Podiatry Institute Manual

PODIATRY

INSTITUTE•

THE P.I. MANUAL A Handbook of Podiatric Medicine and Surgery

2nd Edition

The Podiatry Institute Decatur, Georgia D. Scot Malay, DPM, MSCE, FACFAS, Editor

Podiatry Institute Publishing, Inc. Decatur, Georgia

©2006 by The Podiatry Institute, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system or transmitted in any form or by any means electronic, mechanical, photocopy, recording, or otherwise without the prior written consent of the publisher. For information write Podiatry Institute Publishing, 2675 North Decatur Road, Suite 309, Decatur, GA 30033.

Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the editor and publisher are not responsible for errors or omissions, or for any consequences from application of the

information in this book, and make no warranty, express or implied, with respectto the contents of the publication. The reader is urged to check the package insert of all drugs for current recommendations regarding indications and dosage, and for added warnings and precautions.

20<0811.08

Contents

Chapter 1. Selected Anatomy & Normal Physiology Osteology Arthrology Myology Tendons, Sheaths and Bursae Neurology Angiology Chapter 2. Basic Pathophysiology Skin Wounds and Healing Bone Healing Cartilage Healing Tendon, Ligament and Joint Capsule Healing Peripheral Nerve Wounds and Healing Chapter 3. Selected Diseases and Pathological Conditions Dermatoses and Common Skin Pathology Bacterial Infection Acquired Immunodeficiency Syndrome (AIDS) Peripheral Vascular Diseases Diabetes Mellitus Thyroid Disease Hepatitis Arthritides Neurological Disorders Neoplasms Selected Emergency Situations Basic Cardiac Life Support

1

2 6 12 13 17

22 24 29 29 30 33 40

51 52

59 60 61 61

68 71

81 86

Chapter 4. Selected Diagnostic Techniques History and Physical Examination Diagnostic Imaging Clinical Laboratory Testing Neurological and Electroneurodiagnostic Evaluation Vascular Examination Biomechanics

94 101 104 106

Chapter 5. The Peri operative Patient Preoperative Phase Intra-operative Phase Postoperative Phase

116 116 117

89 89

iv

Contents

Chapter 6. Fundamental Techniques and Procedures Suture Materials Biopsy Techniques Plastic Surgery Techniques Bone Grafting and Orthobiological Agents Selected Endoscopic Techniques Laser Surgery Microsurgery Selected Tendon Lengthening and Transfer Internal Skeletal Fixation External Skeletal Fixation Hemostasis Anesthesia Padding, Straping, Bracing and Prostheses

'.-,.

123 124 126 131 134 137 140 140 146 152 154 157 161

Chapter 7. Basic Reconstructive Foot and Ankle Surgery Toenail Surgery Sunbungual Exostosis Hammertoes Bunion Deformity and Hallux Abductovalgus Hallux Limitus/Rigidus Hallux Varus Hallux Interphalangeal Arthrodesis First Metatarsocuneiform Exostosis Intermediate (Central) Metatarsalgia & Deformities Fifth Metatarsal Surgery and the Tailor's Bunion Heel Surgery Ankle Equinus Nerve Entrapments and Acquired Neuropathy Amputations

184 191 192 193 194 196 198 204 208 213

Chapter 8. Major Reconstructive Foot and Ankle Surgery Collapsing Pes Valgo Planus Pes Cavus Rheumatoid Foot and Pan Metatarsal Head Resection Ankle and Pantalar Fusion Total Ankle Replacement

214 219 223 225 228

163 165 166 171

Contents

v

Chapter 9. Congenital Deformities and Juvenile Surgery Macrodactyly Syndactyly Polydactyly Congenital Hallux Varus Congenital Hallux Abductus lnterphalangeus Congenital Curly (Underlapping) Toe Congenital Overlapping (Fifth) Toe Cleft Foot

229 229 231 232 232 232 232 233

Brachymetatarsia

233

Metatarsus Adductus

234

Talipes Equinovarus

237

Congenital Calcaneovalgus Congenital Vertical Talus Tarsal Coalition Pediatric In-Toe Deformity Pediatric Toe-Walking Gait

239 239 241 242 242

Micromelia

242

Congenital Hemihypertrophy Ostechondroses

242 243

Chapter 10. Management of Foot and Ankle Trauma Selected Soft Tissue Injuries ~~ffis

Chapter 11. Foot and Ankle Disability and Rehabilitation Disability

Chapter 12. Evidence~ Based Medicine and Clinical Research Levels of Clinical Evidence and Clinical Research Design Options

244

m

282

285

The Building Blocks of Clinical Evidence

286

Fundamental Elements of Scientific Publication

286

Appendices Oral Exam TestTaking Algorithm Informed Consent Hospital Admission Orders Hospital Postoperative Orders Hospital Discharge Orders

293 294 294 295 295

Ch. 1

Selected Anatomy & Normal Physiology

Selected Anatomy & Normal Physiology OSTEOLOGY Table 1-1: LEG AND FOOT OSSIFICATION DATES

OSSICLE

PRIMARY OSSIFICATION CENTER APPEARS (YEARS)

EPIPHYSIS APPEARS (YEARS)

OSSIFICATION CENTERS FUSE (YEARS)

Proximal phalanx

Birth

2-3 (base)

15-21

Middle phalanx

Birth

2-3 (base)

15-21

Distal phalanx

Birth

2-3 (base)

15-21

1st metatarsal

Birth

2-3 (base)

15-18

2nd metatarsal

Birth

2-3 (head)

15-18

3rd metatarsal

Birth

2-3 (head)

15-18

4th metatarsal 5th metatarsal

Birth

2-3 (head)

15-18

Birth

2-3 (head)

15-18

5-12 (apophysis)

15-20

Medial cuneiform

3-4

Middle cuneiform

3-4

Lateral cuneiform

Birth-1

Cuboid

Birth-1

Talus

Bith

Calcaneus

Birth

Navicular

3-4

Sesamoids

9-11

Fibula

Birth (shaft)

2 (distal) 3-4 (proximal)

11-14 14-21

libia

Birth (shaft)

2 (distal) Birth (proximal)

17-19 19-21

ACCESSORY OSSICLES These are developmental anomalies, often separations of normal processes or tubercles, and need to be differentiated from avulsion fractures if there is a history of injury.

2

Pertinent Anatomy & Normal Physiology

Ch. 1

Table1-2: ACCESSORY OSSICLES ACCESSORY OSSICLE

lOCATION

Os tibiale externum

Posteromedial aspect tuberosity of navicular, within insertional

{accessory navicular)

fibers of tibialis posterior.

Os Vesalianum

Proximal to well-formed tip of the tuberosity of the 5th

metatarsal

base; to be differentiated from fracture of the tip of the 5th metatarsal base, or nonunited or fragmented apophysis.

Os peroneum

Sesamoid bone within the peroneus brevis tendon insertion at

the 5th metatarsal base. Os supranaviculare (talonavicular)

Dorsal apsect oftanlonavicular joint.

Os intermetatarseum

Between the medial cuneiform and the 1st and 2nd metatarsal bases.

Os sustentaculi

Posterior aspect of sustentaculum tali.

Os calcaneus secondarius

Dorsum anterior process of the calcaneus, at the junction of the calcaneus, cuboid, head of the talus and the navicular.

Os trigonum

The separated posterolateral tubercle of the talus; to be distinguished from the intact trigonal process and fracture thereof !Shepherd's fracture).

Os sublibulare

Distal to the tip of the fibular malleolus; to be distinguished from an avulsion fracture of lateral malleolus.

Os subtibiale

Distal to the tip of the tibial malleolus; to be distinguished from an avulsion fracture of the medial malleolus.

Os cuneo~ 1~ metatarsale-1 ~p lantare

Plantar aspect of the 1stmetatarsal~medial cuneiform articulation.

ARTHROLOGY Interphalangeal Joints IIPJ) (Fig. 1.1) Ginglymus (hinge) joints with capsule that is hooded dorsally by the fibrous extensor expansion and the plantar ligament {flexor plate); reinforced with medial and lateral collateral ligaments running obliquely from the head of one phalanx to the base ofthe next, in a proximal~dorsal to distal~plantar direction. A plantar IPJ sesamoid may be present. lesser Metatarsophalangeal Joints IMTPJ) (Fig. 1.2) Spheroidal joints contained within a capsule that is contiguous with the extensor hood expansion dorsally, and the thickened flexor (plantar) plate. The capsule is reinforced medially and laterally by collateral and suspensory ligaments. The collateral ligament runs obliquely, proximal~dorsal to distal~plantar, from the metatarsal head to the phalangeal base. The suspensory ligament is a continuation of the extensor hood expansion that descends vertically to the plantar plate, which is tethered to the adjacent MTPJ flexor plate by the deep transverse intermetatarsalligament. A plantar sesamoid may be invested within the flexor plate of a lesser MTPJ.

Ch. 1


Figure 1.1

Figure 1.2

Slip from EHL or Ant. Tib.

ha!licus brevis

Tib. sesamoid lig.

Transverse

metatarsallig. lntersesamoidal

Figure 1.3

Plant. tib .. sesamoid lig. Flexor hallicus longus

3

4


Pattern of dorsal tarsometatarsal ligaments

Pattern of dorsal intermetatarsalligaments

Ch. 1

Pattern of intermetatarsal ligaments

Internal cuneiform

Cuboid

Navicular

Plantar tarsometatarsal ligaments

Pattern of interosseous tarsometatarsal ligaments

Figure 1.4 First Metatarsophalangeal Joint (1ST MTPJ) (Fig. 1.3) The 1st MTPJ is of particular importance because of the sesamoid apparatus and its

relationship to the deformities of hallux valgus and varus. The tibial and fibular sesamoids are tethered by the intersesamoidal and plantar sesamoidal ligaments, present medially and laterally, running from each sesamoid to the proximal phalangeal base. The conjoined head of adductorhallucis inserts plantarlateral intothefibularsesamoid, the 1stMTPJ lateral ligaments, and the base ofthe proximal phalanx. Tarsometatarsal Joints (TMTJ, USFRANC'S JOINT) (Fig. 1.4) Complex consisting of arf1culations of the metatarsal bases with the cuneiforms and the cuboid, stabilized by insertion of the base of the 2nd metatarsal (keystone) into the intercuneiform recess. The complex Is arched dorsally in both the frontal and sagittal planes. There are 3 capsular elements: medial, inveSting the interface between the 1st metatarsal base and medial cuneiform; intermediate, investing the interface between the·2nd and 3rd metatarsal bases and the intermediate and lateral cuneiforms; and lateral, investing the interface between the 4th and 5th metatarsal bases and the cuboid. The capsule is reinforced by dorsal intercuneiform and cuneocuboid, tarsometatarsal, intermetatarsal base, and plantar tarsometatarsal ligaments. Lisfranc's plantar ligament runs obliquely from the medial cuneiform to the 2nd metatarsal base plantarly. Calcaneocuboid Joint (CCJ) Saddle-shaped interface invested in capsule reinforced with dorsal, lateral, and medial ligaments. The medial ligament is actually the lateral, or calcaneocuboid, portion of the bifurcate ligament. The joint is also supported by the extracapsular long plantar calcaneocuboid ligament, which extends from the calcaneal tuberosity to the bases of the 2nd-5th metatarsal bases. Talocalcaneonavicular Joint(TCNJ) Commonly referred to as the talonavicular joint, an essentially condylar joint complex that suspends the head of the talus in the midfoot's acetabulum pedis. The acetabulum pedis

Ch. 1


5

consists ofthe concavity ofthe posterior surface of the navicular, the anterior and middle facets ofthe sustentaculum tali of the calcaneus, and the plantar calcaneonavicular (spring) ligament. The TCNJ's capsule is reinforced by the spring ligament, the calcaneonavicular portion of the bifurcate ligament and dorsal talonavicular ligaments. The spring ligament is

crucial to arch support. Midtarsal Joints (MTJ) Complex consisting of the talonavicular and calcaneocuboid joints, and functions reciprocally with the subtalar (talocalcaneal) joint. The STJ and MTJs are generally considered a reciprocating complex. The transverse (Kite's angle) and sagittal plane radiographic cyma lines are useful guides to subluxation of the MTJ. Subtalar Joint (STJ) A modified ginglymus \hinge) joint displaying triplanar motion that occurs primarily in the frontal plane, as inversion and eversion. Anatomically, the STJ is defined as the interface between the posterior facets of the calcaneus and the talus. Functionally, the STJ includes the posteriorfacets of the calcaneus and talus, as well as the anterior and middle calcaneal facets of the sustentaculum (an anatomical component of the talocalcaneonavicular joint), and the sinus tarsi. The sinus tarsi consists ofthe dorsal concavity of the neck of the talus and the plantar sulcus between the posterior facet and the sustentaculum tali of the calcaneus. The sinus tarsi is widest laterally, and is reinforced posteriorly by the talocalcaneal Y-ligament, which also envelops the FHL tendon between the posterior processes ofthe body of the talus. The posterior facets are stabilized anteriorly, medially, and laterally by ligaments. The interosseous talocalcaneal ligament is situated posteriorly in the sinus Oust anterior to the posterior facet), and resists supination ofthe STJ. The cervical ligament is located at the anterolateral aspect ofthe sinus tarsi, between the talus and calcaneus, and resists supination of the STJ. Talocrural (Ankle) Joint A modified ginglymus (hinge) jointthat displays triplanar motion that occurs primarily in the sagittal plane, as dorsiflexion and plantartlexion. The ankle mortise consists of the concave distal tibial-bearing surface (plafond), the triangular facet of the lateral malleolus, the comma-shaped facet of the medial malleolus, and the anterior portion of the distal tibiofibular syndesmotic ligament The capsule may communicate with the peroneal tendon sheath, and is reinforced by the deltoid ligament (medial collateral) and the lateral collateral ligament. The deltoid ligament consists of the deep anteriortibiotalar component; and superficial tibionavicular, tibiocalcaneal, and posterior tibiotalar components. The lateral collateral ligament consists of the intra-capsular anteriortalofibular (ATFL), and the extracapsular calcaneofibular (CFL) and posterior talofibular (PTFL)Iigaments. The ATFL resists ankle plantarflexion, and anterior subluxation (anterior drawer stress) of the talus out of the mortise. The CFL is deep to the peroneal tendons, and inversion injury often disrupts both the CFL and the peroneal sheath. Clinically and radiographically, anterior drawer and inversion stress manipulation ofthe latera! collateral ligaments, and more commonly MRJ, are used to assess the injured ankle.

Tibiofibular Joints The tibiofibular joints include the proximal, interosseous, and distal tibiofibular joints. The proximal joint is planar, and supported by anterior and posterior ligaments. The interosseous


6

Ch. 1

membrane (10) consists of obliquely oriented, dense fibrous connective tissue running from proximal-medial to distal-lateral from the tibia to the fibula. The fibula is also situated slightly posterior to the tibia, !important when transferring tendon through the 10 membrane). The distal tibiofibular joint is supported by anterior, 10, and posterior ligaments. The tibiofibular joints allow motion in frontal and transverse planes, and resists ankle dorsiflexion as the

wider anterior portion of the talar dome engages the mortise.

MYOLOGY The intrinslc pedal muscles comprise 41ayers ln the plantar vault, innervated by the deep peroneaiiEDB; 2nd, 3rd and 4th dorsal ID), medial plantar IFDB, FHB, abductor hallucis, 1st lumbrical), and lateral plantar lOP, abductor digiti minimi, flexor digiti minimi, aJIIO, alllumbricals exceptthe 1st, and adductor hallucis) nerves. Plantar layer I

Abductor Ha/lucis origin------medial calcaneal wall. insertion------tibial sesamoid and medial base of proximal phalanx of hallux (Fig. 1.5). Flexor Digitorum Brevis

origin---calcaneal tuberosity, divides at base of proximal phalanx. insertion-plantar surface of middle phalanx IFig. 1.6).

Abductor Digiti Quinti origin---lateral calcaneal wall. insertion---lateral aspect base of proximal phalanx (Fig. 1.7).

I

I.

plantar nerve plantar artery

plantar artery

Figure 1.5

Figure 1.6

Figure 1.7

Ch. 1


7

Plantar Layer II Quadratus Plantae origin------2 calcaneal heads.

insertio{}-lateral aspect of FDL tendon before it divides IFig. 1.B).

Lumbricales origin------1st, from medial aspect of FDL to 2nd toe; 2nd, from contiguous aspects of 1st and 2nd FDL tendons; 3rd, from contiguous aspects of 2nd and 3rd FDL tendons; 4th, from contiguous aspects of 3rd and 4th FDL tendons.

insertion-media! aspect of mid-portion of proximal phalanges and fibrous expansion of the dorsal hood of the 2nd-5th toes IFig. 1.9).

plantar artery

Figure l.B

Figure 1.9


8

Ch. 1

Plantar layer Ill Flexor Hallucis Brevis

origin--media[ arm from tendons oftibialis posterior inserting into the metatarsal bases, and lateral arm from the cuboid, 3rd cuneiform,· peroneus longus tendon, and long and short plantar ligaments. insertion-base of proximal phalanx on medial and lateral aspects, after investing 1st MTPJ

sesamoids and plantar plate !Fig. 1.10). Adductor Hal/ucis

origin-oblique head arises from 2nd, 3rd, 4th metatarsal bases. insertion-into fibular sesamoid, plantar plate, and lateral aspect base of proximal phalanx origin-transverse head arises from plantar plates of 3rd, 4th, 5th MTPJs. insertion-into fibular sesamoid, plantar plate, and lateral aspect base of proximal phalanx !Fig. 1.11).

Flexor Digiti Minimi Brevis origin-plantar aspect of cuboid and 5th metatarsal base. insertion-plantar aspect base of proximal phalanx of 5th toe IFig. 1.12).

JIFl/--FiJ·s1 plantar metatarsal

artery

Figure 1.10

Figure 1.11 Superficial branch of lateral plantar nerve Lateral--j~

plantar artery

Figure 1.12

Ch. 1


9

Plantar layer IV Dorsa/Interossei (10)

origin---1st, adjacent surfaces of 1st and 2nd metatarsals; 2nd, adjacent surfaces of 2nd and 3rd metatarsals; 3rd, adjacent surfaces of 3rd and 4th metatarsals; 4th, adjacent surfaces of 4th and 5th. insertion-1st, base of proximal phalanx of 2nd toe medially; 2nd-4th, lateral aspect of bases of proximal phalanges oftoes 2, 3, and 4(Fig. 1.13). Plantar Interossei (10)

origin-medial aspect of 3rd, 4th, 5th metatarsal shafts and bases.

inseltion-medial aspect of bases of proximal phalanges of toes 3, 4, and 5(Fig. 1.14).

Dorsal metatarsal arteries

Plantar metatarsal arteries

Superficial-b/1it'&~~

branch of lateral

plantar ne!Ve

Deep branch

of lateral plantar nerve

Figure 1.13

Figure 1.14

Dorsal Intrinsic Muscles

Extensor Digitorum et Hallucis Brevis origin-lateral aspect of the calcaneal sulcus and the cervical ligament; forms four slips that course distally. insertio/'1------lateral aspect of EDL tendons to 2nd through 4th toes, and dorsal aspect of the proximal phalanx otthe hallux or the lateral aspect ofthe EHLtendon. EDB is innervated by the deep peroneal nerve.

EXTRINSIC PEDAL MUSCULATURE Anterior Leg Compartment The anterior leg compartment contains the muscles tibialis anterior \TA), extensor ha!lucis longus (EHL), extensor digitorum longus (EDL), and peroneus tertius (PT). Each of these is innervated by the deep peroneal nerve and supplied by the anterior tibial artery. The tendons of these muscles traverse deep to the transverse and cruciate crural ligaments.

10


Ch. 1

Tibialis Anterior (TAl

origin--most medial ofthe anterior crural muscles, from the lateral superior condyle and shaft of the tibia, 10 membrane, deep crural fascia, and intermuscular septum adjacentto EDL

insettion-90% into the medial cuneiform,-10% into the base of the 1st metatarsal Extensor Digitomm Longus (EDL)

origin-superior lateral condyle of the tibia and the proximal% of the fibula, 10 membrane, crural fascia, and intermuscular septae common to TA and PL; the tendon divides into four major slips that course distally insertion-into each of the 4 lesser toes. In the digit, the tendon divides into a central slip that inserts into the dorsal central aspect of the base of the middle phalanx~ and medial and lateral collateral slips that course along the medial and lateral aspects of the middle phalanx before they reunite and insert as a single tendon into the dorsal surface of the distal phalanx. The tendons also yield medial and lateral fibrous expansions at the level of the head of the metatarsal and MTPJ, creating the dorsal hood that also serves as an insertion point for the dorsal and plantar 10 and the lumbricales.

Extensor Hal/ucis Longus (EHL) origin--inferior to TA and EDL, from the fibula, 10 membrane, and adjacent intermuscular septae. insertion--dorsal aspect of base of the distal hallucial phalanx

Extensor Hallucis Accessorius origin-medial aspect of EHL in the distal leg, ankle, or foot.

insertion-dorsa! and medial aspects of the base of the proximal hallucial phalanx. Peroneus Terlius origin-inferior third ofthe anteromedial surface of the fibula and the 10 membrane.

insertion-base of the 5th metatarsal. lateral Leg Compartment The lateral leg (peroneal) compartment contains both the peroneus longus (PL) and peroneus brevis IPB). The muscles are supplied by the peroneal artery and the superficial peroneal nerve, and they traverse deep to the peroneal retinaculum distal to the lateral malleolus. Peroneus Longus (PL) origin--head and proximal half of the fibula, deep crural fascia, and the anterior and posterior peroneal septae. The muscle is superficial to the peroneus brevis at the myotendinous junction proximal to the lateral malleolus, and must be retracted when harvesting the underlying brevis for some lateral ankle stabilization. The tendon then courses around the lateral malleolus, to the plantar-lateral aspect of the cuboid, where it turns medially into the peroneal groove deep to the long plantar calcaneocuboid ligament. inseJtion---plantar-latera! aspect of the base of the 1st metatarsal. Peroneus Brevis (PB) origin--anterior to PL from the distal 2/3 of the fibula, and the anterior and posterior peroneal septae; just distal to the latera! malleolus, the PB tendon is superior and anterior to the tendon of PL. insertiof}-base of the 5th metatarsal.

Ch. 1


11

Superficial Posterior leg Compartment The superficial posterior leg compartment contains the triceps surae, which converge to form the tendoAchillis that inserts into the posterior aspect of the calcaneus. The muscles include gastrocnemius and soleus, and are innervated by branches of the tibial nerve, and supplied by the posterior tibial artery. The triceps surae plantarflex the ankle, with some inversion, and extend the knee by virtue of the femoral origin of gastrocnemius.

Gastrocnemius origin------as two heads, larger medially, from the medial and lateral condyles of the femur posteriorly.

insertion------as Achilles tendon into the central third of the posterior surface of the calaneus. Soleus origin-head and proximal third of the fibula and the middle third of the tibia above the popliteal line. insertiof}-----as Achilles tendon into the central third of the posterior surface of the calaneus.

Plantaris origi(}-medial to the lateral head of the gastrocnemius at the lateral condyle of the femur, coursing lateral to mediaL

inseraan---medial aspect of the tendoAchillis and, along with the Achilles, into the calcaneus. Deep Posterior leg Compartment The deep posterior leg compartment contains tibialis posterior ITP), flexor digitorum longus IFDL), and flexor hallucis longus IFHL). The muscles are innervated by the tibial nerve, and

supplied by the posterior tibial artery. The tendons of these muscles traverse deep to the flexor retinaculum \laciniate ligament) to enter the plantar vault. Tibialis Posterior (TP) origf(}-from the posteromedial aspect of the fibula, the posterior aspect of the tibia distal to the popliteal line and lateral to the vertical line, the 10 membrane, and adjacent intermuscular septae; FHL and FDL both overlap the belly ofTP; and TP passes through the first !medial) canal of the tarsal tunnel. insertion----primarily into the tuberosity of the navicular, with additional slips inserting into the plantar aspect of the intermediate 3 metatarsal bases and everytarsa! exceptthe talus.

Flexor Digitorum Longus (FDL) origin--from the posterior aspect of the tibia distal to the solealline, and from fascia ofTP; the tendon traverses the second canal of the tarsal tunnel to enter the foot where it first crosses superficial to FHL, and then over TP, where it shares a vinculus {master knot of Henry) with FDL; thereafter, FDL splits into 4 slips. insertion----into the plantar aspect of the distal phalanx of the lesser 4 toes. Flexor Hallucis Longus (FHL) origin-from the distal2/3 ofthe posterior surface of the fibula, the posterior aspect of the peroneal septum, the anterior surface of the deep transverse intermuscular septum !separating the superficial and deep posterior groups), and the fascia aboutTP. The tendon courses through the fourth canal of the tarsal tunnel. insertion-into the plantar aspect of the base of the distal phalanx of the hallux.

12


Ch. 1

TENDONS, SHEATHS liND BURSAE Tendon Structure Tendons consist of dense regular connective tissue made up oftropoco!lagen units, created by fibroblasts, and organized to form collagen fibers. The fibers are supported within

endotenon, and grouped into fasciculi which are contained within an outer epitenon. The epitenon defines the anatomical tendon. Go!gi tendon organs within tendon fibers inhibit skeletal muscle contraction when excessive tension is registered. The organized tendon is further surrounded, outside of the epitenon, by a loose, areolar and highly vascularized

paratenon, wherever the tendon courses a straight line. Paratenon is contained deep to, and adherent to, the deep fascia \muscle fascia); or it is adherent to a neighboring intermuscular septum (fascia) betvveen intact skeletal muscle bellies; or it may be adherent to deeper periosteum. Tendon Sheath and the Gliding Mechanism A tendon sheath exists where a tendon changes direction, such as about the ankle deep to the extensor, peroneal, and flexor retinaculae. The sheath is distinct from paratenon and Consists of a fibrous outer septum with a synovia! lining, much akin to joint capsule. Synovial fluid bathes the tendon within the sheath. Within the sheath, on the tendon's deep {non-friction) surface, a synovium lined fold of connective tissue called mesotenon, conveys vascularity and further supports the tendon. Mesotenon attaches to the epitenon at the hilus. At the proximal margin of the tendon sheath a double fold of paratenon, termed a plicae duplicata, invaginates a short distance into the sheath and adheres to epitenon. Similarly, at the distal margin of the sheath, a single fold of paratenon, termed a plica simplex, protrudes into the sheath. As muscle contracts, the plicae unfold and elongate as the tendon glides within the sheath as the tendon changes direction, or within paratenon where the course is straight Tendon Blood Supply Tendon has three primary sources of blood supply: proximally, at the myotendinous junction perimysial blood vessels from the muscle belly; centrally, from paratenon and/or mesotenon; and distally, insertional periosteal vessels from bone. Synovial fluid within the sheath, and local lymphatics within the paratenon, also nourish and drain metaboliTes from the tendon. Occasionally, a condensed, highly organized fibrous connection, know as a vinculus, may also convey vascularity between closely approximated tendons. The Master Knot of Henry, between the tendons of FHL and the more superficial(plantar) FDL, at a level consistent with the distal margin of the sustentaculum, is just such a vinculus. Vinculi also exist between FHB and FDL near their phalangeal insertions. Subfascial and Subcutaneous Bursae

A variety of bursae occur in the foot and ankle. Bursae protect tendon and muscle from excessive friction or pressure caused by adjacent muscle, ligament or bone, or external forces in the case of an adventitious bursa. Subfascia! bursae include the retrocalcaneaf or pre-Achilles bursa, those at the insertions ofTA, TP, and the 10; and those between the bellies of adductor digiti minimi and the 5th metatarsal, and the belly of FHB and the medial cuneiform. Subcutaneous bursae are usually adventitious in origin, and may present at the

Cll. 1


13

head of the 1st and 5th metatarsals, plantar to the tuberosity of the calcaneus (present in about 50% of specimens), at the medial and lateral malleoli, and occasionally posterior to tile insertion of tile Achilles tendon.

NEUROLOGY The lower extremity nerve supply originates in the lumbosacral spine, and specifically involves spinal nerve roots L4-S3. The spinal nerve roots traverse the lumbosacral plexus to form the sciatic nerve, which divides into the tibial nerve and the common peroneal nerve near the junction of the middle and distal thirds of tile thigh.

Table1.3. MOTOR INNERVATION TO THE LEG AND FOOT

MUSCLE

PERIPHERAL NERVE

Tibialis anterior Extensor digitorum longus Extensor hallucis longus Peroneus tertius Gastrocnemius Soleus Plantaris Popliteus Fexor ha!lucis longus Flexor digitorum longus Tibialis posterior Peroneus longus Peroneus brevis Extensor digitoum brevis Abductor hallucis Flexor digitorum brevis First lumbricalis Flexor hallucis brevis Abductor digiti quinti brevis Quadratus plantae Second, third, fourth lumbricales Adductor hallucis Flexor digiti quinti brevis Plantar interossei First, second dora! interossei Third, fourth dorsal interossei

Deep peroneal Deep peroneal Deep peroneal Deep peroneal 1ibial 1ibial 1ibial 1ibial 1ibial 1ibial 1ibial Superficial peroneal Superficial peroneal Deep peroneal Medial plantar Medial plantar Medial plantar Medial plantar lateral plantar Lateral plantar Lateral plantar lateral plantar lateral plantar lateral plantar Deep peroneal, lateral plantar Lateral plantar

SPINAL LEVEL

u,5 u,5 u.5 u,5 S1,2

Su Su

u.5s, s, u,5

Sz,3

L5Su L5Su Su S2.3

s2.3 S2,3 S2,3 S2,3 S2,3 S2,3 S2.3 Su S2,3 Su,3 S2,3

14


Ch. 1

COMMON PERONEAL NERVE The common peroneal nerve trifurcates near the head of the fibula, forming the lateral sural cutaneous nerve, the deep peroneal nerve, and the superficial peroneal nerve.

lateral Sural Cutaneous Nerve This nerve ultimately anastomoses with the medial sural cutaneous branch of the tibial nerve, to form the sural nerve. The Deep Peroneal Nerve (Anterior Tibial) (Fig. 1.15) This nerve begins atthe peroneal muscular hiatus between the fibula and peroneus longus, then passes deep to EDL on the 10 membrane to innervate TA, EHL, EDL, and PT. At the ankle, it divides into medial and lateral terminal branches.

The lateral terminal branch passes deep to, and innervates, EDB and then yields three interosseous branches which supply the 2nd, 3rd, and 4th dorsaiiO. The medial terminal branch runs parallel and lateral to the DP artery. The nerve divides at the first interspace into two dorsal digital nerves supplying adjacent sides of the great and second toes, and the first dorsal interosseous muscle {which is also innervated by the lateral plantar nerve). The muscular branches of deep peroneal nerve supply all anterior leg muscles, including peroneus tertius. The Superficial Peroneal Nerve The superficial peroneal nerve supplies both the peroneus longus and brevis muscles, then divides to form the medial and lateral dorsal cutaneous nerves.

The medial dorsal cutaneous nerve (Fig. 1.16) divides into two dorsal digital nerves, the medial dorsal digital branch that communicates with the medial terminal branch from deep peroneal nerve, to supply the medial aspect of the hallux. The lateral dorsal digital branch supplies the adjacent aspects of the 2nd and 3rd toes dorsally. The lateral dorsal cutaneous (Lemont's) nerve divides into a medial branch that supplies the adjacent sides of the 3rd and 4th toes, and a lateral branch that supplies the adjacent sides of the 4th and 5th toes.


Ch. 1

15

,s ,I

Dorsal proper

digital nerve

~

c

c

[

\.

Saphenous

nerve Medial terminal nerve branch of the deep peroneal nerve

Figure 1.15

Medial

Communicating

branch

dorsal~~~~~~r-.~:=~~o~~~~rve

cutaneous nerve

Intermediate dorsal

Figure 1.16

digital

Medial plantar nerve

Abductor hallucis

Figure 1.17

Figure 1.18

16


Ch. 1

TIBIAL NERVE The tibial nerve traverses the calf deep to the intermuscular septum between the superficial and deep crural compartments, and in the distal third of leg runs parallel and medial to the tendoAchillis. The tibial nerve yields the medial sural cutaneous nerve that unites with the lateral sura! cutaneous branch of the common peroneal nerve, to form the sural nerve. The Sural Nerve The sural nerve courses distally through the leg, then posterior and inferior to the lateral malleolus, en route to the lateral aspect of the foot and 5th toe. Just distal to the lateral malleolus, the sural nerve sends a communicating branch dorsally to anastamose with the

intermediate dorsal cutaneous nerve. The tibial nerve also provides articular branches that innervate the knee and ankle. In the calf, the tibial nerve innervates the popliteus, gastrocnemius, soleus, plantaris, TP, FOL, and FHL muscles. Prior to bifurcation into the medial and lateral plantar nerves, the tibial nerve yields the medial calcanean branch that emerges through the laciniate ligament to innervate the skin of the heel medially and plantarly.(Fig. 1.17) The medial calcanean nerve can be injured or entrapped in scar tissue following medial exposure (DuVries incision) of the heel, such as in plantar calcaneal spur surgery. The division of the tibial nerve into the medial and lateral plantar nerves usually occurs near the dorsal margin of the tarsal tunnel, however the bifurcation can occur at any level deep to the laciniate ligament, and occasionally it occurs proximal to the ligament In many cases oftarsal tunnel syndrome, operative inspection reveals a far distal bifurcation of the tibial nerve at the porta pedis where the medial plantar nerve enters the anterior chamber, and the lateral plantar nerve enters the posterior chamber, of the calcaneal tunnel which is the distal continuation of the tarsal tunnel deep to abductor hallucis. The anterior and posterior canals are separated by a fibrous septum coursing from the deep sutface of abductor hallucis to the medial wall of the body of the calcaneus plantar to the sustentaculum tali.

PlANTAR NERVE SUPPLY Medial Plantar Nerve(Fig. 1.18) The medial plantar nerve is usually slightly larger than the lateral plantar nerve, and traverses the 3rd canal of-the flexor retinaculum along with the medial plantar vessels. The medial plantar nerve yields cutaneous branches innervating the medial aspect of sole; muscular branches that supply FOB, FHB, abductor hallucis and the 1st lumbrical; the proper digital branch to the plantar-medial aspect ofthe hallux; and three common digital nerves that yield proper digital nerves to the contiguous surfaces of the 1st and 2nd, 2nd and 3rd, and 3rd and 4th toes. The 1st common or 2nd proper digital nerve yields a branch to innervate the 1st lumbrical muscle. The 3rd common or 4th proper digital nerve yields a branch that communicates with the lateral plantar nerve, and is often the site of Morton's neuroma. The proper digital nerves supplythe digital pulp, and the tips and sides ofthe toe, including the nail matrix.

The lateral Plantar Nerve The lateral plantar nerve courses through the porta pedis deep to the plantar fascia, and yields muscular branches to quadratus plantae and abductor digiti minimi; cutaneous

Ch. 1


17

branches to the lateral aspect of the sole; a superficial branch that divides into common and proper digital branches, and a deep branch. The proper digital branch supplies the lateral aspect of the 5th toe; and the flexor digiti minimi brevis as well as the 3rd plantar and 4th dorsa liD muscles. The common digital branch usually communicates with the digital branch of the medial plantar nerve (often the site of Morton's neuromaL before dividing into proper digital branches to the contiguous surfaces of the 4th and 5th toes. The deep branch of the lateral plantar nerve supplies all of the 10 muscles except the 4th dorsal and 3rd plantar in the 4th intermetatarsal space, all of the lumbricales except the 1st lumbrical, and adductor hallucis. Saphenous Nerve The saphenous nerve is the terminal continuation of the femoral nerve, and courses through the thigh to emerge from the adductor canal to become subcutaneous and continue distally along the anteromedial aspect of the leg and foot It yields a branch to the skin over the ankle, and a branch that courses distally to innervate the medial aspect of the tarsus and greattoe. ANGIOLOGY ARTERIAL SYSTEM The arterial supply to the lower extremities originates with the abdominal aorta, which bifurcates into right and left common iliac arteries, which then further divides to form internal and external iliac arteries. The external iliac artery becomes the femoral artery at the distal margin of the inguinal ligament. The femoral artery is palpable in the groin, and courses distally through the thigh to become the popliteal artery, which is palpable in the popliteal fossa. The popliteal artery yields muscular, cutaneous, and articular (knee) branches. The popliteal artery bifurcates to form the anterior and posterior tibial arteries at the lower border of popliteus. The anterior tibial artery courses through the crural 10 membrane to enter the anterior compartment of the leg where it descends to the ankle, where it becomes the dorsalis pedis artery. The anterior tibial artery courses between TA and EDLin the superior third of the leg, between TA and EHL in the middle third, deep to the tendon of EHL just proximal to the ankle and between the tendons of EHL and EDL atthe level of the ankle. The branches of the anterior tibial artery include: 1. Posterior recurrent tibial artery, posterior to 10 membrane 2. Anterior recurrent tibial artery, which joins the circumpatellar network 3. Muscular branches to TA, EDL, EHL, and peroneus tertius 4. Anterior medial malleolar artery 5. Anterior lateral malleolar artery The anterior leg muscles are supplied by muscular branches of the anterior tibial artery. The anterior medial malleolar artery anastomoses with branches of the posterior tibial and medial plantar arteries. The anterior lateral malleolar artery anastomoses with the perforating branch of the peroneal and lateral tarsal arteries.

18


Ch. 1

The dorsalis pedis artery, the second largest source supplying the foot, continues to the 1st intermetatarsa1 space, where it courses as the deep plantar branch to join the plantar arch IFig. 1.19). The branches of the dorsalis pedis artery include: 1. lateral tarsal artery; supplying EDB

2. medial tarsal artery 3. arcuate artery; yielding the 2nd, 3rd, and 4th dorsal metatarsal arteries

4. 1st dorsal metatarsal artery 5. deep plantar perforating branch The dorsal metatarsal arteries lie in the corresponding intermetatarsal spaces, deep to the extensor tendons and dorsal to the dorsal 10 muscles. Except the first dorsal

metatarsal artery, which yields the deep plantar perforating artery, the metatarsal arteries yield posterior and anterior perforating branches at the Ieve! of the metatarsal base and MTPJ, respectively. The arteries continue distally as common digital arteries, which divide into proper dorsal digital arteries that are of smaller diameterthan the plantar digital arteries. The posterior tibial artery, the largest source supplying the foot, is a terminal branch of the popliteal artery and courses through the leg to the third canal of the flexor retinaculum, then divides into medial and lateral plantar arteries deep to abductor hallucis in the calcaneal canals IFig. 1.20). The branches ofthe posterior tibial artery include: 1. circumflex fibular artery, which supplies soleus 2. peroneal artery, which supplies soleus, TP, FHL, PL, PB, and the fibula; and the perforating peroneal branch !third largest source supplying the foot) that pierces the 10 membrane proximal to the ankle to join with branches of the anterior tibial artery 3. nutrient artery to tibia, the largest nutrient artery in the body 4. muscular branches to soleus, TP, FHL, FDL 5. communicating artery that anastomoses with peroneal artery 6. medial malleolar branches 7. medial calcanean branches, which supply tendoAchillis and medial heel 8. medial plantar artery, medial to the medial plantar nerve 9. lateral plantar artery, which becomes the plantar arch and supplies all of the muscles of the sole, except abductor hallucis, FOB, and 1st dorsaiiO muscle. The plantar arch courses lateral to medial toward the first intermetatarsal space, where it anastomoses with the deep plantar perforating branch of the dorsalis pedis artery. The plantar arch separates the 3rd and 4th muscle layers, and yields anterior and posterior perforating arteries that anastomoses with corresponding perforators from the dorsum. The plantar arch yields 4 plantar metatarsal arteries, the first of which consists of the union ofthe lateral plantar and deep plantar branches. The plantar metatarsal arteries become common and then proper digital arteries to the corresponding toes. The plantar digital arteries are larger than the dorsal digital arteries. In the hallux, the lateral plantar digital artery is the largest, while in the lesser toes the medial plantar digital arteries are largest In the hallux, the dorsal digital arteries extend to the toe tip, as do the plantar digital arteries, the dorsal and plantar hallucial digital arteries supplying the hallux equally distal to the interphalangeal joint In the lesser toes, dorsal digital arteries extend to the level of the proximal ITPJ, while plantar digital arteries extend to the toe tip and then retrograde to supply the dorsal aspect of the toe, including the nail bed (Fig. 1.21).

Ch. 1

Pertinent Anatomy & Normal Physiology Proper dorsal

I

Lateral tarsal artery

artery

arteries

F"•Latecall calcaneal arteries

Figure 1.19

Figure 1.20 Proximal

nail fold

Lateral digital artery

Figure 1.21

Distal and proximal arches

19

20


Ch. 1

VENOUS SYSTEM The dorsal venous system of the foot and ankle consists of superficial and deep networks. The deep dorsal venous plexus converges to form the medial marginal vein. The superficial dorsal venous plexus is immediately subcutaneous, and contains the dorsal venous arch. The dorsal veins drain into the greater and lesser saphenous veins. On the plantar aspect, a superficial venous plexus drains into the deep venous plexus, which ultimately converges into the medial and lateral plantar veins, and communicates with the dorsal system via perforating veins.

lYMPHATIC SYSTEM Superficial lymphatics drain the skin of the toes, sole and heel, forming a medial system that drains into the inguinal lymph nodes and a lateral (rays 3-5) system that drains into the popliteal lymph nodes. The deep lymphatic system forms collecting ducts located dorsally, laterally (peroneal), and plantarly, and drain into major lymphatics corresponding to the adjacent anterior tibial, peroneal, and posterior tibia! vessels. The deep system drains primarily into the popliteal lymph nodes.

CUTANEOUS ANATOMY The skin consists of the epidermis and dermis (Fig. 1.22). The dermis consists of both reticular and papillary layers, and contains microcirculatory elements (arterioles, capillaries, venues, glom, and lymphatics), nerves and the annexed. Skin annexed include echini sweat glands and ducts, hair follicles and arrestor pile muscles, sebaceous glands at the base of the hair follicle (pilosebaceous gland), and the toenails and perionychium. Near the nail bed, arterioles shuntdirectlyto venules via the Hoyer-Susquet canal, to effect the glomus body important in temperature regulation. Eccrine glands are present on all pedal skin surfaces, and are innervated by sympathetic nerves. Pilosebaceous glands are only present on dorsal skin. Deep in the dermis, near the subcutaneous fat-superficial fascia junction, lie the Pacinian (Pacini-Vater) corpuscles important in touch-pressure sensation. The epidermis serves as a barrier, and contains five strata: basale, spinosum, granulosum, lucid urn, and corneum. Melanocytes with dendritic processes exist amongst the living cells of the stratum basale, and are responsible for melanin production which serves to protect underlying living cells from the mutagenic effects of UV radiation. langerhans immune cells, much like macrophages, as well as Merkel's sensory cells also exist in the epidermis. Relaxed Skin Tension lines (RSTl) (Fig. 1.23) The skin's intrinsic tension is oriented such that maximum tension is directed parallel to the long axis of the extremity. Intrinsic skin tension is generated by the forces of underlying bone and soft tissue prominence, as well as joint motion and extrinsic forces upon the skin. RSTLare oriented perpendicular to the long axis of the leg and foot, and can be clinically identified with the pinch test As a rule, elective skin incisions should be made parallel to the RSTL, as long as the exposure allows access to the underlying target structures and does not unduly violate vital structures (vessel, nerve, tendon).


Ch. 1

21

Epidermis Papillary granulosum

layer

1:5''?.'1~'f);j";fi'i1f--St<-spinosum

IK.'P.Cf0 :l'9""!!l-- Str. bas ale

Subcutaneous connective

tissue

Figure 1.22

j ___

_( Plantar

Medial

Figure 1.23

22

Basic Pathophysiology

Ch. 2

BASIC PATHOPHYSIOLOGY WOUNDS ANIJ HEALING This section will describe wounds and healing of a variety of tissues, including skin, bone, cartilage, tendon, ligament joint capsule, and nerve. Wound healing relies upon an adequate vascular supply and angiogenesis. Angiogenesis entails endothelial proliferation with resultant capillary budding.

SKIN WOUNDS AND HEALING Healing Phases Dermal wounds include Punctures, Abrasions, Incisions, and Lacerations (PAIL); as well as contusions, pressure injuries, mechanically or chemically induced and hypersensitivity related bullae, burns and frostbite. The epidermis repairs by means of epithelial cell mitosis that continues until contact inhibition occurs. The underlying dermis heals in three phases: inflammatory, fibroproliferative, and maturation. Inflammatory Phase

The inflammatory (substrate or lag) phase begins immediately upon wounding, comprises approximately 10% of the healing process, and is also referred to as the substrate, or lag phase because specialized blood cells and proteins necessary for healing are recruited and migrate to the wound at this time. After initial vasoconstriction, usually lasting several minutes, vasodilatation and erythema predominate during the inflammatory phase, which lasts for 3 or 4 days. Angiogenesis and capillary budding occur while fibroblasts lay down collagen in a random fashion, and tensile strength begins to return to the damaged skin. Superficially, epidermal epithelialization occurs concomitantly with dermal inflammation, and mitosis continues until contact inhibition occurs between epithelial cells, which ultimately seal the wound surface. Fibroproliferative Phase

The fibroproliferative (fibroblastic) phase comprises approximately 20% of the healing process, and lasts from the 3rd to 4th day, until the 14 to 21 day. Granulation tissue, which consists of new collagen and capillary buds, predominates and continues to form until the wound contracts and epithelialization is complete. Collagenation rapidly increases during this phase, and fibroblasts are the primary cell type present in the wound. The tensile strength of the wound approaches only about 35% of the local skin's original strength after 14 days and, at this point, the wound's main source of tensile strength comes from suture material used for primary closure. Maturation Phase

The maturation (remodeling) phase comprises approximately 70% of the healing process and lasts from approximately 3 weeks until one year post injury. During this phase, randomly arranged collagen fibers that were laid down during the fibroproliferative phase are microscopically debrided via macrophage enzymatic breakdown. New fibers are produced and aligned in response to mechanical forces, and wound contraction occurs in a centripetal direction (toward the center of the wound). Linear scar contraction occurs

Ch. 2


23

from both ends of the scar toward the center. This is important when planning an elective skin incision. The long axis of the anticipated scar should be oriented parallel to the axis of motion of the underlying joint. A scar that is perpendicular to the joint axis may cause a joint contracture due to scar contraction, often seen with a posterior longitudinal ankle or a dorsal longitudinal MTP joint incision. Skin Ulcers Dermal wounds that develop secondary to pressure, (typically chronic, non- traumatic weight-bearing or decubitus pressure), can result in ulceration. Technically, skin ulceration is defined as an open wound where the full thickness of skin is violated. The International Association for Enterostomal Therapy

(classifies pressure-induced cutaneous compromise) Stage 1: Epidermis intact, however erythema remains longer than 30 minutes after pressure relieved. Reversible with intervention. Stage II: Partial thickness skin loss, including epidermis and perhaps superficial dermis. There is surrounding induration, and local bullae or vesicles with erythema, tenderness (if not insensitive), and the base of wound is moist and necrosis free. Stage Ill: Full-thickness skin loss, through the dermis into subcutaneous fat and superficial fascia, effecting a crater. Necrotic eschar filling the crater and covering the base must be debrided in order to accurately stage the depth and properly categorize the wound. The central wound base is generally nontender. There is often undermining of the margin, sinus tract formation, local exudate, and a surrounding halo of erythema. Ascending cellulitis and infection may also be present Underlying osteomyelitis or, in the presence of an ischemic limb, subcutaneous gas or necrotizing infection should also be ruled out Stage IV: Deep crater with penetration through deep (muscle) fascia, with associated involvement of musc!e, joint and/or bone. Again, the wound base is usually nontender. Possible associated dissecting abscess, necrotizing infection, and osteomyelitis must be ruled out Wagner Classification of Neurotrophic Ulceration

(categorizes diabetic and neuropathic ulcers) Grade 0: Skin intact, osseous deformity present, at risk. Grade 1: Localized superficial ulcer. Grade II: Deep ulcer extending to tendon, joint and bone. Grade Ill: Deep abscess with osteomyelltis. Grade IV: Gangrene of toes or forefoot. Grade V: Gangrene of foot extending from forefoot to proximal to midfoot.

24


Ch. 2

Keloids and Hypertrophic Scars Keloids are reactive fibrous proliferations that develop at sites of cutaneous injury. They occur more commonly in black individuals and the predilection is hereditary. Fibrous proliferation extends beyond the area ofthe original skin injury and can be debilitating. The lesion is thought to develop due to irregular wound granulation associated with abnormal capillary endothelium, and the presence of excessive myofibroblasts. Excessive col!agenation and decreased collagenase activity may also contribute to fibrous

proliferation. Hypertrophic scars are similar to keloids, however they remain within the area of the original injury and tend to reduce in size over time. lntralesional injection of glucocorticosteroid and surface compression, preferably with elasticized silicone polymer, may reduce keloids and hypertrophic scars. Peptic ulcer, fibromatosis, and enostosis may be present. Elective surgery should be considered cautiously in patients with a history of hypertrophic scar or keloid formation.

Morphea and Systemic Sclerosis Morphea is represented by one or more hardened, linear, plaques of atrophic skin.lt can be idiopathic or posHraumatic and develops with an initial purple or pink margin. Morphea responds to intralesional steroids. Systemic sclerosis (formerly Scleroderma) affects cutaneous as well as multi~organ connective tissue hardening. In the skin, typically in the extremities, there is sclerosis, stiffening of small joints, Raynaud's phenomenon, ulceration and calcinosis (calcinosis cutis). Other findings include esophageal, Gl tract, pulmonary, cardiac, and renal sclerosis.

BONE HEALING

Fractures Fractures are described according to their location and orientation within the specific bone. Incomplete fractures, wherein a portion of the bone's cortex remains intact are termed green stick fractures, and generally develop secondary to flexural deformation of a long bone. Similarly, a stress fracture results in bending without overt radiographic fragment separation. A bone scan can be useful if diagnosis is in question. Incomplete fractures are diagnosed primarily by clinical examination, and with subsequent radiographic evidence of secondary bone callus. Complete fractures can be transverse, oblique, spiral, and comminuted, with fracture stability and management varying with the fracture pattern. Fracture stability, in descending order, is as follows: Transverse> Oblique> Spiral> Comminuted

Ch.2


25

Transverse and oblique fractures can be closed-reduced and immobilized, whereas spiral and comminuted patterns are extremely difficult to adequately reduce and maintain in a closed fashion. When a fracture violates a joint surface, open reduction and

stabilization is most often the besttreatmentoption. Growth plate injuries and open fractures also deserve special consideration. Fracture repair is initiated with closed reduction and immobilization. Charnley's sequence of closed reduction is as follows: 1st) increase the

deformity, 2nd) distract, 3rd) reverse the deformity and realign, and 4th) maintain

correction with Immobilization.

Callus !Secondary) Bone Healing Bone heals via either callus bone healing or primary bone healing, and requires an intact vascular supply. Callus bone healing, which may also be referred to as secondary bone healing, occurs in six phases: hematoma formation, hematoma organization, fibrocartilaginous callus, primary bone callus, primary bone callus absorption, and remodeling (maturation). The hematoma phase lasts 1to 3 days, and consists of hematoma formation between fracture fragments. Hematoma organization lasts from 3to 10 days, and entails inflammation with recruitment of osteoclasts and osteoblasts. The fibrocartilaginous callus phase lasts from 10 days to 6 weeks, depending upon the degree of immobilization and fragment stability; and consists of osteoclastic phagocytosis of necrotic bone, chondroblastic and osteoblastic differentiation into cartilage (low oxygen tension) or bone (high oxygen tension), and neovascularization derived primarily from endosteal, and to a lesser degree periosteal, blood vessels. Fracture instability leads to progressive irritation !fibrocartilaginous) callus formation, and delays the development of bone. The primary bone callus phase lasts from 6 to 10 weeks, and includes condensation of the fibrocartilaginous callus into bone that bridges the fracture interface. Primary bone callus absorption lasts from 2.5 to 4 months, and includes new bone remodeling into secondary bone callus. The remodeling, or maturation phase entails alteration of bone in response to applied forces in accordance with Wolff's law, and continues from about 4 months post~injury. Primary Bone Healing Primary bone healing requires fracture reduction, rigid stabilization, and preservation of fragment vascularity. When bone fragments are reduced and rigidly stabilized, the fibrocartilaginous callus phase can be by-passed and new bone formation and remodeling occur simultaneously via Haversian remodeling. Primary bone healing can occur via either contact or gap healing. Contact healing involves stabilization of bone~to~ bone contact, while gap healing involves stabilization of the fragments with maintenance of a small (up to 2mm) gap between the bone ends. Stabilization is enhanced by compression, which increases friction between bone fragments and promotes rigidity. Fracture stability can be achieved in a variety of ways (see Internal and External Fixation of Bone). Haversian remodeling is the underlying process of normal bone healing. When fracture fragments are reduced and stabilized, capillary budding from Haversian canals occurs at points of contact and bridges the fracture interface by means of the cutting cone; which consists of a leading tip of osteoclasts that phagocytose osteoid, a central capillary emanating from the Haversian canal, and osteoblasts that are organized about capillary margins and lay down lamellar new bone.


26

Ch. 2

Avascular Necrosis

There are many causes of bone necrosis including trauma (accidental and surgical), steroid therapy, occlusive vascular disease, venous thrombosis, collagen vascular disease

\rheumatoid, arteritis), status~post renal transplant, sickle~cell anemia, pancreatitis and chronic alcohol abuse, radiation therapy, hyperuricemia and gout, hyperlipidemia,

barotrauma (Caisson's diseaselr osteoporosis and osteomalacia. The process involves acute ischemia of bone, necrosis, then revascularization and new bone formation. Bone scans, if used early and with fine localization, may show a cold spot due to ischemia. Generally, however, bone scans are hot, which is consistent with new bone accretion associated with healing. An MRl can be useful in establishing the diagnosis of AVN.

Radiographic Classification of AVN ofthe First Metatarsal Head (or Head of the Femur)

Stage 1: Pre-collapse Early Intermediate Late: Stage II: Collapse Early: late: Stage Ill: Arthritis Early: Late:

normal density, localized cold bone scan relative sclerosis of dead bone, due to surrounding hyperemia and disuse osteoporosis true sclerosis due to new bone accretion, hot bone scan mild step defect, loss of articular sphericity fragmentation of articular surface and metaphysis

joint space narrowing, subchondral cysts and sclerosis, osteophytosis sclerosis, ankylosis, articular erosion

Clinical Signs and Symptoms of AVN Stage I : usually asymptomatic, or perhaps minimal pain and stiffness Stage 11: usually significant pain and stiffness, occasionally asymptomatic Stage Ill: pain and stiffness are most typical

The differential diagnosis of AVN includes arthrosis, RSOS, and infection. The ESR is usually not elevated due to AVN and RSOS. The medical treatment of AVN consists of protective or non-weight bearing, electrical bone growth stimulation, vasodilators, NSAIDs to inhibit platelet aggregation, and avoidance of steroids. Surgical treatment of AVN includes debridement of necrotic bone or core decompression and replacement with autogenous bone graft, revascularization with a pedicle muscle graft, and resection with endoprosthesis or arthrodesis. Rates of AVN of the first metatarsal head following distal first metatarsal osteotomy have been reported to range from less than 1% to greater than 40%. Steps for the prevention of AVN include preservation of periosteal and capsular attachments, accurate hemostasis, avoidance of immediately subchondral osteotomies, rigid stabilization of metaphyseal osteotomies, protective or non-weight bearing, use of sharp blades and osteotomes, and routine serial radiographs following osteotomy or fracture.

Ch. 2


27

Delayed Union, Nonunion and Pseudoarthrosis Following fracture, excessive motion and/or inadequate vascularity can lead to formation of hypertrophic irritation callus, malunion, delayed union, nonunion, or pseudoarthrosis. Conditions such as Puget's disease, osteitis fibrosa cystic a, rickets, hyperparathyroidism, osteomalacia and osteoporosis, and debilitated or compromised host (immuno~

compromised, antimetabolite or steroid therapy, anemia, anticoagulation therapy, elderly patient, chronic cigarette smoker) can also impede bone healing. The presence of irritation callus rules out primary bone healing, and indicates instability between fragments.

Delayed union simply means the fracture has not healed within a reasonable period, and can be identified radiographically by the presence of unchanged irritation callus and persistence of a fracture cleft Causes of delayed union, and ultimately nonunion, include inadequate fracture reduction and/or immobilization, overly-aggressive soft tissue iperiosteal) stripping or injury, osteomyelitis, and local vascular compromise. Delayed unions and non unions are determined primarily via serial radiographic inspection, combined with clinical evidence of persistent edema and pain. Depending upon clinical needs and indicators, a delayed union is treated with continued immobilization and non-weight bearing, revisional surgery for callus channelization or bone grafting or re-fixation (internal and external), and employment of electrical bone growth stimulation IEBGS).

A nonunion is classically defined as failure to achieve stable fracture healing after 8 to 9 months of management. It is not necessary to wait 8 or 9 months before intervening surgically, either revisional or as an initial operation, when treating a delayed union, however appropriate non-surgical intervention should be applied before deciding to go to the operating room. Non unions are classified as either atrophic or hypertrophic. The atrophic nonunion, also termed non-reactive, displays radiographic evidence of bone ends rounding off and the absence of bone callus. Atrophic nonunions are classified as comminuted, with multiple fragments and gapping; torsion wedge, where a necrotic butterfly fragment impedes healing; and simply atrophic, where the ends are wasted or markedly rounded. Devitalized and/or septic bone requires surgical excision and often bone grafting for repair: Hypertrophic nonunions display radiographic evidence of the bone ends flaring or mushrooming; and are classified as elephant foot, where there is maximum widening at the interface; horse hoof, where there is moderate callus flaring; and oligotrophic, where there is minimal reactive callus. A pseudoarthrosis is a nonunion with a fibrocartilaginous interface between the fracture fragments. An articular fracture nonunion may develop into a synovial pseudoarthrosis. A pseudoarthrosis can also be classified as infected, previously infected or non-infected; as well as metaphyseal or diaphyseal. A bone scan or MRI can be useful in confirming vascularity at the delayed or nonunion site. Diffuse increased uptake of radionuclide is seen at the hypertrophic nonunion, and may display a biphasic pattern if elephant foot or horse hoof hypertrophy are present. An lndium-1111abeled white-blood cell scan can also be useful in the evaluation of suspected infected pseudoarthrosis or nonunion. If the fracture cleft is large enough, or in the presence of a large-enough synovial pseudoarthrosis, a bone scan may reveal a cold cleft. Otherwise, bone scans are not of much use in distinguishing between delayed and nonunions. CT scans, linear tomography, MRI, stress fluoroscopy, and intramedullary venography, can also be used to evaluate a delayed or nonunion of

28


Ch. 2

bone. In regard to noninvasive measures, overall, MRI provides the most diagnostic and anatomical information regarding a suspected nonunion or pseudoarthrosis. ACT scan is particularly valuable when trying to identify intervening fracture fragments.

Treatment of a hypertrophic nonunion involves immobilization and non~weight bearing, bone growth stimulation (BGS), and continued monitoring. The decision may also be made to operate. An atrophic nonunion, or an infected or synovial pseudoarthrosis, requires

operative intervention for resection of necrotic or problematic tissue, bone grafting or reapproximation of bone, followed by application of BGS and immobilization and non-weight bearing. BGS is ineffective in the treatment of pseudoarthrosis, or, if the gap between fragments is greater than 1/2 the diameter of the bone. Bone Growth Stimulation (BGS) Electrical bone growth stimulation (EBGS) and low-intesity ultrasound (LIUS) bone growth stimulation can be used in the treatment of nonunion, failed fusion, congenital pseudoarthrosis, and fresh fractures (see package insertforthe specific device, for precise FDA-approved indications and contraindications). EBGS and UUS are not effective in the presence of acquired synovial or infected pseudoarthroses, when the gap between bone margins is greater than 1/2 the diameter ofthe bone, or when sepsis is advanced. BGS is contraindicated in the presence of neoplastic bone disease. A "hot" bone scan or MRI should be observed prior to use of BGS. BGS is founded on the fact that areas of bone growth and fracture healing display electronegativity due to stress-generated (piezoelectric) polarity in collagen. In the presence of electronegativity, low-intesity ultrasound, and strain-generated potentials, bone forming growth factors are upregulated and new bone formation induced. BGS can be achieved using any of a number of effective devices (Table 2.1).

Table 2.1_ OPTIONS FOR STIMULATED OSTEOGENESIS

TYPE

METHOD

USE

DEVICE

Invasive

Direct current (20 uA)

24n*

EBI OsteoGen

Noninvasive

Pulse electroinagnetic fields IPEMF) (mV)

3-10 hrs/ day

EBI Bone Healing System, Orthofix PhysioStimLite

Combined PEMF (mV)

30 min/day

Don Joy Orthologic

Capacitative coupling 19 volt dry cell, skin patch electrodes)

24n*

EBI OrthoPak

Low energy ultrasound (30 milliwatts/cm2)

20 min/day

Smith & Nephew Exogen

* 24n = 24 hours/day, 7 days/week, or until power source is exhausted.

Ch. 2


29

The precise method of BGS to be used is determined based on the surgeon's

experience and the patient's needs and abilityto properly use the device. The devices vary

in regard to size, weight, application, precision with which the energy is directed at the target bone, and ease of use. Despite technical differences between the individual

stimulators, all of the devices have been clinically proven to work. In regard to the surgically implantable direct current device, issues of compliance are obviated by the fact that the stimulator, along with the hermetically sealed power supply, stimulate bone growth constantly until the battery is exhausted 124-36 months). Furthermore, with the implantable stimulator, cathode configuration can be varied according to the specifics ofthe anatomical site, and the cathode and lead wire should not contact any hardware used to stabilize the healing bone. The implantable EBGS requires subsequent surgical retrieval of the power pack and lead wire. In regard to the capacitative"coupled device, 2 electrodes are affixed (adhesive patches like EKG leads) to the skin surface on either side of the nonunion, which may require windowing the cast or using an external fixator to enable access to the target site. The device runs constantly, as long as the batteries !supplied by EBI) are changed daily. Like the capacitative-coupled EBGS, L!US requires access to the skin surface so that u[traqsound gel can be applied driectly over the target bone, and this may warrant windowing the cast or using an external fixator. PEMF devices only need to be secured in close proximity to the target bone, and they induce electrical current in the bone by means of a surrounding magnetice field. These devices can be worn outside of a bandage, cast or immobilizing splint

CARTILAGE HEALING Hyaline cartilage consists of chondrocytes within a glycosaminoglycan matrix, along with type II collagen fibers. Fibrocartilage contains type I collagen. Cartilage does not have a direct blood supply, however it requires synovial fluid for nutrition on its superficial (articular) surface. Cartilage is viscoelastic due to canals through which synovial fluid flows, allowing deformation in response to compression and shearing loads. Cartilage wounds can be partial or full-thickness, and can be difficult to heal. Following articular fracture or cartilage injury, necrotic cartilage is phagocytosed by macrophages arriving at the wound via inflammation. Healing thereafter occurs by means of limited chondrocyte mitosis and, for the most part, metaplasia of mesenchymal stem cells into fibrocartilage or near-hyaline cartilage. Ideal joint repair increases the likelihood of hyaline-like Imore type II collagen) cartilage repair. Undifferentiated stem cells arrive at the cartilage defect via disruption of the subchondral cortical bone plate, whether via fracture or by means of surgical perforation, from medullary sinusoids of adjacent epiphyseal and metaphyseal bone. Healing requires restoration of joint capsule and ligaments, perforation and realignment of the subchondral bone plate for support and vascularity, and motion under reduced pressure (non-weight bearing motion). Partial thickness wounds require sculpting (saucerization) of any jagged or elevated cartilage margins, and perforation of the subchondral plate. Necrotic fragments should be excised. TENDON, LIGAMENT AND JOINT CAPSULE HEALING Tendon, ligament, and joint capsule heal by means of lag (substrate), fibroproliferative, and maturation phases. The lag phase occurs during the first two weeks; is enhanced by immobilization; and entails inflammation and fibroblastic splinting, with the majority of tissue strength due to sutures. Fibroplasia and vascularization increase during the 2nd week,

30


Ch.2

and strength exists primarily due to sutures and immobilization is still required. The fibre proliferative icollagenation) phase occurs during week 3, and consists of a marked increase in fibroplasia. At this time, moderate collage nation strength can sustain gentle passive motion or isometric (in cast or brace) exercises. The remodeling {maturation) phase begins after 4 weeks, with collagen realignment and remodeling yielding moderate (not full) strength. Gradual, progressive strengthening occurs with subsequent passive and active exercises. PERIPHERAL NERVE WOUNDS AND HEALING Peripheral nerves respond to injury with inflammation, collagenation, and Wallerian

degeneration. Fibroblasts within the connective tissue sheaths respond to inflammation with increased collagenation. Seddon's Classification of Nerve Injury Neuropraxia-the myelin sheath is disrupted by blunt trauma or compression, causing physiologic blockade of saltatory conduction. Thickly myelinated, large diameter, rapidly conducting nerve fibers are most susceptible. A differential paralysis can develop, wherein deep tendon reflexes, skeletal muscle function, vibratory and two-point discrimination are lost, while pain and temperature sensation, and autonomic function persist. Repair can take days to months, and is usually perfect as the nerve sheaths and axons remain intact, and only the myelin must regenerate. Axonotmesis-involves disruption of axons, with maintenance of supporting connective tissue sheaths. Causes include prolonged compression, traction, ischemia, and toxins. Wallerian degeneration occurs with distal axon degradation via phagocytic Schwann cells, while the proximal portion of the axon and nerve cell body convert from the production of neurotransmitter to making macromolecules for axon regeneration. Axon.otmesis affects heavily myelinated fibers equally as well as unmyelinated fibers. Nerve fiber regeneration occurs at the rate of 1 mm per day from the point of injury. Because the endoneural scaffold and supportive sheaths remain intact, the budding neurite (new axon) can grow down its corresponding distal endoneural tube, en route to the nerve's end organ. Functional recovery is generally good, but diminishes as the distance from the point of injury to the end organ increases. The more proximal the lesion, the less likely it is that normal function will return. An injury at the sciatic level is less likely to fully regenerate compared to injury of the posterior tibial nerve at the level of the ankle. Proximal lesions affect a wider distribution and convey a worse prognosis. 1\feurotmesis-involves disruption of nerve fibers as well as the supportive connective tissue sheaths of the nerve trunk, and is therefore the most devastating form of injury. Causes include sectioning injuries such as laceration, gunshot wound, open fracture, severe traction or avulsion, punctures, and injection oftoxin. Because the di~al endoneura! tubes are disrupted, it is difficult or impossible for budding neurites to bridge the defect and grow into corresponding endoneural tubes and properly innervate end organs. Confused reinnervation is often the case, as neurites that do manage to bridge the defect grow into endoneural tubes that previously corresponded to other nerve fibers. Even with surgical intervention to resect necrotic tissue and fibrosis, and to realign fasciculi, regeneration is imperfect at best and almost impossible without surgical repair. For this reason, nervesuturing techniques are essentiaL Nerve fiber regeneration occurs at 1 mm per day, and axon exhaustion can occur with far proximal lesions. In the case of nerve excision, such as

Ch.2


31

in the treatment of Morton's neuroma, the distal segment of the nerve trunk is excised and budding neurites have no chance of achieving reinnervation. A stump neuroma will always form at the point where the nerve is sectioned, and can be minimized with epineuroplasty (closure of the epineurial cuff). Entrapment Neuropathy Nerve entrapment involves impingement of a peripheral nerve trunk by neighboring anatomic structures, typically where the nerve traverses a fibro-osseous tunnel. Classical impingement sites include the posterior tibia! nerve and its branches in the tarsal and calcaneal tunnels and the plantar common and proper digital nerves in the intermetatarsal spaces {Morton's neuroma). Injury takes the form primarily of neuropraxia and, in severe cases, axonotmesis. Prolonged entrapment leads to the development of a neuroma-incontinuity. Inflammation of surrounding connective tissues can lead to perineural fibrosis.

Signs and symptoms include Tinel's sign, which is pain and paresthesia within the entrapped nerve's distribution upon percussion or palpation of the nerve trunk at the point of entrapment. Percussion or palpation of the entrapped nerve may also effect proximal radiation of paresthesia along the nerves course (Val!eix sign). Generally, sensory abnormalities occur before autonomic (sudomotor, vascular smooth muscle, arrector pili) dysfunction, and skeletal motor dysfunction is usually lastto occur. Electroneurodiagnostic testing may show decreased nerve conduction velocity and electromyographic evidence of fibrillation due to entrapment. It is important to note that electrical testing may be normal despite functional entrapment with a great deal of symptomatology when the patient is weight bearing or active. Differential diagnoses include radiculopathy, metabolic or hereditary polyneuropathy, compartment syndrome, musculoskeletal pathology, and complex regional pain syndrome (causalgia and RSDS). Treatment includes protection of the nerve from external forces, anti-inflammatory medication administered systemically as well as local corticosteroid infiltration about the nerve trunk, ultrasound therapy, other pharmacological therapy, and surgical decompression when non-surgical measures have failed to satisfactorily alleviate pain. Pharmacological approaches are variable, and include: CapsaiciiJ-topical, to diminish substance Pat C-type fiber terminals Tricyclic antidepressants-oral, effect selective neurotransmitter blockade; watch for anticholinergic effects such as dry mucus membranes, insomnia, palpitation, lightheadedness, and cephalgia; available as: amitriptyline, imipramine, dsipramine, nortriptyline, paroxetine, and trazodone Anticonvulsants-oral, effect selective neurotransmitter blockade; with side effects similar to those noted for tricyclics; available as: carbamazepine, diphenylhydantoin, gabapentin, pregabalin, and cymbalta Local anesthetics----such as mexiletine \oral administration) and lidocaine (IV administration or via transcutaneous patch application) Adrenergic agonists-such as clonidine transdermal patch Aldose reductase inhibitors-these can be particularly useful for diabetic neuropathy, and include: sorbinil, tolrestat, epalrestat Other agents-including prostaglandin E1, and B-complexvitamins


32

Ch. 2

The mainstay of surgical treatment involves external neurolysis, with subsequent nerve repositioning or excision. Nerve ensheathing in silicone, or capping, is of questionable benefit and usually effects symptoms of entrapment. External neurolysis alone is often adequate for symptomatic relief, and is periormed using Ioupe magnification and fine-tipped instruments. Specific entrapment neuropathies of the lower extremity include: saphenous nerve where it emerges through the adductor canal, common peroneal nerve nearthe head of the fibula {Fig. 2.1) {Maisonneuve fracture, constricting BK cast, lateral decubitus position, traction injury with associated ankle sprain); superficial peroneal nerve where it emerges through deep fascia proximal to the ankle (compartment syndrome, athlete or jumper with peroneal muscle herniation through deep fascial hiatus [Henry's hiatus] at emergence of superficial peroneal nerve (Fig. 2.2) [Henry's mononeuritis]), deep peroneal nerve deep to the transverse or cruciate crural ligaments (anteriortarsa! tunnel}, sural nerve near the lateral malleolus (any ankle sprain, or surgical approach to the lateral aspect of ankle or heel, tendoAchillis surgery). tibial nerve and its branches deep to the flexor retinaculum {tarsal tunnel syndrome), and the plantar nerves plantar to the deep transverse intermetatarsalllgaments !Morton's neuroma).

\I

I Saphenous nerve and vein

peroneal nerve

Figure 2.1

Figure 2.2

Ch.3

Selected Diseases and Pathological Conditions

33

SELECTED DISEASES AND PATHOLOGICAL COII.IDITIOI\IS DERMATOSES AND SKIN PATHOLOGY The skin forms a barrier to the outside environment, serving as a protective layer from UV radiation (melanocytes, dendrites and melanin), thermal and mechanical trauma, and microbiological inoculation. It also retains moisture, participates in the immune response, and regulates temperature. The epidermis consists of the following five strata, (listed from deep to superficial): st. basale (the basal layer), st. spinosum, st. granulosum, st. lucidum, and st. corneum. Melanocytes located in the basal layer expand via dendritic processes that contain melanin, which absorbs UV-B and thereby protects underlying living cells from radiation-induced mutation. Merkel cells in the epidermis serve as sensory neurotransducers, and Langerhans cells of the epidermis participate in the immune response. The dermis is composed ofthe papillary and reticular layers. The papillary dermis and basal layer of the epidermis adhere along an undulating interface of rete ridges and valleys. The papillary dermis conveys capillaries (responsible for the pin-point hemorrhages noted upon debridement of a verruca) and nerve endings; while the reticular dermis contains the skin adnexae, microcirculatory vessels, and nerves. Deep in the dermis, near the subcutaneous layer, are also found Pacinian corpuscles {Vater-Pacini units) that participate in deep touchpressure sensation. The skin adnexae include: eccrine sweat glands; pilosebaceous units consisting of sebaceous gland, hair and follicle, and the arrector pili muscle, all of which are under autonomic control; and the nail unit consisting of matrix, bed, folds and plate. The glomus body is srtuated atthe toe tip, partially between the nail bed and distal phalanx, and consists of an arteriole-to-venule capillary bypass (Susquet-Hoyer shunt) that participates in thermoregulation, and may become tumorous.

Primary Skin Lesions Macule-flat, discolored, well circumscribed, up to 1 em diameter Patch--larger or coalesced macules, > 1 em diameter Papule-slightly elevated Idue to inflammatory dermal infiltrate). well circumscribed, up to 1 em diameter Plaque-larger or coalesced papules,< 2 em diameter Nodule-well circumscribed, firm elevations,> 2 em but< 3 em diameter Tumor--well circumscribed elevation> 3 em diameter Vesicle-serous fluid-filled, elevated,< 1 em diameter Bulle-serous fluid-filled, elevated,> 1 em diameter Imay be hemorrhagic) Cyst-sterile intradermal mass of fluid or other material, contained within a defined wall, such as a mucus, epidermoid inclusion, or sebaceous cyst Burrow-intra-epidermal tunnel formed by scabies or other insect/parasite Secondary Skin Lesions Scale-thin, plate-like, cornified compact epithelial cells Excoriation---superficial loss of skin Erosion-gradual epidermal breakdown, sometimes referred to as a superficial ulcer that heals without scarring Ulcer-local excavation or surface defect created by sloughing of inflamed necrotic skin Crust-a scab, caused by surface drying of exudate or secretions

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Ch. 3

Fissure-abnormal cleft or deep groove, usually hyperkeratotic superficially with an open or hemorrhagic dermal wound deep in the recess Scar-cicatrix, or the mark remaining after a dermal, or deeper, defect or other morbid process has healed (hypertrophic, keloid) Pustule--visible accumulation of pus within or beneath the epidermis, frequently in an eccrine duct or hair follicle (pus is a liquid inflammatory product consisting of leukocytes and serous transudate, along with bacterial and other proteins) Abscess-a collection of pus in a cavrtyformed by disintegration of surrounding tissue Furuncle-an accumulation of pus in the skin and succutaneous tissue, also known as a boil; typically caused by Staph. entering through a follicle, associated with a painful, nodular inflammation of skin with corium erythema and subcutaneous edema Carbuncle--a cluster of boils (furunc!es) affecting skin, associated with subcutaneous necrosis and multiple draining sinuses

Sinus tract-a cavity or channel connecting an abscess to the skin surface or adjacent tissue layers (a fistula generally refers to a channel or tract connecting a deeper organ to another organ or tissue layer, or the skin surface) Hyperkeratoses (HPKs) Non~mechanically induced diffuse keratoses are usually bilateral, symmetrical, plantar and palmar, and often inherited. Characteristics include 4:1 ratio of stratum (st.) corneum to st Malplghil {germinative layers of the epidermis, st. basale and st spinosumL with the granular layer, between the st. spinosum and st. lucidum of the epidermis. Common non~mechanical diffuse HPKs include: Psoriasis-maculopapulosquamous, silvery scales on erythematous base, Auspitz sign (bleeds when scale removed), elbows and knees Unna Thost disease--bilateral, symmetrical, palms and soles, dominant inheritance Mal de Maleda-torme fruste (partial expression) of Unna Thost, recessive inheritance, with nail, ocular and dental involvement. Vohwinke/'s disease (keratoma mutilans hereditarium)--diffuse, honeycombed, rippled keratosis of soles, star burst keratoma on knees. associated digital contracture and pseudo ainhum Keratosis pfantarum su/catum--status~post immersion toot with Dermatophilus congolensis Pachyderma periostosis-keratosis of soles, periosteal hyperostosis, associated with alveolar cell carcinoma Alcoholic keratosis-mosaic, honeycomb dystrophic keratosis with sympathetic component Hauxthausen's disease (keratosis climactericum)-commonly on heels, erythematous base, in postmenopausal women, associated with hypertension and hyperuricemia Moccasin foot-chronic, dry, hyperkeratotic T. rub rum dermatophytosis Hyperkeratosis traumaticum marginus os calcis (housewives heel)-secondary to prolonged weight bearing barefoot or in an open back slipper failing to support the heel (no counter) Keratoderma blenorrhagica---chronic inflammatory maculopapular and scaly dermatosis associated with Reiter's syndrome (urethritis, iritis, arthritis), usually in young males, localized to palms, soles and digits


Ch.3

35

Mechanically induced diffuse keratoses can be unilateral or bilateral on the soles,

and show a 1:1 ratio of st. corneum to st. Malpighii with the granular layer intact. The underlying dermis is usually fibrous, with dilated capillaries and eccrine sweat ducts, and perineural fibrosis. There are typically about 400 eccrine ducts per cm 2 of plantar skin. This is often observed in patients with global anterior pes cavus with callus extending across the entire ball of the foot.

Non-mechanically induced punctate keratoses characteristically display increased st. corneum, a normal st. Malpighii, an intact st. granulosum, and loose underlying dermis. Genetically determined forms include keratosis punctata of Hallopeau, which is dominantly inherited, and displays hundreds of evenly distributed punctate keratoses, bilateral and symmetrical, with truncated, macular and verrucoid lesions. Acquired punctate keratoses are generally few in number, asymmetrical, and localized to skin creases. Acquired forms include: Arsenical keratoses--arsenic intoxication (Cruveiler~Baumgartener disease), affecting palms/soles, with hepatic failure; associated in past with certain asthma preparations, wines, and seen in coal miners Secondary syphilis-palms/soles, maculopapular, evolves to punctate keratoses Darier's disease-greasy, vegetative lesions, punctiform on palms/soles, external auditory meatus, cheeks Aigner's syndrome (form fruste of Albers-Schonberg disease}-----punctate keratoses of palms/soles with osteopetrosis Hanhart's syndrome-punctate keratoses of palms/soles, with multiple lipomas Basal cell nevus syndrome-pink (ham colored) pits with ice pick, punctate keratoses

Non-mechanically induced punctate keratoses of unknown etiology include heloma neurofibrosum, which displays keratinous filaments, typically about the perimeter of the heel, resembling mosaic verruca, with banana~like projections, single or multiple, and very painful. Mechanically induced punctate keratoses characteristically display a 1:1 ratio ofst corneum to st. Malpighii, a parakeratotic plug with atrophy of underlying granular layer, dilated eccrine sweat ducts, dermal fibrosis, capillary ectasia and perineural fibrosis. Included are: Parakeratosis plantaris discretum of Steinberg---translucent keratinous plug with surrounding white (macerated) rim of blocked eccrine duct Vamp disease-typically overlying EHL, or another extensor, tendon, where shoe vamp chronically irritates skin resulting in parakeratosis, loss of granular layer, and often a sinus tract due to draining bursa or tendon sheath

Dermatitides Dermatitis has many causes and forms, and is typically treated with topical or systemic corticosteroid, local care, and protection. Atopic dermatiti~a chronic pruritic eruption common in adolescents and adults, attributed to allergic, genetic and psychogenic causes; common to flexor surfaces, displaying crusts, lichenification, and excoriation Nummular (coin~like} dermatitis-of unknown etiology, affects extensor surfaces, buttocks and legs, and displays papulovesicular eruption, forming crusts Lichen simplex chronicus (focalized neurodermatitis}-----due to repeated scratching, most common in females and Asian individuals, with well~demarcated scaly erythema

36


Ch.3

Contact dermatitis-an acute inflammation caused by contact with an allergen effecting delayed hypersensitivity, and usually well-demarcated with a raised margin Dyshidrosis--any disorder of eccrine sweat ducts, such as pompholyx. Pompholyx ("bubbles") is a skin eruption, typically on the sides of fingers and toes, palms and soles, consisting of discrete 1 to 2 mm intra-epidermal vesicles with surrounding erythema, associated with intense itching, lasting 1to 2 weeks intermittently ldreactian (id rash}-a remote rash associated with a primary lesion caused by cutaneous sensitization resulting in a distant site allergic reaction to circulating allergen, such as dermatophytid or syphilid Stasis dermatitis-affects the distal leg, ankles and hindfoot, secondary to chronic venous insufficiency (valvular incompetence due to dilation of vein) or lymphedema, with cyanosis, erythema, pruritus; progressive over years, and may eventually ulcerate Purpura and other Hemorrhagic Lesions Purpura are a group of disorders characterized by brown, red or purple subepidermal hemorrhages. Petechiae are pinpoint, macular, round, purple or red, intradermal or submucous hemorrhages. Purpura are larger than petechiae{< 1 em), but smaller than ecchymosis(> 1 em). Ecchymosis, are large hemorrhages causing black and blue marks or bruises. Purpura are caused by thrombocytopenia, amyloid, steroids (capillary fragility), rheumatic vasculitis (leukocytoclastic angiitis), polyarteritis nodosa, serum sickness, SLE, Henoch-Schonlein disease, and hemorrhagic fever (Ebola virus). Splinter hemorrhages occur in the nail bed, and may be indicative of subacute bacterial endocarditis. Papulosquamous Eruptions These are characterized by slightly elevated, erythematous and scaly lesions, and include: linea pedis---dermatophyte or other fungal or yeast infection Psoriasis---chronic, hereditary, recurrent papulosquamous eruption occurring on the scalp and extensor surfaces, displaying a red macule, papule or plaque covered with silvery scales, removal of which effects local bleeding (Auspitz sign) Secondary syphHis-maculopapular and pustular eruption caused by T. pallldum infection, a venereal disease; the primary stage being a hard chancre, from which the bacteria spread systemically via lymphatics and blood. Secondary syphilis occurs 612 weeks after initial infection, displays fever, copper-hued multiform papular skin eruptions (syphilids), iritis, alopecia, mucous patches, and severe arthritis. Tertiary syphilis is late stage generalized disease affecting the CNS, bones, joints, and parenchymal organs Lichen planus-wide, flat, violaceous, itchy skin papules with a characteristic sheen, occurring in persistent patches, of unknown etiology (viral or psychogenic are suspected). The scaling lesion of Lichen planus may demonstrate Wickham's striae (network of white lines) Pffyriasis rose.r---fine, branny, scaling pink oval maculas aligned with skin creases

Benign Pigmented Skin lesions A nevus is a well-demarcated, stable, malformation of hereditary origin, involving epidermal, skin adnexal or vascular elements. A nevus containing melanin is said to be pigmented. Pigmented nevi include: Junctional nevus---brownish, smooth, hairless, macular or slightly elevated, 1to 8 mm diameter, occurring on any skin surface, histologically displaying nests of melanocytes "dropping off" into the dermis

Ch.3


37

Compound nevus-raised, flesh~colored to brown, often papillomatous, may contain hairs, with melanocytes in the epidermis (newly formed) and dermis (older) Intradermal nevus-similar to compound, typically more papillomatous, with hairs, and all melanocytes are in the dermis (older) Nevi evolve from epidermis to dermis, associated with elevation and involvement of skin appendages (hair). Nevus flammeus (port wine stain, or capillary hemangioma) is a diffuse, poorly demarcated area of pink/red/blue/purple capillary dilation in otherwise normal skin (not melanocytic). Livedo, or livedo reticularis, is vascular congestion causing mottled cyanosis, often caused by cold exposure but may be permanent secondarytovenular dilation.

