. Danish. 33. Moher D, Pham B, Jones A, Cook DJ, Jadad AR, Moher M, Tugwell P, Klassen TP. Does quality of reports of randomised trials affect estimates of intervention efficacy reported in meta-analyses? Lancet. 1998;352:609-13. 34. Coombs RRH. Prospective trial of conservative and surgical treatment of Achilles tendon rupture. J Bone Joint Surg Br. 1981;63:288. 35. Majewski M, Rickert M, Steinbruck K. [Achilles tendon rupture. A prospective study assessing various treatment possibilities]. Orthopade. 2000;29:670-6. German. 36. Thermann H, Zwipp H, Tscherne H. [Functional treatment concept of acute rupture of the Achilles tendon. 2 years results of a prospective randomized study]. Unfallchirurg. 1995;98:21-32. German. 37. Kocher MS, Bishop J, Marshall R, Briggs KK, Hawkins RJ. Operative versus nonoperative management of acute Achilles tendon rupture: expected-value decision analysis. Am J Sports Med. 2002;30:783-90. 38. Haggmark T, Liedberg H, Eriksson E, Wredmark T. Calf muscle atrophy and muscle function after non-operative vs operative treatment of achilles tendon ruptures. Orthopedics. 1986;9:160-4. 39. Helgeland J, Odland P, Hove LM. [Achilles tendon rupture. Surgical or nonsurgical treatment]. Tidsskr Nor Laegeforen. 1997;117:1763-6. Norwegian. 40. Paes E, Weyand F, Tuncay N. [Management of Achilles tendon rupture. A comparative study of the adaptation suture and the plantaris tendon interweaving technic]. Unfallchirurg. 1985;88:303-7. German. 41. Steele GJ, Harter RA, Ting AJ. Comparison of functional ability following percutaneous and open surgical repairs of acutely ruptured Achilles tendons. J Sport Rehab. 1993;2:115-27. 42. Weber M, Niemann M, Lanz R, Muller T. Nonoperative treatment of acute rupture of the achilles tendon: results of a new protocol and comparison with

TRE A T M E N T O F A C U T E A C H I L L E S TE N D O N R U P T U RE S

operative treatment. Am J Sports Med. 2003;31:685-91. 43. Weber O, Schmidgen A. Semifunctional postoperative treatment of Achilles tendon rupture. Trauma und Berufskrankheit. 1999;1:258-63. 44. Wellner K. [Modified Kirchmayr suture in comparison with the Silfverskjold folding-plasty in primary management of covered Achilles tendon rupture]. Beitr Orthop Traumatol. 1990;37:107-12. German. 45. Kakiuchi M. A combined open and percutaneous technique for repair of tendo Achillis. Comparison with open repair. J Bone Joint Surg Br. 1995; 77:60-3. 46. Kern O, Bouillon B, Lobach R. On the therapy of fresh rupture of the achilles tendon operative-functional vs. conservative functional therapy. Hefte zur der Unfallchirurg. 1996;262:199. 47. Thermann H, Hufner T, Tscherne H. [Achilles tendon rupture]. Orthopade. 2000;29:235-50. German. 48. Thermann H, Zwipp H, Milbradt H, Reimer P. [Ultrasound sonography in the diagnosis and follow-up of Achilles tendon rupture]. Unfallchirurg. 1989;92:26673. German. 49. Thermann H, Zwipp H, Sudkamp N. Operative versus conservative functional treatment of rupture of the achilles tendon. Hefte zur Unfallheilkunde. 1989;207:398. 50. Thermann H, Zwipp H. [Achilles tendon rupture]. Orthopade. 1989;18:32133. German. 51. Thermann H. Conservative functional treatment. Chirurgische Praxis. 2001; 58:83-95. 52. Thermann H. Functional treatment concept for fresh rupture of the achilles tendon. Hefte zur der Unfallchirurg. 1996;248:4873. 53. Thermann H. Rupture of the Achilles tendon. Conservative vs operative. Trauma und Berufskrankheit. 2000;2:160-6. 54. Thermann H, Zwipp H. Conservative treatment of fresh rupture of the achilles tendon. Hefte zur Unfallheilkunde. 1992;222:83-94. 55. Zwipp H, Thermann H, Sudkamp N, Tscherne H, Milbradt H, Reimer P, Heintz P. [An innovative concept for primary functional treatment of Achilles tendon rupture]. Sportverletz Sportschaden. 1990;4:29-35. German. 56. Mortensen NH, Saether J, Steinke MS, Staehr H, Mikkelsen SS. Separation of tendon ends after Achilles tendon repair: a prospective, randomized, multicenter study. Orthopedics. 1992;15:899-903. 57. Mortensen NH, Sorensen L, Pless S. Below-knee versus above-knee cast after Achilles tendon repair—a prospective controlled trial. Acta Orthop Scand. 1996;67:38. 58. Maffulli N, Tallon C, Wong J, Peng Lim K, Bleakney R. No adverse effect of early weight bearing following open repair of acute tears of the Achilles tendon. J Sports Med Phys Fitness. 2003;43:367-79.

TREATMENT

OF

MOBILE

FLAT FOOT BY DISPLACEMENT OF THE CALCANEUS

E. KOUTSOGIANNIS, From

The

purpose

treatment

to

mobile

flat

and

foot.

an

the

side.

He

believed

that

Bristol,

simple

and cases

calcaneal

angle

old

between

of a medial

severe

flat

one.

foot.

the

wedge.

The

Only

long

one

the

basic

principles

were

patient,

the

than

normal

and

there

navicular

flat

foot

or from

for

some

years,

In

of the and and 96

mobile

flat foot

flat

foot

the

in cerebral

calcaneus

lying on a lower level producing a prominence bones

in the

navicular

bone,

the

cuneiform

as

description

of the

Lord however,

insertion same

shows that the ground,

is a subluxation

effective

was

calcaneus

the

thirteen calcaneal

the

given

and

reported had

with failed

medial to

(Fig.

pillar which 1).

lies

than normal. medially just of the foot is sometimes

THE in

of

osteotomy

graft

patient

floor.

cases

in the

outer

suffered

from

the inferior the talus is

at the tab-

joint.

palsy.

OF

by

1967). Gleich’s and downwards

of a tibial

whether

an

wear in patients measures have

In many

patients

with

the latter

condition

tendo calcaneus as a supplementary procedure at the same time. osteotomy of the calcaneus has been practised in the Bristol clinical the operation having been first performed here by the late Mr Pridie.

ANATOMY

medially, its head

first

axis

In 1923

supplementary procedures. calcaneal osteotomy with

less horizontal

mobile

osteotomy

prevent abnormal shoe in which conservative

FIG. 1 Radiograph of a foot in the standing position surface of the calcaneus is almost parallel with

he elongated the Displacement

Englaizd

Simon, Spindell, Litchman and Scala posterior fragment forwards, medially

normal

excision

for

GREECE

of the

others all required (1960) advocated

Dwyer

advocate

those

Silver,

the

by

osteotomy

alone;

by

restore

achieved

calcaneal

Hospital,

shape

for

displacement

to

was

is to

improve

(quoted

involved attempt

This

paper

Southmead

warrant surgical treatment. of calcaneal osteotomy is an

1893

iii

technique

this fatigue,

It is reserved

the symptoms The concept

Gleich in

of

relieve

the

LARISSA,

OSTEOTOMY

FLAT

valgus;

The behind

area

FOOT its

superior

talus is rotated the navicular

is lost,

and

added

a subluxation

subluxation

THE

articular

is produced between

JOURNAL

surface

is

tilted

medially and downwards, bone. Hence the alignment

OF

between

the

BONE

AND

navicular

JOINT

talus bone

SURGERY

TREATMENT

The

forefoot

The

distorted

flattening

MOBILE

of which

the

may the

is pronated

may

tendo

the

valgus

known

evertor

OF

mid-tarsal

THE

joints

clinical

2) valgus

deformity

97

CALCANEUS

(Fig.

2).

deformity

comprising:

of the heel,

in consequence

1)

action,

7). or

the

the

line

talus

of

passes

5).

OPERATION

is to displace

medially

(Fig.

deformity,

through 4 and

of the operation

of the calcaneus

Technique-A

an

at the

well

3); and

acquires

transmitted calcaneus (Figs.

weight-bearing

abducted the

(Fig.

OSTEOTOMY

represented.

upon

aim

slightly

arch

THE

The

DISPLACEMENT

to aggravate the condition (Fig. or the valgus may predominate

be equally

weight-bearing medial to the

BY

produces

calcaneus

tend planus

FOOT

and

anatomy

Consequent

part

FLAT

at the longitudinal

which Either they

OF

and

the

thus

to restore

The

patient

posterior normal

6).

tourniquet

is used.

lies prone

with a sandbag under the lower shin to allow free movement of the ankle. A lateral incision is made, parallel to and a little behind and inferior to the peroneal tendons,

upper

of

being

care

The

end

the

calcaneal

inferior

margin

taken

of the

not

tendon

of

to damage

incision and

the

held

apart

by

bone

spikes

are inserted

the

overlies its

the

lower

calcaneus.

end

The

a self-retaining

sural

retractor

nerve.

lateral

margin

reaches

the

skin

edges

and

two

are small

and below the calcaneus in order to expose its superior, lateral and inferior surfaces. The periosteum is incised and elevated in the line of the

skin

incision

above

to allow

a broad osteotome. the periosteum is

The divided

subperiosteal osteotomy along

allow the to divide displacement. When

displacement envisaged. the long plantar ligament

displaced

medially

the

osteotomy

has

until

completed

entails is held

a displacement by

53 B,

VOL.

G

one NO.

or

flattening

between two

1, FEBRUARY

Kirschner 1971

FIG. 2 Radiograph of a weight-bearing foot showing that the mid-talar line passes medial to the forefoot and not through the shaft of the first metatarsal as it should in the normal.

and to

border

the

lies in a line

FIG.

Severe

with

open aspect

It may be necessary to obtain sufficient

been

its medial

osteotomy

is prised the medial

of the longitudinal

a third wires,

to a half inserted

posterior with

fragment

of

the sustentaculum

the

calcaneus

tali.

This

is

usually

3 arch

in a mobile

flat

foot.

of the width of the calcaneus. The obliquely from the postero-inferior

displacement surface

of

98

F. KOUTSOGIANNIS

FIG. 4 FIG. S The weight-bearing line and relation of the talus to the calcaneus seen viewpoint in a normal foot (Fig. 4) and a flat foot (Fig. 5). The displacement in Figure 6.

Before

operation

there

is valgus

of the heels

(Fig.

is neutral

7) but after (Fig.

operation

FIG.

6

from a postero-superior at operation is shown

on both

heels

the position

8).

V --

FIG.

9

The arch before operation

FIG.

(Fig.

9) and afterwards

THE

(Fig.

JOURNAL

10 10).

OF BONE AND JOINT SURGERY

TREATMENT

OF MOBILE

FLAT

FOOT

BY DISPLACEMENT

OSTEOTOMY

OF THE

99

CALCANEUS

-

II

FIG.

A lateral operation

radiograph (Fig. 12)

before the

to show

talo-navicular

bone,

Routine

the

care

ankle

a new weeks.

only

subluxation

decreased

and

there

line approximates

that

the

ends

is undertaken

is

the

flat

arch

improvement

of

II). After longitudinal

(Fig.

the

to the normal.

of

and

and

the

wires

a padded

are

buried

below-knee

beneath

the

plaster is applied

skin. with

position.

care-Three

weeks

plaster are

mobilise.

is

the mid-talar

to ensure

skin

in neutral

below-knee Radiographs

to

taken

of the

held

Post-operative

free

being

closure

the talo-navicular

subluxation

arch:

the

12

FIG.

operation

after

is applied. then taken,

Occasionally

operation

the

The patient out of plaster,

physiotherapy

sutures

and

the

is allowed to bear and if union has

wires

are

weight occurred

removed

and

in this for three the limb is left

is required.

FIG. 13 FIG. 14 Marked abduction of the forefoot before operation (Fig. 13). After operation (Fig. 14) there is a decrease of the abduction of the forefoot and the mid-talar line approximates to the normal.

CLINICAL In

the

patients. years over years.

and

Bristol

All

at the

The mean eight males.

53 B,

patients

months.

seventeen

neurological VOL.

the

to a few

clinical

age

All

there

were

traced

and

examined.

range

was

nine

The time was

had

age

of operation; twelve

simple

abnormalities. NO.

1,

FEBRUARY

1971

years

mobile

was

MATERIAL

area

a total

one when

was these

flat

foot

of to

thirty-four

The fifty-five

thirty-nine two

with

are

feet

operated

follow-up

time

years

but

only

years

and

the

excluded.

a marked

on

There

valgus

in nineteen

ranged two

other were

element

patients

was

from

six were

fifty-five

eleven

females

and

without

100

E. KOUTSOGIANNIS RESULTS

The

Shape and The of

results

were

of the foot.

judged

on

three

Hee/-Seventeen

criteria: patients

the

shape

(thirty

foot,

the

lost

had

(six

some failed

patients)

arch before operation (Figs. to show any improvement.

9 and Forefoot

parallel difficult

with the improvement of the longitudinal to demonstrate in the photographs, it was Fatigue-This was recorded as definitely improved pleased to be able to indulge in normal activities dancing.

In

Shoe

addition

wear-In

The

the

parents

of the

Failures-None

deformity

young

features

heel.

These

angle

a proper

appearance-Standing of the

Improvement and

the

in

subluxation. forefoot.

the

and after operation. the calcaneus was

severely

considerably

probably

seen

radiographs

effect of operation. appearance of the

This Figures

heel

Arch-

most

deformed was found

abduction-This

wear.

flat feet to run

arch. Although the improvement easily apparent on the radiographs. in seventeen patients. They were such as walking, running, football

due

before foot

was

to a tight

and

after

always

after with

very and

or

to

to dorsiflex are

with

of

valgus

tendon

operation

elevation

operation.

persisting

inability

associated

in the

the

calcaneal

improvement can be divided into components 1 1 to 14 illustrate the typical radiographic

Only very slight improvement in the lateral radiographs.

was

improved.

was no problem with footwear particularly appreciative. in the two patients (four feet) were

shoe of the

(Figs. 7 and 8). (thirteen patients),

the osteotomy. In both cases there was heel in neutral position and the knee straight.

the

assessment

tabo-navicular arch

improved

failures

was

Nine

and

deformity

at

with

Radiographic

gait

there were

children

displacement

right

in the

patients

of these

of the

inadequate

spring

seventeen

10).

fatigue

valgus

with this the eversion element in the pull of the calcaneal tendon longitudinal arch showed some improvement in twenty-five feet whom

the

of the

feet)

to

essential

for

decrease

in the

: the longitudinal appearance before the

anterior

end

of

CONCLUSION

1

.

Thirty-four

cases

of

calcaneal

osteotomy

for

mobile

flat

foot

in

nineteen

patients

are

reviewed. 2.

The

function

3.

The

operation

was

the the

thirty-four flat foot

markedly

was

feet. deformity

improved

successful

it was was

in seventeen

in correcting

less successful severe.

My thanks are due to Mr A. L. Eyre-Brook of this paper. They and Mr H. K. Lucas, access to their patients and records.

of the

the

valgus

in improving

the

and Mr D. M. Jones Mr M. P. McCormack

nineteen

patients.

deformity

of the

longitudinal

heel

arch,

in thirty

especially

of when

for their help and criticism in the preparation and Mr H. E. D. Griffiths kindly gave me

REFERENCES DWYER,

F. C. (1960):

Reference

Osteotomy

to Cerebral

Palsy.

of the

In

Calcaneum

in

Septembre 1960. Soci#{233}t#{233} Internationale de Chirurgie Imprimerie des Sciences. Low, J. P. (1923): Correction of Extreme Flatfoot. Value 4-9

of Posterior SILVER, C. M., Valgus and

Varus

of Grossly de

Orthop#{233}dique

(Gleich

Operation).

Journal

of Osteotomy

Everted

Chirurgie

Feet

with

Orthop#{233}dique,

p. 892.

et de Traumatologie,

of the

American

THE

of Os Calcis Medical

JOURNAL

and

Special

New

York,

Bruxelles:

Displacement 81, 1502. S. D., SPINDELL, E., LITCHMAN, H. M., and SCALA, M. (1967): Calcaneal Osteotomy for Deformities of the Foot in Cerebral Palsy. Journal of Bone and Joint Surgery, 49-A, 232.

Fragment SIMON,

the Treatment

Huiti#{232}me Congr#{233}s Internationale

Inward

Association,

OF

BONE

AND

JOINT

SURGERY

Pathophysiology/Complications O R I G I N A L

A R T I C L E

Probe-to-Bone Test for Diagnosing Diabetic Foot Osteomyelitis Reliable or relic? LAWRENCE A. LAVERY1 DAVID G. ARMSTRONG2

EDGAR J.G. PETERS3 BENJAMIN A. LIPSKY4

OBJECTIVE — We sought to assess the accuracy of the probe-to-bone (PTB) test in diagnosing foot osteomyelitis in a cohort of diabetic patients with bone culture proven disease. RESEARCH DESIGN AND METHODS — In this 2-year longitudinal cohort study, we enrolled 1,666 consecutive diabetic individuals who underwent an initial standardized detailed foot assessment, followed by examinations at regular intervals. Patients were instructed to immediately come to the foot clinic if they developed a lower-extremity complication. For all patients with a lower-extremity wound, we compared the results of the PTB test with those of a culture of the affected bone. We called PTB positive if the bone or joint was palpable and defined osteomyelitis as a positive bone culture. RESULTS — Over a mean of 27.2 months of follow-up, 247 patients developed a foot wound and 151 developed 199 foot infections. Osteomyelitis was found in 30 patients: 12% of those with a foot wound and 20% in those with a foot infection. When all wounds were considered, the PTB test was highly sensitive (0.87) and specific (0.91); the positive predictive value was only 0.57, but the negative predictive value was 0.98. CONCLUSIONS — The PTB test, when used in a population of diabetic patients with a foot wound among whom the prevalence of osteomyelitis was 12%, had a relatively low positive predictive value, but a negative test may exclude the diagnosis. Diabetes Care 30:270 –274, 2007

I

ndividuals with diabetes have an ⬃25% lifetime risk of developing a foot complication (1), the most common of which is skin ulceration. Over half of these foot wounds may eventually become infected, which greatly increases the risk of lower-extremity amputation (2–5). While most diabetic foot infections involve only the soft tissue, bone involvement occurs in 20 – 66% of cases (6 – 8). Furthermore, foot infections complicated by osteomyelitis generally have a worse outcome and often require surgical resec-

tion and prolonged antibiotic therapy (6,7). While diagnosing osteomyelitis is important, it is unfortunately also difficult. Clinical and laboratory signs and symptoms are generally unhelpful (6,7). Bone infection may not show up on plain radiographs in the first 2 weeks, and any X-ray abnormalities detected may be caused by the neuropathic bone disorders that frequently occur in diabetes. More accurate imaging studies, such as radionuclide scans or magnetic resonance imaging, are

● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ●

From the 1Department of Surgery, Scott and White Hospital, Texas A&M University Health Science Center College of Medicine, Temple, Texas; 2Scholl’s Center for Lower Extremity Ambulatory Research (CLEAR) at Rosalind Franklin University of Medicine and Science, North Chicago, Illinois; the 3Department of Infectious Diseases, Leiden University Medical Center, Leiden, the Netherlands; and the 4VA Puget Sound Heath Care System and the Department of Medicine, University of Washington, Seattle, Washington. Address correspondence and reprint requests to Lawrence A. Lavery, Department of Surgery, Scott and White Hospital, 703 Highland Spring Lane, Georgetown, TX 78628. E-mail: [email protected]. Received for publication 26 July 2006 and accepted in revised form 19 October 2006. Abbreviations: PTB, probe to bone. A table elsewhere in this issue shows conventional and Syste`me International (SI) units and conversion factors for many substances. DOI: 10.2337/dc06-1572 © 2007 by the American Diabetes Association. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

270

expensive and not universally available (9 –21). In 1995, Grayson et al. (22) described a clinical technique they used in diabetic patients with a foot infection consisting of exploring the wound for palpable bone with a sterile blunt metal probe. Their most important finding was that the probe-to-bone (PTB) test had a positive predictive value of 89%, leading them to conclude that a positive test usually made imaging studies for diagnosing osteomyelitis unnecessary (22). Since then, many have considered a positive PTB sufficient evidence for osteomyelitis. In the study by Grayson et al., however, the prevalence of osteomyelitis in their population with “severe limb-threatening infections” was 66%. Furthermore, the investigators did not obtain a bone specimen for analysis, the criterion standard for the diagnosis, from all patients and used histopathological rather than microbiological confirmation to diagnose osteomyelitis. To assess the value of the PTB test in an unselected population of individuals with diabetes, we conducted the test as part of a prospective cohort study of foot complications in diabetic patients and confirmed the presence of osteomyelitis by bone culture. RESEARCH DESIGN AND METHODS — As part of a diabetes disease management program to study and prevent lower-extremity complications and in cooperation with two large primary care physician groups in south Texas, we prospectively enrolled 1,666 patients in an observational trial over an 8-month period. As part of a systematic screening program, we documented each patient’s medical history for all potential foot complications and screened them for established risk factors (23). Patients were then seen at regular intervals (i.e., every 2–12 months, depending on their foot risk classification) for routine foot care and repeat evaluations (24). In addition, all patients were instructed to immediately return to the foot clinic if they developed any foot complication. We followed the patients for an average of 27.2 months (range 4 –32) and tracked all pertinent clinical outcomes, verifying all hospital

DIABETES CARE, VOLUME 30, NUMBER 2, FEBRUARY 2007

Lavery and Associates Table 1—Characteristics of patients with diabetic foot wound by osteomyelitis status Osteomyelitis Age ⬎70 years Male Diabetes duration (years) BMI (kg/m2) Peripheral neuropathy Peripheral vascular disease Wound depth Full thickness skin To fascia or tendon To bone/joint Ulcer duration (days)

Yes (n ⫽ 30)

No (n ⫽ 217)

P value

Relative risk

95% CI

51.3 58.6 17.0 ⫾ 10.1 28.7 ⫾ 6.2 83.3 43.3

52.6 52.1 13.0 ⫾ 9.6 29.6 ⫾ 7.3 72.4 37.8

0.85 0.51 0.03 0.53 0.2 0.6

0.99 1.26 1.03 0.98 1.79 1.22

0.97–1.01 0.63–2.53 1.00–1.06 0.93–1.04 0.71–4.47 0.62–2.40

10.0 3.3 86.7 267 ⫾ 284

73.7 17.1 9.2 169 ⫾ 268

0.75 ⬍0.001 0.06

1.00 1.43 30.71 1.001

0.15–13.37 9.73–96.93 1.000–1.001

Data are percent or means ⫾ SD.

admissions and lower-extremity amputations with claims data. The disease management program’s foot clinic was the primary source for foot care, as well as for referral and consultation for diabetesrelated lower-extremity complications. This project was approved by our institutional review board. We defined a foot wound as a full thickness lesion involving any portion of the foot or ankle (25–27). We excluded wounds characterized as blisters, minor lacerations, or abrasions (n ⫽ 16). We defined a wound infection clinically, by criteria consistent with the International Working Group guidelines (28), i.e., the presence of wound purulence or at least two signs or symptoms of local inflammation or systemic symptoms of infection with no other apparent cause. We evaluated all wounds to determine the extent of soft tissue involved and for any evidence of bone infection (osteomyelitis) (6,29,30). As part of this evaluation, each patient underwent the PTB test, conducted by one of two experienced podiatrists using a sterile probe to gently explore the wound. We defined a positive test as palpating a hard or gritty substance that was presumed to be bone or joint space. Each patient with a clinically infected wound also underwent a series of plain radiographs and had additional imaging studies as indicated. If, based on the clinical examination (other than the PTB test) and imaging studies, we thought bone infection was possible, the patient underwent bone biopsy. Using aseptic techniques, we obtained specimens for culture, either in the clinic or operating room, following standard surgical skin preparation with betadiene. We obtained bone specimens by needle aspirate, curet-

tage, or rongeur at the time of debridement or through sites that were noncontiguous with the wound. Specimens were transferred to a sterile container or transport tube with culture media and quickly transported to the clinical microbiology laboratory. We used the results of bone culture to determine the presence or absence of bone infection. A positive culture was defined as growth of any organism from the bone specimen. Although our data forms did not specifically record information on antimicrobial treatment in all cases, most patients presented with an acute wound and were not receiving any antibiotic therapy. We followed all patients with a foot wound until it either healed or required surgical intervention. To assess the value of PTB in diagnosing osteomyelitis, we calculated the sensitivity, specificity, and positive and negative predictive values of the test using the results of the bone culture as the criterion standard. We calculated statistical values using SPSS version 11.0 for Macintosh (SPSS, Chicago, IL) and Diagnostic and Agreement Statistics DAG Software (Mental Health Research Institute, Parkville, Victoria, Australia). RESULTS — The demographic and clinical characteristics of the patients we enrolled are shown in Table 1. Over a mean of 27.2 months of follow-up, 247 (14.8%) of the 1,666 enrolled patients developed a foot wound and 151 (9.1%) developed 199 foot infections. One patient with cellulitis did not have a wound, precluding conducting the PTB test. All of the patients with osteomyelitis presented with signs and symptoms of a soft tissue foot infection. Bone infection was docu-

DIABETES CARE, VOLUME 30, NUMBER 2, FEBRUARY 2007

mented in 30 patients, representing 20% of the 150 infected patients and 12% of all 247 with a foot wound. The PTB test was performed in all of the 247 patients with a wound; it was positive in 46 (18.6%), 26 (56.5%) of whom had osteomyelitis. The test was positive in 26 (86.7%) of the 30 with culture-proven bone infection, as well as in 20 (9.2%) of the 217 without osteomyelitis. Among the 150 patients with a clinically infected wound, the test was positive in 46 (30.7%). There were no complications attributable to the PTB test. The values for sensitivity, specificity, and positive and negative predictive values of the PTB test for all patients with a foot wound and for the patients with a clinically infected foot wound are shown in Table 2. The sensitivity was 87% for both groups (i.e., all wounds and infected wounds), while the specificity was 91% for all wounds and 87% for infected wounds. The negative predictive value was extremely high (96 –98%), but the positive predictive value was only 57– 62%. The positive likelihood ratio was 9.4 for all wounds and 6.5 for infected wounds, similar to the values for the negative likelihood ratios for both populations. CONCLUSIONS — Osteomyelitis of the foot in individuals with diabetes is often difficult to diagnose. Bone biopsy is considered the criterion standard for the diagnosis. While histopathological definitions may be useful for diagnosing osteomyelitis, most prefer microbiological methods (6,31). Many clinicians (and patients) are hesitant to undertake this invasive and rather expensive procedure. Thus, clinicians have sought clinical evi271

PTB test for diabetic foot osteomyelitis Table 2—Statistical analysis of the PTB test for diagnosing osteomyelitis in all foot wounds and in clinically infected wounds

Statistic Sensitivity Specificity Positive predictive value Negative predictive value Positive likelihood ratio Negative likelihood ratio

All wounds value (n ⫽ 247)

Infected wounds value (n ⫽ 150)

0.87 (0.71–0.96) 0.91 (0.89–0.92) 0.57 (0.46–0.62) 0.98 (0.96–0.99) 9.40 (6.05–14.61) 6.81 (2.73–16.97)

0.87 (0.69–0.96) 0.87 (0.79–0.92) 0.62 (0.46–0.76) 0.92 (0.91–0.99) 6.50 (4.03–10.48) 6.50 (2.60–16.23)

Data in parentheses are 95% CI.

dence to help them determine what patients were likely to have diabetic foot osteomyelitis. Unfortunately, local inflammatory signs and symptoms may be blunted because of diabetes-related vascular insufficiency, peripheral neuropathy (32), and leukocyte dysfunction (33). While clinical findings (34) or elevations in hematological inflammatory markers (e.g., white blood cell count, erythrocyte sedimentation rate [35], or C-reactive protein [36]) may be helpful (37,38), these are not sufficiently accurate for diagnosis (3,4,35,39 – 45). Furthermore, evaluating published reports of the sensitivity, specificity, and predictive value of various diagnostic methods is complicated by inconsistent operational definitions and outcome measures, as well as the variability in the prevalence of osteomyelitis in the populations studied (46). It is not surprising, therefore, that the clinical assessment for diagnosing osteomyelitis has a reported sensitivity ranging from 0 to 54% (9,20,47,48). Various imaging studies, especially magnetic resonance, certainly enhance the accuracy of diagnosing osteomyelitis, but these are expensive, time-consuming, and not universally available (49,50). Thus, clinicians have sought a simple inexpensive bedside test to help determine which patients should undergo more extensive evaluations. Since its introduction, the PTB technique has been widely used for evaluating diabetic patients with a foot wound. Palpation of bone with a metal probe is a simple bedside procedure predicated on the concept that if the probe can reach the bone, so can infectious bacteria. In the report by Grayson et al. (51) on 76 hospitalized patients enrolled in a diabetic foot infection antibiotic trial, 66% were found to have osteomyelitis, defined by histology on bone biopsy (in most subjects) and by surgical exploration or ra272

diological imaging (in the rest). They calculated that the PTB test had a sensitivity of 66%, specificity of 85%, positive predicative value of 89%, and a negative predictive value of 56% (22). Our study evaluated more than three times as many patients with a foot wound and more than twice as many with a foot infection. Unlike in the study by Grayson et al., our patients were identified (and largely treated) in an outpatient setting. Furthermore, in all of our patients, osteomyelitis was defined exclusively by a positive bone culture. We found very little difference in positive and negative predictive values when we compared PTB results in all patients who had a wound with the subset who had clinical signs of infection. In our patient population, the PTB had high sensitivity and specificity, but because of the lower prevalence of osteomyelitis, our positive predictive value was only 57– 62%. Thus, a positive PTB only slightly increased the probability of osteomyelitis over tossing a coin. The negative predictive value, however, was considerably higher, at 96 –98%. A negative test, therefore, argues strongly against the diagnosis of osteomyelitis. These results confirm the importance of disease prevalence in assessing any test for making the diagnosis of diabetic foot osteomyelitis (46). At least three factors may have contributed to the apparent disparity in outcomes between our study and that of Grayson et al. (51). First, the lower positive predictive value in our population may be attributable to their lower prevalence of osteomyelitis (20 vs. 66%) (46). Second, all of the patients in the Grayson et al. study required hospitalization for severe foot infections, which required parental antibiotics. Our study population was derived from patients who mostly presented in a clinic setting, and only 61% of patients with a foot wound had evidence of infection. Third, when bone

biopsy was performed by Grayson et al., they histologically defined osteomyelitis (in 46 of 50 cases by the presence of inflammatory cells, fibrosis, necrosis, and reactive bone), while we defined it microbiologically (by a positive culture of a bone specimen). Because most of our patients presented with an acute foot wound, we believe that few were receiving antibiotic therapy, enhancing the value of a microbiologically based diagnosis. Thus, it is possible that they missed cases of osteomyelitis that did not have histological changes (false negatives) or that we included cases that represented microbial contamination (false positives) of the bone specimen. Our patient population is probably more representative of those in a typical clinical practice where the PTB would be most commonly used. Our study had several potential limitations. First, we did not perform histological examination of the bone specimens to compare against the culture results. Rather, we elected to use a positive bone culture as our criterion standard. We did so because it is often difficult to obtain an adequate core of bone from the small bones of the feet (especially toes) to allow histopathological analysis and because the criteria for histologically diagnosing osteomyelitis are not well-defined. Furthermore, because we believe that most of our patients were not receiving antibiotic therapy at the time the bone biopsy was taken and they underwent careful wound cleansing and debridement before the procedure, we thought that the risk of false negative or positive results was low. Additionally, for samples collected in this study and in our greater clinical experience, readings of histological specimens often refer to signs of inflammation or inflammatory cells but do not specifically describe osteomyelitis. Second, we did not conduct a bone biopsy on patients with a foot wound in whom there was no suspicion of bone involvement. While work in this area suggests that bone biopsy is both safe (52,53) and helpful (49), we believed it would be unethical to do this procedure on patients with no suspicion of osteomyelitis. As previously stated, none of the patients who did not undergo a biopsy were later found to have developed osteomyelitis. Because the average follow-up for patients in this population was 27 months and our group was the sole source of diabetic foot referral, it was unlikely that we missed any cases of bone infection. Third, the PTB was con-

DIABETES CARE, VOLUME 30, NUMBER 2, FEBRUARY 2007

Lavery and Associates ducted by one of two podiatrists, but we did not test the interrater reliability. We were only able to find two other studies in the literature of the PTB test in patients with a diabetic foot wound. In a recent brief report, Shone et al. (54) described 81 patients with 104 foot wounds on whom they did the PTB test. They did not diagnose osteomyelitis by bone biopsy but rather clinically (mostly by physical examination and plain X-rays, with bone histology in a minority). Their patients included both those in whom the diagnosis had already been made and those in whom it was made later. Interestingly, their results were similar to ours, i.e., PTB had a positive predictive value of 53% and a negative predictive value of 85%. They diagnosed osteomyelitis in 19 (24%) of their patients, a prevalence similar to that in our study (20%). Balsells et al. (55) performed a PTB test in a series of 33 episodes of foot ulceration (on 28 diabetic patients) that required the patient to be hospitalized. Among the 21 who had osteomyelitis (defined by either positive nuclear medicine scans or characteristic X-ray changes associated with a foot ulcer), only 7 (33%) had a positive PTB. Unfortunately, they reported no data on the results of PTB in the 12 patients who did not have bone infection, limiting the ability to evaluate the test’s accuracy in this study. If we are to use the PTB test in clinical practice, we must understand both its value and limitations. Unfortunately, some have inappropriately generalized the results from the study by Grayson et al. to all foot (and even other) wounds in various clinical settings (56,57). We have also observed clinicians using devices and methods for the test that are quite different from those described in the original study. Furthermore, there are no data on the interrater or intrarater reliability of the test. Perhaps most importantly, clinicians must realize that the prior prevalence of osteomyelitis greatly affects the usefulness of the PTB test. In a population with “limb-threatening” infections and a high prevalence of osteomyelitis, a positive PTB is probably quite helpful in diagnosing bone infection. In more typical clinical settings, however, this is less likely to be true, and the PTB test is a better tool to exclude osteomyelitis. We need further studies on this test to answer the remaining questions and to help understand its value in different settings.