Vesicles and Bullae

Table 3.1. CAUSES OF BULLOUS ERUPTIONS COMMON BUllOUS DISORDERS

UNCOMMON BULLOUS DISORDERS

Physical (heat, friction, cold) Excess sun or UV exposure Drug-induced photosensitivitv Systemic drug reaction Infection (bacterial, fungal, viral)

Pemphigus Epidermolysis bullosa Dermatitis herpetiform is Bullous lichen planus Toxic epidermal necrolysis Diphtheria cutis

Contact dermatitis Eccrine dysfunction (pomphylox) Erythema multiforme

Herpes infection--results in clusters of small vesicles, with H. simplex Type I occurring on skin or perioral, and Type II affecting genitalia. There is often a prodromal fever, and lesions can be recurrent Herpes zoster is caused by the same virus that causes varicella (chicken pox), which resides in the dorsal root ganglion, and erupts in a unilateral, tense vesicular, usuaHytruncal, inflammation in the dermatomal distribution of the affected spinal nerve root, frequently painful, and occasionally associated with post-herpetic neuralgia (shingles). Erythema multiforme--an urticarial eruption of immune origin, displaying red to purple, raised bullae, classically with target or iris lesions, severe forms of which are termed Stevens-Johnson syndrome, and can be fatal. Pemphigus-typically occurs in middle to older aged persons of Jewish descent, considered autoimmune or viral, with vesicles and bullae On skin and mucus membranes, treated with steroids, chronic, and often with high morbidity or death. Epidermolysis bullosa-typically occurs early in life (1 to 2 years) at sites of previous skin trauma, typically minor, can be fatal in an infant, and treated with supportivemeasures. Dermatitis herpetiformis {Duhring's disease}-a chronic, systemic vesiculobullous eruption on the extremities and torso, wrth associated enteritis, large concentrations of lgA, and considered autoimmune. Toxic epidermal necrolysis {scalded skin syndrome)-can affect all ages with epidennal necrosis and slough or peeling, often caused by staphylococci, and treated in a fashion similar to burns. Can also be a drug reaction, most notably with the use of Allopurinol, NSAIDs, Sulfonamides and measles vaccine.

38


Ch. 3

Nodular or Granulomatous Lesions Necrobiosis lipoidica diabeticorum-------disp!ays dermal edema and collagen distortion, yellow-brown pigmentation, loss of elasticity, well-circumscribed annular pretibial patches in diabetics, histologically showing palisading granuloma. Granuloma annulare---annular, hard, reddish, perimalleolar or dorsal. nodular lesion,

benign and. recurrent, occasionally related to diabetes, histologically showing palisading granuloma.

Erythema nodosum----acute inflammatory skin disease with tender red, pretibial nodules, successive patches over a few weeks, considered an allergic reaction, frequently seen with tuberculotoxin, streptococcal infection, drug reaction, coccidiomycosis and psittacosis. Sarcoidosis-chronic, progressive, systemic granulomatous disease of unknown etiology, affecting any organ system, a common cause of pulmonary hilar adenopathy, histologically showing noncaseating epithelioid cell tubercles (tuberculin negative usually). Angiolipoma-we!l vascularized, benign tumor of mature fat cells, often localized aboutthe tibial plateau and malleoli. Neurilemmoma is a peripheral nerve sheath tumor of myelin. Glomus tumor-reddish~blue nail bed lesion displaying myoepithelial cells and dilation of the Sequet-Boyer canal in the subungual papillary dermis, rarely observed beyond 25 years of age. Eccrine spiradenoma---deep, benign, solitary nodule arising from the coil of an eccrine gland, covered by normal appearing skin and associated with paroxysmal pain. Leiomyoma---benign arrector pili smooth muscle tumor (more commonly, uterine fibroid). Leprosy (Hansen's disease}--due to Mycobacterium leprae infection, causing asymmetrical, maculopapular, hypopigmented, circumscribed skin granulomas that often progress to digital ainhum and spontaneous amputation. Leprosy is diagnosed bacteriologically and histologically, and treatment entails diaminodiphenylsulfone (Dapsone or DDS) combined with rifampin, or clarithromycin and clofazimine. Ulcerative Skin lesions Hypertensive ulcers-localize to the lateral malleolar, digital, and dorsal areas,

are punched-out secondary to occlusion or spasm of arterioles, and are very painful. Treatment entails control of underlying HTN and local care. Venous stasis ulcers-localize along the saphenous vein secondary to venous hypertension caused by valvular incompetence, display stasis dermatitis with surrounding hyperpigmentation and eczematous vesicles and crusts, and are irregularly shaped with granular base and may become secondarily infected. Treatment consists of venous compression, elevation, cleansing, and protection. Decubitus ulcers-display a well-circumscribed, undermined margin; are localized to bony prominences and are associated with immobility and pressure. They are often tender, and respond well to cleansing and pressure relief. Mal perforans ulcers-punched out, nontender (insensitive), undermined and related to repetitive pressure. They respond well to supportive measures unless underlying bone infection develops. Sickle cell ulcerations-localize perimalleolar, are recurrent due to sludging of sickled RBCs and infarction. They are associated with hyperpigmentation and inflammatory infiltrate effecting induration, and are very painful.

Ch. 3


39

Skin Lesions Predisposed to Malignant Transformation or Association Actinic (solar) keratosis-sharply outlined, red or flesh colored macule, or slightly raised, verrucous or squamous growth on sun exposed surfaces. It may develop into a cutaneous horn, or evolve into squamous cell carcinoma. It is considered to be of UV mutation origin and is seen in the middle aged to elderly, usually in light

skinned individuals (also called solar or senile keratosis). Parakeratosis of Mibelli--rare chronic hereditary skin disease of the hands and feet,

with hypertrophy of the st. corneum about the eccrine sweat ducts. It may become dysplastic and effect squamous carcinoma. Xeroderma pigmentosu!TI---rare, familial recessive trait, that is often fatal, affecting skin with atrophy and pigmentation. It is associated with skin and eye photosensitivity has its onset in childhood with development of affiliates (freckles), telangiectasia, papilloma, hyperkeratoses, melanoma and carcinoma. Ataxia telangiectasia (Louis Bar syndrome)-hereditary progressive ataxia. It is associated with oculocutaneous telangiectasia, pulmonary disease and respiratory tract infection, and ocular muscle dysfunction. Malignant Skin Lesions

See selected neoplasms. Nail Disorders (Onychopathy) Congenital Defects Anonychia---------absence of one or more nail plates, associated with ichthyosis. Macronychia-anomalously large nail plate, otherwise normal in appearance (may also be acquired secondary to acromegaly, COPD or pulmonary hypertrophy [clubbing ofthe digits]). Micronychia-anomalously small nail plates, otherwise normal. Onychoheterotopia--nail growth in abnormal location, such as the dorsal or plantar skin of the toe or foot Pachyonychi&-abnormallythick, heavily striated longitudinally, occasionally lytic nail p!ates jean also be acquired secondary to repetitive microtrauma). Polyonychia-extra or supernumerary nail plate on a single toe, with one or more matrices. Synonychia-a single nail shared by two or more syndacty!ized digits.

Traumatic Conditions HangnaiJ.....-.periungual, filamentous epidermal spicule. Subungual hematoma-damage to the nail bed causes hemorrhage that fills the potential space between nail plate and bed, may be associated with simple or complex bed laceration, open phalangeal fracture, and should be drained (hand cautery perforation) if acute and painful or throbbing, or requires removal of the nail plate for repair of the bed if more than 25% ofthe visible nail plate displays hematoma or ifthe plate is substantially unstable. Onychophagi&-nail biting. Onychocryptosis-a late effect of matrix distortion due to acute trauma or repetitive microtrauma, wherein the plate grows into the adjacent nail fold, or when the nail is cut incorrectly and the adjacent fold is pushed by external forces into and over the plate. Onychophosis represents nail fold hyperkeratosis prior to dermal violation and paronychia.

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Ch. 3

Onychogryphosis-distal plantar curvature, with thickening or clubbing of the nail plate, a late effect of matrix and/or bed disruption, either acute or chronic. Leukonychia--white spots due to chronic microtrauma effecting plate separation from the bed, with a change in the refractive index of light; to be distinguished from white superficial onychomycosis. Onychia or paronychia--nail fold inflammation, red and swollen, tender and often with drainage, usually due to onychocryptosis. Onycholysis--separation ofthe plate from the bed, can be traumatic or secondaryto bed hypertrophy or accumulation of subungual debris, as in onychomycosis.

Metabolic and Systemic Conditions That Affect the Nails Hyperthyroidism--koilonychia, onycholysis, fingernails more so than toenails. Psoriatic arthritis-------pitting and onycholysis, discoloration, subungual hyperkeratosis, splinter hemorrhages; usually treated with systemic control of arthritis, local protection and palliative care. Hypertrophic pulmonary asteodystrophy-
INFECTION local signs of infection are those of inflammation, and include rubor (redness), tumor (swelling), calor (heat), and dolor (pain). The patient may display antalgic guarding of the infected lower extremity. Wound drainage should undergo Gram's stain and culture and sensitivity testing. Constitutional signs and symptoms of infection include fever, chills, malaise, loss of appetite, and Gl distress. The CBC shows a "left shift" wherein the total WBC count is elevated above 10,000, and granulocytes rise above 70%, and immature leukocyte bands are identified in the peripheral smear. Blood cultures are indicated when the oral temperature is 102° F(37° C) or greater, taken from three separate sites at30 minute intervals, if chills and/or hypotension occurs, or whenever septicemia is suspected. Blood cultures have been reported to be positive in up to 50% of septic arthritis and osteomyelitis cases. A variety of microorganisms can infect the lower extremity. Aerobic organisms include gram-positive coagulase producing Staph aureus {the most common infecting organism of skin and soft tissue). coagulase negative Staph epidermidis,beta-hemolytic group A Strept. (usually nonsuppurative with intense cellulitis and lymphangitis); gram negative aerobes E col£ Klebsiella, Pseudomonas, Enterobacter, and Serratia. Anaerobic organisms include Bacteroides, Clostridium, and facultative Staph. and Peptostreptococcus. Anaerobic infections develop when aerobic organisms metabolize 02, thereby enhancing conditions for anaerobes. Common synergistic organisms include:

Ch. 3


41

S. aureus, S. epidermidis, Peptostreptococcus, Corynebacterium, Bacteroides, and Clostridia. Signs of anaerobic infection include foul smelling (fetid), brown, watery,. exudate; necrosis, subcutaneous gas effecting soft tissue crepitus (readily observed on standard radiographs), and there is great risk for tissue loss and permanent dysfunction, as well as limb loss. Identification of infecting organisms requires culture and sensitivity testing (C&S). An open or draining wound presents exudate that can be swabbed for aerobic and anaerobic C&S. Clinical suspicion (immunocompromised, chronic or recurrent infection, sickle-cell anemia, concomitant infection elsewhere in the patient) should guide the practitioner to obtain special microbiological testing when indicated, including acid fast {mycobacteria) chocolate agar (Neisseria), and fungal C&S. Specimens can also be obtained via joint or abscess aspiration, aspiration of sterile saline infiltrated dermis and subcutaneous tissue when frank pus is absent (rather unreliable), and excisional biopsy with deep swab of infected bone or sinus tract base. Whenever aspirating for C&S, it is important to try to obtain the specimen through noncellulftic overlying tissues if possible. This is particularly true when aspirating a joint. Aspiration requires aseptic skin preparation, and may be enhanced with fluoroscopy. Sinus tract cultures are not reliable for identifying actual underlying causative organisms in cases of osteomyelitis, where it has been reported that a sinus tract C&S growing Staph. aureus correlates with the underlying causative organism only 50% of the time. Identification of other organisms from a sinus tract C&S correlates <50% with underlying causative organism in cases of osteomyelitis. Bone cultures are the most definitive diagnostic tool in cases of suspected osteomyelitis, and should correlate with bone biopsy. It is often useful to discuss the matter of biopsy and C&S directly with the pathologist and infectious diseases specialist whenever a question arises regarding diagnosis. There are several specific types of skin and soft tissue infections. Cellulitis displays erythema, edema and pain, and is often caused by Strep. Cellulitis can exist as an isolated infectious process, or in conjunction with deeper and more extensive types of infection. Pure cellulitis is usually treated without incision and drainage (I&D). The patient can be treated with appropriate oral or IV antibiotics depending on severity. Common Cutaneous Bacterial Infections Ecthyma- Group A streptococci (S. pyogenes)superficial infection due to minor trauma or poor hygiene, with pustule formation, crusts and erythema, may ulcerate. The treatment is topical mupirocin ointment (Bactroban) and 1st generation cephalosporin or erythromycin. Impetigo- staphylococcus or streptococcus superficial infection, usually in children, pustules with yellowish purulence, crusts. It is readily spread by contact with purulent lesions. Usually treated with topical mupirocin ointment and oral lst generation cephalosporin or erythromycin. Erythrasma- intertriginous superficial infection caused by Corynebacterium minutissimus, displaying maceration, scaling, fissuring, and erythema. Wood's lamp reveals coral red fluorescence. It is treated with dilute povidone iodine soaks and oral erythromycin.

Necrotizing Fasciitis Necrotizing Fasciitis involves infection dissecting along fascial planes, superficial to muscle; and most often is caused by peptostreptococcus, S. aureus, Strept pyogenes, Clostridium, and Bacteroides. Anaerobic muscle infection can cause myonecrosis with subcutaneous gas, exotoxin release, myoglobinuria and renal failure, and bacteremia.

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Ch.3

Myonecrosis (gas gangrene) Myonecrosis is the most morbid and potentially lethal soft tissue infection of the lower extremity. Necrotic muscle fails to display the four Cs: contractility (muscle stimulation with the electrocoagulator causes visible contraction), capillary bleeding (bright red blood), color (beefy red), and consistency (firm).

Osteomyelitis Osteomyelitis is defined as infection of bone and marrow. Osteomyelitis is distinguished

from infectious osteitis, which is suppuration of cortex without marrow involvement; and infectious periostitis, which is periosteal contamination and inflammation. Osteomyelitis is confirmed primarily by bone culture and, to a lesser degree, by bone biopsy (inflammatory biopsy may be false positive). As a rule, osteomyelitis requires surgical debridement followed by at least six weeks of antibiotic therapy. In some cases, based on clinical observation, a four week (or less) course of antibiotics may be sufficient following definitive bone debridement. A variety of classification systems exists for osteomyelitis including the Waldvogel, Cierny, and Buckholz systems.

Waldvogel Classification of Osteomyelitis Waldvogel described a classification based loosely upon the pathogenesis of the disease. The categories are Hematogenous Osteomyelitis, Contiguous Osteomyelitis, and Osteomyelitis associated with vascular insufficiency. Hematogenous Osteomyelitis ~ result of bloodstream dissemination of bacteria emanating from an identifiable focus of infection or developing during transient bacteremia unrelated to infection. This is most comrnon in patients between the ages of 1 to 20 years,-and over 50 years. Blunt trauma to long bone (femur>tibia>humerus) precedes this form of osteomyelitis in 33% of cases. Acute Hematogenous Osteomyelitis (AHO)- can be effected by Streptococcal skin infection, often associated with measles or chicken pox in childhood. Similarly, otitis media due to Hemophilus, Staph.~ or pneumococcus can hematogenously spread to bone. AHO localizes in metaphyseal bone due to the paucity of phagocytes and sludging venous sinusoids. AHO in the infant (0 to 1 year) can involve the joint, as capillaries traverse the epiphysis and effusion develops in 60~70% of cases. Group B Strept, Staph. au reus, and E coli are the most common organisms in AHO in the infant. In the child, AHO usually does not involve the joint space and most commonly localizes around the hip, shoulder, and ankle (distal lateral tibial metaphysis is intra-articular, and can lead to septic arthritis with osteomyelitis). Extensive cortical damage and involucrum develop, rarely is there damage to the growth plate or joint, and Staph. epidermidis is causative in 60~90% of cases of AHO. In patients with sickle~cell anemia or Sc hemoglobinopathy, Salmonella is most common; and Hemophilus influenza is most common in children less than two years old. In the adult, AHO is usually seen in patients older than 50 years of age. Pseudomonas is common in IV drug abusers developing AHO; and in adults using IV catheters, suffering urinary tract and pulmonary infection, or within two .years following major surgery. Joint infection may accompany AHO in the adult. Cases of AHO displaying purulence upon aspiration, or failing to respond favorably within 36 hours of initiating antibiotic therapy warrant operative intervention.

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43

Contiguous Spread Osteomyelitis~ results from direct contamination of bone due to spread of bacteria from contiguous tissue, is the most common form of osteomyelitis observed in podiatric cases; generally involves patients over 40 years of age; and may occurfollowing puncture, laceration, ulceration, or surgical intervention. Postoperative Contiguous Spread Osteomyelitis- includes acute postoperative osteomyelitis {observed within one month of surgery), delayed postoperative osteomyelitis (observed between one month and two years of surgery), and late postoperative osteomyelitis (not observed until at least 2 years after surgery). Most commonly, postoperative osteomyelitis is ofthe delayed or late sort, usually growing Staph. or mixed flora. In all forms of contiguous spread osteomyelitis, adjacent soft tissue or bone infection must be identified. A thorough search for a nearby ulcer or sinus tract is important

Direct Inoculation Osteomyelitis~ is caused by contamination of bone without adjacent soft tissue infection, and is either traumatically or surgically induced. A distinction between postoperative contiguous spread osteomyelitis should be made. Vascular Insufficiency Osteomyelitis- occurs in patients with peripheral vascular disease, wherein associated gangrene and ulceration are usually present. May involve anaerobes, and myonecrosis should be considered. Has features similar to contiguous spread osteomyelitis, however the overriding distinguishing factor is peripheral vascular disease. The Cierny-Mader classification of OM combines anatomic and physiologic categories in an effort to direct therapy. Twelve different stages of osteomyelitis can be described by combining the different categories (Table 3-2).

TABLE 3-2. THE CIERNY-MADER CLASSIFICATION OF OSTEOMYELITIS.

Anatomical category

Physiological category

I. Medullary II. Superticial

A. intact local vascularity and systemic immune competence B. Compromised local vascularity and/ or systemic immune competence C. Host not a surgical candidate, as operative risks outweigh potential benefits

Ill. Localized IV. Diffuse

Bucholtz classified osteomyelitis using 7 categories (Table 3-2).

TABLE 3-3. THE BUCHOLTZ CLASSIFICATION OF OSTEOMYELITIS.

Category A B

c

D

E

F G

Etiology, anatomical site, and physiological type Wound induced Mechanogenic Physeal OM Ischemic limb Combination of A-D Septic arthritis with adjacent OM Chromic OM with osteitis

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Ch. 3

Pus Periosteum Bone abscess Dead and dying bone (sequestrum)

A

B

Involucrum

c

D

Figure 3.1 Diagnostic Imaging Of Infection-radiographic signs of infection inctude increased soft tissue density and volume associated with inflammation and, in cases of OM, include osteolysis, involucrum, cloaca, and sequestration (Fig. 3.1). Osteolysis is not visible as radiolucency until 30-50% of osseous mineralization has been washed away by

inflammatory hyperemia. This generally takes 10-14 days after the onset of symptoms. Thereafter sclerosis and periosteal new bone formation, known as involucrum, surrounds necrotic and infected bone, known as sequestrum, and ultimately a channel, known as a cloaca, forms in new bone as bacteria proliferate and exudate drains. Chronic OM involves the presence of microbes living in dead bone (sequestrum), surrounded and contained within new bone (Involucrum). Eventually, after trauma or some other instigating factor, an ncute flare-up can develop with drainag·e, and signs and symptoms of acute infection. Chronic osteomyelitis can lay dormant for many years (reportedly> 50 years) before a flare-up occurs. In the presence of a chronic draining sinus due to OM (or other causes), squamous cell carcinoma (SCC) can develop in the epithelium along the sinus tract as a longterm seque!!um. Radionuclide studies can be useful in the evaluation of suspected OM, and include WB'C scans labeled with Tc-99 or 1n-111.ln most cases, bone scintigrams become positive within 48-72 hours. In patients with Charcot neuroarthropathy, or suspected fibrous nonunion, bone and joint infection may be strongly suggested with identification of a "hot" ln-111 or Tc-99 labeled WBC scan (Indium and Seratec scans, respectively). MRI may be the most useful imaging method when considering OM, however positron emission tomography {PET) scans have been shown to be even more

Ch. 3


45

sensitive and specific for Charcot neuroarthorpathy, in comparison to MRI scans. None of the imaging methods can be used to definitively ascertain OM, although alone and in combination, they can be very helpful. Definitive diagnosis OM is made by means of biospy, and bone gram stain and C&S. Treatment of Infection-the treatment of any infection, including OM, entails adherence to several general principles, including the 5 Ds: 1) decompression, 2) drainage,

3) debridement, 4) dressings, and 5) drugs. Decompression is achieved with incision and drainage 0&0) or removal of operatively-placed sutures, following surgical preparation. Drainage is achieved with copious lavage, debridement and excision of necrotic and/or grossly infected tissue, removal of implanted materials or foreign bodies, removal of unstable internal fixation devices, open packing with fine-mesh gauze, or partial or complete closure with drain placement, and use of an appropriate dressing. Tourniquets are generally not used when performing 1&0. The extent of infection is thoroughly explored and drained, and definitive cultures and stains are obtained from the deep tissues. In cases of OM, a small margin of apparently uninfected bone can be debrided and sent for pathological inspection. In any infection, drainage is allowed to proceed as long as necessary, usually a minimum of 48to 72 hours, with dressing changes consisting of lavage and debridement as indicated by wound appearance.lf necessary, additional debridement can be carried out by a return to the operating room, which is frequently necessary in cases involving necrotizing infection. Care should be taken to avoid performing a delayed primary closure too soon. Antibiotic Therapy-antibiotics are the primary drugs used in the treatment of infection. Consideration must be given to the spectrum of coverage, frequency of administration, toxicity, duration of treatment and cost. Prior to ascertaining the microbiological results of definitive culture specimens, empiric antibiotic therapy is initiated (Table 3-4). In cases of OM, antibiotic therapy is usually continued for 6 weeks following final debridement A Hickman, Broviac or PICC (peripherally inserted central catheter) can be used for longterm IV therapy. Monitoring the course of treatment of infection requires attention to fever, antibiotic levels, renal and hepatic function, wound appearance and pain, complete blood count(CBC) and differential, erythrocyte sedimentation rate (ESR), insulin requirement in the diabetic, and C&S results. Antibiotic impregnated calcium sulfate, or polymethylmethacrylate (PMMA), beads may be packed in the wound and used in conjunction with IV antibiotics. Antibiotic beads are usually made in the OR, using gentamycin, vancomycin, clindamycin, or another antibiotic, and packed in the debrided bone to increase local concentration of antibiotic. The wound is closed over the beads and, after 10-20 days (or sooner or later, depending upon wound appearance), the patient returns to the operating room tor bead removal, further debridement, and placement of more antibiotic beads if needed, or reconstruction and closure. A previously infected wound is ready for closure after achieving at least one negative culture, and the wound looks clean with beefy red granulations, no evidence of purulence or sinus tract, and resolution of marginal erythema. In some cases, delayed primary closure can be undertaken without first ascertaining a negative wound culture, as a wound that is clinically ready for closure usually has some degree of surface contamination. Closure may be achieved by means of secondary intention, or via delayed primary closure, skin graft, or flap. Previously infected wounds are generally closed over a drain of some sort, or only partially closed. Depending upon the specifics of the infection, use of the wound vacuum, as well as hyperbaric oxygen therapy, should also be considered.

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Ch.3

Diabetic Polymicrobial Infection-diabetic polymicrobial infection can be limb and life threatening. Plantar space infection may develop, with abscess dissection along fascial

planes of the plantar vault into the posterior compartment of the leg, or through an intermetatarsal space into the dorsum then into the anterior leg. The patient must be evaluated for constitutional signs and symptoms of septic shock, including incoherence or confusion, hypotension, tachycardia, and extreme hyperglycemia and ketoacidosis. Hospital admission and inpatient management are usually in order. It is useful to obtain a serum g!ucose level, CBC and differential, ESR, urinalysis, biochemical levels other than glucose, EKG, foot/leg and chest X-rays, blood cultures x3 from 3 separate sites 30 minutes apart, other labs and tests that may be warranted by the patient's individual condition, medical and anesthesia consultation and co~management, and supportive therapy in preparation 'for surgical debridement. Orders should also include NPO, wound and skin isolation, IV LR at KVO via 18~gauge IV catheter, specific medications (chronic and acute), non~weight bearing, on call to operating room for 1&0. The patient, and/or a family member, must be informed of the emergent nature of the condition, and possible consequences. Empiric antibiotic therapy should be initiated prior to identifying definitive culture results, and coverage should include anaerobic, aerobic, gram(+) and gram(~) organisms. A useful initial regimen consists of a combination of amoxicillin~clavulonate, clindamycin, and a quinolone (see Table 3-4). Intravenous antibiotics, such as ticarcillin-clavulonate, could also be used until definitive cultures are identified. It can be helpful to obtain an infectious disease consultation, as well as consultation regarding the potential benefits of hyperbaric oxygen therapy (HBOT). Incision and Drainage (I&D}-once the patient is prepared for surgery, 1&0 is performed in the operating room. The patient should be supine, without a tourniquet, and an orthopedic prep of the lower extremity performed. The wound or abscess is then probed to determine its extent and confines, after which a wide incision is made in order to allow drainage. Exploration entails inspection of all undermined or abscessed areas. In cases of diabetic plantar vault infection, decompression of the vault requires opening the deep fascia adequately enough to drain the medial, central, lateral, and deep plantar spaces, as necessary. Deep specimens are obtained for gram stain and C&S, necrotic and infected tissues are excised and biopsied, and foreign bodies are removed. IV antibiotics may be altered based upon the results ofthe gram stain, however empiric therapy usually does not change until definitive culture results are known. Copious lavage, sometimes using a pulsed, power-flushing system, is perfomed after initial sharp debridement. Close inspection is paid to all tissues prior to open packing with fine mesh gauze, then application of sterile dressing. Subsequent daily or BID dressing changes are performed with lavage and curettage of the wound, and additional specimens obtained for C&S as indicated by the appearance of the wound. If the patient and wound are not responding to the treatment, then there is either persistent abscess or the choice of antibiotic is incorrect An MRI could help detect an unrelieved abscess. A return to the operating room for additional debridement is performed whenever indicated, based on the patient's progress. The goal is to achieve a beefy red granular base, with no purulence or malodor, with decreased edema and erythema and pain, and no residual undermining or tunneling. Closure occurs thereafter via either continued secondary intention healing, or delayed primary closure, or the use of a skin graft or flap. In some cases involving aerobic infection, especially those with deep or large defects, as well as those with considerable drainage, vacuum-assisted wound closure can be helpful. The wound vacuum can also be used over skin grafts and flaps.

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47

Chronic Pedal Wound-when a patient presents with a chronic pedal wound, perhaps with intermittent drainage that has lasted for months, consideration should be given to the possibility of previous puncture wound or osteomyelitis. Common sites for chronic pedal wounds include the digits, metatarsal ball, 5th metatarsal base, heel, and perimaHeolar areas. Protective sensation should be determined, since chronic ulceration is very commonly associated with the insensitive foot {mal perforans ulcer). Puncture wounds that have penetrated the sole of the shoe are likely to involve Pseudomonas aeruginosa, although Staph aureus remains the most common pathogen in barefoot punctures and in children. As with a!I chronic wound, diagnostic images should be obtained, and consideration should be given to the potential benefits of wound margin biospy and surgical debridement. Radiographs are obtained, as are labs (as noted above for the diabetic infection), and consideration given to a bone scan, or aCT or MAl scan. When indicated, the patient is taken to the operating room for 1&0 and exploration. Do not dissect through the site of a chronic draining sinus tract if possible, when exploring bone that may not be infected. A dorsal approach can be useful in the case of a chronic plantar wound, as long as the nidus of infection is not obscured from inspection. If there is any concern about compromising drainage of the abscess, then simply excise the entire sinus tract The important point is to explore the involved area and obtain appropriate samples for gram stain and C&S, as well as soft tissue and bone biopsy. After obtaining specimens for C&S, then initiate IV antibiotics, lavage, pack open, and initiate daily wound care.

Fungal infection-fungal infections are extremely common in the foot and !ower extremities, and must be differentiated from other causes of papulosquamous eruption \secondary syphilis, psoriasis, pityriasis rosea, contact dermatitis) when localized to the glabrous skin. Fungi are eukaryotic and reproduce bv spore formation, grow as hyphae and form a mycelium. Some organisms, such as Candida, are dimorphic and grow as either yeast or fungal hyphae depending upon the host environment Fungi that infect humans are categorized as either dermatophytes (superficial) or deep pathogens. The most common pathogenic fungi affecting humans are the Fungi lmperfecti, although other groups can infect the compromised host. Identification of the infecting fungus is made via skin shaving or nail fragment exam for hyphae or yeast using KOH (potassium hydroxide) to dissolve keratin from skin scrapings, or periodic acid Schiffs (PAS) stain; and by means of fungal C&S using Sabouraud's dextrose agar (SDA). Superficial mycoses include tinea pedis, candidiasis (thrush), onychomycosis, tinea corporis, tinea cruris, tinea capitis, tinea axillaris, and tinea versicolor. linea pedis is usually responsive to topical antifungal cream application for 2~6 weeks, with agents such asterbinafine and econazole proving to be effective. Patients are encouraged to try oveHhe~counter antifungal preparations (tolnaftate, undecylenic acid, miconazole, c!otrimazole) for minor conditions oftinea pedis, if they have not already done so. Candida species often infectthe nail bed in compromised hosts, and cause paronychia and pseudo-clubbing due to chronic digital inflammation. Onychomycosis typically presents as either white superficial onychomycosis (WSO), which is usually caused by Trichophyton mentagrophytes or yeast and is least common; distal subungual onychomycosis (DSO), which is usually caused by T rubrum and is most common; and proximal subungual onychomycosis IPSO), which is also usually caused by T rubrum and is rare and usually associated with systemic disease or HIV. Onychomycosis must be distinguished from mechanically induced nail dystrophy, psoriatic pitting and flaking, lichen planus and pterygium, COPD induced clubbing, dystrophy due to peripheral vascular

48


Ch. 3

disease, and subungual exostosis. Whe·n harvesting nail and nail bed fragments for fungal tissue examination and C&S, it is imperative to obtain plenty of nail bed fragments from deep to the nail plate. Palliative treatment of onychomycosis includes nail plate debridement and regular application of topical antifungal (ciclopirox 8% lacquer or miconazole 2% solution, or similar agents), however cure rates are usually< 75~80% with topical therapy, although debridement alone is known·to improve foot~related quality of life. Cure is more likely with oral administration of either terbinafine (250 mg PO QD x 3 months) or itraconazole (200 mg PO QD x 3 months), or perhaps fluconazole (as an adjunct for the treatment of yeast). it is prudent to check liver enzymes and CBC, current medications, and past medical history, prior to initiating oral antifungal therapy. Chemically induced hepatitis has been greatly diminished using the newer systemic antifungal agents, as therapy is only administered for 3-4 months, generally. Drug interactions (certain antihistamines, anti-lipid agents, and others) must also be considered prior to initiating oral antifungal therapy. The active metabolite of the agent is maintained in the substance ofthe nail for 6-9 months, and the ultimate appearance of the nail plate cannot be truly assessed until 6-12 months following initiation of oral therapy. Prevention of recurrent onychomycosis may require periodic maintenance use of topical therapy, and concurrent debridement is a crucial part of any treatment plan. Deep mycoses include mycetoma and madura foot, sporotrichosis, and blastomycosis; caused by Madurefla mycetoma, Sporothrix schenkii, and Blastomycoses, respectively. Deep fungal infections are granulomatous, with papular and nodular inflammation of the subcutaneous tissues and overlying skin, sinus tract formation, foul odor, and secondary bacterial infection may ensue. Treatment may require excision of infected tissue, including amputation, and systemic administration of amphotericin-8 (sporotrichosis), sufonamide and other oral antifungal agents (mycetoma, madura foot, blastomycosis).

Septic Arthritis (see Arthritides) Antibiotic Therapy-antibiotic therapy varies from community to community, and the clinician is encouraged to be familiar with the characteristics of the organisms in his/her own community. The local hospital's antibiotic susceptibility and causative organism prevalence report can be a useful guide to therapy, and the county health department also monitors organisms responsible for reported infections. Although it is often necessary to initiate therapy empirically, it is always adviseable to obtain a culture from the lesion if this is possible. Once again, appropriate specimens should be obtained for isolation of the causative organism and determination of its susceptibility to antibiotic therapy. Bacterial cultures are particularly important in cases of severe infection, in diabetic or compromised hosts, and for chronic or recurrent infection wherein previous culture and sensitivity has not been performed. In all cases of infection, ongoing assessment of the response to therapy must be undertaken. Therapy is generally continued for 10-14 days for soft tissue infections, and 6 weeks for OM, and the treatment should be honed to the individual patients specific local and systemic requirements. The following information is meantto serve as a general guide to antibiotic therapy for infections involving the foot. ankle and leg. Since organisms and antibiotcs evolve and change frequently, the reader is encouraged to check with appropriate updated literature, such as the drug package insert, for specific indications and dosages.

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49

Methicillin-resistant Staphylococcus aureus(MRSA)-community acquired methicillinresistant Staphylococcus aureus (MRSA) represents an ever-increasing proportion of wound infections, particularly in children. MRSA resists the cidal effects of beta lactam antibiotics such as penicillin and cephalosporin, including cephalexin, ceftriaxone, and amoxicillin-clavulanate; and the organism may also resist the static effects of

erythromycin, clarithromycin, and azithromycin. Potentially useful oral agents include clindamycin, trimethoprim-sulfamethoxazole, doxycycline, and linezolid; IV agents include vancomycin or daptomycin; and mupirocin can be used topically. Rifampin can also be used, however not as a sole antibiotic. For limb- or life-threatening MRSA infection, high-dose IV antibiotic therapy using vancomycin or daptomycin, perhaps combined with gentamicin, should be considered. Some strains of MRSA display "inducible resistance" to agents such as clindamycin, and these can oftern be identified using the "D test." A positive "D test" is associated with an increased risk of antibiotic resistance, and careful clinical follow~up is important. In an effort to prevent colonization and relapsing infection, 4~6 weeks of therapy may be necessary. Postoperative Infection------overall, the prevalence of postoperative infection ranges from

1~2% of clean, elective bone surgical cases, and most of these involve Staph. aureus. In cases involving implant infection, Staph. epidermidis, with its glycocalyx, is also common. Other causative species associated with postoperative infection include Proteus, Pseudomonas, B-hemolytic Streptococcus, Klebsiella, Serratia, Enterobacter, E. coli, and Bacteroides. In general, when stable osteosynthesis implants are present in cases of acute postoperative infection, metallic fixation devices are left in place unless they are associated with loose or necrotic bone (hence, loose or unstable). Chronically infected hardware should be removed and osteomyelitis therapy instituted. Puncture Wounds-the status of the patienfs tetanus prophylaxis should be ascertained whenever a puncture wound is encountered. Appropriate diagnostic measures combined with local wound care and antibiotic therapy are basic elements in the treatment of puncture wounds. In general, antibiotic therapy should cover Staph. aureus, and other gram(+) organisms, with appropriate attention to 1&0 if edema, cellulitis, induration, pain and Hx suggest abscess. The use of cephalexin, dic!oxacillin, or amoxicillin/clavu!onate should be considered. Punctures also convey the risk of anaerobic infection, and radiographs should be inspected for the presence of subcutaneous gas, primarlly hydrogen sulfide. Gas~ forming infections are usually necrotizing and require timely 1&0, and hyperbaric oxygen therapy may also be useful (see Necrotizing Infection, above). For punctures that involve penetration through the sole of the shoe, coverage of Pseudomonas sp. should be considered, and potentially useful agents include aztreonam + clindamycln, or imipenem + ci!istatin, piperacillin +tazobactam, or ampicillin+ sulbactam (see Table 3~4). Empiric Antibiotic Therapy-the following table (Table 3.4) is meant to provide guidelines for empiric antibiotic therapy, and the reader is encouraged to obtain definitive specimens for C&S, and to be familiar with the detailed information contained in the package insert for the specific antibiotic used.

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Ch. 3

TABLE 3-4. EMPIRIC DRUGS OF CHOICE fOR PREDOMINANT BACTERIA SEEN IN ADULT FOOT AND ANKLE SURGERY.* Organism Gram(+) Staphylococcus (methicillin sensitive)

Therapy of Choice

Alternate Therapy

cephalexin 1250 mg PO OlD) cefazolin (1-2g IV q8h)

Streptococcus

clindamycin (300 mg PO OlD) vancomycin 115 mg/kg IV ql2h) dicloxacillin 1250 mg PO OlD) nafcillin 12 grams IV q4h) azithromycin 1500 mg as a single dose on day 1, followed by 250 mg daily on days 2-5) clindamycin 1300 mg PO OlD)

penicillin (penicillin V 0.25-0.5 grams PO TID-OlD, or penicillin G 1.2-20 million units IM/IV per day) cephalexin (250 mg PO OlD) vancomycin 115 mg/kg ql2h IV) cefazolin (1-2g IV q8h) vancomycin 115 mg/kg IV q12h) clindamycin (300 mg PO OlD) doxycycline (0.1 gram PO/IV q12h) minocycline 10.1 gram PO ql2h) linezolid (600 mg PO/IV q12h) TMP/SMX 11 OS tab PO BID) gentamicin 12 mg/kg load followed by 1.7 mg/kg IV q8h) [if limb- or life threatening] ampicillin (250 mgamoxiclllin-clavulonate 1 gram PO TID) l875/125mg PO q12h x 14 days) vancomycin (15 mg/kg IV q12h) gentamicin (2 mg/kg IV load Streptomycin 115 mg/kg IM q24h) followed by 1.7 mg/kg IV q8h) piperacillin/tazobactam (3.375 grams IV q6h) combination ciprof!oxacin i500750 mg PO BID), rifampin (10 mg/kg/day up to 600 mg/day PO single dose), gentamicin 12 mg/kg load fullowed by 1.7 mg/kg IV q8h) or ceftriaxone (1-2 grams IV once daily) chloramphenicol (0.25-1 gram PO/IV q6h up to 4 grams/day)

Staphylococcus \methicillin resistant)

enterococcus vancomycin resistant enterococcus

!

-

Ch. 3


51

Gram(-)

Escherishia coli, Proteus cephalexin (250 mg PO QID) ECSM group

ciprofloxacin (500-750 mg PO BID)

Pseudomonas aeruginosis

ciprofloxacin (500-750 mg PO BID)

Anaerobic infection Bacteroides

Diabetic foot infection polymicrobial

ciproftoxacin (500-750 mg PO BID) cefazolin (1 gram IV qBh) 3rd generation cephalosporin (such as ceftriaxone 1-2 grams IV once daily) aztreonam (1 gram qBh2 gram IV q6h) TMP/SMX (1 DStab PO BID) ceftazidime (2 grams IV q8h) aztreonam (2g IV q8h) gentamicin (2 mg/kg load followed by 1.7 mg/kg IV q8h)

metronidazole (500 mg PO q6-8h)

clindamycin (300 mg PO GID)

amoxi cilli n-c Iavu Ion ate (875/125mg PO q12h x 14days) cefazolin (1-2 grams IV qBh) +metronidazole (500mg PO/IV q6-8h)

ampicillin sulbactam (1.5-3 grams IV q6h) ticarcillin clavulonate (3.1 grams IV q6h) piperacillin tazobactam (3.375 grams IV q6h) lmipenem cilistatin (500mg IV q6h)

vancomycin (15 mg/kg q12h IV)+ aztreonam (2g IV q8h) + metronidazole (500mg PO/IV q6-8h)

*Specific dosages, serum drug level monitoring, creatinine and other appropriate serum laboratory tests, culture and sensitivity, adjunct therapy, and clinical reassessments should be individualized to the specific patient The reader is encouraged to consider the factthat recommended antibiotic therapy often varies overtime and geographic area.

ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) AIDS is caused by infection with the cytopathic human immunodeficiency virus (HIV) retrovirus (RNA virus), which causes cell death. The CD-4 surface glycoprotein is the essential molecule recognized by the retrovirus, on the surfaces ofT41ymphocytes, monocytes, and macrophages. T-helper lymphocytes also become infected and destroyed, which greatly impairs the immune system. Natural killer lymphocytes are also destroyed, which impairs immune surveillance against neoplasms and virus infected cells. Approximately 40% to 50% of patients infected with HI\/, and possessing less than 400T-helper cells, develop AIDS within 2 years of HIV infection. Eighty-five percent of patients with T-helper cells less than 200, will develop AIDS within 2 years of infection.

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Ch. 3

Four Stages of Hl\llnlection Stage 1- manifesting acute HIV, wherein the patient displays general malaise and "mono-like" symptoms Stage II - chronically infected wrth HIV, often asymptomatic while developing antibodies to HIV Stage Ill- persistent generalized lymphadenopathy Stage IV- serious manifestations of immunodeficiency, frequent serious infections

and debilitation Subgroups ol Manifestations of Hill Infection Subgroup A- Constitutional symptoms Subgroup B- Neurological syndromes Subgroup C- Associated with infectious diseases C(1)- Defect in cell mediated immunity (Pneumocystis pneumonia) C(2)- Less profound infections Subgroup D -Secondary cancers (e.g. Kaposi's sarcoma) Subgroup E- Chronic lymphoid interstitial pneumonitis The treatment of AIDS includes supportive measures, as well as suppressive and disease modifying agents such as AZT. Therapeutic regimens have been shown to be most effective when disease modifying agents are used in synergy. Maternal transmission of the disease to the fetus has been controlled with AZT. Treatment regimens are very expensive. Any patient suspected of being HlV positive should be counseled regarding the importance of testing to confirm the presence of antibody, then appropriately referred for infectious disease consultation. Social setvices consultation is also important as various agencies may be able to assist with therapy. Regardless of whether or not you suspect a patient of being HIV positive, univers.al precautions are the standard of care in ALL aspects of health care.

SElECTED PERIPHERAL VASCULAR DISEASES Raynaud's Phenomenon Raynaud's phenomenon is an episode of small arterial and arteriole constriction resulting in acral pallor, cyanosis, or both color changes; with subsequent rubor due to hyperemia after the vasospasm has subsided {white, blue, and red coloration pattern).ln severe cases, prolonged vasospasm can effect cutaneous digital gangrene. The condition is usually bilateral, however it may rarely be unilateral. It is more common in females. Serious organic disease (atherosclerosis) is not usually present in the vessel in Raynaud's phenomenon. When a specific cause for the vasospasm, such as trauma, connective tissue disease, or neurogenic, cannot be identified after several years of suffering, then the condition can be termed Raynaud's disease (also known as primary Raynaud's phenomenon). Secondary Raynaud's phenomenon can be attributed to trauma, either acute or repetitive microtrauma; neurogenic due to nerve entrapment such as thoracic outlet, carpal or tarsal tunnel syndromes; occlusive arterial disease such as thromboangitis obliterans, arteriosclerosis obliterans, or status-post arterial thrombosis or embolism; thermal injury such as trench foot (cold and wet); or for miscellaneous conditions such as scleroderma, lupus erythematosus, RA, dermatomyositis, Fabry's disease, cryoglobulinemia (as in multiple myeloma or chronic leukemia), hemoglobinuria, myxedema, neoplastic disease, hepatitis B, pheochromocytoma, and ergotism. Treatment consists of protection, maintaining warmth,

Ch.3

Sele~;ted

Diseases and Pathological Conditions

53

use of vasodilators (Procardia, alpha~adrenerg.ic blocking prazosin, norepinephrine

depleting methyldopa, and reserpine), topical nitroglycerine and antibiotics. Frostbite and Cold Injury Frostbite implies freezing of the skin. Superficial frostbite is also termed chilblains, and is a mild cold injury. Classifications of frostbite 1st degree (chilblains)- skin frozen, no blisters 2nd degree -skin frozen, blisters formed 3rd degree- skin frozen and necrotic, ulceration, subcutaneous exposure 4th degree- skin and subcutaneous tissue frozen and necrotic. The treatment of chilblains is re-warming in 105-108° Fwhirlpool for 30 minutes, and administer analgesic (meperidine). Blisters are left intact unless they have ruptured, wherein they are treated as burns with cleansing debridement, Silvadene and dry sterile dressing. The treatment of more advanced or deep frostbite is rapid rewarming in 108~ 110° F water, administer antibiotic (cefazolin), tetanus prophylaxis, and analgesic (meperidine). It is important to protect the frozen part until proper thaw and care can be administered, and to avoid thaw followed by refreeze. PosHreezing sequella include vasomotor instability and cold hypersensitivity, paresthesia, depigmentation, hyperhidrosis, and atrophy. Arteriosclerosis Obliterans (Atherosclerosis Obliterans, ASO~ASO is the primary cause of occlusive lower extremity vascular disease, with the main lesion being atherosclerotic plaque occlusion of the superficial femoral or femoral level arteries. It is most common in males age 50-70 years, and more likely in patients with diabetes mellitus, hypertension, cigarette smokers, and/or hyperlipidemia. Pathological findings include atheromatous plaque formation, with secondary thrombosis. Symptoms include intermittent claudication, rest pain, cold intolerance, ulceration and gangrene, ischemic neuropathy, disuse atrophy, joint stiffness and contracture. Aorta or iliac artery occlusion causes buttock, hip and thigh pain; occlusion of the femoral artery and its branches causes thigh and calf pain; and popliteal and tibial artery occlusion causes calf, ankle and foot pain. Findings include diminished peripheral pulsation, discoloration (dependent rubor, pallor, or cyanosis), exaggerated distal cooling, edema, atrophy, cutaneous compromise, intrinsic atrophy, ulceration, and gangrene. The ankle-brachial index (ABI, Table 3-51. toe pulse pressure and amplitude, and TcPO, are diminished. Healing is generally anticipated if: ABI >.5, toe pressure >40 mm Hg, TcP0,>30 mm Hg, and toe pulse amplitude >4 mm. Duplex Doppler ultrasound noninvasive vascular testing, magnetic resonance angiography, and perhaps an arteriogram if surgical care warrants, can assist in the diagnosis. Treatment includes con~ trol of associated systemic disease (HTN, hyperlipidemia, anemia, arrhythmia). avoiding cold exposure, exercise to tolerance, hemorheologic agent (pentoxifylline, cilostazol), antiplatelettherapy (aspirin, clopidogrel, ticlopidine, dipyridamole), vasodilating agents (a and ~~adrenergic blockers, calcium channel blockers), peripheral angioplasty or vascular reconstruction, or amputation. Operative intervention is warranted whenever claudication, rest pain, or non~helaing wound is present. Peripheral arterial disease is often associated with carotid, coronary, and renal vascular insufficiency.

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Ch.3

TABlE 3-5. ANKLE-BRACHIAL INDEX (ABI) CATEGORIES.* Ratio >0.96 0.81-0.95 0.051-0.8 ,0.05

Category Normal Mild obstruction

Moderate obstruction Severe obstruction

*Misleading, elevated ratios may be observed in cases of noncompressible arteries. Thromboangiitis Obliterans (TAO, Buerger's Disease)

TAO is a segmental inflammatory, obliterative disease of medium sized arteries and veins (posterior tibial), most common in the lower extremities of males who smoke cigarettes, the cause of which is unknown. TAO results in gangrene. Treatment involves arresting

progression of the disease by avoiding tobacco products, administering anticoagulants and corticosteroids; followed by effecting vasodialation with Procardia or other agents; and surgical management of gangrenous wounds.

Monckeberg's Medial Calcific Sclerosis This is a form of non-atheromatous degenerative arterial disease observed in middle-age to elderly males. There is fine calcification of the tunica media, which may lead to a non-compressible vessel, and effect a misleadingly high ankle/arm index. This occurs in the aorta and other large vessels. Venous Thrombosis and Pulmonary Embolism-the deep veins of the lower extremity include the plantar arch, posterior tibial, peroneal, anterior tibial, sura!, popliteal, superficial femoral, and deep femoral. Venous thrombosis, particularly ofthe deep system at or above the popliteal fossa, is associated with pulmonary embolism (PE), and for this reason can be fatal or extremely morbid. Predisposing factors fOr venous thrombosis include congestive heart failure, malignancy, trauma, surgery, pregnancy, and thrombocytosis. Other risk factors include cigarette smoking, oral contraceptive use, obesity, advanced age, bed rest or confinement, and paraplegia. Deep venous thrombosis prophylaxis should be instituted in patients at risk (Tables 3-6 and 3-7). Lower extremity deep vein thrombophlebitis {OVT, also known as venous thromboembolism, or VTE) presents with deep, aching pain and tightness in the calf or thigh. Pain upon active dorsiflexion ofthe ankle, or resistance to ankle dorsiflexion is known as Homan's sign, and is a nonspecific and unreliable clinical diagnostic maneuver. Tenderness upon calf or thigh muscle compression is a more specific test for DVT, when associated with edema and local increase in skin temperature. Superficial thrombophlebitis, which conveys a lower likelihood of PE, more commonly displays local heat, edema. erythema, and a palpable cord consistent with the thrombosed vein. Application of a tourniquet above the suspected thrombosis may cause pain at the level ofthrombosis within 30~45 seconds, and is strongly suggestive of DVT. Comparison of calf circumference wiH often show enlargement of the affected side. Constitutional findings may include temperature elevation 139.5'-40.5" C), chills, and malaise. Arterial embolism is usually more painful early on, with less swelling, exaggerated distal temperature decrease, and early sensory deficit. Severe venous thrombosis effecting retrograde arterial flow decrease may result in phlegmasia cerulea dolens, which can result in pedal ischemia and gangrene. Coagulation studies are usuarty

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55

normal unless full blown disseminated intravascular coagulation (DIC), familial

antithrombin Ill deficiency, or lupus erythematosus clotting inhibitors exist The laboratory diagnosis of DVT hinges on venous non-invasive duplex Doppler examination, and

magnetic resonance venography or contrast venography may be employed if ultrasound is equivocal. Radioactive 125 1-fibrinogen scanning, in conjunction with occlusion impedance plethysmography is also a sensitive combination for DVT of the calf. Use of the 0-dimertest may also be useful, however combined clinical and venographic tests are more reliable. An accurate diagnosis of DVT is made upon identification of predisposing factors and clinical observation, combined with duplex Doppler ultrasound and, perhaps, magnetic resonance venogram or contrast venography. Prevention of DVT is recommended, and can be achieved in several different ways (Tables 3-6 and 3-7). Prophylactic therapy in the !ow-risk patient involves mini-dose subcutaneous administration of 5000 units of heparin every 8 or 12 hours beginning about 60 minutes preoperatively. Adjunct physical measures include support hose, intermittent sequential pneumatic compression of the lower extremity, leg elevation with the knee flexed, and out-of-bed activity at an early stage after surgery. In high-risk patients, DVT prophylaxis is administered preoperatively with mini-dose heparinization, however in the postoperative phase, the heparin dose is adjusted upward to keep the PTT within 4 seconds of high norma!. Despite statistically more postoperative hemorrhage, this form of DVT prophylaxis appears to be worthwhile in the high-risk patient A baseline platelet count is recommended prior to mini-dose heparinization, and should be monitored periodically if it is observed to be low. High-risk patients may also be prophylaxed with a combination of mini-dose heparin and dihydroergotamine, which causes venular constriction and rapid venous return. Other prophylactic combinations include heparin and antithrombin Ill administration, and the use of low molecular weight heparin administered once daily has been shown to be effective and popular (see risk stratification and ·guidelines for prophylaxis, below). Coumadin, which inhibits the vitamin !<-dependent clotting factors II, VII, IX, X, and proteins C and S, can also be administered preoperatively and during the postoperative phase to effect DVT prophylaxis.

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56

TABLE 3-6. DVT RISK STRATIFICATION (ASSIGN POINTS BASED ON PROCEDURE, DISEASE, AND OTHER PATIENT-RELATED FACTORS). Risk factors

•

Operating room time> 105 min

•

Tourniquettime >90 min Rearfoot or ankle surgery Age 40-60 years Pregnancy or postpartum <1 month

•

Varicose veins

• • •

Obesity (>20 lbs over ideal body weight) Diabetes meHrt:us Hypertension Hyperlipidemia Smoker Polycystic ovary syndrome Immobilized in BK or AK cast for> 1 week

• • •

•

Risk factor points assigned

Patient confined to bed for >72 hours Central venous access Age >60 years Oral contraceptive use Hormone replacement therapy Inflammatory bowel disease

2

Congestive heart failure •

Ankle, pi!on or tibial fracture

•

Severe sepsis/infection

3

Mu~iple

trauma Acute spinal cord injury

Cancer treatment Currently treated or history of DVT or PE

5

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57

TABLE 3-7. DVT RISK STRATIFICATION AND GUIDELINES FOR PROPHYLAXIS. Risk

points 0

1-2

3-4

Risk stratum Low

Moderate

High

Very high

Clinical features •<40yearsold • Minor surgery <30 minutes

Prophylaxis

• Patient education • Early ambulation

• 40-60 years old +minor surgery • General anesthesia >30 minutes • Minor surgery + 1 or more other risks

• Patient education, early ambulatlon, elastic

• >60 years old+ minor surgery+ no other risks e >40 years old+ minor surgery+ any other risk

• Patient education, early ambulation, elastic stockings •Intermittent pneumatic compression (ifNWB) ., Low dose unfractionated heparin (5000 units sq), or low molecular weight heparin (enoxaparin 30 mg sq q 12 hours or 40 mg sq qd) • Mechanical therapy starting 1-2 hours before surgery, or 12-24 hours postop if needed to achieve adequate hemostasis • Continue therapy throughout hospitalization and up to 7-14 days, then decide duration based on degree of immobilization, ROM and WB status

• > Past PE, cancer or major trauma •>40yearsoldt major surgery+ any other risk factor

• Patient education, early ambulation, elastic stockings •Intermittent pneumatic compression (ifNWB) • Low molecular weight heparin (enoxaparin 30 mg sq q 12 hours or 40 mg sq qd), or fondaparinux, or adjusted dose heparin • Warfarin (therapeutic when INR 2-3) • Start therapy 1-2 hours preop, or 12-24 hours postop if needed to achieve adequate hemostasis • Continue therapy 10-14 days or entire time of immobilization • Encourage early ROM and/or WB if indicated

stockings •Intermittent pneumatic compression (if NWB) • Low dose unfractionated heparin (5000 units sq), or low molecular weight heparin (enoxaparin 30 mg sq q 12 hours or 40 mg sq qd) • Mechanical therapy starting 1-2 hours before surgery, or 12-24 hours postop if needed to achieve adequate hemostasis • Continue therapy while inpatient or during initial recovery, then decide whether to extend 7-14 days

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Ch. 3

Treatment of DVT involves assessment of the PT and PTT, followed immediately by IV infusion of heparin 5000~ 10,000 units. Thereafter, heparin is infused continuously at a rate of 800-1500 units per hour, maintaining the PTI at2-2.5 times the baseline value, and the INR at 2.0-3.0. The patient is maintained at bed rest with the lower extremities elevated at 15 degrees to 20 degrees above the level of the heart. It takes approximately one week for thrombi to become firmly adherent to endothelium and thereby diminish the risk of PE. Coumadin is started as soon as longterm anticoagulation is planned, and takes 3-5 days to

become therapeutic monitoring the PT. The patient is maintained in an anticoagulated state for 4-6 weeks for the treatment of isolated calf DVT, and for 3-6 months for more proximal vein thrombosis. Clinical and/or venographic evidence of clot propagation indicates the need for vascular surgical consultation regarding the potential benefits of Greenfield filter (umbrella) placement in the inferior vena cava. Moreover, thrombolytic therapy, or phlebectomy in rare instances, may be indicated. Postphlebitic syndrome may ensue, and involves venous insufficiency, chronic venous stasis dermatitis, permanent ca!f enlargement and predisposition to recurrent superficial and deep thrombophlebitis, postphlebitic neuritis, and the need for indefinite use of support hose and perhaps other physical measures.

Chronic venous insufficiency(postphlebitic syndrome, chronic venous stasis) affects the skin and subcutaneous tissues of the legs and ankles; and may occur secondary to DVT, varicose veins, cavernous hemangioma, congenital A-V fistula, or pelvic neoplasm obstructing venous outflow from the lower extremity. Findings include edema, stasis dermatitis with hyperpigmentation, eczema, induration, pain, and ulceration. Ulcerations are usually peri-malleolar, and display sharply demarcated or "punched-out" margins (local tissue hypertension). Squamous cell carcinoma may develop. Treatment consists of elevation, application of an Unna-paste bandage, antibiotics as indicated, diuresis, and protection. Consideration should be given to the potentially beneficial effects of topical corticosteroid on inflamed, non-ulcerated skin. Atypical skin lesions should be biopsied. Skin grafting, often in combination with vein surgery wherein varicosities are ligated or sclerosed, and incompetent perforating veins are bypassed via direct connection of superticial veins to deeper veins, may also be usefuL Pulmonary Embolism IPE} PE is very common and a leading cause of death in the US. Lower extremity DVT accounts for 60-80% of PEs. Thrombi embo!ize from the lower extremities, traverse the pelvis and inferior vena cava, then enter the right side of the heart, and subsequently obstruct the pulmonary vessels. Pulmonary infarction ensues thereafter. Clinical signs and symptoms vary with the degree of pulmonary occlusion and infarction, and include crushing chest pain, dyspnea, tachypnea, tachycardia, low grade temperature elevation 138" C [101" F]}, neck vein distension, ipsilateral diaphragm elevation on standard chest X-ray, a positive ventilationperfusion lung scan ("'I or 51Cr}, S-T segment depression (cardiac hypoxia} and other EKG changes, arterial blood gas abnormalities such as decreased P02 and PC02 and Ph, increased serum LDH and bilirubin in the presence of normal SGOT. The differential includes acute Ml and pneumonia.

Treatment includes immediate anticoagulation with IV administration of 5,000-10,000 units of heparin, followed by continuous infusion of 800-1500 units/hr while monitoring the PH Supportive measures include administration of D2, bed rest, and analgesia; while

Ch. 3


59

proceeding with definitive diagnostic measures. Thrombolytic therapy, or surgical phlebectomy, may be indicated. Septic pulmonary emboli may be observed as a

complication of infected pelvic thrombosis, indwelling catheter, transvenous pacemaker, arteriovenous or ventriculovenous shunts, or in cases of IV drug abuse.

Fat embolism is most common after long bone or pelvic fracture. Cerebral infarction symptoms of restlessness, confusion, stupor and coma may accompany pulmonary symptoms of dyspnea and tachypnea; in conjunction with fever, lipuria, and the appearance of chest and conjunctival petechiae. The treatment of fat embolism includes supportive measures identified previously for PE (heparin also activates lipase), in addition to large doses of corticosteroid.

Catheter embolism is also possible when central venous catheterization is performed. Surgical excision is usually indicated in patients that can sustain operative intervention. lymphedema Lymphedema is swelling of soft tissues due to an increased quantity of lymph, which is also associated with increased tissue fluid found outside of the blood and lymphatic capillaries. Primary (idiopathic) lymphedema is noted to be present at birth (congenital), seen early in life (lymphedema praecox), or observed late in life (lymphedema forme tarde). Congenital lymphedema can be hereditary (Milroy's disease) or non-familial (simple congenital). Consideration should be given to congenital or acquired hemihypertrophy. Secondary lymphedema is of either the obstructive or inflammatorytype. Obstructive lymphedema occurs secondary to either malignant occlusion, or surgical radiation-induced disruption, of lymphatic channels and/or nodes. Nontropical inflammatory lymphedema is highlighted by recurrent lymphangitis and cellulitis, fever and chills, adenopathy, and is attributed most commonly to streptococcus infection (although trichophytosis, and other microbes may be causative). Tropical secondary lymphedema is attributed to filariasis. Chronic lymphedema may cause fibrosis, verrucous dermatitis, ulceration, elephantiasis, and/or lymphangiosarcoma (rare). The differential diagnosis for lymphedema includes hypothyroid myxedema, CHF, nephrotic syndrome, and hypoproteinemia. Clinical acumen and historical interview are the mainstays of diagnosis, and biopsy may be beneficial. Treatment should be instituted as early as possible, and is primarily medical, although surgery may be indicated rarely. Medical treatment consists of elevation of the edematous part, diuresis (furosemide), prophylactic anticoagulation with subcutaneous heparin, and observation of serum potassium. Antibiotics may also be indicated. After initial reduction of the extremity, customized support hose measured and fabricated for regular wear, and longterm diuresis may be maintained. If medical therapy fails, vascular consultation regarding surgical efforts aimed at improving lymphatic drainage or excision of edematous tissues may be entertained.

DIABETES MELLITUS Diabetes mellitus (OM) affects about 10 million people in the US. It is a leading cause of blindness, renal disease, PVD, peripheral neuropathy, lower extremity ulceration and amputation, and death. In DM, the ability to oxidize carbohydrates is diminished or lost, usually due to pancreatic dysfunction, particularly of the islets of Langerhans, with resultant disruption of insulin function. Classification includes insulin-dependent diabetes mellitus (lOOM, Type 1, juvenile-onset [although it can develop in adulthood]), and non-insulin

60


Ch.3

dependent diabetes mellitus (NIDDM, Type 2, adult-onset}.IDDM is caused by autoimmune destruction of pancreatic beta cells, and must be treated with insulin replacement NIDDM can be divided into obese and non-obese groups, the obese group displaying the possibility of returning to euglycemia associated with weight loss and dietary control. Gestational OM is observed during pregnancy, and usually subsides postpartum. Findings include hyperglycemia, polyuria, polydipsia, polyphagia, emaciation, weakness, acidosis due to dysfunctional fat metabolism, dyspnea, ketonuria, and coma. lmmunopathy accompanies long-standing hyperglycemia. Diabetic ketoacidosis or non ketotic hyperosmolar coma may result from prolonged or severe hyperglycemia. Diabetic retinopathy and nephropathy are the result of small vessel diseases associated with long-standing hyperglycemia. Diabetic peripheral neuropathy produces pain and paresthesia, pedal insensitivity, anhidrosis, vasodialation, brittle hyperkeratosis, mal perforans ulceration, and Charcot neuroarthropathy. All patients suspected of having OM, or previously diagnosed with the disease, should undergo pedal monofilament esthesiometer testing to determine whether protective sensation is present Diabetic dermopathy creates thin, atrophlc, and friable skin in the pretibial region, wounding of which results in post-inflammatory hyperpigmentation. Necrobiosis lipoidica diabeticorum also affects the pretibial area as an atrophic plaque with telangiectasia, and microscopically displays palisading granuloma formation.·The laboratory diagnosis of DM hinges on an abnormal glucose tolerance test, and/or repetitively high fasting blood glucose measurements. C-peptide assay can be used to distinguish endogenous insulin, and Type 2 OM, from exogenous insulin (administered for therapy), since exogenous insulin doe not contain C-peptide. The GAD 65 antibody assay can also be used to distinguish Type 1from Type 2OM. Therapy includes effortsto identify the cause, after which dietary controls and exercise are instituted (as indicated). Patient education is a crucial partofthe management of DM. Oral hypoglycemic agents may be used in conjunction with dietary control, and include sulfonylureas (chlorpropamide, tolbutamide, tolazamide, and acetohexamide), as well as metformin. Insulin preparations are indicated when the blood glucose level is not adequately controlled with diet and oral medication, and in cases of Type 1 DM. Adjusting the administration of insulin requires close communication between the internist and the patient, and often entails lifestyle alteration. In the peri-operative period, a sliding scale of insulin, based on the blood glucose value, can be useful until a regular regimen is resumed. The goal of therapy in the perioperative phase is to maintain plasma glucose between 150-250 mg%. Pancreas and islet cell transplantation can also be used in an effort to cure DM.

THYROID DISEASE Hypothalamic thyrotropin-releasing hormone stimulates pituitary release of thyroid stimulating .hormone, which activates thyroidal uptake of iodine and production of thyroxine (T,} and triiodothyronine (T,}, which exert negative feedback inhibition of pituitary thyroid stimulating hormone release. Thyroid hormones regulate metabolism. Enlargement of the thyroid gland is referred to as a goiter, and may be associated with overactive or underactive function. Hypothyroidism can occur due to surgical or medical (radioactive iodine) ablation, or inflammation (Hashimoto's disease) of the thyroid gland; or secondary to hypothalamic or pituitary dysfunction (tumor, CVA, trauma, other}. Hypothyroidism effects myxedema, which specifically presents as non-pitting edema, associated with facial changes that include swelling and a thickened nose, dry or hoarse voice, dry and waxy skin, and mucinous deposition in tissues. Hypothyroid patients display fatigue, general malaise, weight gain, bradycardia, and may become comatose (myxedema coma) in severe disease. Thyroid

Ch.3


61

supplementation with T• (Synthroid) and T, (Cytomel), or natural preparations, as well as supportive therapy are used as indicated. Hyperthyroidism, or Grave's disease, effects exophthalmos (lid lag), tachycardia, profuse diaphoresis, nervousness, restlessness, fine tremors, emaciation, and psychosis. Treatment involves supportive measures and drugs that alter hormone metabolism or the end-organ effects of the hormone. Thyroid storm is a medical emergency wherein severe hyperthyroidism effects organ damage and death. Drugs

that inhibit hormone formation and release include thiourea derivatives that block organification of iodine, iodide which blocks thyroid hormone synthesis, and lithium which blocks release of thyroid hormone. Propranolol controls the peripheral manifestations of thyroid hormone. Radioactive iodine destroys thyroid tissue, thereby decreasing thyroid function and possibly effecting hypothyroidism (which can be treated with thyroid supplementation).

HEPATITIS Inflammation of the liver can be caused by trauma, toxins, autoimmune disease, and viral infection. Liver dysfunction results in inability to detoxify a wide range of substances, failure to produce blood elements, such as platelets, and inadequate bile production, resulting in faulty digestion. Acute hepatitis lasts< 6 months, and can result from trauma, vascular insult, viral infection {cytomegalovirus, Epstein-Barr, Herpes simplex, adenovirus, hepatitis A virus [infectious jaundice, due to picornavirus], hepatitis E viruses [common during pregnancy]), bacterial or parasitic infection (Rocky Mountain spotted fever, Leptospira, toxoplasmosis, and Q fever), toxicity (alcohol, carbon tetrachloride, APAP, minocycline, isoniazide, ketoconazole, methyl-dopa, nitrofurantoin, ch!orambutol, penicillin, anesthetics, mushroom toxin), collagen vascular disease (SLE), and metabolic or inherited disorder (Wilson's disease, alpha 1-antitrypsin deficiency). Chronic hepatitis lasts > 6 months, and can result from any of the conditions that cause acute hepatitis, if the condition persists or treatment fails, or the most common forms are related to the hepatitis viruses B, C, and D. Hepatitis B, due to hepadenovirus, results in chronic disease in approximately 15% of those infected; is transmitted via blood transfusion, sexual intercourse or exchange of body fluids, tattooing, needle sharing, and mother-to-child via breast feeding; is successfully treated (remission) in about 45% of those infected, with alphainterferon, pegylated interferon adefovir, entecavir, telbivudine and lamivudine; causes cirrhosis and hepatocellular carcinoma. A vaccine exists that conveys immunity to hepatitis B virus. Hepatitis C(formerly non-A non-B), due to flavivirus, often results in chronic hepatitis that evolves to cirrhosis. Hepatitis Cis transmitted through contact with blood, and It crosses the placenta; and it may remain inactive for 10-20 years. Hepatitis C viral loads can be made undetectable with a combination of interferon and ribavarin, and the response to therapy has been shown to vary with viral genotype. There are other hepatitis viruses, as well.

ARTHRITIDES Rheumatoid Arthritis Rheumatoid Arthritis IRA) is a constitutional disease with inflammatory changes throughoutthe connective tissues. It is generally a wasting disease with muscle and bone atrophy. Chronic proliferative inflammation of the synovium exists and causes irreversible damage to joint capsule and cartilage, which are replaced by granulation tissue. Radiographically

62


Ch. 3

there is joint space narrowing, periarticular demineralization, bone erosion, "punched out" periarticular lesions, subluxation, deformity (arthritis mutilans), and osteoporosis. RA primarily affects the small joints of the hands and feet, most commonly the PIPJs and MTPJs. It can also present in the hindfoot and ankle, with progressive metatarsal joint and subtalar joint subluxation and ankle pes valgus. Frequentlythe posterosuperior process of the calcaneus is involved.

Clinical manifestations include post~static dyskinesia (pain that is worse after periods of immobility) and non-weight bearing, as well as stiffness. Post-static dyskinesia is a hallmark of any type of arthritis. Pain and stiffness often subside somewhat after motion has proceeded and the joint "warms up." Prolonged activity thereafter can lead to worsening of pain. Constitutional symptoms of weight loss, fever, coldness, numbness, tingling, fatigue and malaise are common. The cardinal objective findings are bilateral, symmetrical sma!! joint swelling (fusiform, sausage fingers and toes), tenderness to palpation (or even barometric pressure), and pain with motion. Swelling due to synovia! hypertrophy is palpably spongy or rubbery, and often crepitant. Synovitis may lead to effusion. Limited motion over a long period is associated with muscle wasting, contracture, fibrosis, and ankylosis. Subcutaneous rheumatoid nodules {palisading granulomas) may form in areas of bony prominence, weight bearing or contact. Diagnosis ofRA is based on disease characteristics overtime. Classic RA displays 7 of the fo!!owing symptoms, the first 5 presenting for at least 6 weeks: morning stiffness, painful range of motion in at least one joint, swe!!ing in at least one joint, swe!!ing of at least one other joint, symmetrical joint swelling wfth simultaneous involvement of the same joint on both sides ofthe body (except PIPJs), subcutaneous nodules, X-ray changes typical of RA {peri-articular osteopenia, joint narrowing, bone whittling), positive agglutination test (rheumatoid factor), poor mucin clot precipitate, characteristic histologic changes in synovial membrane, characteristic histologic granulomatous nodules. Five of these findings in combination represent definitive RA, 3 represents probable RA. Possible RA is represented by any 2 of the following tor3 weeks: tenderness or pain with motion, morning stiffness, history of joint swelling, subcutaneous nodules, elevated ESR or CAP, or iritis.

Exclusions to RA include: 1. Malar rash typical of systemic lupus erythematosus ISLE) 2. Rash typical of drug reaction 3. High concentration of lupus erythematosus ILEI cells 4. Histologic evidence of polyarteritis nodosa 5. Trunk or neck or pharyngeal weakness or swelling or dermatomyositis 6. Definite scleroderma 7. Rheumatic fever 8. Tophi or gout 9. Septic arthritis 10. Reiter's syndrome 11. Tubercle bacilli in joint 12. Shoulder-hand syndrome 13. Hypertrophic pulmonary osteodystrophy 14. Clinical picture characteristic of neuropathy 15. Homogentisic acid in urine 16. Histological evidence of sarcoidosis 17. Positive Kveim {sarcoid antigen) test


Ch.3 18. 19. 20. 21.

63

Multiple myeloma Characteristic skin lesions of erythema nodosum Leukemia or lymphoma Agammaglobulinemia

Lab Testing for RA includes CBC with slight to moderate normocytic hypochromic anemia, white count decreased or, in acute cases, elevated (PMNs may be increased with left shift), chronic normal to slight decrease ESR, moderate to marked increase rheumatoid factor (RF) with this agglutination test positive 75% after several months to a year, normal uric acid, altered plasma proteins (fibrinogen and globulin increased, albumin and total protein and AJG ratio decreased), normal Ca++ and P04, and the synovial fluid is cloudy with increased WBCs and decreased viscosity. The differential diagnosis includes any po!yarthritic inflammatory disease with constitutional signs and symptoms.

Osteoarthritis Osteoarthritis (OA) can be idiopathic and defined as primary OA; or the result of repetitive mechanical strain, and defined as secondary OA. Secondary OA is also termed degenerative joint disease or "wear and tear" arthritis, and is generally not inflammatory beyond the confines of the joint Chronic subtalar joint and metatarsophalangeal joint hyperpronation is a common cause of degenerative joint disease in the foot, with resultant pes valgus, forefootsupinatus and hallux limitus/rigidus, plantar fascitis, flexor stabilization induced hammertoes, and medial Lisfranc breakdown. Any joint can be subject to degenerative joint disease, particularly when subjected to weight bearing or in the post~traumatic phase. There are three cardinal roentgen signs of OA, including joint space narrowing, subchondral sclerosis, and osteophytosis. The classic dorsal "flag" of hallux rigidus (dorsal bunion), first metatarsal-cuneiform exostosis, and the anterior tibial exostosis are examples of advanced osteophytosis. Clinical manifestations include PSD, joint pain without acute inflammation, stiffness, fine and/or coarse crepitus, and symptoms that worsen with weight-bearing activity. Although range of motion may be diminished, there is rarely ankylosis. OA usually affects middle-aged or older individuals, with history of insidious onset (unless post-traumatic), with gradual progression. The differential diagnosis includes rheumatoid arthritis, gout, and Charcot neuroarthropathy. GoutyArthritis Chronic hyperuricemia can result in monosodium urate crystal deposition in joints and soft tissues. The four main etiological forms of gout include: 1. primary metabolic gout- chronic over-production of uric acid, often dietary in origin 2. secondary metabolic gout- myeloproliferative disease with high rate of cellular turnover causing over-production of uric acid 3. primary renal gout- under-excretion of uric acid due to primary kidney disease 4. secondary renal gout- under-excretion of uric acid due to renal disease other than primary kidney lesion (certain diuretic medications). Serum uric acid levels of7 mg/dl for males and 6 mg/dl for females indicate a supersaturated state wherein crystals may precipitate In joints and the kidneys. Clinical forms ofgouty arlhritisinclude acute gouty arthritis, intercritical or quiescent, and chronic gouty arthritis. Acute gouty arthritis presents as monoarticular, sudden onset and intensely painful inflammation (red, hot, swollen, excruciating pain), stiffness and antalgic guarding, and overlying cutaneous desquamation. Chronic gouty arthritis presents

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insidiously with gradual, progressive tophus formation; intermittent acute gouty attacks; and is associated with indurated tophus formation (advanced monosodium urate

deposition) in subcutaneous and/or tendon, auricular helix, and the small joints of the hand and foot; and advanced deformity (bunion, hammertoes, nodular lesions) effecting

cutaneous compromise. A draining tophus reveals a white, chalky exudate of monosodium urate crystals. The diagnosis of gout is confirmed by the presence of strongly birefringent

monosodium urate crystals identified on joint aspiration. The presence of a phagocytosed monosodium urate crystal within a granulocyte is pathognomonic, and termed the "martini sign." Serum uric acid, which is chronically elevated in chronic gout is normally 8 mg%; however the serum value can actually be within the normal range during an acute gouty attack. Roentgen signs of acute gouty arthritis consist primarily of increased soft tissue density and volume; while chronic gouty arthritis reveals punched out or "rat bite" defects of bone at the capsular attachment. Overtime, chronic erosion and ankylosis may develop. The most common locations of gouty arthritis are the first MTPJ, posterior heel at the Achilles insertion, the plantar inferior calcaneus, other pedal articulations (lesser MTPJ, MTJ), the ankle; the hand, wrist and elbow, and knee. The differential diagnosis includes pseudogout; suppurative arthritis, acute bursitis, and rheumatoid arthritis.

Oral therapy consists of indomethacin 50 mg Q 6 hours x 24 hours, followed by 50 mg Q 8 hours x 24 hours, followed by 25 mg Q 8 hours x 24 hours. Alternatively, one may use colchicine (inhibits PMN migration) 0.5 mg Q 1 hour or 1 mg Q 2 hours until the symptoms subside, or Gl distress develops, or a total of 6 mg has been administered without relief. Colchicine can also be administered intravenously as an inltia12 mg bolus followed by 1 mg IV Q 6 hours for two additional doses. In surgical or traumatized patients with a history of acute gouty arthritis, prophylactic therapy using colchicine can be administered as 0.5 mg PO Q8 hour for one week, beginning two days preoperatively. Patients with hyperuricemia require medical evaluation, including 24 hour urine uric acid analysis, and may benefit from longterm anti-hyperuricemic therapy. ln such patients, if the uric acid excretion is less than 700 mg/24 hour period, then probenecid sulfinpyrazone is used; and if the uric acid excretion is over700 mg/24 hours, then Allopurinol is used regularly for an indefinite period oftime. 1\nkylosing Spondylitis The criteria for the diagnosis of ankylosing spondylitis include: 1. Limited motion of lumbar spine in anterior and lateral flexion and extension 2. History of pain or presence of pain in dorsolumbar junction or in lumbar spine 3. Limitation of chest expansion to one inch or less Definite ankylosing spondylitis is confirmed by the presence of bilateral sacroiliitis associated with at least one clinical criteria. Probable ankylosing spondylitis exists in the presence of bilateral sacroiliitis associated with none of the clinical criteria. Common symptoms include low back pain, prolonged back stiffness, ascending back pain, heel pain, peripheral joint pain, fatigue, and diminished vision and/or eye pain. Roentgen signs vary with duration of the disease. Early signs include sacroiliac joint blurring, joint space narrowing and widening, subchondral sclerosis, diffuse osteoporosis of spine, apophyseal joint sclerosis, and straightening of spine. Advanced ankylosing spondylitis reveals apophyseal joint erosion, squaring of vertebrae, narrowed disc space, vertebral collapse, pelvic whiskering, and pubic symphysis involvement Terminal roentgen signs include

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intervertebral disc calcification, paravertebral ligament calcification, vertical syndesmophytes, sacro-iliac joint fusion, and bamboo spine. Reiter's Syndrome This is a seronegative \no presence of rheumatoid factorL asymmetrical arthritis that presents with one or more of the following: urethritis, cervicitis, dysentery, inflammatory

eye disease (iriditis), and mucocutaneous disease consisting of balanitis or oral ulceration or keratoderma blenorrhagica. Characteristics include synovitis, symphysitis and

enthesitis; asymmetrical lower extremity arthritis with predilection for small joints of the teet and the ankle, pericalcaneal enthesitis, knee and sacroiliac disease; bone erosion with osteophytosls, and paravertebral. ossification. Diagnostic tests suggestive of Reiter's syndrome include negative rheumatoid factor, demonstration of HLA 8~27 in the serum, Pekin cells in synovial fluid and neutrophilia in prostatic fluid, and unilateral sacroiliitis. Psoriatic Arthritis Psoriatic Arthritis is an often severe polyarthropathy that is more common in females (3:2 M:F ratio), and can affect patients of any age. Patterns of psoriatic arthritis include polyarthritis with DIPJ involvement and nail disease, symmetrical seronegative polyarthritis simulating rheumatoid arthritis, monoarthritis or asymmetrical oligoarthritis, sacroiliitis and spondylitis, and arthritis mutilans. Diagnostic features include papulosquamous skin lesions and nail dystrophy (pitting, onycholysis, flaking, hypertrophy, nonsuppurative paronychia); DIPJ arthritis, fusiform digital swelling (sausage toes), unilateral sacroiliitis, simultaneous exacerbation of cutaneous psoriasis and arthritis, absence of subcutaneous nodules, and serum negative for rheumatoid factor. Roentgen signs include bone resorption with "pencil-in~cup" IPJ osteolysis and mineral resorption (DIPJ involvement with erosion and expansion of base of distal phalanx with proximal osteolysis), oligoarthritis, sacroiliitis, and spinal column involvement.

Charcot Neuroarthropathy (Neuropathic Arthropathy) Causes of Charcotneuroarthropathy include central nervous system defect, such as syphilis (check fluorescent Treponema! antibody if suspect this with charcot foot), syringomyelia, meningomyelocele, post-traumatic degeneration, multiple sclerosis, and spinal cord compression. Peripheral nervous system disorders such as Charcot-Marie-Tooth disease, diabetic peripheral neuropathy, alcoholic peripheral neuropathy, tuberculous or lepromatous infection, amyloidosis, pernicious anemia, and steroid-induced neuropathy. An unusual disorder known as congenital indifference to pain can also effect neuroarthropathic joint disease. Pathologically, Charcot joints have been attributed to, primarily, autonomic denervation with loss of vasomotor tone, hyperemia, increased bone perfusion and loss of bone mineralization. The loss of proprioception, joint relaxation and hypotonia, recurrent microtrauma, possible major injury, resultant malallgnment, cartilage fibrillation, and subchondral plate fragmentation have also been sited as components of the development of Charcot joint disease. Ankle equinus is a primary deforming influence in many cases of pedal Charcot degeneration. The foot is usually warm, dry, and swollen. Other effects of peripheral neuropathy, such as increased hyperkeratosis and keratin stiffness, loss of sudomotortone (anhydrosis), protective touch-pressure sensation (5.1 0 or red West-Foot monofilament esthesiometer), and intrinsic muscle atrophy (intrinsic minus foot), also contribute to pedal breakdown. Increased blood flow results in abnormal venous pooling and edema.

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TABLE 3-8. HARRIS AND BRAND ClASSIFICATION OF INSENSITIVE FOOT DEFORMITY.

Pattern I II Ill IV

v

Anatomical apex of pedal breakdown Calcaneal Talar Midtarsal Lateral hindfoot(calcaneocuboid) Usfranc (tarsometatarsal)

Harris and Brand have divided tarsal destruction in the insensitive foot into five patterns. Pattern 1- Calcaneal, Pattern II - Talar, Pattern Ill - Midtarsal, Pattern IV- Lateral hindfoot, and Pattern V - Lisfranc. As degeneration progresses, cartilage debris is

imbedded in synovium and detritic synovitis develops from deposition of cartilage and bone fragments, and shards of bone and cartilage can migrate into soft tissue along

the extremity. Other causes of detritic synovitis include silicone polymer degradation, osteonecrosis, calcium pyrophosphate deposition {pseudogout), psoriatic arthritis, and osteoarthritis. Microscopic evidence of shards of cartilage and bone in synovium is diagnostic of Charcot joints. Extreme angular deformation of the joint leads to ligamentous and capsular rupture, gross fracture, and progressive deformation. Treatment must encompass systemic medical management in conjunction with local care. Nonwweight bearing using bedrest, patellar tendon bearing bracing, and total contact casting; as well as antibiotic prophylaxis or therapy, and surgical management of cutaneous wounds and bone and joint deformity, are all components in the coordinated treatment of Charcot neuroarthropathy. Prior to surgery for stabilization of deformed joints and fractured bone, it is necessary to achieve a state of quiescence. Equinus deformity is addressed, and the mainstay of surgical reconstruction is arthrodesis in conjunction with electrical bone growth stimulation. Fixation methods for neuroarthropathic bone include internal fixation, external fixation, and intramedullary nailing of the tibia. Careful perioperative management is critical. Septic Arthritis Septic arthritis usually presents as a monoarticu!ar, erythematous (unless vascular compromised), lower extremity disease with the knee as the primary site of involvement. Etiologies include contiguous spread, direct implantation, hematogenous sources, or surgical contamination. Contiguous spread septic arthritis occurs when osteomyelitis is present in metaphyseal or epiphyseal bone, with resultant bacterial spread into subchondral bone leading to eventual joint infection. Hematogenous spread is common in children, and often the result of otitis media or upper respiratory tract infections. Direct implantation of bacteria into the joint may occur due to puncture wound. Postsurgical joint infection is most likely when endoprosthesis are used. Common infecting organisms include S. aureus, H. influenza, and others. Septic arthritis correlates with patient age as follows: S. au reus is the most common organism in all patient populations; Streptococcus and gram negative organisms are most common in neonates, Hemophilus influenza is most common in children 6 months to 5 years of age, Neisseria is most common in teenagers; and in adults, less than 5% of cases are caused by E coli, Proteus mirabilis, and P aeruginosa. (P aeruginosa is common after puncture injuries); while sickle cell anemia patients are predisposed to Salmonella; and the compromised host (burn wounds, drug addict, HIV positive, chemotherapy, steroid therapy) is susceptible to Serratia marcescens. Patients with pyarthrosis present with an

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extremely painful, hot, and swollen joint that they will antalgically guard. The patient may also exhibit varying signs of septicemia. The onset of symptoms and joint destruction are

frequently rapid and, therefore, timely diagnosis and treatment are necessary in order to salvage the joint The differential diagnosis in children includes acute rheumatic fever and/or a flare up of juvenile rheumatoid arthritis. In adults consideration should be given to the possibility of joint trauma, gout, pseudogout, or foreign body synovitis. Useful clinical lab findings include neutrophilia with left shift, elevated ESR, positive CRP; and blood cultures are positive in 50% of cases. Roentgen signs include increased soft tissue density and volume, effusion and juxta~articular osteopenia. A Tc-99 bone scan, in combination with a Ga-67 scan, may be helpful in making an early diagnosis, despite the lack of specificity. An ln-111 labeled leukocytes scan is both specific and sensitive for infection, and may be used instead of Ga-67. Joint aspiration should be performed when septic arthritis is considered, however care should be taken to avoid aspiration through an area of distinct overlying cellulitis or infection, as this technique may actually inoculate a sterile arthritic joint with bacteria. A sterile surgical prep of the overlying skin is mandatory before joint aspiration is performed. In order of importance, aspirate should undergo the following studies: C&S (aerobic and anaerobic, and fungal), gram stain and acid-fast stain, examination for crystals, WBC count and differential, glucose concentration. In a septic joint the WBC will usually be higher than 100,000, with the exception of gonococcal arthritis wherein the WBC count is usually less than 50,000. In septic arthritis, the differential cell count consists of 90-95% neutrophils. In additional to lab analysis, the aspirate is grossly inspected for color, consistency, and clarity. In septic arthritis, the clarity and color will vary from cloudy yellow to creamy white or gray. The treatment of septic arthritis is much the same as that for an abscess, wherein incision and drainage, foreign body removal and debridement are performed. Controversy exists as to whether or not adequate drainage and cleansing can be performed via multiple repeated needle aspirations and lavage. This technique has also been criticized for potential cartilage damage due to needle trauma as well as pain and anxiety related to multiple aspirations (particularly in young patients). Open surgical joint drainage and debridement allows for direct visualization, lysis of adhesion or scar tissue, removal of necrotic and infected tissue, placement of drain tube, placement of antibiotic impregnated PMMA beads if osteomyelitis is present, and thorough inspection of the joint confines. The criticism of open drainage and debridement is that it promotes arthrofibrosis and dysfunction due to scar formation. In a child, arthrotomy may be reserved in case of failed drainage using multiple needle aspirations and lavage. Arthrotomy should be performed in patients with suspected osteomyelitis, infected endoprosthesis, long-standing infection or resistance to previous aspiration/lavage, or in the septicemic or endotoxic patient. Following arthrotomy the wound is initially immobilized and packed open. It is important to avoid dessication of the joint tissues, and BID wound lavage and fresh dressing applications are used until the acute inflammatory episode subsides (24 to 48 hoursLafter which gentle passive range of motion should be initiated. Early motion is critical in preventing significant arthrofibrosis and limited motion. Presumptive antibiotic therapy should cover S. au reus (intravenous cefazo!in or nafcillin, or cl!ndamycin in patients sensitive to PCN), and any other suspected organisms based on clinical history. Antibiotic therapy is adjusted in accordance with definitive C&S results, and should be continued IV for a minimum of two weeks. If the patient is responding well, then conversion to oral antibiotics is made at approximately two weeks, and continued until a full antibiotic course of four weeks is completed (oral antibiotic being administered from the second through fourth weeks).

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SELECTED NEUROLOGICAL DISORDERS

Familial Sensorimotor Polyneuropathy (CharcotwMarie-Tooth Disease) Familial Sensorimotor Polyneuropathy is also know as Gharcot-Marie-Tooth Disease (GMT) and Peroneal Muscular Atrophy. GMT disease is a progressive, familial, symmetrical, peripheral polyneuropathy that affects males five times more often than females, and presents in varying degrees from mild to severe. Severe cases may display significant cardiac dysrhythmia, Friedreich's Ataxia, and often do not survive beyond adolescence. GMT involves distal muscle atrophy that begins in the feet and hands then legs and arms. Lower extremity involvement is often more pronounced, and observed earlier, than is upper extremity involvement Classically, the peronii, tibialis anterior, long extensors, pedal lumbricals and interossei are gradually denervated as the disease progresses, leading to muscular atrophy and the "stork leg" or "wine goblet" appearance of the legs. Muscle wasting effects drop foot, pes cavus \more specifically, cavo-adductovarus), steppage gait, recurrent lateral ankle ligamentous sprains that eventually develop into chronic instability, claw toes and MTPJ subluxations, and mechanically induced cutaneous compromise. Peripheral touch-pressure sensation, deep tendon reflexes, and voluntary muscle function are diminished. Electroneurodiagnostic testing will show markedly slowed conduction velocity (normal conduction 45 to 55 m/sec), while EMG reveals increased fibrillation potentials. Muscle biopsy reveals atrophy. Neurological consultation and genetic counseling are in order. Conservative treatment is aimed at increasing stability, and includes cavus-mold orthoses, digital retainers, ankle sleeve, drop foot bracing (MAFO or similar device), and palliative skin and nail care. ReconstrucTive surgical intervention addresses the pes cavus, digits, and drop foot; and usually combines stabilization arthrodesis, or sometimes osteotomy, with tendon transfer. Arthrodesis is generally preferred whenever progressive neuromuscular disease is treated. Arthrodesis yields a stable bone mass upon which the transferred tendons can function. When heel varus is mild, the Dwyer osteotomy combined with heel cord lengthening and Ste!nd!er stripping \release of plantar intrinsics and fascia from calcaneus) may be adequate; however triple arthrodesis and tendon transfer from the posterior or medial leg compartment to the dorsum of the foot (tibialis posterior through the interosseous membrane) offers more correction and longterm improvement Digftal stabilization, in the form of lesser toe PIPJ and hallux IPJ arthrodesis, in conjunction with MTPJ relocation, is also very usefuL Consideration may also be given to first metatarsal dorsiflexory base osteotomy. Dejerine Sottas Disease (Hypertrophic Interstitial Polyneuropathy) Clinically .this disease is similar to CMT, with distal muscle weakness of the lower extremities with associated sensory deficit, and decreased deep tendon reflexes. Pedal deformities include pes cavus and claw toes, and the patient may display kyphoscoliosis. The most distinctive feature ofthis disorder is palpable and sometimes visible enlargement of the peripheral nerves. Nerve biopsy (usually sural nerve) will confirm the diagnosis. Roussy-Levy Syndrome Patients with this disease have been compared to patients with CMT disease, with the addition of an essential tremor that is most prominently expressed in the hands. This is a familial, slowly progressive, symmetrical neuromuscular disease. Clinical findings include areflexia, intrinsic pedal muscle atrophy, pes cavus and claw toes, clumsy gait and poor equilibrium, and the presence of the previously noted essential tremor.

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Refsum's Disease This disease is the result of abnormal lipid metabolism wherein phytanic acid accumulates in the serum, which results in elevation of serum phytanic acid to levels up to 50 times greater than normal. Associated findings include ichthyosis, night blindness, and a

preceding febrile illness. Peripheral muscle paresis, areflexia, dropfoot, pes cavus, and

claw toes are also observed. Friedreich's Ataxia This is typically a more severe and disabling disease than CMT disease, and the onset is noted early in life (childhood) and progresses until the patient is essentially incapacitated by

middle-age. Hallmarks ofthe disease are ataxia, unstable gait, and pes cavus with clawtoes. Muscular Dystrophy I MDI Muscle fibers atrophy and become necrotic, resulting in weakness, clinically evident muscle atrophy (decreased girth), areflexia, and secondary muscle contracture. Mental impairment may also be present There are three types of MD: 1. Duchenne's pseudohypertrophic MD- most common, muscles appear large and firm because of fatty conversion, affects only males, and the onset is between 1-3 years of age with subsequent rapid progression 2. Facioscapulohumeral MD 3. Limb girdle MD -Ankle equinus and equinovarus deformities are common foot conditions seen in patients with MD, although pes valgus may also appear. Classically individuals with MD display Gauer's sign when they raise themselves from seated or recumbent position, where in they "climb up themselves" by pushing their hands/arms against their knees and thighs, thereby pushing the torso upward. Myelodysplasia(Spina Bilida) These disorders comprise a group of developmental deformities of the spinal cord and vertebrae that most commonly affect the lumbar and sacral levels, and include: 1. spinal bifid a with meningocele The meningeal sac protrudes through an open neural arch vertebral defect and extends to the subcutaneous layer. 2. spina bifid a with myelomeningocele Other elements ofthe spinal cord and nerve roots have also protruded 3. myelocele Even the skin fails to enclose the cord protrusion, resulting in the most severe form of spina bifida. 4. spina bifida occulta The neural arches of the vertebra have not completely closed, however all of the neural elements remain within the spinal canal. Pathologically, the spinal cord defect effects motor, sensory and autonomic functional deficits observed in the lower extremities. The dynamic muscle imbalance tends to worsen over time, resulting in equinus, equinovarus, and equinovalgus, and marked rotary deformities of the lower extremities. Associated findings include urinary bladder paralysis


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(which requires catheterization during operative intervention) which may be associated with chronic urinary tract infection; and profound anesthesia and lack of protective

sensation, often with mal perforans ulceration.

Poliomyelitis The polio virus affects the anterior horn cells (!ower motor neuron) of the spinal cord, resulting in some degree of lower extremity flaccid paralysis (areflexia, hypotonia, and weakness). The central neJVous system defect in poliomyelitis is non~progressive,

however the disease can lead to contracture that changes overtime. Common deformities include equinovalgus, and others, and tibiocalcaneal and pantalarfusion can be useful. Cerebral Palsy (CP) Classically, a congenital neuromuscular disorder caused by an intracranial brain lesion,

and identified early on in the patients life. Three types of CP 1. Spastic CP Upper motor neuron disease effects hyperreflexia, clonus, and extensor plantar response, typically anterior leg compartment weakness, dropfoot, pes cavus, clawtoes, and steppage gait with circumduction. This is the most common form of spastic CP, and affects approximately 65% of CP patients.

2.

Athetoid CP This form affects approximately 20% of patients with CP, and is associated with a slow, worm-like hypertonia due to upper motor neuron disease.

3.

Ataxic CP Ataxic affects about 15% of CP patients, and is associated with tremor and atonia.

UMN disease causes more spasticity in muscles that cross more than one joint, such as gastrocnemius. Muscles of flexion, adduction, and internal rotation tend to overpower those of extens·lon, abduction, and external rotation. Talipes equinova!gus, or equinovarus, is common. Complex regional pain syndrome (CRPS)-This is a serious chronic pain condition, the hallmark symptom being unrelenting, progressively worsening, intense pain out of proportion to the severity of the injury or inciting event Patients with CRPS often display allodynia, wherein they relate pain caused by what would have otherwise been a nonoxious stimulus, and hyperpathia, wherein a stimulus that would typically be considered painful is much more painful. CRPS usually affects an arm, leg, foot or hand, and the pain may evolve to include the entire, dystonic extremity. Although CRPS affects men and women, it is more common in young females. CRPS is thought to be the result of peripheral and central nervous system dysfunction. CRPS I, often referred to as reflex sympathetic

dystrophy syndrome (RSDS), occurs with tissue injury that does not involve direct, underlying nerve trauma. CRPS IJ, often referred to as causalgia, is associated with known trauma involving a known anatomical nerve trunk. The clinical signs and symptoms of CRPS 1and II are the same. Characteristic signs and symptoms include color and teperature changes involving the skin, associated with sharp and burning pain, swelling, and sweating. Associated with these symptoms are exquisite skin sensitivity, vasomotor instability that causes the affected part to be colder or warmer than the contralateral limb, discoloration that includes mottled blue, pallor, purple; textural changes that include thin,

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shiny skin; hypertrophy or atrophy of digital hair and nail growth; fusiform digital swelling and stiffness, dystonia that affects the ipsilateral extremity and may extend to other extremities; symptoms may be heightened by emotional stress, and depression secondary to chronic pain is common. Although there is no definite cutoff between symptoms and signs that define distinct stages of CRPS, many clinicians categorize Stage 1 as lasting from 1-3 months and characterized by sharp, burning pain, myalgia and dystonia, temperature and color changes, and increased hair growth. Stage 2 extends from 3-6 months and is associated with worsening pain, edema, nail dystrophy and diminished hair growth, muscle atrophy and weakness. Stage 3 extends beyond 6 months and entails irrevesible skin and bone atrophy (Sudek's atrophy of bone), and permanent pain and limb contracture. The pathophysiology of CRPS is notfully understood, although it is believed that the sympathetic nervous system plays an important role in maintianing the pain, as pain receptors in the affected limb become sensitive to catecholamines. It has also been theorized that CRPS represents disruption of the healing process secondary to an abnormal immune response to injury. Due to the complexity of symptoms and similarities with other conditions, the diagnosis of CRPS can be difficult to make, especially early in the course of the disease. There is no single diagnostic test for CAPS, and it is important to rule out other conditions so that the diagnosis can be made by exclusion. A triphasic bone scan may be useful, and often shows a splotchy uptake of radiotracer in cases of CAPS. Supportive therapies include the use of topical analgesics, anticonvulsant and antidepressant medications, corticosteroids and opiate analgesics. Physical therapy and movement are encouraged. Sympathetic nerve blockade, using phentoloamine or local anesthetic; sugical sympathectomy, only if blockade afforded prolonged and marked relief; spinal cord stimulation, using an implantable generator with a stimulating electrode along the spinal cord; and spinal intrathecal local anesthetic and/or analgesic pumps, may be usefuL The prognosis tor patients with CAPS varies from person to person, and outcomes range from permanent pain and disability to spontaneous remision and revovery.

NEOPLASMS Any enlargement oftissue, whether edematous, hypertrophic or neoplastic, can be referred to as a tumor. Whenever dealing with neoplasm, a high index of suspicion should be maintained tor potential malignancy. Malignancy of epidermal germ eel! origin is termed carcinoma, whereas those of mesenchymal origin are referred to as sarcoma. Any lesion, even what is thought to be persistent pyogenic granuloma, chronic onychocryptosis, resistant verruca, or a diffuse subcutaneous mass that does not respond to reasonable therapy should be more closely inspected. Closer inspection may involve radiographs or MRI, lab testing, or biopsy. Consultation may also be helpful. In general, any lesion suspected of being malignant warrants oncologkal consultation and systemic evaluation for lymph node, lung, Gl, bone, and other sites of potential metastasis or regional dissemination. Proper biopsy technique is crucial. General considerations in the assessment of a neoplasm include coloration, change in appearance, presence of symptoms such as pain or pruritus, hemorrhage, location superticial(freely moveable below or within the skin) or deep (fixed) to the deep fascial (muscle fascia), sensory or motor disturbance, vascularity or pulsatile nature of the lesion, status of the popliteal and inguinal lymph nodes (tender and/or enlarged), and the presence of metastatic disease elsewhere in the body. Diagnostic imaging, such as standard radiographs, MRI and CT scans may be helpful, and a chest X-ray should be obtained whenever cancer is considered, as the lungs are the

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primary site of sarcoma (and many carcinoma) metastasis. Clinical lab testing, including CBC and differential, biochemical profile, tumor antigen testing, and ESR may be helpfuL Needle biopsy (not fine needle) can be helpful if multiple core specimens are obtained from different sites within the lesion, and incisional biopsy through the mid portion of the soft tissue mass is routinely performed. Whenever performing an incisiona! biopsy for suspected sarcoma (or carcinoma), the biopsy channel to the lesion should be oriented longitudinally in line with the suspicious mass and within a region to be fully excised with subsequent definitive surgical excision of the lesion. Moreover, it is important to avoid dissection into adjacent fascial compartments, in an effort to maintain natural anatomical barriers to spread of malignant cells. The oncological surgeon can, in many cases of sarcoma, preserve adjacent intact muscle compartments protected by intact deep fascia, when appropriate biopsy technique has been used. Attention to such detail may be the difference between muscle compartment resection from the foot into the leg, versus BK or AK amputation. Selected Neoplasms Epidermal (epidermoid)inclusion cyst~ precipitated by skin trauma, wherein e-pidermis is forced into underlying dermis and continues to desquamate and build up degenerating keratin within the dermis. This leads to slow development of a firm, round, subcutaneous nodule that is often seen on the sole or toes. Pilar and sebaceous cysts are inclusion cysts around the hair follicle. Eccrine poroma ~ a sweat gland tumor that is nodular and may drain serous fluid.

Squamous cell carcinoma {SCC)- a malignant epithelial neoplasm with predilection for skin and mucous membranes. The lesions display erythematous margin, nodules or shallow ulceration. There are several variations, including verrucous carcinoma, prickle cell carcinoma, epidermoid carcinoma, and epithelioma cuniculatum. SCC is more common in light-skinned individuals than in African-Americans, usually localizes to sun-exposed surface or previously scarred, burned, or irradiated skin; is usually seen in patients over the age of 40 years, 5% affect the foot and leg, rarely invade deep to bone and rarely metastasize, and there is a 95% cure rate with adequate excision. sec can develop in a chronic, non-healing wound or ulcer, Oncological consultation and possibly adjunct radiation or chemotherapy may be in order. Basal cell carcinoma (BCC)- the most common skin cancer, usually observed on sunexposed surfaces in the 30to 50 year-old patient, more common in women, lighter- skinned individuals, involving basal cells of the epidermis, very slow growing and unlikely to metastasize unless ignored or neglected.lt is also referred to as basal cell epithelioma due to its failure to metastasize. Four types include superficial, pigmented, nodular, and morpheaform. BCC has been known to form in scar tissue. Appears as a shiny nodule with surface telangiectasia. There is a 99% cure rate with adequate excision or ablation via cryogen, electrodesiccation, or radiotherapy. Routine follow~up is required after eradication, and there is a 35% recurrence rate within 5 years. Bowen's Disease (carcinoma in situ)- an in situ squamous cell carcinoma involving skin and mucocutaneous junctions; appearing as a crusty, nodular looking plaque. When the superficial crust is curettaged, the lesion appears dull red and moist It may appear as a

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keratotic lesion on the plantar surface, and pathologically the basement membrane is intact (CAin situ). Proper excision is curative. Bowen's disease is often associated with internal malignancy, and oncological consultation is in order. Dermatofibroma·

this fibrous skin tumor rarely occurs in the foot, appears flesh-colored,

and may be observed as a periungual angiofibroma which is also referred to as Koenen's fibroma and associated with tuberous sclerosis, cafe au !a it spots and mental retardation.

Plantar fibromatosis- this is a benign and reactive lesion of fibrous tissue (plantar fascia) affecting the plantar aspect of the foot. The lesions are firm and nodular, and may resemble a low grade fibrosarcoma due to its fixed nature. Isolated excision is associated with a 65% recurrence rate, and total excision of the affected band of plantar fascia is indicated if padding and accommodative insole has failed to yield pain relief when weight bearing. There is no distinct benefit to injection therapy. Plantar fibromatosis is also known as Lederhaus disease, and associated with people of a Germanic heritage. These individuals may also have Dupuytren's palmar contracture or Peronies penile fibromatosis.

Fibrosarcoma- these are firm, fixed small nodular to expansive irregular lesions that may occur in the lower extremity. Fibrosarcoma may metastasize, and radical excision, amputation, and oncological management are required. Lipoma- these are composed of mature fat cells with thin capsular structures, and may lead to adjacent nerve entrapment They are commOnly observed about the malleoli and knee, and are amenable to excision. Liposarcoma- a malignant lesion, often with vascular infiltration and termed angiolipoma. Treatment is excision and oncological management Ganglion cyst- the most frequently encountered tumor affecting jointtissue, and may also affect the tendon sheath or nerve connective tissue (usually epineurium). These are generally of traumatic etiology (perhaps distant incidental trauma), with myxoid degeneration of connective tissue effecting gelatinous fluid that gels over time. A history consistent with size change and aggravation by activity is common. The ganglion may entrap adjacent vital structures and tendon. When in the popliteal fossa, a ganglion is referred to as a Baker's cyst Conservative treatment consists of padding and gentle compression, aspiration of cyst contents and local infiltration of acetate corticosteroid. Lesion may recur after reduction in size and symptoms, and additional injection therapy or surgical excision may be effective. Ganglions are seen in a!l age groups, even in the very young. Digital mucous cysts~ a small cystic lesion overlying a digitaiiPJ, resembling a ganglion cyst, and observed in the 30 to 80 year age group Inot typical in young individuals). The lesion stems from myxoid degeneration of the underlying joint capsule, and treatment may require IP arthroplasty. Leiomyoma- a well-encapsulated, firm, rubbery-textured smooth muscle tumor arising from erector pili or vascular smooth muscle. The treatment is usually excision or obseJVation overtime.

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Rhabdomyoma- a benign tumor of skeletal muscle that occurs usually in young patients. The treatment is excision. Rhabdomyosarcoma- a malignant tumor of skeletal muscle that occurs usually in the 5th to 6th decade of life. The treatment is oncological consultation, adjunct radiation and/or chemotherapy, and appropriate excision or amputation. Giant cell tumor of tendon sheath- a true benign neoplasm of synovial structure which is actually a variation of pigmented villonodular synovitis (PVS). It is usually seen in the 30 to 50 year age group, and is the second most common tumor oftendon after the ganglion cyst. Observation or excision is the recommended treatmen~ and it is importantto note thatthere is a high rate (25%) of recurrence following excision. Synovial sarcoma- this malignancy arises from joint capsule, tendon, or bursa; and is usually seen in youngsters and adolescents, aged 10 to 40 years. The knee and ankle predominate, and radical excision, or perhaps amputation, is indicated after oncological consultation and consideration to adjunct radiation and/or chemotherapy. The ankle is frequently involved with a periarticular synovial sarcoma in the periarticular soft tissues. Unlike piezogenic papules, synovial sarcoma is present as a subcutaneous nodule even in the non-weight bearing attitude. The tumor can be of a fibroblastic (spindle cell) or epithelioid cell type, and tissue specific antigens can aid the pathological diagnosis. Wide excision, sometimes in conjunction with radiation or chemotherapy, is usually indicated after biological staging is determined.

Schwannoma- a slow-growing benign, encapsulated tumor that develops within the nerve sheath, often of traumatic origin. The tumor causes axon compression and nerve fiber dysfunction. Microsurgical excision under Ioupe magnification is the indicated treatment Neurofibroma- a benign, circumscribed, but not encapsulated neoplasm originating in the nerve trunk, also of Schwann cell origin. The lesions are often multiple, pedunculated, and nontender. Consideration must be given to von Recklinghausen's disease. Neurofibromas may undergo malignant transformation.

Hemangioma- the most common benign vascular tumor observed in the feet There are several distinct types of hemangioma. As with most vascular lesions, they are diascopy positive (blanch when pressure is applied to the skin surface encompassing the lesion). The capillary, or strawberry, hemangioma is the most common form. It is observed in the newborn and may resolve as the child matures. The cavernous hemangioma is a large lesion consisting of a thick, extensive proliferation of vessels which may involve a large portion of the foot, and thereby pose serious surgical problems relative to excision. Arteriography is useful in the evaluation of a suspected hemangioma. Kaposi's sarcoma~ is a vascular malignancy comprised of a proliferation of capillaries and connective tissue, seen traditionally in males over the age of 50 years, and of Mediterranean descent There is also a high incidence in patients suffering with AIDS. The lesions are bluish, or purple nodules or plaques. Treatment is observation (pending general medical status) or excision.

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Glomus Tumor- a benign, neuro-arterial neoplasm that is usually localized to the periungual (nail bed) region, the hallmark of which is extreme pain, and a reddish or bluish color. Treatment is excision.

Malignant Melanoma Melanocytes have dendritic processes and are of epidermal germ cell origin. They function to produce "sun~protective" melanin pigmentthatguardsthe underlying living cells of the basal layer of the epidermis from the mutagenic effects of UV radiation. Lower extremity melanoma is more common in women, while men more commonly display melanoma on the torso. Melanoma is most commonly seen in the 30 to 60 year age group. Sun exposed surfaces are most susceptible, however the palms and soles, particularly in individuals with dark skin, can be affected. Anatomic sites prone to sun exposure include: "BANS" (back, arms, neck, scalp). Diagnostic signs focus.on the size, shape, color, location, and duration of the pigmented lesion. Benign pigmented skin lesions of the lower extremity should be less than 5 mm in diameter, homogenous in color, smooth or regular in contour, and present for as long as the patient can remember. Plantar and periungual pigmented lesions warrant an especially high index of suspicion. Any lesion on the foot that is greater than 5 mm in diameter, heterogenous in color, or displaying an irregular or notched border should be biopsied if it has not been present since birth. Melanoma grows in a radial phase and an invasive or vertical phase. The vertical growth phase correlates with metastasis. Melanoma in the horizontal or radial growth phase appear macular, while the vertical growth phase is associated with a more aggressive tumor. Poor prognostic indicators include lesions displaying a whitish or amelanotic co! or, tumor regression (notched border), progressive nodu!arity (consistent with deeper invasion of the dermis), change in size or shape, ulceration, hemorrhage, pain, or pruritus, should be considered malignant and treated after accurate identification.

Four Main Clincohisto/gic Types 1.

2.

3.

4.

Superticial spreading melanoma (SSM) may develop on any portion ofthe body with peak incidence around the 5th decade. Comprises about 70% of cutaneous melanomas. Classic SSM displays the "red, white, and blue" of advanced malignancy showing tumor regression. These are very common on the trunk of males. Lentigo mallgna malignant melanoma (LMM) is the slowest growing lesion, seen on sun exposed surfaces. LMM comprises about 15% of MM, and is most common in the elderly (mean age 70 years). The lesion is macular with color variegation. Nodular melanoma (NM) is highly malignantwith primarily a vertical growth phase only. NM comprises about 12% of cutaneous melanoma, and is seen most commonly in males approximately 50 years of age. The appearance is uniformly blue, black, or dark brown, with a nodular appearance. Ulceration is rare with NM. Acrallentiginous melanoma (ALM) shows predilection for plantar, palmar, and nail bed or grooves. Hutchinson's sign (pigment changes in the eponychium of subungual melanomas), whereas melanotic whitlow involves subungual melanoma. The peak incidence of ALM is the 7th decade. ALM accounts for about 3.5% of cutaneous melanomas.


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Staging Stage I Stage II

malignant melanoma involves a primary lesion, or one with local satellite within 5 em malignant melanoma entails in transit metastasis and regional lymph node involvement (identified by palpable adenopathy or node biopsy)

Stage Ill malignant melanoma entails distant metastasis. Melanoma can go anywhere in the body including the choroid of the eye and internal parenchyma. The most important determinant of survival rate for malignant melanoma is clinical staging. Survival of a clinical Stage !lesion is far more likely than survival of a clinical Stage II lesion, whereas clinical Stage Ill lesions are usually lethaL

Clark's Levels and Breslow's Thickness Pathological staging systems of malignant melanoma include Clark's levels and Breslow's thickness (Tables 3-9 and 3-10). The deeper the level, or thicker the lesion, the more likely is there to be metastasis, and therefore the prognosis worsens as the lesion thickens or progresses deeper into or through the skin.

Identification of the Breslow thickness has been shown to correlate better with survival rate. TABLE 3-9. CLARK'S LEVELS. level I

Microscopic appearance of melanoma Involvement of epidermis with no involvement deep to the basement membrane

II

Penetrates the basement membrane

Ill

and enters the papillary dermis Fills the papi!lary dermis and cancer cells line up against, but do not penetrate into the reticular dermis

·

IV

v

Penetrates into the reticular dermis Fills the reticular dermis and enters the subcutaneous fat layer

TABLE 3-10. BRESLOW MELANOMA THICKNESS AND CORRESPONDING SURVIVAL Thickness (mm)

5-year survival rate(%)

0-0.75 0.76-1.5 1.51-2.25 2.26-3.0 >3.0

83-100 37-90 37-83 44-72

9-55

The most important service the podiatrist can provide in regard to malignant melanoma

is timely and accurate recognition and biopsy, thereafter followed by appropriate consultation and/or definitive surgery or referral to an oncological surgeon. Clinical Stage I lesions can be definitively excised by the podiatric surgeon, whereas Clinical Stage II lesions, with regional lymph node involvement, require node dissection and the expertise of a general or vascular surgeon familiar with melanoma.

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Biopsy of a suspected malignant melanoma should be performed, when possible, using an excisional technique that provides 1to 3 mm of norma! appearing skin about the lesion, and the biopsy must include subcutaneous fat (full-thickness skin). For small lesions, local anesthesia is infiltrated in a proximal V-b!ock fashion in normal appearing tissue. Two semi-elliptical incisions are made about the lesion from proximal to distal, the resultant dimension of the lesion being about 3:1 length:width. The proximal normal margin of skin should be marked with a suture for pathological orientation. For larger lesions, where complete excision is not possible without creating a large defect, incisional or punch biopsy should be employed. The incisional or punch biopsy should be oriented in a faShion that will allow the biopsy wound to be excised in toto when subsequent definitive surgery is performed. The incision a! or punch biopsy must still be ful!~thickness skin and include underlying subcutaneous fat. Select the most clinically malignant appearing site of the lesion, and get enough of the lesion for pathological inspection. As with any biopsy of suspected malignancy, timely diagnosis and appropriate follow-up are mandatory. It is proper to perform an incisional biopsy when indicated, as long as definitive care is subsequently administered. Definitive treatment, based on clinical and pathological assessment, always includes oncological consultation prior to definitive surgical ablation of the lesion. Malignant melanoma can be a systemic disease, therefore chest X-ray and constitutional evaluation are needed. In many cases, it is best to administer chemotherapy prior to definitive surgical excision, in an effort to decrease the tumor and minimize the risk of metastasis. Survival rates may increase with adjunct preoperative radiation or chemotherapy. Guidelines for definitive excision are depicted in Table 3-11.

TABLE 3-11. GUIDELINES FOR DEFINITIVE EXCISION OF MELANOMA.* Melanoma depth (mm)

Recommended margin of normal appearing skin {em) about definitive excision

< 0.76 0.76- 4.0 >4.0

2 3 5 (with excision of underlying deep fascia)

*Closure may require use of a skin flap or graft

The definitive treatment of a subungual melanoma is digital amputation at the level of the metatarsophalangeal joint Therapeutic lymph node dissection remains somewt"lat controversial for clinical Stage II melanoma, particularly with lesions of Clark's Levell! and Ill, however it has been recommended for lesions of Clark's Ieveii I - V, and the decision has to be made by the oncological surgeon after discussion of adjunct chemotherapy, prognosis and morbidity related to inguinal node dissection. Bone Tumors

Radiographic Characteristics Three common radiographic patterns of bone destruction 1. Geographic bone destruction represents the least destructive, slowly developing and usually benign process. There is a zone oftransition that separates the lesion from normal appearing bone.


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3.

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Moth-eaten bone destruction represents a more rapidly destructive, malignant process such as sarcoma or osteomyelitis. The transition between the lesion and normal bone is wide and less well-defined.

Permeative bone destruction represents the most aggressive and rapidly progressive, malignant process. The zone of transition between tumor and normal bone .is very wide and almost imperceptible radiographically.

Other important radiographic characteristics of bone tumors include the type of trabecular pattern, the periosteal reaction, position of the lesion both relative to anatomic location as well as.the transverse plane (cross sectional) location within the bone.

Trabecular patterns of some bone tumors giant cell tumor of bone~ delicate, and thin trabeculae chondromyxoid fibroma- coarse, and thick trabeculae aneurysmal bone cyst~ delicate, and horizontal, parallel trabeculae non~assifying fibroma- loculated trabeculae intramedu!fary hemangioma~ striated, or radiating trabeculae Periosteal patterns of new bone formation solitary bone cyst- a monolayer of new bone formation adjacent to the tumor and separated from pre-existing cortex osteogenic and Ewing's sarcoma- multiple, concentric layers ("onion skin") of new bone growth, sometimes creating a Cadman's triangle wherein periosteal elevation adjacent to pre~existing cortex radiographically depicts an angle with the apex pointing in the direction of normal bone (also seen in other expansile lesions of bone cortex, such as osteomyelitis) osteogenic sarcoma~ radiating spicules, or star burst pattern of new bone growth multiple myeloma and Ewing's sarcoma~ hair~on-end radiating spicules of new bone growth.

Transverse plane locations within the bone enchondroma and solitary bone cyst- centrally located giant cell tumor of bone, osteogenic sarcoma, chondrosarcoma, fibrosarcoma, and chondromyxoid fibroma- eccentrically located within the medullary canal, arising to one side of the central axis of a long bone; non-ossifying fibroma and osteoid osteoma -located in the cortex periosteal sarcoma osteochondroma~ lesions located in the periosteal region Characteristic anatomic sites of tumor development diaphyseal lesions- solitary and aneurysmal bone cysts, giant cell tumor of bone, Ewing's sarcoma, enchondroma, non-ossifying fibroma, osteoblastoma, eosinophilic granuloma, and fibrous dysplasia metaphyseal lesions~ solitary bone cyst, osteogenic sarcoma, osteochondroma, chondrosarcoma, non~ossitying fibroma, and chondromyxoid fibroma epiphyseal lesions- chondroblastoma, intra osseous ganglion cyst, giant cell tumor after epiphyseal plate closure, and hemangioma.

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In general, malignant bone tumors radiographically display moth eaten or permeative cortical destruction, periosteal new bone formation, and adjacent soft tissue swelling

(increased density and volume). CT scans and MRis can also be helpful in determining the location, confines, and type of tissue involved in bone tumors. Arteriography can be useful in determining vascular involvement, and aids in limb salvage planning when compartment resection or amputation is considered. Laboratory findings consistent with bone tumor formation and destruction include leukocytosis and anemia, elevated ESR, elevated serum Cat+, elevated alkaline phosphatase (osteoblastic activity), and increased total serum protein (multiple myeloma). Definitive diagnosis is made with appropriate bone biopsy, which may involve fine needle aspiration or, more reliably trephine plug(s) or en bloc excision of representative bone.

Treatment of benign bone tumors varies from observation to surgical resection and repair, depending upon symptomatology, the presence of pathological fracture, and prognosis. The treatment of malignant bone tumors always involves oncological consultation and management, as adjunct radiation or chemotherapy may be used in conjunction with appropriate resection or amputation. Longterm (life~long) follow-up is a required part ofthe management of malignancy, regardless of tissue type. Cartilaginous Tumors of Bone Enchondroma· usually a well-defined, asymptomatic, centrally located medullary lesion, seen in the 3rd to 4th decade. This tumor often appears as a lytic lesion in fingers and toes, and pathologic fracture may occur. If pain develops, consider chondrosarcoma. Multiple enchondromatoses are associated with Oilier's disease.

Periosteal (juxtacortical) chondroma - usually observed in children, wherein the juxtacortical soft tissue mass erodes or saucerizes the bony cortex. Chondroblastoma ~ usually observed in 15 to 30 year-old age group, commonly localized to the calcaneus or epiphysis of a long bone, with a well~defined osteolytic appearance. Chondromyxoid fibroma- usually observed in 2nd to 3rd decade, this lesion appears as a sharply-outlined, coarsely trabeculated, round, lytic lesion of the metaphysis. Osteochondroma~ the most common benign growth of bone occurring anywhere in the skeleton, typically in the 2nd to 4th decade, originating in the metaphysis, displaying a cartilaginous cap over new bone proliferation, and rarely associated with malignant transformation. Chondrosarcoma~ a malignant cartilaginous tumor of bone. It can arise from malignant transformation of an enchondroma, periosteal chondroma, or osteochondroma. It is rare in children, and is usually observed in the 5th to 6th decade. lt is the second most common malignant tumor of bone, following osteogenic sarcoma. Bone destruction appears moth eaten, with speckled medullary and soft tissue calcification (in general, soft tissue calcification in the presence of suspected tumor is an ominous radiographic sign), and metastasis to the lungs is common. Treatment of this lesion involves oncological management for radiation and/or chemotherapy, as well as appropriate resection or amputation.

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Bone Forming Tumors Osteoid osteoma- usually observed in children and young adults, marked by nocturnal pain alleviated with aspirin, displaying a round osteolytic defect surrounding a central

radiodense (sometimes lucent) nidus that is usually no larger than 1 em in diameter. This lesion is common in the foot.

Osteoblastoma- usually observed in 2nd to 3rd decade, larger than osteoid osteoma, more common in males, rapidly growing, metaphyseal or diaphyseal lesion the pain of which is not responsive to aspirin. Osteogenic sarcoma- the most common malignant bone lesion, usually appearing in the 2nd to 3rd decade, often affecting the metaphysis of the femur (40%) or tibia (16%). It is rapidly expansile with a star burst pattern of periosteal new bone formation, cortical erosion, and formation of Cod man's triangle. It can develop from Paget's disease of bone, which involves haphazard new bone formation and bone resorption, effecting a "woven bone" appearance, usually in males over the age of40 years, and is of unknown etiology (perhaps viral). Very high levels of serum alkaline phosphatase and urinary hydroxyproline are observed in Paget's disease. Connective Tissue Tumors Non-ossifying fibroma- usually observed in the lstto 2nd decade, eccentrically located in the metaphysis, with a sharply demarcated, lobulated osteolytic lesion displaying a sclerotic border.

Fibrosarcoma- usually observed in the medullary canal (67%) of a long bone in a young male, displaying osteolysis with minimal new bone formation. Speckled soft tissue calcification may be present

locally Aggressive Tumor Giant cell tumor- usually obse!Ved in the 3rd to 4th decade well after growth plates have closed (skeletally mature), localized to the diaphysis as well as metaphysis and epiphysis Displays thin, delicate trabeculae that have a "soap bubble" appearance, expanding into adjacent cortex, and known to undergo malignant transformation. Tumors of Vascular Origin Hemangioma- usually observed in the 4th to 5th decade, occurring in any bone. Displays a cystic lesion surrounded by a "spoke wheel" appearance of periosteal new bone formation. Glomus tumor- usually obse!Ved in the 4th-5th decade, often very painful, localized to the distal phalanx, and may require IPJ disarticulation. Tumor and Tumor-like Bone Lesions of Unknown Origin Solitary bone cyst- these are simple, or unicameral; cystic lesions of bone, often observed in the calcaneus or metaphyseal bone, in the 1st to 2nd decade, and contain a pinkish fluid upon aspiration. This is the most common fluid filled cystic lesion of bone.

Epidennoid cyst- usually obse!Ved in the 2nd to 4th decade, it is an isolated lytic lesion, usually of the distal phalanx.

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81

Aneurysmal bone cyst· a benign, blood-filled lesion that is usually observed in the 1stto 3rd decade. It is expansile, with horizontal, parallel trabeculae that are readily observed on MRI. The lesion is difficult to distinguish from malignancy.

Ewing's Sarcoma- usually observed in age group 5 to 25 years. It is a highly destructive lesion of cortical bone, with both "onion skin" and "hair-on-end" appearance. It displays a high rate of metastasis. It is the 4th most common malignant tumor of bone, and is rare in African-Americans. Pathological fracture is common. Metastatic Bone Disease Breast and prostate cancer often metastasize to bone, including the bones of the feet. Any musculoskeletal pain in an individual with history of previous malignancy warrants a high index of suspicion and careful examination. Leukemia, although rarely arising primarily in the foot, may effect secondary pedal osteolytic lesions, and is associated with leukocytosis, anemia, fatigue and malaise, adenopathy and splenomegaly.

SELECTED EMERGENCY SITUATIONS If a life-threatening event occurs in the office setting, the local emergency medical service (EMS) should be notified (911) immediately so thattransportto the hospital can be achieved in a timely fashion. The patient's vital signs should be monitored and recorded throughout the event, and medications administered during the event should be recorded. Following emergency treatment of any medical crisis, the patient must undergo immediate systemic medical evaluation and ongoing treatment should be provided as indicated. Medical emergencies occur, and the best treatment is prevention and preparation. Syncope Syncope is caused by temporary cerebral anoxia, often caused by bradycardia secondary to parasympathetic overtone. lt is related to emotional stress and pain, often associated with injection therapy. Trendelenburg positioning usually serves as adequate prevention. Signs and symptoms include pallor, hypotension, tachycardia, mydriasis, and diaphoresis (cool and clammy skin). Treatment consists of Trendelenburg positioning, loosening tight clothing, cool compress to forehead, aromatic spirits of ammonia, oxygen administered at 4 to 6 !/min, and monitor vital signs.

Hypersensitivity Reactions Hypersensitivity (allergic) reactions are caused by release of histamine, with resultant vasodilatation and increased vascular permeability, and bronchospasm. If the reaction progresses, airway constriction, hypotension and shock may ensue. There are four major types urticarial rash, angioneurotic edema, asthma attack and anaphylaxis.

Utticarial rash presents with wheals, hives and pruritus. Treatment involves removal of the allergen, and administration of 50-75 mg diphenhydramine (Benadryl) IM, followed by 50 mg PO q 6 h PRN. Angioneurotic edema presents with marked mucous membrane edema resulting in swelling of the eyelids, cheeks, lips, pharynx, and larynx. As the upper airway swetls, hoarseness and stridor (laryngospasm), wheezing (bronchospasm) and cyanosis develop. Treatment involves withdrawal ofthe allergen, and administration of 0.2-0.5 cc epinephrine SC q 15 min


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as needed, in addition to 50-75 mg diphenhydramine IM, and 8 mg dexamethasone (Decadron) IM for late effects. Asthma attack presents with wheezing due to bronchospasm, effecting dyspnea, and initial flush then cyanosis. Treatment involves administration of 2 puffs of aerosol

bronchodilator (Ventolln, Proventil), which asthmatic patients often carry themselves, or 0.3-0.5 cc epinephrine 1:1,000 SC q 15 min x3, in conjunction with aerosol bronchodilator.

Anaphylaxis results in rapid respiratory and cardiovascular collapse, and requires rapid administration of epinephrine in order to avoid a severely morbid or fatal reaction. Signs and symptoms include laryngospasm, bronchospasm, hypotension, nausea, diaphoresis, pruritus, urticaria and angioedema, and unconsciousness. Treatment involves withdrawal of the allergen, Trendelenburg position, maintain airway, 02, and administer epinephrine 1:1,000 SC or sublingual 0.3- 0.5 cc and repeated q 5-15 minutes until an adequate response is observed, try to establish IV access. The sublingual route of administration is acceptable when lV access is not attainable {inject into posterior ventral portion ofthe tongue where it is vascularized with larger vessels). Inject .25 cc 1:1,000 epinephrine about site of previous injection of allergen, or apply BP cuff proximal to site of allergen injection (release every 10 to 15 minutes). If hypotension does not respond to epinephrine, administer metaraminol (Aramine) 0.5- 5 mg IV. If bronchospasm persists, administer aminophylline 250 mg IV over 10 min.lf convulsion occurs, administer diazepam (Valium) up to 10 mg slow IV infusion titrated until the seizure is controlled, or administer short-acting barbiturate pentobarbitallOO mg IV. Be prepared to support and maintain respiration whenever IV diazepam or pentobarbital are administered.

Toxic Reactions to Local Anesthetics Toxic reaction to a local anesthetic involves initial central nervous system {CNS) stimulation due to inhibition of inhibitory neurons, resulting hypertension, tachycardia, and skeletal muscle twitching that may progress to convulsion. Treatment consists of administration of Oz to counter hypoxia and resist convulsion, maintain airway and, in the office, give diazepam (Valium) 10 mg slow IV titration. Following initial CNS excitation, CNS depression may develop as the toxic level of local anesthetic proceeds to suppress CNS function. Pathologic findings include hypotension, weak and rapid pulse, shallow, slow respiration, loss of speech, confusion, delirium, and coma. Treatment involves airway maintenance and administration of 02, ephedrine 0.5 cc IV or lM.Ifthe reaction proceeds to cardiovascular collapse also administer atropine 0.4 mg IV, and commence BCLS and/or ACLS.It is lmportantto know the toxic dose of the local anesthetic being administered. The maximum allowable dose of local anesthetic varies with epinephrine co-administration \Table 3-12), and readers are encouraged to be familiar with the toxic dosages of the agents thatthey use.

TABLE 3-12. MAXIMUM LOCAL ANESTHETIC DOSAGES.* Maximum dose (mg)

local anesthetic

Plain Lidocaine Bupivacaine

W~h

epinephrine

300

500

175

225

"In order to calculate the proper volume of local anestheitc for injection, the following mass per volume proportions are helpful: there are 2.5 mg/ml in a0.25% solution, 5 mg/ml in a 0.5% solution, 10 mg/ml in a 1% solution, and 20 mg/ml in a 2% solution_

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Hypertensive Crisis Hypertensive crisis can develop as a result of progressive, neglected hypertension, head injury or encephalitis, drug induced, pheochromocytoma, dissecting aortic aneurysm {will rapidly drop if aneurysm ruptures), or associated with renal and/or heart failure. Diastolic pressures of 130~140 mm Hg are considered emergent and require immediate treatment with diazoxide (Hyperstat) 300 mg IV infused rapidly over 10 seconds. The patient is

transported to the hospital as soon as possible. Hyperventilation Hyperventilation is cased by anxiety and emotional stress, perhaps related to anticipation of pain or injury, and results in blowing off C02 and development of respiratory alkalosis. Signs and symptoms include rapid, shallow breathing, vertigo, confusion, paresthesia (often affecting the forearms and hands), and carpopedal spasm. Treatment is to reassure and have the patient rebreathe into a brown paper bag so that C02 is elevated. Sedation with 510 mg of diazepam PO (or slow IV infusion) may be helpful in a prolonged event.

Seizure Seizure can result from pre-existing seizure disorder, head trauma, encephalitis, or toxic effect of medication, such as a local anesthetic. Signs and symptoms include aura, CNS stimulation, and grand mal epilepsy with tonic-clonic spasms, coma, post-ictal aphasia, and somnolence. Treatment focuses on protecting the patient from injury during the seizure and allowing the seizure to run its course. Avoiding head injury as the patient convulses or falls is important. If easily achieved, a padded tongue depressor may be placed in the mouth to prevent laceration of the tongue due to jaw compression, however it is not advisable to force anything into the mouth for fear of inducing injury (dental damage). If the patient becomes cyanotic or the seizure fails to subside, or status epilepticus occurs (one seizure is immediately followed by another), then administer diazepam 5-15 mg IV via slow infusion with attention to respiratory support as indicated. Alternatively, 50 mg (2 ml of 2.5% solution) of IV sodium thiopental may be administered. Phenytoin (Dilantin)300 mg IV slow push may also be administered. 02should also be administered. The patient should thereafter be transported to the hospital for neurological evaluation. It is important to know how well-controlled your patients with epilepsy are, and when the patienfs last seizure took place. Insulin (Hypoglycemic) Shock Insulin shock is caused by an acute episode of hypoglycemia or hyperinsulinism. Signs and symptoms include anxiety, confusion, diaphoresis, tachycardia, nausea, convulsion, and coma. Treatment consists of administration of oral glucose either as an instant glucose preparation or via fruit juice or a candy bar. An ampule of 050 may also be administered IV if oral administration has not resolved the crisis. Most experienced diabetic individuals know the warning signs of hypoglycemia, and take counter-actions in a timely fashion. Hypoglycemia may occur in a patient who was running late for a morning appointment and failed to eat breakfast after taking their insulin. Acute Adrenal Crisis

Acute adrenal crisis can occur as a manifestation of insufficient corticosteroid administration in a patient who regularly takes steroids for treatment of a steroid-responsive disease, or as the initial presentation of previously undiagnosed adrenal insufficiency {Addison's disease). Patients on chronic, regular corticosteroid supplementation or replacement therapy require

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administration of exogenous corticosteroid in the perioperative period. These patients have suppression or inadequate function of their hypothalamic-pituitary axis for any of a variety of reasons, often due to the therapeutic use of corticosteroids for the treatment of rheumatoid arthritis and other auto-immune diseases, asthma and other forms of COPD, or malignancy. The body's own production of corticosteroid is suppressed after exogenous administration of just 7.5 mg/day of prednisone over a 7 day period. Symptoms of adrenal insufficiency include hypotension, syncope, nausea and

vomiting. Cardiovascular collapse can develop if corticosteroid is not administered in a timely fashion. Serum cortisol level should be drawn as soon as possible, without delaying administration of 100 mg hydrocortisone IV, followed by 100 mg, or 15 mg/kg, IV every 8 hours. The most common complicating effects of steroid therapy, in particular chronic steroid use, are related to inhibition ofWBC function and diminished fibroplasia, both of which negatively impact soft tissue and bone healing. In the acute postoperative period, steroid supplementation can decrease the white count and mask infection, and also diminish epithelialization and wound contraction. Consideration can be given to supplementing with vitamin A to try to counter some of the detrimental affects of corticosteroids on wound healing. All patients requiring daily maintenance corticosteroid administration should continue on their regular maintenance dose, and receive supplemental corticosteroid during the peri operative period. For cases involving local anesthesia with or without lV sedation, IV administration of 100 mg hydrocortisone 30 to 60 minutes preoperative, then again postoperative in the recovery room for cases lasting greater than one hour, is generally adequate. Alternatively, 15 mg prednisone can be administered orally at 0600 the day of surgery, then again at 1600the day of surgery, and a final supplemental dose of 15 mg orally at 1600 on postoperative day number one. For patients undergoing general anesthesia, 100 mg hydrocortisone can be administered HS the evening before surgery, then again preoperative prior to starting the case, and then Q 8 hours over the first 24 hours postoperative, and continued on a Q 8 hour basis up to the second -fourth postoperative day, depending upon the physical and mental stress of the surgery. Steroid supplementation should be tapered down to the regular maintenance level if supplemental steroid has been administered for more than 3 days. Other supplementation regimens may be better suited for an individual patient, and consultation with the patient's internist is helpful. Alcohol Withdrawal Alcohol withdrawal can occur in individuals of all walks of life, and is precipitated by Illness or injury that precludes access to ethanol. Signs and symptoms include tremulousness, irritability, nausea, anorexia, hallucination, and seizure. These can develop as early as 3~5 hours or up to 48 hours after the last drink. Delirium tremens is characterized by autonomic hyperactivity resulting in hyperpyrexia, diaphoresis, and tachycardia; in conjunction with tremulousness, hallucination, agitation, and confusion. Delirium tremens conveys serious risk of injury and/or death. Treatment of alcohol withdrawal consists of chlordiazepoxide llibrium)25-100 mg PO q 6h or diazepam {Valium) 5~20 mg PO q6h; observation, protection, and reassurance. Adjuncttherapyfor malnutrition and social service intervention is also indicated.

Airway Obstruction Airway obstruction is caused by a foreign body in the airway, or angioedema- induced oropharyngeal occlusion. Signs and symptoms include choking, gagging, violent inspiratory

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85

effort, suprasternal notch retraction, cyanosis, respiratory arrest, and cardiac arrest.

Treatment involves establishing an airway via inspection and sweeping the oropharynx, performance of the Heimlich maneuver, placement of an oral airway or endotracheal intubation, or emergency cricothyrotomy. Once an airway is established, BCLS and/or ACLS

may be indicated. The patient is transported to the hospital as soon as possible. Respiratory Arrest Respiratory arrest is caused by airway obstruction or drug toxicity. Signs and symptoms include apnea, cyanosis, and coma. The so-called "cardinal triad" of barbiturate toxicity or narcotic overdose consists of apnea, miosis and coma (the patient is usually cyanotic as well). Respiratory arrest that is not rapidly alleviated will be rapidly followed by cardiac arrest Even a brief period of airway obstruction or respiratory arrest in an individual with coronary artery disease can effect angina pectoris, myocardia! infarction, and/or cardiac arrest Respiratory arrest is treated with BCLS wherein the airway is established and artificial respiration (rescue breathing) administered. Transport the patient to the hospital as soon as possible. Pulmonary Embolism (PEl PEcan cause acute, crushing chest pain and a sense of impending doom. See Venous Thrombosis and PulmonaJY Embolism Malignant Hyperthermia Malignant hyperthermia is a severe, adverse reaction to general anesthesia (intra-

operative) that occurs in approximately 1:20,000 patients, and displays a familial tendency. lfthere is a family history, the CPK should be assessed preoperatively for elevation (almost 80% correlation). Amide local anesthetics should be avoided in patients with a history of malignant hyperthermia. The reaction occurs upon exposure to inhalant anesthetic agents, and results in hypertonicity and skeletal muscle fasciculation, jaw clenching and rigidity, hyperpyrexia, tachycardia, tachypnea, variable blood pressure, cardiac dysrhythmia, hyperhidrosis, cyanotic mottling of the chest and extremities, and dark blood observed in the surgical wound. Treatment consists of immediate cessation of anesthetic agent, hyperventilation with 100% 02 at 8·10 liters per minute, and IV bolus administration of Dantrolene sodium at 1 mg/kg up to a maximum of 10 mg/kg. The EKG is monitored and procainamide may be administered to stabilize the myocardium. Physical measures to cool the body are instituted to counter brain·injuring hyperpyrexia. Cooling efforts include IV administration of cool saline, application of ice to the groin and axillae, ice water lavage of the stomach, rectum, and bladder. Administration of sodium bicarbonate may be indicated to counter acidosis and hyperkalemia. Kidney function is maintained at 2 ml/kg/hr using IV furosemide or mannitoL Insulin may be administered to assist in providing the cells with glucose for on·going metabolism. Following control of the acute crisis, Dantrolene sodium is administered orally over the next 2·3 days. Angina Pectoris

Angina pectoris is caused by coronary artery disease or obstruction. The patient usually has a family as well as personal history of such crushing chest pain, and may already be medicated for their disease. Anxiety, emotional or physical stress usually precipitate angina pectoris, and the characteristic crushing chest pain that lasts 3 to 5 minutes in the presence

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Ch. 3

of stable vital signs. The pain may radiate to the left arm and wrist The patient may also display diaphoresis, dyspnea, nausea, and weakness. Treatment consists of administration of 100% at 61iters/minute, sublingual nitroglycerine INTG)1/150 tablets every 10 minutes as needed. Loosen tight clothing, sitthe patient in semi-Fowler's position, and transport the

o,

patient to the hospital as soon as possible. Myocardiallnlarction IMI) Ml is caused by respiratory arrest or coronary artery disease, and is usually preceded by 3to 5 minutes of angina pectoris with its associated signs and symptoms, as well as a sense of impending doom. Cardiac dysrhythmia may also develop. Treatment consists of

administration of 100%02 at61iters/minute, morphine sulfate 5-10 mg IV push, or 10-15 mg

IM, while monitoring the BP and securing IV access and initiating infusion of 05W at KVO IB hour) rate. Preparation is made to administer BCLS or ACLS, and to transportthe patient to the hospital. Cardiac Arrest Cardiac arrest is caused by myocardial infarction and/or respiratory arrest. Signs and symptoms include unresponsiveness, apnea, and absence of carotid artery pulse, and clinical death with the pupils fixed and dilated, and facial, acral and chest cyanosis. Treatment involves BCLS, ACLS, and transportation to the hospital as soon as the patient is ready. The treatment protocol involves all of the interventions defined previously for MI.

BASIC CARDIAC LIFE SUPPORT Basic Cardiac Life Support IBCLS) consists of establishment of the airway, rescue breathing, and circulatory support with external chest compression (cardiopulmonary resuscitation CPR).Table 3-13).

TABLE 3-13. CARDIOPULMONARY RESUSCITATION I CPR) PROTOCOLS.

Age of victim Adult Adult Child Infant

Number of rescuers 1 2

2 2

Compression-to-ventilation ratio 15:2 5:1 5:1 5:1

If the required equipment and medications are available, additional support can be administered based on the recuers' level of training and experience. The EKG is observed in a "quick-look" fashion via the defibrillator paddles, or an Automatic External Defibrillator reads the rhythm without visual display, and identification of a lethal dysrhythmia warrants defibrillation in the adult at200-360 joules delivered 12 joules /kg in a child) for ventricular fibrillation.

ADVANCED CARDIAC LIFE SUPPORT Advanced Cardiac Life Support IACLS) entails application of algorithms with a degree of automaticity, however permutations of the algorithms may be helpful on an individualized basis.

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87

Statistics show that: the majority of cardiac arrests occur in patients wfth pre~existing coronary artery

disease 20% of cardiac arrests are the first and last manifestation of the disease 30% of victims have a second arrest within one year if they survive resuscitation but do not follow-up with treatment 50% suffer another arrest within the second year if left untreated the most common cause of arrest is ventricular fibrillation {V-fib)

1-2% of all hospital admissions suffer cardiac arrest and 50% are resuscitated 33% survive at least 24 hours, but only 15% survive to leave the hospital 95% die if the resuscitation extends longer than 15 minutes most codes are called \terminated) after 30 minutes if no significant positive response is noted 56% of out-of-hospital arrest victims survive if ACLS is administered within 4 minutes the prognosis for survival worsens in ascending order as follows: V-tachycardia > V-fib. >bradycardia/asystole; CPR without appropriate drugs, such as epinephrine, is inadequate to sustain adequate perfusion of the brain and heart. The ABCs (Airway, Breathe, Circulate) of cardiopulmonary resuscitation (CPR): 1. Identify unresponsiveness 2. Call for help 3. Position and establish airway 4. Check breathing 5. Begin rescue breathing with 2 full breaths 6. Check circulation by palpa~ng the carotid pulse 7. Activate emergency medical service (EMS) 8. Begin chest compressions according to victim's size/age 9. Continue basic cardiac life support or implement advanced cardiac life support (ACLS) and/or transport

Airway and ventilation protocol: 1. Heimlich maneuver--if obstruction is suspected, implement the Heimlich maneuver 2. Head back-jaw thrust-this is the standard approach to establish unobstructed airway patency 3. Rescue breathing-"mouth-to-mouth" ventilation, using appropriate protective shield \Pocket-mask or similar device) 4. Supplemental oxygen-administer 90% 02 at 10 liters/minute via line to mask or nasal cannula 5. Ventilation-use an Ambu bag-valve-mask if airway remains patent 6. Endotracheal intubation or laryngeal mask airway (LMA) insertion-resortto more secure airway management if head back-jaw thrust is insufficient; consider a nasotracheal intubation if cases involving oral trauma 7. Spontaneous ventilation-if spontaneously ventilating, reduce to 20-40% 02 via nasal cannula

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Ch. 3

Emergency IV access:

Line size-attempt to obtain z16 gauge access to facilitate administration of emergency medications Srte-a central line is preferable to peripheral access Number of lines-as a rule, 2 sites may be useful, especially in a prolonged resuscitation effort Vein options-dorsal hand or antecubital, subclavian or internal jugular vein, and femoral vein (keep in mind, during CPR there is decreased flow inferior to the diaphragm) Catheter methods-Seldinger guide wire and sheath dilator, typically the easiest; catheter-over-needle (Angiocath®), catheter-through-needle (lntracath•) Cut down-as a last resort, sharp dissection to expose and catheterize either the saphenous or axillary vein can be undertaken The EKG and cardiac dysrhythmia: Conduction system-sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, left and right bundle branches Electrocardiogram-P wave= atrial depolarization, PR interval= time between atrial and ventricular depolarization, ORS complex= ventricular depolarization EKG and cardiac rate-each small grid square= 0.04 seconds, there are 5 large squares/second, 31arge squares approximates 90 beats per minute EKG tracing-monitor quick-look paddles or lead-2to determine rate, rhythm, and axis of the dominant pacer Dysrhythmias and cardiac life support: Normal sinus rhythm (NSR)----range 60-100 regular beats per minute Sinus tachycardia-response to exercise, hypovolemia, fever, anxiety, hyperthyroidism, sympathomimetic, etc. Sinus bradycardia-response to vagal overtone or atropine, sinoatrial node defect hypotension, ventricular ectopy, local anesthetic toxicity, etc. Premature atrial contractions {PACs)-ectopic atrial pacer cause irregular rate; response to sympathomimetic stimulant or a-agonist hypoxia, etc. Atrial tachycardia and fibrillation-atrium fails to effectively contract at 400-700 beats per minute, as does ventricle at 150-200 beats per minute; due to myocardial infarct or other disease; requires digitalis and/or cardioversion Junctional rhythm-AV node acts as latent pacer after 1-1.5 second delay, typically effects rate of 40~60 beats per minute Premature ventricular contraction {PVC)-due to ectopic ventricular focus or foci, runs of PVCs are ominous Ventricular tachycardia-3 or more ventricular beats, rate> 100 beats per minute Ventricular fibrillation-this results in no cardiac output and is lethal; coarse waveform represents recent fibrillation, whereas fine waveform indicates late fibrillation Ventricular asystole-flat line waveform due to cessation of ventricular contraction. Atrioventricular block~conduction blockade between the AV node and the bundle of His, effecting wide ORS segment and decreased cardiac output)

Selected Diagnostic Techniques

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89

SELECTED !JIAGNOSTIC TECHNIQUES HISTORY AND PHYSICAL EXAMINATION The most importanttool in making an accurate diagnosis is a properly executed history and physical examination (H&P). The astute practitioner listens to the patient See Oral Exam Test Taking Format for a useful H&P form.

DIAGNOSTIC IMAGING Radiation Safety Radiation safety procedures and an understanding of the effects of ionizing radiation are

important matters tor all office personnel participating in preparation of diagnostic images. X-rays are high energy electromagnetic radiation that can effect mutation of cellular genetic material. There is no safe dose of ionizing radiation, and therefore exposure must be limited while maximizing the diagnostic benefit of the image. Pregnant women should not electively be radiographed, and alf subjects should wear protective lead apron, and the examiner should use a similar apron, thyroid shield, cornea protection, and lead gloves when manipulating the extremity under examination. Variable factors in the imaging process include: kV (kilovoltage), mS (milliseconds), collimation, distance between the foot (part), the film, and the X-ray source. Scatter radiation must be minimized to reduce environmental radiation not used for creation of diagnostic images. Fluorescent film screens are used with blue or green light sensitive films to further decrease the amount of ionizing radiation required to obtain a useful diagnostic image. Automatic or manual film processing requires exposure of the exposed film to developer, fixer, and then a water rinse followed by drying. Poor quality images are unacceptable practice, as useful diagnostic information is compromised at the expense of patient and environmental radiation exposure. Use of a radiation dosimetry service enables one to accurately monitor environmental and personal exposure. Radiographic Views

Standard pedal radiographic views are taken with the patient weight bearing, with the feet in the angle and base of gait. This allows reproducible and reliable images, from which standard angles and relationships can be assessed. Variations can be useful, depending upon specific needs. The primary views of the ankle include the mortise and lateral projections. Ankle views do not necessitate positioning the foot in the angle and base of gait. Contralateral radiographs can be obtained for comparison, particularly when evaluating the skeletally immature, or when concerned about secondary centers of ossification. Dorsoplantarfoot~ the patient standing on film cassette, beam angled 15° from vertical and aimed atthe navicular.

Lateral foot~ the foot is posrtioned beside (against) the film cassette, which is vertical to the substrate, beam angled 90° from vertical and aimed at the midfoot. Lateral oblique foot- the patient standing on film cassette, beam angled 45° from vertical

and aimed at the lateral aspect of the foot. Useful in assessment of the calcaneus, cuboid, fifth metatarsal and little toe.

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Ch. 4

Medial oblique foot- the patient standing on film cassette, beam angled 45° from vertical

and aimed at the medial aspect of the foot. An unconventional view, useful in assessment

of the medial aspect of the foot, the first metatarsal and hallux and, in particular, the plantar medial border of the foot. It is also useful in evaluation of the tuberosity of the calcaneus, as in the case of suspected plantar heel spur.

Calcaneal axial- the patient standing on film cassette, beam angled 45° to vertical and aimed at posterior aspect of the heeL Modifications include Harris and Beath projections, wherein the beam angle ranges from 10° above and 10c below the lateral view declination angle ofthe posterior facet of the STJ las determined by a scout lateral view) or, more simply, 30°, 45° and 60° from vertical. Useful in assessment of the posterior aspect of the calcaneus, suspected calcaneal fracture or inspection of the posterior facet of the STJ or the sustentaculum.

Sesamoidal or metatarsal axial- the patient standing on orthoposer with the film vertical to the substrate, and the toes dorsiflexed against the film. The hindfoot is supported with enough radiolucent foam to elevate the heel above the substrate, with the beam angled from posterior-to-anterior parallel to the substrate and aimed at the metatarsal heads. Positioning devices are available to aid in stabilizing the patient for these views.

Isherwood views- a rarely used set of three non-weight-bearing views that display the STJs. The lateral oblique view shows the anteriorfacet, the medial oblique view shows the middle and posterior facets, and the lateral oblique axial view shows the posterior facet. CT and linear tomography are more typically used, as positioning for Isherwood views is difficult and time consuming. Other sets of radiographic views used to image the STJs, and generally superseded by linear and axial tomography, include Anthansen and Broden projections.

Mortise ankle- the heel is backed against the vertical film cassette, with the foot medially rotated 15", the beam angled parallel to the substrate and aimed at the ankle. This is the standard view for assessment of the tibiotalar and tibiofibular joints, and the dome of the talus and tibial bearing surtace.

lateral ankle- the medial aspect of the foot is positioned against the vertical film, the beam angled parallel to the substrate and aimed at the ankle.

Anterior-posterior ankle- the heel is backed against the vertical film cassette, with the toes pointing straight ahead, the beam angled parallel to the substrate and aimed at the ankle. The lateral malleolus is rotated posterior to and superimposed behind the tibia in this view, and the distal tibiofibular syndesmosis is obscured. The mortise view is much more useful for evaluation of the tibiotalar and tibiofibular joints.

Medial oblique ankle- oriented the same as in the AP or mortise of the ankle, however the foot is medially rotated 45a, thereby further opening the tibiofibular syndesmosis. Lateral oblique ankle- oriented the same as the AP or mortise of the ankle, however the foot is laterally rotated 45°. May be used to assess the medial malleolar cortex and the media! aspect of the talus.

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91

Stress Radiography Stress radiography can be performed with static radiographs, or dynamically under fluoroscopic image intensification. Stress radiographs are used to identify occult fractures and ligamentous instability, and can be used to evaluate any bone or joint in the leg, foot or ankle. The examiner should wear protective gloves, thyroid shield, and body apron whenever stress fllms are made. Anteriardrawerofthe ankle- with the patient supine, the lateral aspect of the foot is placed against the film cassette and the heel is cupped with one hand while the opposite hand stabilizes the anterior aspect of the tibia. The foot is rotated medially about 15°, thereby allowing visualization of the talar dome, while the talus is pulled forward out of the mortise. The distance between the nearest point on the posterior aspect ofthe dome of the talus and the most posterior margin of the distal tibial bearing surface is measured, and a distance of > 4 mm is indicative of disruption of the anteriortalofibular ligament. A Telos apparatus can be useful for applying anterior drawer in a reproducible fashion.

Inversion ankle stress (talartilt)~ with the patient supine, the ankle is oriented in a fashion similar to that used in the mortise view, while the tibia is stabilized medially and the talus lhindfoot with the STJ stabilized) forced into the tibial malleolus in an effort to stress the lateral collateral ligaments. The angle created between the plane of the distal tibial bearing surface and the dome ofthe talus is measured. Angles< 5° are considered normal, between 5-20° may be normal or abnormal, and larger angles are suggestive of lateral collateral ligament disruption. Loose bodies may be identified between the tibia and talus. Stress ankle dorsiflexion (charger)- a weight-bearing lateral view of the ankle is taken with the ipsilateral knee flexed and the ankle relatively dorsiflexed, This is used to depict osseous ankle equinus. Fluoroscopy Fluoroscopy (image intensification) is used to obtain quick radiographic images of operative maneuvers and stress manipulation, fracture reduction, fixation placement, foreign body localization, and trocar or pin placement The C-arm must be used with a radiolucent segment in the OR table. Computerized Axial Tomography (CT) And Magnetic Resonance Imaging (MRI) CT and MRI are useful imaging techniques following review of standard radiographs. Linear tomography {non-axial linear slices) can also be useful, however it is not readily available currently. Computerized tomography (CT) or computerized axial tomography (CAT scan) use high-energy ionizing radiation (X-rays), multiple projections, and a computer to generate images, and is best suited to cortical bone imaging. Magnetic resonance imaging (MRI) uses low energy radio waves traversing the body within a magnetic field, and a computer to generate images. T1 ~weighted \fat) images are dependent on the fat content of the tissue, while T2-weighted \water, inflammation) images are dependent on the water content of the tissue and are especially useful in the presence of pathological inflammation or fluid accumulation. Both CT and MRI can be enhanced when combined with contrast medium.

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Ch. 4

Comparison of CT and MRI for Selected Pathological Conditions

Tarsal coalition- MRI is best, as not all coalitions are cortical bone Arthritis, tendinitis, and other inflammatory processes- MRI is best, as it allows early visualization of peri-articular and soft tissue changes Avascular Necrosis- MRI is preferred, and the hallmark MRI sign is a well-defined region of decreased intensity within medullary bone on both T1- and T2-weighted images. CT could be used to show advanced AVN wherein joint space has collapsed

with cortical bone defect Infection- MRI is sensitive, but not specific, tor imaging soft tissue abscess and osteomyelitis (medullary). MRI does not image subcutaneous gas. CT is useful for ·Imaging cortical defects, sequestrum, cloaca, involucrum, and intraosseous or subcutaneous gas. Neoplasm- MRI is superior for evaluating bone marrow and soft tissue; while CT is best for cortical bone, calcification, endosteal thinning, and fine periosteal reactions. Trauma- MRI is preferred for imaging soft tissue injury, in particular tendon, ligament and cartilage. CT is superior for imaging cortical bone, especially when comminution or growth plate (physeal) injury is suspected. Osteochondral lesions may warrant both CT and MRI. When in doubt as to the preferred imaging technique, simply consult with the radiologist.

Contrast Jmaging Contrast imaging using radiopaque contrast dye injected into a joint space or tendon sheath can be used to assess surface defects such as osteochondral fracture or tendon and sheath disruption. Hypersensitivity (to the contrast medium), possible sepsis, and the invasive nature of the procedure, the need for ionizing radiation and limitations related to patient positioning, are all potential disadvantages of both arthrography and tenography. MRI as well as CT scanning, despite their cost, offer excellent diagnostic images and have almost replaced contrast imaging of the ankle and peroneal sheath. Arthroscopy and endoscopy also offer diagnostic, and therapeutic, modalities applicable in the management of the foot and ankle. Ultrasonography Ultrasonography can be used for localization of foreign bodies following puncture wound, as well as identification of fluid or solid mass in the subcutaneous tissues. Radionuclide Scans Radionuclide scans are used to image bone physiology, and are usually performed using technetlum-99, ga!lium-67, or indium-111. Most scans show increased scintigraphy within 48-72 hours after the infection or other osteitis has begun. Tc-99 has a half-life of about 6 hours. Only the technetium scan labels hydroxyapatite crystals in living bone, and is therefore termed "a bone scan." Ga-67 is used to label white blood cells and plasma proteins, and is used to identifyWBC accumulation (pus, infection) in bone or other tissues. Gallium is not used as an isolated study, and is usually combined with a Tc-99 scan performed about 24-72 hours earlier. An increased uptake of Tc-99 without increased uptake of Ga-67, correlates 85% with the absence of osteomyelitis. If both Tc-99 and Ga-67 scans show increased uptake, then there is about a 70% correlation with osteomyelitis being present. ln-111 is used to tag the patienfs neutrophils, after first drawing blood and separating the PMNs. The labeled neutrophils are then infused back into the patient, and


Ch.4

93

the scan performed 18 to 24 hours later. ln-111 scans are positive in cases of osteomyelitis and .negative in cases of osteoarthropathy. Since ln-111 is tagged to neutrophils chronic osteomyelitis, which is primarily an accumulation of lymphocytes, may present as a false negative indium scan (infection present despite a negative scan). An ln-111 scan may be useful in trying to distinguish postoperative infection from pseudoarthrosis or nonunion.

Bone Scans Bone scans (Tc-99) are imaged in atriphasic fashion, wherein a scintigram is made atthree specified times following administration of the radioisotope. The radio angiogram (first or immediate phase, blood flow images), is measured immediately following infusion of radionuclide and shows dynamic flow to the area. The blood pool image (second phase) is measured about 20 minutes after infusion, and shows increased scintigraphy in the presence of hyperemia. The first two phases are "hot" in both bone and soft tissue infection, or other causes of inflammation and hyperemia. The blood flow image correlates with perfusion of the part, and would not show uptake of radionuclide in the presence of ischemia. The delayed image (third phase) is measured about three hours after infusion of radionuc!ide, and correlates with skeletal uptake of the isotope. The delayed image often identifies activity related to infection or other persistent bone pathology, such as pseudoarthrosis or hypertrophic nonunion. Moreover, longer term delayed TC-99 bone scans, imaged at 24 hours !fourth phase), may be used to image infection in patients with PVD, diabetes mellitus and Charcot neuroarthropathy. Neuroarthropathy may present "hot" scans in all four phases. Soft tissue infections are usually "hot" in only the first two phases. Furthermore, a Tc-99labeled WBC scan (Seratec) can also be used to image bone infection, particularly in patients with diabetes mellitus or suffering postoperative infection. In any case, a scan is a sensitive but nonspecific imaging technique that must be combined with other diagnostic imaging techniques and clinical, as well as surgical, diagnostic measures.

Standard Radionuclide Bone Imaging Combinations

Acute Osteomyelitis Tc - 99m Scan

Ga- 67 Scan In -111 Scan

Phase I + Phase II ++ Phase Ill +++ Positive focal uptake Positive focal uptake

Inactive Chronic Osteomyelitis Tc - 99m Scan

Ga- 67 Scan In- 111 Scan

Phase I +/Phase II + Phase Ill +++!persists in longer delayed imaging)

Negative Negative

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Ch. 4

Acute Cellulitis Tc- 99m Scan

Ga- 67 Scan In -111 Scan

Phase I +++ Phase II ++ Phase Ill + Positive diffuse uptake Positive

Septic Arthritis Tc- 99m Scan

Ga- 67 Scan ln-111Scan

Phase I +++ Phase II +++ Phase Ill +/Positive focal uptake Positive

CARTILAGE IMAGING Contrast arthrography-contrast agent (iodine for X-ray or CT, or gadopentetate dimeglumine for MRI); direct, pseudo-direct (via peroneal sheath to ankle joint), indirect methods; enhances visualization of articular cartilage margins and small cortical abnormalities; entails need trauma, possible infection and hypersensitivity to local anesthetic and contrast agent. High resolution delayed gadolinium~enhanced MRI of cartilage (HR-MRI-dGEMRIC) with fat suppression is currently the best method of cartilage imaging short of arthroscopy. The following methods are under development for clinical use, and are currently experimental research tools that show superb cartilage detail: high frequency ultrasound, diffraction enhanced imaging (MRI), gradient MRI, T1 rho time relaxation MRI, T2 time relaxation MRI, optical coherence IR tomography, and positron emission tomography (PET).

CliNICAl lABORATORY TESTING Complete Blood Count Complete blood count (CBC) with differential cell count is a general screening for a variety of conditions. CBC includes: Hemoglobin (Hgb)- normal range is 13.5-17 gm/1 00 ml for males and 12.5-16 gm/100 ml for females. Values below 11 gm/100 ml are considered to represent anemia, and should be evaluated. Elevation above 18 gm/100 ml may represent polycythemia, and increases blood viscosity and increases risk of thrombosis. Hematocrit(Hct)- normal range is 40-54% for males and 37-47% for females. Varies with the

Hgb. fled blood cell count- normal range is 5.4± 0.8x 106 /mm 3 for males and 4.8 ± 0.6 x 106/mm' for females. The RBC count increases in individuals living at high altitudes, in environmentally hot work places, and in athletically fit individuals.

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Corpuscular indices and anemia normocytic

macrocytic

microcytic/

hypochromic Mean corpuscular volume

82-92

95-150

50-80

Mean corpuscular Hgb

25-30

30-50

12-25

Mean corpuscular Hgb concentration

32-36

32-36

25-30

Remember the phrase "90, 30, 30," for normal MCV, MCH, and MCHC values. Normocytic anemia can be observed with acute hemorrhage, hemolytic anemia, and abnormal hemopoiesis. Macrocytic anemia occurs with pernicious anemia, sprue,

pregnancy, antimetabolic therapy, and other megaloblastic conditions. Microcytic anemia occurs with iron deficiency or malabsorption, hemorrhage, and increased iron metabolism.

White blood cell count- normal range 5,000 -10,000/ mm3. Causes of leukocytosis include: acute infection, metabolic acidosis, gout, uremia, heavy metal toxicity, tissue necrosis or injury (burns, gangrene, tumor, myocardial infarction, pulmonary embolism), secondary to hemorrhage or menstruation, and myeloproliferative diseases. Causes of leukopenia include: adverse drug reactions to Thorazine, phenylbutazone, various antifungals and antibiotics; pernicious anemia, aplastic anemia, and certain severe infections (septic shock). Differential white cell count- segmented neutrophils 40-60%, band neutrophils 0-5%, lymphocytes 20-40%, monocytes 4-8%, eosinophils 1-5%, basophils 0-1%. Some causes of neutrophilia include acute infection, necrosis, pain, exercise or post-convulsion, anoxia, hemorrhage, sunburn. Some causes of neutropenia include overwhelming infection, marrow depression, antimetabolite therapy, and autoimmunity. Lymphocytosis may indicate viral syndrome, hepatitis, chronic TB, and measles. Monocytosis occurs with leukemia, Hodgkin's disease, collagen vascular diseases and arthritides, sarcoidosis, subacute bacterial endocarditis, and other infections and wounds. Eosinophilia is indicative of allergy, asthma, eczema and urticaria; parasitic infection; scarlet fever; pemphigus and dermatitis herpetiformis; leukemia and pernicious anemia. Eosinopenia is seen in Cushing's disease, excess ACTH, chronic steroid therapy, postoperative state, shock, and labor. Basophilia occurs in polycythemia, chronic myelogenous leukemia, chicken-pox, small-pox, hypothyroid myxedema, and renal disease.

Platelet count- normal range is 140,000-340,000/ mm1 Platelets are elevated in collagen vascular disease, iron deficiency anemia, acute infection or injury, hepatic disease, cardiac disease, malignancy and polycythemia Vera. Important Labs in Rheumatoid Disease

Erythrocyte sedimentation rate (ESR)- normal anticoagulated blood shows very little settling, however, elevated globulin and fibrinogen associated with inflammation leads to Rouleaux formation and the clumped red cells settle rapidly. An elevated ESR is indicative of a measurably higher column of red cells settled at the bottom of the tube wrthin a set time. The ESR can be used to distinguish inflammatory from non-inflammatory conditions, and is used to monitor resolution of inflammation during the course of therapy.

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Ch. 4

The ESR is very sensitive, however, nonspecific. The ESR is elevated in acute infection, rheumatoid arthritis, polyarteritis, ankylosing spondylitis, septic arthritis, acute

gout, metastasis, and other connective tissue diseases. C~reactive protein {CRP)- is a glycoprotein that reacts with C-mucopolysaccharide of many pneumococci. It is commonly produced during the acute phase of inflammation. It rises before the ESR, and normalizes in the presence of NSAIDs, aspirin and steroids. It rises in

acute flare of rheumatoid arthrftis, Strep. infection, in the last half of pregnancy, and in females using an IUD and/or oral contraceptives. Antinuclear antibody (ANA)- appears months after onset of connective tissue disease,

and may have its greatest value in monitoring SLE. It is more accurate than the LE cell test because it is unaffected by steroids. The significance of ANA titers less than 16 is uncertain, as healthy persons may display titers in this range. Elevated ANA titers suggest connective tissue disease, while absent or low titers do not rule out connective tissue disorders. High titers are common in SLE, scleroderma, and mixed connective tissue disorders, and Raynaud's phenomenon.

Pattern

Associated Antigens

Clinical Conditions

Homogenous

Deoxyribonucleoprotein

Collagen-Vascular OS

?articulated

Extractable Nuclear Antigen

Mixed C.T. OS., scleroderma, SLE, Malignancy

Peripheral

Native DNA and Histones

Active SLE with Nephritis

Nucleolar

Nucleolar RNA

Scleroderma, Raynaud's

Positive ANA is found in the following percentages in the following diseases

Systemic lupus erythematosus Rheumatoid arthritis Sjogren syndrome Systemic sclerosis Liver cirrhosis Polymyositis Dermatomyositis Malignancy Bullous pemphigus Polyarteritis nodosa or ulcerative colitis Waldenstrom's macroglobulinemia Drug reaction Myasthenia gravis

(100%, high titer) I< 60%, very low titer) (75%, low titer) 138%, low titer) (45%, low titer) 120%, low titer) (20%, low titer) (18%, low titer) (rare, low titer) (rare, low titer) (rare, low titer) (rare, low to high titer) (rare, very low titer)

Rheumatoid factor (RF)- lgM or lgG auto-antibodies that react with the Fe portion of denatured human lgG. There are two methods of measurement: latex fixation {75% sensitive and 75% specific for RA at 1:80 dilution), and sheep cell agglutination (75% sensitive and 95% specific for RA at 1:160 dilution). RF is found in the following

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97

percentages: Sjogren syndrome (75-100%), adult RA (70-80%), juvenile RA (10%), SLE (20-40%), scleroderma 15-10%1, polyarteritis nodosa and dermatomyositis I0-5%). Lupus erythematosus (LEI cell - mature polymorphonuclear neutrophil that has phagocytosed a spherical, homogenous inclusion derived from another neutrophil.

Characteristic of SLE, and observed in the following percentages : SLE (70-80%), Sjogren syndrome 110-20%), RA 15-10%1, scleroderma and polyarteritis nodosa and dermatomyositis I0-5%).

Serum complement series of enzymatic proteins that combine with antigen-antibody w

complexes and effect lysis when the antigen is an intact cell. Complement remains normal in Sjogren syndrome, scleroderma, polyarteritis nodosa, and dermatomyositis; is normal or decreased in SLE; and normal or slightly elevated in acute phase of RA. Anti-streptolysin 0 (ASO)- antibody against streptolysin "0" of group A streptococci {Strept. pyogenes). It is present in 80-85% of patients with acute rheumatic fever or other streptococcal infection. HL-A 827- histocompatability antigen found in the following percentages in the following diseases: ankylosing spondylitis (90%), Reiter's syndrome (75%), psoriatic arthritis and juvenile RA (high concentration). HL-A 815- histocompatability antigen found in 33% of patients with SLE.

Uric acid (UA)- elevated in gout, malignancy, renal disease, and familial hyperuricemia. Normal is 7-9 mg% in males, and slightly less in females. UA may be normal in the acute stage (first 10 days) of gouty arthritis, as much has precipitated out ofthe serum into the affected joint. Monosodium urate (gouty) crystals are needle-shaped, and form the "martini sign" when phagocytosed by a neutrophil.

Calcium pyrophosphate~ crystals are rhomboid, and observed in pseudogout Joint Fluid Analysis Joint Fluid Volume

Normal

Group-1 Increase

Group-11 Increase

Group-Ill Increase

Clarity

Clear

Clear

Cloudy

Opaque

Color

Clear

Yellow Opalescent

Yellow Green

Yellow

Viscosity

High

High

Low

Variable

WBC/mm3<

200

200-2000

2000-100,000

> 100,000

% PMNs

<25%

<25%

>50%

> 75%

Culture

1-1

1-)

1-1

1+1

Mucin Clot

Firm

Firm

Friable

Friable

Glucose lmg%)

=Serum

=Serum

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Ch. 4

Differential Diagnosis Based on the Joint Fluid Analysis Chart Group~!:

Non-inflammatory conditions such as DJD, trauma, osteochondritis dissecans, osteochondromatosis, neuropathic hypertrophic osteoarthropathy {Charcot), resolving or early inflammation, hypertrophic pulmonary arthropathy, and pigmented villonodular synovitis.

Group-11: Inflammatory conditions such as RA, gout, pseudogout, Reiter's syndrome,

ankylosing spondylitis, psoriatic arthritis, arthritis associated with ulcerative colitis or Grahn's regional enteritis, rheumatic fever, SLE, and progressive systemic sclerosis.

Group-Ill: Septic arthritis due to bacterial infection. Hemarthrosis results in a hemorrhagic joint fluid specimen, and can be caused by hemophilia and other bleeding diatheses, ligamentous trauma with or without fracture, neuropathic arthropathy, pigmented vfllonodular synovitis, synovioma, hemangioma, and other neoplasms.

Coagulation Studies

Partial thromboplastin time (PTT)- normal range is 25-35 seconds. Used as a reliable screening test however may not detect subtle defects. Also used to monitor heparin anticoagulation therapy. The PTI can be used to evaluate the three stages of coagulation, with the exception of factor VII or platelet factors. The PTI remains normal in von Willebrand's disease, platelet dysfunction, and thrombocytopenia. The PTT is prolonged by defects in clotting factors I, II, V, VIII, IX, X, XI, and XII. Prothrombin time (PT)- normal range is 11-16 seconds. The PT is used to monitor longterm Coumadin !Warfarin) anticoagulation therapy. The PT is prolonged with defects in factors I, II, V, VII, and X; as well as in vitamin-K deficiency, fat malabsorption \steatorrhea, colitis, jaundice), salicylate orwatfarin therapy, and advanced hepatic disease.

Bleeding time- normal range {Duke) is 1-4 minutes. The bleeding time is prolonged in thrombocytopenia, abnormal platelet function, and von Willebrand's disease. Clotting time- normal range (Lee-White) is 3-6 minutes in a capillary tube, and 6-17 minutes in a test tube. This is a routine, nonspecific screening test used to determine the presence of major clotting deficiencies.

Urinalysis It is preferable to evaluate the first morning specimen. Physical and chemical properties are assessed.

Color- normal is amber to pale yellow. Black urine is noted in alkaptonuria, malignant melanoma, and malaria. Red urine is noted in hematuria, hemoglobinuria, methemoglobinuria, and myoglobinuria. Blue urine may be noted in porphyria. Brown to green urine may occur with bilirubinuria. Dark brown urine occurs in sickle cell anemia. Acidic urine appears orange.

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99

Odor- normal urine smells like ammonia. A putrid odor may indicate bacteria. Mousy urine occurs with phenylketonuria (PKU). Asparagus effects a peculiar urine odor.

Clarity- generally the urine is relatively clear, with some sediments. Cloudy urine may represent infection, crystaluria, hemorrhage, or cellular debris. Specific gravity- normal range is 1.003- 1.026.

pH- normal is 4.6- 8.0

Urine chemistries- glucose, ketones, protein, and drug by-products and metabolites can a!! be measured. Microscopic findings- blood and epithelia cells, casts, crystals, and bacteria can be identified.

Serum Chemistries Calcium- normal is 8.5-10.5 mg%. Elevated in primary hyperparathyroidism or secondary to chronic renal failure, metastatic bone disease, lymphoma or multiple myeloma, sarcoidosis; or lung or renal carcinoma that produce parathormone; or hypervitaminosis D (excessive intake of cod liver oil), diuretic use, or acidosis. Decreased in hypoparathyroidism, chronic renal failure (perhaps postoperative, and classically seen with simultaneous elevation of phosphorous), malabsorption or steatorrhea, alkalosis, pancreatitis, and when EDTA used to anticoagulate the blood specimen.