References 1. Singh N, Armstrong DG, Lipsky BA: Preventing foot ulcers in patients with diabetes. JAMA 293:217–228, 2005 2. Lavery LA, Armstrong DG, Wunderlich RP, Boulton AJM, Tredwell JL: Diabetic foot syndrome: evaluating the prevalence and incidence of foot pathology in Mexican Americans and non-Hispanic whites from a diabetes disease management cohort. Diabetes Care 26:1435–1438, 2003 3. Armstrong DG, Lipsky BA: Advances in the treatment of diabetic foot infections. Diabetes Technol Ther 6:167–177, 2004 4. Armstrong DG, Lipsky BA: Diabetic foot infections: stepwise medical and surgical management. Int Wound J 1:123–132, 2004 5. Lavery LA, Armstrong DG, Wunderlich RP, Mohler MJ, Wendel CS, Lipsky BA: Risk factors for foot infections in persons with diabetes mellitus. Diabetes Care 29: 1288 –1293, 2006 6. Lipsky BA: Osteomyelitis of the foot in diabetic patients. Clin Infect Dis 25:1318 – 1326, 1997 7. Lipsky BA, Berendt AR, Deery HG, Embil JM, Joseph WS, Karchmer AW, LeFrock JL, Lew DP, Mader JT, Norden C, Tan JS: Diagnosis and treatment of diabetic foot infections. Clin Infect Dis 39:885–910, 2004 8. Norden C: Bone and joint infection. Curr Opin Infect Dis 9:109 –114, 1996 9. Vesco L, Boulahdour H, Hamissa S, Kretz S, Montazel JL, Perlemuter L, Meignan M, Rahmouni A: The value of combined radionuclide and magnetic resonance imaging in the diagnosis and conservative management of minimal or localized osteomyelitis of the foot in diabetic patients. Metabolism 48:922–927, 1999 10. Rubello D, Casara D, Maran A, Avogaro A, Tiengo A, Muzzio PC: Role of anti-granulocyte Fab’ fragment antibody scintigraphy (LeukoScan) in evaluating bone infection: acquisition protocol, interpretation criteria and clinical results. Nucl Med Commun 25:39 – 47, 2004 11. Harvey J, Cohen MM: Technetium-99labeled leukocytes in diagnosing diabetic osteomyelitis in the foot. J Foot Ankle Surg 36:209 –214, 1997 12. Devillers A, Garin E, Polard JL, Poirier JY, Arvieux C, Girault S, Moisan A, Bourguet P: Comparison of Tc-99m-labelled antileukocyte fragment Fab’ and Tc-99mHMPAO leukocyte scintigraphy in the diagnosis of bone and joint infections: a prospective study. Nucl Med Commun 21: 747–753, 2000 13. Devillers A, Moisan A, Hennion F, Garin E, Poirier JY, Bourguet P: Contribution of technetium-99m hexamethylpropylene amine oxime labelled leucocyte scintigraphy to the diagnosis of diabetic foot infection. Eur J Nucl Med 25:132–138, 1998

DIABETES CARE, VOLUME 30, NUMBER 2, FEBRUARY 2007

14. Unal SN, Birinci H, Baktiroglu S, Cantez S: Comparison of Tc-99m methylene diphosphonate, Tc-99m human immune globulin, and Tc-99m-labeled white blood cell scintigraphy in the diabetic foot. Clin Nucl Med 26:1016 –1021, 2001 15. Poirier JY, Garin E, Derrien C, Devillers A, Moisan A, Bourguet P, Maugendre D: Diagnosis of osteomyelitis in the diabetic foot with a 99mTc-HMPAO leucocyte scintigraphy combined with a 99mTcMDP bone scintigraphy. Diabetes Metab 28:485– 490, 2002 16. Sarikaya A, Aygit AC, Pekindil G: Utility of 99mTc dextran scintigraphy in diabetic patients with suspected osteomyelitis of the foot. Ann Nucl Med 17:669 – 676, 2003 17. Yuh WT, Corson JD, Baraniewski HM, Rezai K, Shamma AR, Kathol MH, Sato Y, el-Khoury GY, Hawes DR, Platz CE, et al.: Osteomyelitis of the foot in diabetic patients: evaluation with plain film, 99mTcMDP bone scintigraphy, and MR imaging. AJR Am J Roentgenol 152:795– 800, 1989 18. Enderle MD, Coerper S, Schweizer HP, Kopp AF, Thelen MH, Meisner C, Pressler H, Becker HD, Claussen C, Ha¨ring HU, Luft D: Correlation of imaging techniques to histopathology in patients with diabetic foot syndrome and clinical suspicion of chronic osteomyelitis: the role of high-resolution ultrasound. Diabetes Care 22:294 –299, 1999 19. Williamson MR, Quenzer RW, Rosenberg RD, Meholic AJ, Eisenberg B, Espinosa MC, Hartshorne MF: Osteomyelitis: sensitivity of 0.064 T MRI, three-phase bone scanning and indium scanning with biopsy proof. Magn Reson Imaging 9:945– 948, 1991 20. Newman LG, Waller J, Palestro CJ, Hermann G, Klein MJ, Schwartz M, Harrington E, Harrington M, Roman SH, Stagnaro-Green A: Leukocyte scanning with 111In is superior to magnetic resonance imaging in diagnosis of clinically unsuspected osteomyelitis in diabetic foot ulcers. Diabetes Care 15:1527–1530, 1992 21. Lipsky BA, Baker PD, Landon GC, Fernau R: Antibiotic therapy for diabetic foot infections: comparison of two parenteralto-oral regimens. Clin Infect Dis 24:643– 648, 1997 22. Grayson ML, Gibbons GW, Balogh K, Levin E, Karchmer AW: Probing to bone in infected pedal ulcers: a clinical sign of underlying osteomyelitis in diabetic patients. JAMA 273:721–723, 1995 23. Armstrong DG, Lavery LA, Vela SA, Quebedeaux TL, Fleischli JG: Choosing a practical screening instrument to identify patients at risk for diabetic foot ulceration. Arch Intern Med 158:289 –292, 1998 24. Peters EJG, Lavery LA, Armstrong DG: International Working Group’s diabetic foot 273

PTB test for diabetic foot osteomyelitis

25. 26.

27.

28.

29. 30.

31.

32. 33.

34.

35.

36.

274

risk classification: validation in a large population based cohort. Diabetologia 48 (Suppl. 1):A97, 2005 Lavery LA, Armstrong DG, Harkless LB: Classification of diabetic foot wounds. J Foot Ankle Surg 35:528 –531, 1996 Armstrong DG, Lavery LA, Harkless LB: Validation of a diabetic wound classification system: the contribution of depth, infection, and ischemia to risk of amputation. Diabetes Care 21:855– 859, 1998 Oyibo SO, Jude EB, Tarawneh I, Nguyen HC, Harkless LB, Boulton AJ: A comparison of two diabetic foot ulcer classification systems: the Wagner and the University of Texas wound classification systems. Diabetes Care 24:84 – 88, 2001 International Working Group on the Diabetic Foot: International Consensus on the Diabetic Foot. Apelqvist J, Bakker K, Van Houtum WH, Nabuurs-Franssen MH, Schaper NC, Eds. Maastricht, the Netherlands, International Working Group on the Diabetic Foot, 1999 Lipsky BA: Diabetic foot infections: pathophysiology, diagnosis, and treatment. Int J Dermatol 30:560 –562, 1991 Lipsky BA: Evidence-based antibiotic therapy of diabetic foot infections. FEMS Immunol Med Microbiol 26:267–276, 1999 Zuluaga AF, Galvis W, Saldarriaga JG, Agudelo M, Salazar BE, Vesga O: Etiologic diagnosis of chronic osteomyelitis: a prospective study. Arch Intern Med 166:95– 100, 2006 Edmonds M, Foster A: The use of antibiotics in the diabetic foot. Am J Surg 187: 25S–28S, 2004 Oncul O, Yildiz S, Gurer US, Yeniiz E, Qyrdedi T, Top C, Gocer P, Akarsu B, Cevikbas A, Cavuslu S: Effect of the function of polymorphonuclear leukocytes and interleukin-1 beta on wound healing in patients with diabetic foot infections. J Infect. In press Schinabeck MK, Johnson JL: Osteomyelitis in diabetic foot ulcers: prompt diagnosis can avert amputation. Postgrad Med 118:11–15, 2005 Kaleta JL, Fleischli JW, Reilly CH: The diagnosis of osteomyelitis in diabetes using erythrocyte sedimentation rate: a pilot study. J Am Podiatr Med Assoc 91:445– 450, 2001 Upchurch GR Jr, Keagy BA, Johnson G Jr:

37.

38.

39.

40.

41.

42.

43.

44.

45.

46.

47.

48.

An acute phase reaction in diabetic patients with foot ulcers. Cardiovasc Surg 5:32–36, 1997 Pakarinen TK, Laine HJ, Honkonen SE, Peltonen J, Oksala H, Lahtela J: Charcot arthropathy of the diabetic foot: current concepts and review of 36 cases. Scand J Surg 91:195–201, 2002 Lee SS, Chen CY, Chan YS, Yen CY, Chao EK, Ueng SW: Hyperbaric oxygen in the treatment of diabetic foot infection. Changgeng Yi Xue Za Zhi 20:17–22, 1997 Leichter SB, Allweiss P, Harley J, Clay J, Kuperstein-Chase J, Sweeney GJ, Kolkin J: Clinical characteristics of diabetic patients with serious pedal infections. Metabolism 37 (Suppl. 1):22–24, 1988 Armstrong DG, Lavery LA, Sariaya M, Ashry H: Leukocytosis is a poor indicator of acute osteomyelitis of the foot in diabetes mellitus. J Foot Ankle Surg 35:280 – 283, 1996 Lavery LA, Armstrong DG, Quebedeaux TL, Walker SC: Puncture wounds: the frequency of normal laboratory values in the face of severe foot infections of the foot in diabetic and non-diabetic adults. Am J Med 101:521–525, 1996 Armstrong DG, Perales TA, Murff RT, Edelson GW, Welchon JG: Value of white blood cell count with differential in the acute diabetic foot infection. J Am Podiatr Med Assoc 86:224 –227, 1996 Bagdade JD, Root RK, Bulger RJ: Impaired leukocyte function in patients with poorly controlled diabetes. Diabetes 23:9 –17, 1974 Molinar DM, Palumbo PH, Wilson WR, Ritts RE: Leukocyte chemotaxis in diabetic patients and their first degree relatives. Diabetes 25:880 – 889, 1976 Lipsky BA, Berendt AR, Embil J, De Lalla F: Diagnosing and treating diabetic foot infections. Diabetes Metab Res Rev 20 (Suppl. 1):S56 –S64, 2004 Wrobel JS, Connolly JE: Making the diagnosis of osteomyelitis: the role of prevalence. J Am Podiatr Med Assoc 88:337– 343, 1998 Darouiche RO, Landon GC, Klima M, Musher DM, Markowski J: Osteomyelitis associated with pressure sores. Arch Intern Med 154:753–758, 1994 Newman LG, Waller J, Palestro CJ, Schwartz M, Klein MJ, Hermann G, Harrington E, Harrington M, Roman SH,

49.

50. 51.

52.

53.

54.

55.

56. 57.

Stagnaro-Green A: Unsuspected osteomyelitis in diabetic foot ulcers: diagnosis and monitoring by leukocyte scanning with indium in 111 oxyquinoline. JAMA 266: 1246 –1251, 1991 Ertugrul MB, Baktiroglu S, Salman S, Unal S, Aksoy M, Berberoglu K, Calangu S: The diagnosis of osteomyelitis of the foot in diabetes: microbiological examination vs. magnetic resonance imaging and labelled leucocyte scanning. Diabet Med 23:649 – 653, 2006 Tan PL, Teh J: MRI of the diabetic foot: differentiation of infection from neuropathic change. Br J Radiol. In press Grayson ML, Gibbons GW, Habershaw GM, Freeman DV, Pomposelli FB, Rosenblum BI, Levin E, Karchmer AW: Use of ampicillin/sulbactam versus imipenem/ cilastatin in the treatment of limb-threatening foot infections in diabetic patients. Clin Infect Dis 18:683– 693, 1994 Senneville E, Melliez H, Beltrand E, Legout L, Valette M, Cazaubiel M, Cordonnier M, Caillaux M, Yazdanpanah Y, Mouton Y: Culture of percutaneous bone biopsy specimens for diagnosis of diabetic foot osteomyelitis: concordance with ulcer swab cultures. Clin Infect Dis 42:57– 62, 2006 Kessler L, Piemont Y, Ortega F, Lesens O, Boeri C, Averous C, Meyer R, Hansmann Y, Christmann D, Gaudias J, Pinget M: Comparison of microbiological results of needle puncture vs. superficial swab in infected diabetic foot ulcer with osteomyelitis. Diabet Med 23:99 –102, 2006 Shone A, Burnside J, Chipchase S, Game F, Jeffcoate W: Probing the validity of the probe-to-bone test in the diagnosis of osteomyelitis of the foot in diabetes (Letter). Diabetes Care 29:945, 2006 Balsells M, Viade J, Millan M, Garcia JR, Garcia-Pascual L, del Pozo C, Anglada J: Prevalence of osteomyelitis in non-healing diabetic foot ulcers: usefulness of radiologic and scintigraphic findings. Diabetes Res Clin Pract 38:123–127, 1997 Caputo GM, Joshi N, Weitekamp MR: Foot infections in patients with diabetes. Am Fam Physician 56:195–202, 1997 Embil JM, Trepman E: Microbiological evaluation of diabetic foot osteomyelitis. Clin Infect Dis 42:63– 65, 2006

DIABETES CARE, VOLUME 30, NUMBER 2, FEBRUARY 2007

This is an enhanced PDF from The Journal of Bone and Joint Surgery The PDF of the article you requested follows this cover page.

Changes in tibiotalar area of contact caused by lateral talar shift PL Ramsey and W Hamilton J Bone Joint Surg Am. 1976;58:356-357.

This information is current as of December 24, 2007 Reprints and Permissions

Click here to order reprints or request permission to use material from this article, or locate the article citation on jbjs.org and click on the [Reprints and Permissions] link.

Publisher Information

The Journal of Bone and Joint Surgery 20 Pickering Street, Needham, MA 02492-3157 www.jbjs.org

Changes

in Tibiotalar

Caused BY PAUL

L. RAMSEY,

M.D.*,

by Lateral AND

Iro,,i

t/U

WILLIAM Alfred

I.

A carbon black transference technique to determine the contact area in twenty-three

used

dissected tibiotalar neutral position and millimeters laterally. area

occurred

eral displacement, cent. With further contact change

initiah

one

millimeter

the average reduction lateral displacement

area was progressivehy reduced for each increment of shift was

Fractures in widening

sult

the

In an effort tulated the

to explain

such

that the area of the tibiotalar

faces

poor

result.

changes

unsatisfactory

of contact between joint is altered and

We

laterally

results,

of

may reas seen after talar 1,3.6

we pos-

the articular may contribute

surto

ankle

Materials

mortise. and

Twenty-three lower extremities amputated for peripheral vascular disease were studied. Any specimen with infection or gangrene involving the articuhar cartilage of the ankle

joint

was

not

end ofthe tibia both completely

with

To determine ticular

and the talus as separate free of all soft-tissue

surface

the

area

with respect to plantar flexion, dorsiflexion, and lateral tilt. A compression clamp mounted

position

medial bathroom

scale

of seventy

the load

was

kilograms

was

released,

to deliver an axially-directed load on the joint for thirty seconds. When a deposit of carbon black was pres-

356

on the

S

Box

±

Thomas

269,

Wilmington. Jefferson

and on a

used

talus, marking the area of contact end of the tibia. The outline of the deposit wax wrapping paper placed on the talus, ent

components, attachments.

of contact, the distal tibial arwas coated with powdered carbon black and with the talus, which was placed in neutral

rearticulated

area

of contact

contact

area

with

the talus

specimen.

the tibia

was

The

determined

tibia and then with and six millimeters

maintain spacers

placed leading

the exact milled to

between the talus edge of the spacer

between

on the of

the talus

first

and

in normal

it laterally (Fig. 1).

displacement the appropriate

and medial flush with

by

rela-

displaced

during testing, width were

malleolus, the anterior

with border

the of

the articular cartilage. Each spacer was fixed in place by means of a threaded central extension that was passed through a drill hole in the medial malleolus and held securely with a nut tightened against the medial aspect of the malleolus. In this way, the position of the spacer and its apposition to the articular surface of the medial malleolus was maintained during each test. With respect to position, the talus was adjusted so that it was as near neutral as could be determined by inbased

was

in neutral

The

design

each

on the tibiotalar position

of the

specimen

prior

relationship

while the foot soft tissues.

of the

to removal

compression

was

retested

plantar flexion-dorsiflexion each increment of lateral

device ensured it was in the same and of medial-lateral displacement.

that when degree of tilt for

used.

The fibuha was removed and all soft tissues about the ankle were excised, including the ligaments and capsule. The tibia was transected five centimeters above the ankle joint. The anatomical unit to be tested thus included the distal

the

the same

spection

Methods

to measure squares.

not leave a permanent stain permits repeated examinations

To metallic

the rate marked.

DELAWARE

Carbon black does cartilage and therefore

but less

studies residual result

WILMINGTON,

Wilmington

tionship to the one, two, four,

therefore attempted to measure the contact area as the talus is dis-

in the

M.D.t,

Institute,

being 42 per of the talus the

in this

occurring

placed

of hat-

or ligament injuries about the ankle of the medial part of the mortise

on roentgenograms 2 Long-term follow-up ankle injuries have shown that significant displacement predisposes to an unsatisfactory

Shift

ferred to graph paper counting the enclosed

articulations, with the talus in displaced one, two, four, and six The greatest reduction in contact

during

of Contact

Talar

HAMILTON, duPont

ABSTRACT:

was

Area

Delaware 19899. Hospital. Philadelphia.

with the distal was traced on and then trans-

Pennsylvania

19104.

Results The

contact

areas

(range,

mean,

and

standard

devia-

tion)

are listed in Table I. The considerable variation in the areas of contact can be explained by the normal biological variations in the different specimens. This variation renders the measured paring the changes fore, the measured lateral area

displacement

contact areas of little value when comin area in different specimens. Therecontact areas with each increment of were

expressed

as percentages

obtained with no displacement. The mean decrease in contact

area

was

of the

42 per

cent

with one millimeter of lateral talar shift, 14 per cent with between one and two millimeters, 9 per cent with between two and four millimeters, and only 3 per cent with between four tact

and six millimeters. With no talar displacement, extended across the breadth

on the lateral side talus was displaced

and narrow laterally, THE

JOURNAL

the area of tibiotalar of the talus and was

conwide

on the medial side. Once contact was only apparent OF BONE

AND

JOINT

SURGERY

the on

CHANGES

IN

TIBIOTALAR

AREA

OF

CONTACT

CAUSED

talus viewed from above. showing the contact Note the rapid decrease in contact area and the change lateral displacement the major contact is on the medial

the medial

and lateral

no demonstrable tern of contact was

broad

The

findings ,

and

degrees

marked but

of the talus,

decrease

contact

displaced of the

no measurements The unsatisfactory

was

there

narrow

(Fig.

TABLE

being

1).

TIBI0TAI.AR

Lateral Talar Displacement

Range

(,z,ii)

((.,p2)

left

to

side

I

CONTACT

ARIA

Mean

Standard

(ei2)

Deviation (,p2)

2.3-6.7

4.40

1.21

study

I

1.0-5.0

2.50

0.95

2

1.1-3.3

I .89

0.50

4

0.9-3.0

1.53

0.59

6

0.7-2.5

1.37

0.45

expand

those

in a previous

the talus was tilted laterally laterally two millimeters. tibiotahar

were

contact

recorded. clinical results

area

was

sometimes

2 and A noted

importance relationship

of of

restoring the talus

right).

but with

0

as-

sociated with slight widening of the ankhe mortise and the 42 per cent reduction in the area of contact between the tibia and talus with one millimeter of lateral displacement emphasize the roentgenographic

357

SHIFT

Discussion in this in which

area

TALAR

areas with zero. one, two, four, and six millimeters of talar displaccnient (from in its pattern. With no displacement the major area of contact is on the lateral side.

contact in the mid-portion. Also, the patwas reversed so that the medial contact area

and the lateral

investigation 4

prominences

LATERAL

I

FIG. A left

BY

the normal to the medial

mahleolus

after

ankle

injuries.

Since

the stress

per unit

area

increases as the total contact area decreases, a decrease in contact area may be a factor contributing to a poor result after ankle fracture or dislocation when talar displacement is one millimeter or more.

References 1. BR0DIF.

I. A. 0. D.. and DENIJASI, R. A.: The Treatment of Unstable Ankle Fractures. J. Bone and Joint Surg.. 56-B: 256-262. May 1974. 2. DENHAM, R. A.: Internal Fixation for Unstable Ankle Fractures. J. Bone and Joint Surg., 46-B: 206-211. May 1964. 3. Jo, GREGORY: PATZAKIS. M. J.: and HARVEY, J. P., JR.: Precise Evaluation ofthe Reduction ofSevere Ankle Fractures. Technique and Correlation with End Results. J. Bone and Joint Surg. . 56-A: 979-993. July 1974. 4. MullER. M. E.: ALLGOWER, M.; and WII.I.ENEGGER, H.: Technique of Internal Fixation of Fractures, p. 1 14. New York, Springer. 1965. 5. WII.l.ENE;ER, H.: Die Behandlung der Luxationsfrakturen des obenen Sprunggelenks nach biomechanischen Gesichtspunkten. Helvetica chir. acta, 28: 225-239, 1961. 6. WilSoN, F. C.. and SKII.BREw, L. A.: Long-Term Results in the Treatment of Displaced Bimalleolar Fractures. J. Bone and Joint Surg.. 48-A: 1065-1078, Sept. 1966.

VOL.

58-A,

NO.

3, APRIL

976

FOOT& ANKLEINTERNATIONAL Copyright O 2002 by the American Orthopaedic Foot &Ankle Society, Inc.

Incidence of DVT Following Surgery of the Foot and Ankle Gregory Solis, M.D.; Terence Saxby, FRACS (Orth) Jacksonviffe, FL and Brisbane, Austrafia

return for the first postoperative follow-up, had a history of DVT or pulmonary embolus, or were currently taking a blood thinner (warfarin or heparin).

ABSTRACT A prospective study was undertaken to establish the incidence of deep vein thrombosis (DVT) in patients who had undergone surgery of the foot and ankle. All consecutive patients who underwent foot and ankle surgery in the senior author's practice had duplex ultrasound performed of the bilateral calves at the first postoperative visit. Of 201 patients, deep calf clots were found in seven patients (3.5%), but none of these showed progression on follow-up ultrasound or extension proximal to the calf. By the authors' criteria, none of the studied patients required treatment. The authors feel that the rate and progression of DVT after foot and ankle surgery is low and does not require routine prophylaxis. Factors associated with risk of DVT formation were postoperative immobilization, hindfoot surgery, tourniquet time and advancing age.

MATERIALS AND METHODS

The study group consisted of all patients undergoing foot and ankle surgery by the senior author (T.S.) commencing in May 1999 in a practice that is exclusive to disorders of the foot and ankle. During this period, 209 patients were treated but seven patients did not have the first follow-up in the author's rooms, as they lived in country towns some distance away, and one patient had surgery on the tibia, leaving 201 patients in the study group. All of the study patients answered a survey of potential risk factors for DVT. All patients undergoing surgery had a duplex ultrasound of the bilateral lower extremities from the popliteal vein distally upon the first postoperative visit (average 10.55 days, range six to 18 days after surgery). The senior author's standard routine at the time was to screen all postoperative patients with ultrasound. All ultrasounds were performed in the same institution using Advanced Technology Laboratories Ultrasound System with a Linear Array 7.4 MHz Broad-band Transducer. Patients were only excluded if they did not return for their postoperative visit, if they had a history of prior DVT or pulmonary embolism, or patients on anticoagulants (heparin or warfarin) for other reasons. The senior author's standard practice is to give prophylactic anticoagulants to patients with prior DVT or PE, which is the reason these patients were excluded. No patients in the study were treated with perioperative DVT prophylaxis, nor were any patients found to be on blood thinners (heparin/coumarin) prior to the surgical procedure. Therefore, no patients were excluded based on these criteria. The procedures were classified with regard to location using the same criteria as Mizel et aI.l4 Forefoot was defined as extending from the proximal metatarsal to distal phalanx, midfoot from proximal metatarsal to Chopart's joint, hindfoot as talus and caicaneus and ankle as tibiotalar joint and distal leg. Any procedure on more than one area was graded as being the most prox-

INTRODUCTION

Deep vein thrombosis (DVT) following orthopaedic surgery can be a significant cause of morbidity and mortality. The risks have been studied extensively in the literature, particularly with respect to total joint arthroplasty of the lower extremities. This problem has not received nearly as much attention for surgery of the foot and ankle and is generally not regarded as a significant problem in this field of surgery. The actual incidence of DVT following foot and ankle surgery is largely unknown.'O By prospectively studying a series of 201 eligible, consecutive patients undergoing surgery of the foot and ankle with postoperative ultrasound of the legs, the authors hoped to determine the incidence of, and risk factors for, DVT formation in this population. Patients were ineligible for this study if they failed to

Corresponding Author: Terency S. Saxby, FRACS Holy Spirit Hospital 259 Wickham Terrace Brisbane, Qld. 4000 Australia Phone: 0738346640 Fax: 07 3834 6641 E-mail: forefootQbigpond.com

41 1

4 12

SOLS AND SAXBY

imal location that was involved. Procedures were also scored as being bony or soft-tissue only, with combined procedures being placed in the bony category. If a DVT was detected and restricted to the caif, a repeat ultrasound was performed in one week. Where no progression was found, no treatment was instituted."7Progressionof the clot, or any clots found proximaf to the calf, would be treated with heparinization followed by ~ournadin.~' No patients in this study had progression of thrombus or DVT proximal to the calf, and therefore none required treatment. All results were analyzed with statistical software @AS {2QOl] SASe Proprietary Software Release 8.2 [TS2MO] SAS fnstitute Inc. Cary, NC, USA). Wald Chisquare testing was used to analyze the association of a number of variables (Table I ) with the formation of DVT, as well as occfusive DVT as a subset of DVT. Variables were tested as Binomial Factors, Continuous Variables and Categorized Variables. Characteristics of risk factors analyzed are outlined in Table 1. Body Mass lndex was calculated as BMI=Weight(Kg)/Height2(meters)and stratified into the following categories: 48.5, 18.5 to 25, 25 to 30, 30 to 40 and 40+, according to National Institute of Health obesity guidelines10 Age was categorized by decade (10-19, 20-29 etc.), The variables of hindfoot procedures and immobilization appeared linked and were tested as four groups: 1. Nonhindfoot surgery without immobilization, 2. Hindfoot surgery without immobilization, 3. Nonhindfoot surgery with immobilization, and 4. Hindfoot surgery with immobilization. RESULTS

The study population consisted of 201 patients, 83 male and 118 female, with an average age of 45.69 years (range, 13 to 83). Forefoot surgery accounted for 46.6% of the procedures, midfoot 8.9%, hindfoot 18.32% and ankle 26.18%. Bony procedures accounted for 550A of the total procedures, 80% done under general anesthetic, and 33.5% had postoperative immobilization. In the present study population, the rate of DVT was found to be low. Of 201 patients, 53 (6.5%) had positive ultrasound. In six f3.074) of these patients the findings were only in the superficial veins and muscular plexuses. These were not considered clinically significant and were not included in the final analysis. Seven of 201 (3.5% total population) had true DVT (peroneal, anterior tibial and posterior tibial venous thrombi). Five of these seven (2.5% of total population) patients had thrombi that were occlusive, eliminating ail blood flow in the vein. DVTs involved an average of 1.57 of the six veins (two each peroneal, anterior tibia1 and posterior tibialf in

each affected patient, with a range from one to th{ee. One of the seven had thrombus in the contralateral limb but not the operated side. None of the seven patients had any clinical symptoms associated with the DVT (pain, palpable cords, swelling or Homans' sign). Wald Chi-square testing was used to analyze the variables for association with DVT formation, and also with occlusive DVT (ODVT) formation (Table 2). Factors found to be associated with DVT formation were: hindfoot surgery fp=0.02), hindfoot surgery combined with immobilization (p=0.02), and increased tourniquet time fp=0.03). Age was also associated, both as a continuous variable (p=0,051f and a variable categorized by decade @=0.04). Testing was also done to analyze the incidence of occlusive DVT as a separate entity, scoring nonocclusive DVT as normal. Hindfoot surgery was again associated (p=0.04) as was combined hindfoot surgery with immobilization (p=0.03). Unlike the risks for all DVT, neither age nor tourniquet time were associated with the subgroup of occiusive DVT formation. Body Mass lndex was not associated with overall DVT formation, but was associated with occlusive DVT (ODVT). BMI was associated strongly with ODVT in all three modes tested: BMb30 (p=0.04), as a continuous variable (p=O.Ol) and when grouped in the N!H categories of obesity (p=0.02).

Deep vein thrombosis can be a significant cause of morbidity and mortality following orthopaedic surgery. Studies of total hip and knee replacements have found high incidences of DVT in untreated populations, but the incidence foilowing foot and ankle surgery is mostly unknown'4and is largely regarded as a low The practical questions most surgeons would wish to know are what is the risk of thromboembolism, and is routine prophylaxis indicated. Mizel et al.'"ave undertaken the most extensive study to date regarding DVT following foot and ankle surgery, evaluating over 2,700 patients. In this study they found an incidence of DVT of 0.22% and an incidence of nonfatal pulmonary emboli of 0.15O%. While this multicenter study was very significant in terms of the large number of patients, it did suffer two flaws. First, radiological studies to detect DVT were used only on patients who had clinical symptoms of thrombi or embolism. Because clinical detection alone is inaccurate and many thrombi may be a s y m p t o m a t i ~ , ' ~ " " ~ ~ ' ~ ~ ~ ~ the true incidence of thrombi is likely to have been under-reported. The incidence of clinically significant events, however, would be expected to be accurate. Second, the use of thromboembolism prophylaxis was "determined by the treating surgeon." This means that

Foot & Ankle InternationalNol. 23, No. 5/May 2002

DEEP VEIN THROMBOSIS AFTER SURGERY

413

Table 1: Variables analyzed for association with the occurrence of Deep Vein Thrombosis (DVT) and Occlusive Deep Vein Thrombosis (ODVT) Binomial Factors Continuous Categorized Risk Factor (yeslno) Variables Variables Gender (Male) X X Smoker X Oral contraceptive pill X Hormone replacement therapy X History of cancer X Family history of DVT X Blood disorderlclotting problems X Procedure on Bone (v. soft tissue alone) General anesthetic X Postoperative immobilization X X Location-forefoot X Location-midfoot X Location-hindfoot X Location-ankle x (>=30, obese) x (BMI units) x (NIH categoriesa) Body Mass Index (BMI) x (by decadeb) x (in years) Age X Tourniquet time (min) "ational Institute of Health BMI categories: 4 8 . 5 , 18.5 to <25, 2 5 to <30, 3 0 t o <40 a n d 40+ "0-19 years, 20-29 years, 30-39 years etc.

the incidence of DVT in untreated patients undergoing foot and ankle surgery is still unknown, as the two groups were not separated. All patients in this study underwent postoperative ultrasound to detect thrombosis, and no patient received any perioperative DVT prophylaxis. The patients only had calf ultrasound performed. While this may have missed proximal clots, the authors feel that the majority of proximal clots propagate from the The authors believe that checking the calf only would give a higher incidence of thrombosis than in studies that check only the thigh. Studies have shown that ultrasound may be less sensitive (48 to 57%) in the calf compared with the thigh (62%) as well as in asymptomatic patient^'^.'^ of which both conditions apply to this study. Thigh veins were not tested as part of the senior author's protocol, partly as a cost-saving measure. This study was a prospective evaluation of all patients undergoing surgery of the foot and ankle without any DVT prophylaxis. A low incidence (3.5%) was found in this study of thrombus formation in the deep venous system of the calf, none of which showed any progression on follow-up ultrasound. No patients were found to have clinical symptoms consistent with thrombosis or pulmonary embolism at the postoperative visit. In this study, the risk factors found to be associated with DVT formation following foot and ankle surgery were: hindfoot surgery with or without immobilization, increasing age and tourniquet time. Factors found asso-

ciated with occlusive DVT following foot and ankle surgery were hindfoot surgery with or without immobilization and increasing BMI. Age was not found to be associated with occlusive DVT, and BMI was not found to be associated with overall DVT formation, only occlusive DVT. A similar study with larger numbers of patients in the various groups would give more power to the study. This study shows that: 1. DVT following foot and ankle surgery is rare, but more prevalent than previously suggested, 2. They are mostly asymptomatic, and 3. They do not progress proximally. Based on these findings and review of the literature, the authors agree with Mizel et aI.l4 that routine DVT prophylaxis is not indicated in patients undergoing foot and ankle surgery. Even in higher risk patients (hindfoot surgery, obese, elderly or increased tourniquet time) the lack of clot progression or symptoms would lead us to believe that prophylaxis is not indicated routinely in these patients. Based on the results of this study, the senior author no longer performs routine ultrasound screening of postoperative patients. REFERENCES 1. Agnelli, G; et a!: Clinical Outcome of Orthopaedic Patients with Negative Lower Limb Venography at Discharge. Thrombosis and Haemostasis, 74(4):1042-4, 1995. 2. Agnelli, G: PostdischargeProphylaxis for Venous Thromboernbolism Among Highrisk Surgery Patients. Vascular Medicine 351-56, 1998.