Phosphorus ~ normal is 2.5-4.5 mg%. Elevated in chronic renal failure, diabetic ketoacidosis, fracture healing, acromegaly, growing children (physiological), and hypervitaminosis D. Decreased in negative nitrogen balance (simultaneous decreased BUN and alkaline phosphatase), hepatic disease, Fanconi syndrome, osteomalacia, and with longterm IV glucose infusion in a non-diabetic patient. Glucose~ normal is 65-110 mg%. Elevated in diabetes mellitus (serum phosphorous remains normal), Cushing's disease, corticosteroid administration, pheochromocytoma, and brain injury or tumor. Decreased in hyperinsulinism, pancreatic islet cell tumor, Addison's disease, bacterial septicemia, and advanced hepatic necrosis.

Blood urea nitrogen (BUN)- normal is 10-20 mg%. Elevated in renal failure (with or without obstructive uropathy}, dehydration, G.l. bleed. Decreased in hepatic failure (urea production reduced), carbon tetrachloride toxicity, and associated with a negative nitrogen balance. Uric acid- normal is 2.5~8 mg%. Uric acid is the end-product of purine metabolism, and may precipitate out of serum into the tissues as monosodium urate crystals, which is responsible tor acute gouty arthritis as well as chronic tophaceous gout. Elevated in conditions where there is excessive purine intake (tyramine, cheese, dark beer, game meats), over-production of uric acid (rapid cell proliferation as in neoplasms such as lymphoma or leukemia; extensive tissue necrosis), or under excretion of uric acid (renal disease), eclampsia, starvation, thiazide diuretics, lead poisoning, and metabolic acidosis. Decreased with use of uricosuric agents, Fanconi syndrome or Wilson's disease.

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Ch.4

Cholesterol- normal is 150-275 mg% (this is controversial). Elevated in obstructive jaundice, hypothyroidism, nephrosis, uncontrolled diabetes, endotoxic shock or gram negative septicemia, and pregnancy. Decreased in malabsorption syndromes, hepatic disease (about 2/3 of the cholesterol is esterified in the liver), hyperthyroidism, anemia, septicemia, and chronic stress.

Albumin - normal is 3.5-5 gm%. Hyperalbuminemia iS rare. Decreased in protein malnutrition, hepatic failure, renal disease (nephrosis), Gl wasting (diarrhea) or mal-absorption, burn wounds, or extensive exfoliative dermatitis.

Total protein - normal range is 6-8 gm%. Hyperproteinemia is typically caused by an elevation of globulin, as in collagen vascular disease, chronic infection, or malignancy such as multiple myeloma. Hypoproteinemia results from the same causes of hypoalbuminemia. Note the following general formula for total protein: 3 gm% globulin+ 4 gm% albumin= 7 gm% total protein Lactate dehydrogenase- normal is 90-200 mU/mL Lactate dehydrogenase catalyzes lactic acid t pyruvic acid in the citric acid cycle (glycolytic cycle). Increased in cytolysis and cytonecrosis (acute myocardial, pulmonary, renal, hepatic, skeletal muscle, and major organ infarction); pernicious anemia, malignant neoplasm, and sprue. Decreased with radiation therapy. Bilirubin- normal is 0,1-1 mg%. Elevated in jaundice (hepatic, obstructive, or hemolytic), Crigler~Najjar

syndrome and Gilbert's disease. Hemolysis and hemorrhagic or hematoma due to pulmonary injury or other major trauma will elevate serum bilirubin.

Alkaline phosphatase - normal is 30-85 mU/mL Elevated in the growing individual; bone diseases such as sarcoma, fracture healing, Paget's disease, metastatic carcinoma to bone (usually norma! in osteomalacia}; other metastatic disease, histiocytosis, pulmonary embolism, and congestive heart failure. Decreased hypophosphatasia, an inherited condition similar to rickets however, the alkaline phosphatase and leukocyte counts are decreased. Also decreased in magnesium deficiency, chronic diarrhea, malabsorption, uncontrolled diabetes mellitus with magnesium deficient parenteral fluid administration, malnutrition, and pernicious anemia.

Serum glutamic-oxa/oacetic transaminase(SGOT)- normal is 10-50 mU/ml. SGOT is found in liver> heart> skeletal muscle> kidney, pancreas, red blood cells, and lung. Elevated in cardiac and hepatic disease {myocardial infarction, liver cancer or injury or hepatitis), acute tubular necrosis, acute pancreatitis, hemolytic anemia, leukemia, myonecrosis or injury, pulmonary injury or riecrosis, and dermatomyositis. Decreased in conditions with elevated serum lactate or pyruvate such as beriberi, thiamin deficiency, diabetic ketoacidosis, and liver disease. Serum glutamic-pyruvic transaminase (SGPT)- normal is 5-35 mU/mL SGPT is found primarily in the liver, and is elevated in liver disease. Microbiological Testing Culture and sensitivity (C&S) ~ used to identify micro-organisms involved in an infectious process. Standard C&S involves aerobic and anaerobic testing. Acid fast, chocolate agar,

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101

sheep's blood, fungal culture, and other specific test media may be indicated based on individual case requirements. Sensitivity of an organism to a particular antibiotic is determined by Kirby-Bauer disk sensitivity, wherein antibiotic impregnated disks are placed on the culture medium surface and areas of "no growth" are observed surrounding disks containing antibiotic that kill the bacteria. Minimal inhibitory concentration (MIC) and minimal bactericidal concentration (MBC) are also used to test sensitivity to specific antibiotics, wherein the inhibitory concentration stops cell growth and the cidal concentration kills the organism.

Gram's stain- used to identify the presence of bacteria, their morphology, and staining characteristics. Wound exudate suspected of infection should be stained as follows: 1. Gentian violet~ H20 rinse 2. Alcohol- H20 rinse 3. Gram's iodine - HzO rinse 4. Safranin - HzO rinse. Microscopic observation should reveal granulocytes indicative of inflammation, and the presence of bacteria. The combination of granulocytes and bacteria is indicative of infection. Antibiotic selection is made based upon bacterial morphology and staining. Gram-positive bacteria appear violet-purple (gentian violet), while gram-negative bacteria appear red (Safranin). Interpretation of the Gram's stain is particularly important when considering anaerobic bacteria, as it can be difficult to grow such organisms in the microbiology lab. KOH prep- squamous epithelial cells are dissolved in keratinolytic potassium hydroxide, leaving microscopically evident fungal hyphae and/or spores and yeast Also known as a tissue exam for fungus. PAS- periodic acid Schiff stain forfungal hyphae/spores and yeast Acid fast staining- for suspected tuberculin infection (Mycobacterium tuberculi).

Blood agar culture medium- for certain fastidious microbes, such as Neisseria. Chocolate agar- predisposes to growth of Neisseria. NEUROLOGICAL AND ELECTRO-NEURODIAGNOSTIC EVALUATION The basic clinical neurological examination involves sensory, motor, and autonomic testing and observation. The exam involves touch-pressure (anterior spinothalamic tract and peripheral sensory organs) monofilament esthesiometer testing of the skin surfaces, wherein absence of the ability to appreciate touch-pressure of 10 kg/cm 2 is indicative of lost protective sensation. Testing lighttouch with cotton or brush stroke is less reliable in comparison to the use of the monofilaments.(Fig. 4.1) Posftion sensation, proprioception, is tested at the first MTPJ and ankle levels, wherein the patient notes the position of the joint without looking atthe part. Vibratory sensation is tested with the 128 cycles/second tuning fork. Proprioception and vibratory sensation test the dorsal column-medial lemniscus pathway. Pain and temperature assessment with pin prick and a warm or cold water-filled test tube, respectively, tests the lateral spinothalamic


102

Ch.4

1. Medial and intem1ediate femoral cutaneous nerves 2. Posterior femoral cutaneous nerve

3. 4. 5. 6. 7. 8.

Lateral sural cutaneous nerve Saphenous nerve Superficial peroneal nerve Sural nerve Medial calcaneal branch of tibial nerve Medial plantar nerve

6

9. Lateral plantar nerve 10. Deep peroneal nerve

Figure 4.1 pathway. Deep tendon reflexes are tested at the patellar (L2-4) and Achilles (S1-2)1evels. The reflexes are graded as silent or absent (0) hyporeflexic 1+1 normoreflexic (++} hyperreflexic but not necessarily pathological (3+) multiple clonic contractions (4+)

sustained tonic contraction {5+) Deep tendon reflexes test the integrity of the spinal reflex and the muscle spindle. The plantar stroking superficial reflex should effect mild down going contraction of the toes, whereas hallux dorsiflexion and lesser digital fanning represents the Babinski sign which is indicative of upper motor neuron immaturity or lesion. Skin temperature may be increased due to vasodilatation, in conjunction with dryness due to sudomotor denervation, in the presence of peripheral neuropathy. Generally, sensory dysfunction is noted before autonomic dysfunction, both of which precede motor dysfunction, secondary to peripheral neuropathy, injury or nerve entrapment The clinical assessment of muscle strength involves inspection for atrophy or hypertrophy, and placing the joint acted upon by the muscle4endon complex in the end range of motion position, thereby providing the tendon maximum mechanical advantage and yielding the most accurate clinical test of muscle strength. The grading system for gross (clinical) manual muscle testing is: Grade 5 "normal" strength, full resistance at end range of motion.

Ch. 4


103

Grade 4 "good" strength, mild-moderate resistance at end range of motion, often graded 4+ or 4Grade 3 "fair" strength, able to move against gravity only Grade 2 "poor" strength, able to move only after gravity eliminated

Grade 1 "trace" strength, can visualize or palpate contraction without joint motion Grade 0 "zero" strength, no clinical evidence of muscle contraction Muscle strength testing is important when considering tendon transfer. Other techniques useful in the assessment of muscle strength include biometric testing using machines such as Cybex or Biodex, which yield information detailing povver, endurance, and strength. Resting muscle tone is idealized to optimize synergistic muscle contractions to effect movement. Abnormal, Involuntary Movements

Myoclonus- rapid, abrupt, often cyclic, skeletal muscle contractions resulting in major movement of the part. Tremor- more refined, smooth, rhythmic movement, generally of the fingers or toes. Athetoid movement- slow, worm-like writhing and twisting movement associated with rest and intentional motion.

Choreiform movement- rapid, jerking movement associated with rest and intentional motion.

Fasciculation- overt twitching of bundles of muscle fiber within a 1arger muscle belly, nonpathologic when associated with fatigue. During the gait cycle, biphasic contract'10ns of TA, EHL, EDL, and Peroneus Tertius occur during the first 10% of contact at heel strike to decelerate, t::hen again at push off through propulsion and into swing. The peroneii fire at about 15-20% of stance and throughout propulsion. The FDL, TP, and FHL similarly fire at about 15-20% of stance and throughout propulsion. A variety of abnormal gait patterns also exist, and are often associated with specific pathological conditions, including:

Equinus -ankle plantarflexion in swing and, when advanced, stance; associated with dropfoot, pes cavus, and extensor substitution. Spastic/Circumducted- the lower extremity is adducted, medially rota1:ed, and flexed atthe hip and knee, with ankle plantarflexion; associated with cerebra! palsy, cerebral vascular accident, spinal cord lesion, familial diplegia, and other upper motor neuron lesions. Ataxic- unstable, widened base of gait to enhance stability, with the single limb widely swung and then crossing the midline in stance; associated with cerebellar disease, Friedreich's ataxia, tabes dorsalis, syringomyelia, multiple scler()sis, and diabetic polyneuropathy.

Steppage- swing phase dropfoot requires high elevation of the thigh and leg, with hip flexion, in order to have the forefoot c!ear the ground: associated VI./ ith CVA, CP, familial

104


sensorimotor neuropathy (CMT),

Landry~Guillain-Barre

Ch. 4

syndrome, and other paralytic

dropfoot conditions.

Waddling -widened base of stance, lumbar lordosis, external hip rotation, and imbalance; associated with muscular dystrophy (Duchenne's, Becker's, and limb-girdle), and

congenital dislocated hip.

Trendelenburg- pelvic tilt toward the swing phase side with scoliosis pointing (convexity) toward the affected side (weight bearing); associated with gluteus medius injury or

paralysis, or dislocated hip. Festinating- shuffling, shortened and rapid stride, seemingly falling forward, uncoordinated arm swing, actually moving slowly; associated with Parkinson's disease and similar conditions. Major Patterns of Neurological Deficit Upper motor neuron disease- (above the anterior horn cell of the spinal cord) hyperreflexia, clonus, superficial plantar response is upward with Babinski's sign, resting skeletal muscle hypertonicity or rigidity; gait is steppage with spasticity and circumduction.

Lower motor neuron disease -I at or below the anterior horn cell) deep tendon reflexes are absent or hyporeflexic, muscle tone is decreased, superficial plantar response is silent; gait is flaccid. Ataxia -loss of coordinated skeletal muscle synergy, "drunk" appearance in gait or stance, or inability to move the contralateral heel along the tibial crest voluntarily. Neurological consultation, EMG, and NCV testing is usually indicated when a neurological defect is suspected or identified. Nerve conduction velocity can be measured for sensory nerves !e.g. sural, saphenous, lateral femoral cutaneous) in an antidromic fashion; while motor nerves (common peroneal, posterior tibial, medial and lateral plantar) are measured from proximal to distal and tend to conduct impulses at about40 meter/ second. Nerve injury, entrapment, or demyelinating disease can decrease nerve conduction velocity. Electromyography depicts on an oscilloscope skeletal muscle electrical activity associated with needle electrode insertion. Denervated muscle shows increased fibrillation potentials. Results in the intrinsic foot musculature are variable.

VASCULAR EXAMINATION The basic clinical vascular evaluation involves inspection ofthe skin color, temperature, turgor, and digital trichosis; as well as palpation of the arterial pulse at the popliteal, posterior tibial and dorsalis pedis levels. If indicated, arterial pulSe at the perforating peroneal, femoral, and abdominal aortic levels are also assessed. Edema is noted to be either pitting, brawny or spongy. The skin barrier is inspected for areas of open compromise or gangrene. Vasospastic instability may elicit livedo reticularis, while arterial insufficiency may elicit dependent rubor associated with intermittent claudication or even rest pain.

Ch. 4


105

Non~lnvasive Vascular Examination The non-invasive vascular examination is performed with the duplex Doppler ultrasound machine, and correlated with the clinical findings. The non-invasive arterial exam measures

segmental arterial pressures and waveform analysis. Ipsilateral segmental pressure

differences indicative of a 20-30 mmHg pressure drop from the proximal to the distal segment, are strongly suggestive of occlusive disease. Moreover, arterial pulsation waveforms should be triphasic with a dicrotic notch, or at least biphasic. Monophasic Doppler

tracings and sounds are indicative of arterial occlusive disease with decreased flow. Determining the ankle systOlic pressure involves pneumatic cuff placement above the

ankle and elevated until no arterial pulsation can be identified with the Doppler ultrasound over the PT artery. The cuff is then deflated until the ultrasound identifies flow in the PT artery, and the pressure recorded. The maneuver is repeated while measuring the opening

pressure in the DP artery, and then again for the peroneal artery. The highest of the three values is used as the "ankle" systolic pressure. Forefoot and digital systolic pressures, as well as pulse volume recordings using infrared sensors on the toe pulps can also be determined. Transcutaneous oxygen tension and thermography also offer tools for assessment of pedal perfusion. The ankle/arm ratio (also know as ankle/brachial index or ischemic index) is calculated by dividing the ankle systolic opening pressure by the arm systolic opening pressure. Deceptively high opening pressures can be measured in the presence of medial calcific sclerosis.

Ankle/Arm Ratio Guidelines in the Non-Diabetic Patient Ankle/Arm Ratio >0.96 0.31 - 0.95 0.25 -0 .3 0- 0.3

Clinical Finding Normal Intermittent claudication

Rest Pain Impending gangrene

Ischemic Index Guidelines for Reconstructive Surgery

Foot

If ankle/arm index< 0.75, then generally do not operate. If ankle/arm index> 0.75, then check toe/arm index. If ankle/arm index> 0.75 and 1De/arm index< 0.65, then generally do not operate. If ankle/arm index> 0.75 and toe/arm index> 0.65, then may operate. If can't get measurement on toe because of deformity, use forefoot/arm index.

If ankle/arm index> 0.75 and forefoo1/arm index> 0.65, then check Doppler flow of digital arteries. Hallux:

If ankle/arm index> 0.75, and toe/arm or forefoo1/arm index> 0.65 and two of four digital arteries identified with Doppler, then Qenerally may operate.

Lesser Toe: If ankle/arm index> 0.75 and toe/arm or forefoo1/arm index> 0.65 and either both dorsal arteries and one plantar or both plantar arteries identified with

Doppler, then generally may operate.

106


Ch. 4

Invasive arterial testing, in the form of angiography with radiopaque contrast media, is usually obtained only if reconstructive vascular surgery is being entertained. Infusion of contrast medium is not a risk-free undertaking, and conveys the risk of hypersensitivity reaction, as well as renal failure in dehydrated or predisposed individuals. Digital subtraction angiography can further enhance identification of patent and occluded vessels. Although noninvasive, MRI can also be used to evaluate blood vessels and yields considerably accurate images. Venous non-invasive Doppler assessment is used when deep vein thrombophlebitis is suspected, and a venogram may further enhance identification of a thrombosis, particularly one that is propagating or associated with embolism and consideration is given to surgical intervention.

BIOMECHANICS Biomechanics is the study of mechanical laws as they pertain to the human musculoskeletal system and, in particular, bipedal locomotion. Basic terms include: 1. Cardinal body planes sagittal (SP), frontal (FP), and transverse (TP) 2. Axes-

frontotransverse, allowing motion in the SP frontosagiltal, allowing motion in the TP sagittotransverse, allowing motion in the FP

3. Motions-

pronation and supin8.tion (triplanar) inversion and eversion (FP) adduction and abduction (TPI internal rotation and external rotation (TP) dorsiflexion and plantarflexion (SP) flexion and extension (SP)

4. Positions-

pronated, supinated, inverted, everted, abducted, adducted, externally rotated, internally rotated, dorsiflexed, plantarflexed. When a position is fixed, it is referred to as flexion, extensus or extension, adductus, abductus, varus, valgus, elevatus, supinatus, equinus, calcaneus.

Motion is described as occurring in the cardinal planes of the body or foot, in a plane 90° to the axis of motion. Single plane motion occurs in the plane perpendicular to the axis that lies at the intersection of the remaining two planes. Triplanar motion occurs in a plane perpendicular to an axis that courses through all three cardinal planes (oblique to all planes). Triplanar motion of the foot is said to be pronatory/supinatory (pronatory), and the axis is directed from posterior-lateral-plantar to anterior-medial-dorsa!. Pure SP motions include dorsiflexion and plantarflexion, while pure transverse plane motions include adduction and abduction, and pure frontal plane motions include inversion and eversion.

Biomechanical Examination The examination begins with open chain visual inspection, then patient active motion, followed by manipulation and palpation, followed by gait analysis. Special testing, such as

Ch.4


107

pedobarographic, kinematic, and other motion analysis methods may also be used. Visual inspection is used to identify gross positional and structural features. Examination may proceed as follows: hip, knee, ankle, subtalar joint, metatarsal joint, 1st ray, 1st metatarsophalangeal joint, forefoot-to-hindfoot relationship, then on to other assessments of specific concern.

Hip -is a diarthrosis that allows enarthrous gliding, rotation, angulation, and circumduction. Motion occurs in all three body planes: TP (sagittal-frontal axis): Internal and external ROM FP (sagittal-transverse axis): Abduction/adduction ROM SP (frontal-transverse axis): Flexion/extension ROM (including hyperextension).

The mechanical axis of the hip runs from the center of hip to knee, with the mechanical axis of the femoral shaft running from a line between greater and lesser trochanters, relative to the plane of femoral condyles. Examination of the hip should reveal the following:

Adult Hip Range of Motion - Int. Rot. " Ext. Rot., with hip flexed or extended. The neutral hip should align femoral condyles on the FP. Normal SP hip flex./ ext. at birth is 150°, and about 100° after puberty. If limited in extension, then hamstrings are likely tight; if limited in flexion, then Iliopsoas is likely tight; excessive internal to external range of motion indicates tight adductors; excessive external to internal range of motion indicates tight abductors; and asymmetrical limitation of motion may indicate congenital or neglected hip dysplasia or limb length inequity. Total range of motion decreases with age.

,j

Knee- motion occurs aboutthls ginglymus jo.mtwith only two degrees of freedom \axes) of motion: SP flexion-extension, and TP internal and external rotation. 5-6o of TP motion occurs with SP flexion-extension of the knee. Motion occurs predominantly in the SP about a frontal- transverse axis, and to a lesser degree about the frontal-sagittal. FP motion is indicative of collateral ligament damage. The patella enhances quadriceps leverage. In non-weight bearing (open kinetic chain) rotation of the knee, the tibia rotates on the femur. In weight bearing \closed kinetic chain), the femur rotates on the tibia. The lateral femoral condyle rotates around the medial condyle, with motion occurring between the tibia and meniscus. Therefore, for internal rotation, the lateral tibial condyle moves anteriorly on the lateral meniscus. For external rotation, the lateral tibial condyle moves posteriorly on the lateral meniscus. The greatest degree of rotation is available when the knee is flexed at 90°. Examination of the knee should reveal the following: 1. Knee position on the FP when hip and STJ neutral, with end range of motion 180', and fixed 2. Flexion or hyperextension may indicate compensation for ankle equinus. 3. Genu valgum may effect compensatory hindfoot supination, but generally over time acts as 4. A strong pronatory influence on the hindfoot 5. Genu varum must be distinguished from tibial varum, and pro nates the hindfoot. 6. Genu recurvatum may be due to cruciate ligamentous laxity or compensation for ankle equinus. Thigh hamstrings or gastrocnemius can effect genu flexion deformity.

108


Ch.4

Ankle- range of motion occurs about a pronatory axis running from the latera! to medial malleolus, normal range being 20°-30° dorsiflexion OF and 30°-50° PF. The axis is primarily at the junction ofthe FP and TP. deviated in the TP by about 12'-15" of malleolartorsion, thereby allowing primarily SP OF Iflexion) and PF !extension). The articulation represents a mortise (medial malleolus, distal tibial bearing surface, lateral malleolus) and tenon (talar body) joint. Range of motion is assessed by asking the patient to actively take the ankle joint through OF/PF range of motion in the sagittal plane, followed by circumduction of the ankle or figure-of-eight motion. Examination of the ankle should reveal the following: Ankle range of motion should allow 25-30° PF, and lOa or more dorsiflexion with the knee extended. Increased ankle dorsiflexion when the knee is flexed is indicative of limitation by gastrocnemius (equinus if < 10°). The Silfverskiold test is then performed, and the presence or absence of gastrocnemius or gastro soleus equinus, or bony (talotibial exostosis) equinus, is determined. Pseudo equinus, due to plantarflexed forefoot results in functional ankle equinus due to retrograde ankle dorsiflexion in weight bearing. Compensation for ankle equinus may result in normal heel-off due to adequate subtalar joint/metatarsal joint hyperpronation, early heel-off if only partially compensated by hindfoot pronation, or no heel-off whatsoever (no heel contact) if uncompensated in the foot (usually associated with genu recurvatum or fixed flexion).

Subtalar Joint- range of motion occurs about a pronatory axis deviated 42° from the TP I nearly equidistant from the horizontal TP and the vertical FP), and 16o from the SP. STJ is minimal in the SP, as the axis almost lies in this plane. Inversion/eversion and adduction/ abduction motion is greatest and almost equidistant in both the FP and TP, respectively. A higher pitched subtalar joint axis would allow more TP motion, while a lower pitched subtalar joint would allow more FP motion. The subtalar joint is an oblique hinge diarthrosis with trip!anar motion. Motion from maximum pronation to maximum supination defines an arc, with 2/3 of the arc supinated from the neutral position, and 1/3 pronated from the neutral position. Normal subtalar joint range of motion is 30°-35°, with about 10°-15° eversion and 20°- 30° inversion. Pronation of the subtalar joint in open kinetic chain (non-weight bearing) entails abduction, eversion, and dorsiflexion of the calcaneus on the talus; whereas pronation in the closed kinetic chain (weight bearing) attitude entails adduction, inversion, and plantarflexion of the talus on the calcaneus. Range of motion is assessed by observing normal excursion of 2/3 inversion to<< eversion with the ankle joint DF and the metatarsal joint maximally pronated and locked on the hindfoot It has been estimated that a minimum subta!ar joint range of motion of 8°-12° is required for normal ambu!ation. The neutral position of the subtalar joint, as determined by a posterior bisector of the calcaneus, is the point 1/3 of the way from maximum subtalar joint pronation, and 2/3 of the way from maximum inversion. Calculation of subtalar jointISTJ) neutral position INP) is as follows: NP STJ" eversion ROM -!total ROM/3). A positive value indicates a valgus or neutral position A negative value indicates a varus or neutral position.

Ch.4

Selected Dlagnost'1c Techniques

109

Example If there is a maximum of 12° STJ eversion, and 18° maximum inversion, then the tROM = 30". NP STJ = 12'- 30"/3= 12'-10"= NP STJ of2'varus To identify STJ NP, we need to know the point from which there is twice as much supination as there is pronation:

total (STJ ROM /3) x 2 =inversion from NP, and (inv. from leg)-( inversion from neutral)= NP Example If the calcaneus can evert 1Oo from the leg bisection and invert ZOo from the leg bisection, what is the NP of the STJ? total STJ ROM= 10" t 20" = 30", 30"/3 x 2 = 20" inversion from NP, so (inv. from leg)- (inv. from neutral)= 20"- 20" = 0" = NP Examination of the subta!ar joint should reveal: Subtalar joint motion, as described previously, ideally 20° inversion (supination) and 10° eversion (pronationL with subtalar neutral being 1/3 the range from maximum eversion and 2/3 the range from maximum inversion. The posterior bisector of the heel should be

perpendicular to the ground with the subtalar joint neutral. In a subtalar joint varus deformity, there is more than 2/3 of the range of motion in the direction of varus {example 25° inversion with supination, 5° eversion with pronation, so inversion of calcaneus to ground), resulting in excessive compensatory subtalar joint/metatarsal joint pronation in stance {compensated rearfoot varus). Compensated rearfoot varus can also effect excessive subtalar joint pronation in a subtalar joint varus combined with tibial varum deformity {eg. 25° inversion with sup-ination, 5° eversion with pronation, in presence of 5° tibial varum). if the calcaneus is perpendicular to the ground when the subtalar joint is maximally pronated. A partially compensated rearfoot varus {eg. 30° inversion with supination, oo eversion with pronation, so tibial varum), when the subtalar joint cannot fully evert to perpendicular (remains in 5° varus, in this particular example). Metatarsal joint (MTJ)- range of motion occurs about oblique (OMTJ) and longitudinal (LMTJ) pronatory axes. The OMTJ axis lies 52" from the TP and 57' from the SP, coursing from the mid-lateral aspect of the calcaneus to the TNJ. Primary motions are abduction/ adduction and DF/PF, with minimal inversion/eversion. The oblique MTJ (OMTJ) axis allows predominantly OF/PF and adduction/abduction, with minimal inversion/eversion. The longitudinal MTJ axis allows predominantly inversion/eversion with minimal DF/PF and abduction/adduction. Both the OMTJ axis and LMTJ axis allow triplanar motion. Range of motion is assessed with the forefoot loaded in OF and eversion at the 5th metatarsal head, and the subtalar joint in neutral position. The plantar tangent to the hindfoot should be perpendiculartothe posterior bisector of the calcaneus, while allowing the medial column to seek its own level. Pronation of the STJ will unlock the MTJ and allow hypermobility of the first ray (forefoot supinatus). The LMTJ (Hicks' axis)lies 9" from the SP and 15" from the TP, coursing from the posterolateral aspect of the calcaneus to the 1st metatarsal-cuneiform joint. Being so close to the SP and TP, the axis provides a primarily inversion/eversion in the FP. Normal metatarsal joint range of motion is 4°-6°. Forefoot supinatus occurs primarily

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around Hicks' LMTJ axis. When the STJ is pronated, the MTJs become parallel, allowing the head of the talus to decline plantarly relative to the navicular. Examination of the MTJ should reveal: MTJ motion with STJ pronation, the plantar aspect of the forefoot everts relative to the hindfoot as the MTJ unlocks and becomes more mobile. With STJ supination, the plantar aspect of the forefoot inverts relative to the hindfoot, and MTJ motion is limi!Bd. lithe forefoot remains inverted to the rearfoot, forefoot varus exists.lfthe forefoot remains everted to the reartoot, forefoot valgus exists. Forefoot valgus may be rigid or flexible. Forefootsupinatus describes the compensatory inversion of

the forefoot on the rearfoot associated with hyperpronation olthe STJ and OMTJ, the inversion of the forefoot occurring around the LMTJ axis.

1st ray- range of motion occurs about an axis coursing 45° from the SP and 45° from the FP in a posterior-dorsal-medial to anterior-plantar-lateral direction, allowing motion aboutthe medial cuneiform-navicular and 1st metatarsal-cuneiform joints. 1st ray range of motion is assessed with the subtalar joint in neutral position, while manipulating the head of the 1st metatarsal through its OF/PF SP excursion. Examination of the 1st ray reveals: normal 1st ray motion is 5 mm (10°) in both dorsal and plantar directions, as compared to a normal second ray. As the 1st ray dorsiflexes, it inverts; and when it plantarflexes, it everts, in a 1:1 ratio. This motion is important in determining hypermobility of the 1st ray. McGiamry has noted that transverse plane

mobility of the 1st ray is comparable to sagittal plane mobility of the 1st ray, and is indicative of the ability to reverse buckle the 1st MTPJ and thereby reduce the 1st IMA via Reverdin osteotomy. Moreover, hypermobility of the 1st ray, with resultant forefoot supinatus, may indicate the need for 1st metatarsal-cuneiform arthrodesis as compared to 1st metatarsal base wedge osteotomy in the correction of metatarsus primus varus and hallux abducto valgus or other deformities. A plantartlexed 1st ray reveals maximum dorsiflexion below, or plantar to, the level of

the 2nd metatarsal, resulting in a valgus attitude of the forefoot to the rearfoot. It is important to assess the relation of the 1stthrough 5th, and 2nd through 5th, relative to the reartoot. The forefoot valgus may be rigid or flexible. A rigid plantarflexed 1st ray effects forefoot valgus, with retrograde supination of the metatarsal joint and, if severe enough, even supination of the subtalar joint. Associated deformities include hallux malleus (hallux

hammertoe). with EHL and FHL mechanically advantaged relative to EHB and FHB; as well as sesamoiditis (usuaHy tibial), lateral ankle and knee strain, symptomatic Haglund's

deformity (pump bump), and children may display an intoe gait This also results if a 1st metatarsal-cuneiform fusion or 1st metatarsal base osteotomy effects too much plantartlexion.

A flexible plantarflexed 1st ray effects a flexible forefoot valgus, which does not function plantartlexed when the 1st ray is loaded. The 1st ray may function at the level of the lesser metatarsals if the MTJ unlocks with hindfootpronation. Associated findings may include submetatarsa\1 and 5 hyperkeratosis, tibial sesamoiditis, and flexor stabilizing lesser hammertoes. Metatarsus prim us elevatus exists when the 1st ray is positioned above, dorsal to, the level of the lesser metatarsals, specifically the 2nd metatarsal, and is associated with hallux limitus/rigidus, hallux equinus, dorsal bunion, lateral dumping of late midstance and propulsive phase weight bearing and sub-second metatarsalgia and hyperkeratosis, as

well as 5th toe dorsolateral HO and perhaps 4th interspace HM or HO. The 1st met. may be elevated relative to the 2nd, even in the presence of overall forefoot varus. An elevated 1st

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ray may be congenital, or acquired secondary to longstanding hyperpronation of the STJ/MTJ (hindfoot), or iatrogenic following fracture or base osteotomy. Hallux limitus may also be caused by an excessively elongated 1st metatarsal, 1st MTPJ injury, metabolic

arthritis, or sesamoid adhesion. Prolonged metatarsus primus elevatus effects medial column collapse and pes valgus over time.

5th ray- axis of motion is oblique to all three body planes and is therefore pronatory/supinatory, run'ning from proximal-plantar-lateral to distal-dorsal-medial, 20° from the TP and 35° from the SP, and predominately allows SP and FP motion. The 5th ray everts with dorsiflexion and inverts with plantartlexion.

Intermediate rays- consist of the 2nd through 4th rays, which have frontal-transverse axes and therefore allow motion only in the SP. MTPJ function is divided into 1st and lesser groups, all of the MTPJs functioning primarily, or initially, as ginglymus joints with predominantly SP dorsiflexion/plantarflexion although TP rotation is also allowed about a vertical axis. The 1st MTPJ range of motion should display 65° {as measured from a position parallel to the substrate, or 20-21 o from the long axis of the 1st metatarsal which is declined relative to the substrate, in essence making a full range of motion from the long axis of the metatarsal being 65" + 20-21" = 85-86") for normal propulsion, and firm plantarflexion stabilization of the metatarsal (relative plantarflexion) is required in propulsion otherwise 1st ray hypermobility and lesser digital flexor stabilization will result. The initial25" of 1st MTPJ dorsiflexion occur with the joint acting strictly ginglymus, however reciprocal 1st metatarsal plantart!exion is required for dorsiflexion> 25°, which causes the frontal-transverse axis to move proximally and dorsally Ipath of the evolute) as the joint behaves arthrodial in late midstance and propulsion. Lesser IVITPJs- should achieve 15° dorsiflexion in propulsion with good plantarflexion stabilization against the substrate, and similarly require reciprocal metatarsal p!antatilexion and proximal~dorsal migration of the transverse axis (evolute) for greater dorsiflexion. Ontogeny as it Relates to Biomechanics of the Lower Extremity The femoral segment displays a FP angle of inclination relating the head and neck of the femur to the long axis of the femoral shaft birth, 150-160"; 6 years to adult, 125". The TP angle of declination relates torsion within the shaft of the femur from the head and neck to the distal condyles. Femoral antetorsion refers to twisting of the femur such thatthe condyles of the femur are internally rotated relative to the frontal plane and the head and neck. The angle between the head and neck of the femur and the femoral condyles is normally 30 - 40" of anteversion at birth and 8-12° in the adult, representing a gradual retrotorsion as the femur untwists with maturation. Concomitant with the retrotorsion is femoral anteversion, or inward twisting to the thigh segment to counter the more proximal retrotorsion, thereby keeping the femoral condyles on the FP. Delayed derotation can effect in-toe, and is often seen in the older female child and clinical presentation of the "reverse tailor's" sitting position, increased medial femoral range of motion, and knock-knee. Treatment includes proper sitting habits, Ganley femoral de rotation splint (4 to 8 years), and femoral de rotation osteotomy in the older child. Knee flexion diminishes the therapeutic influence of any pedal splinting directed at the femur, and appropriate pediatric orthopedic consultation is in order whenever significant deformity

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Ch.4

exists. The angle between the head and neck ofthe femur and the FP is normally60° external at birth, and 80-100" external in the adult. Terminology pertaining to the femur includes: antetorsion- internal femoral torsion,

anteversion - internal femoral position, retrotorsion - external femoral torsion, and retroversion- external femoral position.

The knee alignment- varies with age as follows: birth, genu varum; 1-3 years, straight; 3-6 years, genu valgum; 7-13 years, stralght; 13-18 years, genu valgum, > 18 years, straight> 60 years genu valgum.1ibial varum is a FP inverted angulation of the lower leg to the ground in static stance. Tibial valgum is a FP everted angulation of the lower leg to the ground in static stance. The malleoli- form a 0" angular relation to the FP at birth, followed by an external growth torque of 18-23°true tibial torsion or 13~18° of malleolar position, malleolar position being about 5° less than true tibial torsion, occurring in the transverse plane. We measure malleolar position because we can not actually measure tibial torsion clinically. As a guide, external malleolar position should be as follows 0-10" from birth to 1 year, 8-13" frorn 1-5 years, and 13-18" from 6 years to adulthood. The hindfoot relationship~ of talus to the calcaneus during fetal development reveals a FP movement of the talus over the calcaneus from a parallel position (clubfoot TEV represents cessation or limitation of the movement away from parallel). The talar head becomes less plantatflexed relative to body of calcaneus, which is importantfor development of normal TP TCA, cyma line, talar declination angle, CIA, and MTJ position.

Growth in length and width of metatarsals and phalanges- is ongoing from fetal to adult stages, and includes FP eversion torsion of metatarsals lw5, and TP abduction of 1st metatarsal to lesser metatarsals: fetal- 1st metatarsal adducted 50°, birth~ adducted 6°, by 4 years to adult~ 7-9° (if> 7~9°, get metatarsal prim us adductus or varus with juvenile HAV). The TP relation of the lesser metatarsals to the tarsus reveals: birth ~ 25° adducted, adult -15-18" adducted. Metatarsus adductus is 15-35" at birth, and 15-22" in the adult. Structural and Positional Deformities of the Lower Extremities Forefoot varus ~ is a structural deformity of the forefoot in which the plantar plane of the forefoot is inverted relative to the supporting sutface and the vertical posterior bisector of the calcaneus when the subtalarjointls neutral and the metatarsal joint maximally pronated and locked. It is associated with compensatory hyperpronation of the STJ/MTJ; submetatarsal 2~5, especially 4~5, hyperkeratosis; tailor's bunionette, flexor stabilization induced hammertoes, adductovarus 4th and 5th toes, HAV, metatarsus primus elevatus, plantar fascitis, and heel spur syndrome, and hallux limitus, medial knee strain and internal rotation secondary to compensatory hyperpronation of the hindfoot. Biomechanical treatment generally entails supporting the deformity, thereby nullifying the need for compensation in the foot, while posting the reatfootto allow 2~4° of motion. Flexible forefoot valgus~ is a structural deformity wherein the plantar plane of the forefoot is everted relative to the supporting sutface and the vertical posterior bisector of the calcaneus when the subtalar joint is neutral and the MTJ maximally pronated and locked. It is associated with compensation via supination about the LMTJ axis (forefoot supinatus); sub~

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113

metatarsal1 and 5 hyperkeratosis; tibial sesamoiditis, flexor stabilization hammertoes, and adductovarus 4th and 5th toes. Biomechanical treatment generally entails supporting the deformity, thereby nullifying the need for compensation in the foot, while posting the rearfoot to allow 2 to 4n of motion.

Rigid forefoot valgus~ is a structural deformity wherein the plantar plane of the forefoot is

everted relative to the supporting surface and the vertical posterior bisector of the calcaneus when the subtalar joint is neutral and the MTJ maximally pronated and locked. lt is associated with compensation via supination about the OMTJ axis and subtalar joint axis; hallux malleus, tibial sesamoiditis, lateral ankle and knee strain, symptomatic Haglund's deformity (pump bump), and children may display an intoe gait Biomechanical treatment generally entails supporting the deformity and using a 1st ray cut out, thereby nullifying the need for compensation in the foot, while posting the rearfootto allow 2-4° of motion. Reatfoot varus- is a structural deformity wherein the calcaneus is inverted relative to the substrate when the subtalar joint is neutral and the MTJ maximally pronated and locked. It is associated with lateral ankle sprain, compensatory pronation of the hindfoot only to vertical (not a profound degree of pronation), submetatarsal 4-5 hyperkeratosis, adductovarus 4th and 5th toes, tailor's bunionette, Haglund's deformity, and HAV. Reatfootvalgus- is a structural deformity wherein the calcaneus is everted relative to the substrate when the subtalar joint is neutral and the MTJ maximally pronated and locked. It is associated with submetatarsal2 hyperkeratosis, HAV, plantarfascitis, flexor stabilization. Metatarsus prim us elevatus- is a structural deformity wherein the 1st metatarsal displays a resting position dorsal to the 2nd metatarsal and plane of the lesser metatarsals. It is associated with hallux limitus/rigidus, hallux equinus, dorsal bunion, lateral dumping of late midstance and propulsive phase weight bearing and sub-second metatarsalgia and hyperkeratosis, as well as 5th toe dorsolateral HD and perhaps 4th interspace HM or HO. Forefoot supinatus- is a fixed position of supination of the forefoot about the LMTJ axis, when the subtalar joint is neutral and the MTJ maximally pronated and locked. It is associated with plantar fascitis, and limited MTJ available range of motion.

Ankle equinus- is the condition of inadequate dorsiflexion range of motion ofthe foot on the leg. It is considered present when < 10° of ankle dorsiflexion is available, and the Si!fverskiold test is used to determine the influence of the Achilles tendon as a whole and the gastrocnemius muscle and aponeurosis separately. Osseous talotibial blockade may also be present Equinus deformity is associated with early heel off, knee flexion throughout stance (unless damaging hyperextension-genu recurvatum occurs), compensatory hyperpronation of the hindfoot with plantar fascitis, flexor stabilization, adductovarus 4th and 5th toes, HAV, and extensor substitution ifthe equinus persists as a dropfootthrough swing phase. Tibial torsion- is measured as malleolar position with the malleoli forming< 13-18° of external malleolar position, malleolar position being about 5° leSs than true tibial torsion, in the transverse plane. External malleolar position is as follows 0-1 0" from birth to 1 year, 8-13° from 1-5 years, and 13~ 18° from 6 years to adulthood. Internal tibial torsion often affects the left lower extremity (in utero pressure from maternal vertebral column) in males,

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and treatment involves serial casting to above the knee, taking care to stabilize the hindfoot

and ankle in neutral position. Genu valgum (knock knee)- is an angular deformity of the knee usually observed in obese female children, and may be associated with coxa vara or uncompensated medial or compensated lateral femoral torsion, tibial torsion, pes valgus, deformation (depression) of the lateral tibial plateau with hamstring or quadriceps or calf pain and DJD in the adult. Genu varum (bowleg)- is an angular deformity of the knee usually observed in cases of

Rickets due to vita min-D deficiency and abnormal Ca and Ph metabolism, or due to Blount's osteochondrosis deformans wherein the medial tibial condyle is flattened and fragmented (present at birth to 24-30 months).

Femoral anteversion- refers to positioning of the femur such that the condyles of the femur are internally rotated relative to the frontal plane and the head and neck of the femur. The angle between the head and neck of the femur and the femoral condyles is normally 30- 40" of anteversion at birth and 8-12° in the adult, representing a gradual retrotorsion as the femur untwists with maturation. Delayed de rotation can effect in-toe, and is often seen in the older female child with the clinical presentation of the "reverse tailor's" sitting position, increased medial femoral range of motion, and knock-knee. Treatment includes proper sitting habits, Ganley femoral derotation splint (4 to 8 years), and femoral derotation osteotomy in the older child. Knee flexion diminishes the therapeutic influence of any pedal splinting directed at the femur, and appropriate pediatric orthopedic consultation is in order whenever significant deformity exists. Unequal limb length- may be structural within the thigh, leg or both femoral and tibial/ fibular segments; or functional secondary to scoliosis induced pelvic tilt with lower side of pelvis effecting functionally longer limb, unilateral supination or pronation of the foot. Compensation for limb inequity involves pedal pronation on the longer side, along with ipsilateral inferior pelvic tilt (tilts downward) due to hyperpronating hindfoot, ipsilateral shoulder tilt downward, scoliosis, ipsilateral head tilt toward longer limb, increased stance phase on the longer side. On the short side, the hindfoot supinates, pelvis rises, shoulder rises, and there is less stance phase weight bearing. Radiographic Findings Related to Biomechanics Radiographic signs of hyperpronation of the foot include: increased TP and SP talocalcaneal angles, increased talar declination, decreased calcaneal inclination, decreased forefoot adductus and increased abductus due to unlocked MTJ, anterior break in the midtarsal cyma line, decreased (<70%) talonavicular articulation congruity, and medial column breach in sever pes valgus. Radiographic signs of a supinated foot are opposite to those seen with pronation, and include a bullet sinus tarsi, and a more parallel relation of the talus and calcaneus. An acquired rocker bottom foot, due to equinus or severe pes valgus, displays plantar articular gapping and dorsal jamming. Basic Gait Analysis Phases of the gait cycle include stance 162%) and swing (38%1. The stance phase is subdivided into:

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115

contact- which occurs from heel contact to forefoot contact and entails 27% of the stance phase and 17% of the entire gait cycle, and is associated with the foot serving as a pronating mobile adapter, with initial vertical force being about 125% of body weight

midstance- (entails 40% of the stance phase) wherein the foot conve rtsto a rigid !ever for push-off, and the vertical force decreases to about 75% of body vveight; propulsion- (33% of stance) which consists of heel off and toe off, wherein the vertical force again reaches about 125% of body weight and the foot is a rigid supinated, tight-packed lever. Swing phase- requires external leg rotation and ankle dorsiflexion, and hip and knee flexion. At heel contact, we note hip extending, knee flexing, ankle pi a ntatflexing, and STJ neutral and pronating. At midstance, we note hip flexing, knee extending, ankle d orsiflexing, STJ supinating and MTJ pronating. Double support occurs atthe beginning and end of each stance phase in walking gait, wherein both feet are on the ground, and this occurs at t:he 1st 0-12% and again at50-62% of the gait cycle, or 25% of the entire cycle. Double float, or an airborne phase, occurs in running gait

The phasic activity of the lower extremity musculature is as follows, rei ative to the gait cycle: hip adductors fire from heel contact to midstance and again from heel off to midswing hip abductors fire through late swing to prior to heel off hamstrings fire from late swing to 25% of stance; quadriceps femoris fire from hee contact to 25% of stance and again from toe off through early swing triceps surae fire from 15-20% of stance to toe off peroneal musculature fires from 15-20% of stance to toe off; and the anterior leg musculature fires from swing to midstance

116

The Perioperative Patient

Ch. 5

THE PERIOPEilATIVE PATIENT The perioperative period is divided into preoperative, intraoperative and postoperative phases. Planning a safe and efficacious course for the patient requires that attention be paid to many details. Open and frank discussion with the patient and their family, and consult-

ants, is important relative to achieving a smooth operative cOurse. PREOPERATIVE PHASE Considerations in the preoperative phase include the history and physical IH&PI, accurate

diagnosis and treatment protocol, the decision to operate, and informed consent. Informed Consent Contains: Review of the diagnosis Planned surgery or procedure The possibility of other intervention based upon operative findings

Potential risks and complications Alternatives to the surgery or procedure Postoperative course and expectations Permission for observers in the operating room and for photography Safe Medical Device Act Identification that no guarantees have been made Signature by the patient, a witness, and the surgeon Appropriate systemic medical evaluation should also be obtained preoperatively, and discussion with the patient's physician should be undertaken as indicated. PreOperative consultation, physical therapy, attainment of postoperative medications and/or special equipment, such as a bone growth stimulator for home use, notification of social services if home wound care or lV antibiotic administnition and testing are anticipated, should also be considered. Special medical considerations include thrombophlebitis prophylaxis, corticosteroid supplementation, prevention of gout, and infection prophylaxis with preoperative administration of antibiotics. If the procedure is anticipated to last more than 2-3 hours, urinary catheterization ·may be performed. The preferred anesthesia should be discussed with the patient and, if there is a question, the anesthesiologist. The operating room personnel should be notified ofthe need for special equipment and studies, such as the C-arm and diagnostic imaging, specific instruments or implants, power lavage, tubes for aerobic and anaerobic C&S, frozen section, drains, bandages, and splinting/casting materials. The patient should fully understand the planned postoperative course, analgesia, weight-bearing status, rehabilitation schedule, time off from work, and prognosis.

INTRA-OPERATIVE PHASE The intra-operative phase entails those activities that take place once the patient is in the operating room. The details ofthis period are documented in the operative report, the record of anesthesia, and the circulating nurses notes. Attention is paid to achieving surgical

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117

anesthesia, patient positioning, hemostasis, extensile exposure, wound exploration and inspection of pathological anatomy, alteration of planned procedure if indicated,

intraoperative imaging to assess correction and fixation, wound closure and bandaging/splinting, and control of any complications (hemorrhage, break of sterile field, malignant hyperthermia, ischemia) that may have arisen during the course ofthe procedure.

POSTOPERATIVE PHASE

The postoperative phase entails the period commencing in the recovery room until the patient is discharged from your care. Obviously the early postoperative period \first 1 to 3 days) is most critical relative to the possibility of systemic complications. The surgeon's postoperative orders detail planned care of the patient once the anesthesiologist has transferred the patient from the recovery room. The surgeon must also document the procedure and findings of the surgery in the operative report Standard Postoperative Orders Can Include 1. 2.

3. 4.

5. 6. 7. 8. 9.

Vital signs (VS Q shift after return to floor) Activity (CBR with side rails up; absolute NWB operated foot at all times; BRP NWB operated foot with assistance; PT for gait and transfer training NWB operated foot). IV fluids (maintain IV D% LR at KVD until fully reactive/stable. Convert to Heparin lock after D/C IV). Medications, including antibiotics, analgesics for moderate and severe pain, anti~inflammatory, anti-emetic, stool softener/bowel stimulant, hypnotic, and the patient's regular medications. Respiratorytherapy Drain management Diet Discharge planning Other orders specific to the case

Postoperative Complications Postoperative complications are variable, and range from mild problems to life- threatening crises. Complications can occur despite the best planning and technique. It is the surgeon's responsibility to point out, within reason, the possible complications related to a specific procedure, and to be on the look-outforthe development thereof in the postoperative phase. The best approach to the management of a postoperative complication is straight-forward identification of the problem, notification of the patient and documentation in the medical record, and treatment. Consultation may certainly be in order. A postoperative complication is defined as any untoward event occurring within thirty days after the surgery. Complications may affect the surgical wound and various organ systems, including pulmonary, gastrointestinal, cardiovascular, and urinary systems. The phrase "wind, water, wound, walk, wonder," reminds the surgeon ofthe most common postoperative complications and the postoperative day during which the specific complication usually occurs.

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118

Postoperative Day

Complication

first day second day third day fourth day fifth day

pulmonary urinary wound calf DVT anything is possible

Ch.5

Pulmonary complications- include atelectasis, aspiration, and pulmonary embolism. Pulmonary complications are more likely following general anesthesia, and in patients who are obese or those with a history of COPD or regular cigarette smoking. Such patients should undergo preoperative pulmonary function testing, and the anesthesiologist should be notified of the results. Postoperative pulmonary assessment notes respiratory rate and effort, in conjunction with auscultation ofthe lung fields.

Atelectasis is the condition of collapse of the adult lung, and is usually due to bronchial occlusion (secretions) and subsequent absorption of air as alveolar perfusion continues. Atelectasis may occur during or after general anesthetic.

Aspiration occurs when gastric c.ontents are admitted into the trachea, bronchial passages, and lung, resulting in airway inflammation and pneumonitis. Aspiration may occur in relation to administration of a general anesthetic, when the patient's gag reflex is muted. Atelectasis and aspiration pneumonitis effect localized pain, dyspnea, and fever. Auscultation may reveal abnormal breath sounds. A chest X-ray should be obtained. Respiratory therapy to enhance ventilation is indicated for mild atelectasis, and will usually suffice. Therapy ranges from simple incentive spirometry lTriflow) to medicated breathing treatments. Aspiration pneumonitis is treated with appropriate respiratory therapy, corticosteroids, and antibiotics.

Pulmonary embolism associated with lower extremity DVT, is the most devastatingpostoperative pulmonary complication. See Chapter 3. Urinary complications- include retention and urinary tract infection. Postoperative assessment involves observation of fluid input and output, blood pressure and heart rate, and suprapubic palpation and percussion.

Retention is common in elderly males at bed rest, particularly if there is concomitant benign prostatic hypertrophy or history of urinary stricture secondary to previous traumatic urethral catheterization, infection or surgery. Atropine or other anti~ cholinergic in high doses associated with general anesthesia can cause urinary retention. Similarly, prolonged surgery and anesthesia, with administration of IV fluids may lead to bladder distention (average bladder volume is about 500 cc). Cases anticipated to last 3 or more hours should entail placement of a Foley catheter after general or spinal anesthesia has been achieved. If the patient has not voided by six hours postoperative, examine for bladder distention (palpation and percussion) and initiate treatment by encouraging the patient to stand (works we!! in males). If patient remains unable to void, then pass a straight catheter once to evacuate the bladder and measure the volume. If the urine volume is< 300 cc, discontinue catheterization. If the urine volume is 500 cc or more, consider placement of an indwelling catheter until the patient is more ambulatory and comfortable.

Ch.5

The Peri operative Patient

119

Urinary tract infection can be caused by prolonged urinary retention, or urinary catheterization. Care should be taken to employ aseptic technique whenever passing a urinary catheter. Females are more likely to develop urinary tract infection, and many have previous history of urinary tract infection. Treatment entails adequate hydration, and antibiotic therapy after obtaining a clean catch, midstream urine specimen for C&S.

Wound complications Fixation failure or loss of surgical correction usually requires a return to the operating

room to rectify anything but the minimal deformity. Circumferential bandage or cast compression. An excessively snug or tight circumferential bandage or cast can induce pain that is unresponsive to analgesia, cutaneous compromise and pressure ulceration, neuropraxia; and requires cast and bandage replacement in order to effect relief.

Hemorrhage will usually cease with protection, rest, ice, compression, and elevation. If hemorrhage persists beyond one or two bandage reinforcements, then consideration should be given to a return to the operating room for exploration and hemostasis. Hemoglobin and hematocrit levels will decline secondary to significant hemorrhage, and preparation for transfusion should be considered if the hemoglobin drops below 9 grams. (It is rare and quite problematic for a patient to require transfusion following foot and/or ankle surgery.) Observation of the patienfs vital signs may indicate the need to increase IV fluid administration above the KVO rate. Dehiscence may be superficial or deep, and can usually be managed wfth local wound care and secondary intention healing, as long as hematoma or infection does not warrant intervention that is more aggressive. Hematoma and infection warrant, at the least, selected suture removal, swab specimen of any exudate or drainage for Gram's stain and C&S, CBC with differential, observation of systemic temperature and blood glucose, close wound monitoring, and possibly oral antibiotic therapy, for minimal or equivocal findings. If the signs of inflammation associated with suspected hematoma and/or infection are significantly advanced, or not responding within 24-48 hours to initial intervention, then a return to the OR for wound inspection and cleansing debridement may be warranted. Actual therapy will depend upon the local and systemic merits of the individual case. It is better to error on the side of over-aggressiveness, rather than miss the diagnosis and place the patient at more risk. Infection is highlighted by unusual amounts of pain, often unresponsive to analgesic medication, on or about the 2nd to 3rd postoperative day. Hemolytic Streptococcus may cause fever and wound infection within 24 to 48 hours of the surgery. Consideration should be given to an acute gouty attack in the hyperuricemic patient with history of gout, and to an excessively tight bandage or cast. Excessive pain at the operative site always warrants inspection. Nonsuppurative wound infection can be difficultto identify, even with close observation of the surface of the well-coapted incision, and a high index of suspicion should be maintained. Systemic signs of


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Ch. 5

endotoxin release and/or septicemia should be suspected, and include Gl distress, general malaise, cutaneous rash and/or desquamation (toxic shock syndrome),

myalgia, cephalgia, and pyrexia.

Postoperative ischemia~ usually identified in the digits as a "blue toe." Other common areas of postoperative ischemia include skin islands (actually isthmuses or bipedicle flaps) situated between two long, parallel skin incisions. Causes of blue toes include venous congestion, dissecting hematoma, and arterial occlusion or microcirculatory vasospasm. Venous congestion effects a cyanotic, often warm, diascopy positive toe that may respond well to eleVation and perhaps loosening of constriction bandages and flexion of the knee. Ice, nicotine, and caffeine should be avoided whenever dealing with a blue toe.

The term dissecting hematoma may be a misnomer, however it refers to the condition wherein hematoma has separated and filled the potential space between intact and viable dermis and overlying epidermis. The condition has also been described with intradermal dissection. In this condition, the epidermis displays a dark appearance consistent with hematoma observed through the thin, translucent epidermis. The basal layer of the epidermis may also become necrotic, and the epidermis will eventually slough. The digit may be anesthetic, cool, and stiff. The important clinical distinction, related to dissecting hematoma, is the possibility of misconstruing the toe as being gangrenous throughout. It is prudent to carefully inspect and debride the superficial layers of the skin to ascertain whether deeper tissues are viable. Arterial Doppler assessment of the digital vessels may also be useful when considering the possibility of dissecting hematoma. Occlusive vascular ischemia due either to functional vasospasm or organic disruption of the flow (thrombus, embolism, impingement or laceration), effects a cold toe that initially displays pallor followed by cyanosis and then gangrene. The ischemic toe will usually blanch upon application of pressure {diascopy positive), however subpapillary venous plexus refill time will be greatly delayed. If blood flow is restored prior to the development of necrosis (3~6 hours), pink or red cutaneous hyperemia will be observed. Vasospasm can be effected by surgical manipulation, often noted with vessel traction and pin stabilization across the MTPJ; or seen in patients with a history of Raynaud's phenomenon and subjected to a cool operating room and lavage fluids; or due to the local use of dilute epinephrine in a patient with Raynaud's phenomenon or treated with tricyclic antidepressant or MAO inhibitor. Counter measures include dependency, loosening tight bandages, avoidance of nicotine and caffeine and ice, adjustment or removal of a pin positioned across the MTPJ, reflex heat(K-pad) applied to the abdomen and or thigh, posteriortibial nerve or ankle block with plain bupivacaine, and oral (Procardia) and/or intra-arterial (Priscoline} vasodilator following vascular consultation.

Postoperative OVT See Chapter 3

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Gastrointestinal complications- include nausea and vomiting, constipation, gastritis and reflux esophagitis, fecal impaction, and postoperative jaundice. Severe bowel obstruction or postoperative paralytic ileus usually only occurs following abdominal surgery. Postoperative assessment of the belly entails observation, auscultation for bowel sounds, and palpation for tenderness, guarding, and rebound. Postoperative nausea and vomiting may be the result of anesthetic or narcotic influence on the central chemoreceptor trigger zone, or due to peptic ulcer disease or gastritis in predisposed patients or those medicated with anti-inflammatory drugs. Excessive emesis can effect dehydration, and IV fluids should be administered. Drugs such as Compazine, Tnlafon, Phenergan, Dramamine, Tigan, and Emeticon can be used to control postoperative nausea, and may be administered in suppository form. Drug interaction with analgesics, sedative/hypnotic, and antidepressants should be considered whenever administering centrally~acting antiemetics.

Constipation often results from inactivity, and commonly occurs in elderly patients who are immobilized in bed. Bulk laxatives such as bran Metamucil or Senokot or stool softeners such as Co/ace, Doxinate and DDS, are preferred over bowel stimulants such as Milk of Magnesia or Dulcolax. Encouraging fluids and out of bed activity are indicated. Rarely is an enema necessary. Fecal impaction is rare following foot and ankle surgery and may present as postoperative diarrhea.lfthe digital rectal examination reveals hard stool, then an oil retention enema may be helpful. Digital disimpaction may also be necessary.

Gastritis and/or reflux esophagitis is common in patients maintained NPO and positioned supine with the legs elevated, especially in those with hiatal hernia and/or previous PUD. Treatment is elevation of the head and oral administration of antacid (Riopan, Rolaids, TUMS)and/or H2 receptor antagonist such as Pepcid. Diarrhea can often be controlled with bismuth (Pepto-bismol). Postoperative jaundice usually associated with nausea, warrants assessment of hepatic enzymes and review ofthe anesthetic record. If right upper quadrant pain is marked (colic), then general surgical consultation and cholecystogram or ultrasound is indicated.

Cardiac complications - uncommon in association with elective foot and ankle reconstructive surgery, and are most likely to occur in patients with pre-existing coronary artery disease, dysrhythmia, congestive heart failure, or patients with significant pulmonary disease. Postoperative cardiac evaluation involves vital sign assessment, and auscultation. Rarely fluid overload can precipitate congestive heart failure, and pretibial, perimalleolar, and pedal pitting edema should be observed. Arrhythmias are most commonly observed during general anesthesia and are usually related to periods of hypoxia or myocardial sensitivity to the anesthetic agent (halothane, enflurane). Consultation with the anesthesiologist is in order in patients with a history of significant cardiac disease, and a recent chest X-ray and EKG are in order. In patients with a cardiac murmur, prophylactic antibiotics are indicated, and an updated echocardiogram may be

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useful pending cardiology consultation. ln patients with a history of coronary artery

disease or CVA, elective surgery is avoided for at least six months following a documented

myocardial infarction.

Postoperative nerve entrapment- can occur even after strict attention has been paid to avoidance and protection of peripheral nerve, secondary to norma! wound healing and fibrosis effecting scar entrapment of the nerve trunk. This generally takes three weeks or more to become symptomatic, as wound healing and fibroplasia progress. Sharp, burning,

shooting pain and paresthesia noted earlier in the postoperative phase may indicate specific nerve trunk trauma due to sectioning, traction, or heavy-handed retraction causing neuropraxia or intraneural hemorrhage. Postoperative fever- is anticipated early on, especially following general anesthesia. Fever is defined as a core (rectal) temperature of 37.8° C(100° F), or greater. Temperatures of 38J° C (101° F), or higher, indicate a major constitutional problem, and can result in severe central nervous system damage. In searching for the cause of postoperative systemic temperature elevation, considerations include: recent general anesthesia; possibility of pulmonary atelectasis or aspiration, UTI, constipation; catheter sepsis {IV, urinary); 0\IT and PE; wound infection or injury; drug reaction or serum sickness. The physical examination should identify sites of inflammation and potential cause of the febrile state. In addition to the clinical examination and discussion with the patient, testing should include CBC with differential; urinalysis; C&S of wound drainage or exudates, urine, blood, oropharynx and sputum; and a chest X-ray. The treatment of hyperpyrexia (fever> 38.5° C) involves administration of antipyretic such as acetaminophen or aspirin (600 mg PO Q 6 h PRN), and use of a cooling blanket If the patient remains hyperpyrexic and symptomatic, then consider discontinuing all medication, consult infectious disease specialist, and re-evaluate the patient.

Chronological Sequence of Postoperative Temperature Alteration Intraoperative & first 12 to 24 hours postop

Elevated temperature due to malignant hyperthermia, or typically postoperative hypothermia.

1st postop day

Postoperative hypothermia, postanesthesia overshoot, atelectasis I pneumonitis

2nd postop day

Benign postoperative fever, urinary tract infection, pulmonary, DVT

3rd postop day

Wound infection, benign postoperative fever, and constipation.

Any time in the postop phase

Drug fever, catheter sepsis, transfusion reaction, cold, or flu.

Ch. 6

Fundamental Techniques and Procedures

123

FUNDAMENTAL TECHNIIJ.UES AND PROCEDURES SUTURE MATERIALS and WOUND CLOSURE Sutures are used to reapproximate sectioned tissue, whether it is skin, superficial or deep fascia, muscle, tendon or ligament, nerve sheath, blood vessel, or bone (stainless steel wire [SSW]). The ideal suture material is strong enough to resist disruptive tensile forces, nonallergenic and non-toxic, pliable enough to handle easily and to stay fixed once tied. Sutures that communicate between the external surface of the skin, and the subcutaneous and/or intradermal layers should also be inert, non-wicking, and easily removable after the tissues have healed. The decision to use an absorbable or nonabsorbable suture material varies with the specific requirements of the operative procedure.

Absorbable sutures-these are made of materials that break down in the tissues over varying time periods, ranging from 1~ 10 weeks. Since most soft tissues, excepttendon, heal in 3~4 weeks, sutures that degrade at a rate that provides tensile strength up to 3~4 weeks are commonly used in foot and ankle surgery. Classically, absorbable sutures were made from sheep or beef intestine, and known as catgut. Plain gut can be strengthened by the addition of chromium salts that slow down degradation by collagenase, or it can be heat~treated to Increase the rate of degradation (rapid gut). Although it is not likely, disease transmission, such as bovine spongiform encephalopathy (mad cow disease), is possible with catgut, which is a xenogeneic materiaL Although many surgeons prefer the behavior of gut suture, monofilament or braided multifilament synthetic polymers comprise the majority of absorbable sutures used nowadays. Synthetic polymers, such as polyglycolic acid, lactic acid and caprolactone, are relatively inexpensive, non~reactive due to hydrolysis rather than collagenase degradation, nontoxic and nonallergenic, and they handle very well. Immunological reaction to synthetic absorbable suture is rare, however when it occurs a sterile abscess can form, and the material may not rapidly orfu!ly absorb. Monofilament absorbable sutures are often used in the deep tissues during delayed primary closure of previously infected or contaminated tissues. Sutures range in size (gauge), as defined by the US Pharmacopeia (USP), from #11-0 (smallest) monofilament nylon used for ophthalmologic and neurosurgery, to #5 (largest) braided polyester used for ligament repair. Some suture materials are also coated or impregnated with antimicrobial agents, to minimize risk of infection. Non-absorbable sutures-these are made of materials that are not degraded by the body, such as silk, polypropylene, polyester and nylon, and are often used for skin closure (where they can readily be removed after the skin has healed), or in tissues where prolonged strength is require, such as tendon or ligament, or myocardium and blood vessel. Due to the inert nature of many of these materials, there is less inflammation and less scar formation, so they are often preferred for skin closure. Stainless steel wire can be used for intra osseous suture, cerclage, and tension banding. Suture needles-needles used for suturing are available in a number of shapes, namely: half curved, quarter circle, 3/8 circle, 5/8 circle, compound curvature, and straight (Keith needle). Separate needles with eyelets for threading suture are known as traumatic needles. Atraumatic needles have the suture material swaged to the needle by the manufacturer. Needles can also be smooth and round or oval, or they may have a cutting edge on the concave surface ofthe curve, or on the convex surface of the curve (reverse

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cutting needle). The body of the needle maytapertoward the tip, or retain the dimension of the body and form a blunt tip (forfriable tissue). The tip ofthe needle can be round, oval, or diamond-shaped. Generally, a non-cutting, atraumatic needle is used for reapproximation of friable tissues, whereas a cutting needle is often used for dense and durable tissues such as fascia and joint capsule.

Suture (stitching) techniques and remova~some of the most common suture techniques include the simple interrupted stitch (almost always applicable). horizontal and vertical mattress stitches {excellent margin eversion, however can strangulate), running and

running lock stitches, figure-of-8 stitch, baseball stitch, and the running subcuticular stitch. Running subcuticular skin closures are usually reinforced with adhesive skin strips. Skin sutures that are designed to be removed, are generally taken out according to the following schedule: face 3-5 days, scalp or trunk 7-10 days, limbs 10-14 days, over a joint 14-20 days, plantar 20-22 days. Care of the operative site varies with anatomical location, and wound healing progress. Stitch maneuvers suitable for tendon include the Bunnell, Kessler, and other lateral trapping methods. Nonabsorbable multifilament sutures are often used to reap proximate tendon to bone, and a variety of tendon anchors are available forth is (see section on tendon transfers). Tissue adhesive---cyanoacrylate ("liquid suture" or tissue glue) can be used as an alternative. to suture material for wound margin reapproximation where there is minimal tendency toward margin disruption. Cyanoacrylate polymerizes when it comes in contact with tissue fluid, forming a flexible adhesive bond between the wound margins. When used for skin closure, cyanoacrylate is reinforced with adhesive skin strips.

BIOPSY TECHNIQUES

lncisional Biopsy---incisional biopsy removes only a selected portion of the lesion in question, while an excisional biopsy removes the entire lesion (theoretically). Obviously, a margin of supposedly "normal" tissue is excised around the lesion in question when an excisional biopsy is performed. Actual pathological assessment of the margins of the biopsy is necessary to determine whether a "clean" margin was created. When performing an incisional biopsy, it is important to select representative portions of the lesion, and more than one sample may be harvested. It is important to accurately identify the samples relative to position about the lesion, and a diagram is helpful in this regard. The pathologist would also benefit from review of the diagram when dealing with a difficult lesion. The surgeon should not struggle to procure a margin of normal appearing tissue in the incisional specimen at the risk of missing representative lesion. Scabs, crusts, and vesicles should be preserved in the specimen, and not destroyed in the surgical preparation of the skin. Most skin biopsies can be performed under !a cal anesthesia, and dilute epinephrine (1:100,000 or 1:200,000 dilution) may aid hemostasis, if it is not contraindicated in the particular patient. The local anesthesia should not be infiltrated directly into the lesion, for fear of spreading potential malignancy or infection, although it has been shown that direct injection below or through a lesion appears to cause no significant microscopic alteration. The area is then prepped and draped in the usual s terile fashion, priOr to biopsy.

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Punch Biopsy--the punch biopsy is a convenient and effective method of tissue extraction and may be either incisiona! (usually), or excisional when dealing with a large punch and a smaller lesion. In the lower extremity, the 4-mm punch is typically employed, and standard punch sets include punches ranging from 2-8 mm. It should be noted that removal of a specimen <4 mm in diameter might allow the histological confirmation of a tumor, however it is generally considered inadequate for the accurate diagnosis of an inflammatory process. When using the punch, the skin surrounding the lesion/s should be stretched taut, perpendicular to the wrinkle lines before the circular punch is inserted. The punch is firmly pressed downward into the lesion with a rotary back and forth cutting motion until it is well into the subcutaneous tissue, thereby providing a full-thickness skin biopsy. To remove the cylindrical specimen from the skin, gently grasp the biopsy plug with forceps, or a 27-gauge needle, and cut the base with scissors or scalpel and then place the sample into 10% formalin. Simple pressure is adequate for hemostasis. A punch biopsy defect of :24 mm diameter may require suture closure, whereas a defect <4 mm will heal via secondary intention with adhesive skin strips and a sterile dressing. A linear defect usually heals more readily than a round defect.

I '

Shave biopsy---the shave biopsy is used to remove that portion ofthe lesion elevated above the plane of surrounding tissue and is useful for biopsy or removing many benign epidermal growths. It is not indicated for biopsies of suspected melanoma, although it can be used to identify the presence of malignancy without providing adequate tissue for microstaging of a melanoma. However, it can be used as a convenient procedure for diagnosis of basal cell epithelioma !basal cellcarcinoma). The preparation is as noted previously for biopsy, and a #15 blade is used to shave the lesion/sand a margin of apparently normal surrounding tissue. The specimen is retained in 10% formalin. Pressure is applied to effect hemostasis. Curettage-curettage is a useful technique, distinguishable from the shave biopsy, for removal of cutaneous lesions such as warts, seborrheic keratosis, and even malignancies such as basal and squamous cell carcinomas. The curette is a spoon-like instrument with a sharp rim. Typically, the 4-mm curette is used. A variation on this technique is excochleation using a blunt instrument, such as a Freer elevator, when removing a lesion that has a clear and separable margin with the adjacent normal tissue. An isolated verruca is ideal for excochleation, as this provides an excellent specimen for biopsy and prepares the base for ablative surgery (acid, cryogen, or laser).

Surgical excision------excisional biopsy should be considered whenever the lesion displays active (spreading) margins and the border with normal appearing skin is to be surveyed, or if the lesion is friable or very sclerotic, or whenever it is necessary to include full-thickness skin to the level of, and including a portion of, the subcutaneous fat layer {e.g. in suspected panniculitis, erythema nodosum, or melanoma). In theory, excisional biopsy is curative, and may be used whenever excision of a lesion is desired. Local anesthesia is achieved as described previously for incisional biopsy. With the exception of the smallest lesions (<4 mm), the planned incisions should be marked on the skin. The most common technique involves the use of two semi- elliptical incisions to create a wedge of intervening tissue to be excised. The length of the ellipse should be three to four times the width, with the long axis of the wedge parallel to crease lines and, therefore, RSTL. Surrounding margins may be undermined in order to decrease tension with closure, and weight bearing on the

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Ch. 6

plantar skin should be avoided for 2·3 weeks, varying with the size of the wound and progress of healing. When malignancy is suspected, it is importan~to avoid contamination of surrounding tissue planes with cellular elements of the lesion in question. A sarcoma

can often be adequately eradicated with wide excision, compartment resection, or amputation. Violation of adjacent soft tissue barriers at the time of biopsy may make subsequent definitive therapy more ablative than it originally need to have been. A frozen section may be used to identify the presence or absence of tumor in a particular specimen, and perhaps yield identification ofthe specific 1ype of tumor present It is often difficult to accurately identify the specific tumor from a frozen section specimen only, however the presence of dysplasia and anaplasia can usually be determined. A frozen section must be planned with the pathologist and OR team. If a local excisional biopsy is performed, and the frozen section pathology report yields a diagnosis of malignancy, then an adequately wide excision should only be attempted for very small and well-defined lesions. By definition, sarcomas are usually invasive and not differentiated from adjacentsofttissues. Carcinomas localized to the skin may be more readily isolated and amenable to definitive excision and eradication at the time of excision aI biopsy. Definitive treatment such as wide excision and coverage with a muscle flap, or amputation, is determined by oncological consultation and additional testing to ascertain tumor staging. Additional radiographs and CT scans of the part as well as the lungs, MRl, and other tumor specific tests are often warranted. Adjuvant radiation and/or chemotherapy may be administered both before and after definitive excision, and is determined by the oncologist. Definitive surgery is planned and carried out in a timely fashion. Plastic surgical consultation and co-management is often needed in order to effectively cover the defect created by wide excision, and a free muscle flap (serratus, or other suitable donor site) in conjunction with skin grafting may be indicated.

PlASTIC SURGERY TECHNIQUES

Elective skin incision planning and execution--elective skin incisions should take into consideration exposure of underlying target tissues, preservation of vital structures, and relaxed skin tension lines (RSTL). As long as adequate exposure is not compromised, the incision should be made parallel to RSTL An incision made parallel to RSTL will be subjected to less gapping tendency, and should therefore form less scar. RSTL run perpendicular to the long axis of the extremity and vital structures. When a transverse incision fails to yield adequate exposure, an incision that is oblique to RSTL is considered better than one perpendicular to RSTL, wfth respect to gapping and scar formation. Difficulty may arise when RSTL are in a transverse direction and the exposure needs to be longitudinal, as in the case of excision of the plantar fascia for treatment of fibromatosis. In such a case, a zigzag incision can be used to effect longitudinal exposure while remaining oblique to RSTL over the short segments of the zigzag.

Primary intention closure--involves direct wound margin reapproximation secured with skin sutures. It results in immediate closure that seals with epithelium after 24-48 hours, and usually results in a fine-line scar. Primary skin closure requires wound margin mobility that allows approximation ofthe edges. Secondary intention closure--involves wound granulation, contraction and epithelialization, and slowly progresses over several days to weeks, depending upon local and systemic factors. This is often the preferred method of closure following incision and

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drainage of an abscess or osteomyelitis, or when the wound presents chronic contamination and necrosis, such as ulceration in a debilitated patient Tertiary intention (delayed primary) closure----involves an initial period of secondary intention healing, followed by additional surgical wound debridement and primary

intention suture closure. Primary, secondary or tertiary intention healing are the preferred methods of wound closure, and should be attempted whenever clinically indicated. Indications include a clean wound with beefy red granulations and resolution of surrounding cellulitis and edema. Generally, other methods of closure, such as skin plasty, grafts, and flaps, entail a greater risk of dehiscence, dysvascularity, slough or other complication, and should be reserved for those cases where simpler methods are deemed inadequate.

Skin Graftintrskin grafts consist of epidermis and varying thicknesses of dermis. The graft is said to "take" when it has successfully revascularized and effectively covered the recipient site. The thicker the graft, the more difficult it is to achieve" graft take." Contrarily, a thinner graft usually takes more rapidly. Moreover, thicker grafts are more durable and contract less while healing, whereas thinner grafts are less durable and contract considerably more. Skin grafts are most frequently autogenous, with the patient serving as his/her own donor. For foot and ankle reconstruction, ipsi- or contralateral leg, thigh, buttock, or the anterior aspect of the abdomen, can serve as donor skin graft procurement sites. Donor skin can be meshed to provide for larger surface coverage at the recipient site. Skin grafts can also be allogeneic {from another individual ofthe same species), xenogeneic (the donor is of a different species, commonly porcine), or isogeneic (the donor is an identical twin). By definition, a graft is detached completelywhen transferred from the donor site to the recipient bed. There are 3 phases of skin graft healing (Table 6-1).

TABLE 6-1. PHASES OF SKIN GRAFT HEALING. Phase Plasmatic

Time period 24-48 hours

Inosculation

48-72 hours

Remodel/reinnervate

3 days to several months

Key events Fibrin adhesion between graft and recipient site Microvasculature traverses fibrin layer Collagenation, collagen remodeling, reinnervation

Split-t/Jickness skingraft(STSG}--these can be thin, intermediate thickness, orthick. A thin STSG measures 0.008-0.012 inches in thickness, while an intermediate graft measures 0.012-0.016 inches, and a thick graft measures 0.016-0.020 inches. Thin STSGs contract as much 50-70%, and are often used as temporary coverage for large wounds. Intermediate STSGs are most versatile and frequently used in coverage of foot and ankle wounds. Thick STSGs only contract about 10~ 15%, however demand markedly increased recipient bed vascularity, and have a higher risk offailure.lntermediate and thick STSGs can be used to cover weight bearing and contact areas. Full-thickness skin graft (fTSG)-these contains the entire epidermis and dermis, including dermal appendages such as sweat glands and hair follicles. The subcutaneous

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Ch.B

fat and superficial fascia are not included in a FTSG. FTSGs are very durable and contract minimally, however take rather poorly in comparison to STSGs. A FTSG can be considered for coverage of a weight- bearing surface, and can be harvested from a pinch of skin over the sinus tarsi, anterior anlde, or medial arch. The inguinal region and popliteal fossa are also potential donor sites. Full-thickness pinch grafts consisting of skin from the sirius tarsi are useful for coverage of small defects in plantar and contact areas of the foot.

The recipient site must be prepared in order to increase the rate of skin graft take, and this should be done prior to harvesting the graft. The recipient site must be free of fibrosis, necrosis, infection, and active hemorrhage. A beefy red, confluent granulation tissue base is the ideal recipientsutiace. Bare tendon, bone, and cartilage are inadequately vascularized for graft support, and a period of secondary intention healing is required to allow for the formation of a granulation tissue surface. In cases involving large or deep wounds, temporary coverage may be achieved with a skin substitute (see below), prior to subsequent autogenous skin grafting. After the recipient site is prepared, the autogenous skin graft is harvested (procured) from the donor site manually using a Goulain or Hum by knife, or via use of a pneumatic powered Brown or Pagget dermatome. Although the graft can be stored for up to 21 days in lactated Ringer's solution at 0-5° C. After procurement, attention should focus on getting the graft to the recipient site in a rapid (immediate) and efficientfashion. The graft may be incised in a fashion similar to pie crusting, wherein small incisions are made to allow expansion and seroma drainage. For large recipient sites, the graft may also be meshed, in a 1:1.5 ratio using_ the graft masher, in order to increase the area of coverage and enhance drainage of wound transudate through the mesh incisions. Mesh ratios of 1:3, 1:6, and 1:9 can also be achieved, however these ratios make for sparse coverage of the recipient site and are only used when a large surtace requires coverage. After meshing, the graft is placed in contact with the recipient bed, maximizing contact and eliminating dead space. The graft is then secured with several simple interrupted sutures of 4-0 or 5-0 chromic gut at the margins. A small amount of excess graft may overlap adjacent intact skin margins. The graft-recipient intertace is then secured with a tie~over stent dressing. The tie-over stent dressing employs fine-mesh nonadherent gauze placed directly over the skin graft, followed by coverage with fluffed gauze or mineral oil impregnated cotton balls, then covered with a flat gauze barrier secured with evenly-spaced silk sutures that convey gentle pressure over the graft In many cases, immobilization and non-weight bearing are indicated, and the graft is typically not disturbed until 5-7 days. The graft donor site is dressed with nonadherent gauze, after assuring hemostasis (topical thrombin spray can be used), and redressed when the recipient site is inspected. Application of a wound dressing consisting of porcine-derived extracellular collagen, elastin, glycosaminogtycan, and glycoprotein (such as Oasis®lr can enhance donor site healing. Complications related to skin graft healing usually develop secondary to disruption of the grafHecipient interface with resultant failure to achieve revascularization. Causes include seroma formation, infection, and inadequate immobilization. A dysvascular recipient site is doomed to failure. Failure to achieve inosculation results in graft necrosis, and this usually leads to contamination and subsequent infection if appropriate treatment (debridement, antibiotic therapy, and revision) is not initiated. Reverse dermal grafts are sometimes used for nail bed reconstruction, and require inverting an intermediate STSG prior to application to the recipient bed.

Skin substitutes-----a number of options exist for skin coverage that do not involve harvesting autogenous skin. These materials typically employ combinations of collagen,

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129

glycosaminog!ycan (GAG), silicon elastomer, and water. One such option (Integra®) is a bilayer skin substitute that consists of a biodegradable type I collagen-GAG co-polymer dermal analog combined with an epidermal analog consisting of a thin silicone polymer that behaves in a fashion similar to normal skin. The cross-linked collagen and GAG matrix maximizes ce!!ular in growth and degrades in a predictable fashion. After neodermis formation, the silicone epidermal analog is removed and replaced with a thin STSG.In some cases, use of the bilayer skin substitute obviates the need for subsequent use of an autogenous skin graft. Other skin substitutes include combinations of keratinocytes and fibroblasts, harvested from neonatal foreskin orxenogenic sources, in a collagen matrix, and these are often used In the treatment of large cutaneous wounds such as those due to burn injuries.

Skin flaps----flaps differ from grafts in that a vascular pedicle is maintained or, via micro~ surgical reanastomosis, reconstructed. Flaps are defined as either local or distant. In the foot and ankle, defects larger than 2.5 cm 2 are generally covered with a skin graft, while smaller defects are amenable to use of a local skin flap. Flaps are advantageous for full thickness defects, poorly vascularized recipient wounds, and coverage of bony prominence or contact areas. Sensation can also be restored when an innervated flap is used. Skin flaps are classified according to their blood supply. Random pattern skin flaps are perfused by the random dermal-subdermal plexus of vessels, and require a pedicle width equal to the length of the flap. The Z-plasty and V-Y pia sty are techniques that create random pattern, local, rotational or advancement skin flaps. Axial pattern skin flaps are supplied by an identifiable (Doppler) cutaneous artery, such as the lateral calcaneal artery flap used to cover heel defects, or the sural artery flap used to cover Achilles tendon defects, and can be rather long in comparison to the pedicle width. Axial pattern flaps can be of the island design, or actually distant flaps when the vascular origin is sectioned and later reanastamosed atthe recipient site. Local flaps----these are mobilized from adjacent skin, and are of either the rotational or advancementtype. Rotational flaps are semicircular and are mobilized about a pivot point where the flap is attached to its pedicle. A larger semicircle imparts less tension on the pivot, and tension can be alleviated at the pivot by means of a back cut or creation of a Burrow's triangle. The single and bilobed rotation flaps are commonly used for coverage of smaff pedal skin defects. Advancement flaps are mobilized via direct extension without rotation, and include the Y~V, V~Y, single, and bipedic!e flaJJs.

Distant flaps----these originate from a vascular pedicle in one area of the body and, via maintenance of the pedicle or sectioning with subsequent microvascular reanastomosis, are used to cover a remote defect. For example, a crossed leg flap uses skin mobilized from the contralateral calfto cover a pedal defect; or a section of latissimus dorsi, complete with its arterial supply and overlying fascia and skin may be harvested to cover a pedal defect. In the crossed leg technique, the calf donor skin remains attached at its pedicle while the legs are skeletally fixated and the flap sutured to the contralateral pedal recipient site. Once the ftap has healed and attached to the recipient bed, the donor side pedicle is sectioned and the skeletal fixation removed. Currently, it is more common to use the microvascular free flap, ratherthan the crossed leg method. The serratus free flap is commonly used by plastic reconstructive surgeons to cover large pedal defects, and requires microvascular reanastomosis and coverage of the muscle with a STSG.

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Ch. 6

Skin plasties-these employ !ocal flaps and are used to redirect skin, and alter skin tension and volume. Scar tissue and contracture can be redirected and lengthened with the Z·plasty !Figure 6-1). The arms of the Z are of equal length, with the apices forming a 60' angle, in order to achieve approximately 75% increase in skin length with resultant

decreased tension. Multiple Z-plasties, resulting in a W-plasty, can be used to further elongate skin and relieve tension. The V-Y plasty results in skin lengthening after flap mobilization. The skin defined by the V-incision is mobilized and elongated, and the resultant wound is sutured closed in the shape of a Y. As a rule, the wider the V's base, the greater the vascular pedicle. Skin can also be shortened or reduced by means of a Y~V plasty. Redundant skin can be excised via the creation of an elliptical wedge using two semi~elliptical skin incisions. This is often useful in digital surgery, in particular when derotation of a frontal plant deformity is desired {Figure 6-2). Fasciocutaneous flaps are useful in the leg, in particular for coverage of defects about the Achilles tendon. Muscle flaps are useful for coverage of weight bearing or contact areas of the foot and ankle, and convey excellent vascularity and provide a robust base over which skin can grow. Identification and preservation of the muscle's vascular supply is critical to the success of the flap. The heel and first metatarsal head area are amenable to coverage with FOB and/or FHB (Figure 6-3), the medial and lateral malleoli with abductor hallucis and abductor digiti minimi, respectively.

A_______ ------~

Figure 6.1

Figure 6.2

.A!fr.. '?'__

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131

Figure 6.3

BONE GRAFTING AND ORTHOBIOLOGICAL AGENTS

i,

Bone grafting may involve transplantation of viable bone that is expected to remain viable in the recipient host, whereas implantation implies transfer of non-living bone or tissue (freeze-dried bone) to the host recipient bed. An autograft originates in the recipient host;

an isograft originates in an identical twin; an allograft or homograft is viable bone originating in a donor of the same species, while an alloimplant or homoimplant is nonliving bone from the. same species; and xenograft or heterograft (or implant) implies bone from a donor of another species (and are not recommended for general use). Autogenous bone grafts are advantageous because of immunocompatabi!ity and transfer of osteoconductive (trabeculae and porous channels), osteoinductive (chemotactic and transformation factors), and osteogenic (viable cells) properties. Disadvantages associated with autogenous bone grafts pertain to creation of stress risers at the donor site with potential for fracture, as well as creation of another surgical wound that is subject to potential hematoma, infection, or other wound complication. Moreover, the host may not have adequate bone to donate, and the osteogenic quality varies with site and age. Autogenous bone is favored for use in the repair of failed unions, previous infection, or donor site/host morbidity. Allogeneic bone is suitable for orthotopic use, backfill of donor site void, and in cases wherein donor bone is limited or harvestthereof is contraindicated. There are 3 physiological elements critical to bone graft healing, including: 1) osteoconduction, 2) osteoinduction, and 3) osteogenesis !Table 6-2). Osteoconduction pertains to the porous nature of trabecular bone, which provides the scaffold upon which cells migrate and reside. Osteoinduction pertains to the chemotactic and differentiating

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influence that bone morphogenetic protein, and other growth factors, has on belie growth. Osteogenesis pertains to the bone generating properties of undifferentiated stem cells, osteocytes and chondrocytes (via enchondral bone formation). Autogenous bone grafts

can take the form of cancellous, cortical, or corticocancellous bone Table

6~3.

More

specifically, bone grafts function in the treatment of delayed union, nonunion and

pseudoarthrosis; to augment skeletal defects created by trauma or surgery, such as to fill a void after cancellous bone biopsy or cyst evacuation; to facilitate arthrodesis and to effect bone block limitation of motion; and to enhance reconstruction by means of osteotomy, as with the Evan's latera! calcanea! (column) lengthening, or in the repair of brachymetatarsia. To a certain degree, restoration of segmental bone defects using autogenous bone grafts has been replaced by means of callus distraction, and the use of bone graft substitutes.

TABLE 6-2. PHYSIOLOGIC PROCESSES OF BONE GRAFT HEALING. Process Osteoconduction

Elements and function Pores (10-1000 microns) that mimic cancellous bone; scaffold for bone growth

Source Cancellous bone, bioceramics (CaP04, CaS041, hydroxyapatite (coralline and natural coral grafts), extracellular matrix scaffolds (collagen or GAG+ HA + TCP), polymers IPGA), alloys (1i)

Osteoinduction

Bone morphogenetic proteins 2 & 7, plateletand fibroblast-derived transforming growth factors; recruit and transform mesenchymal

Autogenous bone, allogeneic stem cells or recombinant demineralized bone matrix, autogenous platelet rich plasma or bone marrow aspirate

Osteogenesis·

Living osteocytes, osteoblasts, chondrocytes, chondroblasts, and undifferentiated mesenchymal stem cells

AutOgenous bone, fresh marrow or cloned cells

TABLE 6-3. STRUCTURAL TYPES OF BONE GRAFTS.

Structure Cortical

Graft characteristics Dense, compact bone containing few viable cells; provides stable graft that can be secured to surrounding bone with fixation devices

Cancellous

Spongy bone containing viable cells to stimulate osteogenesis and rapid incorporation; no structural strength; excellent back-fill

Corticocancellous

Provides stability and osteogenesis; includes grafts such as those harvested from the calcaneal body and iliac crest; excellent reconstructive graft

Harvesting bone graft-when harvesting an autogenous bone graft, plenty of irrigation is used for coo!ing during osteotomy in an effort to preserve viable cells. A sharp osteotome is ideal for harvesting autogenous bone graft. The graft is procured and placed in a sterile

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container and covered with a sa!lne moistened sponge. The graft should not be submerged

in saline solution. Prophylactic antibiotic therapy should be used whenever bone grafting is planned. The graft is usually harvested from the ipsilateral lower extremity. Suitable sites for harvesting autogenous bone graft material include the iliac crest, greater trochanter, proximal and distal tibia, calcaneus, fibula (midshaft is almost all cortical), and rib. Donor site morbidity is a notorious complication, and occurs in up to 25-45% of cases wherein the iliac crest is used to procure autogenous corticocancellous bone, and pain at the donor site has been reported to last up to 5 years postoperative. Furthermore, the use of autogenous bone increases operative blood loss, duration of anesthesia and surgery, wound complications related to a second operative site, including nerve entrapment

Healing of bone grafts.--bone graft healing requires mechanical stability, vascularity, and close contact between the graft and recipient site. Incorporation takes place by means of creeping substitution between viable bone and graft. Chondrogenesis and angiogenesis take place by 5-7 days, and calcification occurs by 10-14 days, and osteoblasts lay down osteoid from 15~50 days. Vascular in growth occurs over an approximately 2 em distance by 6-10 weeks, while mineralization occurs over approximately 1 em in that same time period, and it takes about 3-4 months to fully mineralize. Non~weight bearing may be required for 3~4 months, and electrical or low-intensity ultrasonic bone growth stimulation may be helpful. Complications of bone grafting include a failure rate reported to be 15-20%. Failure to incorporate is usually due to inappropriate application or graft selection, and mechanical instability. Whenever grafting a nonunion site, or in cases involving prior wound sepsis, an autogenous graft is preferred. Allografts and alloimplants function best as a spacer for in growth of vessels and new bone. Allografts and alloimplants may convey immune incompatibility in rare cases, however they are sterile and readlly avallable without creating another wound in the host tissues. Composite bone grafting employs both autogenous and allogeneic graft materials.

Bone graft substitutes------alternatives to autogenous bone alone include: 1) extenders, which consist ofosteoconductorthat serves to increase the volume of graft in addition to the usual autogenous graft (osteoconduction); 2) enhancers, which consist of osteoconductor and osteoinductor, and serve to expand volume and recruit stem cells; and 3) substitutes, which convey osteoconduction, osteoinduction, and osteogenesis, and replace bone. Osteoconductors serve to mimic trabecular bone, with pore sizes that range from 100-1000 microns. These are available in different forms, and vary in strength ranging from weak tricalcium phosphate and calcium sulfate {more porous, rapidly incorporation) to stronger (more dense, slower incorporation) coral hydroxyapatite and calcium carbonate. The pores serve as a scaffold upon which stem cells and blast cells adhere, and capillary in growth is promoted. These are often sterile and noninfectious and nonimmunogenic, if totally synthetic. However, they are usually combined with allogeneic material to induce bone healing. Osteoinductors include demineralized bone matrix (DBM), which contains chemotactic BMP 7 (osteogenic protein 1) and BMP 3 (osteogenin); as well as transforming growth factor B, which converts undifferentiated stem cells to chondro- and osteoblasts; as well as other growth factors (insulin-like GF, fibroblast GFs, platelet-derived GF, granulocyte colony stimulating factor, and others). These are antigen~extracted allogeneic, and treated with either electron beam or gamma ray sterilization. Combinations of osteoconductor with osteoinductor come in different forms, including crunch (DBM + cancellous chips), flexible gel strips and sheets, paste, and putty. Osteogenesis requires

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mesenchymal stem cells, chondroblasts (enchondral bone formation), fibroblasts (collagen), and osteocytes. A bone marrow aspirate, preferably from the proximal tibia,

femur or ilium, can be obtained by aspirating with a Jansheedy needle in 4 cc increments, with sequential advancement across the metaphysis; or aspirate 2 or more separate sites

and centrifuge to concentrate the MSCs. SELECTED ENDOSCOPIC TECHNIQUES Endoscopy involves the use of fiberoptic cameras and small surgical instruments to

evaluate and treat the intra-articular and periarticular compOnents of a joint, as well as other corporeal spaces. Endoscopy has been shown useful in the ankle, however subtalar and metatarsophalangeal arthroscopy can also be undertaken. Moreover, endoscopic plantar fasciotomy has been shown to be useful is certain cases of recalcitrant plantar fasciitis and heel spur syndrome, and it has been experimentally used for sectioning of the deep transverse ~ntermetatarsalligament in the treatment of intermetatarsal neuroma, as well as neurectomy and tarsal tunnel decompression. The value of endoscopy in making an accurate diagnosis of joint (ankle) pathology is well-established. Arthroscopy is indicated when CT and MR imaging remain equivocal, or when these studies indicate the need to biopsy or manipulate intra-articular structures. Endoscopic techniques have advanced a great deal in the past 35 years, and the application of Tiber optics, smaller systems, and intra-articular laser ablation have contributed to newer approaches to long recognized pathologies such as joint instability and cartilage degeneration.

Ankle atthroscopy--this can be used in both acute and chronic conditions of the joint. As with any surgical intervention, proper patient evaluation (H&P) is prerequisite to arthroscopy. Clinicallabtesting, including CBC and differential, ESR, rheumatoid factor, and other indicators of arthritis may be indicated. Non-invasive imaging and testing includes standard and stress radiographs (anterior drawer, inversion stress) radiographs, CT scan, MRI, bone scan and/or other radionuclide imaging, and possibly an arthrogram ortenogram, may be indicated prior to making the decision to intervene arthroscopically. The potential benefits of arthroscopic intervention must be weighed against the potential complications, and the potential benefits of open arthrotomy should be considered. In general, arthroscopic indications increase with thE) ski!! ofthe surgeon, however adequate exposure and completion of the job at hand should not be compromised by the decision not to open the joint in a traditional fashion. Complications related to arthroscopy are the same as those of open surgery, however there is potentially less likelihood of infection and damage to surrounding vital and connective structures. This, in turn, implies the potential tor less joint fibrosis and a faster rehabilitation. Infection, nerve injury and RSDS, excessive joint distraction, hematoma, phlebitis, recurrent deformity and/or pain, and painful scar have been encountered following arthroscopic surgery. Instrumentation for ankle arthroscopy-small joint arthroscopic instruments have improved a great deal since their introduction in the late 1970s. The arthroscope consists of an eyepiece and a lens that is introduced into the joint. Fiberoptic systems enable the confines of the joint to be explored and viewed videographically. Cannulas serve as portals through which instruments, the video camera, and a light source are passed. Power instruments include osteotomes, shavers and abraders; and more recently the laser and radiosurgical instruments. Hand instruments include osteotomes, probes, curettes, knives, punches,

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135

rasps, forceps, staplers, suture drivers, and magnetized rods. Adjunct instruments include distractors, both invasive and noninvasive, and the pressurized distention system. Arthroscopic ankle anatomy------anatomic considerations pertinent to ankle arthroscopy

include topographical landmarks and internal joint structures. Vital structures, including vessels and nerves, as well as the tendons and ligaments about the ankle are marked on the skin surface. Portals of entry for the ankle include: anteromedial, anterolateral,

anterocentral, posterocentral, posterolateral, and accessory portals (Figure 6-4). The posteromedial portal is avoided for fear of neurovascular injury. The posterocentral portal perforates the Achilles tendon. Ankle anatomy is subdivided into anterior and posterior joint pouches. The anterior joint pouch contains the medial, anterior, and lateral gutters. The medial gutter contains the medial malleolus, medial margin of the talus, anterior talotibial ligament !the floor of the medial gutter), and the posterior talotibial ligament Iseen upon application of valgus stress). The anterior gutter (anterior ankle) contains the anterior tibial margin !lip), medial ankle bend, medial talar shoulder, tibial synovial recess, tibial plafond, tibial capsular reflection, talar sagittal groove, lateral talar shoulder, tibiofibular synovial recess and synovial fringe, and the anterior-inferior tibiofibular ligament The lateral gutter contains the lateral talar articular surface, medial fibular articular surface, anterior tibiofibular ligament IATFL), and the posterior talofibular ligament (seen upon application of varus stress). The posterior joint pouch, when viewed through the sagittal groove, contains the posteriortibiofibular ligament, posterior capsular surface, medial ankle bend, medial gutter, and the posterior talar dome. When viewed through the posterolateral portal, the posterior joint pouch contains the posterior tibial margin (lip), posterior talar dome, talar sagittal groove, posteriortibiofibular syndesmotic ligament, labrum media ankle bend, medial malleolus, and the posteriortibiotalar ligament Ankle arthroscopy allows the surgeon to address a wide range of joint pathology (Table 6-4). Soft tissue maladies amenable to arthroscopic inspection and manipulation include meniscoid ligaments (Collin's lesion), capsular adhesions, fibrous bands, and synovitis. It is possible to do an adequate ankle synovectomy in patients with rheumatoid arthritis, entirely via the arthroscope. The articular surtace may be treated for chondromalacia, subchondral erosion, and other chondral defects. Amenable bone pathologies include

Posteromedial

Figure 6.4

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osteochondral lesions and subchondral bone cysts. Other pathological ankle conditions amenable to arthroscopic intervention include transchondral talar dome injuries, avulsion

fractures of the medial, posterior, and lateral malleoli; ligamentous and capsular repair; talotibial exostosis, fractures of the tibial bearing surface and margin (lip); foreign body retrieval, joint biopsy, and ankle arthrodesis (perhaps in conjunction with a trans-Achilles portal, medial malleolar osteotomy, and cannulated screw fixation), can be undertaken by means of arthroscopy. Although applicable to the treatment of many conditions ofthe ankle, arthroscopy is particularly useful in the treatment of osteochondral defects and torn cartilage. Because small portals are used to access the joint, recovery after arthroscopy is often more rapid than that following open arthrotomy, and complications are generally considered to be less likely. It may be possible to repair ta!ar dome and tibial bearing surface fractures without osteotomlzing the malleoli. Despite the use of smaller incisions, ankle arthroscopy still conveys a risk of infection, hematoma, nerve injury, and damage to intact articular structures, and there are associated risks related to anesthesia and tourniquet use. The postoperative course may involve non-weight bearing and immobilization, depending upon the specific reconstruction undertaken, however early return to weight bearing and ROM rehabilitation exercises are the norm.

TABLE 6-4. ClASSIFICATION SYSTEMS FOR CHONDROMALACIA. System Collins

Goodfellow

Bauer & Jackson

Subcategories Grade I Grade II Grade Ill Grade IV Superficial Type I Type II Type Ill Type IV Deep Type I Type II Type Ill Type IV Type 1 Type 2 Type 3 Type4 Type 5 Type6

Description of cartilage defect Fraying Fibrillation and fissure Deep, extensive fissure Full thickness defect Shallow erosion loss of superficial layer Exposed subchondral bone Exposed deep matrix Cartilage softening Blister formation Exposed matrix Exposed bone linear crack Stellate fracture Flap defect Avulsion with exposed bone Fibrillation Fibrillation & subchondral erosion

like most surgical maneuvers, arthroscopy requires training and repetition to become fluent and successful in its application. After achieving satisfactory surgical anesthesia, instrumentation is delivered into the joint via tubes placed through the small incisions, at various locations about the ankle. Typically, the arthroscope, various instruments, and suction are employed simultaneously. Specific operative interventions include joint inspection, chondroplasty, synovectomy, biopsy, fragment excision, subchondral bone plate perforation or microfracture, instillation of medications, graft and suture placement, application of fixation devices, and other maneuvers as indicated by the pathology at hand.

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137

Specific procedures amenable to arthroscopic application include: debridement and

fragment removal' for repair of anterior ankle impingement, excision of ost8ochondral fragments, abrasion chondroplasty, excision and repair of anterolateral gutter meniscoid ligament, and release of posttraumatic arthrofibrosis. Most of the time, patients are positioned supine, with the ipsilateral knee flexed at90°,

for ankle arthroscopy, although the specific position can vary with the needs of the procedure and anesthesia. The joint is usually distracted (.... 1.5 mm) using the sterile

noninvasive foot strap and approximately 25 pounds of tension. Distraction forces >30 pounds, or for periods >1 hours, may cause dorsal cutaneous and/or anterior ankle neuropraxia, although this can result from even lesser force and duration, and each patient should be assessed forth is in follow-up after the anesthesia has subsided. An ingress pump, set to 45-50 mm Hg pressure, and egress suction can be used to maintain a continuous flow of saline through the articular cavity. The egress line may be fitted with a filter to procure particulate matter flushed from the joint during the arthroscopic procedure. The 2.7 mm arthroscope is ideal, however a 4 mm arthroscope can also be used. The 3.5 mm shaver works well in most cases of ankle arthroscopy. The instruments are introduced to the articular cavity by means of a transdermal incision made with a #15 blade scalpel. The scope is usually positioned, initially, through an anteromedial portal situated medial to the tendon of tibialis anterior at the level of the tibiotalar interface. Care should be taken to avoid injury to the large saphenous vein and nerve. After penetration of the skin, an 18-gauge needle is used enter the joint, and saline is infused through this cannula. After instilling saline into the joint, an anterolateral portal, situated immediately lateral to the intermediate dorsal cutaneous branch of the superficial peroneal nerve and the tendon of peroneus tertius, is made using the scalpel and 18-gauge needle. It is helpful to tent the soft tissues and to transilluminate the skin and subcutaneous tissues wh:h the arthroscope, in order to inspect for the course of any nerve in the area of the planned placement of the anterolateral portal. After making the standard anterior portals, a systematic inspection of the articular cavity includes identification of the deltoid ligament and medial malleolus, the joint space between the talar dome and the medial malleolus !medial gutterL the dome of the talus, the distal tibial bearing surface, the anterior joint cavity (anterior gutter), and the syndesmosis between the distal tibia and fibula (anterior talofibular ligament, anterior and posterior tibiofibular ligaments, and the associated talar and fibular articular surfaces). The endoscope (small arthroscope) can also be used to inspect and manipulate other joints and cavities in the foot, including the STJs, first metatarsophalangeal joint, pre-Achilles space, intermetatarsal spaces (sectioning of the deep transverse intermetatarsalligament), proxima! plantar fascia (endoscopic plantar fasciotomy), and other areas depending upon the surgeon's skills and the patient's needs. Generally, the diagnostic and therapeutic benefits related to implementation of the endoscope diminish as the joint or cavity decreases in size, primarily due to technical limitations related to the size ofthe instrumentation and the surgeon's skills.

LASER SURGERY A variety of surgical lasers are used today, however the C02 laser remains the mainstay in cutaneous and musculoskeletal surgery in the foot and ankle. Fundamental physical properties of laser surgery are based on Planck's quantum mechanics and Einstein's stimulated emission theories. LASER stands for Light Amplified Stimulated Emission Radiation. Laser light is monochromatic and coherent, wherein all of the light waves line up


138

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so that the peaks and troughs are equidistant in space and time. The laser beam

\electromagnetic radiation) is characterized by its frequency (Hz, or cycles per second), wavelength (nanometers), time of application (milliseconds to picoseconds), power density (watts per cm 2), and amount of energy delivered to the tissues (joules, or watts per

second). The coherent light is collimated by the flberoptic or articulated arm delivery

by the operator. The time of exposure to the laser beam is controlled by gating the delivery system to allow passage of light as a continuous beam, a

system, and can be aimed

single pulse, or repetitive pulses varying from milliseconds to picoseconds. The interval between pulses allows the tissue to dissipate energy as heat, with the minimal thermal relaxation ratio being 1:10 on:off. Ttssue absorption varies primarily with the wavelength and tissue type, wherein light with a shorter wavelength has higher energy, and therefore penetrates deeper or creates more heat in the same tissue. The specific wavelength is determined by the specific element or elements used in the "active lasing media." The lasing, or active media may be (with helium and nitrogen), or Nd-YAG (neodymium with yttrium, aluminum and garnet), or other elemental gases. Tissue interaction with laser light varies from one tissue type to another. For instance, skin and soft tissue may readily vaporize, while bone and cartilage heat up and their protein content denatures with resultant necrosis, in response to the same laser beam. lt is therefore important to select the proper laser and settings for the tissue being manipulated. In foot and ankle surgery, the a variety of lasers may be useful (Table 6-5).

co,

TABLE 6-5. TYPES Of LASERS USED IN FOOT AND ANKLE SURGERY.

Laser C02

Holmium-VAG non-contact tip Nd-YAG non·contacttip Nd-YAG contacttip

Characteristics and applications Far infrared wavelength, readily absorbed by water and therefore only used for superficial (0.1 mm) penetration such as cutting, ablation, and coagulation of skin and nail lesions Middle infrared wavelength, absorbed by bone and cartilage, penetrates 0.4-0.6 mm, and used for lesion ablation in more dense tissue Near infrared wavelength, poorly absorbed, penetrates 6-8 mm, deep lesion ablation and coagulation Near infrared wavelength, penetrateS 5~200 microns, superficial cutting or incision

KTP (potassium, titanium, phosphate) non-contact tip

532 micron wavelength, absorbed by dermal vessels and superficial lesions such as verrucae, penetrates 0.5 mm in pigmented skin and up to 4 mm in nonpigmented skin, used for ablation

KTP contact tip Argon non-contacttip

Penetrates 1-2 mm, used for incising skin 488-514 micron wavelength, penetrates 0.5-1 mm, absorbed by dermal vessels and superficial skin lesions such as verrucae, used for ablation of dermal lesions

Cu vapor, non-contact tip

478 micron wavelength, penetrates 0.5-1 mm, absorbed by dermal vessels and superficial skin lesions, used for ablation of dermal lesions

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139

Safety with lasers-------laser safety entails special attention to instrumentation, eye protection and personal shielding, vapor evacuation and filtration, and aiming technique. ANSI publication 136.3 serves as a standard reference for laser safety. Specific eye safety precautions vary with the wavelength of the laser beam as follows:

Class !-direct visualization of the beam does not cause ocular damage Class 11-prolonged direct visualization will cause ocular damage

Class Ill-direct visualization causes immediate ocular damage Class IV-directvisualization causes immediate, severe ocular damage ranging from corneal burn to retinal ablation and blindness All medical lasers are categorized as Class IV. They pose a fire hazard, damage the unprotected eye, and are harmful to unprotected skin. Damaging effects can be caused by director reflective laser exposure. Smoke plume evacuation systems should entail vacuum suction atthe point of creation, and 0.2 micron dual filtration with carbon. Personnel in the OR should wear proper body and eye protection, and a filtration mask. The door to the OR must indicate the presence ofthe medical laser potential hazard.

Specific /aserprocedure~surgicallasertechniques are used primarily for lesion ablation and soft tissue dissection (Table 6~6). As with any other form of dissection or tissue ablation (scalpel, radiosurgery, cryotherapy, coblation), violation of the dermis results in tissue repair with scar formation. Incisions are made with a focused beam directed in a repetitive, linear fashion. Lesion ablation is achieved with a defocused beam directed in a cross-hatched linear or back-and-forth fashion, or in an ever-increasing radial circle fashion beginning centrally in the lesion. Periodic curettage may assist lesion ablation, as non~vaporized eschar may accrue. It should be noted that, with the exception of skin lesions, lasers are generally used to assist with dissection and lesion ablation, while standard techniques of dissection and arthroscopy are employed to expose lesions and underlying target structures. Patients should understand this concept of "laser assisted" surgery. Appropriate lesion biopsy should be obtained prior to laser ablation. Appropriate sterile bandage, with topical application of silver sulfadiazine cream, and follow-up are part of the aftercare.

TABLE 6-6. COMMON LESIONS AND PROCEDURES AND APPLICABLE lASERS. Lesion

Laser

Verruca

CO,, Argon, Nd-Yag, KTP

Cavernous hemangioma

Nd-YAG bare fiber

Hypertrophic scar or keloid Cutaneous granulomatous lesion

co, co, co,

Nail matrix ablation

C02, Argon, Nd-YAG

Synovitis, scar, chondromalacia, osteophyte

Holmium-VAG

Tattoo removal

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Ch. 6

MICROSURGERY Microsurgical techniques are valuable when manipulating peripheral nerves, veins and arteries. These techniques can be used in cases of trauma, peripheral neurosurgery (neuroma, tarsal tunnel, nerve entrapment), plastic reconstructive surgery (flaps), or

whenever magnification ofthe surgical field is desired. Magnification can be achieved with the operating microscope (4-30x) or, more typically, by means of Ioupe magnification (2.5-16x). Loupes also enhance inspection of the surgical field when foreign body exploration is undertaken. Microsurgical instruments, namely forceps, scissors, and

needle holders, enhance the surgeon's ability to manipulate structures under magnification. Typical suture gauges include 7-0 to 9-0 nylon. Specific vascular and neurological repair techniques are learned and practiced in residency and fellowship training, and microsurgical techniques courses.

SELECTED TENDON LENGTHENING AND TRANSFER PROCEDURES Balance of muscle power-all of the joints of the foot and ankle are influenced by the muscle~tendon units that cross each joint. The ultimate position of a functional joint, both at rest and during function, is determined primarily by the forces created by the muscle~ tendon units acting upon the faint An accurate clinical assessment of the strength of the muscle(s) in question must be documented. Every time a muscle~tendon unit is manipulated (transferred), there is a change in the overall balance of the joint. To effectively restore function, deforming influences must be removed and it may be necessary to stabilize (arthrodesis) deformed or dysfunctional joints upon which the transferred tendons can work (e.g. it is common to combine triple arthrodesis with major tendon transfers crossing the ankle). Furthermore, there is only a fixed amount of power available to influence a joint, and the total amount of power cannot be increased via transfer. One can expect at least 1/2 grade decrease in strength following tendon transfer {see manual muscle strength testing, in the section describing diagnostic techniques). Rarely would a muscle weaker than grade 4 be considered for transfer, unless another tendon transfer augments it. Only a muscle~tendon unit of satisfactory strength and range of contraction is suitable for transfer.

Muscle and tendon anatomic and physiologic factors~see Chapter 1

Atraumatic tendon surgical technique-specific methods exist for handling tendon, all of which are meant to enhance healing and ultimate function. These include: A. Maintain tendon moisture (avoid desiccation) B. Prepare the recipient site for transfer prior to harvesting the tendon; C. Establish physiological tension in the transferred tendon (See Blix curve); D. Use available, naturally occurring tendon sheaths and retinaculae to direct and maintain the course of the transferred tendon; E. Preserve the vascular supply to the transferred tendon by avoiding excessive traction on the muscle belly, or overcrowding tendons within a sheath or fibroosseous tunnel or hiatus in the interosseous membrane of the leg; and F. Enhanced rehabilitation based upon an understanding of tendon healing.


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141

Blix Curve---depicts the relationship between muscle length and strength of contraction, and shows that physiologically a muscle's ideal resting length allows for optimum strength of contraction (Figure 6-5).1n Blix's contractile force curve, the actual contractile force of muscle is greatest at about 120% of its resting length. Tension falls off markedly in both directions, indicating that muscle must have optimum length for function, and deviations

from this length will reduce the contractile force of the muscle. A muscle subjected to excessive resting tension will undergo fiber degeneration, while inadequate tension predisposes to muscle weakness. Muscle tensile strength is approximately 75 psi, while tendon tensile strength is 8,600-18,00 psi. Comparing tension versus length, as the length increases beyond resting length, tension increases up to a point after which tension decreases as the muscle belly fails to sustain force. Thereafter, tension actually rises as the strength of the tendon, not the muscle, sustains the load. In some cases, it may be desirable to use the transferred tendon as a sling or suspensory ligament, and not a gliding, functional tendon. Direction of pu/.1-:-the direction of pull determines the influence of the transferred tendon on affected joints. The effect of various tendons on the foot and ankle can be schematically summarized in Figure 6-6. Tendon anchors and reattachment techniques include the hole and button, hole and bone plug, 3-hole intra osseous, 2-hole intra osseous, side-to-side, Bunnell, lateral trap, and various commercially available anchors (Statak'M, Mytek®, Permanent Bone Anchor®, and Tenodesis"" Screw System Ontetference screw), to name a few). Complications-complications of tendon transfer may include muscle spasm (diazepam is useful in the early postoperative phase), stenosing tenosynovitis and adhesion, overcorrection, under- correction or weakness, loss of correction, bowstringing, and neNe entrapment.

Inversion

)Eversion

'""':::-

EHL

'

0

TA

'

t

'' '

Total tension

'

Dorsiflexion ----.

I

~I

"

I

c

'6, 1:' Contractile

-~

~

0

~

i

;::,1

~:

.,

CI:I

force

AJ\ _/ Plantartlexion

I 1 1

/

Passive /\ strength)' /

_ _......-

Length~

Figure 6.5

TP

Figure 6.6

EDL

0

'' '

. /

.$;'Y AJ

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Ch.6

Tendon lengthening procedures-these include the open Z-tenotomy, which is commonly used on the long digital extensor when correcting a hammertoe with a significant MTPJ contracture. Ankle equinus is corrected using the gastrocnemius recession or lengthening of the entire tendoAchlllis. The Baker tongue-in-groove gastrocnemius recession is used when the Silverskiold test reveals limited dorsiflexion only when the knee is extended, indicative of gastrocnemius tightness. The tendoAchillis lengthening (TAL) is used when the Silverskiold test reveals limitation of ankle dorsiflexion with the knee extended and flexed, indicative of gastrosoleus equinus. The TAL is commonly performed as an open frontal plane Z-lengthening. Common Tendon Transfers

Jones Suspension (figure 6-7) Goals-eliminate cock-up hallux, enhance ankle dorsiflexion Indications-cock-up hallux, weak tibialis anterior, loss of sesamoid function Adjunct procedures--hallux IP arthrodesis, Heyman-Janes panmetatarsal suspension Complications-recurrence of deformity due to tendon regeneration Attercare-BK weight bearing cast 2-3 weeks Hibbs Suspension (Figure 6-8} Goals-decrease MTPJ buckling and increase ankle dorsiflexion Indications-anterior weakness (mild), flexible anterior cavus with extensor substitution, claw toes often with associated IPK Contraindications-posteriorweakness, weak interossei, gross EDL weakness, structural rigidity, osseous instability Aftercare-BK weight bearing cast 4-6 weeks Tibialis Anterior Tendon Transfer (TATT) (figure 6-9) Goals-decrease forefoot supinatory twist, increase true ankle dorsiflexion Indications-recurrent clubfoot, flexible anterior cavus, dropfoot (GMT) Contraindications-excessively weak TA (<4), pes valgus, weak PL, severe anterior cavus with clawtoes Aftercare-BK weight bearing cast 3-4 weeks Sp/it1ibialis Anterior Tendon Transfer (STATT) (Figure 6-10) Goals-increase true ankle dorsiflexion, decrease long extensor swing phase overload, and decrease adductocavovarus forefoot deformity Indications-flexible anterior cavus, extensor substitution, c!awtoes; spastic posterior ankle equinus, equlnovarus (CP), anterior weakness dropfoot, flexible cavovarus, overpowering inverters Contraindications-excessively weak TA (<4), pes valgus, weak PL, severe anterior cavus with c!awtoes Aftercare-BK weight bearing cast3-4weeks

Ch.6


143

Figure 6.8

Figure 6.7

A

c

Figure 6.9

144


------------------~

Ch.6

------------------~

1. Suitable case 10. Atraumatic technique

I 2. Understanding the anatomy

3. Supple local-11:1);1'5' I tissue

necessary

c 11. Preserve blood supply and innervation

12. Adequate
9. Preserve the gliding mechanism

D

14. Careful postoperative management

E

Figure 6.10 Tibialis Posterior Tendon Transfer (TPTT) (Figure 6-11I Goals-eliminate dropfoot, eliminate flexor substitution (triceps surae weakness) Indications-anterior muscle weakness, dropfoot, non-spastic equinovarus, recurrent clubfoot peroneal nerve palsy (CMT), and triceps surae weakness Contraindications-spastic TP, pes valgus, rigid clubfoot Technical considerations-interosseous window aperture, phase conversion, often combined with arthrodesis Aftercare-BK cast3weeks non-weight bearing, then additional3 weeks weight

bearing, begin ROM at4weeks Peroneus Longus Tendon Transfer (PLTT) (Figure 6-12) Goals----increase ankle dorsiflexion, eliminate PL cavus influence Indications-anterior muscle weakness, dropfoot, and flexible cavus Technical considerations-easy phase conversion, caution sural and intermediate dorsal cutaneous nerves Contraindications-posterior weakness, pes valgus

Aftercare-same as forTPTI (above)


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A

c Figure 6.11

Figure 6.12

E

F


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Peroneus Brevis into Talus Tendon Transfer (PBIT)

Goals-suspend talar neck, eliminate flexible vertical talus Indications-type I vertical talus, severe pes valgoplanus Contraindications-rigid pes valgoplanus, immature talus, or compromised talar neck circulation Technical considerations-may be combined with closing adductory wedge osteotomy oftalar neck, medial arch tendosuspension (McGiamry-Young), and Evans lateral column lengthening

Aftercare-up to 8 weeks, BK cast, non~weight bearing Murphy Anterior Advancement ot the TendoAchil/is (Figure 6-13) Goals-eliminate spastic posterior ankle equinus, shortens ankle lever arm 48% and MTPJ lever arm only 15% lndications-CP induced dropfootwith triceps surae contracture ankle equinus Contraindications-osseous ankle equinus Technical considerations-heel prominence, routing deep to FHL, McGiamry modification involves medial-to-lateral intra osseous suture through calcaneus, recurrent deformity, and weak propulsion Aftercare-up to 5-6 weeks, BK non-weight bearing cast with ankle and STJ neutral

Figure 6.13

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INTERNAL SKELETAL FIXATION Fracture, or osteotomy stability is determined by intrinsic and extrinsic factors. Intrinsic factors include fracture configuration, and bone composition and quality. Certain fracture configurations are intrinsically more stable than others. A transverse fracture is said to be intrinsically stable, whereas a greenstick or torus fracture is said to be potentially stable, and a spiral or comminuted fracture is said to be unstable. Unstable fractures tend to displace when subjected to an axial load, resulting in shortening. Metaphyseal cancellous bone fractures are generally more stable than cortical diaphyseal fractures due to the composition of metaphyseal bone yielding more friction between the fragments. Healthy bone stock without osteoporosis, provides intrinsic bone quality that enhances internal fixation device.purchase and fragment stability. Extrinsic factors that affect stability relate to surrounding soft tissues, including: 1) tendons, ligaments and periosteum-which either aid manipulation and reduction of a fracture, or prevent successful reduction due to interposition between fragments; 2) when multiple fractures exist, soft tissue attachments between larger fragments can be instrumental in providing satisfactory realignment and stabilization; 3) vassal rule (phenomenon)-fixation of the dominant fracture affords stabilization of the subordinate fracture, as classically depicted with reduction and stabilization of the lateral malleolus and subsequent spontaneous reduction of the posterior malleolus in certain ankle fractures; and 4) extrinsic mechanical forces that affect fracture stability include bending, torsion, shear, and axial tension and compression. Cortical bone tends to fail {fracture) on its tension surface. The goals of internal fixation include anatomic reduction, stable internal fixation, atraumatic technique with vascular preservation, and active mobilization in the postoperative phase in an effort to avoid cast disease and fibrosis. Internal fixation devices do not effect faster bone healing, however they create compression between fracture fragments which, in turn, increases friction and enhances stability, the result of which is improved healing without complication {less likely not to heal). Biomaterials used for skeletal fixatio~a number of biomaterials are suitable for skeletal fixation. Key features of metallic biomaterial alloys include strength, ductility and malleability, and corrosion resistance. The basic composition of surgical stainless steel (316L [low vacuum] or 316 LVM [low vacuum remelt]) consists of iron, with carbon added for hardness (carbon steel), and molybdenum, nickel, and chromium added to enhance workability and application to bone fixation {these elements make the alloy less brittle), and to impart resistance to corrosion. Chromium oxide forms the surface passive layer that resists loss of metallic ions in the aqueous environment of the tissues. Specifically, most of the implantable fixation metals come in the form of Austenitic stainless steel. Cutting edges and some wear surfaces are composed of Martensitic stainless steel, which is harder and less malleable and less ductile. Cobalt-chromium alloys are. also particularly resistant to compression and shearing wear and, as such, are often used in the fabrication of he wear surfaces of joint endoprostheses. Titanium (99% pure) also serves as a useful metallic implant, due to its ductility and malleability, a Young's modulus that is suitable for skeletal fixation, and a passive tiTanium oxide passive layer that readily forms and resists corrosion. Although surgical stainless steel and titanium implants are both considered appropriate for permanent implantation, titanium is generally considered more appropriate for such use due to its inert nature. As a rule, dissimilar metals should not be placed in direct contact, due to the risk of galvanic corrosion. Other forms of corrosion include fretting between hardware

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components that are in direct contact, such as the interface between the land at a screw head and screw hole of a metal plate. Resorbable forms of fixation are often composed of poly IL·Iactide) acid IPLLA) or poly·p-dioxanone IPDS).

Splintage-----this is commonly used to effect fracture or osteotomy stability. Splintage generally does not create rigidity, an.d secondary or callus healing is usually noted. K-wires and Steinmann pins, as well as stainless steel wire suture and staples are usually used for splintage. K-wires range in diameter from 0.035-0.062 inches, with the 0.045 and 0.062 inch wires being used most commonly in the forefoot Steinmann pins are larger, with the most frequent sizes used in the hindfoot and ankle being 0.078 inches or larger. Advantages of single pin fixation include application when dealing with small fragments and physeal plates. Disadvantages include poor resistance to distraction and rotary forces, however this can be diminished by using additional pins in divergent directions; and the tendencyfor smooth pins to migrate upon weight bearing or motion. Pin stability can be enhanced with proper bending and burying, or with bandaging when the pin exits the skin. Threaded K-wires offer resistance to distraction and pull out, but care must be taken to prevent separation of the fracture fragments as the far fragment is penetrated. This is accomplished by compressing the fragments together (preloading) prior to positioning the wire across the fracture or osteotomy. Repetitive three-point bending, or pin flexure, can cause metal fatigue and wire failure. This is more likely in narrower and threaded K-wires. Use of a built-up surgical shoe, or non-weight bearing, may be needed to prevent pin failure. Stainless steel wire suture can also be used to effect splintage. Wire size is measured in gauges from 18 to 30 l!arger numbers" smaller gauges). with 18 and 24 gauge wire being commonly used in foot and ankle surgery. Wire fatigue and failure can occur with repetitive or excessive twisting or bending. Proper instrumentation, including use of a wire twister, decreases the likelihood of inadvertent wire breakage. Application of an intra osseous wire loop can be used to stabilize small fracture fragments in bones with thick cortical walls Ito prevent pull through). Wire loops should be placed perpendicularto the fracture and at 90° to each other for maximum stability (double box wire loops). Cerclage wire is used to prevent telescoping of an oblique diaphyseal fracture, or as a gathering influence to control small fragments when used with other forms of fixation (plates and screws). Stainless steel wire suture can be used for: 1) intraosseous wire fixation, 2) cerclage wiring (circumferential placement around a diaphysis), and 3) tension banding. Staple fixation can also be used to effect splintage. Staples are designed to be used almost exclusively in cancellous bone, and cortical bone should be predrilled to avoid fracture during staple placement. Staples resist distraction forces across the osteotomy or fracture, but do not withstand shearing or bending forces very well. Two staples oriented at 90° apart provide excellent stability. During staple insertion, the surgeon should use a minimum of mallet strikes in an effort to prevent loss of contact between the bone and staple. A staple extractor set is needed to remove a staple that has been properly seated against the cortex. Absorbable fixation pins can also be used to achieve splintage. Bioabsorbable fixation devices have become popular and they are particularly useful for treatment of osteochondritis and chondral fragments, as well as for use in metatarsal osteotomy fixation. Poly-p-dioxanone IPDS), and poly IL-Iactide) acid (PLLA). are useful bioabsorbable materials that come in a variety of forms for bone fixation in the foot and ankle. These materials have been shown to be biocompatible and safe, even in the phalanges when used for arthrodesis and fracture stabilization. They are radiolucent and can be used in

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diameters that yield an elastic modulus similar to that of bone IPLLAI, enable loading in standard wire drivers, allow for cutting with a bone sectioning forceps or scalpel, and

degrade in a predictable fashion with creeping bone substitution. OrthoSorb® pins (DePuy division of Johnson & Johnson, New Brunswick, NJ) are made of PDS, and they are available as straight pins in 1.3 mm and 2.0 mm diameters, as wei! as a tapered pin that is swaged to a metallic guide pin. The.Arthrex®Trim-lt Pin"' and Trim-It Drill Pin'" IArthrex, Inc., Naples, Florida) are made of PLLA and are available as a 1.5 mm pin, and a 2.0 mm pin with a metal cutting tip.

Rigid internal fixation-rigid fixation provides absolute stability and promotes primary (non-callus) bone healing. Rigid internal fixation can be achieved with interfragmental compression screws, plates, and tension band wires.lnterfragmental compression is either static or dynamic. Static interfragmental compression is achieved when tension is placed upon a prestressed implant that in turn converts the tension to compression at the osteotomy or fracture interface, and is best represented by the interfragmental compression screw. Contact of the screw head with the near cortex, and purchase of the distal cortex with the screw threads, places tension along the screw shaft as the threads try to pull (!a g) the head into the bone. The screw resists this axial tensile force and, in turn, imparts compression across the bone interface. Dynamic interfragmental compression employs a combination of static force in conjunction with physiologic loads that naturally occur about the part in question, thereby effecting compression across the fracture interface. The classic example of this is the fractured patella, wherein a tension band wire is place across the transverse fracture on the anterior (tension) surface and the knee slightly flexed to convert the tension in the wire to compression between the fracture fragments. Lag screw---this fixation device is used to achieve static interfragmental compression. A lagged screw is one that engages only the far fragment with its threads. Compression occurs as the head of the screw contacts the near cortex and the threads purchasing the far fragment pull the fragments together. The screw itself then sustains tension throughout its mass, as the thread end and head are relatively pushed apart by the bone cortices. The tension within the screw is, in turn, converted to compression between the fragments. There are different types of lag screws, including partially and fully threaded cortical screws and cancellous screws. Cortical screws have a finer thread pitch, thereby increasing the number of threads purchasing bone per unit length of screw. Increased thread purchase increases friction between the screw and bone and, in turn, between the bone fragments. Increased friction enhances rigidity, and promotes primary bone healing. In order to create the lag effect using a fully threaded screw, it is necessary to overdrill the near cortex to create a gliding hole. The Swiss AD (Arbeitsgemeinschaft fUr Osteosynthesefragen, or Association for Osteosynthesis) screws display an asymmetrical (buttress) thread design, which increases purchase and minimizes pullout A screw's size is determined by the diameter of its threads, with the core diameter actually being less than that of the threads. Cortical screws are available in 1.5 mm,2.0 mm,2.7 mm,3.5 mm, and 4.5 mm sizes. Cancellous bone screws are only partially threaded so that overdri!ling of the near cortex is not necessary to produce interfragmental compression. The first rule of fixation states that all of the purchasing threads of a lag screw must purchase only bone of the distallfar) fragment. Threads that cross the osteotomy or fracture line can distract the fragments and maintain a gap. Cancellous screws display a wider pitch and a thinner core diameter, and sizes include 4.0

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mm, 4.5 mm, and 6.5 mm long and short thread pattern screws. Various companies make both cortical and cancellous bone screws that are cannulated, which makes for ease of placement and obviates the need to place temporary stabilization pins that can often impede placement of permanent fixation.

Screw placement-this should ideally be perpendicular to the fracture or osteotomy interface. In reality, this orientation is not always practical. When a lag screw is placed perpendicular to an oblique fracture line, axial loading can cause telescoping and

shortening (Figure 6-14). When a single screw is used, it is often helpful to orientthe screw midway between perpendicular to the long axis of the shaft of the bone and perpendicular to the fracture/osteotomy interface. Long oblique or spiral fractures, wherein the fracture length is 2~3timesthe width of the bone, are amenable to multiple screw fixation with each screw being placed perpendicularto the fracture interface at each level along the shaft The first screw should be placed centrally and perpendicular to the long axis of the bone. Secondary screws are placed on each side of the initial screw and perpendicular to the fracture line (Figure 6-15).

Screw insertion-this proceeds in a specific fashion that, as a rule, should not be altered. To achieve the lag effect with a fully threaded screw, the following sequence is used: 1. Guide hole is drilled through botlt fragments with a K-wire or a drill bit. 2. The near cortex is then overdri!!ed to the diameter of the screw to be inserted, which allows the threads to pass through the near cortex without purchasing. 3. The far cortex thread hole is then enlarged to a diameter that is less than that of the threads, and just slightly larger than the core diameter of the screw's shaft. This requires use of the concentric drill guide {T-sleeve). 4. Countersink the near cortex to fitthe undersurface of the screw head and minimize the development of a stress riser. 5. Depth gauge measurement to determine proper screw size, and add 1-2 mm to assure at least 1-2 thread purchase of the far cortex. 6. Tap (cut) the thread pattern into the far cortex to enhance buttress thread purchase, using an alternating method of 3 clockwise rotations followed by 1/2 counterclockwise rotation to periodically clear the tap flutes of cortical bone. Appropriate drill guides and tap sleeves should be used to assure proper orientation and prevent soft tissue injury ithe tap has a predilection to becoming wrapped with adjacent soft tissues). 7.1nsertscrewto 2-fingertightness.

Figure 6.14

Figure 6.15

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When inserting a partially threaded screw, the sequence is the same as just described for the fully threaded screw, with the exception of not overdrilling. Variations on the

sequence of instrumentation can be effective, however the surgeon is cautioned against this, as each step in the sequence is meant to maximize stability.

-

Plates-these offer another means of achieving rigid internal fixation and, in certain applications, can be used to achieve axial compression. In most cases, plates are used

to effect splintage and to provide protection of

~

a reduced and fixated fracture/osteotomy 1 that is already stabilized with interfragmental t compression provided by lag screws. In this way, the plate acts as a neutralization shield that sustains forces and protects the reduced and stabilized fracture from bending, torque, axial tension and compression, and shear Figure 6.16 forces. Axial interfragmental compression can only be achieved with a plate if the plate is prestressed, and the fracture is relatively transverse in orientation. An oblique fracture will shorten and displace under axial compression. In order to effect axial compression using the plate, standard 1/3 tubular plates must be eccentrically drilled \load screw principle), so that when the undersurface !countersink) of the screw head engages the plate, the plate is pushed away from the osteotomy/fracture as the screw seats into the bone and through the plate. A 1/3 tubular plate must be pre-bent prior to achieving axial compression via load screw placement Pre-bending involves bending the plate away from the bone cortex, so that as the screws seat and lag the plate to the bone, there is no tendency to gap the far cortex as the near cortex is placed under greater axial load !Figure 6-16).

-- --

Dynamic compression plate-this is thick and wi!l not allow gapping of the far cortex, and the hole/slots in the plate are designed to allow the creation of axial compression as the screws seat Whenever possible, the plate should be applied to the Tension side of tlle bone. When using the load screw technique, the first plate hole away from the fracture, after lagging the plate to the bone on the other side of the fracture, is offset drilled away from the fracture interface. Once this screw is seated, axial compression is achieved, and the remaining dri!l holes may be concentrically drilled. It may be possible to get a bit more axial compression by offset drilling the next distal screw, however it is necessaryto first loosen the first load screw prior to securing final purchase with the distal load screws. Neutralization is a method by which a relatively unstable fracture can be afforded more stability while subjected to axial compression, despite the long oblique or spiral fracture orientation. Some fractures, such as long spiral, oblique, or comminuted fractures, are simply not amenable to axial compression. lnterfragmental compression can be obtained between certain fragments using Jag screws. Once lag screw interfragmental compression is achieved, the fixation is protected from shear, flexure, and torsion about the fracture with the use of a plate to neutralize force applied to the bone. A neutralization plate can be applied using any size plate, as long as the plate is well molded. Tubular plates work best for this application. When applying a neutralization plate, all screw holes are drilled concentrically. You can use a separate interfragmental screw and you can use a lag screw through the neutralization plate.

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Buttress plating-this is used in the fixation of unstable fractures, wherein the strong (thick) buttress plate is used to maintain alignment of the fragments despite the lack of intrinsic stabilityieither tensile or compressive) within the injured bone. Buttressing precludes the use of interfragmental compression, and gap healing may occur. The buttress plate

essentially serves as a bridge between larger fragments with intervening small fragments "leaning againsrthe plate. Devitalized bone fragments should be removed and replaced by cancellous bone graft under protection of a buttress plate.

Tension band wire fixation---this usually combines the splintage afforded by two smooth K-wires with stainless steel wire tension, to effect dynamic interfragmental compression. The tension in the stainless steel wire is converted to compression at the fracture interface. This is useful at the fifth metatarsal base, malleolar fractures, and the patella. Classically, dynamic interfragmental compression is created with an eccentrically positioned tension wire used in conjunction with a load beam that converts the tension Jn the eccentric wire to compression across the fracture interface, usually requiring joint positioning that effects wire tension (Figure 6-17). A plate placed on the tension side of a fracture also acts as a tension band.

Figure 6.17

EXTERNAL SKELETAl FIXATION External skeletalfixatio~an external fixator can be used to achieve static interfragmental compression, as long as the fracture/osteotomy/arthrodesis interface is relatively transverse. A variety of external fixators are available tor use in the leg, ankle and foot. In oeneral, these devices are of uniplanar, mu!tiplanar or circular designs. They can also be miniaturized for use in the metatarsus and toes, or for focal use in the tarsus. Hybrid systems, combining uniplanar and multiplanar elements are also ava1lab!e. The devices can be used to distract and elongate bone, and to correct deformity. External fixation (EXFX) devices yie!d a great deal of stability, while allowing periodic adjustment of the compressive or distraction load. EXFX can be useful in the acutely injured patient when temporary skeletal stabilization of the traumatized extremity is required while other injuries, including head trauma, are managed. The external fixator can be used to provide interfragmenta! compression, or it can be used to splint or maintain distraction of an open, comminuted fracture. EXFX can also be used to span a joint or osseous segment that has

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been debrided or resected for the treatment of infection or neoplasm. These devices are also used for limb-lengthening by means of corticotomy and callus distraction and other reconstructive interventions for deformity correction, and have been shown is some case series to be useful in cases of Charcot reconstruction. EXFX can be achieved with unilateral ieccentric), and multiplane and circular frames. In some cases, such as those involving pilon fracture repair, EXFX can be combined with limited dissection internal fixation to effect satisfactory results. The frame is applied to the bones via pins or wires, or half pins (pin-screws), that are positioned proximal and distal to, and as close to the fracture/osteotomy/fusion interface as is possible. EXFX stability can be enhanced, and pin/wire loosening at the metal-bone interface can be reduced, by maximizing pin diameter and radial preload, avoiding overdrilling of the pin tract, and using pins coated with hydroxyapatite. Pin diameters ranging from 4.5-6 mm are uSually sufficient for fixation of the adult tibia, and the diameter of the bone should be >2/3 the diameter of the pin in order to minimize the risk of fracture. Most tibial segments can be adequately stabilized with 2-3 pins separated as far as possible within the segment, with one pin being placed as close as possible to the fracture/nonunion, bone graft interface. As a rule, 3 pins provide more stability to an osseous segmentthan do 2 pins; and, pins oriented in different planes maximize stability. The distance of the extremity to the frame should also be minimized, without compromising the adjacent cutaneous barrier. External fixators are also used to effect dynamization, wherein cyclic micromovement is produced with a lever arm at 3-6 weeks after initial stabilization, thereby stimulating callus formation (secondary bone healing) while maintaining alignment When dynamization is desired, consideration should be given to the optimal length of the frame at the time of initial application, so that shortening can be achieved when adequate bone healing has occurred.

Disadvantages of EXFX include the bulky size of the devices, and the rather high rate of pin tract infection. It can also be difficultto properly place the fixation pins, or pin-screws (halfpins), so that they do not span adjacent joints or violate neurovascular structures. As a rule, it is important to use safe zones for pin placement so that neurovascular structures are not damaged. It is also importantto try and minimize placementthrough muscle bellies, although this becomes necessary at certain locations. Pin and wire placement can be enhanced with the use of intraoperative image intensification fluoroscopy. In the tibia, proximal to the tibial tubercle and> 1 em distal to the knee joint, a safe zone extends from the posteromedial to posterolateral border of the proximal tibia. Care should be taken to avoid violation of the space immediately adjacent and posterior to the head of the fibula, wherein lies the common peroneal nerve, and the space posterior to the tibia, wherein lies the posterior tibial nerve, artery and vein. Transfixation wires can be inserted through the anterior portion of the fibular head, aiming approximately 30° lateral-tomedial into the proximal tibia to exit just medial to the patellar tendon. A second transfixation wire can then be placed from lateral-to-medial in the frontal plane, anterior to

the head of the fibula and the medial collateral ligament. When halfpins are used, they can be positioned obliquely through the medial or lateral portions of the anterior half of the

proximal tibia, or through the head ofthe fibula into the proximal tibia. Immediately inferior to the tibial tubercle, the anterior and posterior tibial arteries are vulnerable to impalement if placement of medial-to-lateral transfixation pins is attempted, or if a pin is directed into the distal aspect of the popliteal fossa or the posterior leg, therefore these methods are not recommended at this level. A transfixation wire can be directed through tibialis anterior and the anterolateral aspect of the tibia, taking care to

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avoid injuring the saphenous vein and nerve. Halfpins can also be positioned obliquely through the medial portion of the proximal tibial metaphysis. At the midshaft level of the tibia, to the junction of the middle and distal thirds of the

tibia, care should be taken to avoid injuring the tibial artery, venae commitans, and nerve located medial to the midline along the posterior surface of the tibia. Here, a transfixation

pin can be directed posteromedia!lythrough the crest of the tibia, avoiding violation ofthe posterior surface of the tibia. Again, it is important to avoid violating the saphenous vein and nerve medial to the crest of the tibia. It is also safe to place an additional wire through the anterior muscle compartment from lateral-to-medial, just posterior to the tibial crest. It is best to align these pins carefully, so as not to redirect and repetitively perforate skeletal musculature. Just proximal to the ankle, care should be taken to avoid injuring the deep peroneal nerve and the anterior tibial artery, adjacent to the lateral surface of the tibia. Placement of tran;fixation pins through the fibula should be limited to the anterior portion of the fibula, and avoid the perforating peroneal nerve lateral to the tibia, and the saphenous nerve and vein medial to the tibia. At this level, it is also useful to position a tibiofibulartransfixation halfpin through the tibia into the fibula, once again taking into consideration the position of the petiorating peroneal artery. It can also be helpful to stabilize the relationship of the foot to the leg, particularly when fracture/dislocations warrant stabilization of the foot, or when reconstructive efforts require immobilization of the ankle or protection of the foot from plantar weight bearing. Purchase of the talus can be achieved with halfpins or transfixation pins, and it is best to position these through the neck of the talus, between the talonavicular joint and the anterior margin of the posterior facet of the talus. Purchase of the calcaneus, either with halfpins or transfixation pins, should be localized to the tuberosity and take into consideration the contents of the tarsal tunnel, the STJs, and the insertion of the Achilles tendon, all of which should be avoided. When using the llizarov technique, pins/wires are positioned obliquely, and this requires elongation of the half ring with a footplate, or plates, and the addition of a distal half ring oriented perpendicular to the substrate. The foot frame can be constructed of 2 half rings that can be stabilized with a transtarsal fixation pin situated dorsa! to the plantar vault and plantar to the dorsal neurovascular bundle; or, the first and fifth metatarsals can be purchased with 2-3 halfpins. Pin (or wire) tract infections are not uncommon when many pins/wires are used, and the EXFX frame is left in place for >3-4 weeks. If the pin remains stable, and there is no radiographic evidence of radiolucency about the pin, then the pin is usually left in place and local pin tract care and, at the surgeon's discretion, oral antibiotic therapy can be useful. If the pins/wires display loosening and radiolucency, then removal and bone curettage, and implantation of vancomycin- or gentamicin-impregnated calcium sulfate (or PM MAl beads, as well as IV antibiotic therapy, may be useful therapies.

HEMOSTASIS

Anatomic dissectiort--anatomic dissection is the foundation upon which target structures and pathological anatomy are identified, tissues manipulated, and hemostasis achieved in foot and ankle surgery. Anatomic dissection enables the surgeon to avoid tourniquet application in almost any forefoot surgical case. The majority of bleeders are identified in the subcutaneous layer, superficial to the deep fascia. The process involves skin incision,

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transdermal dissection, separation of the superficial fascia and subcutaneous fat layer, deep fasdal incision, then joint capsular and/or periosteal incision. Specific capsular and deep muscular vessels are generally few and well known, and attention should be focused upon these vessels when necessary. Hemostasis is achieved via ligature application using a hand tie or instrument tie, when the lumen of the vessel is grossly visible. Electrocoagulation can be readily used for vessels with a smaller lumen diameter. Anatomic dissection is usually performed using the scalpel, however limited sectioning can be achieved with the radiosurgical electro-sectioning unit

Dilute vasoconstrictor (epinephrine~dilute epinephrine can be used to enhance hemostasis in certain cases when indicated. Epinephrine diluted 1:200,00-1: 400,000 in the local anesthetic solution can be infiltrated in the subcutaneous tissues aboutthe surgical site. Contraindications include any evidence of ischemia or PVD, organic occlusive or vasospastic (Raynaud's phenomenon), connective tissue disease such as scleroderma, vasculitis, concomitant use of MAO inhibitor or tricyclic antidepressant agent, pregnancy (which usually contraindicates any elective surgical intervention), or distal tissue injury. Tourniquets-these can be used, in conjunction with anatomic dissection, to achieve hemostasis. Application of the pneumatic cuff is performed in a smooth and even fashion, over a well-padded limb, after exsanguination via three minutes of elevation at 45°, or distal-to-proximal application of an Esmarch bandage. The cuff is applied at the ankle isupramalleolar) or thigh !junction of proximal and middle thirds) level tor foot and hindfoot/ankle surgery, respectively. Sterile tourniquets are available, although proper draping will allow application of a nonsterile ankle cuff for forefoot surgery. Inflation pressure-there are 3 variables used to determine tourniquet inflation pressure: patient age, systolic blood pressure, and the size of the extremity. The usual pressure range for a thigh tourniquet is 300-375 mmHg. The usual pressure range for an ankle tourniquet is 70-100 mm Hg above the preoperative systolic blood pressure, or approximately 225-250 mm Hg tor the average size adult, or approximately 125-150 mm Hg for children. Insufficient pressure may effect a "venous tourniquet" that only inhibits venous return, while allowing arterial perfusion, congestion and stagnation of the blood in the extremity, which can be problematic. The pneumatic tourniquet pressure register should be checked regularly with the mercury manometer to assure proper pressure measurement The tourniquet should remain inflated no longer than 90 minutes on the ankle, or 120 minutes on the thigh. The tourniquet can be re-inflated after a 20 minute "breathing period/' however for most foot and ankle surgery, this is usually not necessary. The "breathing period" enables hyperemic limb perfusion and restoration of norma! pH, pC02, and p02. If it becomes necessary to deflate the tourniquet additional times during a prolonged case, each tourniquet inflation period should be shorter and each "breathing period" should be longer 115 minute increments). Potential complications of tourniquet application include paralysis, ischemia, clotting dysfunction, thrombophlebitis, and cutaneous compromise. Paralysis may result from neuropraxia induced by excessive pressure or prolonged inflation, inadequate pressure allowing creation of a venous tourniquet that allows perfusion of the vasonervorum and intraneural hemorrhage; or prolonged ischemia. Limb ischemia lasting greater than three hours effects some degree of sublethal muscle damage. Tourniquet induced alteration ofthe clotting mechanism hinges on the


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llberation of plasminogen activators secondary to non~physio!ogical pressure applied to venous walls and limb hypoxia that, in turn, results in fibrinolysis. Increased fibrinolytic activfty peaks at approximately 15 minutes post-deflation, and normalizes at approximately 30 minutes post-deflation. The combination of post-deflation hyperemia and increased fibrinolytic activity effects increased hemorrhage in the first 30 minutes following tourniquet deflation. Thrombophlebitis is rarely seen following proper use of the pneumatic cuff in patients with no previous history of thrombophlebitis or venous stasis. Chemical irritation of the skin can occur if the tourniquet padding becomes soaked with povidone iodine or any other antiseptic solution used to prepare the skin for surgery.

Topical hemostatic agents-these topical agents, when placed in contact with blood, effect clotting.

Topical thrombin---bovine~derived prothrombin that is activated by tissue thromboplastin. It catalyzes conversion of fribrinogen to fibrin monomers and polymers and, ultimately, a fibrin clot Can induce hypersensitivity due to bovine origin. Used to cause rapid, direct coagulation of capillaries and small vessel {minor) bleeding. Available in a spray bottle, or blotted on bleeding surfaces. Not for intravascular use. Absorbable gelatin (Gelfoam"}-sterile, purified porcine skin collagen gelatin that is H20 soluble, pliable, and non~antigenic. It is not intrinsically hemostatic, however absorbs many times its weight in blood, providing tamponade and pressure, thereby slowing bleeding. Once clot forms, the gelatin serves as a framework for granulation. The gelatin is absorbed in 4-6 weeks. Used for small vessellminor), capillary, and venous bleeding. It is deal for small dead space control, however it can interfere with bone and dermal healing. Oxidized cellulose (Surgicef®}-when impregnated on a knitted fabric, oxidized cellulose can be used to rapidly clot capillary, venous, and small arterial bleeding impregnated knitted fabric. It is removed after the clot forms, and any residue left in the tissues is absorbed via liquefaction in about2 weeks. It is non~antigenic, non~toxic, and also antibacterial. It will inhibit bone healing if placed interfragmental. Microfibrillar collagen (Avitene®}-this is the dry, sterile, HCI acid salt of purified bovine corium collagen, and it rapidly causes clot formation via the extrinsic clotting pathway. It can be antigenic due to bovine origin. It can be used to stop brisk bleeding, and is applied with gentle compression. It is more expensive than the other topical hemostats described, above. It is notto be used between bone fragments, as it will inhibit osteosynthesis. Drains and dressing~itis advisable to use an appropriate wound drain, whenever closure entails reapproximation of deep layers, in particular those layers deep to the deep fascia. Drains are of 2 basic types: gravity and c1osed~suction. Gravity drains include fine~mesh gauze and latex or non~latex, or silicone, rubber drains in various sizes and shapes. These are typically pulled from the wound after several days, usually at the time of the first dressing change, and may be appropriate following delayed primary closure. Closed suction drains, using either a vacutainer or bellows chamber, are appropriate for deep wounds with considerable muscle oozing, or when larger volumes of drainage are expected. Negative pressure wound closure (Wound VAC®) is often useful in achieving closure of open wounds, and is not indicated for use in wounds closed by primary intention.


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157

Wound dressings should also serve to absorb any drainage, serous or hemorrhagic, that exude from the closed wound. To this end, the bandage should splint the healing tissues, absorb drainage, and avoid excessive pressure or strangulation of circumferentially wrapped tissues. For almost every tendon or osseous surgery performed on pedal

structures, bringing the bandage materials above the ankle can help to stabilize the tissues, as well as prevent the bandage from coming loose. ANESTHESIA

Local Anesthetics--these agents are either esters or am ides. Esters are formed from an alcohol and acid by removal of water, and am ides are formed from an acid by replacing the hydroxide group with the amide group (NH3). Amides are detoxified in the liver and consequently their effects last longer. Esters are metabolized in the blood stream by

pseudocholinesterase and are more quickly detoxified, and they display a high potential for hypersensitivity. When using local anesthesia, it is important to convert the concentration of the solution(% solution) to milligrams of local anesthetic agent (Table 6-7). TABLE 6-7. CONVERTING CONCENTRATION(% SOLUTION) TO MASS (MilliGRAMS) OF LOCAL ANESTHETIC. Percent(%) solution

Milligrams (mg) ollocalanesthetic

0.25% 0.5% 1%

2.5 5 10 20

2%

General guidelines for the use of local anesthesia include: 1) having knowledge of the patient's medical and allergy history, 2) knowledge of the toxic dose of the particular local

anesthetic being used, 3) use the smallest concentration of local anesthetic necessary to effect anesthesia (a higher concentration does not last longer), 4) a larger volume of local anesthetic may be necessary to anesthetize a larger diameter nerve, 5) allow enough time for the anesthetic to take effect (each anesthetic agent has an intrinsic time lag before anesthesia sets in), G) concomitant use of dilute epinephrine is helpful when a large volume of local anesthetic would otherwise be necessary (when epinephrine is not contraindicated), 7) infiltration should be done with frequent aspiration to assure avoidance of intravascular infusion ofthe local anesthetic, 8) patients who are scheduled for procedures using local anesthesia should be maintained NPO preoperatively so that conversion to sedation or general anesthesia can be undertaken if deemed necessary, 9) avoid local infiltration into an infected or traumatized area since local anesthetic onset is delayed by lower pH !inflammation and/or infection), and 10) each foot should be injected separately when long duration bilateral cases are planned. Local anesthesia used in conjunction with IV sedation is usually adequate for many forefoot surgeries. The local anesthetic dose can be adjusted under certain circumstances, including: 1) use half of the standard adult dose for debilitated or elderly patients, 2) use Clark"s rule for children, where the child"s weight in pounds is divided by 150 and multiplied by the adult dose, and 3) use Fried's rule for infants, where the infant's age in months is divided by 15 and multiplied by the adult dose. Standard local anesthetic dosages are depicted in Table 6-8.


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TABLE 6-8. STANDARD LOCAL ANESTHETIC DOSAGES FOR USE IN AN AVERAGE ADULT(> 25 YEARS OF AGE, 70 KG MALE OR 60 KG FEMALE).

Duration of action

Class

name

Procaine

Novocaine®

0.75-1 hour

1000

Ponto caine®

2·3 hours

Ester Ester

750

Tetracaine

75

100

Local anesthetic

Proprietary

Maximum single dose (mg) Plain With epinephrine

Lidocaine

Xylocaine®

1-Zhours

Amide

300-350

500

Mepivacaine

Carbocaine®

1-3hours

Amide

400

500

Bupivacaine

Marcaine®

3-12 hours

Amide

175

225

General Anesthesia

General anesthesia causes reversible unconsciousness via CNS depression starting at the cerebral cortex, and proceeding through the basal ganglia, cerebellum, medulla oblongata, and finally, the spinal cord. The anesthesiologist must look for several potentially complicating factors in patients anticipating general or IV sedation anesthetics, in particular cardiovascular disease such as hypertension, coronary artery disease, valve dysfunction or arrhythmia; endocrine disorders such as diabetes me!litus, adrenal insufficiency, or thyroid disease; pulmonary disorders such as COPD, regular cigarette smoking, or chronic cough; Gl concerns such as the last time the patient ate or drank, or whether or not denture plates are present; history of hepatitis; and history of personal or familia! neuromuscular disorder or anesthesia-related adverse reactions, such as malignant hyperthermia. The stages of anesthesia are depicted in Table 6-9.

TABLE6-9. STAGES OF ANESTHESIA. Stage 1-amnesia and analgesia 2-delerium

Plane 1

2 3 1

3-surgical anesthesia

2 3 4 4-medullary paralysis

2

Physiological effects Preanalgesia, memory and sensation intact Partial amnesia and analgesia Total amnesia and analgesia Unconscious, mydriasis, irregular breathing, involuntary skeletal muscle movement Sleeping, residual lid reflex, eyes fixed centrally, regular breathing Pupils dilating, full analgesia, heart rate and BP stable Partial intercostal paralysis, tachycardia and hy potension, hypotonia Complete intercostal paralysis and respiratory arrest, requires artificial ventilation Reversible respiratory paralysis Irreversible cardiovascular and respiratory arrest

Anesthetic agents are used with such frequency that they are improved upon regularly, and new agents become available with regularity. lnhalational agents used to


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159

achieve general anesthesia historically include diethylether, methoxyflurane, and chloroform. More recently, the following agents have been used: Enflurane-supports the cardiovascular system, can be used with epinephrine, does not induce emesis, however can be hepatotoxic.

lsoflurane----maintains heart rate, allows rapid induction and emergence, can be used with epinephrine, does not induce emesis, may be hepatotoxic, however often induces shivering. Halothane--allows rapid induction, acts as a bronchodilator, is nonemetic, however

can be negative inotropic, arrhythmogenic and it sensitizes the myocardium to catecholamines, can be hepatotoxic, often induces postoperative shivering, and is associated with malignant hyperthermia. Sevoflurane---very fast onset and offset, minimal mucus membrane irritation,

excellent cardiovascular stability, an agentthat replacing isoflurane and halothane in everyday general anesthesia. Desflurane--extreme!y fast onset and offset due to very high volatility, however may

be associated with tachycardia, limited potency, and relatively high cost. Nitrous oxide--a low-potency inhalant gaseous anesthetic that has little effect on the heart, liver, kidneys, and lungs, as long as hypoxia does not develop. Nitrous oxide provides profound analgesia, without sensitizing the myocardium, and allows rapid induction and emergence. There is, however, no muscle relaxation and nitrous oxide has been associated with fatal agranulocytosis and spontaneous abortion after prolonged administration. The patient receiving nitrous oxide should be ventilated with 100% 02 during emergence, in order to prevent postanesthetic delayed-diffusion hypoxia. Sedative and hypnotic agents are usually administered as induction and maintenance agents before or in addition to an inhalational anesthetic, in an effort to diminish anxiety, initiate, and maintain CNS depression. Traditionally used agents include barbiturates, benzodiazepines, and narcotics. Neuroleptanalgesia effects somnolence, psychological indifference, amnesia, analgesia, and loss of voluntary movement. As with all IV sedativehypnotic agents, careful assessment at the patient's respiration is mandatory, and supportive measures are often necessary. fentanyl-a short-acting narcotic that depresses respiration, effects analgesia, and is reversed by naloxone. Fentanyl is administered 0.05-0.1 mg IM 30-60 minutes pre-procedure, then titrated as indicated.

sedative-tranquilizer that effects peripheral vasodilatation, somnolence, mental dissociation (perhaps dysphoria), and serves as a strong antiemetic. The sedative dose of droperidol is 2.5-10 mg IM 30-60 minutes preprocedure. The combination of droperidol and fentanyl combines the analgesic effects of fentanyl wiTh the tranquilizing and antiemetic effects of droperidol in a 1:50 (fentanyl: droperidol) ratio. Droperidol-a


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Ch. 6

Propofo~an IV· sedative hypnotic agent used for induction and maintenance of anesthesia or sedation, and can be used in conjunction with local anesthesia. Midazola~a

short-acting benzodiazepine CNS depressant often used in

conjunction with analgesia to achieve IV conscious sedation. Midazolam is titrated

IV starting with 1 mg, then increasing up to 2.5 mg over at least two minutes, then via small increments (not to exceed 5 mg) while monitoring the degree of sedation. Other medications used in a balanced anesthesia protocol may include phenothiazine tranquilizers such as promethazine and prochlorperazine. Atropine (atropa belladonna) and scopolamine are premedications used to minimize respiratory secretions and to counter parasympathetic overtone by blocking the vagus nerve whenever a positive chronotropic cardiac effect is desired. Ondansetron is a selective 5-HT3 receptor antagonist with strong antiemetic properties, originally used in patients undergoing cancer chemotherapy, and now regularly used following general anesthesia. Ondansetron is administered 4 mg IV slow infusion over 3-5 minutes, in the treatment of postoperative nausea and vomiting. Paralytic agents such as succinylcholine are used to paralyze the body and facilitate endotracheal intubation, cause a fast onset and short duration depolarizing skeletal muscle blockade. Depolarization can be associated with marked increase intragastric and intraocular pressures, and a rise in serum K+. The rise in K+ can be arrhythmogenic in patients predisposed to high serum K+, such as patients with burn, tetanus, trauma, uremia, or lower motor neuron disease (paraplegia, quadriplegia, and muscular dystrophy, Landry-GuillainBarre syndrome). Depolarization may be associated with rhabdomyolysis, masseter spasm, malignant hyperthermia, and dysrhythmia. Atracurium-besylate is a non-depolarizing neuromuscular blocker that competitively binds with the cholinergic receptor sites on the motor end plate, and is often used when depolarization is contraindicated. Muscle relaxants not only facilitate intubation of the trachea, but aid in ventilation and abdominal dissection by diminishing muscle tone. Skeletal muscle paralysis does not cause amnesia or analgesia, and these conditions must first be achieved via administration of rapid onset IV agents before paralyzing the patient.

Spinal and Epidural Anesthesia--these methods should be considered whenever general anesthesia poses greater risk. Spinal anesthesia should not be attempted in the presence of hypovolemia, anticoagulanttherapy or bleeding diathesis (peridural hematoma and spinal compression), asthma or other GOPD, obesity, pre-existing neuromuscular disease (MS, myasthenia gravis, poliomyelitis, spinal metastasist pre-existing lumbosacral disk disease or DJD, local or systemic sepsis, or in the debilitated host Lumbar epidural anesthesia is achieved by injecting local anesthesia into the spinal epidural space, usually below b. Epidural anesthesia prevents spinal headache, can be maintained 24-48 hours for ongoing anesthesia, rapidly resolves after discontinuing anesthetic, is not associated with hypotension and allows segmental blockade. Spinal anesthesia may propagate proximally and effect spinal headache or anesthetize a broader-than-desired area; however the technique uses less local anesthetic than does an epidural block, and is generally easierto perform than an epidural block. The most common acute complication of spinal anesthesia is hypotension caused by sympathectomy. Late complications include postural headache, lumbago, meningitis, spinal neuralgia, cauda equina syndrome (very rare and due to fibrosis), and epidural hematoma.

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161

Intravenous Block (Bier Block}-Bier block is commonly used for hand surgery, however it is applicable to the lower extremity, as long as the surgeon and anesthesiologist are prepared to handle a possible toxic reaction to local anesthesia. Two pneumatic

tourniquets are placed side-by-side proximal to the operative site after obtaining IV access in the upper extremity. A butterfly needle is then introduced to the dorsal venous arch, secured, and connected to a 10 ml syringe. The extremity is exsanguinated to the distal tourniquet, and the proximal cuff inflated. Lidocaine, or carbocaine, is then infused using 3 ml/kg of body weight of a 0.5% solution 15 mg/ml), through the butterfly catheter. This effects surgical anesthesia regionally in about 5 minutes, and lasts for 60~90 minutes. When the patient begins to complain of proximal cuff tenderness, inflate the distal cuff over the now anesthetized portion of the extremity, and deflate the proximal cuff only after the distal cuff is inflated. Do not deflate both cuffs at the same time. At about 30~40 minutes after infusion of the local anesthetic agent, slow deflation of the tourniquets can be safely performed as enough of the anesthetic has been bound by local tissues and metabolized to avoid a toxic dose in the systemic circulation. Even if the surgical procedure is finished before 30-40 minutes of elapsed time, the tourniquet must remain inflated at least this long before deflation. Patient positioning and safety in the OR are the responsibility of the anesthesia!~ agist and surgeon, and care must be taken to avoid traction nerve palsy, neuropraxia, injury secondary to pinching or crushing small parts (fingers, skin and other appendages) in equipment and the operating room table.

PADDING, STRAPING, BRACING AND PROSTHESES Padding with the use of felt, rolled cotton, felted-foam, various foams and sponge materials, can be very useful whenever mechanical pressure is associated with pain or skin compromise Hichenification, hyperkeratosis, or wound). Standard pads include the metatarsal projection, toe crest medial longitudinal arch pad, heel cobra pad, heel counter pad, heel lift, aperture or pontoon pads, and bunion and bunionette flange padding. Strapping can be used to support musculoskeletal and ligamentous structures, and include standard applications such as the low Dye strap, digital sling-down strap, the Gibney ankle boot, and variations that combine different methods. A number of arch binders, and bunion and hammertoe shields can be customized or obtained commercially. Similarly, a variety of ankle and Achilles braces (McDavid-type lace~up, AircasfM stirrup, Malleotrain® and Achllliotrain®) can be obtained from surgical supply services or via online services. A wide range of braces is available for support and substitution of lost function. The use of accommodative foot orthoses, an extra depth shoe that is anatomically fitted with a roller sole or metatarsal bar can be used for many conditions, in particular the rheumatoid or insensitive foot Simple adjustments for limb length and gait imbalance can be readily applied. Reverse, adduction and straight shoe last, and custom~made shoes are also available. Surgical shoes, forefoot~relief and heel~relief orthoses, healing sandals, removable cast boots (fixed and adjustable, low- and high-top), ankle-foot orthoses IAFOs), Charcot Restraining Orthotic Walkers (CROW), and total contact casts can be used in the post-traumatic, postoperative and chronic settings. Of particular use in cases of dropfoot are molded ankle foot orthoses that fit into the shoes, and the heavier double upright brace with metal stays that are affixed directly to the shoe. The double upright (contoured aluminum) brace is preferable when ankle edema or deformation prohibits the use of a hinged AFO !Richie brace®, or similar device), a gauntlet-style brace (Arizona AFO"'), or a polypropylene molded AFO. The patellar tendon bearing brace, usually of a clamshell

162


Ch.6

design, can also be used to diminish weight-bearing load transfer through the foot Of course, off~loading can be achieved using appropriately fitted crutches or a walker to aid ambulation. Off-loading of the lower extremity can be enhanced with the use of a wheelchair, a Roi!-A-BoufiD or Turning Leg Caddy"'', or, as a last resort, bed rest Braces and

shoe gear need to be periodically inspected, along with the patienfs lower extremities, in order to monitor for the possibility of cutaneous compromise, especially in those with neuropathy and/or vasculopathy, immunocompromise or steroid dependence, and

collagen disorders.

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities

163

RECONSTRUCTIVE SURGERY: BASIC CONDITIONS AND DEFORMITIES NAIL SURGERY The ingrown toenail (onychocryptosis) involves nail pathology wherein the nail plate has

grown into the ungual labia, with or without concomitant infection. Paronychia (also termed whitlow or run-around) consists of nail fold erythema, edema, and pain. Ingrown toenails are commonly classified as self-inflicted or iatrogenic. Self-inflicted is where the patient chronically cuts the nail too short or incorrectly angulates the nail nipper deep to the nail fold. Other causes of ingrown toenails include congenital abnormalities where the matrix is maligned and produces an incutvated plate; primary soft tissue hypertrophy wherein the primary pathology involves the adjacent nail fold, which is enlarged and overlaps the plate; and combinations of incurvated nail plate and nail fold hypertrophy. Nail fold hypertrophy can also develop secondary to chronic plate incurvation and repetitive wound irritation with the formation of a pyogenic granuloma. Treatment options include: Avulsion~ treatment should

involve education as to proper nail trimming technique, as well as acute intervention to alleviate paronychia and allow the wound to heal. No amount of antibiotic will cure an infected ingrown toenail until the offending nail border is satisfactorily removed. The mainstay of treatment for onychocryptosis is avulsion of the offending nail border. This effects temporary removal of the margin, and allows subsequent regeneration over the ensuing months. Avulsion can be performed with, or without, local anesthetic digital blockade, depending upon the extent of plate removal necessary to alleviate the condition and other factors, such as peripheral sensory status. Avulsion is followed by local wound care, perhaps concomitant use of oral antibiotics if paronychia and/or systemic factors warrant doing so. Re~evaluation should be performed between 2 and 3 weeks after avulsion, at which time proper nail trimming technique is reviewed with the patient Temporary removal of the offending border is generally recommended in a firsHime case of ingrown toenail, whereas recurrent onychocryptosis may be best treated with permanent matrix ablation via either chemical or surgical matrixectomy. Phenol and Alcohol (P & A) and Sodium Hydroxide (NaOH) matrix ablatiot>-these techniques of permanent partial or total nail matrix ablation are rather simple, and inflict minimal pain. The P & A involves three 30Hsecond applications (causing the nail bed and matrix to appear ashen gray) of 90% phenol followed by rinsing with alcohol (70-90% isopropyl or ethyl), then copious saline lavage and application of silver sulfadiazine cream and a sterile bandage. The NaOH procedure involves application of 10% NaOH until the matrix and nail bed tissues appear ashen gray-brown (about 20-30 seconds); followed by acetic acid (vinegar) rinse, then copious saline lavage, silver sulfadiazine cream, and a sterile bandage. It is important to avoid excessive hemorrhage during application of either chemical cauterant, as dilution could inactivate the chemical agent. A digital tourniquet can be useful in this regard, and must be removed after applying the chemical. The main disadvantage to both the P&A and NaOH procedures is the creation of a chemical injury that denatures proteins much as a thermal burn would do. The wound remains open and draining for 3-4 weeks. Chemical matrixectomy is generally not performed in the presence of advanced paronychia, and it is recommended that the patient undergo avulsion of the offending border/s followed by local wound care, and perhaps oral antibiotic therapy

164


Ch. 7

(cephalexin), with planned matrix ablation to be performed anytime after resolution of the paronychia and before recurrence of onychocryptosis. It is also advisable to have the patient initiate oral antibiotic therapy 24 hours before the planned matrixectomy.

Matrixectomy techniques (true "open" matrix excisions) employing eponychial and nail fold incision are numerous, and include: Modified Steindler Matrixectomy-a useful technique for incurvated or iatrogenic chronically ingrown toenails. This is often employed afterfai!ed chemical matricectomy, or when an "open" excision is desired. The procedure is used to excise the matrix, and does not address nail fold hypertrophy. Frost Partial MatnXectomy-employs a right angle incision into the nail fold allowing reflection of the fold and exposure of the underlying corner of the matrix, following nail plate avulsion (Figure 7-1. The involved area of nail bed is also excised. The right angle incision is actually rounded gently to avoid slough of the apex. Winograd Partial Matricectomy--uses 2 incisions, one longitudinal through the nail bed, and a second semi-elliptical incision through the adjacent nail fold, to create a wedge of nail fold and bed that are excised after avulsion of the nail plate (Figure 7-2). Hypertrophic ungual labium is readily excised. Ungual Labioplasty-involves a wedge-shaped excision ofthe hypertrophic labium, and is useful only for reduction of nail fold hypertrophy. Suppan Panhypertrophy Matrixectomy-uses a fish mouth incision through the nail folds surrounding the entire nail plate, allowing excision of surrounding hypertrophic folds and underlying matrix and bed.

I~

( Figure 7.1

Figure 7.2

I

Ch. 7


165

D

( ''~--J..'

:·~·~

Figure 7.3 Zadik (Quenu) Matrixectomy-an H-shaped incision is made with the two vertical arms through the nail medial and lateral folds, and the transverse arm through the proximal nail fold (Figure 7-3). The proximal nail fold is then reflected proximally and the underlying matrix and proximal bed excised. The exposure a!lows removal of subungual exostosis if necessary. Closure involves proximal advance of the distal nail bed flap, allowing closure without shortening of the distal phalanx.

SUBUNGUAL EXOSTOSIS Dorsal proliferation of the distal phalanx into the overlying nail plate can effect plate deformation, often described as a pincer nail, with or without associated onychocryptosis (Figure 7-4). Subungual exostosis can be of traumatic origin or, when capped with fibrocartilage, congenital due to osteochondroma. Osteochondroma is usually observed early in life, between 10-25 years of age, onset on or before puberty, and most commonly is observed in females (F: M ratio 2:1 ). Eradication of a symptomatic subungual exostosis or osteochondroma is via nail plate avulsion, and exposure of the phalangeal lesion with a distal fish mouth incision, or via longitudinal or semi-elliptical nail bed incision or excision, respectively. The semi-elliptical incisions are used to create a wedge excision of associated nail bed, when the pathology has caused nailed scar or other lesion. It may not be necessary to perform nail plate avulsion when the exostosis is small, however exposure of the exostosis should not be compromised by trying to preserve nail plate attachment. Osteotripsy may be a useful method for reduction of the osseous prominence. The excised lesion should be submitted en bloc for pathological inspection, and specimens should be obtained for bacterial C&S, as well.

Figure 7.4

166


Ch. 7

HAMMERTOES

Digital contraction deformities include hammertoes, clawtoes, and mallet toes. The deformities can be flexible or rigid, and the Kelikian push-up test is used to assess the degree of flexibility. Anatomic considerations include extrinsic and intrinsic muscufature, with emphasis on the MTPJ extensor hood expansion (Figure 7-5).

Extensor sling Metatarsal head

Capsule

Plantar interosseous

Dorsal interosseous

~ransverse metatarsal

. Lumbncal~ ~

ligament

Flexor tendons

Figure 7.5

Dynamic etiologies of digital contracture include:

Flexor Stabilization-the most common cause of pathological digital contracture (>70%}, itself caused by late stance and propulsion phase hyperpronation; the FDL and FOB fire earlier and longer to stabilize the hypermobile forefoot, thereby overpowering the interossei with resultant dorsal subluxation of the MTPJ; associated with adductovarus fourth and fifth digital deformities.