4 14

foot & Ankle Infernztional/Voi.23, No. 5/May 2002

SOLS AND SAXBY ---

-

-

-

-

DVT (ODVT) on Table 2: Results of logistic regression of incidence of Deep Vein Thrombosis (DVT) or risk factors O DVT DVT Wald Chi-square Wald Chi-square X i ' "

(Probability) ---. 0.47 fn.s.1 0 (n.s.) 0 (n.s.) 1. l 0 (n.s.) 0.31 (ns.) 0 fn.s.) 0 Ins.) 2.06 fn.s.) 0.12 (n.s.j 3.76 (P=0.053) 2.52 (n.s.) 0.25 (n.s.1 5.45* (P=0.02) 0.42 (n.s.1 2.23 ( n s f 3.37 fP=0.07) 2.53 (n.s.) 3.80* (P=0.051) 4.39* (P=0,04) 5.64* (P=0.02) 4.80* (P=0.03)

Risk Factor -Gender Smoker Oral contraceptive pill Hormone replacement therapy History of cancer Family history of DVT Blood disorder/ clotting problems Procedure on Bone fv. so3 tissue alone) General anesthetic Postoperative immobilization Location- forefoot Location- midfoot Location- hindfoot Location- ankle Body Mass Index fBMl)>30 Body Mass Index (continuous] Body Mass Indexb(categorized by National Health Instjfute standards) Age in years (continuous) Age (categorized by decade)" HindfooVlmmobilizationd(categorize4 Tourniquet time in minutes (cantinrraus)

)'(:

'"

rubabi it .I ityf

0 (ns.) 0 fns.) 0 (n.s.) 0.13 (n.s.) 0.81 (ns.) 0 (8s.) 0 fns.) 1.02 (ns.) 0 (ns.) 3.50 (P=0.06) 0 (ns.) 0.71 (n.s.) 4.29* (P=0.04) 0.06 fn.s.1 4.07* (P=0.04) 6.43* (P=O.Ol) 5.68* (P=0.02) 0.99 (ns.) 1.51 (ns.) 4.88' (P=0.03) 3.23

"All Chi-squared values h a v e o n e degree of freedom bl=underweight, ...6=profoundly o b e s e

...

"Decade 0=1-9. 1 = 10-19.. 8=80-89. a~indfootllmmo'bilization ~ e i t h e rHindfoot nor Immobilization 1= Either Hindfoot o r Immobilization 2 = Both Hindfoot a n d Immobilization "Signif~cantat 5% level ns,: Non-significant

i=

-

-

3. Ascani, 8; e i at: Distiibution and Occiusiveness of Thrombi in Patients with Sunteillance Detected Deep Vein Thrombosis after Hip Surgery. Thrombosis and Haemostasis 75(2):239-41, 1996. 4. Bates, SM; Hirsh, J: Treatment of Venous Throboernboiism. Thrombosis and Haemostasis 82(2):870-7, 1999. 5. Davidson, HC; Mauu, D; Gage, BF; Jeffrey, RB: Screening for Deep Venous Thrombosis in Asymptomatic Postoperative Orthopedic Patients Using Color Doppjer Sonography- anaiysis of prevalence and risk factors. Am. J. Roentgenol, 166:659-62, 1996. 6. Hatch, DJ; Magnusson, PG; DiGiovanni, JE: Mini-dose heparin prophylaxis for high-risk patients in pediatric surgeiy J. Am. Podiatry Assoc., 70(2):7343, 1980. 7. Hyers TM; Agnelii G; Hull RD; Weg JG; Morris T A Samama M; Taspon V: AntithromboticTherapyfor Venous Thromboembolic Disease. Chest, 114(5):561S78S, 1998 Supplement 8. Kakkar, VV; Howe CT; Flanc C; Clarke MB: Natural History of Postoperative Deep-Vein Thrombosis. Lancet ,Aug 2 ik230-32, 1962. 9. Kroll, HR; Odderson, IR; Alten, FH: Deep vein thrombi associatedwith the use of plastic ankleloot orthoses. Arch. Phys. Med. Rehabi1.,79:576-578, 1938. 10, National Institute of Health: The Practical Guide: Identification. Evaluation and Treatment of Oveweight and Obesity in Adults, NIH Publication Number 00-4084, October 2000. 11. Paiement, GD; Mendelsahn, C: The risk of venous thrornboembolismin the orthopedic patient: Epidemiologicaland physiological data. Orthopedics, Feb., 20 Suppl: 7-9, 1997. 12,Magnusson, M; Eriksson, 81; Kaiebo, P; Sivertsson, R: Is Colour Doppier

..

Ubmsound a Sensitive Screening Methd in Diagnosing Deep Vein Thrombosis after Hlp Surgery? Thrombosis and Haemostasis: 75(2):242-5. 1396. 13. Mitcheti, LJ: Thron>boembolicComplications of Cast Immobtlrzation lor injuries of the lower extremities. Clin. Grthop., 108:191-5,1975. 14. Mizel, MS; Temple, HT; Michelson, JD; Alvarez, RG; Clanton, TO; Frey, CC; Gegenheimer, AP; Hurwitz, SR; Lutter, LD; Mankey, MG; Mann, RA; Miller, RA; Richardson, EG; Schon, LC; Thompson, FM; Yodlowski, ML: ThromboemboiismAfter Foot and Ankle Surgery- a muliicenier study. Cim. Orihop., 348:160-85. 1998. 15. Paiement, GO; Mendelsohn, C: The Risk of Venous Thromboemboism in the Grihopedic Patient: Epidemiologicaland Physioiogical Data. Oithopedics. Feb, 20 Suppl:7-9, 1997. 16. Servatjoo, P: Deep venous thrombosis. The dilemma of diagnosis. J Am. Podiatr. Med. Assoc., 87(5):224-32 1997. 17. Simon, MA; et al: The Effect of Thigh Tourniquet on the Incidence of Deep Venous Thrombosis after Operations on the Fore Part of the Foot J. Bone Joint Surg., 64Af2]:188-91. 1982. 16. Thomas, AIIL; O'Dwyer, JA: A Phlebographic Study of the lnadence and Significance of Venous Thrombosis in the Foot. Am. J. Roentgenoi. 135 751-754, 1978 19. Wells, PS; et al: Accuracy of Ultrasound for the Diagnosis of Deep Venous Thrombosis in Asymptomatic Patients after Orthopaedic Surgery- a rneta-analysis. Ann Intern Med. 122:47-53, 1995. 20, Wolf, DW: Case records of the California Podiatry Hospital clinicopatholog~cexercise- postoperative thrombophlebitis. J. Am. Podiatry Assn , 69(3):207.:0. 1979.

ARTICLE IN PRESS

Journal of Diabetes and Its Complications xx (2008) xxx – xxx WWW.JDCJOURNAL.COM

Charcot arthropathy of the foot and ankle: modern concepts and management review Dane K. Wukich a,⁎, Wenjay Sung b a

UPMC Comprehensive Foot and Ankle Center, University of Pittsburgh School of Medicine, Pittsburgh, PA 15203, USA b UPMC South Side Podiatric Residency Program, Pittsburgh, PA 15203, USA Received 4 April 2008; received in revised form 14 August 2008; accepted 13 September 2008

Abstract Charcot arthropathy (Charcot neuroarthropathy, diabetic neuropathic osteoarthropathy, or neuropathic arthropathy) remains a poorly understood disease, although recent research has improved our level of knowledge regarding its etiology and treatment. The effects of Charcot arthropathy are almost exclusively seen in the foot and ankle, and the diagnosis is commonly missed upon initial presentation. It has been well established that this complication of diabetes mellitus severely reduces the overall quality of life and dramatically increases the morbidity and mortality of patients. However, there are few high-level evidence studies to support management and treatment options at this point in time. The goal of this study is to evaluate the modern concepts of Charcot arthropathy through a review of the available literature and to integrate a perspective of management from the authors' extensive experience. © 2008 Elsevier Inc. All rights reserved. Key words: Charcot arthropathy; Neuroarthropathy; Neuropathic osteoarthropathy; Diabetes mellitus; Current treatment concepts

1. Introduction Charcot arthropathy of the foot and ankle is a deforming and destructive process that can lead to increased patient morbidity due to gross instability, recurrent ulcerations, and/or amputation (Armstrong & Peters, 2002; Frykberg et al., 2006; Saltzman, Hagy, Zimmerman, Estin, & Cooper, 2005). Charcot arthropathy has been associated with leprosy, toxic exposure, syringomyelia, poliomyelitis, rheumatoid arthritis, multiple sclerosis, congenital neuropathy, and traumatic injury (Gupta, 1993; Johnson, 1967; Sanders & Frykberg, 2007). However, diabetes mellitus has become the most common etiology in the modern era (Miller & Lichtman, 1955). The diagnosed cases of Charcot arthropathy associated with diabetic patients range from 0.08% to 7.5% (Sanders & Frykberg, 2007); however, true prevalence is likely unknown due to cases undiagnosed by untrained ⁎ Corresponding author. Tel.: +1 412 586 1546; fax: +1 412 586 1544. E-mail address: [email protected] (D.K. Wukich). 1056-8727/08/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.jdiacomp.2008.09.004

clinicians (Rajbhandari, Jenkins, Davies, & Tesfaye, 2002). The effects of Charcot arthropathy are almost exclusively seen in the foot and ankle (Frykberg & Belczyk, 2008); however, the supply of scientific data and evidence-based treatments is largely based on retrospective studies. Known as Charcot neuroarthropathy and diabetic neuropathic osteoarthropathy (Sanders & Frykberg, 2007), this complication of diabetes mellitus severely reduces the overall quality of life and dramatically increases the morbidity and mortality of patients (Gazis et al., 2004; Lee, Blume, & Sumpio, 2003).

2. Historical review and epidemiology Sir William Musgrave is believed to have first recorded descriptions of “neuropathic arthritis” as a complication of venereal disease in 1703 (Armstrong & Peters, 2002; Gupta, 1993; Kelly, 1963), but most of the world's medical communities remained unaware of this disease. In 1831, an American physician, John Kearsley Mitchell, reported a case

ARTICLE IN PRESS 2

D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

of “caries [tuberculosis] of the spine” that correlated spinal disease with hot, swollen, and asymmetrical joints (Mitchell, 1831). Silas Weir Mitchell supported J.K. Mitchell's findings by observing similar clinical features from wounded soldiers with spinal injuries during the American Civil War (Mitchell, Morehouse, & Keen, 1864). In 1868, Jean-Martin Charcot recognized the importance of their findings and described a hypertrophic process of destructive arthritis. Fifteen years later, Charcot and Féré (1883) published the first observations of this process in the “short bones and small joints of the foot [la pied tabetique]” (Sanders, 2004). Charcot received universal acclaim at the Seventh International Medical Congress in London, and the prominent Sir James Paget, recognizing the discovery of a distinct pathologic entity, declared that the disease be known as “Charcot's disease” (MacCormac & Klockmann, 1881; Sanders & Frykberg, 2007). However, it was Jordan (1936) who established the link between Charcot arthropathy and diabetes mellitus. The incidence of Charcot arthropathy, defined as the number of new cases over a set period of time divided by the study population initially without the disease (Le & Boen, 1995), was first reported by Miller and Lichtman (1955) to occur more often in diabetic neuropathy patients than in those with other neurologic disorders. The authors accounted that out of 33 patients presenting as new cases of Charcot arthropathy, 17 had diabetes while only 4 had syphilis. Sinha, Munichoodappa, and Kozak (1972) reported an incidence of 1/680 in their series of 68,000 consecutive admissions of diabetic patients over a 21-year period. The authors suggested that the true incidence was much higher due to several patients in the series who were discovered after radiographs had been taken due to unrelated reasons; however, the authors did not specify what those unrelated reasons were. Fabrin, Larsen, and Holstein (2000) reported epidemiological data of spontaneous-onset Charcot arthropathy in a consecutive series of diabetic patients. In this long-term observational study from Denmark, the authors followed an average of 4000 patients over a 10-year period and found the incidence of Charcot deformity to be 0.3% annually. In a smaller cohort study, Lavery, Armstrong, Wunderlich, Tredwell, and Boulton (2003) prospectively reported the incidence of diabetic foot complications in a consecutive series of Americans diagnosed with diabetes while enrolled in a diabetes management program. They found a total incidence of Charcot arthropathy of 8.5/1000 patients per year. However, they suggested that further studies were needed to explain the significant differences between non-Hispanic White Americans (11.7/1000 patients per year) and Mexican Americans (6.4/1000 patients per year). The lower incidence reported in Mexican Americans may be due to failure to recognize the diagnosis, especially in the early stages, thereby underestimating the true rate of incidence. The reported incidence of new Charcot arthropathy cases has remained relatively low among diabetic patients even

though diabetes has emerged as the primary cause (Fabrin et al., 2000; Lavery et al., 2003; Miller & Lichtman, 1955; Sinha et al., 1972). The prevalence of Charcot arthropathy, defined as the number of patients currently with the disease divided by the study population (Le & Boen, 1995), is unknown, and this may be due to the lack of standardized clinical or radiographic diagnostic criteria (Rajbhandari et al., 2002). In a series of 68 patients treated for midfoot Charcot arthropathy (Myerson, Henderson, Saxby, & Short, 1994), the clinicians noted that 25% of the patients referred to their facility had not been diagnosed correctly with active Charcot arthropathy by the referring institution. These patients were initially diagnosed with infection, gout, arthritis, fracture, venous insufficiency, or tumors. There have been estimates of prevalence by various authors ranging from 0.08% of the general diabetes patient population to 13% of patients presenting at a high-risk diabetic foot clinic (Frykberg & Belczyk, 2008). Although there has been much published work on Charcot arthropathy in the literature, there remains little work on actual evidence for drawing conclusions about its prevalence. Charcot arthropathy has also been reported in diabetic patients who undergo transplant surgery. Matricali, Bammens, Kuypers, Flour, and Mathieu (2007) retrospectively reviewed the medical records of 66 patients with diabetes who underwent simultaneous pancreas–kidney (SPK) transplants. They found that 8 of 66 patients (12%) developed a Charcot foot, and they attributed this to long-standing diabetes, high glycosylated hemoglobin (HbA1c) values, and nephropathy. Pretransplant HbA1c values were significantly higher for the SPK group that developed Charcot arthropathy; however, the study did not mention trauma history, neuropathy, or the role of immunosuppressive therapies in these patients. Despite the fact that it has been over 300 years since the first reported case, Charcot arthropathy of the foot and ankle remains a difficult and complex disease to identify, manage, and treat. With the increasing prevalence of diabetes worldwide (Wild, Roglic, Green, Sicree, & King, 2004), health-care providers need to be aware of Charcot arthropathy and its potentially limb-threatening complications in the foot and ankle. The goal of this current concepts review is to examine the available literature and to provide the reader guidance in managing and treating this potentially devastating complication of diabetic neuropathy.

3. Etiology and pathogenesis Diabetic Charcot arthropathy typically presents as a warm, swollen, and erythematous foot and ankle. The appearance of the extremity may be indistinguishable from infection, and almost all afflicted patients have severe peripheral neuropathy. It is this lack of protective sensation that delays identification of bony stress injuries that may

ARTICLE IN PRESS D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

overload the insensate limb, leading to an active Charcot process (Chantelau, 2005; Schon & Marks, 1995; Sella & Barrette, 1999). Charcot (1868) and Charcot and Féré (1883) believed that the disease occurred due to degeneration in the central nervous system, resulting in a neurogenic deficit in bone nutrition. This “neurotrophic theory” stimulated research and interest even though they could not provide any evidence, outside of observational studies, to support this idea (Chantelau & Onvlee, 2006). After many years and several transformations of Charcot's theory, the amount of evidencebased studies supporting the “neurotrophic theory” has been debatable (Banks & McGlamry, 1989). However, there is no debate that his work brought the attention of the medical world to this disease process. Although there have been others who suggested that autonomic denervation would lead to a hyperemic state (Leriche & Fontaine, 1927), Johnson (1966) is credited for describing a variation of Charcot's theory known as the “neurovascular” theory. From his observations of bedridden patients with spinal cord injury, he found radiographic evidence of osteolysis. Johnson contended that a central sympathetic failure initiated a hypervascular reflex that led to a state of overactive bone resorption and mechanical weakening, thus instigating Charcot arthropathy (Chantelau & Onvlee, 2006; Sanders, 2004). In support of this theory, Edmonds, Clarke, Newton, Barret, and Walkins (1985) found a significant increase in the pattern of isotope uptake on bone scans of patients diagnosed with Charcot arthropathy of the foot compared to those of diabetic neuropathy patients without the disease. The authors attributed the increase in uptake to sympathetic denervation. Others have found the same pattern of isotope uptake in patients experiencing acute Charcot arthropathy (ACA), but attributed the findings to bony destruction from an acute inflammatory process (McGill et al., 2000). Using duel-energy X-ray absorptiometry, Young, Marshall, Adams, Selby, and Boulton (1995) demonstrated that the bone mineral densities (BMD) of Charcot-arthropathyafflicted lower extremities were significantly less than those of non-Charcot-arthropathy-afflicted diabetic patients. Although there have been other BMD studies that did not show differences between diabetic patients with Charcot arthropathy and diabetic patients without Charcot arthropathy (Clasen, 2000), Young et al.'s findings were in line with those of others who observed bone resorption in up to 81% of Charcot arthropathy patients (Brower & Allman, 1981; Cundy, Edmonds, & Watkins, 1985). All of the patients with Charcot arthropathy were qualitatively diagnosed with cardiovascular autonomic neuropathy and demonstrated significantly reduced BMD in the afflicted feet. However, there was no difference in lumbar spine BMD values between patients with Charcot arthropathy and patients without Charcot arthropathy. In agreement with previous studies, Young et al. believed that the severity of

3

their somatosensory neuropathy was proportional to that of autonomic neuropathy. However, they did not elaborate as to how the autonomic neuropathy led to increased osteopenia. Nevertheless, Young et al. concluded that their findings supported the assertions of Edmonds et al. (1985). The reduced BMD in Charcot arthropathy patients results in reduced bone strength, predisposing patients to the development of fractures. Herbst, Jones, and Saltzman (2004) separated the pattern of Charcot arthropathy in the foot and ankle into three groups: fracture, dislocation, and combined fracture–dislocation. Although not all Charcot arthropathy patients had reduced BMD in their lower extremity, those within the fracture-pattern group had significantly lower BMD compared to the dislocation group and the combination group. They concluded that reduced BMD in the lower extremity was a specific risk factor for patients developing the fracture pattern, especially in the ankle, but those with normal BMD were more likely to develop a dislocation or combination pattern. Their findings also acknowledged why successful results vary with early surgical treatment between patients within the different groups (Bibbo, Lin, Beam, & Behrens, 2001). Research into the relationship between reduced BMD and the pathogenesis of Charcot arthropathy has led to the investigation of bone resorption mediators. Increases in certain proinflammatory cytokines, which are known mediators of bone resorption, are a contributing factor to increased osteoclastic activity in ACA patients (Baumhauer, O'Keefe, Schon, & Pinzur, 2006). In a study of Charcotarthropathy-reactive bone, osteoclasts were disproportionately increased compared to osteoblasts, and the osteoclasts demonstrated immunoreactivity for interleukin (IL) 1, IL-6, and tumor necrosis factor (TNF) α (Baumhauer et al., 2006; Jeffcoate, Game, & Cavanagh, 2005). Reacting from an initial insult, bone resorption due to a disproportionate increase in cytokines is believed to factor into the pathogenesis of Charcot arthropathy (Baumhauer et al., 2006). By measuring serologic markers, Petrova et al. (2007) demonstrated that the acute inflammatory Charcot foot is a peripheral event and is dissociated from any systemic inflammatory response. They concluded that the local inflammatory response demonstrated by the increase in skin temperature must be related to an increased expression of proinflammatory cytokines that did not consequently lead to a classical systemic acute-phase response. The role of proinflammatory cytokines and the “receptor activator of nuclear transcription factor κB ligand (RANK-L)/osteoprotegerin (OPG)” signaling pathway in Charcot arthropathy pathogenesis provided a modern direction for research and theory (Jeffcoate, 2004; Jeffcoate, 2005a; Jeffcoate et al., 2005). Jeffcoate (2004) observed that in a wide variety of other medical conditions such as osteoporosis and cardiovascular disease, the RANK-L/OPG signaling pathway regulates both bone turnover and vascular calcification. He hypothesized that this pathway

ARTICLE IN PRESS 4

D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

may play the decisive role in Charcot arthropathy. Increased osteoclastogenesis and subsequent osteolysis result in response to RANK-L up-regulation of nuclear transcription factor κB (NF-κB). The glycoprotein OPG, a member of the TNF receptor superfamily, inactivates RANK-L by serving as a decoy receptor, therefore moderating RANK-L activity and NF-κB expression (Jeffcoate, 2004). RANK-L and OPG syntheses are essential features of the regulation of the fine balance of bone homeostasis. A disturbance in the balance between RANK-L and OPG, which might include trauma, surgery, foot ulcers, or iatrogenic factors, is believed to trigger excessive osteolysis (Frykberg et al., 2006; Jeffcoate, 2004). This cycle is fully realized in the insensate limb of a patient who continues to bear weight on the affected foot, thereby continually reactivating the inflammatory process. Mabilleau, Petrova, Edmonds, and Sabokbar (2008) compared osteoclastic activity in active Charcot arthropathy patients to osteoclastic activity in general diabetes patients and healthy control patients using in vitro samples of peripheral blood monocytes (PBM). From these samples of PBM, the investigators used a previously described technique to generate functional osteoclasts in the presence of macrophage colony-stimulating factors and soluble RANKL (Fujikawa, Quinn, Sabokbar, McGee, & Athanasou, 1996; Sabokbar & Athanasou, 2003). They then compared the sample of nine consecutive patients with recent-onset Charcot arthropathy to the samples of eight diabetic patients with no history of Charcot arthropathy and eight healthy control subjects. After excess concentrations of OPG had been added to all the samples, the results indicated that the RANK-L-dependent pathway played a significant role in osteoclastic activity in active Charcot arthropathy, but it also suggested that an alternative non-RANK-L dependent pathway may be involved in combination. Evidence of unregulated activation of RANK-L derived from sympathetic denervation has only been circumstantial (Jeffcoate, 2004). Although some authors have implicated relationships among peripheral somatosensory neuropathy, autonomic sympathetic neuropathy, and osteoclastic activity, there have been no conclusive studies linking them (American Diabetes Association, 2008; Young et al., 1986). Investigators have discovered evidence linking sympathetic autonomic activity to increased osteoclastic activity (Togari, 2002). The findings indicate that decreased sympathetic activity leads to decreased osteoclastic activity, or, in other words, sympathetic failure leads to an unregulated increase in osteoblastic activity. In light of these findings, Chantelau and Onvlee (2006) postulated that peripheral osteopenia of the foot and ankle is not the result of decreased autonomic sympathetic activity. Historically, many have believed that the loss of sympathetic innervation was associated with increased peripheral blood flow, leading to an ACA process (Sanders & Frykberg, 2007). Vascular calcification of smooth muscle cells (Monckeberg's arteriosclerosis) is commonly found in diabetic Charcot arthropathy patients (Jeffcoate, 2005b), and

there are studies linking sympathetic denervation—induced and noninduced—to this calcification (Edmonds, Morrison, Laws, & Watkins, 1982; Goebel & Fuessl, 1983). There is also evidence that the bones of patients afflicted with syphilis who undergo ACA changes have widened haversian canals as a result of the sustained increase in blood flow (Jeffcoate, 2005a). However, the obvious sympathetic neuropathic consequence leading to bilateral changes in ACA patients should be consistently expected (Jeffcoate, Lima, & Nobrega, 2000; Young et al., 1995), but unilateral distribution is the normal finding (Jeffcoate, 2005b). Bilateral involvement has ranged from 5.9% to 39.3% in heterogeneous population studies (Sanders & Frykberg, 2007), but simultaneous bilateral involvement has been reported to be only 0.7% (Fabrin et al., 2000). Another facet of Charcot arthropathy that is not well understood is whether the process may recur in the same or uninvolved limb (Eichenholtz, 1966). Fabrin et al. reported on 20 cases of Charcot arthropathy recurring in the ipsilateral foot and suggested that recurrent stress injuries to the neuropathic foot, regardless of location, may initiate breakdown. This selflimiting process of Charcot arthropathy should not be expected in someone with irreversible autonomic sympathetic neuropathy (Jeffcoate, 2005b). The belief that sympathetic neuropathy acts as a precursor for diabetic bones and joints undergoing a “neurotrophic,” vulnerable, and hyperemic state remains popular among investigators. There is evidence to suggest that patients with type 1 diabetes mellitus and peripheral neuropathy have a greater tendency for osteopenia (Petrova, Foster, & Edmonds, 2005; Rix, Andreassen, & Eskildsen, 1999). Some authors also suggest that autonomic sympathetic neuropathy results in increased peripheral blood flow (Edmonds et al., 1985; Watkins & Edmonds, 1983; Young et al., 1995) and that increased blood flow from arteriovenous shunting occurs in all diabetic neuropathy patients with or without Charcot arthropathy (Boulton, Scarpello, & Ward, 1982). However, investigators have not been able to demonstrate the link between autonomic sympathetic neuropathy and increased osteoclastic activity in ACA through bone circulatory hyperperfusion (Chantelau & Onvlee, 2006). The perspective of Bloomgarden (2005) on clinical diabetic neuropathy was that the effects of autonomic neuropathy on the foot would lead to a state of inefficient circulation and abnormal sweat gland and oil gland functions. Although ulceration would likely occur due to this dysfunctional state, Bloomgarden did not attribute bone destruction in Charcot arthropathy to autonomic neuropathy. In a case series of 47 Charcot arthropathy patients by Pinzur, Sage, Stuck, Kaminsky, and Zmuda (1993), it was noted only half of all patients were also diagnosed with autonomic neuropathy; however, all 47 patients were diagnosed with peripheral sensory neuropathy. In fact, only peripheral somatosensory neuropathy has been consistently seen as a predisposing factor for developing Charcot arthropathy

ARTICLE IN PRESS D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

(Armstrong, Todd, Lavery, Harkless, & Bushman, 1997; Sinha et al., 1972). Shapiro et al. (1998) examined the patterns of peripheral blood flow and the rhythmic contractions of small arteries and arterioles in three groups of patients: those with diabetic neuropathy and ACA, those with diabetic neuropathy without Charcot arthropathy, and healthy control subjects. Despite severe neuropathic findings in Charcot arthropathy patients, they found that the ACA group did not differ in the rate of blood flow when compared to a control group of healthy subjects. Also, there was no significant betweengroups difference in their respective vasomotion, defined as spontaneous rhythmic oscillations of venules and arterioles that theoretically serve to direct the distribution of blood flow (Shapiro et al., 1998). This suggested that these patients would have similar, if not exaggerated, responses to repetitive trauma. They further suggested that the lack of inflammatory response seen with diabetic neuropathy patients without Charcot arthropathy, when challenged with increased local temperature, may actually act as a preventive factor against the development of the disease. Inflammation in response to trauma may explain the central role for the exaggerated hyperemia (Jeffcoate, 2005b). In addition, the reported low incidence among diabetic patients may be explained by the high prevalence of macrovascular disease, which limits the capacity of an inflammatory response. Although there is evidence to suggest that peripheral somatosensory neuropathy and vascular changes are involved in Charcot arthropathy (Armstrong et al., 1997), increased blood flow may be more likely the consequence—rather than the cause—of bony destruction (Chantelau & Onvlee, 2006). In 1886, three notable German physicians, Virchow, Rotter, and Volkmann, disputed Charcot's theory of neurotrophic bone (Anonymous, 1886). They believed that a repetitive trauma sustained by a joint that was unable to sense pain would lead to this disease—the “neurotraumatic” theory. Gupta (1993) noted that the common thread of pathogenesis included continual injuries from minor trauma or isolated major trauma to neuropathic joints. There are many authors who believed that Charcot arthropathy may be triggered in diabetic patients by some type of joint trauma, and they are supported by the identification of the lack of protective sensation as a predisposing factor to the disease

5

(Armstrong et al., 1997; Eloesser, 1917; Horwitz, 1948; Kimmerle & Chantelau, 2007; O'Connor, Palmoski, & Brandt, 1985; Sinha et al., 1972). The current majority of clinicians believe that a combination of these theories may contribute to the pathogenesis of this disease. The debate between “neurovascular" and “neurotraumatic" exclusivity has become an antiquated sidebar to the mystery of Charcot arthropathy. Whether these theories equally contribute to—or whether active Charcot arthropathy is—the sum of two or more unequal parts continues to be explored.

4. The course of Charcot arthropathy: modified Eichenholtz stages Early literature contributions concerning Charcot arthropathy lacked clinical findings that correlated with radiographic descriptions of the disease. Eichenholtz (1966) published a landmark article on Charcot arthropathy based on radiographic appearance and its physiologic course. Dividing the condition throughout its process, he described three separate but linear stages: developmental, coalescent, and reconstructive stages. Shibata, Tada, and Hashizume (1990) modified the Eichenholtz system to include an earlier stage prior to “development.” Several authors have proposed that this early inflammatory phase following injury be called “Charcot in situ,” “pre-Stage 1,” or “Stage 0 Charcot” (Schon & Marks, 1995; Sella & Barrette, 1999; Shibata et al., 1990; Yu & Hudson, 2002). This classification is currently being applied by the majority of foot-andankle physicians to Charcot arthropathy patients in the staging of the disease. Table 1 shows a summary of this Charcot arthropathy classification. Stage 0 Charcot (inflammatory) arthropathy begins with an initial perceived or nonperceived insult to the neuropathic foot-and-ankle complex, producing localized swelling, redness, and warmth (Chantelau, 2005; Shibata et al., 1990). Minimal, if any, radiographic abnormalities may be detected, and Classen, Rolley, Carneiro, and Martire (1976) noted that clinical symptoms may precede radiographic changes by up to 1 year. Diagnosis of this stage with magnetic resonance imaging (MRI) or technetium bone scans may prove to be critical in preventing the disease from

Table 1 Modified Eichenholtz stages a Stage Phase 0

Description

Inflammatory Localized warmth, swelling, and redness; minimal to no radiographic abnormalities; MRI may show nondisplaced pathologic fracture(s) and increased marrow edema to the foot and/or ankle Development Localized warmth, marked swelling, and redness; radiographic presence of bony debris, fragmentation of subchondral bone, periarticular fracture, subluxation, and/or dislocation Coalescence Continued but decreased warmth, swelling, and redness; radiographic presence of absorption of fine debris, new bone formation, coalescence of fragments, fusion of joints (ankylosis), and/or sclerosis of bone ends Remodeling Marked decrease or absence of warmth, swelling, and redness; physically enlarged fixed (“healing”) deformity; radiographic appearance of remodeled and new bone formation, decreased sclerosis, and/or possible gross residual deformity

1 2 3 a

Modified from Eichenholtz (1966).

ARTICLE IN PRESS 6

D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

progressing into the development phase (Chantelau & Poll, 2006). Schon and Marks (1995) proposed that neuropathic diabetic patients be identified as being at risk for Charcot arthropathy even after only minor injury to limbs with loss of protective sensation. Repetitive cumulative injuries to insensate patients may progress into the destructive stage of Charcot arthropathy and may lead to gross foot deformity, ulceration, infections, and/or amputation (Armstrong et al., 1997; Chantelau, Richter, Ghassem-Zadeh, & Poll, 2007). In contrast, patients with intact protective sensation limit the progressive course of repetitive injury by offloading the injured limb. Identification of this prodromal stage may deter further progression into the latter stages of Charcot arthropathy, thus preventing further deformity and complications (Chantelau, 2005; Frykberg et al., 2006). Frequently, Stage 0 patients are misdiagnosed as cellulitis, gout, or deep vein thrombosis due to its clinical appearance and normal radiographic findings, but increased clinical awareness and education of the health-care provider can potentially limit the progression of the disease. Stage 1 Charcot arthropathy (development) is distinguished by marked warmth, swelling, and redness, and radiographic changes are evident in the bone-and-joint architecture (Eichenholtz, 1966). The appearance of bony debris, fragmentation of subchondral bone, subluxation, dislocation, and periarticular fractures are common findings during Stage 1. This stage may also have abnormal laboratory values that indicate overactive osteoclastic and osteoblastic activities (Chantelau & Onvlee, 2006). Stage 2 Charcot arthropathy (coalescence) follows, with decreasing warmth, swelling, and redness, and radiographic signs of healing fracture fragments (Eichenholtz, 1966). Although sometimes difficult to distinguish, Stage 2 Charcot arthropathy is considered separate from Stage 1 Charcot arthropathy, and the clearest detection of Stage 2 is radiographic appearance of osseous debris absorption, coalescence of bone fragments, and/or new periosteal bone formation. Stage 3 Charcot arthropathy (remodeling) results as the final consolidation of fractured and deformed bone without the warmth, swelling, and redness seen previously (Eichenholtz, 1966). This stage is characterized by osseous deformity that can be either stable or unstable. Considered the chronic stage of Charcot arthropathy, osteoclastic and osteoblastic activities are no longer increased, as confirmed by laboratory test (Chantelau & Onvlee, 2006). Radiographic appearance of a mature fracture callus, bony remodeling of major fragments, and decreased sclerosis signify the finality of the permanent deformity. Although Eichenholtz described the Charcot course in linear stages, the time of progression through each stage can vary from weeks to months to years. However, neuropathy remains unchanged throughout the Charcot process, whether active or quiescent (Armstrong et al., 1997; Sinha et al., 1972). ACA initially begins in one joint and may progress to other proximal joints. There have been

case reports of isolated involvement within the body that do not include the foot or the ankle (Bayne & Lu, 1998; Edison & Finger, 2005; Lambert & Close, 2002); however, less attention is paid to these anatomical sites due to lack of readily available data. When multiple joints are involved in Charcot arthropathy, these may be seen at different Eichenholtz stages, and these multiple joint attacks may even course at different progressive rates of destruction (Eichenholtz, 1966). However, a study by Fabrin et al. (2000) showed that recurrent and/or multiple joint attacks were not influenced by any particular location. The lack of data and standardization of assessment for ACA may fuel debate as to whether these cases of “recurrence” may actually be, in fact, true recurrence.

5. Anatomical classifications Several authors have anatomically classified the characteristics of Charcot arthropathy by observing the patterns of destruction to the foot and ankle (Brodsky & Rouse, 1993; Sanders & Frykberg, 2007; Sanders & Mrdjenovich, 1991; Schon, Weinfeld, Horton, & Resch, 1998; Sella & Barrette, 1999). Although this disease has been associated with other bodily sites in the diabetic patient (Bayne & Lu, 1998; Lambert & Close, 2002), it almost exclusively affects the foot and the ankle. Sanders and Frykberg (1991) divided the foot and the ankle into five patterns of destruction for diabetic Charcot arthropathy and correlated different anatomical patterns with the frequency of complications: Pattern I (forefoot)=15%; Pattern II (tarsometatarsal joints)=40%; Pattern III (naviculocuneiform, talonavicular, and calcaneocuboid joints)=30%; Pattern IV (ankle and/or subtalar joint)=10%; Pattern V (calcaneus)=5% (Sanders & Frykberg, 1991). The most severe structural deformity and functional instability are found at the Lisfranc joint and at the ankle/subtalar joints. Destruction at the calcaneus is not commonly seen with Charcot arthropathy (Sanders & Frykberg, 2007), but it may be associated with an isolated pathologic fracture or avulsion injury of the posterior tuberosity (Brodsky & Rouse, 1993). A summary of this anatomical classification is described in Table 2. Brodsky (2007) described an anatomical classification based on the four areas most commonly affected by Charcot arthropathy. Representing about 60% of the anatomical sites that develop Charcot arthropathy, Type I (“midfoot”) is considered the most common site and includes the metatarsocuneiform and naviculocuneiform joints. These are also noted to be associated with symptomatic bony prominences. The second most common site, Type 2 (“hindfoot”), includes the subtalar, talonavicular, or calcaneocuboid joints, where bony prominences are less common. It accounts for 30–35% of anatomical incidence. Type 3 is divided into “A” and “B,” or the ankle and the posterior calcaneus, respectively. Comprising 9% of Charcot

ARTICLE IN PRESS D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

7

Table 2 Charcot arthropathy anatomical classification a Pattern Location I

Description

Forefoot

Involving the interphalangeal joints, phalanges, metatarsophalangeal joints, and/or distal metatarsal bones; commonly occurring pattern, also seen with plantar ulceration; seen as osteopenia, osteolysis, juxtaarticular cortical bone defects, subluxation, and destruction on radiographs Tarsometatarsal joints Involving the tarsometatarsal joints and metatarsal bases, cuneiforms, and cuboid; commonly occurring pattern, with greater frequency in diabetic patients than in patients with leprosy; may be associated with plantar ulceration at the apex of deformity; seen as subluxation or fracture–dislocation, collapse of midfoot, and resultant rocker-bottom foot deformity (consistent with initial features of osteoarthritis) on radiographs; may have dorsal prominence at metatarsal bases; late changes include fragmentation Naviculocuneiform, talonavicular, Involving usually the naviculocuneiform joint and navicular bone but also the other midtarsal joints and bones; and calcaneocuboid joints ulceration may occur at the apex of deformity and may be in combination with Pattern II; on radiographs, seen as osteolysis of naviculocuneiform joints with fragmentation; with osseous debris both dorsally and plantarly Ankle and subtalar joints Involving the ankle joint with or without the subtalar joint and medial or lateral malleolar fracture; considered a severe structural deformity with instability—may even be associated with minor ankle sprain; on radiographs, seen as malleolar fractures, erosion of bone and cartilage with collapse of joint, free bodies in ankle, extensive destruction, and lateral dislocation of ankle Calcaneus Rarely involving only the calcaneus bone and usually involving an avulsion fracture of the posterior tubercle; although no joint is involved, the pattern develops in patients with Charcot arthropathy; on radiographs, seen as osteolytic changes in the posterior calcaneus attachment of the Achilles tendon; avulsion fracture of the posterior tubercle may ensue; osteolytic changes may also occur at the naviculocuneiform joint due to additional stress during liftoff in the gait cycle (this may be due to lack of an Achilles tendon attachment to the calcaneus)

II

III

IV

V

a

Adapted from Sanders and Frykberg (2007).

arthropathy presentations, Type 3A involves the tibiotalar joint and associated bones, and Type 3B, representing less than 2% of presentations (Sanders & Frykberg, 2007), involves a pathologic fracture of the tuberosity of the calcaneus. Brodsky and Rouse (1993) also noted that the breakdown of soft tissues from bony prominences occurred most commonly in Type I patterns, and these ulcers were located on the plantar surface of the foot. Trepman, Nihal, and Pinzur (2005) have noted the obvious lack of inclusion for the forefoot and multiple regions of involvement, and have modified Brodsky's anatomical classification to include these sites. Because of their increased proportion of involvement in Charcot arthropathy, the midfoot and medial column of the foot have been further classified into separate schemes. Schon et al. (1998) evaluated 131 feet from 109 patients to describe the patterns of acquired midfoot deformities, and although many etiologies of midfoot deformities were included, 89 of the 109 patients were diagnosed with Charcot arthropathy. Assessed from the three standard radiographic views, the anatomical location with the most clinically significant involvement would determine the pattern type. Each of the four patterns in this classification was divided into three separate clinical stages ranging in the degree of midfoot collapse, regardless of etiology. The “Lisfranc pattern” has radiographic breakdown involving the first three metatarsocuneiform joints, and as the stages progresses in severity from A to C, the fourth and fifth metatarsocuboid joints become involved. The “naviculocuneiform pattern” is seen when the majority of radiographic deformities occur more proximally and medially at the naviculocuneiform joint. Less significant anatomical deformities can also be seen in the central column and

laterally at the fourth and fifth metatarsocuneiform joints. The “perinavicular pattern” includes the navicular and its surrounding bones, and patients with this pattern may have a tendency toward an adducted forefoot. The “transverse tarsal pattern” involves significant deformity in the talonavicular joint, including the medial and central columns. Unlike the other patterns, the “transverse tarsal pattern” has much larger talocalcaneal and talonavicular coverage angles. By examining the severity of the mechanical malalignment, the healthcare provider could assess the treatment appropriate for the midfoot using radiographic and clinical parameters. It was also noted that the most severe “rocker-bottom” phase in any of the four patterns of Charcot midfoot could lead to ulceration and/or infection at the midfoot (Schon, Easley, & Weinfeld, 1998). The medial column of the Charcot foot was also further divided into five clinical stages using clinical findings, radiographs, and bone scans (Sella & Barrette, 1999). Similar to the modified Eichenholtz classification, the first of the five stages is called Stage 0, and the medial column is swollen, warm, and often painful; however, radiographs are negative for any abnormal findings. Clinical symptoms persist into Stage 1 with radiographic findings of periarticular cysts, erosions, localized osteopenia, and sometimes diastases. Once subluxation is seen, Stage 2 is reached, with the second metatarsocuneiform joint usually involved. Stage 3 is identified with joint dislocation and arch collapse, while Stage 4 represents the healed stage wherein the end result is a sclerotic fusion of involved bones and joints. Although several authors have provided classification schemes with some clinical importance, none has been able to predict outcome (Rajbhandari et al., 2002). These different classifications do add insight into the understanding of

ARTICLE IN PRESS 8

D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

diabetic Charcot arthropathy and do not enable clinicians to accurately describe the stage and location of the disease.

6. Clinical presentation and standard diagnostics The American Diabetes Association (2008) recently released its position statement for standards of medical care and foot care recommendations for patients. The American Diabetes Association (2004) has long recognized the need for the screening and evaluation of the foot and ankle of patients with long-standing diabetes, especially those who have developed neuropathy. These recommendations rely on a keen understanding of the diabetic foot and ankle, with all their possible complications. If the treating physician can recognize Charcot arthropathy without delay, the chances of devastating morbidity and mortality decrease substantially (Chantelau, 2005). The diagnosis of Charcot arthropathy is primarily reliant on clinical presentation, but a physician's high index of suspicion should not be underappreciated (Armstrong & Peters, 2002; Jeffcoate, 2005b; Sanders & Frykberg, 2007). A thorough patient history is essential to any assessment; however, a neuropathic patient's history can be unintentionally misleading. It is therefore up to the clinician to know what questions to ask and what information is important when making an assessment. Special attention must be given to the patient especially if history of any trauma, history of neuropathy, recent swelling, redness in the limb, or a combination of the like is uncovered. Counterintuitively, the history may include pain sensations in an insensate limb but no recollection of any sustained trauma. In a study of 55 patients with Charcot arthropathy, more than 75% complained of pain in the foot upon presentation even though all subjects had a clinical loss of protective sensation to the 10-g Semmes–Weinstein monofilament wire (Armstrong et al., 1997). Repetitive trauma to the foot and ankle may be entirely absent from verbal history even though clinical symptoms prove otherwise. The study found that only 22% of patients were able to recall some specific traumatic event prior to the onset of Charcot arthropathy. The loss of protective sensation may leave the patient unaware of any particular event or reoccurring minor events (Chantelau, Richter, Schmidt-Grigoriadis, & Scherbaum, 2006). It is important to investigate any previous history of infections or ulcers to rule out a recurring acute or chronic infection. The usual presentation of Charcot arthropathy involves a warm, swollen, erythematous foot or ankle in an insensate patient and, because of its similarity to an acute soft-tissue infection, heightened awareness is needed when dealing with the diabetic neuropathy patient population (Armstrong et al., 1997; Pinzur et al., 1993). Most infections in the diabetic foot involve a direct source of inoculation through an opening in the skin, usually caused by neuropathic ulcers (Sanders, 1994; Singh, Armstrong, &

Lipsky, 2005). It may be easy to clinically diagnose an infection with an obvious open wound, but this does not exclude a concomitant Charcot process. Some have observed cases of Charcot arthropathy that may have been triggered by cellulitis, osteomyelitis (OM), and even synovitis (Armstrong et al., 1997; Jeffcoate, 2005b). Positive systemic signs of infection include leukocytosis, elevated C-reactive protein and erythrocyte sedimentation rate (ESR) levels, and recent unexplained hyperglycemia. However, unremarkable clinical tests may not necessarily exclude infection, making distinction between the two difficult. The treatment regimen is therefore dependent on the accurate diagnosis of infection. The Charcot arthropathy patient may present for treatment at any stage of the disease, but the common reasons for seeking medical consultation may be mild and moderate pain, severe edema of the foot, and inability to put their shoe on due to swelling (Wilson, 1991). Chantelau (2005) reported that 19 of 24 patients (80%) were misdiagnosed as sprain, OM, Sudeck's atrophy, deep vein thrombosis, cellulitus, or rheumatoid arthritis instead of Charcot arthropathy, and all continued to bear weight on the involved limb prior to referral to a specialty clinic. Although radiographs may not reveal any bone or joint abnormalities during the prodromal inflammatory stage of the Charcot process, radiographic studies, in correlation with clinical exam, are one of the tools widely used to differentiate the disease (Sanders & Frykberg, 2007). When this initial stage is suspected but not proven, the patient should be prevented from incurring any additional injury to the suspected limb. With immobilization and offloading, the patient is protected while awaiting the results of further investigation. Gouty arthritis and rheumatoid arthritis can be separated from Charcot arthropathy by their radiographic and clinical features (Trepman et al., 2005). Radiographs of the foot and ankle that are taken in the non-weight-bearing position can have obvious variability in image quality and may not show subtle instability compared to radiographs in the weightbearing position. It is recommended that all foot-and-ankle radiographic examinations be obtained in a weight-bearing position if possible. MRI exams are increasingly being used and recommended for diagnosing Charcot arthropathy, especially at the earliest stage (Chantelau & Poll, 2006; Sanders & Frykberg, 2007). Chantelau et al. (2007) evaluated 12 consecutive diabetic patients with polyneuropathy who presented with only mild pain and a swollen foot. All of these patients had plain radiographs that did not demonstrate any osseous abnormality. MRI studies in all these patients revealed bone stress injury with a median involvement of 2.5 bones per foot, which were previously undetected using plain radiographs. Although bone scintigraphy and white blood cell scans have been traditionally advocated for the differentiation and diagnosis of Charcot arthropathy, there is clear evidence that MRI offers the highest diagnostic accuracy (Tan & Teh, 2007). Differentiating between OM and ACA has been noted to be difficult due to similar signal intensity

ARTICLE IN PRESS D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

changes (Marcus et al., 1996). However, there are several MRI features that—with clinical correlation, anatomical distribution, and abnormal appearance—help distinguish these two diagnoses (Tan & Teh, 2007). In OM, the pattern of bone marrow edema tends to involve a single bone with diffuse marrow involvement, but in ACA, the pattern tends to be periarticular and subchondral (Tan & Teh, 2007). Distribution of OM has a focal involvement, usually the weight-bearing surfaces of the toes, metatarsal heads, or calcaneus (Ledermann, Morrison, & Schweitzer, 2002), while ACA usually has several joints/bones involved. Differentiating based on site involvement is helpful; however, it cannot be relied on solely. Deformity is usually present with ACA along with bone debris, but OM does not typically involve deformity unless there is an underlining Charcot process. The clinical presence of soft-tissue disease, ulcerations, soft-tissue abscess, or sinus tract in the foot can improve the overall diagnostic accuracy for OM (Morrison, Schweitzer, Batte, Radack, & Russel, 1998); however, MRI changes without these clinical findings may sway the diagnosis away from OM. The limitations to an MRI exam include the presence of internal fixation devices, associated cost, and lack of available MRI equipment. Bone scintigraphy is highly sensitive, but lacks specificity in the diagnosis of Charcot arthropathy (Schauwecker, Park, Burt, Mock, & Wellman, 1988). It is mainly used to rule out OM in diabetic patients with open wounds that may or may not have bone destruction on radiographs. The determination to use bone scans should be based on “clinical suspicion.” However, when bone destruction is evident on radiographs without an open wound, then there is less need to undergo a three-phase 99technetium scan. However, when MRI is not available for neuropathic diabetic patients with open wounds and if an MRI is not available, the use of a bone scan to rule out OM may be warranted. Some authors recommend using leukocyte-labeled bone scans (111indium or 99mtechnetium hexamethylpropyleneamine oxime) to help exclude OM (Rogers & Bevilacqua, 2008a). Histological specimens can be obtained through wound or surgical intervention, but this is primarily used for research methods only. In diagnosing Charcot arthropathy, Horwitz (1948) found multiple shards of bone and soft tissue embedded in the deep layers of the synovium. One review described findings of abnormal values of bone-specific alkaline phosphatase, type 1 collagen carboxyterminal telopeptide, and urinary desoxypiridinoline cross-links, indicating increased osteoclastic/osteoblastic activities throughout Eichenholtz Stages 1 and 2 (Chantelau & Onvlee, 2006). Baumhauer et al. (2006) found that Charcotarthropathy-reactive bone had osteoclasts disproportionately increased compared to osteoblasts, and the osteoclasts demonstrated immunoreactivity for IL-1, IL-6, and TNFα. Although these laboratory findings may assist a clinician's assessment, it is impractical to obtain histological samples from patients presenting with the initial symptoms. It is recommended that biopsies be collected only when there is a

9

nonhealing wound or suspected bone infection (Sanders & Frykberg, 2007).

7. Nonoperative therapies and medical management The treatment of Charcot arthropathy depends on many factors, including the course or stage of Charcot arthropathy (Eichenholtz, 1966), location(s) of involvement (Sanders & Frykberg, 2007; Sinacore, 1998), presence of ulcers (Saltzman et al., 2005), and ability to achieve a stable and plantigrade foot (Harrelson, 1993). Other factors that could affect treatment options are comorbidities (American Diabetes Association, 2008) such as cardiovascular disease, morbid obesity, nephropathy, or infected ulcer (Armstrong et al., 1997; Saltzman et al., 2005). The goals for every patient undergoing treatment for an acute or quiescent Charcot process should be to maintain or achieve structural stability of the foot and ankle, to prevent ulceration, and to preserve a plantigrade foot. The initial treatment for Stage 0 or Stage 1 Charcot arthropathy is typically offloading in a total contact cast (TCC) (Sanders & Frykberg, 2007). Persistent warmth and increased temperature at the site involved indicate that the Charcot process has yet to progress to Stage 2. One specialty center's experience found that 60% of patients with midfoot Charcot arthropathy had minimal deformity and were treated successfully without surgery (Pinzur, 2004). This finding emphasized that if ACA is treated judiciously, achievement of a stable midfoot without incurring surgery or skin breakdown is possible. It may also be prudent to monitor temperature changes at the site of involvement to detect any areas that may be experiencing repetitive stress (Lavery et al., 2004) perpetuating the Charcot process. Although alternatives devices for immobilization and offloading have been studied, the TCC is considered by many clinicians as the treatment of choice (Armstrong et al., 1997; Frykberg et al., 2006; Myerson, Papa, Eaton, & Wilson, 1992; Pinzur, 2007; Pinzur et al., 1993). Some clinicians have recommended an 8- to 12-week non-weightbearing immobilization in a TCC, while others have allowed weight bearing as tolerated from the start of treatment (Sanders & Frykberg, 2007). Although ambulation after an initial period of non-weight-bearing is often recommended, weight bearing during the acute stage may not adversely affect their Charcot limb. A preliminary study of 10 patients examined whether allowing patients with ACA localized to the midfoot to bear weight was detrimental to their outcome (Pinzur, Lio, & Posner, 2006). The patient population was considered “overweight,” and their large stature did not permit these patients from maintaining a non-weight-bearing status. All 10 patients were permitted to bear weight as tolerated in a TCC, utilizing assistive devices as needed. The authors concluded that the use of “conscientious total contact therapy” and biweekly cast changes allowed all patients to successfully progress into custom shoes. Whether or not

ARTICLE IN PRESS 10

D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

bearing weight, cast changes every week to every 2 weeks is needed to accommodate for decreased edema. Factoring in the increased load stress on the contralateral limb, Clohisy and Thompson (1988) suggested that the nonweight-bearing TCC may actually have unfavorable consequences on the weight-bearing non-Charcot limb. Others have also noted that the increased pressure attributed to a three-point gait may induce unnatural stress patterns, resulting in ulcerations (Lesko & Maurer, 1989). Using a patellar tendon-bearing cast or orthosis can help negate the increased load on the contralateral limb (Saltzman, Johnson, Goldstein, & Donnelly, 1992). Sinacore (1998) found that the different anatomical locations affected by Charcot arthropathy would also affect healing times in TCC. Although patient compliance and delay from diagnosis to treatment were essential factors leading to shorter healing times, Sinacore found that Charcot arthropathy of the hindfoot (mean, 97±16 days), midfoot (mean, 96±11 days), and ankle (mean 83±22 days) took significantly longer to heal in TCC than Charcot arthropathy of the forefoot (mean, 55±17 days). The total time of nonweight-bearing TCC and the immobilization period in a weight-bearing TCC or Charcot restraint orthotic walker (CROW) device may last up to 4–6 months (Frykberg et al., 2006). Once there is bony consolidation, custom inserts or extra-deep shoes can be worn, followed by proper physician visits to ensure no uneven distribution of plantar pressures. Although the TCC is an effective treatment for the ACA process, there have been complications associated with this treatment, usually related to weight-bearing allowance (Guyton, 2005; Wukich & Motko, 2004). In a study of 70 neuropathic patients with 389 TCC changes, Guyton found a complication rate of 6% per cast, and the greatest contributing factor for complications was the diagnosis of Charcot arthropathy. The study concluded that TCC was a safe and reliable technique for offloading and immobilizing the neuropathic foot because of the predictable low rates of minor and reversible complications. Wukich and Motko concluded that minor complications such as irritation and cast tightness should be anticipated, but the avoidance of major complications relied mostly on well-trained casting technique, appropriate follow-up, and proper patient education. After TCC, some patients may benefit from CROW device (Frykberg et al., 2006). The CROW device offers the capacity to offload the forefoot and may replace the initial TCC because of its similar offloading capability (Hartsell, Fellner, & Saltzman, 2001). However, the design of the removable walker device also relies heavily on patient compliance. Armstrong, Short, Nixon, and Boulton (2002) described the “instant TCC” technique that transformed a removable cast walker to one that is less easily removed. Although it addresses the disadvantages of removable walkers in Charcot arthropathy management, the additional plaster around the walker creates a heavier, bulkier, and less practical device. Patients and physicians must be aware of all

possible complications and patient compliance issues before proceeding with Charcot arthropathy management. Saltzman et al. (2005) found that “intensive, nonoperative” treatment for Charcot arthropathy patients varied based on whether the patient presented initially with or without ulceration. The standardized regimen for treatment included immobilization of the foot and ankle and administration of antibiotics, if there was a presenting infected ulcer. After resolution of the infection, patients were placed in a nonweight-bearing TCC. After erythema and warmth had resolved, the patients were braced in a weight-bearing footand-ankle orthosis. Their treatment regimen identified a 3% annual amputation risk due to infection and a 49% annual amputation risk for recurrent ulceration. This retrospective study suggested that not all patients at Stage 0 or Stage 1 Charcot arthropathy would benefit from initial TCC treatment, especially those with a history of prior ulcerations. Bisphosphonates are popular as antiresorptive drugs against osteoporosis, Paget's disease, and other diseases with increased bone turnover (Rogers, 2003), and there have been reports on the possibility of pharmacologic therapy for ACA (Anderson, Woelffer, Holtzman, & Jacobs, 2004; Selby, Young, & Boulton, 1994). One study infused pamidronate intravenously in ACA patients while comparing its effects to saline (Jude et al., 2001). The authors performed a randomized double-blinded placebo-controlled study in 39 patients and found significant reductions in bone turnover markers, temperature, and pain symptoms. However, significant findings in time to ambulation and time to radiographic consolidation were not reported. Pitocco et al. (2005) evaluated the oral efficacy of bisphosphonate compounds for the treatment of ACA patients during a 6-month randomized controlled trial. Their results showed a significant reduction in serum collagen COOH-terminal telopeptide of type 1 collagen and hydroxyprolin (known bone resorption markers) and noted clinical improvements in the Charcot foot at 6 months. Although some consider these studies as strong evidence supporting the use of bisphosphonates in the treatment of early-stage Charcot arthropathy (Pinzur, 2007; Tan, Greenstein, Jarrett, & McGonagle, 2005), these drugs have not been approved by the US Food and Drug Administration for use in Charcot arthropathy patients. The US Food and Drug Administration (2008) has issued an alert regarding bisphosphonate use and the “possibility of severe and sometimes incapacitating bone, joint, and/or muscle (musculoskeletal) pain in patients.” Black et al. (2007) studied the use of bisphosphonates for postmenopausal osteoporosis and reported that “serious atrial fibrillation occurred more frequently in the zoledronic acid [bisphosphonate] group” than in the placebo-controlled group. To be clear, atrial fibrillation has not been reported with the use of pamidronate or other bisphosphonates approved by the US Food and Drug Administration, but only with zoledronic acid. However, with these data, the use of bisphosphonates in ACA patients must be carefully evaluated and all consequences must be examined fully.

ARTICLE IN PRESS D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

A randomized controlled study compared bone turnover and temperature between a study group that received salmon calcitonin nasal spray daily with calcium supplementation and a control group that received only calcium supplementation (Bem, Jirkovska, Fejfarova, Skibova, & Jude, 2006). Although both groups received offloading treatments by a removable contact cast or a cast walker, the study group showed significant reduction in bone turnover compared with the control group during the 3-month follow-up. The advantage of calcitonin may be its direct impact on the RANK-L/OPG system, with fewer complications compared to bisphosphonate use (Bem et al., 2006). Other adjunct therapies have also been offered to help manage ACA. Electric bone growth (EBG) stimulators (Grady et al., 2000; Petrisor & Lau, 2005) have been experimentally applied and clinically tested to promote healing of fractures in the acute phase. In theory, the EBG stimulator generates an increased number of hydroxyl ions, increasing the pH and thus decreasing tissue oxygen pressure (Lavine & Grodzinsky, 1987). This scenario correlates with what has been found in animal studies of bone repair (Brighton & Heppenstall, 1971). In a small case series of 10 patients, Grady et al. found that when their EBG stimulator was used during the initial period of immobilization, there was a clinical decrease in ACA symptoms. The authors also reported radiographic consolidation in all patients in an average of 3.5 months. However, this limited case series did not examine the efficacy of a EBG stimulator compared to immobilization with a TCC during ACA (Pinzur, 2007). Although little evidence has been provided to support the use of EBG stimulators in ACA treatment, its use has been supported as an adjunct therapy during the postsurgical reconstruction period in Charcot arthropathy patients (Hockenbury, Gruttadauria, & McKinney, 2007; Petrisor & Lau, 2005; Saxena, DiDomenico, Widtfeldt, Adams, & Kim, 2005). A series of case reports has described the use of adjunct low-intensity ultrasound for Charcot arthropathy treatment (Strauss & Gonya, 1998). The authors reported a patient who underwent five surgical procedures at the tibiotalar joint and calcaneus without success of healing. Provisional surgery using a retrograde nail across the subtalar and tibiotalar joints was elected, and low-intensity ultrasound was begun postoperatively after initial soft-tissue healing. The outcome revealed complete arthrodesis 5 1/2 months after the application of the ultrasound device. Although these findings were promising, there have been no subsequent studies to validate this method.

8. Integrated strategy for operative treatment and management As the discipline of evidence-based medicine continues to improve patient care and clinical practice, operative treatment for Charcot arthropathy must also integrate

11

individual clinical expertise with the best available external evidence (Sackett, Rosenberg, Gray, Haynes, & Richardson, 1996). Individual clinical expertise relies on the proficiency and judgment acquired through clinical experience and practice with Charcot arthropathy patients. The best available external evidence relies on relevant basic science research and patient-centered clinical research into the accuracy, precision, and safety of therapeutic treatments. However, there is a lack of high-level evidence supporting the basis of surgical therapies in the treatment of Charcot arthropathy patients. Levels of evidence for medical therapeutic studies—from Level 5 (expert opinion) to Level 1A (systematic review of homogenous randomized controlled trials)—were established to better interpret the quality of studies, with grades of recommendations (from A to D) based on the consistency and quality of these studies (Phillips et al., 2001; Wright, Einhorn, & Heckman, 2005). The difficulty of structuring a blinded prospective randomized study in a surgical specialty limits the availability of “high-level” evidence, and the relatively low prevalence of Charcot arthropathy restricts the number of patients per study. Currently, surgeons are carefully constructing an integrated strategy for operative treatment in Charcot arthropathy based on the best available evidence and individual clinical experience. From a literature search on MEDLINE (using the key terms Charcot, arthropathy, neuroarthropathy, osteoarthropathy, surgery, and diabetes) from 1960 to July 2008, approximately 430 articles were cited. Of these articles, 80 reported on operative treatments and/or discussed operative management. Over half of the articles (43 of 80) were noncontrolled retrospective case series (Level 4), one article was a non-controlled prospective study (Level 4), and the rest were expert opinions or case reports (Level 5). There were no controlled or randomized prospective (Levels 1 and 2) or controlled retrospective (Level 3) studies reported on this topic. The current knowledge base for operative management of Charcot arthropathy is based on approximately 1000 patients who have been reported in the literature between 1960 and July 2008. However, this number may be less on closer inspection because some authors may have reported data on the same patients in separate articles. The surgical procedures that were mentioned in conjunction with Charcot arthropathy operative management include amputations; arthrodesis; debridement of ulcers, drainage, or infections; and exostectomies. The optimal surgical management has not reached a consensus due to the lack of robust data supporting any particular approach. However, this has not deterred surgeons from addressing concerns of deformity, ulceration, and joint stability due to the effects of Charcot arthropathy on the foot and ankle. Most clinicians agree that the indications for surgical intervention in Charcot arthropathy include, but are not limited to, recurring ulcer(s), joint instability, pain associated with malalignment, offending exotosis, and potential skin complications from inability to brace or from

ARTICLE IN PRESS 12

D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

a nonplantigrade foot (Burns & Wukich, 2008). At specialty referral centers, Charcot arthropathy patients who undergo minor and/or major surgical procedures have ranged from 14% (Fabrin et al., 2000) to 51% (Pinzur, 1999). Amputation rates of the lower extremity have ranged from 3% to 9%, depending primarily on avoidance of ulceration (Saltzman et al., 2005). One center hypothesized that amputation risk increased with a more proximal location of deformity and complexity of infection (Rogers & Bevilacqua, 2008b). The authors believed that the more proximal is the Charcot deformity and with increasing degree of infection, the more likely is the chance of amputation. However, they did not correlate this hypothesis with patient data. Saltzman et al. found that the majority of amputations were performed in patient(s) who had developed Charcot arthropathy distal to the midfoot (nine cases), compared to more proximal amputations (six cases). This cohort study of 127 limbs reported that the location of Charcot arthropathy did not play a significant role in whether ulceration would occur or whether the likelihood of amputation was necessary. Instead, they found that those with chronic recurrent ulcerations were significantly more likely to require amputations (36%) than those without chronic recurrent ulcerations (6%). Specialty referral centers have the most clinical and surgical experience with Charcot arthropathy patients. These centers may be more “aggressive” in their surgical treatment of Charcot arthropathy. Using benchmark analysis to measure morbidity and resource consumption, Pinzur (1999) justified the use of aggressive therapies to reduce the costs and complications associated with this high-risk patient population. This may include a more intensive offloading regimen or even “early” surgical intervention in order to reduce the morbidity associated with this disease (Saltzman et al., 2005; Simon, Tejwani, Wilson, Santner, & Denniston, 2000). The decision to proceed with surgery should never be taken lightly even if the patient has one or more indications for surgical intervention. Surgical reconstruction of the deformed foot and ankle has historically been recommended after all nonoperative measures to prevent further breakdown had been exhausted (Pinzur et al., 1993). This is due to the perceived greater risk of potential malunion and complications of surgery in patients with Charcot arthropathy. During the acute inflammation and destruction stage, optimal fixation can be difficult to achieve, thus discouraging surgeons from operating during Eichenholtz Stage 1. Simon et al. (2000) reported their results of surgical management of acute midfoot Charcot arthropathy (Eichenholtz Stage 1 or early Stage 2). All 14 patients were treated with adequate anatomical reduction and primary arthrodesis, and all achieved a successful clinical outcome. There are other case series involving arthrodesis for limb salvage that have resulted in relatively successful results; however, these studies involved relatively few patients and arthrodesis of different anatomical sites of the foot and ankle (Bono, Roger, & Jacobs, 1993; Papa, Myerson, & Girard, 1993; Tisdel,