Extensor Substitution-this is associated with pes cavus, foot drop, and anterior compartmentweakness, wherein the EDL overpowers the lumbricales during swing phase, and causes dorsiflexion of the MTPJs; results in a high degree of MTPJ subluxation and retrograde plantar buckling ofthe metatarsus. Flexor Substitution-this is the least common cause of digital contracture, and occurs due to weakness of the triceps surae wherein the deep posterior leg muscles compensate and thereby overpower the interossei during stance phase, particularly during propulsion; the digits are seen primarily in the sagittal plane, with minimal varus rotation; a calcaneus gait may develop and this may be observed following over-lengthening (TAL) of the heel cord. A mallettoe involves sagittal plane plantarflexion of the DIPJ, and may be associated with a long toe. A congenital curly (varus) toe involves adduction contracture and varus rotation of the DIPJ, usually toes 3-5, and radiographs (upon reaching skeletal maturity) may show a delta-shaped middle phalanx. Hammertoes involve dorsiflexion of the proximal phalanx and plantartlexion of the middle phalanx, perhaps with transverse plane deviation in the direction of flexor plate subluxation. The clawtoe involves plantarflexion of both the PIPJ and the DIPJ, and is often seen in cases of extensor substitution (Figure 7-6).

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities MPJ extension

167

MPJ extension

DIPJ flexion

Figure 7.6 Symptoms associated with advanced digital contracture deformity include painful PIPJ motion, painful hyperkeratotic lesion(s), inability to wear regular shoes, contracted painful toe that is short and possibly dorsiflexion deformity of the DIPJ. Radiographic findings include joint narrowing and superimposition at the contracted joint levels, gun-barrel sign on the AP view due to long axis imaging of the phalanx in either dorsiflexion (proximal) or plantarflexion (middle), shortened contracted toe, DJD of the PIPJ and MTPJ, and periarticular osteoporosis. Biomechanica! signs of digital contraction deformity include the presence of hypermobile first ray and other hyperpronation findings (flexor stabilization), or Stage I pes cavus as seen in anterior cavus and dropfoot related extensor substitution. Postoperative management involves the use of a wooden or stiff-soled surgical shoe, perhaps with build-up when the pins cross the MTPJ, and may involve casting depending upon other procedures performed. A variety of nonsurgical options are availablefortreatmentof symptomatic digital contractu res, including the use of larger shoes with an extra-depth toe box, digital retainers such as dorsal (early, flexible deformity) and/or plantar (advanced, rigid deformities) toe crests, sling-down toe-MTPJ splints (Budin splint), sling-down or predislocation taping, pads and shields, and periodic debridement of hyperkeratoses. The use of a supportive insole with a metatarsal projection pad can also help to realign the MTPJs, and enhance nonsurgical treatment of hammertoes. When nonsurgical efforts fail to effect satisfactory relief, then a variety of surgical Interventions can be considered. Like the nonsurgical interventions, operative measures also take into consideration the alignment of the MTPJ as well as that of the IPJs. Surgical procedures for repair of contracted digital deformities include:

Flexor tenotomy-operative procedures for correction of digital deformities will vary depending on the degree of toe and MTPJ flexibility. The reducible lesser digital deformity may be responsive to flexor tenotomy, both long and short (flexor set), however the use of this as an isolated procedure is rarely indicated and does not provide a long lasting correction in most cases. Indications include plantarilexion deformity at the PIPJ or DIPJ that is completely reducible with manipulation. Attention may

168


Ch. 7

only be required at the long flexor and the IPJ capsule proximally and distally. Generally a plantar stab incision is indicated, however a mild contracture may be approachable through a medial or lateral exposure. This procedure can be useful in conjunction with PIPJ arthrodesis in the presence of persistent mallet toe, when the toe is pin-stabilized in a position ofslightDIPJ dorsiflexion.

Extensor tenotomy and capsulotomy--these are also rarely indicated as isolated procedures, and are commonly useful in conjunction with PIPJ stabilization and MTPJ relocation (see sequential release).

Resection arthroplasty--a variety of hammertoe procedures can be used, including the Post arthroplasty wherein the head of the proximal phalanx is resected transversely at the level of the metaphyseal flare. Resection of the base of the proximal phalanx (Gotch and Kreuz) is wrought with complications due to destruction of the intrinsic muscle attachments to the base, and must be combined with adjacent digital stabilization and syndactyly in order to avoid floating or flail toe. Digital stabilization---in general, multiple digital stabilizations, consisting of PIPJ fusion and MTPJ relocation, are indicated for correction of advanced, dynamically induced digital deformities. Such deformities are usually associated with lesser metatarsalgia, concomitant plantar hyperkeratosis (intractable plantar keratoma [IPK] or diffuse plantar tyloma), dorsal PIPJ and distal digital tip and hyponychium hyperkeratosis, mechanical onycholysis and nail dystrophy that predisposes to fugal infection, and rigidity or incomplete relocation with push-up loading. Transverse plane deformity may also be present, in particular when the second toe crosses over or, less commonly, under the hallux in the presence of associated HAV and bunion deformity. The crossover second toe is particularly hard to completely realign. Isolated interphalangeal arthroplasty can be useful in the presence of an unusually long digit that is contracted secondary to shoe crowding, however it is rarely indicated for the treatment of multiple, dynamically-induced hammertoes. Moreover, multiple adjacent PIPJ arthroplasty may IBBd to digital instability and recurrent deformity, in the postoperative phase. It can be useful to approach the deformity by means of sequential release. The sequential release for advanced hammertoe deformity (Figure 7-7) includes the following steps: 1. Long extensor hood recession, 2. Long extensor tenotomy (open Z-tenotomy or transverse), 3. PIPJ capsulotomy and arthroplasty or arthrodesis, 4. MTPJ capsulotomy, and 5. MTPJ flexor plate release (made easy using the McGiamry metatarsal elevator) and repair. The Kelikian push-up test (apply a dorsally-directed force to the plantar surface of the metatarsal head, to simulate ground reactive force) is performed between each step in the sequential release, and progression to the next level of release is not necessary if the digit and MTPJ properly align in a relaxed attitude with simple push-up loading. Full sequential release is used in the correction of advanced clawtoe or hammertoe deformities. It is necessary to perform the Z-tenotomy when advanced dorsal contracture is corrected, otherwise it may be difficult to reapproximate the tendon upon closure. Medial or lateral

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities EDL

8 A Phalangeal head

~cted

c

D

F

G

Figure 7.7

Figure 7.8

169

170


Ch. 7

dislocation of the flexor plate will cause a medial or lateral deviation of the digit upon push-up loading, and is usually related to chronic synovitis and subluxation of the flexor plate to the side of deviation. Flexor plate subluxation must be addressed at the time of sequential release, and an anchor suture may be necessary in order to maintain correct, balance alignment. In some cases, persistent deformity may require MTPJ capsulorrhaphy

with wedge excision of redundant capsule, or metatarsal osteotomy lmedia! or lateral transpositional and/or shortening) for satisfactory correction.

Interphalangeal arthrodesis-this entails several modifications, including end-to-end (non-fixated, described by Soule; K-wire stabilization, described by Taylor and Selig); and peg-in-hole (pike, described by Higgs; or rounded, described by Young) techniques. Arthrodesis is generally indicated in cases of multiple lesser digital deformities, which is the typical presentation when treating dynamically induced (flexor stabilization, extensor substitution, or flexor substitution) contractu res of the toes and MTPJs. Either peg-in-hole or end-to-end fusion can be used, based on surgeon's preference. If shortening is a concern, then the end-to-end fusion may be used, as less shortening is encountered. The peg-in hole may more reliably achieve radiographic fusion mass consolidation, however, the functional result of a fibrous pseudoarthrosis of an end-to-end arthrodesis has been shown to function as well as the radiographically solid fusion in many cases. After resection of the articular surfaces, arthrodesis is completed with pin stabilization, starting the 0.045" (or 0.062" if desired) K-wire at the base of, or hole in, the middle phalanx and driving it distally across the dorsiflexed and straightened DIPJ, then out the tip of the digit centrally. Care is taken to avoid perforation of the nail bed. The K-wire is then retrograded proximally across the PIPJ to the base of the proximal phalanx, then across the realigned MTPJ if indicated by persistent upon push-up loading. Stabilization of the MTPJ is performed with the toe situated half way between the horizontal substrate (parallel to the bottom of the foot), and in line with the metatarsal declination angle. Digital alignment is slightly over-corrected in plantartlexion, and the pin crossing the MTPJ maintained for 3-6 weeks. The PIPJ fusion is stabilized for 5-6 weeks, or until radiographic and clinical evidence of fusion is observed. Placing the pin across the MTPJ requires use of a built-up surgical shoe postoperatively, in order to avoid repetitive mechanical flexure and pin breakage in the MTPJ (Figure 7-8). Interphalangeal arthrodesis can also be achieved using bioabsorbable fixation pins or screws, and other devices made to press-fit or snap-fit once seated in either the proxima! and/or middle phalanges. It is important to keep in mind that if absorbable fixation, or a device that is limited to just the interphalangeal joint/s, is used to achieve digital fusion, attention to the alignment of the corresponding MTPJ may require separate fixation or metatarsal osteotomy, if the push-up test fails to display satisfactory MTPJ realignment After realignment of the toe and MTPJ, the long extensor tendon is re-approximated in corrected alignment, followed by subcutaneous and then skin closure. Flexor tendon transfer (Girdlestone, Foerster and Brown)-can also be useful for the correction of hammertoes and clawtoes, however care must be taken to transfer the sectioned flexor tendon slips from plantar to dorsal on the phalanx in a subperiosteal fashion (to avoid constriction of digftal vessels), or through a drill hole in the phalanx, and it is possible to effect a PIPJ rocker-bottom deformity unless arthrodesis is performed (obviating the need for flexor tendon transfer). Sgarlato's modification of the Girdlestone procedure can be used for the correction of hammertoes and clavvtoes with MTPJ

Ch. 7


171

subluxation, and serves to redirect the long extensor tendon's pull to that of a stabilizing

influence on the toe and MTPJ. Two incisions are used, 1 medial or lateral aspect at the proximal phalanx, and an adjunct dorsal incision more to the side opposfte the medial or lateral incision. The long flexor tendon is split and transferred dorsally in a subfascial fashion and sutured to itself and the dorsal hood expansion as a sling dorsally atthe level of the proximal phalangeal shaft. Care must be taken to transfer the splittendon segments in a subfascial (deep fascia) fashion, in order to avoid circumferential constriction of the subcutaneous neurovascular elements coursing to the toe tip. The transfer results in decreased PIPJ range of motion. Dockery and Kuwada modified the transfer by use of a dorsal-to-plantar drill hole in the anatomic neck ofthe proximal phalanx. Moreover, a rocker bottom PIPJ or swan-neck deformity can be created if too much tension is placed within the transferred long flexor. PIPJ arthrodesis is generally considered a more effective and lasting method to stabilize the digit and convert the long flexor to a stabilizing influence on the MTPJ, particularly for the intermediate lesser digits. A flexor tendon transfer may be applicable to the fifth toe, or in the presence of congenital absence of the middle phalanx.

BUNION DEFORMITY AND HALLUX ABDUCTO VALGUS First metatarsal anatomy pertinentto the bunion deformity and hallux abductovalgus (HAV, hallux valgus) surgery includes the proximal physeal plate, which closes at about 15-18 years of age, the primary nutrient artery situated laterally about 2 em proximal to the articular surface, and the peri-articular soft tissue sleeve and sesamoid apparatus. When the hallux abducts and the first metatarsal adducts (metatarsus prlmus varus), the dorsomedial eminence of the first metatarsal head becomes clinically prominent, and is termed a "bunion." The term bunion basically refers to a bump, traditionally, from the old French buignon, from buigne or "bump on the head." (Similarly, a prominent fifth metatarsal head is often referred to as a bunionette.) Radiographic Angular and Anatomic Relationships Related to HAV~there are a number of angular relationships useful in the assessment of HAV, including:

HalluxAbductusAngle(HAA}--me angle formed by the intersection of the bisection ofthe shaft of proximal phalanx and the bisection of the shaft of first metatarsal, normally 15°, and representative of the relative position of the hallux to the first metatarsal (Fig 7-9). Distal Articular Set Angle (OASA}--the angle formed by the intersection of a line perpendicular to the effective cartilage of the base of the proximal phalanx and the bisection of the shaft of the proximal phalanx, normally 7.5°, and representative of the relative position of the effective cartilage to the shaft of the proximal phalanx. An increase in DASA may indicate lateral deviation in me shaft of the proximal phalanx (Fig 7-10). Proximal Articular Sol Angle (PASA}--the angle formed by the intersection of a line perpendicular to the effective articular cartilage of the metatarsal head and the bisection of the shaft of the first metatarsal, normally 7.5°, and representative of the relative position of the effective cartilage to the shaft of the metatarsaL An increase in PASA indicates lateral deviation (adaptation) ofthe cartilage surface (Fig 7-11).

172

Figure 7.9


Figure 7.10

Figure 7.11

Ch. 7

Figure 7.12

Metatarsus Primus Adductus or First lntennetatarsal Angle (first IMA)--the angle formed by the intersection of the bisection of the shaft of the first metatarsal and the bisection of the shaft of the second metatarsal, normally 8°, and representative of the angular relationship between the first and second metatarsals. An increase in the first IMA makes the head of the first metatarsal more prominent medially, and predisposes to HAV (Rg 7-12).

Hallux lnterphalangeusAngle (HIA)--the angle formed by the intersection of the bisection of the shaft of the proximal phalanx and the bisection of the distal phalanx, normally 10", and representative of hallux interphalangeal joint (HIPJ) or phalangeal deformily (Fig 7-13). Metatarsal Protrusion Distance-the distance between two arcs which, respectively, represent the lengths of the first and second metatarsals. A line representing the bisection of the first metatarsal is extended to intersect with a line representing the bisection of the second metatarsaL A compass is placed at the point of intersection and an arc drawn from the distal portion of the first metatarsal and another arc is drawn from the distal portion ofthe second metatarsaL A positive millimeter distance is used to indicate a longer first metatarsal. A negative distance is used to indicate the second metatarsal being longer than the first Normal is± 2 mm, and represents the relative length between the first and second metatarsals. A longer first metatarsal may be associated with hallux limitus, whi!e shortening may correlate with lesser metatarsalgia (Fig 7-14).

Metatarsus Adductus Angle (MAA)--the angle formed by the intersection of the bisection of the lesser tarsus and the bisection of the second metatarsaL The lesser tarsus is bisected by obtaining the midpoint between the anterior-medial corner of the first cuneiform and the posterior-medial corner of the navicular, and the midpoint between the anterior-lateral corner ofthe cuboid and the posterior-lateral corner ofthe cuboid. The midpoints are then connected and a perpendicular is drawn to this line. The MAA is normally 10-20"; and represents the degree of adduction of the metatarsus. As the MAA increases, the foot becomes more adducted and there is greater chance for development of HAV. Moreover, the first IMA becomes pathologically significant at a lower degree in the presence of increased MAA (Fig 7-15).

Tibial Sesamoid Position (TSP)--the position the tibial sesamoid is compared to the bisection of the first metatarsal shaft, and designated as position 1-7; normally 1-3, and traditionally representative of the need to remove the fibular sesamoid. TSP 4 predicts erosion of the tibial sesamoid against the plantar central crista of the metatarsal

Ch. 7


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head, and relative deviation of the metatarsal head medially so that the fibular sesamoid is positioned in the first intermetatarsal space. When the first metatarsal plantarflexes, a relative distal position of the sesamoids may appear, whereas dorsiflexion causes relative proximal positioning (Fig 7-16). Shape ollhe Metatarsal Head-the intrinsic stability ofthe MTPJ varies with the shape of the metatarsal head. A round head is theoretically most unstable and likely to deviate into HAV; a square head is considered stable, and a square head with a central ridge is considered most stable and may be seen in cases of hallux rigidus (Fig 7-17). First MTPJ Position (Congruous, Deviated or Subluxated)-first MTPJ alignment can be congruous, deviated or subluxated. In the congruous joint, a parallel relationship exists between the effective articular cartilage of the metatarsal head and the phalangeal base. The deviated joint displays extra-articular intersection of the lines representing the effective articular surfaces of the metatarsal head and phalangeal base. The sub luxated (subluxed) joint displays intra-articular intersection of the lines representing the effective articular suliaces of the metatarsal head and phalangeal base (Fig 7-18).

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Structural, Positional, and Combined HAV Delormilies-HAV can be classified as to whether or not the first MTPJ deformity is structural, positional, or a combined deformity based on the formulae depicted in Table 7·1.

Table 7-1. FORMULAE FOR STRUCTURAl, POSITIONAl, AND COMBINED FIRST MTPJ DEFORMITIES. TYPE OF DEFORMITY

FORMULA

PASAAND/ ORDASA

FIRSTMTPJ ALIGNMENT

Structural Positional

PASA + DASA ~ HAA PASA + DASA < HAA

PASAorDASA PASA and DASA

Abnormal, congruent Normal, deviated or subluxed

Combined

PASA + DASA < HAA

PASAorDASA

Abnormal, deviated or subluxed

ANGLE

Example 1: HAA ~ 35", DASA ~ 3", PASA ~ 5" (3 + 5 < 35, so MTPJ displays positional deviation or subluxation, as PASA and DASA are normal). Example 2: HAA ~ 35", DASA ~ 7", PASA ~ 28" (7 + 28 ~ 35, so MTPJ displays a congruous structural deformity, and PASA is abnormal). Example 3: HAA ~ 35", DASA ~ 1", PASA ~ 18" (1 + 18 <35, so MTPJ displays a combined deviated or subluxated deformity, and PASA is abnormal).

Ch. 7


175

Bunionectomies-specific procedures for bunion repair vary a great deal, and it is the surgeon's responsibility to select the best procedure for the patient in question. Procedure selection varies with patient expectations, bone stock, local and systemic tissue status, the degree of deformity relative to the anatomic relationships, and the surgeon's skills. Repair

options are categorized as soft tissue manipulations, hallux osteotomies, and distal, shaft and base metatarsal osteotomies, and combinations thereof. Soft tissue manipulations used for correction of HAV include:

McBride Bunionectomy-this is a versatile and powerful component of many bunion repairs, and focuses on muscleM tendon balance that addresses the underlying pathologic influences in the development of HAV. Preoperative criteria include mild to moderate pain associated with the sesamoid apparatus, first MTPJ range of motion that is essentially free of crepitus or

significant articular degeneration, mild-moderate axial rotation (valgus) of the hallux, prominent dorsomedial bunion, medial bursitis; and radiographic signs such as relative hypertrophy of the medial eminence, deviated to subluxated first MTPJ, and a tibial sesamoid position of 4 or greater. Specific surgical maneuvers used Figure 7.19 in the true McBride bunionectomy include medial exostectomy, excision of the fibular sesamoid, medial capsulorrhaphy, and transfer of the adductor hallucis tendon to the deep surface of the medial capsular flap (Figure 7-19). The modified McBride procedure involves preservation of the fibular sesamoid, with adductor tendon transfer following complete plantarlateral soft tissue release (Figure 7M20). The primary limitation of the McBride procedure is an inability to correct a structural deformity of the metatarsal head. The modified McBride procedure serves as the foundation for many bunionectomies, and is usually combined with f1rst metatarsal osteotomy for the correction of HAV with metatarsus prim us varus. OverM aggressive manipulation ofthe soft tissues using the McBride procedure can overMcorrect and predispose the patient to the development of hallux varus. Proper execution of soft tissue release and realignment about the first MTPJ, in conjunction wtth distal metatarsal osteotomy, can be carried out safely and without the development of capital fragmentAVN.

Figure 7.20

Keller Bunionectomy-this joint destructive procedure is a time~honored technique for alleviation of debilitating pain related to severe, advanced HAV, usually with concomitant DJD and/or hallux rigid us. Indications include apropulsive gait, pain in the first ray and lesser metatarsalgia (lateral dumping) that presents a constant impediment to ambulation,

176


Ch. 7

stiffness, and inhibition of weight bearing or motion. The Keller procedure classically involves resection of the base of the proximal phalanx of the hallux. A number of

modifications of the Keller procedure have come to be appreciated in order to prevent complication, including: re-attachment of the flexor apparatus to the phalangeal shaft, use of a long medial capsular flap that serves as a sling to resist hallux abduction, and

lengthening of the EHL (and brevis). Other variations include use ofthe medial capsularflap as a biological trellis over the metatarsal head (Ganley modification), K-wire nailing for temporary stabilization, and purse string capsular interposition. The main complications related to the Keller procedure are shortening of the hallux, recurrent hallux abductus, hallux elevatus, lesser metatarsalgia secondary to proximal retraction of the sesamoid apparatus, and sub-second metatarsal head IPK. The development of complications is reduced with implementation of the modifications.

Silver (Simple} Bunionectomy--may be used in cases where bump pain and medial cutaneous compromise predominate, especially in the elderly or debilitated host. It does not address sesamoid pain, deep joint pain, or dynamic MTPJ imbalance. Preoperative criteria include a satisfactory first MTPJ range of motion, no crepitus, and often a medial adventitious bursa is present Surgery focuses on simple resection of the dorsomedial eminence of the first metatarsal head while preserving the plantar sesamoidal shelf. Caution should be taken to use a digital retainer postoperatively, so that rapid advance of hallux abductus due to loss at medial capsular-ligamentous tethering of the hallux, is countered. The procedure may convey poor long-term results, and recurrence may occur because the etiology of the deformity is not addressed. The combination of first metatarsal head medial exostectomy and Akin osteotomy for correction of significant HAV, particularly in a young or active patient wherein systematic disarticulation and first MTPJ reconstruction are not addressed, can convey a high rate of recurrent deformity. Hallux osteotomies used for correction of HAV include:

Osteotomy-a closing adductory osteotomy of the proximal metaphysis of the proximal phalanx of the hallux, indicated for correction of true hallux interphalangeus or an increased DASA. The Akin osteotomy is rarely indicated as an isolated procedure, and is usually used in conjunction with more proximal intervention that addresses first MTPJ muscle-tendon balance and/or structural deformity. The Akin osteotomy itself does not directly address a bunion deformity or HAV. Inadequate correction of the first MTPJ cannot be adequately corrected with a ·'cheater Akin," which creates the clinical appearance of a straightened hallux even in the presence of a deviated or sub luxated first MTPJ. The Akin procedure employs a wedge osteotomy in the proximal phalangeal proximal metaphysis, the distal arm of the osteotomy being perpendicular to the long axis of the phalanx and the proximal arm being parallel to the articular surtace of the phalanx Figure 721 (Figure 7-21). Caution should be practiced if the proximal phalanx is short, and the physis should be closed in a young patient The osteotomy is stabilized using a nonabsorbable suture, wire suture, a K-wire, an absorbable pin, or a staple. The Akin is an adjunct procedure to MTPJ realignment Standard Akin

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177

Cylindrical Akin Osteotomy-a cylindrical resection of the proximal phalanx, usually at the junction of the diaphysis and proximal

metaphysis, to correct abnormally high DASA and/or HIA in a very long proximal phalanx. The epiphysis should be closed, and delayed diaphyseal healing is a risk. The Akin is an adjunct procedure to MTPJ realignment(Figure 7·22).

Distal Akin Osteotomy-a closing adductory proximal phalangeal osteotomy positioned in the distal metaphysis, and indicated for the correction of HIA >10-12°, in the presence of a congruous first MTPJ (corrected), and an adequately long phalanx. It can be used even when the proximal physis is open. The Akin is an adjunct procedure to MTPJ realignment (Figure 7·23).

Figure 7.22

Distal first metatarsal osteotomies used for correction of HAV:

Reverdin Osteotomy-a useful technique for correction of high PASA, when used in conjunction with appropriate muscle-tendon balancing of the first MTPJ. The Reverdin can be performed in young patients, however it is most frequently used in conjunction with a true McBride procedure in an elderly patient with an advanced, yet flexible HAV. The osteotomy is an intra-articular closing adductory wedge osteotomy, at the level of the sesamoid apparatus, that preserves an intact lateral cortical hinge. The distal cut is made proximal and parallel to the residual articular cartilage of the metatarsal head, and the proximal cut is made perpendicular to the long axis of the first metatarsal (Figure 7-24). The osteotomy is oriented perpendicular to the substrate {weight-bearing surface), and positioning the osteotomy distal to the sesamoid apparatus may theoretically decrease weight bearing load on the capital fragment. Removal of the medially based wedge of bone decreases articular cubic content, and may enhance range of motion in cases involving hallux limitus. Placement of the osteotomy distal to the weight bearing level of the sesamoids increases the risk of capital fragment AVN. The osteotomy is ideally fixated with 1 or 2 diverging segments of bioabsorbable pin. Alternative fixations include stainless steel wire suture or 2·0 absorbable suture. A K·wire may also be used. The main complications of the Reverdin osteotomy include AVN, sesamoiditis, and first MTPJ stiffness. The Reverdin osteotomy enables first IMA reduction via reverse buckling, wherein the hallux applies an abductory force on the head of the flexible first metatarsal when bandaged in slight overcorrection. Green-Modified Reverdin Osteotomy (distai-L}-a useful modification ofthe classical Reverdin osteotomy, wherein a horizontal plantar osteotomy is made through the metatarsal head, dorsal to the sesamoid, so that the Reverdin cuts do not penetrate the plantar cortex and violate the sesamoidal articular surfaces (Figure 7-25).

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178


Ch. 7

Laird~Modified

Reverdin Osteotomy--combines the Green-modified Reverdin with completion of the osteotomy through the lateral cortex, eliminating the intact cortical hinge

and allowing transverse plane translocation of the capital fragment toward the second

metatarsal in an effort to decrease the first IMA. A K-wire or otherfixator is required to stabilize the capital [ragmen~ and AVN is a risk (Figure 7-26).

Todd-Modified Reverdin Osteotomy-combines the Laird-modified Reverdin with penetration of the plantar cortex to enable sagittal plane correction in addition to transverse plane correction. Peabody Osteotomy-addresses a high PASA using the same osteotomy as described for the traditional Reverdin, however the osteotomy is positioned at the anatomic neck of the first metatarsaL Bone healing is traditionally slower due to a higher degree of cortical bone at the more proximal location.

Wilson Osteotomy-an oblique, through-and-through osteotomy at the surgical neck of the metatarsal, usually oriented from distal~medial to proximaHateral to allow reduction of the first IMA with shortening of the metatarsal. The orientation of the osteotomy can be reversed to elongate the metatarsal, or oriented perpendicular to the long axis of the second ray to avoid shortening or lengthening. The Wilson osteotomy, in the past, was often employed in minimal-incision surgery, and conveys a high risk of malunion, delayed union, and. recurrent deformity or transfer metatarsalgia when not adequately controlled and stabilized. Mitchell Osteotomy-a popular distal metaphyseal, step-down osteotomy wherein the distal arm of 2 parallel cuts does not penetrate the lateral cortex while the proximal arm does. Completion of the osteotomy allows both transposition and angulationa! correction of the capital fragment lt is used for correction of mildly increased first IMA, and dorsal displacement of the osteotomy can be problematic (Figure 7-27) .

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Figure 7.26

Figure 7.27

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179

Austin Osteotomy-perhaps the single most commonly used osteotomy for correction of moderate HAV, wherein the first IMA is usually no more than 16°, and the joint is not degenerated. The procedure consists of a through-and-through, sagittal plane V-osteotomy (chevron), with base proximal and apex distal, situated at the first metatarsal

metaphysis. The osteotomy allows triplanar correction. The apex of the osteotomy is positioned at the center of the imaginary circle of the metatarsal head, and application of a smooth K-wire as an apical axis guide, for many surgeons, enhances control of the saw and predetermines the direction of displacement of the capital fragment. The arms of the V-cut usually intersect to form a 60° angle, however an offset-V, such as the Vogler and Kalish modifications, with the dorsal arm extending proximally to the proximal (Vogler osteotomy) or midshaft (Kalish osteotomy) level of the metatarsal can be used to achieve interfragmental screw fixation and, perhaps correct a higher degree of metatarsus primus adductus by virtue of additional angular correction made available by swiveling the distal fragment upon the proximal portion of the metatarsal. An offset-V osteotomy positioned through the shaft, with the dorsal arm exiting near mid-diaphysis, namley Kalish's modification of the Austin, is readily stabilized with 2 interfragmental compression screws. An offset-V osteotomy positioned through the shaft, with the dorsal arm exiting near the proximal metaphysis, nam!ey Vogler's shaft osteotomy, is ideally suited to enable a significant amount of transverse plane swivel of the dorsal fragment to reduce PASA (Figure 7-28), and may be used to correct rather large degrees of HAA and first IMA. The degree of displacement of the capital fragment in the Austin procedure, and ITs variations, is dependent upon the width of the metatarsal and orientation of the osteotomy. The plantar arm of the osteotomy creates a shelf that resists weight bearing, and the osteotomy is very stable when soft tissues are properly preserved. Fixation of the traditional Austin osteotomy is via buried or percutaneous K-wires, absorbable pins, or lag screws. Although originally described as an unfixated osteotomy, the addition of fixation decreases the likelihood of delayed union, loss of correction, and AVN of the capital fragment. Postoperative care involves weight bearing in a surgical shoe and early return (3-4 weeks) to a soft shoe or sneaker.

A

Figure 7.28

Oerotational Abductory Transpositional Osteotomy (ORATO}-a relatively difficult and infrequently used osteotomy of the metatarsal head that addresses valgus rotation, PASA, metatarsus prim us varus, and sagittal plane (usually elevatus) deformity. The DRATO osteotomy is performed through the cortical bone of the anatomic neck, and requires cast immobilization and K-wire stabilization. Complications, including AVN and delayed union, as well as technical difficulties which have limited the use of this procedure.


180

Ch. 7

Shaft osteotomies of the first metatarsal used for correction of HAV: Off-set V Osteotomy (Vogler}-a weight bearing, sagittal plane V-osteotomy !described above in the discussion of the Austin osteotomy) that extends

through the shaft of the metatarsaiiFig 7-29), allowing correction of a moderate to high first IMA, PASA via swiveling of the dorsal fragment, and application of lag screws or a K~wire or Steinmann pin for stabilization.

Figure 7.29

Gudas-scarf Osteotomy-this Z-plasty osteotomy accomplishes the same goals as does the Vogler

off-set V osteotomy, however it employs 3 bone cuts whereas the V-osteotomy employs just 2 cuts

!Fig 7-30). The osteotomy, and its shortened variation,

the short Z-osteotomy, is amenable to lag screw or pin fixation.

Figure 7.30

Ludlof!Osteotomy-this osteotomy involves a straight oblique transection of the metatarsal shaft from dorsal-proximal to plantar-distal, and is typically fixated wlth lag screws and maintained for 6-8 weeks non-weight bearing. The Ludloff design can be used to elongate the metatarsall-2 mm when indicated IFigure 7-31).

Mau Osteotomy--this osteotomy involves a straight oblique transection of the metatarsal similar to the Ludloff, however the orientation of the osteotomy is reversed \dorsal-distal to plantar-proximal) (Figure 7-32).

B Figure 7.31

Figure 7.32

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181

Proximal osteotomies of the first metatarsal and medial cuneiform, and metatarsocuneiform arthrodesis, for correction of HAV:

Juvara Oblique Base Wedge Osteotomy-employs the hinge axis concept (Figure 7-33) to create an oblique, closing abductory base wedge osteotomy that enables correction in the transverse and sagittal planes. The osteotomy is oblique and measures about twice the width of the metatarsal base. The Juvara is suitable for

correction of a first IMA of> 16°, as long as the bone stock is satisfactory and the metatarsal base not too narrow. It can be used in the presence of an open proximal physis, as long as the osteotomy is positioned distal to the growth plate. A dorsomedial hinge allows

reduction of the first IMA with plantar declination of the distal fragment. Use of a pure medial (vertical) hinge only allows reduction of the first IMA, whereas a plantarmedial hinge allows dorsal excursion along with reduction of the first IMA, and a dorsomedial hinge allows plantar excursion along with reduction of the first IMA. The osteotomy is ideally

suited forfixation using an anchor and lag, 2-screw arrangement. Potential complications include delayed or nonunion,shortening and/or elevatus with transfer metatarsalgia, and medial dorsal cutaneous neuritis (Figure 7-34). There are 3 variations of the Juvara oblique

base osteotomy:

Type A-oblique osteotomy directed from distal-lateral to proximal-medial, with an intact medial cortical hinge, the arms of the osteotomy creating an approximately 15° wedge resection. Type 8-proceeds as described for Type A, however the medial hinge is sectioned after wedge resection and a greater degree of sagittal plane manipulation can be achieved, as well as shortening or lengthening by means of swiveling or sliding the fragments upon one another. Type C-an oblique osteotomy without wedge resection, completing the hinge thereby allowing swiveling and sliding manipulations as in Type B.

Figure 7.33

Figure 7.34

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Ch. 7

Transverse Base Wedge (Louisan-Balacescu) Osteotomy--involves a transverse, closing abductory, base wedge osteotomy of the proximal metaphysis, and maintains an intact medial cortical hinge. The osteotomy is not amenable to lag screw fixation, and crossed K-wires or stainless steel wire suture are applicable, in conjunction with immobilization and non-weight bearing up to 6-8 weeks.

Crescentic Base Osteotomy-uses a crescent shaped saw blade to create a crescentic osteotomy in primarily the transverse plane (TP), offering easy manipulation ol the distal segment into a corrected alignment in the TP. Sagittal plane (SP) correction must

be addressed via orientation of the osteotomyto include motion in the SP. Minimal shortening occurs with this osteotomy if stabiliTy is maintained. Delayed union is the most likely complication, and crossed K-wire, lag screw and stainless steel wire suture fixation can be used in conjunction with immobilization and non-weight bearing for 6-8 weeks (Figure 7-35). Figure 7.35 Proximal Chevron Osteotomy-a chevron osteotomy can be positioned at the base of the metatarsal, and may be useful in regard to correction of the first IMA and a small to moderate amount of angulational correction can also be achieved by means of swiveling. The osteotomy can be fixated in a nuber of ways, including interfragmental compression screw or screws, or splintage methods, and non-weight bearing and immobilization for up to 6-8 weeks are indicated. Ope11ing Wedge (Trethoan) Osteotomy and Bone Graff----this repair can be performed on a short metatarsat and traditionally packs a medial base cortical osteotomy with the resected bone of the medial eminence (autogenous bone graft) to lengthen the medial cortex of the metatarsaL Consideration should be given to harvesting autogenous corticocancellous graft from the calcanean body, as the medial exostectomy may not provide adequate graft material. Alternatively, the use of a suitable bone graft substitute can work well. A staple or K-wire may be used to stabilize (non-compressive splintage) the graft, and immobilization and non~weight bearing up to 6-8 weeks are in order (Figure 7-36). Specialized locking fixation plates (Darco'" plates) are ideally suited to this procedure.

Figure 7.36

Lapidus Procedure (First MetatarsafwCuneiform Arlhrodesis)-applicable when there is DJD, pain and/or instability at the first metatarsal cuneiform articulation in conjunction with a high first IMA and bunion deformity, often observed with a round first metatarsal head. The Lapidus procedure may shorten the first ray, and it is combined with a bone graft for this reason. Fixation is usually via lag screws and a neutralization or load-screw plate applied to the medial-plantar aspect of the metatarsal and, as with the opening wedge procedure, specialized locking fixation plates (Darcor"' plates) are also suited to this procedure. Care must be takentto accurately manipulate the intercuneiform and intermetatarsal articulations as desired, and avoidance of excessive shortening is also important. Immobilization and non-weight bearing lor up to 10-12weeks may be in order (Figure 7-37).

Ch. 7


A

Figure 7.37

183

s·~·

Figure 7.38

Cotton Procedure (Medial Cuneiform Opening Wedge Osteotomy and Gralt)-this procedure addresses excessive first metatarsal-cuneiform adductus, and employs

application of the resected medial exostosis of the first metatarsal head or, more typically a bone graft substitute perhaps combined with ipsilateral calcaneal or distal tibial donor bone, as an autogenous graft placed into the opening medial cuneiform

osteotomy. The osteotomy preserves the lateral cortex of the medial cuneiform. Pin or staple splintage, or locking fixation plates, along with immobilization and non-weight bearing are also employed. Complications include cuneiform AVN, medial dorsal cutaneous neuritis, and TA tendinitis. This procedure may be applicable in the correction of metatarsus adductus, when combined with a closing wedge osteotomy of the cuboid. Epiphysiodesis for Juvenile HAV-this may be applicable for correction of mild juvenile HAV, wherein the first IMA is not greatly increased. Epiphysiodesis represents an effort to control the final position of the first metatarsal by either staple fixation or bone graft interposition at the lateral aspect of the first metatarsal base physis (Figure 7-38). The staple can be removed at a later date, however bone graft consolidation of the physis is permanent. Attention must be paid to standard growth charts, so that adaptation and subsequent growth can be anticipated.

Combination Procedures for Correction of HAV: Logroscino Procedure-application of a closing abductory base wedge osteotomy with the Reverdin osteotomy, for correction of a high first IMA and PASA, comprises the logroscino procedure. Use of an Austin-type chevron osteotomy has also been described in conjunction with a base wedge osteotomy. Obviously, double osteotomy is associated with extensive disruption of periosteal and epiphyseal blood supplies, and conveys a higher risk of bone healing complications. There have been cases reported of AVN of the intervening segment of first metatarsal, usually associated with loss of osteotomy stability proximally.

Stamm Procedure-this procudure involves application of an opening base wedge osteotomy and graft with the Keller procedure, and may be of historical importance only.


184

Ch. 7

go• Dorsal and proximal migration of instant center of motion of 1st MPJ as hallux dorsiflexes.

Neutral

A

8

Figure 7.39

HALLUX LIMITUS AND HALLUX RIGIDUS Hallux limitus/rigidus (HUHR)traditionally implies limitation of first MTPJ motion to less than 65° of dorsiflexfon, with excessive compressive load of the proximal phalangeal base upon the dorsal aspect of the first metatarsal head as the end range of motion is approached (Figure 7-39). More recently, it has been appreciated that at least 35" of first MTPJ dorsiflexion is typically needed for normal walking, and less motion will usually result in pain and inhibited ambulation. Some surgeons refer to any limitation of 1st MTPJ dorsiflexion, in general, as hallux rigidus. Others distinguish between limitus and rigidus, wherein rigid us is reserved for those cases that display minimal to no dorsiflexion. In this manual, we will referto the condition as hallux limitus/rigidus (HUHR). Etiologies of HUHR include metatarsus prim us elevatus related to hypermobile first ray, forefoot supinatus, or iatrogenic metatarsal elevatus following base wedge osteotomy; a long first metatarsal, which may be associated with a distal metaphyseal epiphysis (pseudoepiphysis); immobility of the first ray due to Lisfranc DJD or tarsal coalition; first MTPJ DJD due to osteoarthritis, longstanding HAV, or systemic arthritic involvement of the joint status-post trauma or iatrogenic deformity; and even a short first metatarsal wherein the hallux vigorously plantartlexes {hallux equinus) to stabilize the first ray in stance. Signs and symptoms include pain and swelling, stiffness and crepitus, dorsal bony prominence (dorsal bunion) and HIPJ overload with plantar hyperkeratosis, and lateral metatarsalgia due to antalgic guarding of the painful first ray, apropulsive gait, and fifth toe heloma durum formation. Radiographic signs include subchondral sclerosis, joint space narrowing, flattening of the metatarsal head, and osteophytosis with exostosis (dorsal flag sign) formation. In some cases, the metatarsal head displays a central ridge. It is important to ascertain the status and function of the sesamoids by loading the plantar aspect of the joint while dorsiflexing the hallux. Nonsurgical treatment of HUHR involves use of a metatarsal bar or tapered rocker-sole, orthosis control of hypermobility, and range of motion physical therapy; and these measures are combined with anti-inflammatory intervention, intraarticular chondroprotective agent (chondroitin sulfate and glycosaminoglycan preparations), and alteration of activities. The surgical treatment of HUHR is founded upon adequate chie!ectomy in conjunction with reconstructive osteotomy. Procedures include:

First MTPJ Chielectomy---involves removal of osteophytic proliferation via a dorsomedial, longitudinal capsulotomy. It is necessary to remove osteophytes and spur for-

Ch. 7


185

mation from the dorsal, medial and lateral aspects of the joint including the metatarsal head and the phalangeal base. The metatarsal elevator can be used to release capsular and sesamoidal adhesion plantarly at the flexor plate. loose or degenerated cartilage should be debrided and sculpted to an intact and smooth surface, and exposed subchondral cortical bone should be perforated with multiple 1.5 mm or 0.045" K-wire holes. Fenestration of the cortex enables mesenchymal stem cells from the medullary sinusoids to cover the articular surface and, under conditions of motion with reduced compression, convert to functional fibrocartilage. It is important to understand that chielectomy does not address structural deformity or the etiology that may have contributed to the condition in the first place. First MTJ range of motion is initiated early in the postoperative phase. Chielectomy is usually used in conjunction with metatarsal osteotomy and MTB, and serves as the foundation upon which almost all repairs of HUHR are based. Watermann Osteotom~a dorsally based trapezoidal wedge resection at the surgical neck of the metatarsal, designed to rotate plantar cartilage dorsally and decrease first MTPJ cubic content. Complications associated with the Watermann osteotomy include capital fragment instability, loss of correction, sesamoiditis, delayed and/or nonunion, AVN, and inability to truly rotate the articular surface without creating a transverse angular ridge at the apex of rotation. Excessive shortening of the first metatarsal may also predispose to lesser metatarsalgia. The McGiamry-modified Watermann osteotomy preserves a plantar cortical hinge, while resecting a dorsally based, pie-shaped wedge of metatarsal head that also rotates plantar cartilage dorsally and decreases internal cubic content of the joint \Figure 7-40). Fixation is via absorbable pins or suture, or metallic splintage wires or screws. The hallux may initially be splinted in dOrsiflexion for a few days, however early passive and active range of motion is desirable. The Watermann and McGiamry-modified Watermann are used in conjunction with chielectomy. Modified Green-Watermann Osteotomy-this involves chielectomy, and osteotomy of the metatarsal neck wherein a rectangular section of bone is excised from the dorsal aspect of the surgical neck, while a plantar arm (much like that used for the Austin osteotomy) exits the joint parallel to the substrate posterior to the articular surface IFig 7-41). An axis guide

Figure 7.40

Figure 7.41

186


Ch. 7

can be used to orient the arms of the osteotomy, and the first IMA can be reduced if necessary. This procedure enables shortening of the metatarsal while simultaneously allowing plantar declination ofthe capita! fragment, thereby decreasing the risk of lesser metatarsalgia. The osteotomy also avoids violation of the articular sutface with the osteotomy, decreasing both the risks of sesamoiditis and AVN. Fixation of the osteotomy is performed with lag screws, smooth or threaded K-wires, or absorbable pins. When threaded K-wires are used, they are cut flush to the cmlica! surface and retained indefinitely.

Austin Osteotomy and Variations-this osteotomy has been described above, and is applicable for correction of certain cases of H/HR. The apical axis guide is oriented to effect primarily plantar declination of the capital fragment, which also limits reduction of the first IMA. In the presence of concomitant HAV and HUHR, the Green· Watermann and Austin osteotomies enable simultaneous reduction of the first lMA, although the Green-Watermann osteotomy generally enables greater plantar declination without excessive shortening. The Youngswick modification of the Austin osteotomy entails removal of a trapezoidal wedge of bone from the dorsal arm of the proximal segment of the metatarsal, thereaby allowing plantar declination and some shortening of the first metatarsal. This procedure is versatile and readily stabilized with tapered absorbable pins, a K-wire, or an interfragmental compression screw.

Lambrinudi and Other First Metatarsal Plantarflexory Osteotomies---this employs an oblique wedge osteotomy directed from plantar~distal to dOrsal-proximal in the metatarsal base, with the base distal and the apex proximal, and is designed to correct structural metatarsus prim us elevatus (Figure 7-42). Instability of the first metatarsal-cuneiform joint contraindicates efforts at structural correction distal to the joint, and medial column lisfranc arthrodesis (such as the Lapidus) may be indicated. The osteotomy is fixated with lag screws. Excessive shortening of the first ray may complicate the Lambrinudi, however concomitant over-aggressive plantar declination usually results in weight bearing sesamoiditis. Various modifications of oblique base wedge osteotomy, abductory if reduction ofthe first IMA is indicated, can also be used to achieve plantar declination of the distal segment of the first metatarsal. Furthermore, osteotomy through the cortical hinge allows plantar displacement ofthe distal segment via swiveling in the sagittal plane (Figure 7-43). Oblique and step-down (Giannestras) shaft osteotomies can also be used to effect shortening and plantar declination of the distal segment of the first metatarsal (Figure 7·44). Opening Plantarflexory First Metatarsal Osteotomy--this can be used to correct metatarsus primus elevatus, and involves a dorsally based wedge graft of bone placed into an osteotomy of the dorsal portion of the proximal metaphysis of the first metatarsal base. Autogenous corticocancellous bone graft, or a suitable substitute, is used. Mayo Procedure and Stone Procedure--these involve varying degrees of first metatarsal head resection. The Mayo procedure involves oblique resection, from dorsal~proximal to plantar-distal in the sagittal plane, of the dorsal aspect of the metatarsal head. The osteotomy penetrates the articular surface centrally in the sagittal plane, and includes resection of any medial osteophytosis. The Stone procedure more aggressively resects the dorsal portion of the metatarsal head, and penetrates the articular surface just distal to the

Ch. 7

Reconstructive Surgery of Basic- Conditions and Deformities

187

Figure 7.43

Figure 7.42 Figure 7.44

sesamoids. In effect, the Stone procedure attempts to preserve the plantar cortical surface of the metatarsal head, while eliminating dorsal blockade to hallux dorsiflexion. Heuter Procedure--this involves complete excision of the first metatarsal head, and may be useful tor the treatment of osteomyelitis, or as a component of pan metatarsal head resection. This procedure irreversibly destroys the weight bearing function of the first ray, and is of historical interest only in regard to the treatment of HL/HR. Bonney~Kessel Osteotomy-this procedure involves resection of a dorsally based wedge of bone from the proximal metaphysis of the proximal phalanx of the hallux, however there is very little indication for this procedure as it does not address metatarsus prim us elevatus, degenerative changes of the first MTPJ, or length of the first metatarsaL It has been said thatthis procedure may be indicated in young patients without DJD, however it must be stressed thatfailure to definitively address the biomechanical and structural causes of HUHR may result in progressive first MTPJ degeneration even after apparently correcting lack of hallux dorsiflexion with a hallucial osteotomy. This criticism is analogous to that of the isolated Akin osteotomy in the treatment of HAV.

Base enclavement (Regnauld procedure}-employs creation of a hat-shaped osteocartilaginous proximal phalangeal base graft, in an effort to, theoretically decrease first MTPJ tension and enhance range of motion (Figure 7-45). The hat-shaped graft is harvested, and the proximal phalanx shortened via cylindrical resection of cortical bone, after which the graft is implanted into the residual medullary canal of the phalanx. Care must be taken to avoid proximal retraction of the sesamoids, which are the true weight-bearing level ofthe first ray, and to this end actual relaxation of tension through the first MTPJ may be compromised. The procedure has been shown most useful in repair of the traumatically or iatrogenically deformed first ray with metatarsus prim us varus aggravated by concomitant proximal phalangeal elevatus. Fixation Of the graft, despite its peg-in-hole arrangement can be tenuous, and crossed K-wires may be used.

188


Ch. 7

Figure 7.45 Keller Arthroplasty-the Keller procedure, which has been described above, can also be used to treat HUHR. first Metatarsophalangeal Arthrodesis (McKeever Fusion)-arthrodesis of the first MTPJ is a versatile and time-honored method of achieving a stable, pain-free alignment in the treatment of painful, inhibiting arthrosis (pain, decreased function, and deformity). Indications for arthrodesis include apropulsive gait, flail toe, neuromuscular disease (spastic or flaccid), failed implant, failed Keller, previous bone and/or joint sepsis, and previous intra~articular fracture. The technique is also applicable for rheumatoid forefoot reconstruction when combined with lesser metatarsal head resections and digital stabl!izations, and it can also be used to repair longstanding hallux varus or severe HAV, or Charcot degeneration of the first MTPJ. Contraindications include limited and/or painful HIPJ motion, and inadequate bone stock. It may be combined with HIPJ fusion when the IPJ is already arthritic or deformed. The optimum position affusion is parallel to the second toe in the transverse plane, approximately 15-20° of sagittal plane dorsiflexion (varies with anticipated heel height of shoes/boots), and a neutral frontal plane position. McKeever originally described a peg-in-hole technique, and modifications of this can be employed based on operative findings. However, effort should be made to minimize bone resection and shortening, and the technique of cartilage removal via curettage and perforation of the subchondral plate to expose cancellous bone works well, as long as adequate trabecular bone is exposed. Stabilization of the arthrodesis can be achieved with crossed K-wires (0.045 and/or 0.062"), a single axial retrograded 3/32" or 5/64" Steinmann pin, lag sc·rews, Herbert screws, tension band wire, cerclage wire, or a plate and screws, and there are specialized locking plates available for this procedure, as well. Immobilization and non-weight bearing may be helpful postoperatively, however it may be necessary to use a removable, modified walking cast or brace that floats the hallux, in patients with rheumatoid arthritis or neuroarthropathy. Advantages of first MTPJ arthrodesis include preservation of intrinsic attachments to the phalanx, stability, good cosmesis, improved weight bearing function of the first ray, and spontaneous reduction of the first IMA. Disadvantages include technical difficulties that relate to achieving the optimal position affusion; and post-fusion difficulty kneeling, potential HIPJ overload and degeneration, and potential delayed or nonunion. A bone growth stimulator may be helpful in cases of delayed union or anticipated bone healing difficulties.

Ch. 7


189

First Metatarsophalangeal Endoprosthesis (Implant Atthrop/asty)-patients suitable for first MTPJ end aprosthesis implantation should display adequate neurovascular status, skin coverage, bone stock, and adequate capsular and tendinous structures, as well as an understanding and acceptance of the procedure. Indications also include apropulsive gait, previous joint trauma, stiffness, and pain that inhibit weight bearing. Contraindications to endoprosthesis

implantation

include

dense

peripheral

neuropathy,

advanced

osteoporosis, excessively short proximal phalanx, inadequate joint and/or cutaneous coverage, and allergy to implant materials. Relative contra indications include previous septic arthritis, or a young and active patient. The goals of endoprosthesis implantation include the classic triad of reconstructive surgical goals: 1) decrease pain, 2) increase function, and 3) reduce deformity. Patients undergoing endoprosthesis placement should be informed of the subsequent need for prophylactic antibiotic therapy wheneverthey are subjected to invasive procedures and dental work. Implant design has improved greatly over the past 10~ 15 years, and use of a silicone polymer (Silastic®) joint spacer has given way to functional designs that enhance motion and bear weight during propulsion. Technical refinements related to endoprosthesis of the first MTPJ include reattachment of FHB and the sesamoid apparatus to the proximal phalanx, lengthening of EHL, sectioning FHL, and proper angulation of bone resection. Alternatives to joint implantation for the treatment of HUHR with DJD include Keller arthroplasty and first MTPJ arthrodesis. Complications associated with implants include stress~induced plastic deformation, osseous and implant stress fracture, and microscopic shard production (wear debris) that causes detritic synovitis with marked synovia! thickening. Softer implant materials, especially silicone polymer, are subject to wear~induced shard formation, although all biomaterials will eventually show microscopic wear~and~tear breakdown. Implant arthropathy consists of detritic synovitis, subchondral bone cyst formation, ectopic new bone proliferation, and aseptic necrosis. Host soft tissue inflammatory reactions are of the foreign body granuloma type, as shards are phagocytosed with resultant capsular fibroplasia and encapsulation. (Silicone polymer has also been used in the production of interphalangeal implants and as metatarsal caps following head resection.) Basic implant designs include hemi~implant endoprostheses and total joint replacement models.

Hemi·implant arthroplasty-silicone polymer hemi~implant functions as a spacer (not an endoprosthesis) and is rarely used in the first MTPJ. Indications for the hemHmplant included joint space narrowing, osteophytosis, joint subluxation, and preservation of a satisfactory first metatarsal articular surface, if the subchondral bone plate has good contour and direction and if resection of metatarsal head exostosis will not destroy functional articulating surface. The technique of hemi~ implantation involved dissection of the first MTPJ in a fashion consistent with that described for the Keller bunionectomy. lt is possible to perform a Reverdin or Austin osteotomy when hemi-implanting. The proximal phalangeal base is transacted perpendicular to the long axis of proximal phalanx (5 -10 degrees of abductus is physiologic), and the hub ofthe implant should be wider than the cortical width ofthe phalanx. An excessively wide implant may limit range of motion. The medial capsular flap, which is made long via a vertical incision at aboutthe mid~diaphyseal level (as is done when performing the Keller) of the proximal phalanx, is reattached following implant sizing and placement. The capsular flap is attached via drill holes in the phalanx positioned dorsomedial and plantar medial, while a central plantar drill hole is used to reattach the intersesamoidal ligament or the FHB directly, using 2~0

190


Ch. 7

nonabsorbable suture. The Weil angulated hemi-!mplant incorporates a 15° lateral deviation of the phalangeal base surface, designed to compensate for

deviation of the first metatarsal articular surface (increased PASA).

Total implant arthroplasty (total replacement arthroplasty}-the total implant is applicable, in limited situations, where severe DJD of both articular surfaces has caused hallux rigidus. The Swanson-designed total implant, manufactured by Dow-Corning Wright is made of Silastic® silicone polymer. Contraindications

include a high first IMA and excessive HAA, as the implant cannot stand up to

angular deforming forces over time. Prolonged angular deformation of the implant will result in implant degradation, and/or osseous erosion and/or fracture. Metatarsal length is preserved in an effort to avoid transfer metatarsalgia, and the majority of bone is resected from the phalanx. Titanium grommets are available to fltoverthe implant stems, and function to shield the silicone polymerfrom wear at the bone interface. Sutter Biomedical's Lawrence~designed total implant displays a proxima! stem that is angu!ated 15° dorsally, to correspond to first metatarsal declination; and their La Porta-designed total implants display right, left, and neutral transverse plane sided angulated stems. When performing total implant arthroplasty, the first IMA is corrected via closing abductory base wedge osteotomy when indicated, or via aggressive distal and dorsal first metatarsal resection using the Mayo partial head resection. Complications of total joint implantation include floating or non~purchasing hallux, if too much metatarsal head is removed dorsally; limited dorsiflexion and transfer metatarsalgia, if too much metatarsal head is removed plantarly.

Multicomponent First MTPJ Endoprosthesis-these are designed to resist wear-induced degradation while providing a degree of functional weight bearing and motion in the first ray. They combine high density polyethylene I HOP) and cobalt-chromium ICoCr) and/or titanium alloy. Wear surfaces are made of HOP and CoCr, while scintered stems of titanium provide a Young's modulus compatible with bone. Polymethylmethacrylate bone cement may be used as a leuting agent to secure the implant stems, however is usually not necessary when appropriate broaches are used to seat the device. These systems also employ osteotomy jigs {guides) for preparation of the metatarsal and phalangeal surtaces to assure proper fit without excessive bone loss, and allow near~physiological range of motion while maintaining the weight~bearing level of the sesamoid apparatus. Accumet's great toe implant employs an extended dorsal flange thattheoretically allows anatomic range of motion as the first metatarsal plantarflexes and the hallux glides dorsally. The Biomet two component endoprosthesis combines HDP and CoCr at the wear surfaces. The Bioaction total endoprosthesis is anothertwo~component system made of HOP, CoCr and titanium. and·employs a plantar flange that articulates with the sesamoids and theoretically enhances weight bearing through the first ray. Autologous Cartilage Transplant Procedures (OATS and ACT}-osteoarticular transfer system (OATS) is a surgical procedure used to treat focal cartilage defects. An osteochondral graft is usually harvested as multiple plugs procured from a non~weight bearing surface of the knee, or the head of the talus, or some other non-contact articular site. Once procured, the plugs are transplanted to the recipeint site

Ch. 7


191

in a mosaic fashion. Care must be taken to try and match subchondral cortical contour and cartilage thickness between the donor and recipient sites. The donor site usually heals by secondary intention, and the recipient site heals by means of graft incorporation and fibrocartilage regeneration. It is important to maintain range of motion under reduced pressure, during the healing phase. Another potentially useful method is that of autologous chondrocyte transplant (ACT), which is a procedure that entails collection of normal cartilage cells from, typically, inside the knee and are then sent to a laboratory to grow for several weeks in tissue culture. Once they are grown in the laboratory, the chondrocytes are then transplanted to the recipient site and secured by means of articular reconstruction that will enable reduced weight bearing motion in the postoperative phase. A summary olthe surgical options lor the treatment of H[jHR is depicted in Table 7-2.

TABlE 7-2. A STEPWISE APPROACH TO HAllUX LIMITUS/RIGIDUS. Amount of first metatarsal head

articular degeneration

Surgical options to be used alone or in combination

<50% of central third of distal surface

Arthroplasty Cheilectomy and cartilage sculpting Subchondral drilling (or cultured, autogenous cartilage cell transplant) Arthrodiastasis Reconstructive osteotomy Plantar and proximal displacement (decompression)

?:":50% of centra! third of distal surtace

Arthrodesis Keller-type arthroplasty Endoprosthesis Autologous cartilage transplant (OATS) Cultured cartilage celt transplant

HALLUX VARUS Hallux varus involves an adductus and/or varus deviation of the hallux at the first MTPJ, and is usually observed as a complication of hallux valgus surgery. Contributing iatrogenic influences include excessive resection of the medial eminence (staking the metatarsal head), excision of the fibular sesamoid, overcorrection of the intermetatarsal angle, over-tightening of the medial capsule, and overcorrection of the PASA. The condition can also occur post-traumatically, congenitally or secondary to neuromuscular imbalance. Symptoms include difficulty wearing conventional shoes, pain along the medial aspect of the hallux secondary to shoe pressure, medial arch pain due to abductor ha!lucis spasm, and pain and crepitus and !imitus due to first MTPJ OJO. Clinical signs include adduction and/or varus of the hal!ux, plantart!exion contracture of the hallux IPJ, and EHL contracture effecting dorsiflexion of the MTPJ. Radiographic signs include hallux adductus, a reduced or negative first IMA, possibly staked first metatarsal head and/or absent fibular sesamoid, the presence of a previous osteotomy of the first metatarsal, a negative PASA, and MTPJ DJD (narrowing, sclerosis, irregular contour). Non-surgical treatment includes counter-

192


Ch. 7

~

I

Figure 7.46 bandaging, padding, and shoe weac Not every hallux varus requires surgical repair, however significant deformity should be corrected as early as possible to prevent resultant DJD. There is no single surgical procedure, but rather the causative factor must be determined and corrected along with any secondary deformities that may have developed. Surgical repair entails complete soft tissue release, correction of structural deformity (reverse negative IMA), tendon transfer about the first MTPJ (Figure 7-46), tibial sesamoidectomy, and arthroplasty or fusion in severe or degenerative cases. Arthrodesis is preferred in cases of neuromuscular imbalance or spasticity.

HALLUX INTERPHALANGEAL ARTHRODESIS Hallux interphalangeal arthrodesis is usually used as an adjunct procedure in cavus foot reconstruction, or following excision of the hallucial sesamoids. The deformity of hallux malleolus, or cock~up hallux, can be repaired with hallux interphalangeal arthrodesis. Indications for HIPJ arthrodesis include the presence of partially or nonreducible HIPJ contracture, painful hyperkeratotic or ulcerative lesion overlying the IPJ, transverse or frontal plane hallux deformity, hallux hammertoe, or an abnormally short or long hallux. Signs and symptoms include painful and/or limited HIPJ motion; lichenification, keratoma,

or ulceration; and inability to wear regular shoes. Radiographic findings include the contracted IPJ, joint space narrowing, osteophytosis, and subchondral sclerosis; abnormal hallux interphalangeal abductus angle; abnormal hallux length; and adequate bone stock should be present when arthrodesis is considered. Biomechanical observations associated with the need to fuse the HIPJ include instability of first ray and/or MTPJ causing an abnormal weight-bearing position of the hallux, and severe pronatory imbalance effecting forefoot supinatus, or loss of sesamoid stabilization of the hallux. Surgery should be considered if a digital retainer and balanced inlay with a roller sole have not satisfactorily alleviated symptoms. The surgical approach to the HlPJ is via either a lazy-S, L-shaped, or two semi-elliptical incisions. The joint is resected with attention paid to angulation and length, and planned fixation method. A variety affixation methods can be used, including stainless steel monofilament wire (single or double box loops of 20 or 22 gauge stainless steel wire), two crossed 0.045" K-wires, a single 4.0 mm cancellous lag screw, a single 3.5 mm cortical lag screw, and a 2.7 mm cortical lag screw. Advantages of the stainless steel wire suture technique include relatively easy application and minimal instrumentation, no need for intraoperative radiographs, can be used


Ch. 7

193

in conjunction with first MTPJ endoprosthesis, and it can be used when a sagittal plane deformity of the hallux is maintained. Disadvantages of the stainless steel wire technique include pull~through in osteoporotic bone, requires intact cortical bone adjacentto the fusion, difficulty achieving uniform interfragmental compression, and the wire becomes a permanent fixation device. Advantages of the K-wire technique include easy application and minimal instrumentation, and affords effective splintage even in osteoporotic bone, and it need not be permanent if placed percutaneously, and it can be used when a sagittal plane deformity of the hallux is maintained. Disadvantages of the K-wire include frequent need to confirm alignment radiographically, pin-tract infection, difficulty when used in conjunction with first MTPJ endoprosthesis, and inability to generate interfragmenta! compression. Advantages of screw fixation for HIPJ fusion include interfragmental compression, typically rapid primary bone healing ensues, and earlier mobilization of the first MTPJ is possible. Disadvantages of the lag screw technique include technical difficulties with screw purchase and instrumentation, prominence of the screw head distally at the hyponychium, screw removal is usually indicated (and quite easy), intra-operative radiographs should be taken, not amenable to concomitant first MTPJ endoprosthesis placement with stem of the implant secured in the proximal phalanx, and sagittal plane hallux deformity must be corrected in order to enable the screw to seat properly in the phalanges. Postoperative management includes use of a built-up surgical shoe, cast, and/or non-weight bearing for reduction of push-off loading of the hallux for 6-8 weeks. Percutaneous pins can be removed at about 6-8 weeks pending radiographic and clinical evidence of consolidation. A lag screw inserted from distal to proximal should usually be removed at approximately 8weeks postoperative, unless the screw head has not caused any distal irritation.

FIRST METATARSOCUNEIFORM EXOSTOSIS This degenerative process generally accompanies chronic first ray hypermobility and dorsal jamming atthe metatarsocuneiform joint (MCJ). It can be seen in anterior cavus, as well as forefoot supinatus, and is overall a component of Usfranc DJD. Over time, the dorsal aspect of the MCJ becomes prominent, while plantar gapping occurs. Signs and symptoms include cutaneous erythema, difficulty fitting shoes, medial dorsal cutaneous neuritis, MCJ bursitis, EHL tendinitis and/or vamp disease. Anatomic considerations relating to surgical intervention include the EHL and TA tendons, and the neurovascular bundle. First MCJ exostosis is categorized as depleted in Table 7-3.

TABLE 7-3. FIRST METATARSOCUNEIFORM EXOSTOSIS. Type of metatarsocuneiform exostosis

Clinical description of exostosis Localized dorsal exostosis

II

Dorsal exostosis with MCJ arthritis

Ill

Dorsal exostosis with angular deformity, such as adduction of the cuneiform and first metatarsal

IV

Hyperostosis that extends across the entire Lisfranc joint complex

v

Pseudoexostosis of anterior cavus, wherein an actual exostosis is not present, although the dorsum of the articulation is relatively prominent

194

Reconstructive Surgery of Basic Conditions and Defonnities

Ch. 7

Exposure of the exostosis can be approached from the medial aspect via a curvilinear incision situated between the EHL and TA tendons, and this will allow retraction of the dorsal neurovascular elements while providing access to the dorsal exostosis. Exostectomy is performed with osteotome and mallet or power instrumentation, followed by hand rasping. The articular margins should be saucerized. lf articular degeneration is extensive, then arthrodesis should be considered, and is usually achieved with a combination of lag screws

and a neutralization or

load~screw

plate situated on the

medial~piantar

aspect of the

metatarsocuneiform fusion interface. Specialized locking plates are also available for this fusion. Postoperative care involves application of a compression dressing and mobilization and weight bearing to tolerance following exostectomy, or immobilization and non-weight bearing following arthrodesis.

INTERMEDIATE (CENTRAl, Second-through-Fourth RAYS} METATARSAlGIA and DEFORMITIES The primary causes of lesser ray pathology are dynamic in nature, and include retrograde buckling of contracted digits (flexors stabilization, extensor substitution, and flexor substitution}, hypermobile first ray and hallux limitus/rigidus effecting lateral dumping of weight bearing, and various forms of ankle equinus and dropfoot Isolated structural deformities affecting the intermediate rays are less common, but certainly exist and must be considered when evaluating the patient with lesser metatarsalgia. Isolated structural deformities may be congenitat post-traumatic" or iatrogenic; and include hypertrophic plantar condyle, elongated metatarsal or adjacent brachymetatarsia, isolated metatarsal equinus, or adjacent elevatus. Radiographic inspection of the intermediate lesser metatarsals should include the lateral oblique projection, as this allows comparison of the sagittal plane relationship of the central metatarsals. The metatarsal axial view, and measurement of relative metatarsal protrusion on the weight bearing A~P view, may also be helpful. Signs and symptoms include metatarsalgia, IPK, diffuse tyloma, and MTPJ enthesitis. The differential diagnosis entails functional and structural etiologies, as well as systemic arthritis, intermetatarsal neuroma, MTPJ enthesitis and/or bursitis, stress fracture, thrombocytosis and erythromelalgia. Treatment involves attention to the dynamic etiology, and conservative protection of the metatarsus, as well as anti-inflammatory measures both systemic and local, and physical measures. Application of a metatarsal projection pad to the insole proximal to the metatarsal heads, in conjunction with digital retainers and supportive shoes, perhaps with a roller sole, can be helpful. A forefoot extension with aperture padding may also be used. Surgical intervention usually entails digital stabilization and MTPJ relocation via the sequential release. Isolated metatarsal osteotomy may be used if digital surgery and supportive measures prove inadequate. Caution is practiced when considering intermediate lesser metatarsal osteotomy, as the incidence of recurrence, transfer lesion, floating toe, delayed and/or nonunion are relatively high, especially when osteotomy fixation is notpursued.lntermetatarsal osseous bridging may develop in cases wherein multiple adjacent metatarsal osteotomies are performed, even when fixation, immobilization, and non-weight bearing are employed. Selected lesser metatarsal surgical procedures include plantar condylectomy, distal and proximal osteotomies, shaft osteotomies, and adjunct techniques such as syndactyly and bone grafting. It is important to understand the need for appropriate digital stabilization and MTPJ alignment when it comes to successful management of lesser metatarsalgia, and the foundation role that digital stabilization plays relative to metatarsal surgery. A number of surgical procedures are useful for treatment of intermediate metatarsalgia, and include:

Ch. 7


195

Plantar condylectomy-used to reduce a hypertrophic or prominent plantarlateral metatarsal head condyle, and is rarely indicated as an isolated procedure. The procedure is usually performed via a dorsal longitudinal incision over the MTPJ and is often combined with arthrodesis of the corresponding and adjacent central PIPJ and sequential release of the MTPJs, and syndactyly of the corresponding toe to the adjacent stabilized digit. Syndactyly is an important adjunct procedure, as condylectomy results in decreased MTPJ

cubic content that, in turn, allows the toe to float dorsally due to loss of plantar tethering. The MTPJ capsulotomy enables plantar displacement of the toe and exposure of the plantar condyles ofthe metatarsal head. Use of the metatarsal elevator may expedite this exposure and delivery of the metatarsal head into view. The hypertrophic condyle is then resected with the osteotome and mallet, and the remaining bone smoothed with the rasp. A temporary K-wire may be used to stabilize the toe and MTPJ if necessary. Layer closure ensues, with attention paid to avoiding excessive EDL tension. A built-up surgical shoe will be necessary if the MTPJ is pinned.

Wei/ osteotomy-this is a powerful procedure for shortening and elevating the capital fragment of the metatarsal by means of a dorsal-distal to plantar-proximal oblique osteotomythatcan be fixated with a single 2.0 or2.7 mm interfragmental compression screw from dorsal to plantar. Caution should be taken in regard to the prevention of a postoperative floating toe, which can accompany any shortening or elevating metatarsal osteotomy, or procedure that decreases the internal cubic content of the MTPJ, such as plantar condylectomy. Jacoby V-osteotomy-involves a transverse plane chevron osteotomy, through-andthrough from dorsal to plantar at the surgical neck, with base proximal and apex distal. The approach entails dorsal dissection, digital stabilization, and MTPJ relocation. This osteotomy can also be used to plantar declinate the capital fragment when indicated. The osteotomy is stabilized with a K-wire, either from proximal to distal or through the stabilized digit and MTPJ in an axial (medullary nail) fashion.

Dorsiflexory wedge osteotomy (DFWO}-there are several variations of dorsiflexory wedge osteotomy (OFWO). including distal metaphyseal (surgical neck) osteotomies such as the transverse tilt-up and oblique wedge osteotomies; and the oblique base wedge osteotomy. Distal osteotomies are readily fixated with an axial K-wire used to simultaneously stabilize the corresponding digital arthrodesis and MTPJ relocation. The dorsal-distal to plantar-proximal oblique distal DFWO at the anatomic neck usually involves resection of only a thin wedge !thickness ofthe saw blade) of bone, and can be fixated with a K-wire or a lag screw (Figure 7-47). The same dorsal-distal to plantar-proximal oblique DFWO can be placed atthe metatarsal base, and stabilized with K-wires or a lag screw. Lesser metatarsal shah osteotomy-a variety of shaft osteotomies can be used, often in conjunction with bone grafting. The Giannestras step~down osteotomy is classical!y used to shorten a metatarsal, however it can also be used to elongate. The step-down osteotomy isthrough~and-through, and involves complete exposure of the metatarsal. The osteotomy consists of three cuts oriented in the transverse plane. The proximal and distal transverse arms exit opposite sides (medial or lateral) of the cortex, and are united by a longitudinal central arm. When shortening is desired, an additional proximal and distal transverse cut is made from the shaft segments. The osteotomy can be oriented somewhat in the sagittal

196


Ch. 7

Figure 7.47 plane, in an effort to facilitate !ag screw fixation. Variations on the Ludloff and Mau, Gudas-

scarf Z-p!asty, and offset V-osteotomy, oriented in both the transverse and sagittal planes, have all been used for lesser metatarsal shaft reconstruction. The sliding osteotomies are more suitable to interpositional bone grafting with lag screw fixation.

FIFTH METATARSAL SURGERY AND THE TAILOR'S BUNION The tailor's bunion deformity is observed in the uncompensated or partially compensated rearfoot or forefoot varus foot types, which predispose to hypermobility of the fifth ray in response to ground reactive forces. The plantarflexed fifth metatarsal will adduct, evert and dorsiflex in response to the ground reactive force; and may present with a plantarlateral bursitis, hyperkeratosis, and pain. A congenitally dorsiflexed fifth ray may also result in tailor's bunion symptoms, usually with a dorsolateral or lateral lesion. Weight bearing radiographic analysis of the tailor's bunion deformity will usually display rotation of the plantarlateral tubercle to a more lateral position, consistent with pronatory eversion of the metatarsal. There will often be an increase in both the fourth IMA above 6.5°, and the lateral deviation (bowing) angle above 2.JO. There is often a dumbell-shaped and enlarged fifth metatarsal head, and arthritic changes with osteophytosis may be present. When the foot clinically appears to be very wide, the combination offirst IMA >12" and a fourth IMA >8° is consistent with splayfoot deformity, and the tailor's bunion is often the primary area of patient concern. Surgical goals in the treatment of tailor's bunion focus on elimination of prominent lateral exostosis, either dorsal or plantar; along with correction of structural deviations such as excessive fourth IMA and/or lateral bowing. Adjunct procedures may include correction of an adductovarusflfth hammertoe. Specific procedures for correction oftailor's bunion deformity include:

Lateralexostectomy-this procedure (Fig 7-48), performed performed on mild tailor's bunions as an isolated procedure, or in conjunction with other structural corrections and a variety of fifth metatarsal osteotomies. If an over-aggressive lateral exostectomy is performed (staking the metatarsal head) in the presence of structural bowing or a high fourth IMA, excessive fifth MTPJ laxity will lead to adductovarus fifth toe contracture and retrograde MTPJ buckling with recurrence and worsening of deformity. fifth metatarsal head excisiotr-a radical procedure that involves head resection at the

anatomic neck and usually well tolerated in less ambulatory individuals due to the fifth ray's independent axis of motion; it may be indicated too, in cases of fifth metatarsal head osteomyelitis, tumor or avascular necrosis.

Ch. 7


Hohmann

Reverse Wilson

Figure 7.49

Figure 7.48

Mitchell

Figure 7.51A

197

Figure 7.50

Thomasen's

Figure 7.51 B

Hohmann osteotom~a transverse through-and-through osteotomy at the anatomic neck, usually stabilized with a K-wire (Fig 7-49).

Reverse Wilson osteotomy---an oblique osteotomy from distal-lateral to proximalmedial often floated but better to be stabilized with a K-wire (Fig 7-50).

Mitchell osteotomy---a variation of the first metatarsal osteotomy that may be limited by a narrow fifth metatarsal neck; this osteotomy is at risk for dorsiflexion if subjected to early weight bearing (Figure 7-51A).

Thomasen's osteotomy--a peg-in-hole variation of the Hohmann osteotomy, usually stabilized with a K-wire (Fig 7-51 B).

198

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities j

Figure 7.52

Figure 7.53

Figure 7.54

Reverse Austin osteotomy-a sagittal plane chevron limited by the width of the metatarsal neck and stabilized with a K-wire or absorbable pin (Fig 7-52).

Closing adductory osteotomy at neck (MercadoHistal transverse plane medially based wedge osteotomy with an intact lateral cortical hinge, stabilized wH:h either a K-wire or stainless steel wire suture, or both (Fig 7-53).

Closing adductory base wedge osteotomy (Gerbett}-a transverse plane medially based wedge osteotomy with an intact lateral cortical hinge, fixated with a K-wire and or stainless steel wire suture, or made oblique to facilitate lag screw fixation

Oblique wedge osteotomy-located at the apex of the bowing deformity, fixated with a Kwire and or stainless steel wire suture, or lag screws (Fig 7-54). HEEl SURGERY Approximately 15% of all adult foot complaints are related to disorders of the heel. The circulation to the heel entails the medial calcaneal branches of posterior tibial artery medially, the communicating branches of the peroneal and lateral malleolar arteries laterally and plantarly, and communicating branches posteriorly. The neutral or vascular triangle, of the calcaneus is the radiolucent area observed in the lateral radiograph, inferior to the sustentaculum tali within the body of the calcaneus, where the subtalar pressure trabeculae combine with traction trabeculae formed in response to the pull ofthe plantar fascia and Achilles tendon are seen under sustentaculum tali.

Plantar Fascitis and Heel Spur Syndrome---this condition results tram prolonged, excessive tension in the plantar fascia, usual!ysecondaryto hyperpronation of the STJ/MTJ, and eventually leads to fasciosis at or near the attachment of the plantar fascia to the calcaneus. Overtime, an elongated plantar spur may also develop atthe attachment of the fascia. Stress fracture may lead to development of a prominent plantar protrusion. Chronic inflammation of the fascia, with or without spur formation, may also be associated with distal tarsal (calcanea!) tunnel syndrome. The diagnosis is made based on localization of

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199

focal, deep tenderness to the fascial attachment to the calcaneus, the presence of similar pain upon activation of the plantar windlass (simultaneous dorsiflexion of the MTPJs and ankle, with the knee extended); post-static dyskinesia, and radiographic evidence of a plantar spur in about 75% of cases. A distinct plantar spur need not be ·present to effect pain. Differential diagnostic considerations for plantar heel pain include lumbosacral radiculopathy, systemic arthritis, tarsal tunnel syndrome, subcalcaneal bursitis, contusion

or local trauma, stress fracture, entrapment neuropathy of the lateral plantar nerve and its muscular branch, diffuse idiopathic skeletal hyperostosis (DISH) syndrome, Paget's disease, and heel neuroma. A bone scan may be helpful in resistant cases when stress

fracture is suspected. Conservative treatment combines biomechanical, pharmacological, physical, and surgical therapies (Table 7-4).

TABLE 7-4. TREATMENT HIERARCHY FOR PLANTAR FASCIITIS AND HEEL SPUR SYNDROME. Intervention

Slagel

Stage II

Pharmacological

NSAID Local steroid Oral steroid

NSAID

Biomechanical

Low Dye strap Custom orthotic Prefabricated Roller sole

Stage Ill

Stage IV

Immobilization

orthotic Physical Surgical

Ice Flexibility

Iontophoresis

Night splint Dynamic splint ESWT

Cold ablation

microdebridement, fa scioto my, spur resection;

bursectomy fxtracorporeal Shockwave Therapy(ESWT}-shockwaves consist of high amplitude, fast rising, asymmetrical, low frequency (>500 bar in 33 nanoseconds) sound energy that imparts intense pressure to the target tissues, namely the plantar fascia. Shockwaves can be generated by means of piezoelectric crystals or ceramics, electromagnetic energy, and electrohydraulic vaporization of water. Shockwaves have been used in the treatment of tendinosis calcarea (shoulder), lateral epicondylitis (tennis elbow), cedial epicondylitis (golf elbow), chronic calcifications (thigh, apophysis), patellar tendinitis, ossoue nonunions and pseudarthrosis, nephrolithiasis, and microscopic studies into the potential use in the treatment of cancer and CNS lesions are alos underway. In order to treat plantar fasciitis, shockwaves must deliver 0.26·0.32 mJ/mm2 of energy to the target fascia. This causes physical alteration of small axons, inhibiting impulse conduction, chemical alteration of pain receptor neurotransmitter, and hyperstimulation analgesia (gate control); as well as neovascularization. Resultant tissue absorption and deformation create a wound healing response that, in 3-6 weeks, may relieve chronic pain related to plantar fasciitis. Weight bearing is immediate following ESWT. Potential complications of ESWT include subcutaneous hematoma, skin erosion, swelling, petecchial hemorrhage, pain and

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Ch. 7

paresthesia, and vasovagal syncope. Contraindications to ESWT include pregnancy, children, nerve damage, tarsal tunnel syndrome, tarsal tunnel syndrome, osteoporosis, rheumatoid arthritis, peripheral vascular disease, infection or tumor, bleeding diasthesis,

cardiac pacemaker, and healing fracture. Radiofrequency cold ablation (Coblationm} microdebridement-the plantar fascia can be debrided in an open fashion by means of a small incision over the proximal portion of the fascia, and application of 15-20 high voltage radiofrequency impulses in a saline medium that creates a plasma layer between the concentric electrodes at the tip of the probe, and disrupt the molecular bonds in the target tissue, thereby effecting localized fascia debridement with minimal collateral tissue destruction. Non~weight bearing, or partial weight bearing is employed following cold ablation debridement of the plantar fascia, varying with the nature of the plantar skin incision, surgeon's preference, and the amount of debridement undertaken.

Plantar Fasciotomy and Calcaneal Spur Resection---exposure of the attachment of the plantar fascia to the calcaneus, and the plantar spur, can be achieved through a plantar transverse, longitudinal, or oblique incision. Of historical .interest is the distally-based U~shaped pedicle flap Griffith incision, which can be used to expose the entire plantar aspect of the calcaneus. The medial DuVries approach can also be used, however this incision makes the medial calcanean nerves vulnerable to post-incisional entrapment. The deep plantar fascia is identified and sectioned from the calcaneal tuberosity, and the plantar spur resected. A small segment of the most proximal fibers of the plantar fascia is retained for pathological inspection. It is important to re-establish a normal cortical contour when the spur involves prominent plantar protrusion, even if fascitis has been essentially resolved with conservative measures. Care must be taken to avoid injury to the lateral plantar nerve and its branches, and over~aggressive resection of bone as this could weaken the calcaneus and predispose it to fracture. Other complications include recurrence, hematoma, scar pain, and chronic plantar enthesitis. A compressive dressing is applied, and early ankle range of motion and 3 weeks non-weight bearing ensue. Non~weight bearing is necessary in order to allow the plantar skin wound to heal. A wide range of techniques have been used over the years for the treatment of recalcitrant plantar heel pain, some of which are of historical interest only while others show useful application. Variations on the general theme of fasciotomy and spur resection include minimal incision or semi-closed approaches wherein the fascia is released and the spur remodeled under fluoroscopic guidance, or via topographical guidance and identification of palpable landmarks. Instep plantarfasciotomy, localized to the mid portion ofthe medial band of the plantar fascia, and not addressing the calcaneus, can also be useful in some cases. Historically, spur reduction has been addressed with a countersinking osteotomy, or a rotational osteotomy combined with tendoAchillis lengthening. Endoscopic Plantar Fasciotomy (EPF}-endoscopic plantar fasciotomy has been shown to be a useful option for releasing the fascia, and is based on the theory that the spur need not be remodeled in order to alleviate plantar heel pain. The procedure is performed under local or general anesthesia, and uses a blunt obturator to channel from medial to lateral across the heel after initially making an incision through which the obturator is passed. The deep fascia is visualized by passing a slotted cannula with obturator from medial to lateral and rotating the slot toward the fascia. An L~shaped blade is then inserted from lateral to

Ch. 7


201

medial while viewing through the endoscope, which is inserted from medial to lateral. The blade is turned dorsally at the medial margin of the fascia, and then pulled laterally. Fasciotomy is directly viewed, and several passes of the blade are usually necessary to adequately section the fascia. Care is taken when inserting and removing the L-shaped blade through the lateral incision. The wound is Javaged and skin closure performed, followed by application of a compressive dressing. It is also possible to reduce bony prominence endoscopically with the rota-osteotome and shaver, however this is generally

not done. External Neurolysis-if the cause of plantar heel pain is thought to be entrapment neuropathy of the lateral plantar nerve and/or its muscular branch (inferior calcaneal nerve and calcaneal tunnel syndromeL then external neurolysis of the nerve trunks may be in order. External neurolysis, however, is usually performed in conjunction with fasciotomy and spur reduction. External neurolysis is best performed with the use of fine-tipped instrumentation and Ioupe magnification.

Calcaneal Decompression-decompression of calcaneal intramedullary pressure, via multiple small drill or K-wire holes aligned obliquely from posterior-proximal to anteriordistal (dorsal cortex to plantar cortex) through the cortex of the calcaneal body, has also been espoused as a treatment for plantar calcaneal pain. Currently, this procedure is primarily of historical interest only, although there is some basis to its use. In essence, the decompression holes result in cortical fracture when subjected to the pull of the Achilles tendon and plantarfascia, thereby reducing tension in these soft tissues after resumption of weight bearing. Calcaneal joint depression fracture is an obvious risk of the decompression technique. Haglund's Deformity-this deformity consists of prominence of the posterosuperior aspect (bursal projection) of the calcaneus. It can be structural or positional, or a combination of both. A variety of radiographic observations (Figure 7-55) are used to assess the posterior aspect of the calcaneus. The Fowler and Philip angle (FPA) normally ranges from 44"-69", and an FPA >75° will often present with posterior swelling, cutaneous compromise and prominence just superior to Achilles insertion. Prominence of the posterior aspect of the calcaneus predisposes to the development of retrocalcaneal bursitis, as the constant pre-Achilles bursa becomes repetitively irritated with anl
s T 1) Angle of Fowler & Philip 2) Calcaneal inclination angle 3) Total angle

Figure 7.55

A

Figure 7.56

202


Ch. 7

posterior aspect of the heel to irritate the retrocalcaneal bursa, as this measurement takes into accountthe calcaneal inclination angle (CIA) and posterior structural prominence (FPA). A total angle> 90° correlates highly with retrocalcanea! bursitis and Haglund's deformity. Parallel pitch lines IPPL) have also been used to assess the prominence of the posterosuperior prominence of the body of the calcaneus. An adventitious superficial calcaneal bursa may develop superficial to the Achilles tendon secondary to repetitive mechanical irritation. Kager's triangle is demarcated by the long flexor tendons anteriorly, the Achilles tendon posteriorly, and the superior surface of the calcaneus inferiorly, and Is visualized in the lateral radiograph as a dark, radiolucent triangle with apex pointed dorsally. Kager's triangle represents the pre-Achilles fat pad. Thickening of the Achilles, which is usually about 9 mm wide in the lateral radiograph, due to retrocalcaneal bursitis and/or tendinitis will encroach on Kager's triangle and blur the usually sharp interface with the pre-Achilles fat pad. The calcaneal apophysis usually closes at 14-16 years of age. Biomechanical foot types associated with increased motion between the posterior aspect of the heel and the shoe counter, thereby aggravated by Haglund's deformity, include compensated reatfootvarus, compensated forefoot valgus, and rigid plantatflexed first ray. Symptomatic Haglund's deformity is most commonly observed in young to middleaged females; with pain and cutaneous irritation at the posterior aspect of the heel, radiographic evidence of a cortically intact bursal projection, loss of the pre-Achilles recess indicative of retrocalcaneal bursitis, Achilles tendon widening > 9 mm indicative of tendinitis, and loss of distinction of the posterior margin of Kager's triangle. A tender superficial Achilles bursitis may be present, and causes the classic "pump bump" aggravated by shoes with a tight counter and elevated heel height. Treatment of the symptomatic Haglund's deformity, due either to a prominent bursal projection, a normal posterior contour with a high CIA, or a combination of both, involves initial use of a heel lift inside the shoe and a heel counter pad to shield the tender posterior aspect of the heel. The use of NSAIDs, calf and arch flexibility exercises, orthotic control of hyperpronation, and local infiltration of corticosteroid combined with gel-cast or similar immobilization can be useful for persistent cases. Recalcitrant cases may warrant surgical intervention for excision of chronic superficial and/or retrocalcaneal bursitis, and remodeling of the prominent bursal projection. The treatment of Haglund's deformity and posterior calcaneal spur are summarized in Table7-5.