Marcus, & Heiple, 1995). Successful surgical intervention for ACA has not been established in the hindfoot or ankle, and this may be due to the peripheral BMD deficiency associated with certain Charcot arthropathy patients (Herbst et al., 2004). Overall, the timing of surgical intervention remains controversial due to the lack of high-level evidencebased literature on reconstructive surgery in Charcot arthropathy (Burns & Wukich, 2008). Treatment decisions and expected outcomes are usually based on the anatomical pattern of Charcot arthropathy, stage of the disease, and associated comorbidities. After a mutual decision to proceed with surgical treatment has been made, preoperative assessment of adequate vascularity, nutritional status, and BMD is prudent to achieve the optimal environment for wound healing and successful surgery (Burns & Wukich, 2008). The type of surgical approach depends on many factors, including the amount and location of deformity, ulceration with and without infection, stability, and skill of the surgical team. Although the senior author has vast surgical and nonsurgical experience with Charcot arthropathy patients, the complexity and diverse presentations of the foot and ankle that this center encounters may not mirror those of other specialty referral centers. Fig. 1 summarizes an integrated treatment strategy based on the available literature, coupled with our experience at the comprehensive footand-ankle center. Certain Charcot arthropathy patients requiring surgery may have bony prominences without other major deformities that require only simple exostectomy (Brodsky, 2007). The exostectomy technique has been used successfully in many studies of surgical treatment in Charcot midfoot deformity and ulceration (Brodsky & Rouse, 1993; Catanzariti, Mendicino, & Haverstock, 2000; Laurinaviciene, Kirketerp-Moeller, & Holstein, 2008; Myerson et al., 1994; Pinzur et al., 1993; Rosenblum, Giurini, Miller, Chrzan, & Habershaw, 1997). One recent case series of 20 patients reported that exostectomy procedures were effective and safe for treating Charcot midfoot deformities and ulcerations (Laurinaviciene et al., 2008). Their results were comparable to those of previous studies in terms of exostectomy success. Although there are no controlled studies utilizing this technique, there is a fair amount of evidence to support the use of exostectomy for Charcot midfoot deformity and/or ulceration treatment. If exostectomies fail to prevent recurring ulcerations and if the deformity is unstable, realignment arthrodesis may be used to stabilize the foot and ankle (Zgonis, Roukis, & Lamm, 2007). The forefoot and midfoot prominences may develop from hindfoot influences such as subtalar or ankle joint valgus instability. The literature regarding arthrodesis in Charcot arthropathy provides fair evidence to support its use. As the potential for major complications is higher for Charcot deformity in the hindfoot and ankle because of greater instability (Brink, Eickmeier, Levitsky, & Solomon, 1994; Papa et al., 1993), there is a trend toward the use of

ARTICLE IN PRESS D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

13

Fig. 1. Charcot arthropathy treatment algorithm.

supplemental fixation to increase stability at the surgical site. However, there is insufficient medical evidence to support one form of fixation (i.e., internal vs. external) over another. Because the role of ankle equinus may determine the severity of Charcot deformity, most surgical reconstructions are performed with concomitant lengthening of the Achilles tendon or gastrocnemius muscle (Burns & Wukich, 2008). Achilles tendon contracture has been examined as a factor leading to midfoot collapse in Charcot arthropathy due to lack of adequate dorsiflexion of the foot (Armstrong & Lavery, 1998; Mueller et al., 2004). In order to decrease pressure on the midfoot and forefoot, lengthening procedures of the Achilles tendon have been performed to decrease its power and to provide more available dorsiflexion (Maluf, Mueller, Strube, Engsberg, & Johnson, 2004). However, this decrease in power and forefoot peak pressure has not been shown to be permanent and may return to baseline several

months after the procedure (Mueller, Sinacore, Hastings, Strube, & Johnson, 2003). This is supported by studies on the beneficial biomechanical effect of Achilles tendon lengthening that have been published in various medical journals; however, it appears that the same authors may be reporting the same results and the same patient data in these studies (Hastings et al., 2000; Maluf et al., 2004; Mueller et al., 2004; Salsich et al., 2005). Catanzariti et al. (2000) used adjunctive Achilles tendon lengthening with ostectomies in 9 of 10 Charcot arthropathy patients with lateral midfoot ulcers, but only 38% healed primarily. They also found a 92% primary healing rate with medial midfoot ulcers. Mueller et al. (2003) randomized and controlled an outcome comparison study of diabetic patients with neuropathic ulcerations using TCC with and without Achilles tendon lengthening. Their study, which also included patients with Charcot arthropathy midfoot

ARTICLE IN PRESS 14

D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

deformity, found that those with Achilles tendon lengthening and TCC were 75% less likely to have ulcer recurrence at 7 months and 52% less likely to have ulcer recurrence at 2 years compared to the TCC-only group. Their recommendations were to consider using Achilles tendon lengthening as an adjunctive procedure for limited dorsiflexion of less than 5° and plantar ulcerations at the forefoot of diabetic neuropathy patients. This adjunctive procedure, however, must be done with caution and not indiscriminately, as Achilles tendon lengthening has been shown to increase the risk for heel ulcerations (Holstein, Lohmann, Bitsch, & Jorgensen, 2004). Mueller et al. also found in their study that peak pressure on the heel increased by 34% and skin breakdown was noted in 4 of 31 patients in the Achilles tendon lengthening group. Even in light of possible complications, there appears to be good evidence to support the use of adjunctive Achilles tendon lengthening for certain Charcot arthropathy patients with neuropathic ulcers. Postoperatively, patients should be immobilized until edema and erythema have resolved. Immobilization may be necessary for 5–6 months, at which time patients can be placed into braces or therapeutic shoes with custom inserts (Trepman et al., 2005). Extended duration of bracing may be necessary especially in hindfoot and ankle reconstruction. It is evident from long-term follow-up of reconstructive Charcot surgical techniques that complications such as nonunions, malunions, or amputations can occur despite excellent surgical technique (Fabrin et al., 2000; Pinzur, 1999; Saltzman et al., 2005). Other postoperative complications may include development of Charcot arthropathy in adjacent joints, pseudoarthrosis, postoperative infection, recurrence of ACA, and transfer lesions. 9. Conclusion In the era of evidence-based medicine, Charcot arthropathy of the foot and ankle remains a poorly understood disease, although recent clinical and basic science research has improved our level of knowledge regarding its etiology and treatment. However, there are few high-level evidence studies to support management and treatment options at this point in time. The current goals for clinicians treating Charcot arthropathy include the following: 1. Maintaining a high index of suspicion in diabetic patients with peripheral neuropathy who experience pain or edema with or without a history of trauma. 2. Recognizing ACA and promptly offloading the affected limb in patients in whom the diagnosis is suspected but not proven. 3. Maintaining a stable plantigrade foot that remains free of ulcerations and infection. 4. Educating patients, primary care physicians, and emergency medical doctors about this disease process and the urgency of early diagnosis.

5. Reducing the incidence of amputations and mortality associated with this disease process. 6. Obtaining scientific evidence to identify those patients who are most at risk, to facilitate prompt and early diagnosis, and to initiate routine care. The current evidence for surgical intervention for Charcot arthropathy includes the following: •

There is fair evidence for surgical excision of bones (exostectomy) to reduce pressure from bony prominences. There are Level 4 studies with a consistency of successful results (Grade C recommendation). • There is fair evidence for the arthrodesis of unstable Charcot deformity of the foot and/or ankle as indicated in patients who fail nonoperative treatment. There are Level 4 studies with a consistency of successful results (Grade C recommendation). • There is not enough evidence available to determine any advantage of internal fixation over external fixation, and vice versa, in the surgical reconstruction of Charcot deformities (insufficient data available to grade recommendation). • There is good evidence to support the use of tendoAchilles or gastrocnemius muscle lengthening to decrease forefoot pressure and to improve ankle equinus. There is one Level I study and several Level III and IV studies with a consistency of successful results (Grade B recommendation). References American Diabetes Association. (2004). Preventive foot care in diabetes. Diabetes Care, 27(Suppl 1), S63−S64. American Diabetes Association. (2008). Standards of medical care in diabetes—2008. Diabetes Care, 31(Suppl 1), S12−S54. Anderson, J. J., Woelffer, K. E., Holtzman, J. J., & Jacobs, A. M. (2004). Bisphosphonates for the treatment of Charcot neuroarthropathy. Journal of Foot and Ankle Surgery, 43, 285−289. Anonymous (1886). Sitzung vom 17. November 1886. (in German). Berliner Klinische Wochenschrift, 23, 5. Armstrong, D. G., & Lavery, L. A. (1998). Elevated peak plantar pressures in patients who have Charcot arthropathy. Journal of Bone and Joint Surgery, American Volume, 80, 365−369. Armstrong, D. G., & Peters, E. J. (2002). Charcot's arthropathy of the foot. Journal of the American Podiatric Medical Association, 92, 390−394. Armstrong, D. G., Short, B., Nixon, B. P., & Boulton, A. J. M. (2002). Technique for fabrication of an “instant” total contact cast for treatment of neuropathic diabetic foot ulcers. Journal of the American Podiatric Medical Association, 92, 405−408. Armstrong, D. G., Todd, W. F., Lavery, L. A., Harkless, L. B., & Bushman, T. R. (1997). The natural history of acute Charcot's arthropathy in a diabetic foot specialty clinic. Journal of the American Podiatric Medical Association, 87, 272−278. Banks, A. S., & McGlamry, E. D. (1989). Charcot foot. Journal of the American Podiatric Medical Association, 79, 213−235. Baumhauer, J. F., O'Keefe, R. J., Schon, L. C., & Pinzur, M. S. (2006). Cytokine-induced osteoclastic bone resorption in Charcot arthropathy: An immunohistochemical study. Foot & Ankle International, 27, 797−800.

ARTICLE IN PRESS D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx Bayne, O., & Lu, E. J. (1998). Diabetic Charcot's arthropathy of the wrist. Case report and literature review. Clinical Orthopaedics and Related Research, 122−126. Bem, R., Jirkovska, A., Fejfarova, V., Skibova, J., & Jude, E. B. (2006). Intranasal calcitonin in the treatment of acute Charcot neuroosteoarthropathy: A randomized controlled trial. Diabetes Care, 29, 1392−1394. Bibbo, C., Lin, S. S., Beam, H. A., & Behrens, F. F. (2001). Complications of ankle fractures in diabetic patients. Orthopedic Clinics of North America, 32, 113−133. Black, D. M., Delmas, P. D., Eastell, R., Reid, I. R., Boonen, S., Cauley, J. A., Cosman, F., Lakatos, P., Leung, P. C., Man, Z., Mautalen, C., Mesenbrink, P., Hu, H., Caminis, J., Tong, K., Rosario-Jansen, T., Krasnow, J., Hue, T. F., Sellmeyer, D., Eriksen, E. F., & Cummings, S. R. (2007). Once-yearly zoledronic acid for treatment of postmenopausal osteoporosis. New England Journal of Medicine, 356, 1809−1822. Bloomgarden, Z. T. (2005). Clinical diabetic neuropathy. Diabetes Care, 28, 2968−2974. Bono, J. V., Roger, D. J., & Jacobs, R. L. (1993). Surgical arthrodesis of the neuropathic foot. A salvage procedure. Clinical Orthopaedics and Related Research, 14−20. Boulton, A. J., Scarpello, J. H., & Ward, J. D. (1982). Venous oxygenation in the diabetic neuropathic foot: Evidence of arteriovenous shunting? Diabetologia, 22, 6−8. Brighton, C. T., & Heppenstall, R. B. (1971). Oxygen tension in zones of the epiphyseal plate, the metaphysis and diaphysis. An in vitro and in vivo study in rats and rabbits. Journal of Bone and Joint Surgery, American Volume, 53, 719−728. Brink, D. S., Eickmeier, K. M., Levitsky, D. R., & Solomon, M. G. (1994). Subtalar and talonavicular joint dislocation as a presentation of diabetic neuropathic arthropathy with salvage by triple arthrodesis. Journal of Foot and Ankle Surgery, 33, 583−589. Brodsky, J. W. (2007). The diabetic foot. In M. J. Coughlin, R. A. Mann, & C. L. Saltzman (Eds.), Surgery of the foot and ankle (pp. 1281−1368). Philadelphia: Mosby Elsevier. Brodsky, J. W., & Rouse, A. M. (1993). Exostectomy for symptomatic bony prominences in diabetic Charcot feet. Clinical Orthopaedics and Related Research, 21−26. Brower, A. C., & Allman, R. M. (1981). Pathogenesis of the neurotrophic joint: Neurotraumatic vs. neurovascular. Radiology, 139, 349−354. Burns, P. R., & Wukich, D. K. (2008). Surgical reconstruction of the Charcot rearfoot and ankle. Clinics in Podiatric Medicine and Surgery, 25, 95−120. Catanzariti, A. R., Mendicino, R., & Haverstock, B. (2000). Ostectomy for diabetic neuroarthropathy involving the midfoot. Journal of Foot and Ankle Surgery, 39, 291−300. Chantelau, E. (2005). The perils of procrastination: Effects of early vs. delayed detection and treatment of incipient Charcot fracture. Diabetic Medicine, 22, 1707−1712. Chantelau, E., & Onvlee, G. J. (2006). Charcot foot in diabetes: Farewell to the neurotrophic theory. Hormone and Metabolic Research, 38, 361−367. Chantelau, E., & Poll, L. W. (2006). Evaluation of the diabetic Charcot foot by MR imaging or plain radiography—An observational study. Experimental and Clinical Endocrinology & Diabetes, 114, 428−431. Chantelau, E., Richter, A., Ghassem-Zadeh, N., & Poll, L. W. (2007). “Silent” bone stress injuries in the feet of diabetic patients with polyneuropathy: A report on 12 cases. Archives of Orthopaedic and Trauma Surgery, 127, 171−177. Chantelau, E., Richter, A., Schmidt-Grigoriadis, P., & Scherbaum, W. A. (2006). The diabetic Charcot foot: MRI discloses bone stress injury as trigger mechanism of neuroarthropathy. Experimental and Clinical Endocrinol & Diabetes, 114, 118−123. Charcot, J. M. (1868). Sur quelques arthropathies qui paraissent dépendre d'une lésion du cerveau ou de la moelle épinière. Archive de Physiologie Normale Pathologique, 1, 161−178.

15

Charcot, J. M., & Féré, C. (1883). Affections osseuses et articulaires du pied chez les tabétiques (Pied tabétique). Archives de Neurologie, 6, 305−319. Clasen, S. (2000). Is diabetic Charcot foot related to lower limb osteopaenia? Foot and Ankle Surgery, 6, 255−259. Classen, J. N., Rolley, R. T., Carneiro, R., & Martire, J. R. (1976). Management of foot conditions of the diabetic patient. American Surgeon, 42, 81−88. Clohisy, D. R., & Thompson, R. C., Jr. (1988). Fractures associated with neuropathic arthropathy in adults who have juvenile-onset diabetes. Journal of Bone and Joint Surgery, American Volume, 70, 1192−1200. Cundy, T. F., Edmonds, M. E., & Watkins, P. J. (1985). Osteopenia and metatarsal fractures in diabetic neuropathy. Diabetic Medicine, 2, 461−464. Edison, J., & Finger, D. R. (2005). Neuropathic osteoarthropathy of the shoulder. Journal of Clinical Rheumatology, 11, 333−334. Edmonds, M. E., Clarke, M. B., Newton, S., Barrett, J., & Watkins, P. J. (1985). Increased uptake of bone radiopharmaceutical in diabetic neuropathy. Quarterly Journal of Medicine, 57, 843−855. Edmonds, M. E., Morrison, N., Laws, J. W., & Watkins, P. J. (1982). Medial arterial calcification and diabetic neuropathy. British Medical Journal (Clinical Research Edition), 284, 928−930. Eichenholtz, S. N. (Ed.). (1966). Charcot joints (pp. 3−8). Springfield, IL: Charles C. Thomas. Eloesser, L. (1917). On the nature of neuropathic affections of the joints. Annals of Surgery, 66, 201−207. Fabrin, J., Larsen, K., & Holstein, P. E. (2000). Long-term follow-up in diabetic Charcot feet with spontaneous onset. Diabetes Care, 23, 796−800. Frykberg, R. G., & Belczyk, R. (2008). Epidemiology of the Charcot foot. Clinics in Podiatric Medicine and Surgery, 25, 17−28. Frykberg, R. G., Zgonis, T., Armstrong, D. G., Driver, V. R., Giurini, J. M., Kravitz, S. R., Landsman, A. S., Lavery, L. A., Moore, J. C., Schuberth, J. M., Wukich, D. K., Andersen, C., & Vanore, J. (2006). Diabetic foot disorders: A clinical practice guideline (2006 revision). Journal of Foot and Ankle Surgery, 45, S1−S66. Fujikawa, Y., Quinn, J. M., Sabokbar, A., McGee, J. O., & Athanasou, N. A. (1996). The human osteoclast precursor circulates in the monocyte fraction. Endocrinology, 137, 4058−4060. Gazis, A., Pound, N., Macfarlane, R., Treece, K., Game, F., & Jeffcoate, W. (2004). Mortality in patients with diabetic neuropathic osteoarthropathy (Charcot foot). Diabetic Medicine, 21, 1243−1246. Goebel, F. D., & Fuessl, H. S. (1983). Monckeberg's sclerosis after sympathetic denervation in diabetic and non-diabetic subjects. Diabetologia, 24, 347−350. Grady, J. F., O'Connor, K. J., Axe, T. M., Zager, E. J., Dennis, L. M., & Brenner, L. A. (2000). Use of electrostimulation in the treatment of diabetic neuroarthropathy. Journal of the American Podiatric Medical Association, 90, 287−294. Gupta, R. (1993). A short history of neuropathic arthropathy. Clinical Orthopaedics and Related Research, 43−49. Guyton, G. P. (2005). An analysis of iatrogenic complications from the total contact cast. Foot & Ankle International, 26, 903−907. Harrelson, J. M. (1993). The diabetic foot: Charcot arthropathy. Instructional Course Lectures, 42, 141−146. Hartsell, H. D., Fellner, C., & Saltzman, C. L. (2001). Pneumatic bracing and total contact casting have equivocal effects on plantar pressure relief. Foot & Ankle International, 22, 502−506. Hastings, M. K., Mueller, M. J., Sinacore, D. R., Salsich, G. B., Engsberg, J. R., & Johnson, J. E. (2000). Effects of a tendo-Achilles lengthening procedure on muscle function and gait characteristics in a patient with diabetes mellitus. Journal of Orthopaedic and Sports Physical Therapy, 30, 85−90. Herbst, S. A., Jones, K. B., & Saltzman, C. L. (2004). Pattern of diabetic neuropathic arthropathy associated with the peripheral bone mineral density. Journal of Bone and Joint Surgery, British Volume, 86, 378−383.

ARTICLE IN PRESS 16

D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

Hockenbury, R. T., Gruttadauria, M., & McKinney, I. (2007). Use of implantable bone growth stimulation in Charcot ankle arthrodesis. Foot & Ankle International, 28, 971−976. Holstein, P., Lohmann, M., Bitsch, M., & Jorgensen, B. (2004). Achilles tendon lengthening, the panacea for plantar forefoot ulceration? Diabetes Metabolism Research and Reviews, 20(Suppl 1), S37−S40. Horwitz, T. (1948). Bone and cartilage debris in the synovial membrane; its significance in the early diagnosis of neuro-arthropathy. Journal of Bone and Joint Surgery, American Volume, 30A, 579−588. Jeffcoate, W. (2004). Vascular calcification and osteolysis in diabetic neuropathy—Is RANK-L the missing link? Diabetologia, 47, 1488−1492. Jeffcoate, W., Lima, J., & Nobrega, L. (2000). The Charcot foot. Diabetic Medicine, 17, 253−258. Jeffcoate, W. J. (2005a). Abnormalities of vasomotor regulation in the pathogenesis of the acute Charcot foot of diabetes mellitus. International Journal of Lower Extremity Wounds, 4, 133−137. Jeffcoate, W. J. (2005b). Theories concerning the pathogenesis of the acute Charcot foot suggest future therapy. Current Diabetes Reports, 5, 430−435. Jeffcoate, W. J., Game, F., & Cavanagh, P. R. (2005). The role of proinflammatory cytokines in the cause of neuropathic osteoarthropathy (acute Charcot foot) in diabetes. Lancet, 366, 2058−2061. Johnson, J. T. (1967). Neuropathic fractures and joint injuries. Pathogenesis and rationale of prevention and treatment. Journal of Bone and Joint Surgery, American Volume, 49, 1−30. Johnson, L. (1966). Comment to Williams et al. Arthritis and Rheum, 9, 358−359. Jordan, W. R. (1936). Neuritic manifestations in diabetes mellitus. Archives of Internal Medicine, 57, 307−366. Jude, E. B., Selby, P. L., Burgess, J., Lilleystone, P., Mawer, E. B., Page, S. R., Donohoe, M., Foster, A. V., Edmonds, M. E., & Boulton, A. J. (2001). Bisphosphonates in the treatment of Charcot neuroarthropathy: A double-blind randomised controlled trial. Diabetologia, 44, 2032−2037. Kelly, M. (1963). De arthritide symptomatica of William Musgrave (1657– 1721): His description of neuropathic arthritis. Bulletin of the History of Medicine, 37, 372−377. Kimmerle, R., & Chantelau, E. (2007). Weight-bearing intensity produces Charcot deformity in injured neuropathic feet in diabetes. Experimental and Clinical Endocrinol & Diabetes, 115, 360−364. Lambert, A. P., & Close, C. F. (2002). Charcot neuroarthropathy of the knee in Type 1 diabetes: Treatment with total knee arthroplasty. Diabetic Medicine, 19, 338−341. Laurinaviciene R., Kirketerp-Moeller K., Holstein P.E. (2008). Exostectomy for chronic midfoot plantar ulcer in Charcot deformity. Journal of Wound Care, 17, 53–55, 57–58. Lavery, L. A., Armstrong, D. G., Wunderlich, R. P., Tredwell, J., & Boulton, A. J. (2003). Diabetic foot syndrome: Evaluating the prevalence and incidence of foot pathology in Mexican Americans and non-Hispanic whites from a diabetes disease management cohort. Diabetes Care, 26, 1435−1438. Lavery, L. A., Higgins, K. R., Lanctot, D. R., Constantinides, G. P., Zamorano, R. G., Armstrong, D. G., Athanasiou, K. A., & Agrawal, C. M. (2004). Home monitoring of foot skin temperatures to prevent ulceration. Diabetes Care, 27, 2642−2647. Lavine, L. S., & Grodzinsky, A. J. (1987). Electrical stimulation of repair of bone. Journal of Bone and Joint Surgery, American Volume, 69, 626−630. Le, C. T., & Boen, J. R. (Eds.). (1995). Health and numbers: Basic biostatistics methods (pp. 5−14). New York: Wiley-Liss. Ledermann, H. P., Morrison, W. B., & Schweitzer, M. E. (2002). MR image analysis of pedal osteomyelitis: Distribution, patterns of spread, and frequency of associated ulceration and septic arthritis. Radiology, 223, 747−755. Lee, L., Blume, P. A., & Sumpio, B. (2003). Charcot joint disease in diabetes mellitus. Annals of Vascular Surgery, 17, 571−580. Leriche, R., & Fontaine, R. (1927). Experimental researches upon vasomotricity. Annals of Surgery, 85, 641−646. Lesko, P., & Maurer, R. C. (1989). Talonavicular dislocations and midfoot arthropathy in neuropathic diabetic feet. Natural course and

principles of treatment. Clinical Orthopaedics and Related Research, 226−231. Mabilleau, G., Petrova, N. L., Edmonds, M. E., & Sabokbar, A. (2008). Increased osteoclastic activity in acute Charcot's osteoarthropathy: The role of receptor activator of nuclear factor-kappaB ligand. Diabetologia, 51, 1035−1040. MacCormac, W., & Klockmann, J. W. (Eds.). (1881). Transactions of the international medical congress: Seventh session held in London, August 2–9, 1881 (p. 26). London: Balantyne, Hanson, & Co. Maluf, K. S., Mueller, M. J., Strube, M. J., Engsberg, J. R., & Johnson, J. E. (2004). Tendon Achilles lengthening for the treatment of neuropathic ulcers causes a temporary reduction in forefoot pressure associated with changes in plantar flexor power rather than ankle motion during gait. Journal of Biomechanics, 37, 897−906. Marcus, C. D., Ladam-Marcus, V. J., Leone, J., Malgrange, D., BonnetGausserand, F. M., & Menanteau, B. P. (1996). MR imaging of osteomyelitis and neuropathic osteoarthropathy in the feet of diabetics. Radiographics, 16, 1337−1348. Matricali, G. A., Bammens, B., Kuypers, D., Flour, M., & Mathieu, C. (2007). High rate of Charcot foot attacks early after simultaneous pancreas–kidney transplantation. Transplantation, 83, 245−246. McGill, M., Molyneaux, L., Bolton, T., Ioannou, K., Uren, R., & Yue, D. K. (2000). Response of Charcot's arthropathy to contact casting: Assessment by quantitative techniques. Diabetologia, 43, 481−484. Miller, D. S., & Lichtman, W. F. (1955). Diabetic neuropathic arthropathy of feet; summary report of seventeen cases. AMA Archives of Surgery, 70, 513−518. Mitchell, J. K. (1831). On a new practice in acute and chronic rheumatism. American Journal of the Medical Sciences, 8, 55−64. Mitchell, S. W., Morehouse, G. R., & Keen, W. W. (Eds.). (1864). Gunshot wounds and other injuries of nerves (pp. 119−133). Philadelphia: J. B. Lippincott & Co.. Morrison, W. B., Schweitzer, M. E., Batte, W. G., Radack, D. P., & Russel, K. M. (1998). Osteomyelitis of the foot: Relative importance of primary and secondary MR imaging signs. Radiology, 207, 625−632. Mueller, M. J., Sinacore, D. R., Hastings, M. K., Lott, D. J., Strube, M. J., & Johnson, J. E. (2004). Impact of Achilles tendon lengthening on functional limitations and perceived disability in people with a neuropathic plantar ulcer. Diabetes Care, 27, 1559−1564. Mueller, M. J., Sinacore, D. R., Hastings, M. K., Strube, M. J., & Johnson, J. E. (2003). Effect of Achilles tendon lengthening on neuropathic plantar ulcers. A randomized clinical trial. Journal of Bone and Joint Surgery, American Volume, 85-A, 1436−1445. Myerson, M., Papa, J., Eaton, K., & Wilson, K. (1992). The total contact cast for management of neuropathic plantar ulceration of the foot. Journal of Bone and Joint Surgery, 74A, 261−269. Myerson, M. S., Henderson, M. R., Saxby, T., & Short, K. W. (1994). Management of midfoot diabetic neuroarthropathy. Foot & Ankle International, 15, 233−241. O'Connor, B. L., Palmoski, M. J., & Brandt, K. D. (1985). Neurogenic acceleration of degenerative joint lesions. Journal of Bone and Joint Surgery, American Volume, 67, 562−572. Papa, J., Myerson, M., & Girard, P. (1993). Salvage, with arthrodesis, in intractable diabetic neuropathic arthropathy of the foot and ankle. Journal of Bone and Joint Surgery, American Volume, 75, 1056−1066. Petrisor B., & Lau J. T. (2005). Electrical bone stimulation: An overview and its use in high risk and Charcot foot and ankle reconstructions. Foot and Ankle Clinics, 10, 609–620, vii–viii. Petrova, N. L., Foster, A. V., & Edmonds, M. E. (2005). Calcaneal bone mineral density in patients with Charcot neuropathic osteoarthropathy: Differences between Type 1 and Type 2 diabetes. Diabetic Medicine, 22, 756−761. Petrova, N. L., Moniz, C., Elias, D. A., Buxton-Thomas, M., Bates, M., & Edmonds, M. E. (2007). Is there a systemic inflammatory response in the acute Charcot foot? Diabetes Care, 30, 997−998. Phillips, B., Ball, C., Sackett, D., Badenoch, D., Straus, S., Haynes, B., & Dawes, M. (2001). Levels of evidence. Oxford Centre for

ARTICLE IN PRESS D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx Evidence-Based Medicine. Oxford: www.cebm.net/levels_of_evidence. asp (Accessed August 6, 2008). Pinzur, M. S. (1999). Benchmark analysis of diabetic patients with neuropathic (Charcot) foot deformity. Foot & Ankle International, 20, 564−567. Pinzur, M. (2004). Surgical versus accommodative treatment for Charcot arthropathy of the midfoot. Foot & Ankle International, 25, 545−549. Pinzur, M. S. (2007). Current concepts review: Charcot arthropathy of the foot and ankle. Foot & Ankle International, 28, 952−959. Pinzur, M. S., Lio, T., & Posner, M. (2006). Treatment of Eichenholtz Stage I Charcot foot arthropathy with a weight-bearing total contact cast. Foot & Ankle International, 27, 324−329. Pinzur, M. S., Sage, R., Stuck, R., Kaminsky, S., & Zmuda, A. (1993). A treatment algorithm for neuropathic (Charcot) midfoot deformity. Foot & Ankle, 14, 189−197. Pitocco, D., Ruotolo, V., Caputo, S., Mancini, L., Collina, C. M., Manto, A., Caradonna, P., & Ghirlanda, G. (2005). Six-month treatment with alendronate in acute Charcot neuroarthropathy: A randomized controlled trial. Diabetes Care, 28, 1214−1215. Rajbhandari, S. M., Jenkins, R. C., Davies, C., & Tesfaye, S. (2002). Charcot neuroarthropathy in diabetes mellitus. Diabetologia, 45, 1085−1096. Rix, M., Andreassen, H., & Eskildsen, P. (1999). Impact of peripheral neuropathy on bone density in patients with type 1 diabetes. Diabetes Care, 22, 827−831. Rogers L.C., Bevilacqua N.J. (2008a). Imaging of the Charcot foot. Clinics in Podiatric Medicine and Surgery, 25, 263–274, vii. Rogers, L. C., & Bevilacqua, N. J. (2008b). The diagnosis of Charcot foot. Clinics in Podiatric Medicine and Surgery, 25, 43−51. Rogers, M. J. (2003). New insights into the molecular mechanisms of action of bisphosphonates. Current Pharmaceutical Design, 9, 2643−2658. Rosenblum, B. I., Giurini, J. M., Miller, L. B., Chrzan, J. S., & Habershaw, G. M. (1997). Neuropathic ulcerations plantar to the lateral column in patients with Charcot foot deformity: A flexible approach to limb salvage. Journal of Foot and Ankle Surgery, 36, 360−363. Sabokbar, A., & Athanasou, N. S. (2003). Generating human osteoclasts from peripheral blood. Methods in Molecular Medicine, 80, 101−111. Sackett, D. L., Rosenberg, W. M., Gray, J. A., Haynes, R. B., & Richardson, W. S. (1996). Evidence based medicine: What it is and what it isn't. British Medical Journal, 312, 71−72. Salsich, G. B., Mueller, M. J., Hastings, M. K., Sinacore, D. R., Strube, M. J., & Johnson, J. E. (2005). Effect of Achilles tendon lengthening on ankle muscle performance in people with diabetes mellitus and a neuropathic plantar ulcer. Physical Therapy, 85, 34−43. Saltzman, C. L., Hagy, M. L., Zimmerman, B., Estin, M., & Cooper, R. (2005). How effective is intensive nonoperative initial treatment of patients with diabetes and Charcot arthropathy of the feet? Clinical Orthopaedics and Related Research, 0, 185−190. Saltzman, C. L., Johnson, K. A., Goldstein, R. H., & Donnelly, R. E. (1992). The patellar tendon-bearing brace as treatment for neurotrophic arthropathy: A dynamic force monitoring study. Foot & Ankle, 13, 14−21. Sanders, L. J. (1994). Diabetes mellitus. Prevention of amputation. Journal of the American Podiatric Medical Association, 84, 322−328. Sanders, L. J. (2004). The Charcot foot: Historical perspective 1827–2003. Diabetes Metabolism Research and Reviews, 20(Suppl 1), S4−S8. Sanders, L., & Frykberg, R. (2007). The Charcot foot (Pied de Charcot). In J. H. Bowker, & M. A. Pfeifer (Eds.), Levin and O'Neal's the diabetic foot (7th ed., pp. 257−283). Philadelphia: Mosby Elsevier. Sanders, L. J., & Frykberg, R. G. (1991). Diabetic neuropathic osteoarthropathy: The Charcot foot. In R. G. Frykberg (Ed.), The high risk foot in diabetes mellitus (pp. 297−338). New York: Churchill Livingstone. Sanders, L. J., & Mrdjenovich, D. (1991). Anatomical patterns of bone and joint destruction in neuropathic diabetics. Diabetes, 40(Suppl 1). Saxena, A., DiDomenico, L. A., Widtfeldt, A., Adams, T., & Kim, W. (2005). Implantable electrical bone stimulation for arthrodeses of the foot and ankle in high-risk patients: A multicenter study. Journal of Foot and Ankle Surgery, 44, 450−454.