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203

TABLE 7-5. TREATMENT HIERARCHY FOR HAGLUND'S DEFORMITY OR POSTERIOR CALCANEAL EXOSTOSIS.

Intervention

Stage I

Stage II

NSAID Local steroid* Oral steroid

NSAID

Pharmacological

Heel lift Custom orthotic Biomechanical Heel counter pad Roller sole

Prefabricated orthotic Physical Surgical

Ice Flexibility

Stage IV

Stage Ill

Continued immobilization

Immobilization Iontophoresis

Night splint Dynamic splint Remodel posterosuperior process or spur resection; preserve Achilles or detach; bursectomy

*Support of the ankfe and partial immobilization (gel cast and surgical shoe, cast boot (cam walker}, BK cast} with

weight bearing are ad'Jised whenever corticosteroid is infiltrated about the Achilles tendon.

Surgical repair of Haglund's deformity of the heel involves a lateral paratendinous incision with the patient prone or in the contralateral decubitus position. The procedure is readily performed under local anesthesia with IV sedation, and anatomic dissection yields adequate hemostasis. The sural nerve must be protected within its subcutaneous bed. The deep fascia is incised in a paratendinous fashion, in line with the overlying skin incision. Care should be taken to avoid excessive reflection of the fibrous expansion of the Achilles tendon at its insertion. Plantarflexion ofthe ankle enhances retraction ofthe Achilles. The prominent posterosuperolateral process is resected with an osteotome and mallet and the remaining calcaneal surface is then rasped. "Chasing the bump" prevents creation of a new prominence dUe to over aggressive resection. It is possible to remodel the entire posterior aspect from the lateral approach, however a second medial paratendinous incision can be used if necessary, however a distance of at least 2.5 em should be maintained between the two parallel incisions. A curvilinear or lazy-S incision could also be used. Generally, with Haglund's deformity the single lateral incision will suffice. In the symptomatic, structural cavus foot with a pathologically high CIA, in the presence of a normal posterior contour and bursal projection, the Kelly and Keck osteotomy may be used to resect a dorsally based wedge from the calcaneal body. This procedure brings the posterosuperior aspect of calcaneus anteriorly. The osteotomy is fixated with Steinmann pins, staples or lag screws.

Retrocalcaneal Exostosis with Calcification in the Achilles--the retrocalcaneal exostosis differs from the Haglund's deformity in that it is usually seen in older individuals, is situated distal to the posterosuperior process, and it generally traverses the entire posterior aspect from lateral to medial. The patient should be positioned prone or in the contralateral decubitus position, and the procedure can be performed under local

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Ch. 7

anesthesia if desired. lncisional approaches are variable, including two paratendinous incisions, a central longitudinal posterior or an oblique curvilinear (Dickinson) incision, and it is often necessary to create a central longitudinal tendon-splitting incision in order to remove intratendinous calcification {Figure 7-57). The tendon splitting incision enables the surgeon to expose the posterior surtace of the calcaneus while preserving distal attachments medially and laterally. After remodeling the posterior surface of the calcaneus

and debriding the Achilles, the tendon is reattached with multiple intraosseous tendon anchors and nonabsorbable sutures. Following layered closure, a compressive dressing and short leg cast are applied. The patient is maintained non-weight bearing for 2-4 weeks, and immobiHzation is discontinued at 5-6 weeks followed by gradual rehabilitation. The duration of non-weight bearing and immobilization is determined by individual factors and the extent of tendon reflection. Downey has advocated the use of an inverted V-tenotomy for debridement ofthe Achilles tendon and removal of a posterior calcaneal spur, noting that this method enables the surgeon to readily access the calcaneus and easily reap proximate the tendon.

52% Anterior

Medial@:::> Lateral Posterior

35%

Medial~ Lateral

13%

Medial

€ ) lateral

Calcaneus

Figure 7.57

Figure 7.58

ANKlE EOUINUS The triceps surae consist of the medial and lateral heads of gastrocnemius, plantaris, and soleus. The medial head of gastrocnemius is thicker and broader than the lateral head, and

it extends further distally and attaches to the lateral aspect of the tendoAchillis. Soleus attaches to the medial2/3 ofthe deep surface of the tendoAchillis (Fig 7-58). Plantaris arises from the lateral femoral condyle, and Is absent 7% of the time. Plantaris attaches medially along the Achilles. The tendoAchillis averages 15 em in length and originates near the middle of the leg. Gastrocnemius traverses three joints: knee, ankle, and STJ; while soleus traverses two joints: ankle, and ST.J. The gastrosoleus complex functions in late contact through midstance and into early propulsion, and causes knee flexion and heel lift via

ankle plantarflexion.

Ch. 7


205

Muscular Forms of Ankle Equinus-the muscular forms are caused by skeletal muscle spasm, congenital shortness, and acquired conditions. Spastic equinus is the oldest recognized form of ankle equinus, and is caused by upper motor neuron disease such as cerebral palsy, CVA, and head and spinal trauma. Spastic equinus presents with

hypertonicity, hyperreflexia, and steppage gait Congenital equinus usually presents with toe walking until about 15·18 months of age !usually the first3·6 months after initial walking), and thereafter the equinus subsides. Acquired ankle equinus may develop in response to prolonged casting in plantarflexion, such as following Achilles tendon repair, or due to chronic use of high~heeled shoes. Chronic equinus contracture results in tightness of the deep flexors and peroneal tendons, posterior ankle and subtalar ligaments and capsule. The Silverskio!d test indicates gastrocnemius equinus if ankle dorsiflexion is <10°with the knee extended, but 2'10° with the knee flexed; or gastrosoleal equinus it <10° of dorsiflexion with the knee extended or flexed. Gastrocnemius equinus can be addressed with gastrocnemius recession, while gastrosoleus equinus warrants tendoAchil!is length~ ening !TAL). The end range of motion should be smooth and "soft tissue," as compared to an abrupt, bony end range consistent with osseous equinus. The standard lateral ankle and charger (stress dorsiflexion) radiographs should be checked for talotibial exostosis, which could cause bony blockage to dorsiflexion. Distal tibiofibular synostosis following trauma can inhibit the wider anterior portion of the dome of the talus from gliding through the ankle mortise, thereby blocking ankle dorsiflexion without the presence of talotibial exostosis. Hamstring tightness can also cause ankle equinus, and the knee should be checked for flexion contracture while plantarflexing the ankle (eliminates pull of gastrocnemius on the knee) and passively extending the knee to end range. Pseudoequinus may be present when the cavus foot(anterior equinus) uses available dorsiflexion at the ankle, simply to stand with the forefoot loaded, thereby limiting available dorsiflexion range of motion and functionally inducing equinus deformity. Combined forms of equinus may involve gastrocnemius or gastrosoleus equinus, with bony blockade and/or pseudoequinus. Distal pedal compensation for ankle equinus occurs as hyperpronation of the STJ and MTJ with associated forefoot supinatus, flexor stabilization induce hammertoes and HAV, and serves as one of the most forceful and common deforming influences acting on the foot Failure to compensate with pedal hyperpronation results in genu recurvatum or overt toe walking/standing. Uncompensated equinus also presents as pes cavus, with equinovarus, fixed STJ supination, extensor substitution, and dropfoot In the neuropathic (insensitive, Charcot) patient, equinus deformity leads to tremendous Lisfranc fracture and luxation. Neurological consultation is in order whenever UMN or spastic equinus is noted. Nonsurgical efforts to manage significant equinus deformity are generally not very successfuL Efforts include stretching and flexibility tor nonspastic forms, and possible acceptance of the deformity and use of a heel lift, orthosis, and roller sole.

206


Figure 7.59

Ch. 7

Figure 7.60

Gastrocnemius Equinus-gastrocnemius equinus has been treated with selective dennervation of the gastrocnemius muscle bellles, as well as proximal recession via transection of the medial and lateral heads near their femoral origins. Vulpius and Stoffel described a distal transverse recession of the gastrocnemius aponeurosis, and they later converted the technique to an inverted V-shaped lengthening of the aponeurosis without suturing to underlying soleus muscle. Strayer described a transverse aponeurotic incision with suturing of proximal portion to underlying soleus. Baker described a distally based tongue-in-groove recession of the aponeurosis (Fig 7~59), and sectioned the central soleus aponeurosis deep to the gastrocnemius aponeurosis. Fulp and McGiamry modified the tongue~in-groove distal recession by basing the tongue proximally (Fig 7~60), however Downey and Banks later noted this to associate with atrophy of the medial head of gastrocnemius due to the natural rotation of the gastrocnemius fibers. Gastrocnemius recession is used most effectively in cases of nonspastic gastrocnemius ankle equinus. Distal gastrocnemius recession (Baker) is carried out on the prone or lateral decubitus patient using an approximately 6-7 em longitudinal incision, originating at the palpable myotendinous junction, and positioned just medial to the midline on the posterior aspect of the calf. The incision is deepened through the dermis into the subcutaneous fat, where the sural nerve and Jesser saphenous vein are preserved in their soft tissue bed laterally. The deep fascia and paratenon are incised in line with the overlying skin incision, and reflected as a single layer. Plantaris is transacted on the medial aspect of the wound (originates laterally and traverses from lateral to medial as it propagates distally), and a segment is excised to assure release. The ankle is then slightly plantarflexed to enhance access to the most distal fibers of the aponeurosis, and the tongue-in~groove aponeurotomy is initiated by transacting the medial and lateral thirds of the aponeurosis distally. The ankle is then slightly dorsiflexed to make the remaining intact fibers taut, and the central third of the aponeurosis is transacted proximally. The aponeurosis is then lengthened (recession) by dorsiflexing the ankle with the knee extended until 10o of motion is achieved with the subtalar joint neutral. The central so leal aponeurosis is then sectioned. The wound is the lavaged and the central tongue portion of the aponeurosis is sutured to the medial and

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lateral thirds in the corrected length, using 2-0 nonabsorbable, buried knot sutures

reinforced with 2-0 absorbable sutures to reapproximate the medial and lateral thirds centrally. Paratenon and deep fascia are closed with 3-0 absorbable running lock suture, and smooth gliding function deep to the fascia/paratenon layer is assessed by moving the ankle through its range of motion. The subcutaneous layer and skin are then closed. A BK cast or immobilizing splint is then applied with the knee extended and STJ neutral, and maintained for 3-4 weeks before rehabilitation is initiated. Gastrosoleal Equinus-gastrosoleal equinus has been treated with a variety of tendo-Achillis lengthening (TAL) procedures. The frontal plane Z-lengthening (Fig 7-61) is a commonly used techn)que for TAL, and provides excellent control of length and avoidance of suture irritation of the overlying deep fascia and skin posteriorly. The procedure is performed on the prone or lateral decubitus patient via a 6~8 em longitudinal incision medial to the posterior midline, terminating at the insertion of the Achilles. Deep fascia and paratenon are then incised longitudinally, and the entire Achilles tendon isolated for a distance of 5·7 em from its insertion. A #11 (bayonet) blade is then used to hemisectthe tendon in the frontal p_lane, creating anterior and distal hemisections. The hemisection is converted to a Z~tenotomy by sectioning the posterior hemisection proximally, and the anterior hemisection distally. The plantaris tendon is sectioned at the medial aspect of the Achilles (or alternatively it can be Z-lengthened itself). Attention is directed to residual contracture, and posterior ankle and/or STJ capsulotomy or deep flexor or peroneal tendon lengthening is performed as necessary. The ankle is placed in corrected position, with the STJ neutral, and the tendon sections reapproximated with a combination of 1~0 and 2~0 nonabsorbable and absorbable sutures taking care to bury the knots. Paratenon and deep fascia are then reapproximated with 3-0 running lock absorbable suture, followed by closure of the subcutaneous layer and skin. A BK cast is then applied with the knee extended and the STJ in neutral position.

Figure 7.61 Osseous Ankle Equinus-an anterior talotibial exostosis can be addressed via an open or arthroscopic technique, and involves removal of impeding osteophytosis and spurring until adequate range of motion is achieved. lftibiofibular synostosis inhibits ankle dorsiflexion, then mortise reconstruction may be in order. Murphy Anterior Advancement of the Achilles Tendon-this procedure has been described in Chapter 6, and is indicated in the treatment of spastic triceps surae equinus.

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Selected Peripheral Nerve Entrapments and Acquired Neuropathy Kopel and Thompson have defined peripheral nerve entrapment as an area of nerve trunk impingement due to the surrounding "stress anatomy" at a point where the nerve traverses a fibro-osseous tunnet or constricting soft tissue hiatus. In the lower extremity, a number of entrapment sites are commonly symptomatic, and any peripheral nerve can become

entrapped. Most notable among the common entrapments inferior to the knee are tarsal tunnel syndrome (medial), Morton's intermetatarsal neuroma, and superficial peroneal nerve entrapment at the deep fascial hiatus proximal to the ankle. Tarsal Tunnel Syndrome (TIS)-tarsal tunnel syndrome is classically described as entrapment or compression neuropathy of the posterior tibial nerve and/or its terminal branches, the medial and lateral plantar and medial calcanean nerves. The surgical anatomy of interest includes the flexor retinaculum (laciniate ligament) extending from the medial malleolus to the medial process of the calcaneal tuberosity and the plantar aponeurosis. The porta pedis at the distal aspect of the medial tarsal tunnel is the canal

created by the abductor hallucis muscle belly and its deep fibrous septal attachmentto the periosteum of the medial wall of the calcaneus, through which the medial and lateral plantar nerves pass and enter the plantar vault The division of posteriortibial nerve into its three terminal branches most commonly occurs proximal to the laciniate ligament, however it may divide deep to the laciniate ligament, or even at the distal margin of the tunnel. The distal bifurcation into medial and lateral plantar nerves is often identified in cases of TIS, as the subabductor fibrous septum encroaches on the crotch of the division, and is termed distal tarsal tunnel, or calcaneal tunnel, syndrome. This is often associated with longstanding, recalcitrant plantar fascitis and medial heel pain. The medial calcanean nerve usually emerges through the laciniate ligament, and is primarily a sensory branch. The medial plantar nerve provides sensory innervation to the plantar aspect of the hallux,

second and third toes, medial half ofthe fourth toe, and medial half of plantar aspect ofthe foot. The lateral plantar nerve provides sensory innervation to the plantar-lateral half of the

fourth toe, plantar aspect of the f1fth toe, and the plantar-lateral aspect ofthe foot The plantar nerves provide motor innervation to the intrinsic muscles, and autonomic innervation to sweat glands and vascular smooth muscle.

The etiology of medial TTS is generally thought to be due to overuse or repetitive microtrauma, consistent with impingement of the nerve by the surrounding "stress anatomy." Operative inspection may reveal no particular gross abnormality of the structures, unless a distal bifurcation, or tumor within the tunnel is identified. In the

typical case, longstanding hyperpronation of the STJ and MTJ has effected chronic constriction of the contents of the tunnel. The existence of dilated and tortuous posterior tibial veins within the tunnel may lead to engorgement and concomitant chronic stasis, which can result in peripheral nerve compression and severe nocturnal discomfort which is often associated with calf cramping. Traumatic causes of medial TTS include ankle, talar or calcaneal fracture; recurrent ankle and/or subtalar sprain and subluxation; both of which may lead to chronic, recurrent hemorrhage and fibrosis. Systemic diseases such as rheumatoid arthritjs, hypothyroid myxedema, and even diabetes mellitus predispose to TTS. Space occupying lesions such as lipoma, neurofibroma, neurilemmoma, ganglion, and synovial cyst ioften associated with rheumatoid arthritis), have also been implicated as causes of entrapment within the tunnel. Even hypertrophy of the abductor hallucis muscle belly has been implicated as a cause of TIS. The clinical symptoms associated with medial

TTS include forefoot pain with symptoms localizing to the metatarsal ball and digits plantarly,

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as well as medial and plantar heel pain and paresthesia. Early symptoms include intermittent burning pain, numbness, and paresthesia over the medial side of the heel, the toes and the plantar aspect of the foot As the condition worsens, late symptoms include paresis that will develop into paralysis of the pedal intrinsic muscles (intrinsic minus foot). Proximal radiation of pain (Valleix sign) may propagate up the posterior calf. Pain and paresthesia are generally proportional to the amount of weight-bearing activity sustained during the day. The diagnosis of TIS is not always sharply defined. Important aspects of the diagnosis include history of progressive symptomatology, unless there is a traumatic event relevant to the tunnel; the presence of unilaterallinel's (Hotfman-linel's) sign upon gentle percussion or moderate-deep palpation of the tunnel's contents and, similarly, the presence of a unilateral Valleix sign; application of a venous tourniquet proximal to the ankle will elicit pain and paresthesia on the affected side secondary to venous occlusion with a temporary passive congestion in the presence of intra-tunnel varix; forced eversion of the STJ may elicit symptoms on the affected side in cases related to prolonged hyperpronation; radiographs may provide evidence of previous injury; and appropriate lab testing may be useful in establishing the presence of RA, myxedema, or DM. It is important to rule-out lumbosacral radiculopathy or plexopathy, employing the straight leg raise, Achilles and patellar deep tendon reflexes, and extrinsic muscle strength testing. EMG and NCV testing may be helpful, however need not necessarily be positive for nerve entrapment at this level even in the presence of overwhelmingly suggestive clinical findings. For this reason, treatment decisions are not made solely on the results of electrodiagnostic testing. Conservative treatment of medial TIS entails local anesthetic block of the posterior tibial nerve and local infiltration of corticosteroid into the third canal of the tarsal tunnel, followed by rest and gentle flexibility exercises of the ankle and foot. Support hose may be indicated in case involving dependency-related venous congestion. Functional orthotics may be useful for those patients displaying weight-bearing hyperpronation. Surgical management of medial TIS can be enhanced by avoiding use of a tourniquet as this allows visualization ofthe posteriortibial artery and the tortuous veins that may require ligation. A tourniquet may be used if this is the surgeon's preference. Extensile esposure is gained via a curvilinear incision extending posterior and plantar to the medial malleolus. The incision should be placed at least 1 em posterior to the malleolus. The laciniate ligament is identified, and vessels and nerves in the superficial fascia and subcutaneous fat are observed and protected. The medial calcanean branch, which may pierce the flexor retinaculum at this level and may display multiple branches, should be identified. The flexor retinaculum is then incised and opened in line with the overlying skin incision and the contents identified and documented; afterwhich external neurolysis of the posterior tibial nerve and its branches is performed. Nerve retraction is maintained with a latex drain or vessel loop. The nerve trunks are identified from proximal to distal through the tunnel, including inspection of the porta pedis. Dilation of the porta pedis is enhanced with loupe magnification and microsurgical instrumentation. Abductor hallucis is examined for hypertrophy and hypertrophic tissue may be excised. The posterior tibial veins may reveal varicosities that require ligation and excision. The wound is then flushed, and the laciniate ligament is realigned but generally not sutured directly. The superficial fascia is then reapproximated with absorbable suture of choice, followed by skin closure and application of a gently compressive, sterile dressing. The foot and ankle are allowed to move freely, however weight bearing is avoided for 2-3weeks, depending upon wound and patient progress. A gradual resumption of activity is thereafter undertaken. Complications of TIS treatment include recurrence of symptoms secondary to fibrosis, and consideration

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should be given to burying the nerve in the calcaneus or tibia in cases of severe disability due to recurrent nerve entrapment. This is obviously a serious undertaking, as plantar insensitivity and loss of intrinsic muscle function ensues. Severing the posterior tibial artery, which provides 80% of the arterial supply to the foot is a potential complication that would require microsurgical repair. Other potential complications include nerve laceration,

tenosynovitis, hematoma, and possible infection, as well as dehiscence.

B

Figure 7.62 Morton's Neuroma-this condition is a common cause of metatarsalgia, and must be

considered in cases involving pain in the ball of the foot It is most frequently encountered in the fourth to 6th decades of life and, although any intermetatarsal space can be affected, it is usually localized to the third intermetatarsal sapce. The patient relates sharp, shooting pain with associated aching, brought on by weight-bearing load of the forefoot, insidious in onset, progressively worsening, and intermittent in nature, and seemingly relieved by sitting and massaging the unshod foot for a brief time. Hyperpronating individuals, the obese, and those that wear high-heeled or tight-fitting shoes are prone to entrapment irritation of the common plantar nerve and/or its branches in the intermetatarsal space, just plantar to the transverse intermetatarsalligament (Figure 7-62). The mechanism of nerve entrapment in the intermetatarsal space involves repetitive irritation of the nerve by the neighboring ligament. Identification entails focal tenderness and paresthesia to direct deep palpation, a positive Mulder's strum-click sign, and localization of anesthesia to the contiguous sides of the adjacent toes. Differential diagnoses include MTPJ enthesitis, intermetatarsal bursitis, diabetic peripheral neuropathy, neoplasm, trauma, TIS, and radiculopathy. Nonsurgical treatment measures involve the use of a metatarsal projection pad {proximal to the metatarsal heads), orthoses, local infiltration of corticosteroid, ultrasound with MTPJ range of motion exercises, use of a sneaker with roller sole, NSAIDs, ice after strenuous activity, and rest. Surgical intervention evolves around adequate external neurolysis ofthe involved plantar nerve and, traditionally, excision ofthe common plantar

nerve proximal to the proximal margin ofthe DTIL. Approaches include: 1) the plantar

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longitudinal interspace incision, which yields optimal exposure of the plantar nerve without disruption of the DTIL; 2) the transverse plantar incision, which yields exposure to adjacent interspaces; 3) the web-splitting incision, 4) the dorsallongitudinat which is satisfactory for an interspace into which no previous dissection has been undertaken; and 5) the plantar zig-zag or lazy-S incision, which affords exposure of the plantar metatarsus and vault whenever revisional neurectomy is necessary. Sectioning the DTIL readily exposes the plantar nerve and its branches, and makes IT easy to excise the neuroma, which is typicaly present at the distal margin of the DTIL After identification of the common plantar digital nerve trunk and its proper digital branches to the contiguous surfaces of the adjacent toes, the nerve is inspected for coloration and texture and, usually, resected proximal to the proximal margin of the DTIL. Some surgeons do not excise the nerve, and limit the procedure to sectioning the DTIL or, less commonly, translocating the nerve from plantar to dorsal to the DTIL The latter intervention entails sectioning the ligament, transposing the nerve, and then repairing the ligament It is also possible to section the DTIL by means of endoscopic identification and sectioning using specialized instrumentation, however such intervention neither excises the neuroma nor translocates the nerve trunk. If the nerve is section and the neuroma excised, the proper branches are procured as far distal as possible in each toe, and the common nerve trunk is sectioned as far proximal to the proximal margin of the DTIL as possible. This can be difficult when the dorsal incisional approach is used, however this method of surgical treatment is commonly used. After the common trunk is sectioned, the proximal nerve stump is allowed to retract further proximally in the intermetatarsal space, where it can reside amidst intact intrinsic skeletal muscle bellies. In an effort to further diminish the potential risk of developing a symptomatic stump neuroma, closure of the common trunk's epineurium with 8-0 nylon suture can be undertaken, prior to allowing the stump to retract proximally. All plantar incisions require approximately 3 weeks of non-weight bearing thereafter. Complications of plantar neurectomy include hematoma in dead space, and this is most often associated with the dorsal longitudinal incisional approach. Hematoma predisposes to infection, and may require suture removal and drainage. Vascular ischemia may also develop after neurectomy, and is particularly likely following adjacent interspace dissection. If postoperative ischemia is noted, avoid ice and elevation, nicotine and caffeine, excessive weight bearing, loosen bandage, and administer bupivacaine posterior tibial nerve block, and consider using reflex abdominal or popliteal heat (K-pad), as well as isoxsuprine IV 5 mg- 10 mg with careful assessment of vital signs. Venous congestion may cause cyanosis, and elevation in this case would be helpful. Recurrent intermetatarsal neuroma, also known as amputation or stump neuroma, occurs in all cases of nerve resection. A symptomatic stump neuroma, however, occurs in only about 10~ 15% of cases following excision of an intermetatarsa! neuroma. Efforts to minimize the risk of symptomatic stump neuroma formation include sectioning the nerve proximal to the proximal margin of the DTIL, epineurial closure over a clot of thrombin or cyanoacrylate (not FDA approved) using 8-0 nylon simple interrupted sutures. One may also bury the nerve stump in an adjacent metatarsal shaft. Silicone capping and entubulation have not proven to be reliably effective in preventing symptomatic stump neuroma formation. The ideal location for a sectioned nerve stump is within well-vascularized, protected, intact skeletal muscle bellies, as is the condition within the intrinsics ofthe foot wherein the plantar nerve retracts proximal to the DTIL Permanent numbness of the contiguous surfaces of the involved digits and plantar interspace, as well as loss of sudomotor and vascular smooth muscle tone, are anticipated.

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Terminal Syme operation for total nail removal

Hallux amputation Fourth and fifth ray resection

Transmetatarsal amputation

Lisfranc's amputation

Syme's amputation

Figure 7.63

Chopart's amputation

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Superficial Peroneal Nerve Entrapment (Henry's Mononeuritis}--this is most frequently seen in active individuals, often involved in jumping sports or physically strenuous

occupations, or in older individuals who were once regular participants in such activities. The pathology is localized to the deep fascial hiatus proximal to the ankle where the superficial peroneal nerve emerges to enter the subcutaneous layer. It is usually

aggravated by peroneal muscle herniation through the hiatus, thereby impinging the nerve and causing localized pain and paresthesia over the ankle and pedal distribution of the nerves. Treatment involves local corticosteroid and nerve block, attention to any potential causes of compartment syndrome, and recalcitrant symptoms may require surgical repair ofthe skeletal muscle herniation and transposition of the intact nerve trunk. The branches of the superficial peroneal nerve, namely the intermediate dorsal cutaneous nerve (IDCN, Lemont's nerve) and the medial dorsal cutaneous nerve (MDCN), can also become entrapped and, being located on the anterior aspect of the ankle and the dorsum of the foot, these are particularly vulnerable to direct contusion as well as traction injury associated with ankle inversion. Morever, they are vulnerable to iatrogenic involvement in association with surgical dissection of these areas. Amputations The essential element in determining amputation level is tissue viability. Clinical assessment, duplex Doppler ultrasound, and transcutaneous oxygen tension (Tc-p02) are primary methods used to assess tissue viability, perfusion, and predisposition to healing. The skin is warmed to 44~ C, and a Clark electrode is used to measure Tc-p02. Amputations are likely to heal if the Tc-p02 is at least 40 mmHg, are questionable if the Tc-p02 is between 26-40 mm Hg, and likely to fail if the Tc-p02 is <26 mmHg. Surgical principles specific to amputations include gentle handling of the skin, adequately wide flap pedicle, and avoidance of skin tension or bony prominence. Bone resection and remodeling can be performed with both power and hand instrumentation. Moreover, muscle insertions should be maintained or recreated to avoid contracture deformity and severe muscular imbalance. Preservation of muscle balance usually requires intraoperative decision making on the part of the surgeon. Preservation of TA and PB tendons prevents equinovarus deformity. Isolated digital amputation predisposes to adjacent digital transverse plane drift, and HAV is likely following second toe removal. Hallux amputation predisposes to apropulsive (pedestal) gait. During amputation, stump (amputation) neuroma formation should be prevented by sharp sectioning under tension, with subsequent retraction proximally into well-vascularized and protective skeletal muscle bellies. Epineurial closure may be helpful on large nerve trunks. Planning should include use of a robust, sensate flap to cover the stump. Hemostasis is critical, and vessels with lumens large enough to grossly visualize should be ligated as compared to electrocoagulated. In general, transtibial amputations are regarded as major amputations, and those distal to the tibia are considered minor amputations. Pedal amputations include the following techniques: terminal Syme's amputation, digital amputation and disarticulation, ray resection, transmetatarsal amputation (TMA), Lisfranc amputation, Chopart amputation, Pirogoff amputation, and Symes (ankle) amputation (Figure 7-63). The Symes amputation entails ankle disarticulation with removal of the malleoli and proximal rotation of the heel pad to cover the distal surface of the tibia. The Pirogoff amputation entails sectioning the talus and calcaneus in line with the anterior margin of the tibia, thereby preserving the posterior portion of the calcaneus, heel weight bearing surface, and the insertion of the Achilles tendon.

214

Reconstructive Foot and Ankle Surgery

Ch. 8

RECONSTRUCTIVE FOOT AND ANKLE SURGERY: COMPLEX CONDITIONS AND MAJOR DEFORMITIES Complex conditions requiring major foot and ankle reconstruction often require combination surgery. Repair may require major hindfoot or midfoot, or ankle, arthrodesis and adjunct soft tissue manipulations such as tendon lengthening and/or transfer. These procedures can be

used to correct acquired, degenerative, or post-traumatic conditions, as well as neurologically induced and congenital defects. Selected deformities amenable to major pedal reconstructive intervention include advanced pes valgus, pes cavus, degenerative arthrosis, and the rheumatoid foot. Congenital deformities will be discussed elsewhere. Deformities may be rigid, or flexible and unstable. Selected procedures include triple arthrodesis, ankle and pantalar arthrodesis, and Usfranc arthrodesis. At times, it may be applicable to perform isolated intertarsal arthrodesis, or variations on midtarsal and intercuneiform fusion, as well as partial tarsometatarsal fusion, based upon the needs of the individual case.

Collapsing Pes Valgoplanus (CPVP, Flexible Flatloot)-it is important to note that not all flatfeet are pathological. Isolated sagittal plane arch depression, in the presence of a perpendicular or minimally everted resting calcaneal stance position, is usually asymptomatc and well tolerated throughoutthe individual's life with the exception of posttraumatic degeneration or neuropathy. On the other hand, the presence of hindfoot eversion, or pes valgus, is a strong destructive force during weight bearing and is associated with steadily progressive articular subluxation and degenerative joint disease, TP dysfunction, abnormal shoe wear, and difficulty walking or standing. A variety of etiologies exist for CPVP, including: tibialis posterior muscle weakness, accessory navicular iKidner foot), and chronic TP dysfunction; ligament weakness and laxity; prolonged FF supinatus secondary to hyperpronation ofthe STJ and MTJ IFF and RFvarus, flexible FF valgus, ankle equinus, and other pronating biomechanical foot types); congenital or acquired calcaneovalgus; lower extremity torsional abnormalities such as femoral anteversion; and Charcot collapse in its early stages.

Radiographic findings Associated with CPVP-standard radiographs include: AP view Kite's angle (Kite's talocalcaneal angle) 30-50" reducing to 17-21" by age 5 years, with 75% articulation of TNJ; lateral view CIA 18-21", talar declination angle 21", and lateral talocalcaneal angle of 35- 50". Plana I dominance of deformity in flatfoot: transverse plane dominance with increased Kite's angle, increased cuboid abduction, decreased FF adduction; frontal plane dominance with superimposition of metatarsals, decreased first met declination, decreased height of sustentaculum tali, midtarsal and STJ; sagittal plane dominance with increased talar declination, navicular-cuneiform breach, and increased T-C angle on lateral view. Clinical Signs of CPVP-these include evidence of the Hubscher maneuver Itoe test of Jack). indicative of flexibility. The Hubscher maneuver should cause the flexible flatfoot to reform a medial longitudinal arch when the hallux is dorsifiexed and the patient externally rotates the ipsilateral hip and leg, causing the heel to go into varus. A lateral radiograph can be taken with the heel elevated to see if the medial column reduces, if not, there is a need for medial column work in addition to other reconstructive procedures. In the young child, simply have them attempt raise up on the ball of the foot and observe the heel go into varus, which indicates a flexible deformity that will often respond well to supportive therapy while the skeleton matures.


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Surgical Repair of CPVP-indications for flatfoot surgery include: midfoot and tarsal

instability with associated FF hypermobility (HAV, flexor stabilizing HTs, MTPJ subluxation), metatarsalgia, and plantar fasciitis; postural symptoms extending from the foot to the low back; midfoot and arch pain, especially along TP and TNJ, as well as sinus tarsi; tight heel cord with calf pain and inability to stand for iong periods of time; difficulty walking/running,

or performing other weight bearing activities; decreased activity level of youngster due to symptomatic feet; failed non-surgical treatment such as foot orthoses and calfflexibility and TP exercises. Contraindications to flexible flatfoot reconstructive efforts include rigid flatfoot\convex pes valgus, tarsal coalition, paralytic); osseous equinus and extreme obesity. CongeniTal gastrocnemius or gastrosoleus equinus often accompanies CPVP, and may be contributory in the development of the deformity, and must be addressed with either gastrocnemius recession or TAL, respectively, when the flatfoot is reconstructed. Similarly, metatarsus adductus must be considered whenever medial arch enhancement, with or without lateral column lengthening, is undertaken. Repair of CPVP effects FF adductus as the medial arch elevates and TP becomes more effective. Therefore, it may become necessary to address metatarsus adductus deformity in addition to repair of the CPVP. Reconstruction ofCPVPtypica!!y addresses the triad of deformities including the medial arch, lateral column, ankle equinus, and usually combines osseous and soft tissue manipulations. As a rule, isolated soft tissue manipulations in the medial arch are inadequate without associated osseous stabilization or lateral column lengthening. Surgical options include: Extra~Articular STJ Bone Block Procedures Useful in Young Patients-a variety of extra-articular blocking procedures are available for patients wherein arthrodesis is not desireable.

Chambers procedure-indicated for children <8 years of age, wherein bone graft is

placed in the calcaneal sulcus of the sinus tarsi to inhibit adduction and plantarflexion of the talus on the calcaneus (Figure 8.1). Baker and Hill procedure-calcaneal osteotomy and elevating bone graft under posterior facet, to decrease vertical alignment of STJ and minimize adduction and plantarflexion of talus. Selakovich procedure-opening osteotomy and graft of sustentaculum tali, inhibiting

talar declination and adduction. Subtalar Arthroereisis-STJ arthroereisis is also useful in young patients 4-8 years of age, with CPVP displaying a transverse plane (TP) TC angle >30" and 50% TN articular congruity, heel eversion of 8-10°, and-FF varus of> 10° with superimposition of the metatarsals on the

Figure 8.1


216

Ch.8

lateral radiograph. This procedure can also be used in adults with CPVP, and is often used in conjunction with other reconstructive procedures addressing the medial columnn and triceps sura e. Arthroereisis uses synthetic polymer or metallic implant, rather than bone graft, to block STJ pronation by impinging on the anterior margin of the leading edge of posterior talar facet The implanted blocking plug is usually removed after the child has achieved skeletal maturity and avoided the destructive, adaptive changes related to pathological STJ/MTJ hyperpronation during the formative years. Specific techniques include:

Lelevre------si!icone polymer (SIIastic®) plug positioned from_lateral to medial in the sinus tarsi, thereby elevating the floor of the sinus (calcaneal sulcus) and blocking talar adduction~plantarflexion. The polymeric plug has been criticized for instability, displacement, and implant degradation. StaPeg"-polyethylene plug positioned in the sinus tarsi, and noted to be more stable and durable in comparison to the LeLevre procedure.

Villadot-an hour glass-shaped Sllastic
Maxwe/1-Brancheau M8A"'1itanium Subta/arlmplant---one of several highly refined arthroereisis implants, the MBA"' probably has the longest record of clinical successfuL It is a barrel-shaped, slotted implant made of titanium alloy that is readily implanted by means of limited dissection and accurate sizing. The instrumentation and surgical technique are well··developed. The implant is also easily assessed on standard radiographs. Weight bearing in an immobilizing cast-bootfor approximately 2-3 weeks is commonly undertaken in the early postoperative phase. The implant can be removed at a later date, or it can be retained permanently, depending upon the requirements of the clinical course. Medial Column Procedures--these focus on restoring joint stability, TPfunction, and arch height (eliminate TN or NC fault), and include:

Kidner-excise os tibiale externum and transpose TP to plantar aspect of the navicular.

Young-used to correct TN and/or NC fault in a flexible flatfoot with FF supinatus, wherein theTA is rerouted through a keyhole slot in the navicular. McGiamry and Ruch (Figure 8-2) have enhanced this procedure by specifically including advancementofthe spring ligament, TP, and combining lateral column lengthening using the Evans open calcaneal graft.

Lowman--TN arthrodesis combined with rerouting TA under the navicular and suturing it to the spring ligament.

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217

Figure 8.2

cuneiform combined with cuneiform-first metatarsal arthrodesis, further combined with soft tissue reefing. This procedure results in much

Mil/er-navicular~medial

shortening and it is difficult to achieve satisfactory bone-to-bone apposition without interposition of corticocance!lous bone graft Hoke--navicular to first and second cuneiform arthrodesis.

Cotton--dorsally-based opening wedge osteotomy of medial cuneiform, packed with truncated corticocancellous bone graft; used to plantarflex the medial column.

Lateral Column Lengthenin[rlateral column lengthening enhances the stability and longevity of medial arch reconstruction, and has proven to be highly reliable, readily achieved, and associated with low morbidity and complication. The Evan's calcaneal osteotomy and bone graft, or bone lengthening using corticotomy and callus distraction with an external fixator, are the mainstays of lateral column lengthening. Bone graft extension calcaneocuboid arthrodesis can also be employed. The highly trabecular anterior portion of the body of the calcaneus readily heals, accepts allogeneic corticocance!lous bone graft and bone transport manipulation, and is ideally positioned to influence forefoot adduction (correct forefoot abduction by reducing the calcaneocuboid abductus angle). Once again, attention must be paid to pre-existing metatarsus adductus skewfoot deformity, and the metatarsus adductus may require concomitant correction. Evans Calcaneal Osteotomy and Bone Graft--this is the primary osteotomy used to reduce forefoot abduction in the transverse plane iFigure 8-3). The procedure invo!ves an opening osteotomy approximately 1.5 em proximal to the calcaneocuboid joint (CCJ), preserving the ligaments and capsule of this joint, and directed from lateral to medial through-and-through the anterior portion of the body of the calcaneus. The osteotomy is distal to the posterior facet of the STJ, and it is extra-articular. A trapezoidal block of allogeneic corticocancellous bone graft is then wedged into the osteotomy, advancing the distal aspect of the calcaneus and CCJ, and adducting the forefoot Autogenous bone graft could also be used, however the site is amenable to alogeneic graft, and a secondary donor site wound is not necessary. Alternatively, corticotomy and gradual distal transport of the anterior portion ofthe calcaneus can be achieved, after an initial10-14 days of stabilization, using an adjustable external fixator employing the principles of callus distraction osteotaxis.

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Figure 8.3 Varus-Prod,.acing Calcaneal Osteotomies-varus~producing calcaneal osteotomies are

performed in the posterior aspect of the calcaneus, in patients >3 years of age. Fixation of calcaneal osteotomies, both with and without bone graft, can be achieved with staples, interfragmental compression screws, or absorbable pins (preferably without bone graft); and postoperative non-weight bearing and immobilization are cruciaL Lateral approaches

to the calcaneus require that attention be paid to the course of the sural nerve, lesser saphenous vein, and the peroneal tendons .. Specific procedures include:

Gleich--an oblique calcaneal osteotomy anterior to the posterior cortex that allows medial shift of the posterior segment and relative adduction of the tuberosity and posterior os cal cis.

Dwyer-a lateral opening wedge oriented obliquely from the dorsal-to-plantar margins of the calcaneus, midway between the posterior margin of the posterior STJ facet and the Achilles attachment, incorporating allogeneic or autogenous corticocance!lous bone graft insertion. It has also been described as a medial closing calcaneal osteotomy, however the contents of the tarsal tunnel can complfcate Figure 8.4 the dissection, and the procedure is not commonly done in this fashion. The lateral closing Dwyer osteotomy is a mainstay of pes cavus reconstruction \Figure 8-4). Silver-an opening wedge bone graft pertormed via a lateral approach, wherein the posterior aspect of the calcaneus and tuberosity are shifted plantarly, and medially. Koutsogiannis-a versatile, frontal plane osteotomythrough the body of the calcaneus midway between the posterior lip of the STJ and the Achilles insertion, allowing triplanar correction ofthe posterior calcaneus and tuberosity via primarily medial and plantar displacement.

Ch.8


219

Pes Cavus-the etiology of pes cavus includes: 1. 2.

3. 4.

Muscular diseases such as muscular dystrophy, Peripheral or spinal nerve lesions, such as Dejerine Sottas, Charcot Marie Tooth \familial sensorimotor neuropathy, peroneal muscular atrophy), and polyneuritis and/or trauma to peripheral nerves, Spinal cord defects such as poliomyelitis (often effects paralytic flatfoot, also). spina bifid a with myelomeningocele, diastematomyelia, and spinal tumors, Spino-cerebellar defects, which are usually hereditary, including Roussy-Levy

syndrome, and Friedreich's ataxia,

5.

Pyramidal and extrapyramidal tract lesions effecting spastic and athetoid cerebral palsy,

6.

Supratentorial conditions such as hysteria,

7. 8.

Congenital defects such as talipes equinovarus, and Idiopathic pes cavus.

Etiopathogenesis hinges on muscle imbalances, often with spastic triceps surae and deep posterior musculature, and anterior and peroneal compartment weakness causing dropfoot. The first ray is usually plantarflexed as peroneus longus is unopposed. Extensor substituion results chronic MTPJ subluxation, clawtoes, metatarsalgia, and inability to get the heel to the ground. It is postulated that the extrinsic digital extensors overpower the lumbricales. TP overpowers and supinates the foot and plantarflexes the ankle. Classification of Pes Cavus-the classification of pes cavus can be confusing and cumbersome, and several systems exist, including:

Apex of the Cavus Deformity--a common classification involves identification of the apex of the cavus deformity. Anterior pes cavus can be described by the Sagittal Plane (SP) shape of the foot as it relates to the dorsal apex of the deformity, as follows: metatarsal, tarsometatarsal. lesser tarsal, and forefoot or midtarsal cavus. Subcategories of anterior cavus include isolated medial or lateral column cavus, first and fifth ray respectively, or global cavus wherein all of the metatarsal rays bear weight more or less equally due to transverse plane symmetry of the plantarly declined structures distal to the apex. Combinations of anterior cavus can also exist. Lower extremity compensation for anterior cavus includes digital and MTPJ contraction, effecting hammer and clawtoes and associated subluxation of the MTPJs; dropfoot that often catches or scuffs across the substrate, and metatarsalgia with or without plantar keratoma forma1ion. If the deformity is flexible, then loading the forefoot results in a certain degree of metatarsal and tarsal dorsiflexion that, over time, can become degenerative. Moreover, a certain degree of ankle joint dorsiflexion will also be used to compensate for residual anterior cavus, thereby limiting available dorsiflexion required for late stance propulsion. This relative limitation of ankle dorsiflexion is referred to as pseudoequlnus, and functions to further load pedal structures and lead to symptomatology. Pseudoequinus is more pronounced in rigid forms of anterior cavus. Posterior pes cavus results from structural increase in the calcaneal inclination angle, usuallywith adduction and varus of the hindtoot. Combined pes cavus typically entails fixed frontal plane varus and a non-reducible rearfoot.

220


Three~Stage

Ch.B

Classification of Pes Cavus-perhaps the most useful classification involves

3 stages of pes cavus, and focuses on options for surgical repair after failed non-surgical efforts. The system includes: Stage I Pes Cavus-entails claV\1oes and subluxated or dislocated MTPJs. Repair evolves around digital stabilization with PIPJ arthrodesis and MTPJ relocation with pin fixation. Adjunct procedures involve the Hibbs and Jones tendosuspensions, and perhaps tendon transfer (STATI) to enhance ankle dorsiflexion.

Stage II Pes Cavus---entails those deformities of Stage I cavus, as well as heel varus

and more significantcavoadductovarus localized primarily to the distal to the midfoot Reconstructive options are determined by the degree of flexibility, as determined by the Coleman block testfor heel varus and plantarflexed first ray. Failure to establish a perpendicular relationship of the posterior bisector of the heel to the ground when the lateral column is elevated on a block, to eliminate the varus influence of a rigid plantarflexed first ray on the hindfoot, indicates the presence affixed heel varus that will require corrective osteotomy. Corrective procedures include the Dwyer closing lateral wedge osteotomy of the calcaneus, dorsiflexory wedge o::.teotomy (DFVVO) of the first ray, Jones and/or Hibbs suspension, and tendon transfer to the dorsum of the footto enhance straight ankle dorsiflexion.

Stage Ill Pes Cavus-entalls marked, rigid, cavoadductovarus deformation, often of neurological etiology, associated with adaptive arthrosis and serious dropfoot, and typically requires Cole midfoot osteotomy or triple arthrodesis for correction. The Cole procedure involves a through-and-through, dorsally based wedge resection of bone positioned through the tarsal navicular and cuneiforms, and the cuboid, thereby elevating the forefoot out of an equinus alignment The osteotomy, after reduction, is stabilized with Steinmann pins or staples, and maintained non-weight bearing for up to three months. The triple arthrodesis is a versatile procedure for correction of the most severe cavus deformities. Assessment ofthe Patient with Pes Cavus-assessment of the patient with pes cavus requires a thorough family history that includes inquiry about parents, siblings, and other blood relatives. Neurological examination, typically with neurology consultation prior to surgery, should identify the presence or absence of spasticity, flaccidity, muscular dystrophy, spinal and other CNS defects; as well as familial diseases that may require genetic and social counseling. Nerve conduction velocity and EMG may be in order. Pedal and ankle, as well as spinal radiographs if spina bifida or other defect is suspected, should be obtained. Radiographically, the apex of the cavus deformity should be identified and the deformity classified in this regard. The radiographic evaluation of pes cavus should be performed weight bearing, and include AP, lateral and lateral oblique projections, with consideration given to ankle films. The lateral radiograph will show increases CIA >30°, norma! to posterior break in the SP cyma line, accentuated or bullet-hole sinus tarsi, SP long axis of the neck of the talus passes superior to the long axis of the first metatarsal, and dorsally based wedge shaped cuneiform& An axial view of the calcaneus at 45° should be obtained to rule out a structural heel varus.

Ch. 8


221

Surgical Procedures for Correction of Pes Cavus~procedures for the correction of pes cavus vary depending upon the degree of flexibility. Flexible Pes Cavus-procedures useful for correction of flexible pes cavus include the Steindler stripping, wherein the plantar fascia and intrinsic musculature is reflected from the plantar calcaneal cortex, and may be useful only if the deformity is flexible and not of bony rigidity. A Hibbs suspension may also be combined with the Steindler stripping in a flexible deformity. Tendon transfers such as the STAn and PLH or TPH are often used to balance inverter/everter imbalance in flexible deformity. Digital fusion and MTPJ relocation are crucial to the treatment of both flexible and rigid pes cavus.

Rigid Pes Cavus-for rigid deformity, where the Coleman block test failed to eliminate heel varus or the medial column is rigidly plantarflexed, a first metatarsal base DFWO combined with a Dwyer lateral closing osteotomy of the calcaneus, perhaps with the STATT, is a useful combination (Stage II pes cavus). It may also be useful to transfer TA dorsally into the base of first metatarsal and perform a plantar opening wedge osteotomy with bone graft of the medial cuneiform, along with a Jones suspension of the first ray. If fixed bony equinus is localized to the lesser tarsus and midfoot, the Cole osteotomy is indicated (Figure 8-5). The Cole osteotomy is performed as a dorsally based wedge resection of bone and joint through the navicular-cuneiform and cuboid level. A first metatarsal OFWO may also be necessary, and adductovarus deformity can be addressed by manipulating the forefoot on the hindfoot at the level of the osteotomy. The Cole should only be performed on a skeletally mature foot, as shortening will ensue. The Japas osteotomy can be used for less severe, rigid pes cavus, and involves a transverse plane V-osteotomywith the apex in the navicular and the wings diverging distally through the cuneiforms and cuboid on the medial and lateral aspects, respectively {Figure 8-6). The Japas causes less shortening than does the Cole, however it is difficult to address adducto varus deformity. In youngsters with open growth physes, in the presence of pan metatarsal global equinus, first metatarsakuneiform dorsal opening wedge osteotomy with bone graft, along with pan-lesser metatarsal DFWD may be used.ln the adult, pan metatarsal DFWOs may be considered. The triple arthrodesis remains the most versatile and powerful reconstructive procedure for repair of severe pes cavus, which is often of neurological etiology (Figure 8-7). Charcot Foot Reconstruction-Charcot deformity and treatment are described in Chapter 3. Rheumatoid Foot Reconstruction and Panmetatarsal Head Resection---when treating the patient with rheumatoid arthritis, it is necessary to consider the patient's physiologic age, general medical status, immunocompromise status, bone stock, wound healing capacity, systemic corticosteroid supplementation, and current as well as anticipated weightbearing activity level. The combination of deformities caused by rheumatoid arthritis mutilans is generally referred to as the rheumatoid foot The rheumatoid foot will usually be symptomatic in either the forefoot or hfndfoot/ankle. The majority of symptomatic presentations involve the forefoot, which displays claw or hammertoes, subluxated to dislocated MTPJs, plantar metatarsalgia with or without IPK and/or rheumatoid nodules. Excessive mechanical overload can effect ulceration and underlying bone infection. Hindfoot and ankle involvement usually entails TP synovitis and chronic dysfunction, rheumatoid nodules of the plantar and posterior heel, retrocalcaneal enthesitis, and severe pes and ankle valgus deformity. The patient often adapts a pedestal gait with antalgic


222

A

c Figure 8.5 Figure 8.6

A

E~

Figure 8.7

Ch. 8

Ch. 8


guarding. Fundamental

non~surgical

223

treatments include periodic, palliative skin and nail

care, accommodative foot orthoses, extra-depth shoes with an external roller sole, and other supportive measures that hinge upon adequate systemic disease modulation under a rheumatologist's guidance. Rheumatoid Foot Reconstructive Surgical Techniques-techniques useful for repair of the rheumatoid foot include: synovectomy, excision of rheumatoid nodules, digital stabilization, Keller arthroplasty, pan metatarsal head excision, first MTPJ fusion along with lesser metatarsal head excision, MTPJ and/or IPJ endoprosthesis, and arthrodesis of the greater and/or lesser tarsus and ankle. Systemic corticosteroid supplementation and prophylactic antibiotics are in order. Postoperative non-weight bearing can be difficult, and immobilization can be detrimental to subsequent joint movement. Occupational and physical therapy should also be considered.(Note: digital arthrodesis, Keller arthroplasty, endoprosthesis implantation, and first MTPJ fusion have been described elsewhere in this manua!). In regard to the use of first MTPJ endoprosthesis in rheumatoid patients, multicomponent total joint replacement is common, although the use of silicone polymer total hinged implants can also be useful. In these patients, however, endoprosthesis probably offers little more in comparison to Keller arthroplasty. Importantly, implantation requires the presence of adequate bone stock, and perhaps metatarsal osteotomy to correct angular deformity. Other useful procedures include: Panmetatarsal Head Resection-this is performed to eliminate pain and cutaneous compromise, and maintain a pedestal gait Hoffman described excision of all five metatarsal heads, while Clayton recommended excison of a portion if not all ofthe proximal phalangeal bases 1f they were large or osteophytic. Proximal phalangeal base resection is wrought with subsequent digital instability and may require syndactylization to effect stability. lncisional options include transverse plantar, orfive or three dorsal longitudinal incisions. The more severely dislocated MTPJs and clavvtoes invite a transverse plantar incision with an elliptical excision of redundant plantar skin and postoperative non-weight bearing. The subcutaneous fat layer should remain attached to the skin, and intermetatarsal dissection should be avoided. The five incision approach includes a wound over each metatarsal, while three dorsal incisions are localized to the first ray, between the second and third and between the fourth and fifth toes respectively. Separate dorsal incisions are used to perform PIPJ arthrodesis of the second through fourth and arthroplasty of the fifth. The preferred length pattern after metatarsal head resection is: 2 = 1> 3 >4 > 5. The metatarsals are transacted distally from dorsal to plantar and the plantar cortex rasped smooth. The first metatarsal is also angulated from distal lateral to proximal medial, while the third-fifth metatarsals are angulated from distal medial to proximal lateraL Most commonly, fusion of the PIPJs 2 through 4 and arthroplasty of the fifth toe are performed along with the metatarsal head excision, and for added stability a K~wire is directed through the PlPJ fusion and into the metatarsals. The combination of first MTPJ fusion with lesser panmetatarsal head excisions can be very usefuL Postoperatively, a protective cast boot works well. Some shortening of the foot can be expected, but the patient should maintain an apropulsive gait lislranc Arthrodesis-arthrodesis of all or part ofthe tarsometatarsal joint(TMJ, Lisfranc's joint) is useful in the treatment of post-traumatic or degenerative arthritis, Charcot foot associated with ankle equinus, and other maladies localized to this level (Figure 8-8).


224

Ch. 8

Isolated first metatarsal-medial cuneiform arthrodesis (Lapidus procedure), as previously noted, can be used to stabilize the medial column and may be used to correct severe HAV deformity with associated metatarsal-cuneiform instability, hypermobility of the first ray and long-standing forefoot supinatus. Arthrodesis of Lisfranc's joint complex usually involves 3 dorsal incisions, the first medially over the medial column, the second and third between the second and third, and fourth and fifth metatarsals, respectively. Fixation is achieved with a

plate and interfragmental compression screw pia cement across the first metatarsal-medial cuneiform fusion site, Steinmann pins or crossed K-wires or single interfragmental screws across the lesser metatarsal-cuneiform and cuboid fusion, or perhaps a plate and screws across the fifth metatarsal-cuboid site. Specialized locking plates may also be used at this site. Furthermore, achieving primary rigid internal compression fixation of the medial column, in conjunction with splintage ofthe lesserTMJs, is an example of the vassal rule of internal fixation and serves as a common approach to Usfranc arthrodesis. Triple Arthrodesis-this is a versatile procedure that is applicable in cases that include collapsing pes val go planus, tarsal coalition, convex pes valgus, tarsal arthritis, pes cavus, residual clubfoot, neuromuscular disease, and others. Triple arthrodesis enables the surgeon to orientthe foot in relation to the leg and ankle, and to manipulate the relationship of the forefoot to the hindfoot. It also affords a stable hindfoot upon which the tendons of the extrinsic pedal musculature can function. The classic Oilier incision can be used for the triple arthrodesis, and courses from the tip of the fibular malleolus, across the sinus tarsi then on to the dorsal aspect of the talonavicular joint The Oilier incision is applicable in the cavus foot, however predisposes to difficulty exposing the TNJ in the valgus foot In the valgus foot, a 2-incision approach is preferred, and most surgeons use the 2-incision approach even for pes valgus correction. The lateral incision extends from the tip of the lateral malleolus to the dorsum of the junction between the fourth and fifth metatarsal bases, and provides excellent exposure of the STJ and CCJ. The medial incision extends from the anterior margin. of the medial malleolus longitudinally to the first metatarsal-medial cuneiform joint, and provides excellent exposure of the TNJ and neck of the talus. The lateral dissection proceeds through the superficial fascia to the deep fascia, which is incised longitudinally between EDB and the PB tendon Care is taken to preserve the peroneal sheath. EDB is reflected away from the CCJ, and the intertarsal talocalcaneal ligament and sinus tarsi are evacuated. The lateral aspect ofthe head and neck of the talus are exposed, and the peroneal tendons are retracted plantarly to expose the posterior facet of the STJ. Medially the dissection should avoid the medial marginal vein, and the deep fascial incision is made medial to the tendon ofTA. A medial periosteal and capsular incision exposes both the TNJ and the anterior margin of the ankle. The technique of osseous resection is crucial

A

Figure 8.8

B

Ch. 8


225

when performing the triple arthrodesis {Figure 8~9). Preoperative assessment of the

relationship between the foot and leg enables the surgeon to take into consideration knee and ankle positions so that proper placement of the hindfoot can be achieved. The hindfoot should be positioned in slight valgus, and varus should be avoided at all costs. A varus hindfoot fusion is destined to marked weight bearing difficulties, pain, and ankle instability postoperatively. The foot should be positioned in about 12-15° of pes abductus, when the knee is on the frontal plane. Less pes abductus is needed if the knee is externally rotated, and more may be useful in the presence of medial knee position or tibial torsion. Resection proceeds from the MTJs to the STJs, as MTJ resection enables easier access to the STJ. The foot is held in a reduced attitude and the CCJ and TNJ are resected with the blade parallel to the articulations in most cases. Severe adductus or abductus may warrant transverse plane wedging, however a flush resection preserves bone mass and correction can usually be satisfactorily achieved via translocation of the forefoot on the hindfoot without the need for specific wedge resection. Similarly, a near~para!lel resection ofthe STJs (posterior, medial and anterior facets) is usually adequate, as only slight valgus positioning will suffice. STJ wedging may be more pronounced if the frontal plane deformity is severe. The calcaneus is translocated medially for correction of pes valgus, and laterally for correction of pes cavus. Sagittal plane correction is also corrected primarily via translocation of the forefoot on the hindfoot, after achieving the desired talocalcaneal alignment The calcaneus can also be shifted posteriorly to increase the lever arm for the tendoAchillis and to increase sagittal plane talar declination and thereby increase arch height. Contrari!y, sliding the calcaneus anteriorly relative to the talus dorsiflexes the talus and decreases arch heightAchilles function. The desired alignment is temporarily stabilized with cannulated screw guide pins, and intraoperative radiographs in the AP, lateral, and calcaneal axial projections are obtained and reviewed. The order of stabilization generally

proceeds from STJ to TNJ to CCJ, and is usually achieved with three 6.5-7.0 mm interfragmental compression screws (Figure 8-10). The TC fusion is achieved with a !ag screw directed from the neck of the talus dorsally, into the body of the calcaneus. In a similar fashion, the TNJ and CCJ are stabilized with distal to proximal lag screws. Care is taken to avoid the following fixation hazards: violation of the medial cortex of the body of the calcaneus and entrance of the fixation device into the tarsal tunnel when fixating the TC interface, entrance of the TN fixation into the ankle, and fracture of the dorsolateral cortex of the cuboid with the screw head. Additional intraoperative radiographs should be used to reassess final fixation if any questions exist. The TC lag screw can also be directed from the apex of the calcaneus posteroMplantarly into the body and neck of the talus. The MTJs can also be satisfactorily stabilized, each with two staples oriented 90° to each other. Closure proceeds in layers following placement of drains medially and laterally, and the foot is secured in a BK Jones compression immobilizing dressing. Aftercare involves drain removal after 24 to 72 hours, redressing between 3 to 5 days, and BK cast immobilization without weight bearing for up to 3to 4 months. Mobilization of the ankle and MTPJs can be undertaken in a non-weight-bearing attitude as soon as desired, and immobilized partial weight bearing can be initiated by 10 to 12 weeks pending clinical and radiographic findings. Full weight bearing ensues thereafter, as does conversion to desired shoes. Ankle and Pantalar Fusion-the most common indication for ankle fusion is post-traumatic

arthrosis following ankle fracture, wherein a small proximal and lateral shift of the lateral malleolus has produced mortise incongruity resulting in articular cartilage degeneration. It

226


Ch. 8

Figure 8.9

Figure 8.10

has been shown that a 1 mm shift can result in greater than a 40% decrease in tibiotalar congruity. The most common predisposing causes of the need for pantalarfusion is severe cava adducto varus deformity with chronic ankle instability, and avascular necrosis of the talus for whatever reason. Other indications for ankle and pantalar fusion include destructive bone tumors, infection, and failed ankle endoprosthesis. Evaluation of the patient requires inspection ofthe knee, leg, ankle, STJ and MTJ, and the relationship of the forefoot to the hindfoot and leg. The ideal position of fusion is 90' of the foot relative to the leg, with slight ankle and/or hindfoot valgus, and approximately 10-12' of pes abductus. If tibial varum is present, increase the amount of valgus to adjust for the added varus deformity. The surgical approaches to ankle fusion include Charnley's transverse anterior incision, extending from one malleolus to the other, which is rarely used currently because of risk of injury to anterior neurovascular and tendinous structures. The lateral transmalleolar hockey stick incision is most commonly used, and begins over the junction of the middle and distal thirds of the fibula, then curves distally toward the sinus tarsi for the ankle fusion, and onward toward the junction of the bases of the fourth and fifth metatarsals for pantalarfusion. This approach yields anterior, lateral, and posterior exposure forfibufar osteotomy. An accessory medial incision over the anterior margin of the medial malleolus is usually combined with the transfibular incision to provide anteromedial exposure for resection of the cartilage of the medial malleolus and enables hardware placement through the tibial pilon. When performing ankle fusion, we are looking to position the large cancellous mass of the tibial metaphysis in rigid apposition to the trabecular bone of the body ofthe talus.

Ch. 8


227

Techniques to Achieve Ankle Fusion

1.

Curettage of cartilage with interposition aI bone graft;

2.

Sliding inlay graft from the anterior surface of the tibial metaphysis into the talar

neck/body; 3. 4.

Modified Ga!lie fusion wherein allogeneic graft is inserted anterolaterally and stabilized with a staple; Transmalleolar (either fibular or tibial) with osteotomy to enhance visualization of

5.

the tibiotalar interface; The subtotal fusion for debilitated patients that cannot sustain extensive bone

6.

7.

resection and trephine plug joint resection with dowel graft fusion will suffice; Compression arthrodesis using any of a variety of external fixation devices or interfragmentallag screws; and The Blair tibiocalcaneal fusion which can be useful post*polio or after collapse

of the talus. As with all fusion procedures, Glissane's criteria must be met for successful arthrodesis: 1. 2. 3. 4.

Removal of cartilage, fibrous tissue, or other material hindering raw bone contact; Accurate and close fitting of surfaces; Optimal position of fusion; and Maintenance of apposition in undisturbed fashion until fusion is complete.

The Podiatry Institute technique of ankle and pantarlarfusions entail the use of: 1. 2. 3.

A lateral hockey stick incision; Preservation of the fibula (avoid osteotomy); Cartilage resection with preservation of as much ofthe talar body as possible;

4.

Ancillary medial approach for removal of medial malleolar and talar body

5.

cartilage; Temporary stabilization with cannulated screw guide pins;

6. 7.

Fusion alignment of 90" of the foot to the leg; 10-12" pes abductus and slight ankle/hindfoot valgus;

8. 9.

Intraoperative radiographs in the AP, lateral, and calcaneal axial views; lnterfragmental compression fixation wrth crossing 6.5~7.0 mm cancellous screws; Placement of the fibular on lay graft with interfragmenta! compression screws purchasing the tibia and talus (and calcaneus in pantalar fusion); Be sure to allow a gap between the proximal and distal segments of the osteotomized fibula in order to avoid pseudoarthrosis or nonunion; Repeat intraoperative radiographs to ascertain fixation and bone alignment; Place and activate closed suction drains, bandage and immobilize; Plan to leave hardware in indefinitely or at least6 to 12 months; and Be sure not to penetrate the STJ with fixators if only ankle fusion is performed.

10. 11. 12. 13. 14. 15.

228


Ch.B

Complications of ankle and pantalar fusion include infection (reported as high as 20% in the literature); nonunion, malunion, and pseudoarthrosis; malposition due

to operative

misadventure (most often varus or calcaneus); stress transfer to MTJ and STJ (may need triple later if only ankle fusion originally performed); and limb shortening if bone graft is

not used. Total Ankle Replacement (TAR) Arthroplasty-chronic ankle pain that is not responsive to

other treatments, as well as the potential complications related to ankle arthrodesis, have prompted the quest for a total ankle replacement (TAR) that is reliable and effective. Severe ankle pain, deformity and dysfunction that serves as a constant impediment to weight

bearing ambulation, often due to arthritis secondary to rheumatoid disease, trauma, joint sepsis, or osteoarthritis, can be treated by means of TAR. There are basically 2 types of ankle endoprostheses: 1) 2-part prostheses that are either constrained, semiconstrained or nonconstrained; and 2) multi-axial 3-part prostheses that include a free gliding interposition aI core. These devices have been under development since the 1970s and have yet to be perfected, and the long term results have not be promising for any particular device, so far. Earlier models were secured with cement, however most surgeons prefer cementless models. Common complications of TAR include loosening without the presence of infection, and postoperative dehiscence. Ankle geometry and soft tibial metaphyseal bone contribute to aseptic loosening, and this complication is most common when a constrained system is used. Unconstrained systems, on the other hand, are associated with instability, ankle deformation and subsequent loosening. Difficulties mimicking ankle geometry stem from the factthatthe ankle is not a true ginglymus (hinge) joint, and the path of the center of motion evolves as the ankle goes through its range of motion. Current goals of ankle en do prosthesis design focus attention on the normal contours of the talar dome and the distal tibial bearing surface, and minimization of the amount of bone resection required to secure the implant. A number of options exist for TAR, including the Scandinavian Total Ankle Replacement (STAR) (Waldemar Link GmbH & Co., Hamburg, Germany), a 3-component device; the Agility'" Total Ankle System (DePuy, Inc., Warsaw, IN), a 2-component device; the TNK Ankle (Kyocera Corporation, Kyoto, Japan), a 2-component device; and the Buechel-Pappas Ultra Total Ankle Replacement (Endotec, South Orange, New Jersey), a 3-component device. The main alternative to TAR is ankle fusion, and both procedures aim to alleviate pain while TAR also aims to improve function. While both procedures are designed to reduce pain, TAR is also intended to improve function. If TAR fails, then consideration is given to arthrodesis, the standard therapy option for ankle arthrosis and the mainstay of salvage following failed TAR. Salvage after failed TAR often requires the use of substantia! amounts of bone grafting. To date, unlike the results of hip and knee arthroplasty, the long-term results of TAR have not been as successful. Although there are many case series describing the benefits and shortcomings of different types of TAR, further investigation is necessary to determine the best options for patients with recalcitrant anlde arthrosis.

Congenital Deformities and Juvenile Surgery

Ch.9

229

COIIIGEI\IITAL DEFORMITIES AN II JUVENILE SURGERY Congenital deformities can be familial, inherited traits, or they may present without a known family history. The condition may be idiopathic; or a known etiology such as an identified

genetic defect, intrauterine or birth trauma, hypoxia, teratogenic drug or toxin exposure, tumor or other cause may exist Some defects present as a component of a known

syndrome and other defects, both physical and mental, may be identified. Macrodactyly (Localized Gigantism)--this idiopathic, rare, usually unilateral, congenital defect displays abnormal largeness of a single or multiple adjacent toes. It may be related to or caused by hyperplastic lymphatiC or vascular elements, or neurofibromatosis; and usually occurs as an isolated defect without familial inheritance. In static macrodactyly, the giant digit(s) display a growth rate proportional to the remaining norma! parts. In progressive macrodactyly, the giant digit(s) display a more rapid growth rate than normal tissues. Treatment consists either of partial or total amputation of the giant part, or sequential operations to reduce excess soft tissue and bone in a staged fashion (Figure 9·1 ). Reconstructive efforts can be difficult and convey a high rate of complication.

A~~v {) B

~ D~

c~

Figure 9.1

Syndactyly-this is· the most common congenital deformity of the foot and hand, and is marked by partial or complete persistence of the interdigital web. The condition is familial, and can occur unilaterally or bilaterally. The defect occurs during the sixth to eighth intrauterine week, and most commonly localizes to the second-third toes. Simple syndactyly involves only fusion of the skin and soft tissues of the adjacent toes, while complex syndactyly involves fusion of the soft tissues, nails, and bone. Single syndactyly involves two toes and one web, double syndactyly involves three toes and two webs, and triple syndactyly involves four toes and three webs. Treatment is usually based not on physical dysfunction, but rather on psychological or emotional concerns ofthe older child or adult Surgical desyndactylization can be difficult, and techniques involve creation of dorsal and plantar skin flaps or use of dorsal and plantar W-plasties (Figure 9-2A), or application of a FTSG (Figure 9-28) after incislonal separation. Osteotomy may be necessary in cases of complex syndactyly.

230 _ _ _ ___':C:C,oll\ngl"ellin''ttaa".'lD~e'!'fo~rmm1ilti•'e_s_an_d_J_u_ve~n~ile~S~u~rg~e~rv _ _ _ _ _~~ , Ch. 8

c

B

A

D

Figure 9.2A

B

A

D

c Figure 9.28

Ch. 9


231

Polydactyly-this is a common congenital anomaly consisting of an accessory (supernumerary) digit or digits. The condition is idiopathic and an irregular autosomal dominant inheritance has been suggested. Preaxial polydactyly involves duplication of the hallux, while postaxial polydactyly involves duplication of the fifth toe. Postaxial polydactyly occurs in approximately 80% of cases, preaxial in about 15% of cases, and central ray duplication occurs in about 5% of cases. Mixed polydactyly involves pre- and postaxial duplication, and is observed most often in black individuals. Duplication can be either of an entire extra digit complete with bone (Type A), or of a rudimentary or vestigial toe (Type B). Polydactyly occurs bilaterally in about 50% of cases. Six radiographic patterns are seen with extra digits, including the short block metatarsal, Y-shaped metatarsal, T-shaped metatarsal, normal metatarsal shaft with wide head, partial or complete ray duplication, and normal metatarsal with distal phalangeal duplication (Figure 9-3). Syndactyly can occur in addition to polydactyly (synpolydactyly). Surgical treatment entails identification of the digit that has the most potential for normal growth and function, as duplication can involve bone, tendon, vessels, and nerves. Amputation should allow the foot to assume the most normal contour and facilitate wearing a shoe. Usually, the most medial digit is amputated in preaxial polydactyly while the most lateral digit is amputated in the postaxial state. Amputation for preaxial polydactyly, involving disarticulation of the extra medial toe is associated with the development of postoperative hallux varus, and K-wire stabilization across the MTPJ with recession of abductor hallucis are recommended. In cases of postaxial polydactyly, preserve robust skin (usually plantar) for coverage and closure over the lateral aspect of the new fifth ray. In case of an abnormal metatarsal configuration (Y or T), the prominent portion of bone should be osteotomized flush with the metatarsal shaft, and a wide metatarsal head should be made more narrow with osteotomy perpendicular to the growth physis in an effort to avoid growth disturbance. Central ray duplication can be managed with a dorsal racquet shaped incision at the base of the toe, and disarticulation and/or osteotomy at the appropriate level

Block met

., 1

i~

Nocmal mel w/ J1 digital duplication

Figure 9.3


232

Ch.B

Congenital Hallux Varus-this deformity involves an adductus and/or varus deviation of the hallux at the first MTPJ, and is usually observed as a complication of hallux valgus surgery. Congenital hallux varus can be observed as a consequence of neuromuscular disease, and often accompanies metatarsus primus adductus/varus. The Thompson procedure involves abductor halluc.is recession and tendon lengthening, or actual excision of the muscle, and may be used in the infant or juvenile with congenital hallux varus due to non-spastic contracture of this muscle. This technique conveys risk of overcorrection and hallux valgus. Congenital Hallux Abductus lnterphalangeus (Ungual Phalanx Valgusl-this rare congenital anomaly displays abduction and valgus positioning of the hallux, with the apex of the deformity at the hallux IPJ. Radiographically, the phalangeal primary centers appear at birth, and the secondary center between 2-3 years. By 2-3 years of age, enlargement of the medial aspect ofthe distal phalangeal base can be observed. Surgical treatment entails excision of the medial aspect of the distal phalangeal base and growth p!ate arrest, or Akin osteotomy. Congenital Curly (Underlapping) Toe-this familial, idiopathic anomaly can involve any of the lesser toes and occurs uni~ or bilaterally. Adductovarus underlapping of a lateral toe beneath its medial neighbor is most common, however abduction and vaiQus can also occur. Treatment entails interphalangeal arthroplasty and derotational skin wedge plasty (Figure 9-4 A, B, and Cl. Congenital Overlapping Filth Toe-this anomaly usually affects the fifth toe overriding the fourth, with adduction and varus, and dorsal soft tissue contracture in a proximal and medial direction. The second toe overriding the first is the next most common form of congenital overlapping toe. As the individual matures, IPJ plantar contracture and hammer or claw toe ensues. Nonsurgical treatment includes taping or use of a digital retainer to try to redirect the digit in the infant or youngster. Surgical options include amputation, (which

Figure 9.4A

A

w ~

A Figure 9.48

) B

B '' Figure 9.4C

'

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233

c~

B Figure 9.5 is a rather undesirable approach), as well as sequential release of the deformity and reconstruction. The Butler procedure entails use of racquet-shaped incision, EDL

lengthening, MTPJ capsulotomy (Figure 9-5). The McFarland procedure involves excision of skin of the web between the fourth and fifth toes, EDL lengthening, MTPJ and PIPJ capsulotomy, and syndactyly of the fifth-to-fourth toe. The Podiatry Institute technique involves a dorsal Z-plasty, EDL lengthening, MTPJ capsulotomy, PIPJ arthroplasty, excision of redundant plantar skin wedge, and K-wire stabilization. Cleft Foot (lobster Foot , Claw Foot)-this rare, familial, congenital anomaly displays

absence of part or all of the central rays, effecting a claw-like foot The defect can present either unilaterally or bilaterally. Associated defects include syndactyly, polydactyly, cleft palate, deafness, and many others. Surgical treatment focuses on establishing a functional

limb, and a footthat can be shod. Each case is unique and no specific procedure is always applicable. Surgery usually combines soft tissue and bone surgery, such as skin and bone grafting, arthrodesis and osteotomy. Brachyrnetatarsia-this hereditary anomaly is characterized by premature closure of the epiphyseal plate of one or more metatarsals, and most commonly affects the fourth metatarsal although any or multiple metatarsals can be affected. Associated maladies include Down's syndrome, pseudohypoparathyroidism, and poliomyelitis. The defect is usually not recognized at birth, however becomes evident between 4~15 years of age. Although usually unilateral, brachymetatarsia can occur bilaterally. Surgical treatment has traditionally hinged on one-stage autogenous bone graft elongation of the affected metatarsaL This technique, as well as elongating osteotomy such as the Giannestras step-down, and other sliding shaft designs, are limited by skin and neurovascular compromise secondary to excess lengthening. Skin plasty and Z-lengthening of tendon, as well as staging and soft tissue expansion techniques can be useful in this regard. More recently, bone transport with the mini external fixation has proven to be most effective and very safe as the soft tissues can gradually elongate along with the bone. Postoperative nonweight bearing is used for up to 2~3 months pending radiographic evidence of bone healing.


234

Ch.B

Metatarsus Adductus-this transverse plane deformity displays medial deviation of the metatarsals with the apex of the deformity at Usfranc's articulation. Metatarsus adductus IMAdd) occurs in 1 out of every 1,000 live births, is familial, and the presence of the deformity conveys a 1 in 20 chance that a sibling will also have the anomaly, and it occurs bilaterally in 55% of cases. Clinical findings include a C-shaped foot with convex latera! and concave medial borders in the transverse plane, adducted metatarsals with the more medial metatarsals being more adducted (1>2>3>4>51. a high arch if there is no STJ compensatory pronation, a skewfoot (toes abducted, metatarsals adducted, tarsus abducted) with heel valgus if compensatory STJ pronation is available, separation between the first and second digits, inability to abduct the metatarsals past midline of the foot, hypertonicfty and spasm of tibialis anterior in gait or upon striking in open chain, and possible hyperactivity of abductor hal!ucis.lfthe hindfoot is in rigid equinus and varus, rule out clubfoot. Total MAdd involves all five metatarsals, whereas atavistic MAdd localizes to the first ray, and is termed congenital metatarsus prim us adductus or varus. MPV displays a first intermetatarsal angle of 10° or greater. Radiographic assessment of MAdd is necessary to quantify the degree of deformity. The AP view is used, and the long axis of the lesser tarsus or that of the second cuneiform can be compared to the long axis of the second metatarsai(Fig 9-6). Using the long axis of the lesser tarsus, the normal met-add angle is 15-21°, and 25° when using the middle cuneiform reference. The Podiatry Institute radiographic classification system employs the long axis of the lesser tarsus, and defines met-add as follows: normal(rectus foot) 0-15", mild 16-25', moderate 26-35", and severe >35°. Jn the AP view, long-term compensation will show moderate~severe hallux abductus, cuboid abduction, and digital abductus as toes align with reatfoot, and increased Kite's talocalcaneal angle as the talus adducts medial to the navicular. ln the lateral view of the compensated deformity, an anterior break in the cyma line indicates hyperpronation and is usually associated with a decreased CIA. The uncompensated toot will display characteristics of pes cavus. LTAx

Points plotted for deremination of logitudinal bisection of lesser tarsus.

Figure 9.6

Lesser tarsal axis {LTAx) represents perpendicular to bisector of lesser tarsus. Line "EF" is bisector of lesser tarsus. Line "G" is bisection of second cuneiform.

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Conservative treatment can be effective if instituted in a timely fashion. For patients <3 months of age, manipulation, taping or casting, can be effective. For patients <3 years of age, altering sleeping habits to avoid adduction, use of the Ganley splint or corrective casting are

useful. Cast therapy involves three point bending of the foot in the transverse plane (Figure 9-71, and should be maintained an additional period of time equal to half of the time that was required to eliminate the deformity. If cuboid abduction increases, then over correction is occurring and casting should be discontinued. The BK cast should entail limited padding, and effect abductory force at the first metatarsal head and medial aspect of the heel, with an adductory force applied to the cuboid-fifth metatarsal junction. The hindfoot and ankle are maintained in neutral position. Medial tibial torsion, if present, can simultaneously be addressed with an AK derotating cast The cast is changed every 1-2 weeks. Following correction, a reverse last shoe may be useful for up to 6-12 months. Surgical treatment is indicated in patients >2 years of age who have reached an impasse with nonsurgical methods, and offer treatment options for patients up to 8 years of age. The Heyman, Herndon and Strong (HHS) procedure is performed through either a transverse or three longitudinal incisions, and entails sectioning of the medial 2/3 of the capsule and ligaments of the tarsometatarsal joints, followed by K-wire stabilization and casting. The Thompson procedure can be used in the infant or youngster to correct hallux varus associated with metatarsus primus adductus or varus. Johnson's chondrotomy technique entails laterally based (medial apex) wedge resection (2.5 mm) of the cartilaginous metatarsal base of the lesser metatarsals and a closing abductory base wedge, distal to the physis, on the first ray; in addition to lengthening abductor hallucis. The Lange procedure involves first metatarsal-cuneiform capsulotomy with recession of abductor hallucis, followed by serial casting. The Lichtblau procedure entails sectioning of a hyperactive abductor hallucis, much !ike Thompson's procedure, and is indicated in the equinovarus foot with metatarsus adductus Brown described transfer of tibialis posterior into the navicular from anomalous insertion, combined with medial cuneiform-navicular caps ulotomy. Ghali described an anterior-medial release of the first metatarsocuneiform and naviculocuneiform joints with division of tibialis anterior at the medial aspect of medial cuneiform. Osseous procedures are indicated in patients 8 years of age or older. McCormick and Blount described arthrodesis of the first metatarsocuneiform joint with lateral closing wedge osteotomy of the second, third, and fourth metatarsals and the cuboid. Peabody and Muro described mobilization of the first metatarsocuneiform joint combined with excision of the second, third, and fourth metatarsal bases and lateral closing wedge osteotomy of the fifth metatarsaL Steytler & VanDerWall described pan metatarsal oblique laterally based dosing wedge osteotomies. The Berman-Gartland procedure is a popular technique that employs lateral closing base wedge osteotomies of a!I five metatarsals distal to the growth plates (Figure 9-8). The lepird procedure (Figure 9-9) is a refinement on the BormanGartland technique that varies with the use of through-and-through rotational osteotomies ofthe intermediate metatarsals, combined with lateral closing base wedge osteotomies of the first and fifth metatarsals. The through-and-through osteotomies are made parallel to the substrate and are initially made with preservation of the dorsal-distal-media! cortex, which is completed only after interfragmental screw placement has been positioned and prior to achieving final screw purchase after swiveling the metatarsals into corrected alignment Fowler described an opening wedge osteotomy of the medial cuneiform, and Ganley refined the technique to address a deformed LASA (lisfranc articular set angle)that displays a severely oblique first met-cuneiform articular interface directed from proximal-medial to distal-lateral. Ganley performed a medial cuneiform opening wedge osteotomy with

236


A

Metatarsus adductus angle.

Correction is gained by compressing the reartoot. Metatarsals are then abducted on stable resrfoot.

Figure 9.7

Figure 9.8

Figure 9.9

Ch.B

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237

autogenous bone graft in conjunction with a laterally based closing wedge osteotomy of the cuboid. The resected corticocancellous cuboid bone is harvested for transplant into the medial cuneiform. The osseous work is combined with appropriate soft tissue releases and subsequent casting. Bankhart described excision of the cuboid, and Tachdjian-Grice

described a combination of hindfoot extra-articular arthrodesis with forefoot soft tissue release for correction of skewfoot. Talipes Equinovarus (TEV, Clubfoot}-this is an idiopathic, triplanar deformity thattypically includes ankle equinus, hindfootvarus, and forefoot adduction; in addition to subluxation of the TNJ. Although TEVis the most common form of clubfoot, equinovalgus can also occur. Clubfoot occurs in 1:1,000 live births, with a 2:1 male: female ratio. 50% of cases are unilateral, with the right foot being more commonly involved. The condition is familial, and siblings display 20-30times the chance of having clubfootthan the general public. Acquired forms of clubfoot can be neuromuscular in origin and associated with CP, CVA, meningitis, cord lesion, and post-polio; or post-traumatic following burns, ischemic contracture, and fracture malunion or tendon injury. In clubfoot, the head and neck ofthe talus are adducted 60-90° to the body in the transverse plane, whereas the normal relationship is 15-20°. In the sagittal plane, the head and neck of the talus are plantarflexed 25-30' in clubfoot, whereas the normal relationship is 45-65°. Recenttheory embraces medial rotation of foot under the talus, with the talus staying aligned with the leg (Ganley). The anterior aspect of the calcaneus is observed to be rotated beneath the talus in a medial direction, while the posterior aspect of the calcaneus is rotated laterally. There is associated tightness of the anterior deltoid, tibialis posterior and long flexors, and medial TNJ and NCJ and first metatarsocuneiform joint; as well as tightness of the CFL laterally. Tethering of the tibialis posterior tendon pulls the navicular medially and forces articulation with the medial malleolus. The cuboid, tethered to the navicular by ligament, follows the navicular. Equinus in clubfoot affects the ankle, and is due to tightness of the heel cord, long flexors, and posterior AJ and STJ capsules. The wider anterior portion of the talar dome does not reside in ankle mortise, and may pose difficulty in late term realignment due to tightness of the mortise. Contracted ligaments in clubfoot include: posteriorly, the calcaneofibular, posterior talofibular ligament; and medially, the deltoid, tibionavicular, and calcaneonavicular. Tendon contractures include: posteriorly, the Achilles; medially, TP, FDL, FHL, and abductor hallucis; and laterally, the peroneal tendons. Radiographically, clubfoot displays, in the AP view (Figure 9-10), Kites talocalcaneal angle reduced to 0-15' (normal20-30'), the !alar-first metatarsal angle >15°, which is indicative of TN subluxation. In the lateral view, the sagittal plane TCA 0-35" (normal35-55") with decrease upon dorsiflexion stress (this angle will increase in the normal foot). The Ponsetti method of corrective casting is the mainstay of conservative treatment Much like metatarsus adductus, initial efforts are directed at reducing adductus until the cuboid is anterior to the calcaneus and the navicular is anterior to the talus. Secondly, the varus is reduced until the calcaneus is no longer medial to and inverted in relationship to the talus. Lastly, the equinus is reduced after satisfactory reduction of the adductus and varus components. If a dorsiflexory force is applied before reduction of the adductus and varus, the STJ and MTJ will hyperpronate and subluxation will effect a rocker bottom foot If the equinus resists manipulative reduction, and a nutcracker compression of the midfoot is likely, then posterior release should be performed before continuing to force dorsiflexion. Serial cast therapy should be initiated as early as possible, even in the infant. Neonates may respond to taping alone. Casting is ideal before 6~8 months of age, but can be attempted

238


Ch. 8

I

l

1

Normal foot Talocalcaneal L 20°-40°

Clubfoot Talocalcaneal L 15°

Figure 9.10 even in older children. Clubfoot becomes more resistantto corrective casting after the child begins walking. The typical duration of cast therapy is 6 weeks to 3 months in patients <1 year old, and from 3-5 months in older children. Casting can be continued as long as progressive correction occurs, however surgical intervention should be entertained if impasse is reached. Serial casts are changed approximately every two weeks. The

duration of casting is proportional to the degree of rigidity, and growth must occur for the

deformity to reduce. Surgery entails soft tissue release in the infant and young child. Correction entails release of those structures that are tight, and varies from patientto patient Goals include restoration of the TN, TC, and CC relationships. Consideration should be given to staging the repair in older children and adults, to avoid neurovascular compromise. Turco popularized the one stage posteromedial and circumferential releases (Turco procedure) for clubfoot repair. The Cincinnati incision, or a medial hockey stick approach can be used. The Cincinnati incision may limit posterior exposure. The posteromedial release involves release and/or lengthening of the following: Achilles tendon Z-plasty; posterior ankle and STJ capsulotomy; section CFL and posterior syndesmotic ligament; TP, FDL and FHL Z-lengthening; TN, NC, cuneiform-metatarsal capsufotomy; sectioning the interosseous talocalcaneal (cervical) ligament; abductor hallucis recession; and smooth K-wire stabilization of the relocated TN and TC joints. Circumferential release includes the posteromedial release with additional release of plantar and lateral structures. The plantar release involves reflection of the plantar fascia and intrinsic musculature from the plantar cortex of the calcaneus. Lateral release involves sectioning the bifurcate ligament (Y-Iigament, or calcaneonavicular-calcaneocuboid ligament), and perhaps Z-plasty of the peroneal tendons if indicated. Transfer of tibialis anterior into the lateral cuneiform may also be a useful adjunct. Osseous procedures, performed in conjunction with soft tissue releases, include lateral column shortening techniques such as the Lichtblau anterior

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calcaneal lateral closing wedge osteotomy, the Evans calcaneocuboid wedge resection and fusion, and Ganley's closing abductory cuboid osteotomy. It may be necessary to osteotomize the lateral cuneiform as wei!. In case of neglected clubfoot, triple or pantalar arthrodesis may be useful, howevertalectomywith tibiocalcaneal-tarsal arthrodesis is the most frequently used reconstruction.