17

Schauwecker, D. S., Park, H. M., Burt, R. W., Mock, B. H., & Wellman, H. N. (1988). Combined bone scintigraphy and indium-111 leukocyte scans in neuropathic foot disease. Journal of Nuclear Medicine, 29, 1651−1655. Schon, L. C., Easley, M. E., & Weinfeld, S. B. (1998). Charcot neuroarthropathy of the foot and ankle. Clinical Orthopaedics and Related Research, 349, 116−131. Schon, L. C., & Marks, R. M. (1995). The management of neuroarthropathic fracture—Dislocations in the diabetic patient. Orthopedic Clinics of North America, 26, 375−392. Schon, L. C., Weinfeld, S. B., Horton, G. A., & Resch, S. (1998). Radiographic and clinical classification of acquired midtarsus deformities. Foot & Ankle International, 19, 394−404. Selby, P. L., Young, M. J., & Boulton, A. J. (1994). Bisphosphonates: A new treatment for diabetic Charcot neuroarthropathy? Diabetic Medicine, 11, 28−31. Sella, E. J., & Barrette, C. (1999). Staging of Charcot neuroarthropathy along the medial column of the foot in the diabetic patient. Journal of Foot and Ankle Surgery, 38, 34−40. Shapiro, S. A., Stansberry, K. B., Hill, M. A., Meyer, M. D., McNitt, P. M., Bhatt, B. A., & Vinik, A. I. (1998). Normal blood flow response and vasomotion in the diabetic Charcot foot. Journal of Diabetes and Its Complications, 12, 147−153. Shibata, T., Tada, K., & Hashizume, C. (1990). The results of arthrodesis of the ankle for leprotic neuroarthropathy. Journal of Bone and Joint Surgery, American Volume, 72, 749−756. Simon, S. R., Tejwani, S. G., Wilson, D. L., Santner, T. J., & Denniston, N. L. (2000). Arthrodesis as an early alternative to nonoperative management of Charcot arthropathy of the diabetic foot. Journal of Bone and Joint Surgery, American Volume, 82-A, 939−950. Sinacore, D. R. (1998). Acute Charcot arthropathy in patients with diabetes mellitus: Healing times by foot location. Journal of Diabetes and its Complications, 12, 287−293. Singh, N., Armstrong, D. G., & Lipsky, B. A. (2005). Preventing foot ulcers in patients with diabetes. Journal of the American Medical Association, 293, 217−228. Sinha, S., Munichoodappa, C. S., & Kozak, G. P. (1972). Neuro-arthropathy (Charcot joints) in diabetes mellitus (clinical study of 101 cases). Medicine (Baltimore), 51, 191−210. Strauss, E., & Gonya, G. (1998). Adjunct low intensity ultrasound in Charcot neuroarthropathy. Clinical Orthopaedics and Related Research, 132−138. Tan, A. L., Greenstein, A., Jarrett, S. J., & McGonagle, D. (2005). Acute neuropathic joint disease: A medical emergency? Diabetes Care, 28, 2962−2964. Tan, P. L., & Teh, J. (2007). MRI of the diabetic foot: Differentiation of infection from neuropathic change. British Journal of Radiology, 80, 939−948. Tisdel, C. L., Marcus, R. E., & Heiple, K. G. (1995). Triple arthrodesis for diabetic peritalar neuroarthropathy. Foot & Ankle International, 16, 332−338. Togari, A. (2002). Adrenergic regulation of bone metabolism: Possible involvement of sympathetic innervation of osteoblastic and osteoclastic cells. Microscopy Research and Technique, 58, 77−84. Trepman, E., Nihal, A., & Pinzur, M. S. (2005). Current topics review: Charcot neuroarthropathy of the foot and ankle. Foot & Ankle International, 26, 46−63. US Food and Drug Administration. (2008). Bisphosphonates (marketed as Actonel, Actonel+Ca, Aredia, Boniva, Didronel, Fosamax, Fosamax+D, Reclast, Skelid, and Zometa) 2008 safety alerts for drugs, biologics, medical devices, and dietary supplements. Available at: www.fda.gov/ cder/drug/infopage/bisphosphonates/default.htm, January. Watkins, P. J., & Edmonds, M. E. (1983). Sympathetic nerve failure in diabetes. Diabetologia, 25, 73−77. Wild, S., Roglic, G., Green, A., Sicree, R., & King, H. (2004). Global prevalence of diabetes: Estimates for the year 2000 and projections for 2030. Diabetes Care, 27, 1047−1053. Wilson, M. (1991). Charcot foot osteoarthropathy in diabetes mellitus. Military Medicine, 156, 563−569.

ARTICLE IN PRESS 18

D.K. Wukich, W. Sung / Journal of Diabetes and Its Complications xx (2008) xxx–xxx

Wright, J. G., Einhorn, T. A., & Heckman, J. D. (2005). Grades of recommendation. Journal of Bone and Joint Surgery, American Volume, 87, 1909−1910. Wukich, D. K., & Motko, J. (2004). Safety of total contact casting in highrisk patients with neuropathic foot ulcers. Foot & Ankle International, 25, 556−560. Young, M. J., Marshall, A., Adams, J. E., Selby, P. L., & Boulton, A. J. (1995). Osteopenia, neurological dysfunction, and the development of Charcot neuroarthropathy. Diabetes Care, 18, 34−38.

Young, R. J., Zhou, Y. Q., Rodriguez, E., Prescott, R. J., Ewing, D. J., & Clarke, B. F. (1986). Variable relationship between peripheral somatic and autonomic neuropathy in patients with different syndromes of diabetic polyneuropathy. Diabetes, 35, 192−197. Yu, G. V., & Hudson, J. R. (2002). Evaluation and treatment of Stage 0 Charcot's neuroarthropathy of the foot and ankle. Journal of the American Podiatric Medical Association, 92, 210−220. Zgonis, T., Roukis, T. S., & Lamm, B. M. (2007). Charcot foot and ankle reconstruction: Current thinking and surgical approaches. Clinics in Podiatric Medicine and Surgery, 24, 505−517.

1570 C OPYRIGHT Ó 2008

BY

T HE J OURNAL

OF

B ONE

AND J OINT

S URGERY, I NCORPORATED

Current Concepts Review

The Management of Ankle Fractures in Patients with Diabetes By Dane K. Wukich, MD, and Alex J. Kline, MD

ä

Patients with diabetes mellitus have higher complication rates following both open and closed management of ankle fractures.

ä

Diabetic patients with neuropathy or vasculopathy have higher complication rates than both diabetic patients without these comorbidities and nondiabetic patients.

ä

Unstable ankle fractures in diabetic patients without neuropathy or vasculopathy are best treated with open reduction and internal fixation with use of standard techniques.

ä

ä

Patients with neuropathy or vasculopathy are at increased risk for both soft-tissue and osseous complications, including delayed union and nonunion. Careful soft-tissue management as well as stable, rigid internal fixation are crucial to obtaining a good outcome. Prolonged non-weight-bearing and subsequently protected weight-bearing are recommended following both operative and nonoperative management of ankle fractures in patients with diabetes.

Ankle fractures are among the most common injuries treated by orthopaedic surgeons, with an estimated 260,000 occurring per year in the United States1,2. With an ever-aging population, the number of ankle fractures continues to rise3. While protocols for management of ankle fractures are generally well established, treatment of these injuries in patients with diabetes mellitus poses a challenge for orthopaedists. These patients have unique characteristics, including delayed fracture-healing, impaired wound-healing, vasculopathy, and neuropathy, that all must be taken into account when formulating a treatment plan. As the prevalence of diabetes mellitus has continued to increase, so too has the number of ankle fractures seen in this patient population. While much has been published on the impact of diabetes on the treatment of ankle fractures, the majority of studies have included a small number of patients and have been either retrospective reviews or case-control studies. In this review, we will report the impact of diabetes on the management of ankle fractures. Specifically, we will examine the epidemiology of diabetes as it relates to ankle fractures, the specific characteristics of

diabetes that pose a problem in the management of ankle fractures (impaired wound-healing, delayed fracture-healing, and neuropathy), the information in the literature as it relates to outcomes and complications following the management of these fractures in diabetics, and current evidence regarding the optimal management of ankle fractures in patients with diabetes. A critical analysis of the existing evidence regarding the impact of diabetes on ankle fractures will lead to a better understanding of this problem and the ability to make better decisions for patient management. Epidemiology of Diabetes According to statistics from the Centers for Disease Control and Prevention in 2005, 20.8 million people (7% of the population) in the United States had diabetes mellitus4. In the population over the age of sixty years, 10.3 million (20.2% of the population) were affected. Additionally, 1.5 million new cases of diabetes were diagnosed in 2005 alone4. The prevalence of diabetes increased by 61% between 1990 and 2001, and it is estimated that

Disclosure: The authors did not receive any outside funding or grants in support of their research for or preparation of this work. Neither they nor a member of their immediate families received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, division, center, clinical practice, or other charitable or nonprofit organization with which the authors, or a member of their immediate families, are affiliated or associated.

J Bone Joint Surg Am. 2008;90:1570-8

d

doi:10.2106/JBJS.G.01673

1571 THE JOURNAL

O F B O N E & J O I N T S U R G E RY J B J S . O R G V O L U M E 9 0-A N U M B E R 7 J U LY 2 008 d

d

d

this number will further increase by 165% between 2000 and 2050, with the fastest rates of increase occurring in older and minority subpopulations5. Overall, the estimated cost incurred by the United States economy as a result of diabetes and its complications is more than 100 billion dollars annually 6. Similar increases in the prevalence of diabetes and its associated costs have been reported throughout the world7,8. The authors of a recent study estimated the overall lifetime risk of diabetes developing in an individual born in the United States in the year 2000 to be 32.5% for males and 38.5% for females9. The highest rates were predicted to occur in the Hispanic population (a 45.4% risk for males and a 52.5% risk for females). The diagnosis of type-2 diabetes at the age of forty was predicted to be associated with a decreased life expectancy of 11.6 life-years for males and 14.3 life-years for females. Additionally, the number of quality-adjusted life-years was predicted to be decreased by 18.6 for males and 22.0 for females. Pathophysiology of Diabetes Diabetes mellitus constitutes a heterogeneous group of metabolic disorders that share the common manifestation of hyperglycemia. The diagnosis of diabetes is contingent on a fasting blood glucose level of ‡126 mg/dL (‡7 mmol/L) measured on two separate occasions, random glucose levels of ‡200 mg/dL (‡11 mmol/L) with symptoms (polyuria, polydipsia, or unexplained weight loss), or a positive glucose challenge of ‡200 mg/dL10. Broadly, diabetes can be considered to present in two forms (type 1 and type 2). Type-1 diabetes is caused by the autoimmune destruction of insulin-producing b-cells in the islets of Langerhans in the pancreas. This leads to an absolute decrease in the amount of circulating insulin. Circulating insulin is virtually absent, and pancreatic b-cells fail to respond to normal insulinogenic stimuli. Therefore, exogenous insulin must be administered in order to maintain adequate glycemic control. Type-2 diabetes (formerly known as adult-onset diabetes) is characterized by increased peripheral insulin resistance combined with a secretory defect in insulin by the pancreatic b-cells. Both components must be present for the clinical manifestation of diabetes. Overall, 90% of the cases of diabetes in the United States are type 2, and 90% of these patients are clinically obese. Regardless of the underlying cause of diabetes, the common manifestation is systemic hyperglycemia. In turn, this leads to the glycosylation of proteins and the increased formation of intracellular sorbitol and other polyols. The end product is tissue damage in a number of end organs. Patients all show some degree of immune dysfunction, peripheral neuropathy, nephropathy, retinopathy, and arthropathy. Diabetic Neuropathy Diabetic neuropathy profoundly impacts the management of ankle fractures. In the United States, 10% of diabetic patients have some degree of neuropathy at the time of the initial diagnosis of the diabetes, and up to 40% will be diagnosed with peripheral neuropathy within the first decade following that diagnosis1,11,12. In older patients, in whom ankle fractures are more common, neuropathy is even more prevalent. More than 50% of

THE MANAGEMEN T WITH DIABETES

OF

AN K L E FR AC T U R E S

IN

P AT I E N T S

all diabetic patients over the age of sixty have some degree of peripheral neuropathy 13. The subgroup of patients with a loss of protective sensation in the foot and ankle is at particular risk for complications following an ankle fracture. In general, peripheral neuropathy must be profound prior to the loss of protective sensation. Once protective sensation is lost, the risk of foot ulcerations increases sevenfold because of the increased vulnerability to unrecognized trauma14,15. While the so-called gold standard for diagnosing peripheral neuropathy remains nerve conduction studies, the most commonly used instrument clinically is the 10-g (5.07) nylon Semmes-Weinstein monofilament test16-19. This simple test can identify persons at an increased risk for foot ulceration with a sensitivity of up to 91% and a specificity of up to 86%20-22. Vibration testing with a 128-Hz tuning fork can also be used and may be an even more sensitive predictor of early neuropathy 16. It is important to identify neuropathy in all diabetic patients and particularly in those who have sustained an ankle fracture. The severity of diabetic neuropathic complications is directly related to both the lack of control and the chronicity of abnormal glucose metabolism23. The importance of control is highlighted by the fact that a 1% reduction in the hemoglobin A1C level results in approximately a 25% to 30% reduction in the rate of complications10. Under normal glucose homeostasis, the entry of glucose into the cell is tightly regulated by insulin. However, in diabetic patients, insulin impairment leads to increased glucose levels in the bloodstream and subsequently to increased diffusion of glucose into the cells. The end product of this is the formation of advanced glycosylation end products, which are stable and irreversible. In red blood cells, these can be measured as the hemoglobin A1C level, a marker of long-term glucose control. Ultimately, the effects of hyperglycemia on peripheral nerves are twofold, direct neuronal injury and microvascular damage. On a molecular level, cellular homeostasis relies on the tightly regulated use and production of certain reactive oxygen species (nitric oxide, hydrogen peroxide, and superoxide) that play crucial roles in the normal functioning of the cell. These processes are very sensitive to glycemic control. In the presence of excess glucose, the tight regulation of reactive oxygen species is disrupted and excess reactive oxygen species are produced23,24. Within the nerve cells, the excess reactive oxygen species cause direct injury to both cellular proteins and membrane lipids. Additionally, toxic peroxidation products accumulate and bind to normal cellular nuclear material, leading to increased apoptosis, DNA damage, and decreased axonal transport. Hyperglycemia also ultimately results in a decreased production of neurotrophic factors that are responsible for the health and maintenance of normal nerve function25,26. On the vascular level, chronic excess production of superoxide species leads to a loss of normal nitric oxide function, resulting in vasoconstriction and nerve ischemia. Charcot Arthropathy Charcot arthropathy is defined as a noninfectious, destructive process culminating in eventual dislocation and periarticular

fracture in patients with peripheral neuropathy and the loss of protective sensation27-29. While diabetes is the most common cause of Charcot arthropathy today, it can potentially result from any clinical entity that renders a patient insensate to protective sensation. Although Charcot arthropathy is relatively uncommon, the potentially serious complications following a delayed diagnosis of this condition make early detection extremely important. As recent evidence has highlighted, a high index of suspicion and early intervention can potentially avoid some of the historically poor outcomes30. Charcot arthropathy was originally described in the 1860s by the neurologist Jean-Martin Charcot 28. The hypertrophic, destructive neuroarthropathy that he initially described has since been shown to occur in diabetic patients with peripheral neuropathy. The prevalence of Charcot arthropathy is estimated to be approximately 0.3% among all diabetic patients, although it is thought that this may be an underestimate of its true burden31. The only symptom of diabetes that has been shown to be predictive of the potential for the development of Charcot arthropathy is the loss of protective sensation32,33. Two distinct theories have been postulated as potential causes of Charcot arthropathy: the neurotraumatic theory and the neurovascular theory 27. In reality, the cause is likely multifactorial, and overlap between the theories is certainly feasible. The neurotraumatic theory postulates that an initial injury (either a single macrotraumatic event or repetitive microtrauma) activates the process. The loss of protective sensation leads to continued weight-bearing by the patient and the lack of protective unloading. Eventually, there is a loss of structural integrity, and finally a reparative process begins. The neurovascular theory predicates a state of hyperemia resulting from abnormal vasomotor control secondary to the underlying neuropathy. This leads to an increase in local blood flow and, secondarily, to an increased level of osteoclast stimulation. Eventually, this results in increased bone turnover and a relative local osteopenia, which leaves the osseous architecture susceptible to minor trauma. This theory is supported by the fact that local tissue samples from Charcot joints show an increased osteoclast-to-osteoblast ratio mediated by a local cytokine pathway 34. Recently, overexpression of RANKL (receptor activator of nuclear factor kappa-B ligand) has been implicated as a mechanism for the development of Charcot arthropathy35. The classic clinical description of an early Charcot foot or ankle is one with painless erythema, warmth, and swelling of the involved joints. Many patients still have some degree of pain on initial presentation. Often, a patient with an acute Charcot foot is initially misdiagnosed with an infection secondary to the erythematous, inflamed appearance of the foot. However, these patients lack signs of systemic illness, such as fever or elevated white blood-cell counts. Additionally, the erythema will resolve rapidly with elevation of a Charcot foot but not with elevation of an infected foot. In the absence of an open, draining ulceration as a conduit for deep infection, infection is unlikely to be the cause of the acute inflammation. When observed prior to the development of osseous changes on radiographs, these clinical symptoms are often initially

dismissed as a sprain, contusion, cellulitis, gout, or deep vein thrombosis. The initial classification system described by Eichenholtz was based on clinical and radiographic data of patients with Charcot arthropathy 36. Stage I (development-fragmentation) refers to the initial, acute phase in which the cardinal signs of hyperemia, warmth, and swelling are present. Radiographically, a continuum of joint subluxation and dislocation, articular erosions, and osseous destruction is observed. Stage II (coalescence) is heralded by the resolution of the cardinal clinical signs and the transition from destruction to the reparative process. Radiographically, sclerosis is present and, as the bones begin to coalesce, their inherent stability increases and the deformity ceases to rapidly progress. Stage III (reconstruction-consolidation) refers to the hypertrophic, remodeling phase in which trabecular remodeling and the maturation of the osseous architecture into a stable, almost ankylosed state occur. The Eichenholtz classification ignores the initial phase of inflammatory swelling in which the radiographic appearance remains normal or nearly normal. It is patients with this stage of the disease who are often initially dismissed as having a bruise or strain, and unfortunately this is also the group that can most likely be successfully treated if diagnosed early. Shibata et al. were, to our knowledge, the first to describe Stage-0 neuroarthropathy in their series of patients with leprosy 37. In 1995, Schon and Marks referred to Stage 0 as occurring in patients with neuropathy who sustain an acute fracture38. Chantelau et al. subsequently defined Stage-0 Charcot arthropathy as occurring in the six to twelve-month period in which the clinical signs of a Charcot foot develop without any abnormality seen on plain radiographs39,40. Magnetic resonance imaging at this stage will show a pattern of bone-marrow edema consistent with osseous stress injury. When diagnosed at this early stage, the Charcot foot can be managed with immobilization and non-weightbearing and this can often successfully prevent the development of osseous destruction and deformity 39.

ERROR: undefined OFFENDING COMMAND: get STACK: /3 -dictionary1

This is an enhanced PDF from The Journal of Bone and Joint Surgery The PDF of the article you requested follows this cover page.

The key role of the lateral malleolus in displaced fractures of the ankle IG Yablon, FG Heller and L Shouse J Bone Joint Surg Am. 1977;59:169-173.

This information is current as of November 7, 2007 Reprints and Permissions

Click here to order reprints or request permission to use material from this article, or locate the article citation on jbjs.org and click on the [Reprints and Permissions] link.

Publisher Information

The Journal of Bone and Joint Surgery 20 Pickering Street, Needham, MA 02492-3157 www.jbjs.org

The

Key Role Displaced

BY

ISADORE

G.

YABLON,

LEROY From

The

ABSTRACT:

reason

the

why

M.D.t,

SHOUSE,

Boston

late

of the Lateral Malleolus Fractures of the Ankle* FREDERICK

M.D.t,

University

Medical

degenerative

ar-

thritis developed in some patients who had sustained displaced bimalleolar fractures of the ankle was investigated. reduction

The roentgenograms indicated of the lateral malleolus and

were present. When bimalleolar fractures created in cadavera the talus could be anatomically positioned only when the lateral malleolus was rately reduced. fractures were

Fifty-three patients treated by anatomically

eral malleolus with a four-hole anatomical reduction of the talus in each instance and there were generative for from

six

arthritis months

talus

It has

were reaccu-

bimalleolar fixing the lat-

plate. There was an and medial malleolus no late cases of de-

when these patients were followed to nine years. We concluded that

the lateral malleolus tion of bimalleolar of the leolus.

with

is the key to the fractures, because

faithfully

generally

followed

been

accepted

that

lateral

mal-

reduction

malleolus

unstable usually

bimalleolar fractures of the ankle 1,2 It is further believed that even if the lateral malleolus is intact of

the

ankle

is lost

when

importance

of the

medial

stability

is of paramount

of the

the

in treating

medial

malleolus

M.D.t,

AND

Center,

Universiti

Hospital,

Boston

Materials

and

Methods

Studies

Ankles from fresh muscles, and tendons, were inserted transversely

cadavera and two through

were stripped of skin, heavy Kirschner wires the talus parallel to the

anklejoint.

were

to stabilize

These

wires

used

the foot

and

to measure rotatory and sagittal displacements Four individual specimens were used for each

of the talus. set of exper-

iments

times.

and

separate stability

each

maneuver

was

repeated

five

studies were done, to assess the effects after: (1 ) isolated division of the deltoid

(2) isolated transverse

division osteotomy

Four

on ankle ligament,

of the fibular collateral ligaments, of the medial malleolus at the

(3) level

of the joint with all ligaments intact, and (4) short oblique osteotomy of the lateral malleolus with all ligaments intact. The amount of rotatory displacement was measured with a protractor and determined by the amount of rotation of the Kirschner wires from the longitudinal axis of the

anatomical reducthe displacement

that

HELLER,

MASSACHUSETTS

Laboratory

that incomplete a residual talar

tilt

G.

BOSTON,

in

tibia and fibula. Varus deformity was measured by noting the angle between the tibial plafond and the wires. The final result was expressed as the mean of the values obtamed

is

fractured, especially if the fracture is transverse and at the level of the joint Most relevant publications emphasized that reduction of the medial malleolus should be anatomical and that once it is achieved there is complete reduc-

from each of the individual In a fifth series of experiments,

observations. after the

pins

had

been inserted the medial malleolus was osteotomized at the level of the joint line and an oblique osteotomy was performed on the lateral malleolus to simulate an external

.

tion

of

the

also

stated

displaced

talus

that

residual

any

It

4.5.8.10.12,16.19.22.25.26#{149}

talar

was

displacement

can

be corrected by manually reducing the lateral malleolus after the medial malleolus has been securely fixed in place ‘ 1 In following patients who had sustained displaced abduction-external rotation bimalleolar fractures of the

rotation-abduction gus

and

30

formities

juries.

fracture. degrees

seen

Clinical

age

*

Read

in part

at the Annual

59-A, NO. 2.

MARCH

1977

range

ofThe

American

Academy 2, 1976. Ma.ssachu-

of

was

injuries women

from

nineteen years.

series.

and eleven of the deltoid This

initial

was

placed

then

the

de-

of

such

in-

attempted

rotating

in val-

to create

roentgenograms

was

internally

of thirty-four

in this Meeting

Orthopaedic Surgeons, New Orleans, Louisiana, February t University Hospital, 75 East Newton Street, Boston, setts 02118. VOL.

com-

the

patients

was undertaken in an attempt plication occurred.

this

ankle rotation

by applying

a

as would

be

the ankle,

Material Fifty-three

external rotation were thirty-one

why

The

external

reduction

stress and clinically.

ankle, we became aware that a number of the patients had late degenerative changes in the ankle. The arthritis had its onset one to eight years after the injury. The present study to determine

on

Manual

varus done

of

latter

Forty-two

had a fracture ligament, group

was

who

had

sustained

of the ankle were and twenty-two to eighty-six Open

fractures

patients

had

of the lateral as evidenced treated

by open

abduction-

studied. There men. The age

years, were

with

an aver-

not included

a bimalleolar

fracture

malleolus

and a tear

by lateral

talar

shift.

reduction

and

interI 69

I. G.

170 nal fixation The deltoid

YABLON,

of the lateral malleolus using ligament was not repaired.

quality of reduction roentgenographically. The first leolar fractures with a screw

of

the

F.

G.

HELLER,

AND

LEROY

SHOUSE

a four-hole plate. The stability and

fracture

were

assessed

seventeen patients in this series with bimalhad the medial malleolus reduced and fixed in the conventional manner, in order to de-

INVERSION

termine whether primary reduction of the medial malleolus would reposition the talus. Intraoperative roentgenograms were then obtained. In fourteen patients there was an incomplete these

reduction patients

of the

the

moved, through

following a separate

four-hole

plate

malleolus.

In

screw

in all

replacing patients

revealed

reduced, the screw place but a four-hole malleolus

lateral

malleolus.

malleolus

that

the screw in whom

In

was

reFIG.

the

talus

was

roentgenograms

a

Anterior

obliquely

view of positioned.

displacement, The vertical

1-A

with the fibula intact line represents the axis

but the foot of the fibula.

in the medial intraoperative anatomically

in the medial malleolus plate was also applied

Postreduction

.

and medial

which the lateral malleolus was exposed incision and accurately reduced with

without the three

roentgenograms

talus in the

was left in to the lateral were

obtained

cases.

In order to determine what effect primary anatomical reduction of the lateral malleolus would have on these displaced fractures, in ten patients in this series the lateral malleolus was exposed and reduced under direct vision. The reduction was held in place with a blunt periosteal elevator

and

intraoperative

roentgenograms

were

made

INVERSION

to

observe the position of the talus and medial malleolus. A four-hole plate was then applied to the lateral malleolus and intraoperative stress roentgenograms were made to test the stability of the ankle. Postoperatively, in all cases the extremity was elevated

five

in a canvas

days.

patient

sling

suspended

A below-the-knee was

allowed

from

cast to

walk,

was

a Balkan

then

applied

non-weight-bearing,

frame

for

and

the on

FIG. The

tion. Securely not improve

years.

malleolar force was

Experimental

Findings

When

the deltoid

ligament

instability. were divided

When there

alone

was

divided,

no in-

only the fibular was approximately

collateral liga30 degrees of

external rotatory instability and marked talar instability (Figs. 1-A and 1-B). Resecting the lateral malleolus produced marked rotatory and valgus instability, and this increased as progressively greater force was applied. When abduction-external rotation fractures were created varus

and stress

manual reduction and internally

has been

resected.

fixing the medial malleolus with the position of the talus. However,

a screw when

did the

ankle was forcefully internally rotated after the medial malleolus had been fixed, the talus could be anatomically repositioned; but this occurred by stretching the lateral ligament discontinued

complex. When the the talus resumed

internal rotatory its displaced p0-

sition.

stability of the ankle resulted. Resection of the medial malleolus at the level of the joint line allowed about 10 degrees of rotatory displacement of the ankle but very little valgus ments

1-B

end of the fibula

began to move into position but its progress was arrested because the lateral malleolus began to impinge on the proximal fibular fragment, preventing further internal rota-

crutches. A below-the-knee walking cast was applied after four weeks. The patients were followed for six months to nine years (from 1966 to 1975), with an average of 5.5 years. Twenty-nine patients were followed for more than six

Results

distal

was attempted by applying rotating the ankle, the talus

Clinical

Findings

leolus plate,

In the fifty-three was accurately postreduction

patients in whom the lateral malreduced and fixed with a four-hole roentgenograms revealed an anatomi-

cal reduction of the talus. In the seventeen patients had primary fixation of the medial malleolus, fourteen already mentioned) showed evidence of a residual

who (as talar

tilt. When the screw was removed and the lateral malleolus was anatomically reduced, the talus and medial malleolus were seen to be accurately repositioned (Figs. 2-A through 2-D). No instability was demonstrated on the stress

roentgenograms

duced

and fixed

with

when a four-hole THE

JOURNAL

the lateral plate

malleolus (Figs.

OF BONE

AND

3-C JOINT

was

re-

and 4-B). SURGERY

ROLE

FIG.

OF

LATERAL

MALLEOLUS

2-A

IN

DISPLACED

FRACTURES

2-B

FIG.

FIG.

OF

THE

171

ANKLE

2-C

2-D

FIG.

2-A: Anteroposterior roentgenogram showing a displaced bimalleolar fracture. Fig. 2-B: lntraoperative roentgenogramof the same ankle. An attemptwas made to reduce the talus manually and the medial malleolus is fixed with a screw . Although the repositioning of the medial malleolus is accurate, there is residual talar displacement and incomplete reduction of the lateral malleolus. Fig. 2-C: lntraoperative photograph of the same ankle, demonstrating incomplete reduction of the lateral malleolus. Fig. 2-D: Postreduction roentgenogram. The screw was removed from the medial malleolus and a four-hole plate was applied over the distal part of the fibula after the lateral malleolus was anatomically reduced. The talus is in its normal position and the medial malleolus has been reduced. The radiolucent area between the medial malleolus and the tibia is due to traumatic loss of bone. FIg.

There

was

no

tendon interposition malleolus. There thritis,

the

there

were

tions

which

talus

instance

remained

no cases were

the fractures

of

periosteal

preventing was no evidence in its

eventually

VOL.

3-A: 3-B: it in 3-C:

59-A,

tibial-

of the medial degenerative arposition,

were

3-A

four

and

and

two

suction-irrigation,

after

FIG.

Fig. Fig. holding Fig.

There

by closed

united

posterior

anatomical

of non-union. treated

or

reduction of late

five

infecand

months.

One patient had a superficial but the wound did not become ondary intention. The total ten weeks. All patients experienced the cast was removed, but three

FIG.

weeks.

Seven

2, MARCH

1977

immobilization

this

patients

swelling resolved

still

FIG.

3-B

Oblique roentgenogram of a right ankle showing a displaced bimalleolar fracture. lntraoperative roentgenogram showing repositioning of the talus and medial malleolus position with a blunt periosteal elevator. Postoperative roentgenogram. An anatomical reduction was achieved by the application

NO.

skin slough over the plate, infected and closed by sec-

by accurately of a four-hole

had

time

averaged

of the ankle after in an average of mild

asymptomatic

3-C reducing plate.

the lateral

malleolus

and

172

I.

FIG.

F ig Fig.

G.

YABLON,

G.

F.

HELLER,

4-A

AND

FIG.

LEROY

SHOUSE

4-B

FIG.

5

A : Anteroposterior roentgenogram of a d i splaced bimalleolar fracture. 4-B: lntraopcrative roentgenograrn of the same fracture. An anatomical reduction was achieved by reducing the lateral malleolus and applying a tour-hole plate. A valgus and external-rotation stress was applied. The ankle retains its stability despite the fact that the medial malleolus was not fixed. Fig. 5: Anteroposterior rocntgenogram of the ankle of a patient who had sustained a fracture of the lateral malleolus and a tear of the deltoid ligament. with lateral and rotatory talar displacement. The talus follows the dIsplacement of the lateral malleolus. .

4

-

swelling. support.

Forty-nine patients became ambulatory without Three patients had walked with a cane prior to the

accident healed.

and continued to do so after their Thirty-eight patients regained a full

less

motion

the

remaining

siflexion

within one

average

six

year

of

10

after

patients

cast

lacked

but

of

two

Six

full

plantar

continued

Roentgenograms

removal. 10

postoperatively.

degrees

asymptomatic, walking.

weeks

fifteen

fractures had range of painNine

degrees

patients flexion:

four

pearing

an

demineralization

of

the tarsal bones suggestive of Sudeck’s atrophy. With the exception of these two instances, all patients were able to resume their normal preinjury activities.

and

the

literature

paucity

of communications

describing

late

entity

clinical

techniques

scribed

and

to restore

a number

ankle

ap-

reconstruction

established

of

observais a well

of effective

stability

have

surgi-

been

de-

7.13

It

on

the

may also correlate with these hand, lateral ligament laxity

were

of pain

or lax, in

the deltoid ligament tions. On the other cal

dor-

lacked

to complain

revealed

of

of

ruptured

was

of

interest

to

observe

experimentally

why

anatomical reduction of a displaced bimalleolar fracture could not always be achieved manually. Impingement of the lateral malleolus on the proximal fibular fragment prevented the talus from resuming its anatomical position.

Discussion Unsatisfactory placed

long-term

bimalleolar

others. Cedell reviewed 400 abduction-external that

late

pain,

results

ankle

tinued strated

swelling,

was

bimalleolar

and

the

most In all

erature,

it was

of the

lateral

The sion

of

create

changes

tibiofibular that 44 per

fault

in the

there

and

studies degree

observation

fits

in well

frequency

of ankle

treatment

was

or

talar

instability

medial

ligaof con-

demonmalleolus frac-

in the

lit-

reduction that

malleolus of the

the clinical when

cent

tilt.

surprisingly,

of instability

with

were

of these reported

incomplete

residual

showed,

ligament

an important

by

conservatively

patients

that

malleolus deltoid

treated

symptomatic

found

cadaver the

degenerative

Several authors 14.15.17.21.24 reduction of the lateral

common of the

of dis-

reported

the anterior reported

fractures

to cause pain. that incomplete

tures.

were

the results of treatment of over rotation fractures. He postulated

due to persistent laxity of ment. Phillips and associates thirty-six

of treatment

fractures

findings

the deltoid

did ankle.

divinot This

of a low ligament

is

Anteroposterior and oblique roentgenograms of the ankle of a patient who sustained a tear of the deltoid ligament and a diastasis of the inferior tibiofibular joint. The talus follows the displacement of the lateral malleolus.

THE

JOURNAL

OF

BONE

AND

JOINT

SURGERY

ROLE

OF

LATERAL

MALLEOLUS

Secure fixation of the medial malleolus sion screw did not improve the displaced talus, and the talus could be anatomically forced abduction and occurred by stretching plex. The displaced force, the

DISPLACED

with a compresposition of the reduced only by

internal rotation of the ankle; but this the lateral collateral ligament com-

lateral malleolus, however, position. On discontinuation talus resumed its displaced

In reviewing the ankle which

IN

still

maintained its of the manual position.

our clinical material of other injuries to involved talar displacement with fracture

only of the lateral malleolus or talofibular diastasis, not ineluded in the series described, we found that in many instances the talus followed the lateral malleolus (Figs. 5 and

6).

These

observations

strongly

suggest

that

in un-

FRACTURES

OF

173

ANKLE

ankle in such cases, but this stretches ligament. When external immobilization

the fibular collateral is discontinued,

the lateral ligaments remain in a stretched position and slight to moderate talar instability, which predisposes to the development of late degenerative arthritis, may be the result. On the basis of these studies it would appear that the lateral malleolus is the key to the anatomical reduction of displaced tegrity ankle

bimalleolar

of the medial that

fractures,

of the lateral 18.23 This does medial aspect

the

lateral

malleolus

disregarded There

One

can

lateral malleolus cannot pinges on the proximal the talus can be achieved

mon

as is generally

sues

are

should

in the treatment was no instance

soft-tissue interposition dial malleolus when

resumes

and

that

only

assume

replaced

restoring

malleolus establishes not necessarily lessen

malleolus in contributing of the ankle, but it does

stable bimalleolar fractures, or those fractures in which the lateral malleolus is fractured and the deltoid ligament is torn, the talus remains attached to the lateral malleolus. Reducing the medial malleolus alone may prevent anatomical repositioning of the talus, because in some cases the be accurately reduced when it imfibular fragment. Repositioning of by forcibly internally rotating the

THE

that

this

believed. in their

no longer

its anatomical

be

replacement malleolus was complication Perhaps

original

in-

congruity to the serve to emphasize

of these injuries. in our fifty-three cases

prevented the lateral

the

stability of the the importance

ignored

or

in which of the mereduced9.

is not as cornthe

sites

by

interposing the

tis-

talus

as

it

Surg..

4: 51-

position.

References 1.

A.

ASHHURST,

P. C.,

and

BROMER,

R. S.:

Classification

and

Mechanism

of

Fractures

of

Leg

Bones

Involving

the

Ankle.

Arch.

129. 1922. 2. BONNIN, J. G.: Injuries to the Ankle. London, Heineman, 1950. 3. BRAUNSTEIN. P. W., and WADE. P. A.: Treatment of Unstable Fractures of the Ankle. Ann. Surg. , 149: 217-226, 1959. 4. BURGESS, ERNEST: Fractures of the Ankle. J. Bone and Joint Surg., 26: 721-732, Oct. 1944. 5. BURWELL, H. N., and CHARNLEY, A. D.: The Treatment of Displaced Fractures at the Ankle by Rigid Internal Fixation and Early Joint Movement. J. Bone and Joint Surg., 47-B: 634-660, Nov. 1965. 6. CEDELL, C-A.: Supination-Outward Rotation Injuries of the Ankle. A Clinical and Roentgenological Study with Special Reference to the Operative Treatment. Acta Orthop. Scandinavica, Supplementum I 10. 1967. 7. CHRISMAN. 0. D. , and SNOOK. G. A.: Reconstruction of Lateral Ligament Tears of the Ankle. An Experimental Study and Clinical Evaluation of Seven Patients Treated by a New Modification of the Elmslie Procedure. J. Bone and Joint Surg. , 51-A: 904-912, July 1969. 8. CONWELL, H. E., and REYNOLDS, F. C.: Key and Conwell’s Management of Fractures, Dislocations, and Sprains. Ed. 7. St. Louis, C. V. Mosby. 1961. 9. COONRAD, R. W.. and BUGG. E. I., JR.: Trapping ofthe PosteriorTibialTendon and Interposition ofSoftTissue in Severe Fractures about the Ankle Joint. J. Bone and Joint Surg. . 36-A: 744-750. July 1954. 10. Cox, F. J., and LAXON, W. W.: Fractures About the Ankle Joint. Am. J. Surg. , 83: 674-679, 1952. 11. CRENSHAW. W. H. [editor]: Campbell’s Operative Orthopedics. Ed. 5. St. Louis, C. V. Mosby, 1971. 12. DENHAM, R. A.: Internal Fixation for Unstable Ankle Fractures. J. Bone and Joint Surg., 46-B: 206-211, May 1964. 13. FREEMAN. M. A. R.: Treatment of Ruptures of the Lateral Ligament of the Ankle. J. Bone and Joint Surg., 47-B: 661-668, Nov. 1965. 14. lSEi.IN, MARC, and DE VELLIS. H.: La primaut#{233}du p#{233}ron#{233} dans les fractures du cou-de-pied. M#{233}m.Acad. chir.. 87: 399-408, 1961. 15. KLEIGER, BARNARD: The Treatment of Oblique Fractures of the Fibula. J. Bone and Joint Surg., 43-A: 969-979, Oct. 1961. 16. LEE, H. G.. and HORAN. T. B.: Internal Fixation in Injuries ofthe Ankle. Surg., Gynec. and Obstet.. 76: 593-599. 1943. 17. MAGNUSSON. RAGNAR: On the Late Results in Non-operated Cases of Malleolar Fractures. A Clinical-Roentgenological-Statistical Study. 1. Fractures by External Rotation. Acta Chir. Scandinavica, Supplementum 84, 1944. 18. MULLER, M. E.; ALLGdWER, M.; and WILLENEGGER, H.: Manual ofinternal Fixation. Berlin, Springer, 1970. 19. PATRICK. JAMES: A Direct Approach to Trimalleolar Fractures. J. Bone and Joint Surg. , 47-B: 26-29, May 1965. 20. PHILLIps, R. S.; BALMER,G. A.; and MONK, C. J. E.: The ExternalRotation Fracture oftheFibular Malleolus. British J. Surg., 56: 801-806, 1969. 21. PICAUD, A.-J.: R#{233}fiexions a propos dun traitement chirurgical simple des fractures r#{233}centesde Ia cheville. Rev. chir. orthop.. 39: 570-580, 1953. 22. QUIGLEY, T. B.: Analysis and Treatment of Ankle Injuries Produced by Rotatory, Abduction, and Adduction Forces. In Instructional Course Lectures. The American Academy ofOrthopaedic Surgeons. Vol. 19, pp. 172-182. St. Louis. C. V. Mosby. 1970. 23. SNEPPEN, 0.: Pseudoarthrosis ofthe Lateral Malleolus. Acta Orthop. Scandinavica, 42: 187-200, 1971. 24. SOLONEN. K. A.. and LAUTTAMUS. LEO: Operative Treatment of Ankle Fractures. Acta Orthop. Scandinavica, 39: 223-237, 1968. 25. STAPLES. 0. S.: Injuries to the Medial Ligaments of the Ankle. Result Study. J. Bone and Joint Surg.. 42-A: 1287-1307, Dec. 1960. 26. WIlSoN. F. C.. JR.. and SKILBRED, L. A.: Long-Term Results in the Treatment ofDisplaced Bimalleolar Fractures. J. Bone and Joint Surg., 48-A: 1065-1078, Sept. 1966.

VOL.

59-A,

NO.

2, MARCH

1977

Predislocation Syndrome Progressive Subluxation/Dislocation of the Lesser Metatarsophalangeal Joint Gerard V. Yu, DPM* Molly S. Judge, DPM† Justin R. Hudson, DPM‡ Frank E. Seidelmann, DO‡

Progressive subluxation/dislocation of the lesser toes resulting from idiopathic inflammation about one or more of the lesser metatarsophalangeal joints is a common cause of metatarsalgia that is frequently unrecognized or misdiagnosed. The disorder results from a failure of the plantar plate and collateral ligaments that stabilize the metatarsophalangeal joints and is typically associated with abnormal forefoot loading patterns. The authors refer to this condition as predislocation syndrome and have devised a clinical staging system that is based on the clinical signs and symptoms present during examination. A thorough review of predislocation syndrome and an overview of the conservative and surgical treatment options available for this disorder are presented. (J Am Podiatr Med Assoc 92(4): 182-199, 2002)

Painful instability of the lesser metatarsophalangeal joint has been recognized in both the orthopedic and the podiatric literature as a common cause of metatarsalgia.1-6 The condition is typically described as a progressive, painful subluxation or dislocation of the proximal phalangeal base on the metatarsal head that occurs as a result of weakening of the periarticular structures that stabilize the metatarsophalangeal joint—in particular, the plantar plate. The subluxation/dislocation process can be slow or rapidly progressive. Medial or, less commonly, lateral deviation of the digit may also occur and accompanies dorsal *Diplomate, American Board of Podiatric Surgery; Fellow, American College of Foot and Ankle Surgeons; Director of Podiatric Medical Education and Residency Training, St Vincent Charity Hospital, Cleveland, OH; Faculty Member, The Podiatry Institute, Tucker, GA. Mailing address: 23823 Lorain Rd, Ste 280, North Olmstead, OH 44070. †Director of Externship Program, St Vincent Charity Hospital, Cleveland, OH; private practice, Toledo, OH. ‡Submitted during third-year podiatric surgical residency, St Vincent Charity Hospital, Cleveland, OH. ‡Adjunct Professor of Radiology, Ohio College of Podiatric Medicine, Cleveland; Clinical Professor of Radiology, Ohio University, Athens; private practice, Cleveland, OH.

182

migration of the proximal phalanx. A hammer toe deformity may be found in association with the disorder, but is usually not an early or a significant component. Unlike in the classic hammer toe deformity, a dorsal corn overlying the proximal interphalangeal joint is typically not observed (Fig. 1). Although any lesser metatarsophalangeal joint can be affected, the second metatarsophalangeal joint is affected most often.7, 8 Hallux valgus and first-ray insufficiency may contribute to this problem but are not necessarily precursors or prerequisites.1-6 A long second metatarsal has also been implicated in the development of this entity.1 While pain about any lesser metatarsophalangeal joint may be associated with several systemic and local processes, the idea of idiopathic pain and instability of the metatarsophalangeal joint is relatively new.6, 9 The literature is replete with numerous terms describing the components of lesser toe derangement. The following terms, for example, are slightly modified from a list appearing in Miller10: ● ●

Sub–metatarsal 2/neuroma syndrome Chronic lesser metatarsophalangeal dislocation

April 2002 • Vol 92 • No 4 • Journal of the American Podiatric Medical Association

Figure 1. Classic hammer toe deformity of the second toe with chronic metatarsophalangeal joint subluxation. Note the presence of a classic heloma durum overlying the proximal interphalangeal joint, which is not typically seen in patients with predislocation syndrome.

Floating toe syndrome Lesser metatarsophalangeal joint instability syndrome ● Second metatarsophalangeal joint dislocation/ subluxation ● Monoarticular nontraumatic synovitis of the second metatarsophalangeal joint ● Crossover second-toe deformity ● Second metatarsophalangeal joint instability ● ●

The authors, however, consider many of these to be part of a distinct clinical entity, which they refer to as predislocation syndrome. Once a frank dislocation occurs, more appropriate descriptive terminology should be employed. This article presents the natural history of predislocation syndrome and reviews the conservative and surgical treatment options available for this disorder.

Clinical Presentation Patients suffering from predislocation syndrome typically present with acute, subacute, or, less commonly, chronic focal pain at the plantar aspect of the involved lesser metatarsophalangeal joint or joints. In general, pain is most noticeable during ambulation and subsides during rest.11 Frequently, patients com-

plain that they feel as if they are walking on a “stone bruise” or “lump” on the bottom of the foot in spite of the absence of any obvious plantar lesion. Patients may also complain of swelling about the base of the toe, more impressive plantarly than dorsally. Some patients will note that the toe “feels as though it is trying to go out of position,” and others may have even noted a distinct change in position over the course of several weeks. Rarely is a lesion present over the dorsal aspect of the proximal interphalangeal joint, although mild erythema may be present as a result of shoe irritation of the knuckle pad. Tyloma formation plantarly is rarely present. Some patients mention a recent increase or change in activity level prior to the development of symptoms.1 The current authors have seen this problem develop following participation in such activities as jogging, tennis, and basketball. In other cases, patients may recall a minor traumatic event, such as a misstep on a stair, hole, or protruding object such as a garden hose or an electrical cord prior to the development of symptoms. In a number of cases, the senior author (G.V.Y.) has encountered a history of a misstep climbing up or down stairs or a ladder as an inciting factor. In later stages of predislocation syndrome, severe pain may lead to an antalgic gait, with the patient compensating by walking on the lateral aspect of the foot. Barefoot weightbearing often becomes intolerable, especially on hard surfaces. The authors have found that secondary manifestations, such as lateral column overload and calcaneocuboid joint syndrome, may occur, sometimes becoming as significant as the original chief presenting complaint. A constant lingering or long-lasting throbbing sensation may also develop, regardless of weightbearing status. Frequently, the patient had sought treatment for the problem in the past, often after being treated by a variety of medical and surgical specialists to no avail. Treatments may have been either conservative or surgical. It is not uncommon for the patient to have received a diagnosis of second interspace or adjacent interspace neuromas in spite of the obvious absence of the subjective complaints classically associated with neuromas. Many patients will have undergone neurectomy, some with revisional procedures undertaken for the presumed recurrence of neuroma or stump neuroma (Fig. 2). The failure of these various treatments and continuing disability are very frustrating for patients and may give rise to anxiety about their prognosis.6 Some patients may have been accused of malingering or suspected of having a psychosomatic illness. A few patients or their spouses may even question whether they are imagining the

Journal of the American Podiatric Medical Association • Vol 92 • No 4 • April 2002

183

Figure 2. Foot of a 45-year-old patient who previously underwent two neuroma resections from the second interspace within a 3-month period. This patient subsequently developed complete dislocation of the second metatarsophalangeal joint. Note the persistent swelling of the second metatarsophalangeal joint and toe. The patient denied having had the symptoms attributable to a typical neuroma.

problem and feel as if they are acting like hypochondriacs. Some patients, out of desperation, will plead, “Please tell me I’m not crazy!” Not uncommonly, this unfortunate chain of events results in significant depression and anxiety, further complicating the clinical course of the complaint.

Physical Examination Specific and accurate pain localization during a physical examination is paramount for determining the structures affected. On physical examination of the patient with predislocation syndrome, one finds excruciating pain on palpation just distal and plantar to the metatarsal head that is disproportionate to any other objective clinical findings. Focal pain in this area is thought to result from bursitis or inflammation of the plantar plate.12 Occasionally, inflammation of an intermetatarsal bursa may cause local nerve irritation, resulting in neuritic or neuroma-type symptoms. However, patients presenting with pain caused by inflammation of the plantar plate generally do not have subjective complaints of numbness or shooting pain or objective sensory deficits in the affected digits on clinical examination.11 In addition, on physical

184

examination, the focal point of tenderness is clearly and distinctly the metatarsophalangeal joint area, not the adjacent interspace. An intermetatarsal injection of local anesthetic may be helpful when symptoms are generalized or when the patient has difficulty pinpointing the target area of pain. Active flexor and extensor tendon functions of the affected toe are present with minimal or no compromise. Palpation and range of motion of the metatarsophalangeal joint may elicit capsular crepitus or mobility of a well-circumscribed, bursa-like projection. A painful decrease in range of motion of the joint, particularly in plantarflexion, is often noted.13 Significant malposition is absent in the early stages; however, the astute clinician readily notes subtle changes in position over time. Not uncommonly, the toe manifests a clear tendency toward dorsal migration (not necessarily dorsiflexion), with or without transverse plane deviation toward or away from the hallux (Fig. 3). In most cases, evaluation of weightbearing stance demonstrates subtle but obvious malalignment of the involved digit. Loss of toe purchase, with or without medial or lateral deviation, is typically present. If this condition is left unchecked, the toe will continue to progressively subluxate dorsally, and when this occurs, increased pain plantarly is predictable. Rarely, a callus plantar to the metatarsal head or a corn overlying the proximal interphalangeal joint of the affected toe (as is typically seen with the classic hammer toe deformity that has undergone chronic metatarsophalangeal joint subluxation/dislocation) is present on examination. These keratoses are due to friction and shear of associated osseous structures and to loss of intrinsic muscle balance; they develop only after long-standing dislocation of the toe. Change in local topography is common and often impressive (Fig. 4). Local edema and warmth resulting from inflammation about the metatarsophalangeal joint are typically present; the increased temperature may be measured with skin-surface thermometers and recorded. Subtle edema may be indicated by the obliteration of normal extensor tendon contours. In most cases, the plantar edema is obvious, even profound, and encompasses the entire metatarsophalangeal joint area, frequently extending distally into the sulcus and base of the toe or toes. In the initial stages of predislocation syndrome, the lesser metatarsophalangeal joint may be in good anatomical position without malalignment or contracture. However, as the condition progresses and joint instability ensues, dorsal or transverse plane deviation develops, with subsequent loss of toe purchase. The stages of predislocation syndrome have

April 2002 • Vol 92 • No 4 • Journal of the American Podiatric Medical Association

A

B

Figure 3. Nonweightbearing (A) and weightbearing (B) views of a patient with predislocation syndrome of the right second toe. Note the edema surrounding the metatarsophalangeal joint, obliteration of the extensor tendons to the second digit, and the absence of a significant lesion over the proximal interphalangeal joint. Mild irritation is present. Absence of toe purchase and medial deviation are seen on weightbearing.

been described by Yu and Judge6 and are based on the clinical findings present at the time of examination. In stage 1, there is mild edema plantar, and often dorsal, to the metatarsophalangeal joint. Extreme tenderness is present when the joint is manipulated. No anatomical malalignment is noted clinically. In stage 2, there is moderate edema with noticeable deviation of the affected digit both clinically and radiographically. Often the patient does not realize that the affected toe does not purchase the ground. This becomes quite evident in stance evaluation. In stage 3, moderate edema is present about the entire circumference of the metatarsophalangeal joint and ex-

Figure 4. Edema in a patient with predislocation syndrome of the left third metatarsophalangeal joint. The patient has a congenital syndactyly of the second and third digits, confusing the clinical presentation. Note the absence of similar findings in the contralateral foot.

tends into the toe. More pronounced deviation and possible subluxation/dislocation of the toe are present. While the edema and inflammation eventually subside altogether, the deformity remains unchanged or continues to progress. The end result can be a crossover second-toe deformity, with or without a concomitant hallux abducto valgus deformity. Thompson and Hamilton5 have suggested the use of a vertical stress test, akin to the anterior drawer sign in the unstable ankle joint, to identify and stage sagittal plane metatarsophalangeal joint instability. In this maneuver, the foot is placed in neutral position, and the metatarsal head is stabilized between the examiner’s thumb and index finger. The contralateral hand is used to grip the dorsal and plantar aspect of the corresponding proximal phalanx base. The digit to be tested is manipulated upward with vertical pressure applied by the thumb plantarly. A purely vertical force is applied to the base of the proximal phalanx in the dorsal direction. This is different from testing for dorsiflexion (Fig. 5). A positive vertical stress test result is present when the proximal phalanx can be translocated 2 mm dorsally above the metatarsal head. According to Thompson and Hamilton’s classification scheme, in stage 0 there is no dorsal translocation of the proximal phalanx. In stage 1, the phalangeal base can undergo subluxation dorsally but not dislocation. In stage 2, the phalangeal base can be dislocated but may be manually reduced. In stage 3, the phalangeal base is in a fixed dislocated position. Accurate assessment of the amount of dislocation of the base of the proximal phalanx on the metatarsal head may be quantified on a lateral x-ray.

Journal of the American Podiatric Medical Association • Vol 92 • No 4 • April 2002

185

Figure 5. Positive vertical stress test result with dorsal translocation of the proximal phalanx. Note maintenance of the toe parallel to the plantar aspect of the foot while this maneuver is performed. The examiner must be careful not to confuse dorsal translocation with dorsiflexion.

A thorough history and physical examination are required to rule out all systemic and local problems that may contribute to pain about the metatarsophalangeal joint. Degenerative joint disease, avascular necrosis, rheumatoid arthritis, fat pad atrophy, stress fracture, neuromuscular dysfunction, and neuromas are all common causes of lesser metatarsalgia.2, 12 Only after a detailed history and physical examination and a radiographic evaluation can a primary diagnosis of predislocation syndrome be made (Table 1). Selective laboratory testing may be needed for completeness. It is important to listen carefully to the patient’s subjective complaints, as these will often provide sufficient information for the clinician to suspect this entity as the cause of the patient’s pain, even prior to a physical examination of the area.

Pathomechanics The key developmental factor for idiopathic subluxation/dislocation of the lesser toe is progressive inflammation about the metatarsophalangeal joint with subsequent attenuation and rupture of the plantar plate and collateral ligaments.2, 5 Thus any structural or biomechanical deformity that increases loading forces within the forefoot and results in inflammation of the plantar plate can predispose an individual to progressive weakening of the periarticular structures and resultant joint instability. A long second metatarsal is often cited as a common finding in individuals with instability of the second metatarsophalangeal joint.8, 11 An elongated sec-

186

ond metatarsal (or a short first metatarsal) may alter normal forefoot loading patterns by transferring load from the first to the second metatarsal head (Fig. 6). Hallux abducto valgus may also cause abnormal forefoot loading patterns.2 Lateral deviation of the hallux into the second digit may cause multiplanar deviation of the second toe that results in retrograde buckling at the second metatarsophalangeal joint level on weightbearing. The use of high-heeled shoes or heel lifts, which increase forefoot loading by maintaining the metatarsophalangeal joints in a hyperextended position, have also been implicated in the development of predislocation syndrome in one or more of the lesser digits.1 Biomechanical hypermobility may also predispose a patient to altered forefoot loading patterns. Excessive pronation will alter the axis of insertion of the peroneus longus tendon in such a way that it loses its ability to stabilize the first ray during the forefootloading phase of gait. 13 Accordingly, metatarsus primus elevatus resulting from either biomechanical dysfunction or structural deformity may cause excessive load transfer to the adjacent lesser metatarsophalangeal joint or joints. Similarly, first-ray insufficiency caused by generalized joint hypermobility syndromes, such as Ehlers-Danlos syndrome or Marfan syndrome, may result in overload of one or more of the lesser metatarsophalangeal joints.14 The senior author has also witnessed numerous cases of predislocation syndrome in patients who had undergone surgical correction of hallux abducto valgus deformity in which subtle, but discernible, elevation of the first metatarsal head occurred (Fig. 7). In other cases, the initial presenting complaint was sub–metatarsal 2 discomfort attributed to an asymptomatic hallux abducto valgus deformity. While surgery for the hallux abducto valgus was uneventful, progressive dislocation of the second toe ensued. Patient frustration in such cases is very high. Coughlin1 has identified two distinct populations at risk for developing instability of the second metatarsophalangeal joint: The first group consisted mainly of sedentary women aged 50 to 70 years, with an average age of 60 years. The high proportion of elderly women in this group was attributed to the prevalent use of high-heeled shoes in this population. The second group consisted predominantly of athletic men aged 25 to 64 years, with an average age of 50 years. A majority of this group were found to have a long second metatarsal. Coughlin hypothesized that in the second group repetitive physical activity resulted in inflammation about the second metatarsophalangeal joint that eventually resulted in a weakening of the periarticular structures that stabilize the

April 2002 • Vol 92 • No 4 • Journal of the American Podiatric Medical Association

Table 1. Differentiating Predislocation Syndrome from Common Lesser Metatarsophalangeal Joint Problems Predislocation Syndrome

Other Common Problems

Pain localized to plantar metatarsophalangeal joint Negative tuning fork test X-rays nondiagnostic in early stages Bone scan uptake at metatarsophalangeal joint

Stress Fracture Pain at metatarsal shaft dorsally Tuning fork test elicits pain Conventional x-rays eventually diagnostic Bone scan uptake in metatarsal shaft

Minor trauma or inciting event may be recalled Onset distinctly acute, subacute, or chronic No digital contracture until late stage Positive vertical drawer test Usually no lesions; occasional irritation of the dorsal proximal interphalangeal joint

Plantar to metatarsophalangeal joint, often the second interspace Neuritic symptoms absent Moulder sign absent Subtle or obvious malalignment or malposition of the involved toes May demonstrate significant inflammation of metatarsophalangeal joint and toe, especially plantarly

Hammer Toe No inciting event or trauma Onset insidious over years Contracture at proximal or distal interphalangeal joint preceded pain Negative vertical drawer test Lesions frequently present: heloma durum at proximal interphalangeal joint and/or sub–metatarsal head tyloma Neuroma Classic third interspace Neuritic symptoms: tingling, cramping, burning, shooting pain Positive Moulder sign: palpable click of soft-tissue mass Toes usually have normal alignment and position No edema present

A

B

Figure 6. Anteroposterior (A) and lateral (B) radiographs of a patient who developed sudden dislocation of the second metatarsophalangeal joint following a period of severe pain and inflammation of the plantar aspect of the joint. Note the slightly elongated second metatarsal segment as a possible contributing factor and the presence of a hallux abducto valgus deformity.

Journal of the American Podiatric Medical Association • Vol 92 • No 4 • April 2002

187

A

B

Figure 7. Anteroposterior (A) and lateral (B) radiographs demonstrating dorsal dislocation of the second toe following a distal metaphyseal osteotomy for correction of a hallux abducto valgus deformity. The patient’s initial complaint was pain beneath the second metatarsal segment. An arthroplasty procedure was performed. Owing to persistent symptoms, the patient received multiple injections of steroid and local anesthetic, which resulted in acceleration of the deformity and a steroid-induced avascular necrosis of the third proximal phalangeal base. Note the development of a stress fracture of the second metatarsal and the shortening and elevation of the first metatarsal segment.

toe. The authors believe that both structural alteration and biomechanical dysfunction of the first ray can contribute to the development of this entity at the second metatarsophalangeal joint. The condition can, however, occur in the absence of either of these predisposing factors.

Role of the Plantar Plate in Predislocation Syndrome Stability of the lesser metatarsophalangeal joint is derived from the plantar plate, the collateral ligaments, and the intrinsic and extrinsic foot musculature.15-17 Static stabilization of the metatarsophalangeal joint is derived primarily from the plantar plate and collateral ligaments. The plantar plate is described as a fibrocartilaginous thickening of the metatarsophalangeal joint capsule plantarly that is firmly attached to the base of the proximal phalanx but only loosely attached to the metatarsal head.15 It is composed of type I collagen that is histologically identical to the collagen present in the meniscus of the knee.16 The plantar plate acts as the major distal attachment of the plantar fascia and has attachments to the deep transverse metatarsal ligament and metatarsophalangeal joint collateral ligaments. It

188

also serves as an insertion for both the interosseous and the lumbrical tendons. Inferiorly, the plantar plate has a smooth grooved surface for the passage of the flexor tendons. An anatomical dissection by Johnston et al 15 demonstrated that the plantar plate of the foot is similar in both form and function to the volar plate of the hand. However, those authors noted that the plantar plate is larger and thicker than the volar plate and has a weaker proximal attachment. Deland et al16 also performed an in-depth anatomical dissection of the plantar plate and outlined several possible functions of the structure. First, the plantar plate merges with the plantar fascia distally and is an integral part of the windlass mechanism. Second, its fibrocartilaginous structure helps to absorb compressive loads acting on the metatarsal head. Finally, its central position and multiple attachments act to stabilize the lesser metatarsophalangeal joint in the plantar direction. Through mechanical testing, Bhatia et al17 found the plantar plate to be the main stabilizing force of the metatarsophalangeal joint. The study concluded that the metatarsophalangeal joint collateral ligaments, which have an insertion into the plantar plate, are the second most powerful structures that stabilize the metatarsophalangeal joint. Deland and Sung18

April 2002 • Vol 92 • No 4 • Journal of the American Podiatric Medical Association

performed an anatomical dissection of a medial crossover second toe in a cadaveric specimen in an attempt to fully describe the underlying pathologic anatomy found in the condition. The specimen exhibited rupture of the lateral collateral ligaments, shortening of the medial collateral ligaments, attenuation of the plantar plate, and dorsal medial displacement of both the flexor tendons and the plantar plate. While static stabilization of the metatarsophalangeal joint is primarily the function of the plantar plate, dynamic stabilization is provided by the extrinsic and intrinsic musculature of the foot. It should be noted, however, that the ability of the intrinsic and extrinsic foot musculature to stabilize this joint is dependent largely on the integrity of the plantar plate. When the metatarsophalangeal joint is in a flexed or neutral position, the extensor digitorum longus and extensor digitorum brevis tendons act to dorsiflex the metatarsophalangeal joint through their insertion into the extensor hood apparatus.19 However, with rupture of the plantar plate, the proximal phalanx assumes a subluxated (dorsal) position, and the extensor tendons are mechanically unable to extend the proximal and distal interphalangeal joints. When the metatarsophalangeal joint is maintained in a subluxated (dorsal) position for a prolonged period, the extensor digitorum longus becomes a deforming force at the metatarsophalangeal joint and results in progressive dorsal subluxation and frank dislocation of the toe.2 The flexor digitorum longus and brevis tendons provide flexion at the proximal and distal interphalangeal joints, but are relatively inefficient flexors of the metatarsophalangeal joint.3 In a weightbearing situation, these muscles act to stabilize the toes against the ground and, in doing so, may cause slight dorsiflexion of the metatarsophalangeal joint.19 The flexor tendons are therefore unable to aid in stabilization of the dorsally subluxated toe. Under normal circumstances, the interosseous muscles provide most of the flexion that occurs at the lesser metatarsophalangeal joints.20 However, with dorsal subluxation of the metatarsophalangeal joint, the interosseous tendons migrate dorsal to the axis of the metatarsophalangeal joint and subsequently lose their mechanical ability to provide flexion of the joint.21 The lumbrical muscles also play an important role in the dynamic stability of the lesser metatarsophalangeal joint. These muscles arise from the long flexor tendons and insert into the medial aspect of the extensor hood. According to an anatomical and functional study performed by Jarrett et al,22 the interosseous muscles stabilize the interphalangeal joints in the extended position and maintain the

metatarsophalangeal joint in the plantarflexed position during weightbearing. However, like the interosseous muscles, they too lose their ability to provide flexion of the metatarsophalangeal joint when the proximal phalanx is in a subluxated (dorsal) position.3 Thus, in chronic subluxation of the metatarsophalangeal joint, the long and short flexor, interosseous, and lumbrical muscles provide no dynamic restraint to dorsal dislocation of the toe. The second toe is anatomically unique, having insertions of two dorsal interosseous tendons but no plantar interosseous tendon. The lumbrical tendon has a medial insertion and provides a slight medial pull in the second toe. With chronic inflammation about the metatarsophalangeal joint, progressive dorsal subluxation of the second toe ensues as the plantar plate and collateral ligaments fail in static stabilization of the joint. As a result of the dorsal position of the toe, the normal axes of the intrinsic muscles are lost, rendering them incapable of dynamically stabilizing the joint. The extensor digitorum longus and lumbrical muscles subsequently become a deforming force, contributing to dorsal medial dislocation of the toe. Further explanation for a dorsal medial dislocation following failure of the plantar plate has been provided by Hatch and Burns,23 who performed an anatomical dissection of seven cadaveric specimens exhibiting a crossover second-toe deformity. The authors found that four of the seven specimens demonstrated an accessory medial slip of the extensor digitorum brevis tendon to the second toe and believed that this accessory tendon was a contributing factor in the etiology of the crossover second-toe deformity. The current authors have not found this anatomical variant in several cases of predislocation syndrome that have undergone surgical correction. Anatomically, it is easy to understand why dorsal medial dislocations are most common at the second metatarsophalangeal joint. However, dorsal medial dislocations are also more common than dorsal lateral dislocations at the other lesser metatarsophalangeal joints. The rationale behind this observation is not easily understood, as the other lesser metatarsophalangeal joints have both dorsal and plantar interosseous tendon insertions that directly oppose one another in the transverse plane. Subluxation and dislocation of the lesser toe at the level of the lesser metatarsophalangeal joint, not attributable to the normal progression of the classic hammer toe deformity, are still somewhat of an enigma and continue to challenge physicians who treat foot and ankle problems. The senior author has diagnosed and treated predislocation syndrome involving one or more of the following

Journal of the American Podiatric Medical Association • Vol 92 • No 4 • April 2002

189

digits: second, third, and fourth (Fig. 8). While dorsal subluxation is seen in all of them, the medial or lateral deviation is a peculiar finding not well understood. The authors suggest that an underlying structural metatarsus adductus deformity may influence the type of transverse plane deformity that develops.

Diagnostic Modalities Several imaging modalities are available to assess instability of the lesser metatarsophalangeal joint, although rarely is extensive or expensive imaging required. When there is clinical evidence of subluxation or dislocation, standard radiography is the most practical diagnostic modality and is essential in ruling out local or systemic pathologies that contribute to lesser metatarsophalangeal joint instability and

A

B

C

190

dysfunction. Weightbearing lateral or oblique radiographs clearly indicate dorsal subluxation of the proximal phalanx upon the metatarsal head as the condition progresses. Weightbearing anteroposterior radiographs will demonstrate dorsal as well as transverse deviation of the affected toe. The normal clear space of the lesser metatarsophalangeal joint is 2 to 3 mm, and the joint surfaces should be congruent.2 When dorsal subluxation or dislocation is present, the clear space is obliterated as the concave base of the proximal phalanx migrates dorsally over the convex metatarsal head. Incongruency of the joint space is noticed as the digit deviates in the sagittal and transverse planes. The anteroposterior radiograph will also demonstrate any abnormal metatarsal length patterns that might contribute to the development and progression of this deformity. Cortical hy-

Figure 8. Predislocation syndrome of the third metatarsophalangeal joint. A, Initial radiographic findings were unremarkable; B, a subsequent radiograph demonstrated a complete dislocation of the third metatarsophalangeal joint (arrow); C, note the swelling of the digit and corresponding metatarsophalangeal joint.

April 2002 • Vol 92 • No 4 • Journal of the American Podiatric Medical Association

pertrophy of the affected metatarsal shaft may be present and is believed to be indicative of abnormal forefoot loading.1 However, the authors have not found this to be a consistent finding. Finally, a radiographic vertical stress test may also be used to support the clinical findings of sagittal plane instability. More advanced imaging modalities may be warranted when there is no clear clinical or radiographic evidence of instability. An arthrogram with 0.5 to 1 mL of iodinated contrast material injected dorsally into the metatarsophalangeal joint under fluoroscopy may be used to evaluate the integrity of the metatarsophalangeal joint capsule.24 Rupture of the metatarsophalangeal joint capsule is demonstrated by opacification of the flexor tendon sheath while leakage of the contrast material outside the joint capsule into the intermetatarsal bursa is indicative of collateral ligament rupture.25 Although not typically used, a nuclear medicine three-phase bone scan will show increased tracer uptake at the metatarsophalangeal joint during all three phases.6, 11 The first two phases are decidedly more intense than the delayed phase. This pattern strongly suggests a local inflammatory process, rather than an osseous problem. Additionally, a conventional bone scan may be helpful in identifying a stress fracture not identified on conventional radiographs. The pattern of uptake is different from that seen in patients with predislocation syndrome. A stress fracture would show increased uptake in all phases of the bone scan with the greatest uptake in the delayed phase (3 to 6 hours), which demonstrates a linear pattern within the shaft of the affected metatarsal. In contrast, the pattern of uptake in patients with predislocation syndrome is localized to the metatarsophalangeal joint area. Magnetic resonance imaging (MRI) of the manifestations of predislocation syndrome can be demonstrated on high-field, as well as low-field, magnets. This includes imaging on high-field superconducting extremity images. However, adequate MRI visualization demands a tailored approach. The necessary pulse sequences include sagittal longitudinal relaxation time (sagittal T1), gradient echo transverse relaxation time (gradient echo T2), and short tau inversion recovery (STIR) images and coronal T1 and STIR images, as well as an oblique axial STIR sequence for imaging of the metatarsals and intrinsic muscles of the forefoot. The selection of pulse sequences is very important. Sagittal images are obtained perpendicular to the long axis of the metatarsals. Coronal images, however, require alignment of the first and second metatarsal heads, with imaging of the lesser metatar-

sophalangeal joints obtained parallel to the second through fifth metatarsal heads. The oblique axial sequence is aligned to the dorsal surface of the foot with a lateral down-sloping orientation. To obtain the scan, merely instruct the technologists to perform a STIR sequence in the plane defined by laying their hand on the dorsum of the forefoot region. This combination of pulse sequences provides a simple yet detailed evaluation of the metatarsophalangeal joints and their associated capsuloligamentous complexes, including the plantar plate. The plantar plate and its associated structures are best visualized on T1 and gradient echo image sequences.25 In T1-weighted images, the plantar plate is seen as a smooth, low-signal structure running beneath the metatarsal head and proximal phalangeal base. However, the plantar plate may be difficult to distinguish from the thicker, underlying flexor tendons on T1-weighted images. For this reason, it is helpful to obtain gradient echo images in which the plantar plate is slightly hyperintense relative to the flexor tendons. The MRI findings of plantar plate rupture have been well documented by Yao et al.25, 26 A rupture of the plantar plate will demonstrate increased signal intensity within the plate with a loss of continuity.26 The area of rupture will be isointense with synovium and joint fluid and is typically located adjacent to the metatarsal head (Fig. 9). Synovitis of the flexor tendon sheath and distention of the metatarsophalangeal joint capsule are common associated findings in plantar plate rupture and, if present, are readily identified on MRI.

Figure 9. Typical MRI findings of a patient with predislocation syndrome involving the second and third metatarsophalangeal joints.

Journal of the American Podiatric Medical Association • Vol 92 • No 4 • April 2002

191

Conservative Treatment The goal of conservative treatment for predislocation syndrome is to prevent progression of the deformity and alleviate symptoms. Successful treatment is most often accomplished with a combination of several treatment modalities. Nonsteroidal anti-inflammatory drugs and corticosteroids have been a mainstay for the management of the pain and inflammation associated with this disorder. While a tapered course of oral corticosteroids has been found to be safe and effective, the same cannot be said about repeated intra-articular steroid injections. Dislocation of the toe following repeated intra-articular administration of corticosteroids has been documented in the literature.27 The senior author has witnessed this in several cases where dislocation of the metatarsophalangeal joint was seemingly accentuated by the repeated use of intra-articular steroid injection. The adverse effects of corticosteroid injection directly into periarticular structures have been recorded in the literature. In one study, a single injection of methylprednisone (4 mg) deposited directly into ligamentous tissues destroyed fibrocytes and decreased the tensile strength of the tissues for as long as 1 year.28 The physician must realize that such an injection may weaken the already compromised plantar plate. However, if intra-articular steroids are deemed necessary, the smallest effective dose of a phosphate salt should be used. Generally accepted guidelines recommend that any given joint be injected a maximum of once every 1 to 3 months and no more than two to three times within a 12-month period.29 A number of factors will influence the frequency of injections; these include the type of steroid, the quantity of the steroid, and the clinical entity being treated. The authors strongly discourage the indiscriminate, repeated use of intra-articular steroids for predislocation syndrome. In the authors’ opinion, the use of acetate steroids is rarely, if ever, indicated for the treatment of predislocation syndrome. If intra-articular steroids are employed, splinting of the toe to maintain position and prevent progressive dislocation is strongly recommended. In addition to pharmacologic therapy, offloading the metatarsophalangeal joint and supporting the toe in a proper position are essential to successful treatment. Taping of the digit into a slightly overcorrected rectus position can prevent pain and progression of the deformity. It is believed that this course of treatment stabilizes the digit enough to allow fibrosis of the periarticular structures to occur. However, there are two main drawbacks to taping of the digit: 1) Taping may take several months before stability and

192

pain-free ambulation are achieved; 2) a prolonged course of taping may result in edema and possible ulceration of the digit.11 In short, it is simply not practical. Taping is, however, useful in helping to establish the diagnosis of predislocation syndrome at the initial office visit, provided that the metatarsophalangeal joint has undergone only deviation or subluxation, not dislocation. Taping the toe in the correct position often provides immediate relief of the patient’s symptoms on weightbearing, confirming the diagnosis of predislocation syndrome. Splinting may also be used to maintain proper anatomical alignment of the digit. A metatarsal sling pad stabilizes the proximal phalanx in a plantar direction at the metatarsophalangeal joint level by augmenting the function of the plantar plate and preventing hyperextension or dorsal migration of the proximal phalanx. Accommodative padding may also be used to alleviate symptoms at the affected metatarsophalangeal joint. A longitudinal metatarsal pad with a lesser metatarsophalangeal joint cutout can be used to effectively decrease the weightbearing stress on the metatarsal head. A metatarsal pad applied to the foot or used in the shoe is also helpful, but far less effective than the metatarsal sling pad. It will offload the metatarsal but is insufficient in providing direct splinting of the toe in a plantar direction and fails to prevent further dorsal migration and dislocation. For patients who have received insufficient benefit from taping and padding therapy or are not considered candidates for surgery, shoe modifications may relieve symptoms.3-5, 30 An extra-depth shoe to accommodate the digital deformity combined with a rocker-bottom sole with steel shank to decrease propulsive forces on the affected metatarsophalangeal joint may be effective. A viable alternative option for treating this condition is an extra-depth shoe with a metatarsal bar added to the sole. The authors’ typical regimen for the conservative treatment of predislocation syndrome consists of a combination of oral steroids, nonsteroidal anti-inflammatory drugs, and taping or padding. In cases of significant symptomatology associated with moderate to severe inflammation, oral steroids have been very effective. The authors typically use a tapering dose (from 60 to 10 mg in 10-mg increments) of prednisone, administered in twenty-one 10-mg tablets; this regimen is extremely effective clinically and quite cost-effective. This is followed by a course of nonsteroidal anti-inflammatory drug therapy in conjunction with splinting. Additionally, the authors often employ physical therapy and aggressive manipulation to stretch out the dorsally contracted tissues and decrease inflammation.

April 2002 • Vol 92 • No 4 • Journal of the American Podiatric Medical Association

Crossover taping of the toe in proper position usually provides immediate relief of symptoms in the office (Fig. 10). The patient is permitted to be weightbearing and ambulate. If the patient is comfortable with this taping, the diagnosis is confirmed. A metatarsal sling pad fabricated from 1/8-inch adhesive foam, moleskin, and tube gauze has been very effective for this condition and is worn for weeks to months until the toe stabilizes or is corrected surgically (Fig. 11). Felt should not be used to fabricate these pads because its bulkiness aggravates plantar discomfort and usually makes it difficult for the pads to fit into normal shoes. Foam does not seem to pose this problem. Prefabricated pads are commercially available for single-, double-, or triple-digit control. Where the toe deviates in more than one plane, it can be splinted to the adjacent toe with a multidigit pad by securing the digital straps to one another. Varying degrees of success have been reported with conservative treatment of lesser metatarsophalangeal joint instability. Mizel and Michelson4 treated patients with a combination of a single intracapsular steroid injection and a laced shoe with a steel shank added to the outer sole. They reported a 70% success rate with this treatment regimen for a 75-month follow-up period. Trepman and Yeo30 also used a single intra-articular steriod injection and a rocker-sole shoe modification to treat lesser metatarsophalangeal joint synovitis. That study included 15 joints in 13 patients with no known history of rheumatologic conditions. At follow-up evaluation, an average of 18 months later, nine joints (60%) were asymptomatic, five joints (33%) were improved, and one joint (7%) had progressed to surgery. Mann and Mizel9 treated a group of seven patients with nonsteroidal anti-inflam-

Figure 10. Crossover tape used as a diagnostic tool to evaluate and assess predislocation syndrome.

Figure 11. Metatarsal pad to maintain digital position when metatarsophalangeal joint dislocation has not yet occurred is shown along with the materials used to fabricate it. The materials are 1/8-inch foam, moleskin, and tube gauze. Prefabricated pads are readily available.

matory medications and extra-depth shoes with a metatarsal support. Only one patient responded positively to this course of treatment; the remainder progressed to surgical correction of the deformity. Coughlin1 treated a group of ten athletes with taping for a period of 3 to 6 months combined with a reduction in activity level. Three of the ten patients responded well to this treatment, and six of the remaining seven patients progressed to surgery. One weakness of these studies is the lack of correlation of the stage of the deformity with the clinical outcome of conservative treatment. In the Coughlin study, all of the patients already had a positive vertical stress test result, and eight of the ten patients had either transverse or sagittal plane deviation at the time of initial presentation. It would seem likely that the number of patients requiring surgical correction would be lower if the disorder was identified and treated prior to obvious or frank subluxation. Nonetheless, the literature bears out that conservative treatment will only prevent progression of the deformity and does not permit realignment of the digit once significant malalignment or instability has occurred. In the authors’ experience, significant alleviation of symptoms can be quickly achieved with conservative treatment; however, the complete resolution of all symptoms is less predictable. Digital splinting and pharmacologic management are used for several months in most cases. Early discontinuation of splinting is likely to result in progressive subluxation and dislocation of the metatarsophalangeal joint. As this occurs, secondary contracture of the extensor digitorum longus tendon develops along with dorsal

Journal of the American Podiatric Medical Association • Vol 92 • No 4 • April 2002

193

contracture of the metatarsophalangeal joint capsule. Once flexibility and reducibility of the deformity are lost, surgical intervention becomes the logical next treatment.

Surgical Management In light of the frequent failure of conservative treatment in dealing with subluxation/dislocation of the lesser metatarsophalangeal joint, numerous surgical procedures have been advocated to correct the deformity.2, 3, 9, 31-37 While there is great divergence in the strategies employed to correct the deformity, the basic goal of all of the procedures is release of periarticular contractures and decompression of the metatarsophalangeal joint to reestablish alignment of the digit. Surgical treatment should focus on restoration of plantar plate function and release of the dorsally contracted structures. The design and extent of surgery will vary with the severity of the deformity and the amount of time that has elapsed since the initial diagnosis. Several authors have realized the importance of the plantar plate and collateral ligaments in stabilizing the metatarsophalangeal joint and have developed procedures to correct the deformity at this level. Some surgeons have chosen to correct this deformity with direct primary repair of the plantar plate. A plantar incisional approach is employed with direct visualization of the plantar plate. The attenuated or ruptured site is identified, and direct primary surgical repair is performed with or without concomitant arthroplasty or arthrodesis of the proximal interphalangeal joint and release of the dorsal contracted soft tissue. Ford et al33 have also advocated primary repair of the plantar plate to correct this deformity. Using a biomechanical testing apparatus, they showed that primary plantar plate repair is as effective as a flexorto-extensor tendon transfer in stabilizing the metatarsophalangeal joint. However, the study concluded that performing both procedures together was more effective than performing either procedure individually. Deland et al32 noted the importance of the collateral ligaments in stabilizing the metatarsophalangeal joint and proposed grafting of a partial thickness of the interosseous tendon to reinforce the weakened collateral ligament. Although Deland et al only reported on the procedure as performed in cadaveric specimens, they stated that the benefits of this procedure would include a good range of motion postoperatively, compared with a flexor-to-extensor tendon transfer, and the ability to control the transverse plane alignment of the digits.

194

Numerous authors have advocated other soft-tissue procedures to correct subluxation or dislocation of the lesser metatarsophalangeal joint. Ruch31 has described two different procedures in which the extensor digitorum brevis tendon is transferred to reestablish muscle-tendon balance at the lesser metatarsophalangeal joint. Girdlestone35 is often credited as being one of the first to advocate reduction of the dislocated metatarsophalangeal joint by splitting the long flexor tendon and transferring it to the dorsum of the proximal phalanx. Later, Kuwada and Dockery38 popularized the transfer of the long flexor tendon to the dorsal aspect of the proximal phalanx through a drill hole in the neck of the proximal phalanx. A recent modification of that procedure places the drill hole in the base of the proximal phalanx.39 The benefits of this modification include better reduction of the dislocation owing to a more proximal pull of the flexor tendon and the preservation of the ability to perform either a proximal interphalangeal joint arthroplasty or arthrodesis. The main drawback of all flexor-to-extensor transfer procedures is the decreased dorsal range of motion at the metatarsophalangeal joint that occurs postoperatively. This, however, may also be construed as the main benefit of the procedure, as the goal of treatment is to prevent dorsal migration and dislocation of the toe. Some authors have used a combination of soft-tissue and osseous procedures to correct the deformity. Daly and Johnson40 advocated resection of the bases of the second and third proximal phalanges with subtotal webbing. They believed that subtotal webbing promoted digital stability that was lost as a result of the resection of the bases of the proximal phalanges. Coughlin and Mann11 have recommended relocation of the metatarsophalangeal joint by partial metatarsal head resection and release of the contracted periarticular structures in severe cases of dislocation of the metatarsophalangeal joint. Cracchiolo et al41 reported on 28 cases in which silicone implant arthroplasty was used to correct second metatarsophalangeal joint dislocation. They reported good results in 88% of patients presenting with multiple forefoot deformities. The authors cited transfer lesions as the most frequent complication of the procedure. Other osseous procedures that have been used include oblique osteotomies of the head and neck of the metatarsal, with or without fixation. In a comparison of the results of the Weil and Helal osteotomies in correcting dislocation of the lesser metatarsophalangeal joint, Trnka et al36 concluded that the Weil osteotomy was far superior in maintaining the metatarsophalangeal joint in a corrected position and resulted in fewer malunions. They suggest that this is because

April 2002 • Vol 92 • No 4 • Journal of the American Podiatric Medical Association

the Weil procedure uses stable internal fixation while the Helal procedure allows the metatarsal head to “float” or “seek its own level” after osteotomy. Vandeputte et al42 studied the use of the Weil osteotomy for both intractable plantar keratosis and chronically dislocated metatarsophalangeal joints. Of the 59 metatarsophalangeal joints involved in the study, 33 were chronically dislocated. At follow-up at an average of 30 months postoperatively, patients rated the results as excellent or good in 32 of 37 feet (86%). Two symptomatic transfer lesions occurred, and recurrent dislocations occurred in 5 joints. Vandeputte et al concluded that the Weil osteotomy is simple and efficient for the reduction of chronically dislocated lesser metatarsophalangeal joints. The current authors do not have experience with direct surgical repair of the plantar plate, but have instead chosen to approach this problem by means of various soft-tissue and osseous procedures. A dorsal incisional approach is employed. An arthrodesis of the proximal interphalangeal joint is typically performed. The dorsal soft-tissue release is done in a sequential manner until complete release and relocation of the toe at the metatarsophalangeal joint are achieved. An extensor hood release/recession is followed by a dorsal/medial/lateral metatarsophalangeal joint capsule release. It is not uncommon for a significant amount of synovitis to be present within the joint. Debridement of this inflammatory tissue is performed as needed (Figs. 12 and 13). The toe is stabilized with a Kirschner wire driven across the metatar-

Figure 12. Intraoperative appearance of the second metatarsophalangeal joint following complete relocation of the digit. Note the extensive synovitis within the joint capsule. In addition to soft-tissue release and synovectomy, an arthrodesis of the proximal interphalangeal joint was performed.

sophalangeal joint for 5 to 7 weeks, allowing for softtissue adaptation and stabilization of the metatarsophalangeal joint. If instability of the metatarsophalangeal joint persists following soft-tissue release, a flexor tendon transfer employing the flexor digitorum longus (more commonly) or the flexor digitorum brevis is strongly recommended (Fig. 14). Arthrodesis of the proximal interphalangeal joint alone, although helping to create a rigid beam effect of the toe, may not be sufficient to prevent dorsal subluxation/dislocation of the phalangeal base. Several types of flexor digitorum longus tendon transfers have been well described in the orthopedic and podiatric literature. Several modifications the current authors employ are worthy of discussion. Regardless of the technique of actual transfer, the authors routinely harvest the tendon at the level of the proximal interphalangeal joint that is undergoing arthrodesis. The plantar tissue is incised at the base of the middle phalanx from the dorsal incision. A secondary plantar incision, although commonly used, is not necessary. The split flexor digitorum brevis tendon is retracted medially and laterally, and the flexor digitorum longus tendon identified. The tendon is retracted into the wound, tagged, and transected at the level of the middle phalangeal base. The tendon is transferred by means of one of several techniques. The standard technique is to split the tendon and then transfer each of the two halves around the proximal phalanx and suture them together dorsally. Another technique is to suture the end of the tendon distally, split it proximally, and then simply pass it over the proximal phalangeal neck area, creating a “check-rein” type of configuration.

Figure 13. Clinical photograph 6 months following surgery of the patient shown in Figures 2 and 12.

Journal of the American Podiatric Medical Association • Vol 92 • No 4 • April 2002

195

Figure 14. Traditional technique of flexor digitorum longus tendon transfer. Tendon has been harvested at the proximal interphalangeal joint level, split, and brought around the diaphysis of the proximal phalanx. A simultaneous arthrodesis of the proximal interphalangeal joint will further facilitate plantar stabilization of the digit via the flexor digitorum longus and flexor digitorum brevis.

Figure 15. Modified technique of flexor digitorum longus tendon transfer through a drill hole at the base of the proximal phalanx. The tendon is sutured to the dorsal periosteum and extensor digitorum longus tendon. Simultaneous fusion of the proximal interphalangeal joint can be performed. As shown here, the Kirschner wire is driven through the tendon and across the metatarsophalangeal joint if desired.

The authors’ current recommendation is to pass the tendon from plantar to dorsal through a drill hole at the proximal metaphyseal–diaphyseal junction and secure it to the dorsal periosteal tissues (Figs. 15 and 16). When the digit is stabilized with a Kirschner wire, the wire is driven through the transferred flexor digitorum longus tendon and across the lesser metatarsophalangeal joint. It is important to impart a physiologic tension to the transferred tendon, as excessive tightness can limit the amount of dorsiflexion

at the metatarsophalangeal joint that is available for normal walking. In more resistant and recalcitrant cases, an osteotomy of the metatarsal for shortening or angular correction will be necessary. A variety of techniques can be performed depending on the need for, and extent of, shortening versus angular correction of the metatarsal segment. A through-and-through oblique osteotomy from dorsal distal to plantar proximal allows for shortening as well as rotation if needed. Small

A

B

Figure 16. Preoperative (A) and postoperative (B) clinical appearance of the patient in Figure 15 following correction of the hallux abducto valgus deformity as well as arthrodesis and flexor digitorum longus tendon transfer of the second digit.

196

April 2002 • Vol 92 • No 4 • Journal of the American Podiatric Medical Association

cortical screws are used to fixate the osteotomy. A shortening Z-osteotomy can also be employed. If only angular change of the metatarsal is needed in the transverse plane, a small wedge osteotomy at the metatarsal base can be very effective; a rotational osteotomy can also be employed. The authors generally reserve metatarsal osteotomy for the more severe and fixed deformity where obvious structural deformity (abnormal length or position) is present (Figs. 17 and 18).

Conclusion Instability of the lesser metatarsophalangeal joint is becoming well recognized and accepted in podiatric and orthopedic surgery. It is often the sequela of a chronic inflammation resulting from increased and abnormal weightbearing stresses about the lesser metatarsophalangeal joint. The end result of this derangement is attenuation or rupture of the plantar plate, capsule, or collateral ligaments with subsequent subluxation or dislocation of the digit. This clinical entity has been underrecognized as a cause of lesser metatarsalgia. Although the second digit is most commonly and most profoundly affected (ie, crossover second-toe deformity), the adjacent third and fourth digits can also be affected. Additionally, one or more lesser digits can be simultaneously involved. The clinical signs and symptoms present on examination can help to stage and chart the evolution of

lesser-toe metatarsophalangeal joint subluxation/dislocation. The treatment of predislocation syndrome is dependent on the stage of the deformity. In early predislocation syndrome, conservative treatment with anti-inflammatory medication, shoe modification, padding, and taping may be successful in preventing progression of the deformity. In long-standing deformity of the lesser metatarsophalangeal joint, surgical intervention is warranted when painful fixed subluxation or dislocation is present and conservative treatment modalities have failed or when prolonged conservative care is not desirable. Acknowledgment. The Podiatry Institute and Atlanta Slide Art Productions (Tucker, Georgia) for their assistance in the preparation of the photographs; Michael Dujela, DPM, for his assistance with the preparation of the manuscript.

References 1. C OUGHLIN MJ: Second metatarsophalangeal joint instability in the athlete. Foot Ankle 14: 309, 1993. 2. C OUGHLIN MJ: Subluxation and dislocation of second metatarsophalangeal joint. Orthop Clin North Am 20: 535, 1989. 3. F ORTIN PT, M YERSON MS: Second metatarsophalangeal joint instability. Foot Ankle 16: 306, 1995. 4. MIZEL MS, MICHELSON JD: Nonsurgical treatment of monoarticular nontraumatic synovitis of the second metatarsophalangeal joint. Foot Ankle 18: 424, 1997. 5. T HOMPSON FM, H AMILTON WG: Problems of the second

A

B

Figure 17. Preoperative (A) and postoperative (B) anteroposterior radiographs demonstrating a shortening Z-osteotomy of the second metatarsal and oblique rotational osteotomy of the third metatarsal in a patient with an abnormal metatarsal parabola as a significant contributing factor to the development of digital dislocations. The lines represent the metatarsal break angle.

Journal of the American Podiatric Medical Association • Vol 92 • No 4 • April 2002

197

A

B

Figure 18. Preoperative clinical appearance of the patient shown in Figure 17. Note the complete dislocation of the toes with multiplanar deviation (A) and severe plantar plate inflammation (B). The patient had complete resolution of all symptoms postoperatively.

metatarsophalangeal joint. Orthopedics 10: 83, 1987. 6. Y U GV, J UDGE MS: “Predislocation Syndrome of the Lesser Metatarsophalangeal Joint: A Distinct Clinical Entity,” in Reconstructive Surgery of the Foot and Leg: Update ’95, ed by CA Camasta, NS Vickers, SR Carter, p 109, The Podiatry Institute, Tucker, GA, 1995. 7. B RANCH HE: Pathologic dislocation of the second toe. J Bone Joint Surg Am 19: 978, 1937. 8. D U V RIES HL: Dislocation of the toe. JAMA 160: 728, 1956. 9. M ANN RA, M IZEL MS: Monoarticular synovitis of the metatarsophalangeal joint: a new diagnosis? Foot Ankle 6: 18, 1985. 10. MILLER SJ: “Transverse Plane Metatarsophalangeal Joint Deformity: Another Etiology and Solution,” in Reconstructive Surgery of the Foot and Leg: Update ’98, ed by SJ Miller, KT Mahan, GV Yu, et al, p 124, The Podiatry Institute, Tucker, GA, 1998. 11. C OUGHLIN MJ, M ANN RA: “Lesser Toe Deformities,” in Surgery of the Foot and Ankle, 7th Ed, Vol 1, ed by RA Mann, MJ Coughlin, p 351, CV Mosby, St Louis, 1999. 12. F ISHCO WD: “The Sub-Two Syndrome,” in Reconstructive Surgery of the Foot and Leg: Update ’98, ed by SJ Miller, KT Mahan, GV Yu, et al, p 107, The Podiatry Institute, Tucker, GA, 1998. 13. R OOT ML, O RIEN WP, W EED JH: Normal and Abnormal Function of the Foot, p 218, Clinical Biomechanics Corp, Los Angeles, 1977. 14. COOPER PS: “Disorders and Deformities of the Lesser Toes,” in Foot and Ankle Disorders, Vol 1, ed by MS Myerson, p 308, WB Saunders, Philadelphia, 2000. 15. J OHNSTON RB, S MITH J, D ANIELS T: The plantar plate of the lesser toes: an anatomical study in human cadavers. Foot Ankle 15: 276, 1994. 16. D ELAND JT, L EE KT, S OBEL M, ET AL : Anatomy of the plantar plate and and its attachments in the lesser metatarsophalangeal joint. Foot Ankle 16: 480, 1995. 17. B HATIA D, M YERSON MS, C URTIS MJ, ET AL : Anatomical restraints to dislocation of the second metatarsophalangeal joint and assessment of repair technique. J Bone Joint Surg Am 76: 1371, 1994.

198

18. DELAND JT, SUNG I: The medial crossover toe: a cadaveric dissection. Foot Ankle 21: 375, 2000. 19. M C G LAMRY ED: “Lesser Ray Deformities,” in Comprehensive Textbook of Foot Surgery, 2nd Ed, Vol 1, ed by ED McGlamry, AS Banks, MS Downey, p 321, Williams & Wilkins, Baltimore, 1992. 20. S ARRAFIAN SK, T OPOUZIAN LK: Anatomy and physiology of the extensor apparatus of the toes. J Bone Joint Surg Am 51: 669, 1969. 21. BOJSEN-MOLLER F: Anatomy of the forefoot, normal and pathologic. Clin Orthop 142: 10, 1979. 22. J ARRETT BA, M ANZI JA, G REEN DR: Interossei and lumbricales muscles of the foot: an anatomical and functional study. JAPA 70: 1, 1980. 23. HATCH DJ, BURNS MJ: An anomalous tendon associated with crossover second toe deformity. JAPMA 84: 131, 1994. 24. KARPMAN RR, MACCOLLUM MS: Arthrography of the metatarsophalangeal joint. Foot Ankle 9: 125, 1988. 25. YAO L, DO HM, CRACCHIOLO A, ET AL: Plantar plate of the foot: findings on conventional arthrography and MR imaging. AJR Am J Roentgenol 163: 641, 1994. 26. Y AO L, C RACCHIOLO A, F ARAHANI K, ET AL : Magnetic resonance imaging of plantar plate rupture. Foot Ankle 17: 33, 1996. 27. R EIS ND, K ARKABI S, Z INMAN C: Metatarsophalangeal joint dislocation after local steroid injection. J Bone Joint Surg Br 71: 864, 1989. 28. N OYES FR, N USSBAUM NS, D E L UCAS JL, ET AL : Biomechanical and ultrastructural changes in ligaments and tendons after corticosteroid injection. J Bone Joint Surg Am 57: 876, 1975. 29. G RAY RG, G OTTLIEB NL: Intra-articular steroids: an updated assessment. Clin Orthop 177: 235, 1983. 30. TREPMAN E, YEO S: Non-operative treatment of metatarsophalangeal joint synovitis. Foot Ankle 16: 771, 1995. 31. RUCH JA: “Use of the EDB Tendon for Muscle-Tendon Balance of the Lesser MPJ,” in Reconstructive Surgery of the Foot and Leg: Update ’95, ed by CA Camasta, NS Vickers, RS Carter, p 114, The Podiatry Institute, Tucker, GA, 1995.

April 2002 • Vol 92 • No 4 • Journal of the American Podiatric Medical Association

32. DELAND JT, SOBEL M, ARNOCZKY SP, ET AL: Collateral ligament reconstruction of the unstable metatarsophalangeal joint: an in vitro study. Foot Ankle 13: 391, 1992. 33. F ORD LA, C OLLINS KB, C HRISTENSEN JC: Stabilization of the subluxed second metatarsophalangeal joint: flexor tendon transfer versus primary repair of the plantar plate. J Foot Ankle Surg 37: 217, 1998. 34. GAZDAG A, CRACCHIOLO A: Surgical treatment of patients with painful instability of the second metatarsophalangeal joint. Foot Ankle 19: 137, 1998. 35. GIRDLESTONE GR: Physiotherapy for the hand and foot. J Chartered Soc Physiotherapy 32: 167, 1947. 36. TRNKA HJ, MUHLBAUER M, ZETTL R: Comparison of the Weil and Helal osteotomies for the treatment of metatarsalgia secondary to dislocation of the lesser metatarsophalangeal joints. Foot Ankle 20: 72, 1999. 37. RUCH JA: “A Surgical Technique for the Repair of the Predislocation Syndrome,” in Reconstructive Surgery of the Foot and Leg: Update ’97, ed by NS Vickers, SJ Miller, KT Mahan, et al, p 7, The Podiatry Institute, Tucker, GA, 1997.

38. KUWADA GT, DOCKERY GL: Modification of the flexor tendon transfer procedure for the correction of flexible hammertoes. J Foot Ankle Surg 19: 38, 1980. 39. SCHUBERTH JM, JENSEN R: “Flexor Digitorum Longus Transfer for Second Metatarsophalangeal Joint Dislocation/Subluxation,” in Reconstructive Surgery of the Foot and Leg: Update ’97, ed by NS Vickers, SJ Miller, KT Mahan, et al, p 11, The Podiatry Institute, Tucker, GA, 1997. 40. DALY PJ, JOHNSON KA: Treatment of painful subluxation at the second and third metatarsophalangeal joints by partial proximal phalanx excision and subtotal webbing. Clin Orthop 278: 164, 1992. 41. C RACCHIOLO A 3 RD , K ITAOKA HB, L EVENTEN EO: Silicone implant arthroplasty for second metatarsophalangeal joint disorders with and without hallux abducto valgus deformities. Foot Ankle 9: 10, 1988. 42. VANDEPUTTE G, DEREYMAEKER G, STEENWERCKX A, ET AL: The Weil osteotomy of the lesser metatarsals: a clinical and pedobarographic follow-up study. Foot Ankle 21: 370, 2000.

Journal of the American Podiatric Medical Association • Vol 92 • No 4 • April 2002

199