Congenital Calcaneovalgus-this congenital anomaly presents the foot in an acutely extended position with the dorsal surtace in contact with the anterolateral surface of the leg. The entire foot, including the heel, is in complete valgus to the point that when the neonatal foot is pulled into plantarflexion, the following are noted: flexion is limited to the neutral position, or perhaps slightly beyond; skin and subcutaneous tissues are stretched tightly due to contracture that reveals a prominent, tight band that blanches in comparison to surrounding normal skin; the underlying tendons usually not contracted; the calcaneus (heel) is in valgus with the rest of the foot, and there is no frontal plane deviation of the forefoot in relation to the hindfoot; and the foot is fairly flexible so thatthe heel and midfoot can be brought into a corrected varus posrtion (a nonrigid deformity). Normal neonatal ankle dorsiflexion is approximately 45°, unlike the calcaneovalgus foot that can dorsiflex to become flush with the pretibial surface ofthe leg. Normal neonatal ankle plantarflexion is about 50°, whereas the calcaneovalgus foot only gets to neutral or a few degrees of plantarflexion. Increased plantarflexion of talus will be visible on the lateral radiograph, and Kite's angle will be >35" in the AP view.

TABLE 9-1. COMPARISON OF THE NORMAl FOOT VS. THE CALCANEOVALGUS FOOT. Normal foot

Calcaneovalgus foot

Talus sits on top of calcaneus without overlap of the anterior edges of the bones Bisection of the talus passes through the superior half of the cuboid, on the lateral radiograph

Talus is plantarflexed and the talar head overlaps the anterior edge of the calcaneus Bisection ofthe talus falls plantar to the cuboid on the lateral radiograph If the deformity is severe, the talus lies in a vertical position

As with many pedal misalignments, the parents usually do not seek an opinion or care until the child is 6-8 months of age, when the child first stands. In weight bearing, a complete absence of the arch and severe valgus are noted. Conservative treatment employs corrective casting using two layers of cast padding after applying skin adherent (tincture of benzoin). An assistant holds the foot by the toe tips and maintains as much of an equinus position as possible, while maintaining a neutral relationship of the FF to the hindfoot, and adduction ofthe FFto correctthe TN alignment The cast is then applied from the toe tips to below-the-knee, molding into the arch and aboutthe heel. A lateral X-ray is obtained to confirm reduction, and correction is maintained for 2-3weeks, changing the cast every 3-4 days in the neonate. Congenital Vertical Talus (Congenital Convex Pes Valgus, Rocker Bottom Foot)-this idiopathic anomaly, a form of clubfoot, is characterized by a footthat may actually contact the pretibial surface at birth. The plantar surface is convex (rocker bottom), and the talar head can be identified on the medial plantar aspect of the longitudinal arch, with the hindfoot in equinovalgus. Deforming muscfe groups displaying contracture include

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Ch.S

gastrosoleus complex (ankle equinus); ankle dorsiflexors (TA, EDL, EHL,) and the peroneal tendons; and the peroneii and tibialis posterior are relatively more anteriorly migrated than normal. Ligamentous shortening involves the dorsal talonavicular, tibia-navicular, calcaneofibular, calcaneal-cuboid, interosseous talocalcaneal ligaments; and the posterior AJ and STJ capsules are tightened. The spring ligament conversely, is elongated. Radiographic evaluation employs use of the AP, lateral and forced plantarflexion views (Figure 9-11).1n the lateral view, the long axis ofthetalus appears vertical and parallel to that ofthe tibia while the calcaneus is in equinus and the forefoot dorsiflexed. ln the AP view, the TCA is increased to >40°. The navicular cannot be radiographically evaluated until3-4 years of age, when it ossifies. When it has ossified, the navicular is identified in a dorsally dislocated position. The stress plantarflexion lateral view allows comparison of the first metatarsal on standard lateral and the stress view, so that rigidity of the deformity can be determined. Normally, the talar and first metatarsal axes are parallel; however in the presence of a rigid plantarflexed talus, the talar axis passes through sole of foot and the first metatarsal axis passes dorsal to head of talus. In the forced p!antatflexion view, this relationship will not be reduced. Convex pes valgus is categorized as either Type I or Type II. Type I involves dislocation of the TNJ, subluxation of the TCJ, and a normal CCJ. Type II is more rigid and involves dislocation of the TNJ, subluxation ofthe TCJ and CCJ, and ankle equinus. The differential diagnosis for calcaneovalgus includes talipes calcaneovalgus, severe pes valgoplanus with gastrosoleus equinus, paralytic pes valgoplanus, myelomeningocele, polio, and rigid pes valgus due to tarsal coalition. Associated deformities include cleft palate, arthrogryposis, and spastic equinus due to CP and others. Treatment of congenital vertical talus focuses on restoring the normal TN, TC, and CCJ relationship as soon as possible. This condition is notoriously resistant to nonsurgical treatment. As with talipes equinovarus, manipulation and serial corrective casting (Ponsetti method) are useful. At birth, gentle manipulation is used to stretch the contracted soft tissues. Manipulation entails stretch oftriceps surae and ca!caneofibular ligament via distal and medial traction, plantatf!exion and adduction of the FFto stretch dorsiflexors and everters, and distal traction of the FF and TNJ to effect adductus and varus stretch of the tibionavicular and talonavicular ligaments. The stretch is held for 15 seconds and then released, and the exercise is continued for 15 minutes after which the cast is applied. The cast is changed twice per week for six weeks. As correction ensues, focus more on TN reduction by means of distal FF traction until the head of the talus dorsiflexes and the calcaneus is pulled under the talus. It may become necessary to maintain the closed reduction with percutaneous pin stabilization. If, after 4-6 months of closed reduction,

Figure 9.11

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impasse is reached, then open reduction should be performed. The longer the TN dislocation persists, the more the soft tissue contracture deforms bone and surrounding joints. Surgical repair of congenital vertical talus employs a medial, curvilinear skin

incision extending from the medial aspect of the Achilles tendon at a point 4-6 em proximal to the ankle, around the tip of the medial malleolus, and onward to the junction of the first metatarsal and medial cuneiform. The neurovascular bundle is retracted, after which the Achilles, TA, EHL, and peroneal tendons are Z-plasty lengthened. The tibionavicular, TN, bifurcate, and dorsal calcaneocuboid, calcaneofibular and TC interosseous ligaments are then sectioned, The talar head is manipulated dorsally and the navicular moved in a plantar direction with inversion, A smooth 0,062" K-wire is then driven from the posterior aspect of the talus across the reduced TNJ, and continued anteriorly across the NCJ. The spring ligament is then reefed tightly, and an AK cast used to maintain the correction for 12-16 weeks. The K-wire can be removed around 6 weeks postop. Avascular necrosis of the talus is a possible complication. Excision of the navicular has been effective in the treatment of rigid arthrogryposis in patients 3·6 years of age. In children >6 years old, rigid bone and joint adaptation may indicate the need for triple arthrodesis. Tarsal Coalition-this condition occurs due to failure of differentiation and segmentation of primitive mesenchyme with resultant lack of joint formation. Types of coalitions include: syndesmosis or fibrous, synchondrosis or cartilaginous, and synostosis or osseous. The middle facet talocalcaneal (TC) coalition occurs most frequently, followed by the calcaneonavicular (CN barL and then by the talonavicluar (TN) coalition. The age of onset of symptoms varies as follows with the site of the coalition: TN coalition, 3-5 years; CN bar, 8·12 years; TC coalition, 12-16 years. The 3 predominant symptoms include: 1.

2. 3.

Tonic peroneal muscle spasm, hence the term peroneal spastic flatfoot, with antalgic eversion guarding against STJ motion; Limitation of STJ and possibly MTJ motion; and Pain upon weight bearing or attempted hindfoot motion.

Classically, a rigid flatfoot deformity displays the combination of peroneal spasm, stiffness, and pain. Radiographic evaluation of tarsal coalition, in the lateral view, reveals talar beaking, increased halo effect or sclerotic appearance of sustentaculum tali and crucial angle area of the calcaneus, broadening and flattening of lateral talar process, and diminished or absent joint space of middle and posterior facets. The medial oblique view Oateral projection) is the best view to visualize a CN bar. Isherwood views and the 60° medial oblique are best for visualization of the anterior facet of the STJ. A single 45° calcaneal axial or a set of Harris and Beath views will reveal the relationship of the middle and posteriorfacets, which should be paralleL The presence of a TC coalition wlll make the relationship oblique or obliterate the involved, usually middle or medial, facet space. Secondary articular changes are those of joint space narrowing, osteophytosis, and subchondral sclerosis. These are classically observed atthe dorsal aspect of the TNJ in the form of dorsal exostosis, or talar beaking, in association with a TC coalition; or in the form of the parrot beak sign (anteater sign, calcaneal beak) in association with a CN bar. Wide-angle linear tomography, making images across the STJs at 5 mm intervals beginning at the lateral malleolus, can also be useful. CT scanning and MRI can also be used to identify coalitions, and MRI is particularly useful in cases of fibrous or cartilaginous bridging. Conservative treatment of tarsal coalition entails stabilization of the STJ using

242


Ch.B

strapping, foot orthoses, and cast immobilization in acutely painful cases with marked peroneal spasm. Corticosteroid infiltration into the sinus tarsi may also yield symptomatic relief. Surgical intervention for persistently painful CN bar involves resection of the

coalition and is best performed before 14 years of age. The bar is excised via an Ollier or similar approach to the sinus, and Bagley described transplantation of the EDB muscle belly into the excision site in an effort to avoid the development of rigid fibrosis in the cleft (Figure 9~ 12). Postoperative non-weight bearing and immobilization are used for 4-6 weeks. In cases of TC coalition in a youngster with no secondary arthrosis, consideration can be given to resection of the coalition, and arthrodesis may become necessary in the future. In the adult without significant secondary arthrosis, isolated TC fusion is indicated. In any patient with significant secondary arthrosis, triple arthrodesis is indicated.

Figure 9.12

Pediatric ln~toe Deformity~a variety of conditions can cause an in-toe, or medially adducted gait The most common causes are femoral anteversion, which usually selfcorrects by 3 years of age, and metatarsus adductus. Talipes equinovarus, metatarsus primus varus, juvenile hallux varus, and medial tibial torsion also display ·m-toe. Asymmetry pronounced deformity, pain, or gait imbalance all warrant evaluation. Treatment may range from simple observation to manipulation, reverse last shoe, casting, night splints, or surgery depending upon the cause and degree of deformity. Pediatric Toe~walking Gait~a variety of causes can lead to an equinus or toe-walking stance and gait, including: CP, delayed myelinization of the corticospinal tracts, muscular dystrophy, CMT and other peripheral neuropathies, disease of the basal ganglia such as dystonia musculorum, spinal cord defects such as spina bifida, talipes equinovarus, gastrocnemius or gastrosoleus equinus, prancer syndrome where the child mimics toe walking seen in adults or older children, autism and conditions of mental retardation Micromelia,-this rare congenital defect has been associated with hypoxia, maternal thalidomide intqke during gestation, and involves pathological smallness of the limb. The condition Is usually associated with other defects. No specific treatment is recommended for the extremity. Congenital Hemihypertrophy---this rare, idiopathic anomaly usually displays enlargement of the ipsilateral upper and lower extremities or parts thereof. Possible causes include neurofibromatosis, vascular or lymphatic hyperplasia, AV fistula, malignancy, or benign

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tumor. When indicated, treatment is directed at the identified primary defect, or ablative intervention on the involved limb. Shortening osteotomy, arthrodesis, and soft tissue debulking techniques can be used in one stage or multi~staged procedures. Osteochondroses-these acquired diseases affect grovvt:h centers, both primary and

secondary, and have been attributed to vascular disturbance and/or trauma. Systemic arthritis, infection, certain medications and toxins, and tumors can also disturb the growth center, however the osteochondroses are generally observed as idiopathic, insidious conditions that occur in active youngsters and cause diffuse aching and guarded ambulation. Radiographic inspection may reveal irregularity and fragmentation of the growth center and adjacent physis, and increased soft tissue density and volume. Treatment usually entails rest, ice, compression, and elevation, and appropriate oral anti-inflammatory medication can be helpful. Gel casting and use of a surgical shoe, cast or splint immobilization, protected weight-bearing and follow-up use of foot orthoses may also be used. Specific osteochondroses include: Freiberg's infraction-osteochondritis that usually affects the second metatarsal head, more common in females :::13 years of age, resulting in flattening and widening of the

metatarsal head, and attributed to traumatic disruption of the physeal blood supply. Lushke's disease-osteochondritis of the fifth metatarsal base, observed in children 5-11 years of age. Kohler's disease--osteochondritis of the tarsal navicular, most common in boys 3-6 years

of age. Sever's disease--osteochondritis ofthe calcaneal apophysis, observed in children 8-14 years of age and most common in boys. Osgood-Schlatter's disease-osteochondritis of the tibial tuberosity, most common in athletic boys aged 11-15 years. It is important to rule-out osteosarcoma in this age group and location.

244

Management of Foot and Ankle Trauma

Ch. 10

MANAGEMENT OF FOOT AND ANKLE TRAUMA Basic principles ofthe management oftrauma include a thorough assessment otthe injured patient, triage, and appropriate treatment of specific injuries. Priorities include basic and advanced life support (described elsewhere in the manual), which entail maintenance of an airway, CPR, identification and control of hemorrhage, monitoring vital signs lBP, pulse, respiration, temperature, and level of consciousness), and fluid management Blood should be obtained for typing and cross matching, if the potential for substantial volume depletion exists. While waiting for compatible whole blood, an IV infusion of glucose and water, plasma, plasma expanders, or lactated Ringer's solution may control shock temporarily. Ideally, whole blood should be administered for severe blood loss. Specific injuries of soft tissues and bone should then be determined. Injuries include punctures, abrasions, incisions, and lacerations (PAIL), as well as burns, penetrating trauma, fractures, and dislocations. Tetanus prophylaxis is a consideration in every form of trauma that results in cutaneous compromise. ln general, the injured lower extremity should receive protection, rest, ice, compression, and elevation (PRICE), after assessment of the neurovascular status to the injured limb.

SELECTED SOFT TISSUE INJURIES Cutaneous Wounds-After ascertaining the systemic status of the patient. local tissue factors may be evaluated. Inspection enables identification of pathological anatomy and the presence of foreign body. An open wound is considered "old" and contaminated if care has not been administered within 6 hours after the onset ofthe injury. The status of the skin, vessels and nerves, tendons, bones and joints must all be documented based on the merits of each individual injury. local, regionat and even general anesthesia may be necessary in order to thoroughly identify pathology. The procedure may take place in the office, emergency department. or the operating room. Intravenous conscious sedation with local or proximal field block often suffices for foot and ankle· injuries. local anesthesia should only be infiltrated after assessment of the peripheral neurovascular status, and then only proximal to the injured tissues. A proximal tourniquet is usually preferred as compared to dilute vasoconstrictor in the local block. Normal sterile saline, warm or room temperature, a bulb syringe or 18-gauge needle with a 20-50 cc syringe, and aseptic technique are used for lavage, inspection and local debridement Tissue forceps, scalpel, curette, and other probes may be helpful. Adequate debridement entails removal of all necrotic or heavily contaminated tissue, including small fragments of bone, and foreign bodies. Skin viability is ascertained clinically by a pink dermal coloration, warmth, and capillary bleeding. If necessary, IV administration of 10-15 mg/kg of fluorescein dye followed by observation of the tissues under Wood's light will reveal dye uptake in the tissues by means of fluorescence. Fascia is relatively expendable due to its diminished vascularity compared with other tissues, and it is also prone to infection. For tendon to remain or become viable, it must be covered with intact skin or graft, flap, muscle, or a suitable skin substitute. Muscle viability is determined by the presence of the 4 Cs: color (beefy red), contractility (upon electrical stimulation). capillary bleeding (bright red blood). and consistency (firm, elastic). Specimens should be obtained for C&S, as well as for histopathological inspection of appropriate tissues. Following initial debridement definitive therapy can be determined, or additional debridement may be in order. Specialized vascular and/or neurological consultation may be indicated following initial

Ch. 10


245

debridement, prior to definitive reconstructive efforts. Similarly, infectious disease, internal medicine and any other appropriated consultation that is indicated, could be obtained. Tetanus Prophylaxis-the specific action to be taken is determined by the patient's immunization history, as follows:

1. 2.

3. 4.

5.

6.

7.

If immunization was completed previously, and the last booster was within 1 year; then there is no need to administer tetanus toxoid or immune globulin. If immunization was completed within the preceding 10years without subsequent booster, then administer 0.5 ml tetanus and diphtheria toxoid (adultTd). If immunization was completed >10 years ago, and the last booster was within the preceding 10 years; then administer 0.5 ml ofTd. If immunization was completed >10 years ago, and there has been no booster within the previous 10years, and the wound is minor, relatively clean and treated promptly; then administer 0.5 ml ofT d. If immunization was completed >10 years ago, and there has been no booster within the preceding 5 years, and the wound is dirty or >6-8 hours old; then administer 0.5 ml ofTd and 250-500 units of human tetanus immune globulin (TIG [h]). The 500-unit dosage is used if the wound is considered prone to clostridial contamination, otherwise 250 units is sufficient. The Td and TIG[h] are administered using separate syringes and needles, at distant sites (deltoid and contralateral glutei). If there is no history of immunization, and the wound is minor, clean, and treatment is prompt; then initiate an immunization program with 0.5 ml ofTd and schedule the follow-up booster series. If there is no history of immunization and the wound is dirty or treatment is delayed; then administer 0.5 ml Td and 250 units TIH[h] and follow-up with the booster series. Give 500 units TIG[h] if the wound is clostridia-prone. In addition to Td and TIG[h]. 10-20 million units of aqueous penicillin-G should be administered IV for a tetanus- prone wound, and appropriate cleansing debridement and wound care undertaken.

Nail Trauma-traumatic conditions that affect the nail and associated structures include subungual hematoma, and hematoma with underlying phalangeal fracture; simple and complex nail bed lacerations; and nail bed tissue loss injuries such as partial digital amputation, degloving and avulsion. The majority of nail injuries result from blunt trauma, either stubbing or dropping something heavy on the toe. Treatment can be enhanced by digital or metatarsal ray block with local anesthetic infiltrated into normal-appearing skin proximal to the defect. Subungual hematoma causes throbbing pain as hemorrhage through the nail bed accumulates in the potential space between the plate and bed, and usually requires no more treatment than reassurance and observation. Hematoma will slowly migrate forward with nail growth, and takes 7-9 months in the adult for complete regeneration of a toenail. Painful hematoma in the acute phase may benefit from drainage by perforating the nail plate with a hand cautery, or a narrow rotary bur or#11 scalpel blade. The toe is prepped with antiseptic before drainage, then antibiotic cream and a sterile coverlet afterwards.lfthe subungual hematoma involves greater than 25% of the visible nail plate, and the plate is unstable upon the nail bed, then serious consideration should be given to avulsion ofthe nail plate and inspection ofthe damaged nail bed (Zook's rule). Nail

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Ch. 10

bed lacerations are either simple transverse, oblique or longitudinal lesions; or complex (stellate, crushing), perhaps with apices that will eventually undergo necrosis. Approximately 20% of subungual hematomas are associated with distal phalangeal fracture, which can technically be considered an open fracture after either traumatic or therapeutic nail plate avulsion in the presence of nail bed laceration . .After cleansing debridement the nail bed is sutured with 4-0 or 5-0 absorbable suture in fresh, clean wounds; or nonabsorbable suture in heavily contaminated or longstanding (>6 hours) wounds. The nail bed is bandaged with nonadherent gauze preserving· the cui de sac nature of the proximal nail fold, and appropriate supportive measures are used. Nail bed tissue loss injuries are defined by the Rosenthal classification system, which describes the level of tissue loss as either distalto.the bony phalanx (zone 1), distal to the lunule (zone 2), or proximal to the distal margin of the !unula (zone 3); and according to the direction of tissue loss as either dorsal oblique, plantar oblique, transverse guillotine, tibial or fibular axial, or central gouging (Fig 10-1). Treatment includes cleansing debridement, and coveragewith local transport of adjacent skin by means ofthe Atasoy flap (plantar-to-tip V-Y flap) or Kutler flap (medial and lateral V-Y plasties) after reduction of any prominent distal phalanx. Split- and full-thickness skin grafts can also be used to cover broad defects. Lesions proximal to the DIPJ may require disarticulation. Complications of nail bed injury include delayed nail regeneration; matrix disturbance with Beau's transverse line or ridge,

II

Ill

~c~

A

D

B

c figure 10.1

E

Ch. 10


247

onychocryptosis, and nail dystrophy with onycholysis and secondary fungal infection, canaliformis or split~nail deformity, and an unstable nail. Burns and Frostbite--burns are caused bythermal injury, both hot and cold, and chemical and electrical injury. The severity of a burn depends upon the extent of surface area and depth of skin penetration. Tissue damage is caused by protein denaturation, fluid

extravasation, and edema. The extent of a burn is designated as a percent of total body surface area (TBSA). and the rule of nines is applicable. The body is divided into multiples of 9% (Fig. 10-2). Partial-thickness burns include first and second degree wounds. Full-thickness burns are designated as third degree. First-degree burns involve only the epidermis, show erythema and no blisters, and are painfuL The most common form is sunburn. Second-degree burns are either superficial or deep. A superficial second-degree burn involves injury to the epidermis and a portion of the dermis; and they are erythematous, moist with blister formation and serous drainage, and are very painfuL A deep second-degree burn injures the epidermis and most of the dermis, leaving skin appendages intact It may or may not show blister formation and can be dry and it might display scattered anesthesia. A third degree burn involves full-thickness skin and a portion of the subcutaneous layer, destroying all skin appendages, thrombosing vessels, and appearing dry, anesthetic, whitish and leathery (eschar). A third degree burn can extend to bone. Fourth degree burns are caused by low voltage (<1000 volts) electrical injury, and fifth degree burns are caused by high voltage electricity or radiation injury. Fourth and fifth degree burns involve muscle and bone. Minor burns can be treated outpatient and include all first-degree, second-degree <15% total body surface area (TBSA), and third-degree <2% TBSAwounds. Moderate burns may be treated either in or out of the hospital, based on specific merits of each case, and include second-degree >15% TBSA and third-degree <10% TBSA. Severe burns require inpatient treatment and entail any third-degree burn of the foot, hand or face; seconddegree >30% TBSA, third-degree >10% TBSA, or any burn with associated sepsis,

l)

l)

I

I

Figure 10.2

248


Ch. 10

fracture, or systemic complication such as shock or cardiopulmonary disorder. The goals

of treatment are to stop the burn process, prevent infection, and enhance healing. Fundamentals include airway management, fluid management (IV lactated Ringer's

solution or fresh frozen plasma, monitor urine output along with tetanus prophylaxis, IV and topical antibiotic, analgesia, and escharotomy. Silver sulfadiazine and sulfamyalon (anti-pseudomonal [nosacomia!]), sterile water lavage, and porcine heterograft or biosynthetic skin substitutes may be used. First-degree burns respond weH to topical lotions to moisturize and diphenhydramine and methylprednisolone in a dose pack may be helpful in some cases. Second-degree burns are managed much like abrasions, cleansed, blisters that are very large or already show drainage are debrided, followed by application of topical antibiotic cream and sterile bandage. Third degree, or full-thickness burns require excision of necrotic eschar followed by autogenous split-thickness skin graft(STSG) or temporary coverage with porcine heterograft or skin substitute until the patient can be prepared both locally and systemically for definitive skin grafting or other plastic

reconstruction. Compressive dressings, splints, and early physical therapy for range of motion are crucial therapeutic measures that minimize contracture and edema. Complications of burns include hypertrophic scar, contracture deformity, syndactylization, ischemia, and vasomotor instability. Frostbite is also categorized based on the depth of penetration. First-degree frostbite displays freezing of the epidermis with subsequent pain, erythema and exfoliation, but no blister formation. Second-degree frostbite involves freezing of the entire epidermis and a portion of the dermis, and pain develops after thawing. Third-degree frostbite involves freezing of the entire thickness of skin and displays localized ulceration. Fourth-degree frostbite also involves full-thickness skin freezing, however the extent of injury is more extensive in the extremity, encompassing an entire hand or foot, leg or arm. Superticial frostbite, first- and second-degree, is also termed chilblains. Trench foot implies freezing or near freezing in a wet environment, with vasospastic hypoxia, necrosis and subsequent edema. Systemic hypothermia is described as a core body temperature <90° F, with dehydration, and cardiogenic shock can ensue. Treatment of frostbite entails protection of the part, avoiding friction rubbing to try to stimulate warming frozen tissues, and getting to a place where rewarming and assessment of the core body temperature can be achieved in a definitive fashion. Refreezing is particularly destructive. Rewarming of the frozen part is done in a footbath wfth water at 38A4° C in 15-20 minutes. Administration of IV dextran counters the osmotic imbalance due to local tissue dehydration in the frozen part Tetanus and antibiotic prophylaxis, analgesia, and subsequent sterile bandaging are also in order. Sequelae include cold sensitiviTy, Raynaud's phenomenon, paresthesia and pain, and contracture. Puncture Wounds (see Chapter 3) Gunshot Wounds (GSW) and Penetrating Trauma--gunshot wounds are a form of

penetrating trauma associated with a wide range of defects, both local and systemic. In the lower extremity, low velocity injuries are most common. The projectile creates a path and cavity in the tissues, which varies with projectile mass, velocity, and tissue density and volume. Kinetic energy is equal to half of the mass times its velocity (KE" 1/2 mv2),

therefore both velocity and mass greatly influence the amount of energy sustained by the body part. A low velocity projectile, shot from most handguns, effects a straight and

narrow, or focused path and cavity; whereas a high velocity projectile, shot from a hunting

Ch. 10


249

rifle or military weapon, will yaw, tumble and create a large cavity as it traverses the body part Soft nose or hollow point, as well as jacketed bullets, are designed to deform and fragment upon impact, thereby creating more projectiles that result in more damage. Low velocity projectiles frequently do not create an exit wound, even when bone is not involved. High velocity bullets create entry and exit wounds. Exit wounds are usually larger than the entry defect, since the projectile deforms and fragments, along with the tissues, as it penetrates and traverses the part. When a low velocity projectile encounters bone in the foot, a typical "drill hole" defect can be observed radiographically where the bullet traverses the bone. High velocity bullets shatter small bone into fragments that are often too small to repair. Treatment of GSWs entails triage, identification of the systemic and local tissue status, attention to neurovascular compromise, tetanus and antibiotic prophylaxis, cleansing debridement and removal of necrotic soft tissue and bone, foreign body bullet removal, skeletal stabilization and reconstruction, often requiring bone grafting. Definitive reconstruction may be performed on a delayed basis. Completion of a police report is usually required. Knife wounds represent a form of low velocity penetrating trauma. The path and cavity are very narrow and distinct. Identification of systemic and local pathology proceeds in a fashion similar to that for gunshot wounds, and the management protocol is essentially the same. Animal and Human Bite Wounds~these are crushing injuries that convey special microbiology related to a wide range of organisms and tissue necrosis. Anaerobes and both gram-negative and posrtive organisms may be present. Cleansing debridement with identification of pathological anatomy proceeds in the standard fashion. Peroneal Tendon Dislocation, Stenosis, and Rupture-dislocating peroneal tendons can be caused by forced eversion of the hindfoot with ankle dorsiflexion, a direct blow to the lateral aspect of the hindfoot and/or ankle, or due to congenital absence or defect of the peroneal groove in the lateral malleolus. Symptoms include hindfoot and ankle pain and edema due to peroneal tendinitis, palpable crepitus, and a clicking sensation as the tendon subluxates from behind the fibula and displaces anteriorly. Radiographs may show an avulsion fracture fragment from the lateral malleolus or defect in the peroneal tubercle of the calcaneus. MRI can also be useful, and may reveal a split-tear of the peroneal tendon, tenosynovitis of the peroneal sheath, as well as any associated osseous lesion. Treatment involves cast immobilization in the acute phase for 3-6 weeks, or ankle bracing during strenuous activity in the chronic state. Surgical reconstruction of the peroneal retinaculum IRg. 10-3) orofthe peroneal groove in the fibula IFig. 10-4) may be indicated in recalcorant cases. Stenosing peroneal tenosynovitis can be caused by direct, acute trauma sustained during fibular, talar, or calcaneal fracture; or by chronic microtrauma due to an enlarged peroneal tubercle or constricting retinaculum. Symptoms include pain upon hindfoot/ankle inversion, and stiffness. Signs include point tenderness along the tendon at the point of entrapment, and thick, boggy edema. Diagnostic studies include lateral and calcaneal axial radiographs, peroneal tenogram, or MRI. Treatment involves supportive bracing, corticosteroid infiltration, and perhaps physical therapy; or surgical repair of bone, sheath, and tendon. Postoperative physical therapy may also be in order. Peroneal tendon rupture is uncommon, and may result from laceration, severe hindfoot/ankle fracture/dislocation or, more typically, chronic degeneration. Signs and symptoms include edema and pain in addition to associated injury, as well as absence of


250

Ch. 10

Figure 10.4

Figure 10.3

Figure 10.5 eversion function and inability to plantarflex the first ray. MRI is essential to making the diagnosis, and has replaced the use of the peroneal tenogram in most cases. Longitudinal split-tears may be identified. Treatment entails surgical repair, perhaps with tendon graft, postoperative immobilization, and gradual rehabilitation. Ankle ligamentous Injury--collateral ligament injury involving the ankle is very common. It should be noted that the calcaneofibular ligament (CFL) runs anterior to posterior in the sagitta! plane and angulates 20A0° from the long axis of the fibula, while the anterior talofibular ligament IATFL) courses lateral to medial in the frontal plane (Fig. 10-5). The orientation of the ligaments can be difficultto recreate with secondary surgical repairs, and non physiologic motion may follow such treatment. Causes of ankle instability include post-traumatic ligamentous disruption, osteochondritis dissecans (OCD) of the talar dome, DJD with ligamentous laxity, peroneal subluxation, muscle weakness or paralytic dropfoot, talofibular meniscoid (defective ligament trapped between articulating surfaces), tibiofibular diastasis, nonunion of previous ankle fracture or poorly reduced yet healed fracture (shortened fibula), fixed calcaneal varus, tibial varum, rigid plantarflexed first ray, pes cavoadductovarus, or femoral anteversion or tibial torsion effecting pronounced in toe. Acute Ankle ligament Disruption (lnstabilityf-acute disruption of the lateral collateral ligaments causes immediate ankle instability, and may lead to chronic

Ch. 10


251

instability and arthrosis. Most cases of .acute disruption are treated with non-

operative functional thera pythat involves temporary immobilization for up to 4 weeks, weight bearing ambulation, and gradual rehabilitation for strength and flexibility. Aspiration of hematoma or hemarthrosis may be indicated. Acute ankle instabilfty is determined by the presence of pain, edema, antalgic gait, and clinical and

radiographic evidence of anterior drawer and/or talar tilt In many cases, chronic instability conveys minimal chronic pain despite frequent inversion sprain. Instability can be identified with the stress lateral (anterior drawer) and stress AP (talar tilt) radiographs. Classification of the acute injury is based on the presence or absence of ligament disruption and resultant instability. A first-degree sprain correlates with ATFL rupture, while a second-degree sprain correlates with ATFL and CFL rupture, and a third degree-sprain correlates with ATFL, CFL and posteriortalofibular ligament (PTFL) rupture, although this classification system can be confusing and difficult to accurately determine. Crucial to the diagnosis, however, is the determination that ankle instability is or is not present Anterior drawer of 5-8 mm suggests rupture of the ATFL, 10-15 mm suggests rupture of the ATFL and CFL, and >15 mm suggests rupture of the ATFL, CFL, and PTFL. Talar tilt of> 10" suggests of rupture of the CFL. Surgical intervention may be considered after acute disruption in the patient with an active/strenuous occupation/avocation, positive stress radiography indicative of at least ATFL and CFL rupture, and adequate local and systemic findings to sustain surgery. Primary collateral ligament repair, in the acute or delayed (months to years after disruption) setting, involves a lateral curvilinear incision extending from the posterior margin of the fibular malleolus to the lateral margin of the EDL anteriorly. Dissection should occur between the sural and intermediate dorsal cutaneous nerve trunks. Immediately upon penetration of deep fascia, capsule and ligament will be evident Hematoma is evacuated in the acute phase, and scar dissected in the chronic scenario. Ligament is repaired with suitable suture, and intra-osseous anchors or fracture fragment repair in the case of ligament avulsion, may be indicated. Intraoperative stress anterior drawer and talartilt should be negative. Postoperative immobilization in a weight-bearing attitude, with the ankle in a neutral alignment, for 3-4 weeks followed by bracing and rehabilitation is undertaken. Chronic Ankle Ligamentous Disruption (lnstability)--;;econdary ankle ligamentous reconstruction can be useful in the treatment of chronic instability, and entails reconstructive procedures that approximate rather than truly restore ligaments to their native state. It is difficult to recreate ligaments that mimic the ankle's normal orientation and physiologic motion, despite restoring stability. Traditionally, peroneus brevis has been harvested for ligament reconstruction, however peroneus longus is now more frequently used as the supinatory influence of the first ray on the ankle can be diminished by eliminating the pu!t of peroneus longus while preserving the everter function of peroneus brevis. There are many options, and the surgeon should pursue a reconstruction that best suits the patient's needs. The use of intraosseous tendon anchors and nonabsorbable suture materials are useful in these repairs. Procedures that recreate 1ligament, namely the ATFL, include:

Watson-Jones (Fig. 10-6}----detach peroneus brevis (PB) proximally and suture its belly to peroneus longus, then reroute the distal portion through 2 drill holes that course transversely through the fibula and a single drll! hole in the neck/head of the talus. The tendon is first directed from posterior to anterior through the

252


Ch. 10

proximal fibular channel, then from superior to inferior through the talus, then back through the distal fibular channel from anterior to posterior and sutured upon itself and periosteum atthe posterior aspect of the lateral malleolus.

Lee (Fig. 10-7}-detach PB tendon as proximal as possible and suture its belly to peroneus longus, then reroute the harvested distal portion of tile PB tendon from posterior to anterior through a drill hole in the distal fibula, then suture the

tendon to itself distal to the lateral malleolus.

Nilsonne (Fig. 10-8}-detach PB proximally and suture its belly to peroneus longus. Create a subcortical trough with a gouge in the lateral malleolus while preserving an anterior cortical hinge, then place the tendon into the trough and flap the cortex over the tendon and suture periosteum to stabilize both cortex and tendon. Evans (Fig. 70-9}-detach PB proximally and suture its belly to peroneus longus, reroute the distal portion of the tendon through a drill hole in the fibula from anterior-inferior to posterior-superior, then suture the tendon to periosteum at both ends of the osseous tunnel.

Figure 10.6

Figure 10.8

Figure 10.7

Figure 10.9


Ch. 10

253

Procedures that recreate 21igaments (ATFL and CFL), include: Christman-Snook (Fig. 10-IOHetach a split portion of PB proximally IPS is deep to peroneus longus IPL) at the proximal level of sectioning), then split PB to the

vicinity of the fifth metatarsal base, then reroute the split portion in a subperiosteal and subcapsular fashion to the anterior surface of the lateral malleolus. Next, route the tendon from anterior to posterior through a drill hole in the fibula, then course inferiorly superficial to the peroneal tendons posterior to the lateral

malleolus toward the lateral wall of the calcaneus. Route the tendon through a small channel created in the calcaneus from posterior to anterior and suture the tendon to periosteum and the PB and PL tendons posterior to the fibula.

Split Peroneus Brevis Lateral Ankle Stabilization (SPBLAS) (Fig. 10-11)--this is a modification of the Christman-Snook procedure that involves simply transplanting the split portion of PB into a trephine hole in the lateral aspect of the calcaneus and packing the site with the trephine bone plug rather than suturing the tendon to PB and PL after channeling through the calcaneus. Having converted to the use of PL, this technique is now referred to as the SPLLAS, and proceeds as described previously with the only significant variation being use of a split portion of PL. E!mslie {Fig. 10-12)--tascia lata is harvested and used as a tree graft anchored through a channel in the calcaneus and one in the talar neck, routed through a drill hole in the fibula. A variety of other secondary ankle ligament repairs have also been described, including use of free tendon graft and synthetic ligament substitutes. Over time, however, the delayed primary repair has offered the best physiologic result and should be the surgeon's first choice if enough ligament can be identified and sutured.

Figure 10.10

Figure 10.11

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Ch. 10

Figure 10.12 Achilles Tendon Rupture-this injury is most commonly seen in males, aged 25-40 ("weekend warrior"), and typically occurs in the least vascularized portion of the tendon 2-6 mm proximal to its insertion in adults >25 years of age. The Achilles tendon is surrounded by a richly vascularized paratenon, however has no true tendon sheath (a sheath is only present where tendon changes direction). The mechanism of acute rupture in a previously asymptomatic heel cord is severe traction sustained during weight bearing push-off with the knee extended, or less commonly secondary to severe ankle dorsiflexion (downhill skiing). Chronic degenerative tendinitis, with a long history of pain and inflammation, can predispose to rupture near the insertion and is often associated with calcification ot the insertional fibers and a prominent posterior calcaneal step defect Acute rupture may effect a popping sensation, or the sensation of being struck across the tendon. Pain, edema, and an apropulsive gait with inability to stand on the toes with the heel elevated on the affected side are common findings. Palpation otthe tendon reveals a defect or rent in the tendon, surrounding tenderness and induration, loss of active open chain ankle plantarflexion, and the presence at the Thompson-Dougherty sign. The ThompsonDougherty test involves squeezing the ipsilateral triceps surae and noting absence of passive ankle plantarflexion. Even a small amount ot intact tendon, despite partial rupture, is enough to make the Thompson-Dougherty test negative. Standard radiographs display increased soft tissue density and volume obliterating Kager's triangle. MAl reveals tendon disruption, and may be useful when partial rupture is suspected. Conservative treatment is indicated tor cases of partial rupture, and in patients with limited function or inadequate local tissue factors. Nonsurgical care entails application at a Jones compression dressing to splintthe ankle for 24-72 hours, followed by AK cast applicalion with the knee slightly flexed and the ankle in plantarf!exion for up to 4 weeks, then conversion to a less plantarflexed cast for an additional 4 weeks. Additional cast or removable walking boot therapy, in addition to physical therapy to improve flexibility is thereafter used as needed. Functional therapy, which can be very effective, entails the use of a plantarflexed brace that is gradually converted to a right ankle orientation of the foot to the leg, enabling weight bearing as tolerated by the patient Many cases at complete rupture warrant operative repair, preferably in the acute setting with end-to-end reapproximation or other methods that permit reconstruction. Tendon reapproximation requires the use of a Bunnell or other lateral trapping suture technique to substantially purchase longitudinal tendon fibers and resist tension. Good results have also been obtained with functional recovery using gradually decreasing degrees of weight bearing plantarflexion splinting. Dissection via a

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Ch. 10

posterior incision just medial to the midline, taking care to avoid the sural nerve, and

preserving the paratenon for reapproximation over the repaired tendon is standard. A number of repair techniques are notable, including:

Lynn Achilles tendon repair-this technique involves reapproximation ofthe 2 ends re~ info reed with a flap of free plantaris graft harvested from the same wound and fanned out

over

and

around

the

repair

for

reinforcement

Schuberth

has

recommended lengthening the tendon at the time of repair, to avoid posttraumatic equinus and to hasten rehabilitation. V-to-Yplasty atthe myotendinous junction eases reapproximation and decreases traction across the repair.

Lindholm Achilles tendon repair-this technique of delayed primary Achilles repair employs two proximal, longitudinal flaps from the aponeurosis that are rotated distally and sutured to the distal segment, and themselves, to bridge a fibrotic gap. Transfer of a portion of tibialis posterior and peroneus longus to the distal portion of the Achilles, as wei! as techniques using free tendon grafts, fascia lata, and synthetic tendon mesh have also been described. Compartment Syndromes~increased intracompartmental pressure can cause local muscular and neurovascular damage. The compartment is that area defined by overlying deep muscle fascia, surrounding intermuscular septae, and/or underlying bone and periosteum. The contents of the compartment are skeletal muscle bellies, tendons, bursae, and neurovascular structures. A compartment syndrome develops when the intracompartmental pressure increases to a pathological level, thereby damaging the contents of the compartment and distal structures dependent on blood flow through the compartment. In the foot, there are 3 main longitudinal compartments: 1) medial compartment~containing abductor hallucis and FHB; 2) superficial compartment-which is plantar central and contains FOB; and 3) !atera!~which contains abductor digiti minimi and flexor digiti minimi brevis. The forefoot also houses 5 smaller compartments: 4 intermetatarsal \interosseous) spaces containing the interossei; and the adductor hal!ucis compartment plantar!y. The hindfoot houses a single deep compartment, referred to as the calcanean compartment, which contains the quadratus plantae. In the leg, the peroneal, anterior, and posterior deep and superficial compartments are of concern (Fig. 10-13). Compartment pressure increases due to enlargement of intracompartmental volume, or external pressure that causes a decrease in the compartment volume. The norma! lower extremity intra compartmental pressure, in the normotensive patient, is 4 ± 4 mmHg. During exercise, the intracompartmental pressure may exceed 50 mmHg. Immediately post-exercise, the pressure should be <30 mmHg; and within 5 minutes after cessation of exercise, the pressure should normalize. In the normotensive patient, compartment pressures approaching 100 mm Hg are necessary to occlude arterial pulsatile flow. Any condition resulting in sustained intracompartmental pressure of :::30 mmHg, in a patient who presents 28 hours after injury or the inciting event, and who demonstrates clinical signs and symptoms, should undergo emergency fasciotomy to alleviate compartment syndrome. Signs and symptoms include allodynia, exquisite pain, paresthesia, and pulse!essness {the 3 "P's"). Soft tissue and osseous injury may be present, along with edema, pallor or cyanosis, decreased skin temperature, and sensorimotor deficit The neurological and vascular deficits must be documented prior to

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Ch. 10

Deep oo,;terior-.1. neurovascular

structures Superficial

posterior

Tibialis anterior Extensor digitorum longus hallucis longus

.,.l,enone"' longus and brevis

Figure 10.13 surgical intervention. Distal arterial pulsation may be appreciated even when compartment syndrome causes pain and paresthesia, as the initial vascular compromise occurs at the microcirculatory \arteriolar) level distally. Predisposing injuries include comminuted fracture or crush defect, contusion, Volkmann's ischemic contracture (post~ischemiaL

intracompartmental hemorrhage or hematoma, burn wounds, decubitus stasis secondary to drug overdose and coma, circular bandages and/or casting, abscess and tumor. Diagnosis is confirmed via transcutaneous wick catheter measurement of the intra compartmental pressure, with values of ;::-30 mmHg. Pressure measurements <10 mmHg are indicative of neuropraxia (pulses will usually be palpable). Values of 10-20 mmHg should be remeasured 30-60 minutes after observation, and administration of analgesic, systemic corticosteroid (methylprednisolone or prednisone), and rest If the condition is thoughtto be related to circumferential bandaging or casting, remeasure the compartment pressure 30-60 minutes after cast and bandage removal. Fasciotomy is performed after sterile prep, and may be done in the emergency room or OR, depending upon the merits of the specific case. Compartment decompression in the foot is achieved using 2 dorsal longitudinal incisions located over the second and fourth metatarsals. Dissection is carried through the deep fascia to periosteum, then medially and laterally into the adjacent intermetatarsal spaces where the interosseous musculature is reflected from the corresponding metatarsal. In a similar fashion, other compartments in the foot and leg are opened via fasciotomy. The wounds are then packed open and maintained with local care for 3-5 days, keeping the extremity at bed level with slight knee flexion, after which delayed primary closure or skin grafting is undertaken.

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257

FRACTURES The principles of fracture management include:

Reduction and Immobilization-fractures are described according to their location and orientation within the specific bone. Fractures are caused by pathological bending, twisting, and shearing forces that are applied either directly (direct blow) or indirectly (twisting). Fractures are either closed or open injuries. Radiographic inspection requires at least two or three (preferably), or more views, as well as comparison views of the contralateral extremity in questionable cases involving sesamoids, growth plates, or suspected supernumerary bones. Incomplete fractures, wherein a portion of the bone's cortex remains intact, are termed greenstick fractures and generally occur secondary to flexural deformation of a long bone. Similarly, a stress fracture results in bending without overt radiographic fragment separation. A bone scan can be useful if diagnosis is in question. Incomplete fractures are diagnosed primarily by clinical examination, and with subsequent radiographic evidence of secondary bone callus. Complete fractures can be transverse, oblique, spiral, and comminuted, with fracture stability and management varying with orientation. Fracture stability, in descending order, is as follows: transverse> oblique> spiral> comminuted Transverse and oblique fractures may be amenable to closed reduction and immobilization, whereas spiral and comminuted patterns are extremely difficult to adequately reduce and maintain in a closed fashion. When a fracture violates a joint surface, open reduction and stabilization is most often the best treatment option. Growth plate injuries and open fractures deserve special consideration. Fracture repair is initiated with closed reduction and immobilization, regardless of whether the injury is open or closed. Closed reduction, as described by Charnley, entails the following sequential maneuvers: 1) increase the deformity; 2) distract; 3) reverse the deformity and realign; and 4) maintain correction with an immobilizing splintiFig. 10-14). These general rules apply to all fractures, and may be used as definitive treatment in amenable injuries, or as a temporary intervention to improve neurovascular status in preparation for open reduction and fixation in the OR. Closed reduction can be impeded by soft tissue interposition, such as the tibialis posterior tendon at the medial malleolus. Maintenance ofthe reduction with a castor brace is indicated when closed reduction and immobilization are the mainstays oftreatment.lf open reduction and internal fixation lORI F)

Convex

Figure 10.14


258

Ch. 10

or use of external fixation is employed, the brace may be removable or nothing more than a posterior, sugar tong (medial and lateral stirrup), or anterior splint. The usual

fracture-healing phase lasts at least 6-8 weeks, and protection should be maintained during this period. As a rule, the bone should be stabilized with immobilization extended to one joint above the fractured ossicle. If internal or external forms of skeletal fixation are used, the "one joint above" rule becomes less important. Fractures sustained distal to the MTPJs are usually satisfactorily stabilized with a rigid sole trauma/surgical shoe (such as the Darco® shoe). Stress fractures of the metatarsals respond well to a gel-cast and surgical shoe, and digital fractures can be managed with gauze dressings and a surgical shoe. Acute metatarsal fracture is best treated with below-the-knee iBK) immobilization. Only very stable fractures, due either to fracture pattern, location, or surgical fixation, can sustain weight bearing during the healing phase (compare the fracture to surgical osteotomy design and fixation to help decide how to protect during healing). For this reason, non-weight bearing immobilization is the general rule for foot and ankle fractures. Ambulation with crutches, a walker, or wheel chair or another protective device are standard. Follow-up radiographic inspection is required after initial reduction, and perhaps a few days later (initial follow-upL based on clinical progress, to assure maintenance of alignment, then at about 6-8 weeks, or any time as indicated based on clinical signs and symptoms.

Open fracture Management--open fractures may be associated with severe limb and/or life threatening injuries. Locally, the extent of soft tissue injury must be evaluated. Open fractures convey a 60-70% incidence of bacterial contamination and grovvth atthe time of initial inspection. Open fractures that have gone without treatment for 6-8 hours are considered infected. The Gustilo classification of open fractures is depicted in Table 10-1. TABLE 10-1. THE GUSTILO CLASSIFICATION OF OPEN FRACTURES. Type I

Description of the fracture Fracture with open wound <1 em, clean, minimal soft tissue necrosis, and the fracture is usually transverse or short oblique with minimal or no comminution

II

Fracture with open wound >1 em, clean, minimal soft tissue necrosis, and fractL,Jre is usually transverse or short oblique with minimal or no comminution, commonly associated with crush injuries sustained in motor vehicle accidents, farm or industrial machinery mishaps, and gunshot wounds Fracture with extensive open wound, contamination, and/or necrosis of skin, muscle, neurovascular and surrounding soft tissues; and the fracture is often comminuted

111

The principles of open fracture treatment tallow those stated previously for wound debridement, tetanus and antibiotic prophylaxis, in addition to skeletal stabilization. Appropriate antibiotic therapy entails initial administration of cefazolin 1 or 2 grams IV, followed by 1 gm IVPB Q 8 hr thereafter until definitive cultures are available, depending upon the specifics of the case. If the injury occurred in a farm o'r similar tetanus-prone environment, then cover for Clostridia by administering aqueous penicillfn-G 10~20 million units IV daily in divided doses every 6 hours. Alter antibiotic therapy based on allergy history, and other systemic factors. Use antibiotics for at !east 3 days, and continue therapy for 3 additional days in the noninfected wound if management warrants delayed

Ch. 10


259

primary closure, secondary intention closure, OR IF or in the event that internal or external fixations require alteration. Skeletal stabilization in an anatomic alignment enhances tissue viability, wound healing, and diminishes the risk of infection. Initial treatment varies with fracture stability and neurovascular status, and focuses on manipulative (closed) reduction as described above. Temporary and/or permanentfixation can be achieved with K-wires and Steinmann pins, external fixation, and interfragmental compression screws as deemed indicated based on the specific merits of each fracture. It is preferable to minimize periosteal reflection. If bone grafting is indicated, this can be done immediately in a Type I open fracture, however is best performed on a delayed basis after initial stabilization of the wound. In Type II open fractures, the bone graft is best applied at the time of delayed primary closure when there is no evidence of infection. Application of an external fixator obviates the need to effect stability with a bone graft at the time of initial intervention. If infection does occur after graft transplantation, the autogenous graft may still take. Gustilo recommended autogenous cancellous bone grafting in type Ill open fractures at approximately 3 months after initial therapy, when reactive bone callus formation has diminished. The decision to close the wound is based on factors previously described. Digital Fractures and Dislocations-digital fractures usually occur secondary to dropping a heavy object on the toe, which usually damages the distal phalanx; or by stubbing the toe into a rigid object. which usually fractures the distal phalanx of the hallux or the proximal phalanx of a lesser toe. Hyperplantarflexion injuries often result in IPJ dorsal avulsion fracture. The fifth toe is the most commonly fractured digit, followed by the hallux and then the intermediate toes. Intermediate phalanx fractures are rare in the lesser toes. The medial oblique projection is useful for evaluating the hallux, as is isolation of the toe by elevating it on foam or similar material to eliminate superimposition of adjacent digits. Digital fractures should be stabilized with gauze bandaging, stabilizing the injured toe/s to adjacent healthy digits (buddy splint), and a surgical shoe, much as would be used following digital arthroplasty. Displaced or unstable fragments that are large enough, particularly if intra-articular, can be stabilized via OR IF with K-wires or small lag screws. Distal phalangeal tuft fractures, particularly if comminuted, may require surgical nail plate avulsion, repair of any nail bed defect, and excision of displaced fragments. Distal phalangeal fractures that heal with hypertrophy may require subsequent reduction of prominent bone to eliminate subungual exostosis. Proximal phalangeal base fractures, particularly of the hallux, can predispose to digital floating, and transverse plane misalignment. If hallux abductus develops, consideration should be given to surgical treatment. Hallux interphalangeal joint (HIPJ) dislocation is the essential differential diagnosis in cases of suspected phalangeal fracture, as ft can also result from the same pathological force. In the lesser toes, IPJ dislocation rarely involves the DIPJ, and most commonly affects the PIPJ of the fifth toe. Treatment is closed reduction and buddy splinting usually, unless the reduction is unstable or prevented by protrusion of the phalanx through the IPJ capsule. In this case, open reduction and capsular repair are required. Metatarsophalangeal Joint Fractures and Dislocations-turf toe is a traumatic condition of the hallux and first MTPJ, wherein repetitive hyperdorsiflexion, hyperplantarflexion, hyperadduction, or hyperabduction results in MTPJ sprain without gross change in joint alignment. The injury usually affects athletes, in particular those playing on artificial turf surfaces, although tennis and basketball players can also be affected. Clinically the joint, as well as the HlPJ, appears swollen, indurated, and tender to palpation and motion. Often


260

Ch. 10

there is an associated subungual hematoma and/or digital ecchymosis. Radiographs should be obtained to rule out dislocation, osteochondral or avulsion fracture, or sesamoid

fracture. Treatment consists of PRICE with use of a gauze bandage and surgical shoe. Gradual resumption of strenuous activity is initiated in 7-10 days, and athletic shoes should be evaluated for proper fit. Orthoses may be helpful. Oral anti-inflammatory agents are generally indicated, and corticosteroid injection should be avoided. First MTPJ dislocation-this occurs secondary to hyperdorsiflexion force, and is

categorized as depicted in Table 10-2.

TABLE 10-2. CLASSIFICATION Of FIRST METATARSOPHALANGEAL JOINT DISLOCATION. Type I

11

Description A transverse capsular rupture plantar to the metatarsal head/neck with the proximal phalanx, plantar capsule, and sesamoids displaced dorsally on metatarsal head. The retrograde plantar directed force of the phalanx drives the metatarsal head in a plantar direction, and the HIPJ becomes fixed in plantarflexion. This injury is usually not amenable to closed reduction. A

Same as Type I except that rather than the entire plantar capsule and sesamoid apparatus dislocating distally and dorsally, the intersesamoidal ligament ruptures and the sesamoids sublux to each side of the metatarsal head. Radiographs readily show the sesamoids medial and lateral to the metatarsal head. This injury is amenable to closed reduction, however the soft tissue disruption should be repaired with suture.

B

This injury also displays the sesamoids displaced medial and lateral to the metatarsal head, however rather than rupture of the intersesamoidal ligament, there is avulsion fracture of one of the sesamoids. Closed reduction of the first MTPJ dislocation entails Mayo block of the first ray, then distraction, followed by pushing the proximal phalanx into a congruous relation with the metatarsal head. Correction is maintained with a slipper or BK cast for 3A weeks, then a surgical shoe for an additional 3 weeks. Resistant deformity requires operative repair. The Type liB injury should be casted BK for 6 weeks non-weight bearing. Late term sequelae include sesamoid nonunion and/or sesamoiditis, and surgical excision of the painful ossicle may be necessary.

Lesser MTPJ dislocation---this occurs less often than does first MTPJ dislocation, and dorsal dislocation of the phalanx on the metatarsal head is the usual pattern. Closed reduction is similar to that performed for Type I first MTPJ dislocations. Osteochondral fractures of the firstMTPJ--these can affecteitherthe phalanx base or metatarsal head. Phalangeal osteochondral fractures usually occur due to stubbing with forced transverse plane motion that avulses the intrinsic attachments to the base. Metatarsal head osteochondral fractures usually occur due to hyperdorsiflexion that causes impaction with high shear strain at the dorsal aspect of the head. Treatment entails closed reduction and 6 weeks of immobilization In a slipper or boot cast for small fragments, or ORIF and immobilization for 6 weeks in a cast for larger fragments. Very small fragments can be treated much like a dislocation, with earlier return to weight

Ch. 10


261

bearing and motion. When the joint is opened, loose or torn cartilage should be

remodeled and the subchondral cortical bone fenestrated with a 0.035" K-wire. Late term sequelae include post-traumatic DJD, and arthrodesis or multicomponent

endoprosthesis may be indicated. Sesamoid fractures-these can occur after a fall from a height wherein direct dorsally

directed force pushes the sesamoids into the plantar surface of the metatarsal head while the hallux forcefully dorsiflexes. Cumulative microtrauma can also cause

sesamoidal stress fracture, and is associated with dancing, basketball, tennis and other strenuous activities. The condition is often misdiagnosed and mismanaged. The tibial sesamoid is more commonly fractured, and rarely are both the tibial and fibular fractured in the same joint Moreover, bilateral sesamoid fractures are rare. Symptoms include pain upon direct palpation or first MTPJ range of motion, in particular with dorsiflexion. The differential diagnosis is extensive, and includes: Joplin's neuroma, sesamoiditis, osteochondritis dissecans of the sesamoid, osteochondrosis ofthe sesamoid, bi- or multipartite sesamoid DJD or rupture, turf toe, HAV with eroded crista, and prominent or hypertrophic sesamoid with plantarflexed first ray painful plantar callus. Radiographic evaluation can be difficult, particularly when a bipartite sesamoid is present, 75% of which occur unilaterally. Medial and lateral oblique, sesamoidal axial views, and contralateral comparison views are often helpfuL When in doubt, order a bone scan or MRI. Treatment entails a slipper or boot cast or immobilizing splint and non-weight bearing for 6-8 weeks, followed by transition back to a sneaker using a surgical shoe until asymptomatic. The prognosis for complete healing is guarded, and primary as well as delayed excision of the fracture fragment{s) should be considered. Remember that sesamoidectomy, even partial, conveys the risk of valgus or varus deformiTy for the tibial and fibular ossicles, respectively, especially in cases involving a round metatarsal head. Appropriate muscle-tendon balancing should be performed whenever sesamoidectomy is performed. Removal of both sesamoids will decrease intrinsic muscle strength and hallux purchase, causing a hallux hammertoe or cock-up hallux. Prophylactic fusion ofthe HIPJ should be performed whenever both sesamoids are excised.

Metatarsal Fractures-the principles for management of metatarsal fractures, whether of the first or Jesser metatarsals, at the head, shaft or base, are the same as those stated previously in the general management of fracture discussion. A few points of interest should be noted. It is importantto try and restore the weight bearing balance of the metatarsus, and attention should be paid to length and sagittal plane relations. Transverse and short oblique metatarsal fractures, particularly of the shaft, are amenable to closed reduction and immobilization, and difficult lesions can be pinned either percutaneously or via open dissection. Multiple metatarsal fractures often display spontaneous reduction of those of the intermediate rays upon ORIF of either or both of the first and fifth metatarsals, and fixation of the intermediate metatarsals can be adequately achieved with a single K-wire or no fixation other than casting. This is an example of the vassal rule. A number of different types of metatarsal fractures can be incurred, including:

Fifth metatarsal fractures~these are very common injuries. Keep in mind that the apophysis of the fifth metatarsal styloid appears at 9·14 years and fuses at 12-15 years of age. The physis is oriented almost parallel to the long axis of the fifth metatarsal

262


Ch. 10

shaft. The accessory ossicle, os Vesalianum, appears in the tendon of peroneus

brevis near the base. Of particular interest is the Jones fracture (Fig 10-15), which is caused by medial or lateral cutting or pivoting movementthat produces a transverse fracture distal to the junction of the fourth and fifth metatarsals. This is actually a proximal diaphyseal fracture that is not produced by inversion of the foot and ankle. The Jones fracture is notorious for nonunion, and meticulous fracture management is crucial. In the patient without great physical demands, closed reduction and immobilization for 6-8 week in a BK non-weight bearing cast is indicated. In the athlete or individual that participates in strenuous daily activity, ORIF and BK non-weight bearing cast 5-6 weeks followed by weight-bearing cast for an additional 2-3 weeks is indicated. If delayed union is suspected, maintain non-weight bearing and immobilization and add electrical bone growth stimulation (EBGS).I! a nonunion develops, repair with autogenous cancellous bone graft, electrical stimulation, and cast non-weight bearing. The base of the fifth metatarsal can also fracture into the metatarsal-cuboid joint secondary to forced inversion and traction applied through the tendon of peroneus brevis or the lateral slip of the plantar fascia. The result is an avulsion fracture that enters the tarsometatarsal joint (TMJ). If the fracture is displaced, the ORIFfollowed by weight- bearing BK cast for 6 weeks. lithe fracture is nondisplaced, then closed reduction and immobilize in a non-weight bearing cast for 6 weeks. The fifth metatarsal base can also fracture at the styloid process (Fig 10-16). which is an extra-articular fracture caused by the same force described above for the intra-articular fracture. Treatment is the same as that described above for the articular fracture at the fifth metatarsal base.

Metatarsal stress fracture--this is also known as a march or fatigue fracture, and develops secondary to cumulative that surpasses the bone's ability to respond to repetitive load. This is frequently observed when a person initiates a new exercise program, undergoes basic training in the military (march fracture), suffers with a specific biomechanical abnormality wherein there is loss of adjacent metatarsal support (hypermobile first ray dumping force on the second ray, or following adjacent metatarsal fracture or osteotomy). The onset of pain is usually gradual, but

Figure 10.15

Figure 10.16


Ch. 10

263

exacerbated by recent increased activity. The pain is localized to the affected metatarsaL with associated edema and local heat. Stress fracture usually localizes to the metatarsal neck, and most commonly involves one of the intermediate rays. The differential diagnosis includes neuroma, MTPJ enthesitis, arthritis, and extensor tenosynovitis. Charcot fractures, pathological fracture, and osteoporosis should also be considered. Radiographic findings initially may reveal a small cortical break at site of maximum clinical tenderness. Periosteal reaction usually develops at the stress fracture site, and may become evident at about 10 days or longer from onset of pain. Repeat radiographs at 2-3 weeks after the onset of pain may be needed to confirm diagnosis. A bone scan or MRI should be obtained if standard films are equivocaL Treatment of metatarsal stress fracture entails a gel-cast and surgical shoe or a removable cast-boot for 3-5 weeks, and orthoses may be useful to address biome chanica! abnormalities thereafter.

Lisfranc Fracture Dislocation-this injury constitutes 1% of all reported fractures, however the diagnosis is missed in almost 20% of cases. Anatomical considerations include the "keystone" nature of the second metatarsal base in the intercuneiform recess, which provides a significant amount of stability to the midfoot complex. The tarsometatarsal joint (TMJ) is bound together by a series of transverse dorsal and plantar ligaments, as well as intermetatarsalligaments. There is a distinct absence of an intermetatarsal ligament between the first and second metatarsals. The plantar ligaments are thicker, and dorsal displacement is most common. The ligament attaching the medial cuneiform to the first metatarsal is the largest ligament at this level. The most important ligament of the TMJ is Lisfranc's interosseous ligament, which attaches the base of the second metatarsal medially to the lateral aspect of first cuneiform. Usfranc's ligament is often involved in avulsion fracture of the second metatarsal base. The Hardcastle classification {also know as Oueno and Kuss) is the standard system for identifying TMJ fracture/dislocations (Fig. 10-17), and categorizes these injuries as depicted in Table 10-3.

TABLE ID-3. THE HARDCASTLE CLASSIFICATION OHISFRANC FRACTURE DISLOCATIONS. Type A

(total, homolateral dislocation)

B

(partial dislocation)

C

(divergent)

Description of injury The most common TMJ fracture/dislocation, it displays disruption of the entire TMJ in the sagittal or transverse plane. This injury usually involves lateral displacement of all ofthe metatarsal 1. Medial displacement of the first metatarsal alone or with metatarsals 2, 3, 4, not 5 2. Lateral displacement of one or more of the lesser metatarsals (notthe first metatarsal) Displays the first metatarsal dislocated medially and the lesser metatarsals either partially or totally dislocated laterally in the sagittal and/or transverse planes

Although the Hardcastle classification is most commonly used, Wilson also classified Lisfranc joint fracture/dislocations, as depicted in Table 10-4.


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Ch. 10

Partial Incongruity

Dorsa plantar Type A

Lateral dislocation

Figure 10.17

TABLE 10-4. THE WilSON ClASSIFICATION OF LIS FRANC FRACTURE DISLOCATIONS.

Class

Stage

Description of the fracture

II

Dorsolateral dislocation of metatarsals 2-5 Dorsolateral dislocation of metatarsals 1-5

I

Medial dislocation of first metatarsal

II

Medial dislocation of first metatarsal, dorsolateral

Plantar-flexionsupination-most common

Plantart!exion pronation

dislocation of metatarsals 2-5 Plantarflexion

Dorsal dislocation of second metatarsal base and/or

fracture dislocation base of first metatarsal The mechanism of TMJ injury is usually a crushing force applied to the forefoot with the ankle plantarflexed. The second metatarsal must be dislocated first, either by transverse base fracture or medial avulsion by Lisfranc's ligament, in order to disrupt the TMJ. Clinical findings include localized signs and symptoms of fracture/dislocation, and it is critical to assess the neurovascular status to the forefoot. The foot may appear grossly shorter than the contralateral limb. Radiographs can be difficult to assess, and attention should be directed at the first metatarsocuneiform interfaces, as well as the base of the second metatarsal. One should also look for a compression fracture of the cuboid. Transverse and sagittal plane stress views can add information, and the CT scan has

Ch. 10


265

become a mainstay of diagnostic accuracy in regard to this injury. Treatment begins with

attempted closed reduction and immobilization, if indicated. Distal traction can be achieved by suspending the foot above the table with Chinese finger traps until adequate soft tissue relaxation ensues. Counterweights strapped around the ankle can be used to enhance distraction. An external fixation frame can also be used to effect distraction and stabilization. Attention is directed attrying to relocate the second metatarsal base into the intercuneiform recess, then to reduction of the first metatarsal-medial cuneiform joint depending on the fracture/dislocation pattern. Percutaneous pin stabilization may be attempted after reduction, however this is notoriously difficult If closed reduction fails, it may be due to tibialis anterior or peroneus longus interposition, or due to the avulsion fragment of the second metatarsal base. OR IF may be performed via 3 dorsal incisions: 1) dorsomedial first met-cuneiform, 2) between second and third metatarsals and corresponding cuneiforms, and 3) between fourth and fifth metatarsals and the cuboid. The first metatarsal is generally fixed first, followed by the remaining metatarsals from medial to lateral. Pin stabilization is recommended as follows:

Type A-1 wire stabilizing first metatarsal-cuneiform and a second stabilizing the fifth metatarsal-cuboid joints. Type B (medial type)-2 pins stabilizing the first metatarsal-cuneiform. Type C-2 pins medial and one lateral. A BK cast is then used for 8-12 weeks, the first6-8 weeks being non-weight bearing. The pins are removed after 6-8 weeks. Calcaneal Fractures-this injury is most commonly observed in men aged 35-45 years, and the male to female ratio is 5:1. Calcaneal fractures are associated with spinal fractures 20% of time, with Tl2- L2 the most common vertebral range and L1 the most common vertebra fractured. The most common mechanism is a fall from a height, followed by motor vehicle accident Clinical findings include Mondor's sign, which is plantar ecchymosis extending from the heel into the plantar vault The heel also appears wide and shortened, and the patient is antalgic and unable to bear weight on the injured foot. Bohler's angle is made by the intersection of a line extending from the posterosuperior process of the calcaneus to the posterior margin of the posterior facet of the STJ, and the line extending from the posterior margin of the posterior facet of the STJ to the tip of the anterior beak of the calcaneus (Fig. 10-18). Bohle(s angle is usually 25-40", and is depressed or even negative when the posterior facet is depressed by the talus into the body of the calcaneus in a joint depression fracture. Radiographic signs include disruption ofthe calcaneocuboid joint on the AP view; depression of the posterior facet of the STJ and Bohler's angle on the lateral view; disruption of the posterior facet and widening of the calcaneus with lateral wall blow out on the calcaneal axial view; and fracture of the anterior process on the medial oblique view. Radiographs of the ankle, legs, and vertebral column may also be indicated, and a CT scan of the hindfoot can be very useful prior to operative intervention. The Rowe classification (Table 10-5) deals primarily with extra-articular calcaneal fractures (Fig. 10-19).

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Ch. 10


Lateral talar process

Neutral triangle

Figure 10.18

~ Ia

Ill

lb

ef)

~ lc

._)

~lla Break

~fcactuce ,·,_.

11

Figure 10.19

IV

lib Avulsion

fracture

~ '

v

Ch. 10


267

TABLE 10-5. THE ROWE CLASSIFICATION OF CALCANEAL FRACTURES. Type

Description

Treatment

I

A Fracture of the calcaneal tuberosity

Closed reduction immobilization with BK cast, 6 weeks, weight bearing if non-displaced. ORIF if displaced or unstable

sustained in afall with the heel everted or inverted; can result in splaying and widening that may interfere with the peroneal tendons B Fracture of sustentaculum tali, sustained from fall with twist on a supinated foot; tenderness upon passive or active

flexion and extension of the hallux due to FHL; axial calcaneal X-ray is the

Closed reduction immobilization with BK cast 6 weeks if nondisplaced. ORIF if displaced or unstable

best view. C Fracture of anterior process (most

common Type I fracture); only cal-

caneal fracture where females have higher incidence; this is an avulsion in~

i

Closed reduction and immobilization with BK walking cast for 6 weeks. Excise or ORIF the fragment if symptoms persist

jury of bifurcate ligament; force is

plantarflexion on a supinated foot; seen clearly on lateral or medial

oblique views; may need tomograms to visualize if the fragment is small II

A Beak or avulsion fracture of calcaneus that does not affect Achilles insertion B Avulsion fracture with pull off at Achilles attachment

Ill

Fracture of body without involvement of STJ (most common extra-articular fracture); results from fall with edge of talus going into calcaneus; lateral X-ray and axial views most helpful; axial view determines STJ involvement

IV

Fracture of body of calcaneus involving STJ; this is actually an articular fracture, however fractures in the Rowe classification are still considered as primarily extra~articu!ar

I

V

Central depression fracture with a degree of comminution (also, an articular fracture)

Non-weight bearing BK cast for about 6 weeks in plantarflexion if non-displaced. Must reduce if large and/or displaced; percutaneous pin may work, or ORIF if unstable AK Non-weight bearing cast with knee flexed. ORIF if displaced or unstable

Closed reduction, percutaneous pinning, or OR IF


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Ch. 10

The Essex-Lopresti classification (Table 10-6) describes intra-articular calcaneal fractures (Fig. 10-20). The Essex-Lopresti system of intra-articular fractures describes approximately 75% of all calcaneal fractures that usually result from a long fall from a high place. When the victim hits the ground feet first, the talus is driven down into the

calcaneus, crushing the posterior facet into the body of the as cal cis and splitting the bone like a wedge. Essex-Lopresti Types A and Bare differentiated by the secondary fracture line and the shape of the resultant fragments.

Tongue Type

Figure 10.20

Joint depression type


Ch. 10

269

TABLE 10-6. THE ESSEX-LOPRESTI CLASSIFICATION OF CALCANEAL FRACTURES. Type A !tongue fracture)

PrimaiV fra.cture line Courses from superior to inferior, extending from Gissane's critical angle at the junction of the posterior

facet and the calcaneal

Secondary fracture line Propagates from the primary, posteriorly to exit the posterior cortex, usually proximal to the Achilles insertion

sulcus, to the plantar aspect of the calcaneus B !joint depression)

The same as described above for the tonguetype fracture

Surrounds the posterior facet that is driven like a column into the cancellous bone of the body of the calcaneus, exploding the bone medially and laterally into comminuted fragments

The Sanders classification of calcaneal fractures is probably the most useful in

regard to directing surgical intervention (Table 10-7). To classify the fracture using this system, the frontal plane CT scan is used, and the posterior facet of the subtalar joint is divided into 3 equal segments, from lateral to medial, with the final line collinear with the vertical margin of the sustentaculum tali. The Type I fracture are nondisplaced and involve a fracture of either the lateral, central, or medial segment of the posterior facet. Fractures localized to the medial segment are most difficult to visualize and reduce primarily. Type II fractures involve 2-part split fracture of the posterior facet, and Type Ill injuries involve 3-part split fractures with depression of the posterior facet into the body of the calcaneus. Type IV fractures involve severe comminution of the posterior facet and the body of the calcaneus.

TABLE 10-7. THE SANDERS CLASSIFICATION OF CALCANEAL FRACTURES. Type

Description olthe frontal plane CT appearance of the fracture

I

Nondisplaced fracture of the posterior facet

II

2-part (split) displaced fracture

Ill

3-part Isplit) displaced fracture with joint depression

IV

Severely comminuted fracture with joint depression

Mechanically speaking, the calcaneal tuberosity is situated lateral to the center ofthe talus. When a vertical compressive force is applied,2 primary fracture fragments develop: 1) superomedial or sustentacular fragment !sustentaculum tali), and 2) the tuberosity fragment that contains the lateral1/3 to 1/2 of the posteriorfacet. lfthe pathological force continues, the talus and sustentaculum tali are driven plantar and media!. If the force still continues, then the posterolateral edge ofthe talus is driven into the superolateral aspect of the posterior facet, which is supported by cancellous bone that is crushed and impacted. A lateral wall blowout fracture may also occur, with possible extension into the calcaneocuboid joint. Palmer's three constant components of intra-articular fracture include: 1) vertical shearing fracture, 2) fracture of the lateral cortex, and, 3) depression

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Ch. 10

fracture of the posterolateral STJ. Pedal deformity related to calcaneal joint depression fracture includes: increased calcaneal width making shoe wear difficult, decreased

calcaneal height and length adversely affecting limb length and gait, intra~articularfracture of the STJ with resultant DJD, and sural nerve and peroneal tendon entrapment along the lateral wall of the calcaneus. Initial management involves neurovascular assessment, PRICE, and attempted closed reduction and immobilization if indicated. Simple immobilization, often combined with early weight bearing, eliminates surgical risks and may be indicated in certain patients who are less active and perhaps at high risk for surgical complication. Limited weight be-aring after 1 week, progressing to ful! weight bearing at 612 weeks can be undertaken. Essex-Lopresti described manipulation with skeletal fixation using a pin that enters the body of the calcaneus from the posterior aspect that is then pulled in a plantar direction to try and lift the posterior facet out of the body ofthe calcaneus. This can also be undertaken with more than 1 pin. The pin or pins is/are then secured in the surrounding plaster that is applied AK with the knee flexed. This method is applicable only in tongue fractures, and is not used much because of inaccurate STJ realignment, and subcutaneous compromise at the pin tract. Palmer described a clamp \Palmer clamp) used to squeeze the medial and lateral cortices together, however this did very little to improve the STJ. Palmer also described OR IF with elevation of the posterior facet under direct visualization and manipulation, followed by packing beneath the raised facet with autogenous bone graft, followed by pin stabilization and BK non-weight bearing cast for 12 weeks. Galie described early triple arthrodesis, and indeed this is often a last resort for patients who have developed post-traumatic arthrosis following fracture.lffracture blisters are present, then surgical intervention should be postponed until the skin barrier is healthy. Operative intervention is ideally performed within the first 2-6 hours of injury. The Zwipp incision preserves the peroneal tendons and the sural nerve in an intact soft tissue flap. The Podiatry Institute technique entails a lateral approach with sectioning or preservation of the peroneal tendons, reconstruction of the posterior facet with supporting bone graft, and a combination of buttress plate and lag screw and cerclage wire fixation, as necessary. A number of specialty locking and non·locking plates are available for reconstruction of the fractured calcaneus. Complications of calcaneal fracture, and its repair, include post-traumatic STJ arthritis, ankle joint arthritis, tenosynovitis of peroneals, plantar heel pain due to diminished cushioning effect of fat pad, sural or PT nerve entrapment, shuffling gait with shortened stride, and stiffness. Late salvage of arthrosis following calcaneal fracture often entails talocalcaneal fusion, triple arthrodesis, or extra-articular bone bloc distraction arthrodesis to restore the height of the heel. Talar Neck Fractures-anatomically, 2/3 of the talus is covered with articular cartilage, therefore most fractures of the talus are intra-articular. No muscles or tendons originate from or insert into the talus. The extended neck with its tenuous blood supply is vulnerable to injury. The blood supply to the talus entails:

Body-artery of tarsal canal from the posterior tibial and deltoid branch.

Head and neck-artery of tarsal sinus from perforating peroneal and DP. Posterior talus-calcaneal branches of PT. Avascular necrosis \AVN) is likely to occur when 2/3 of the vascular channels are disrupted. Hawkins noted that it takes until 6-8 weeks after the injury to recognize the presence of AVN, and it may not appear until 1-4 months have passed. Signs and


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271

symptoms oftalar AVN include intractable pain, relative radiographic sclerosis, or opacity of the dead bone, best observed on the AP view of the ankle. Hawkins noted the presence of subchondral bone revascularization as radiolucency in the dome of the talus on the AP

view, and this is referred to as Hawkins' sign and is indicative of healing. The treatment of AVN is non-weight bearing in BK cast for 6-8 months until revascularization occurs, with electrical bone growth stimulation. The Hawkins classification (Table 10-8) oftalar neck fractures can be useful in regard to anticipating the development of avascular necrosis (Fig. 10-21).

TABLE 10-8. THE HAWKINS CLASSIFICATION OF TALAR NECK FRACTURES. Type

Fracture

Clinical characteristics

I

Vertical non-displaced

II

Vertical fracture through neck with dislocation of STJ (not ankle)

Occurrence is 20%, only the blood supply to the neck disrupted, 0-15% incidence of AVN Occurrence is 42%, with 2 areas of disrupted blood supply, neck and body; 15-50% incidence of AVN

Ill

Vertical fracture of neck

fracture oftalar neck

with dislocation of IV

STJ and ankle Vertical fracture of neck with dislocation of STJ, ankle, and TNJ

Figure 10.21

Occurrence is 34%, and all3 sources of talar blood supply are disrupted; 90-100% incidence of AVN

Occurrence is 4%, disrupts all3 areas of talar blood supply; 90-100% incidence of AVN


272

Ch. 10

The treatment of talar neck fractures is based on the degree of injury and blood supply. Hawkins Type I fractures are managed in a BK non-weight bearing cast for 6-8 weeks. Alternatively, an AK cast with the foot plantarflexed for 3-4 weeks followed by a BK cast neutral for an additional 4 weeks can be used. Weight bearing and motion are not initiated until adequate signs of healing are observed radiographically. Hawkins Type II, Ill, and IV fracture/dislocations are initially closed reduced, however OR IF with lag screw fixation of the neck is most effective. Immobilization and WB status are the same as described previously for non-surgical treatment. Complications of talar neck fractures include AVN, degenerative arthritis of the ankle and STJ, nonunion or mal-union, and

infection related to open fracture or surgery. Os trigonum Syndrome and Shepherd's Fracture-as trigonum syndrome and Shepherd's fracture can be very painful and debilitating. The os trigonum is present in 10% of the population. The posterior aspect of the talus displays 2 processes that form a groove through which the FHL tendon courses. The lateral process, also known as Stieda's process or the trigonal process, is the larger of the 2 and develops from a secondary center of ossification atS-11 years of age. Ossification with closure of the physiswill usually occur within one year thereafter. The os trigonum represents failure of the secondary center to unite with the posterolateral process of the body. Fracture of Stieda's process is referred to as Shepherd's fracture, and must be differentiated from a painful os trigonum. Both the os trigonum and Stieda's process are injured by means afforced plantatflexion. The os trigonum may occur bilaterally, so contralateral radiographs may be informative. A fractured posterior process will be jagged with rough edges in the early phase, while the margins of the os trigonum should be smooth. Ankle and first MTPJ range of motion may be painful in both cases. Treatment for both as trigonum syndrome and Shepherd's fracture entails a local anesthetic block, BK weight bearing cast immobilization for 6 weeks, followed by range of motion physical therapy. Recalcitrant cases require surgical excision of the os trigonum or the Shepherd's fracture fragment, via a posterolateral incision that parallels the peroneal and is anterior to the Achilles tendon. Tatar Dome Fractures-talar dome defects can develop secondary to ankle sprain or fracture, and are known to be debilitating in all age groups. The Berndt and Harty classification {Table 10-9) is the standard system for identification of talar dome lesions. Talar dome osteochondral defects develop as a result of shearing under compressive load between the distal tibial bearing sutface and the dome. The injury causes AVN of the subchondral trabecular and cortical bone, which eventually heals with cortical irregularity, and resultant development of post-traumatic arthritis.

TABLE 10-9. THE BERNDT AND HARTY CLASSIFICATION OF TALAR DOME lESIONS. Stage I II Ill IV

Description of the injury A small area of subchondral bone compression A partially detached osteochondral fragment A completely detached fragment, remaining in its crater A displaced osteochondral fragment

The incidence of posteromedial talar dome defect is 56%, while anterolateral defects occur in 44% of cases. Medial lesions are caused by ankle inversion and plantatflexion,

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273

while lateral lesions are caused by ankle inversion with dorsiflexion (Figs. 10-22 and 10-23). Treatment for all Stage I, II, and medial Stage Ill lesions is 6-12 weeks of BK non-weight bearing cast immobilization, with consideration to use of a patellartendon bearing brace and partial weight bearing; and surgical intervention for recalcitrant pain. Stage IV and lateral Stage Ill lesions are treated surgically by means offragment excision, saucerize the crater,

drill hole fenestration of the subchondral bone to aid revascularization and enhance fibrocartilage production. Medial lesions may require medial malleolar osteotomy and subsequent replacement with lag screw fixation. Lateral lesions may be combined with secondary repair of chronic lateral ankle instability if this condition exists. Very large fragments may be amenable to reduction and fixation with either absorbable pin or screw fixation. The use of autogenous osteochondral plug grafts (OATS) harvested from non~ contact articular cartilage from the head of the talus, or the knee, as well as allogeneic grafts, and/or autogenous cultured cartilage cells, provide other reconstructive options. Early postoperative range of motion in a non·weight bearing fashion is indicated, with resumption of weight bearing at about 2-3 weeks postop. Salvage by means of ankle fusion, or total ankle replacement may also be considered {explained elsewhere in this manual). Ankle Fractures-the anterior inferior tibiofibular ligament attaches to the tibia at the tubercle of lillaux. Avulsion fracture of the tibia at this location is termed a lillaux-Chaput fracture. Avulsion of the fibula at the attachment of this ligament is termed a Wagstaffe fracture. The Lauge-Hansen classification (Table 10-10) of ankle fractures provides a functional description of the mechanism of injury. The first word in the system describes the position of the foot at the time of injury, and the second word denotes the pathological motion of the foot relative to the ankle.

Stage I

Stage II

Stage Ill

Stage IV

Anterolateral lesions

Key

Figure 10.22

I Sites of osteochondral fractures

Figure 10.23

274


Ch. 10

TABLE 10-10. THE LAUGE-HANSEN CLASSIFICATION OF ANKLE FRACTURES.

Class

Mechanism

Supination~

Pure inversion of foot in the

adduction (Figure 10-24)

Stage I

II

ankle mortise

Description of the pathology Rupture of lateral collateral ligaments or transverse avulsion fracture of lateral malleolus Talus impacts the medial malleolus causing a vertical (oblique) fracture of the tibia; the tibiofibular syndesmosis remains intact and

diastasis does not occur

Pronation-

Pure eversion abduclion of the foot in (Figure 10-25) the ankle mortise

Rupture of the deltoid ligament (medial clear

space), or transverse avulsion fracture ofthe medial malleolus

II

Rupture ofthe anterior and posterior inferior tibiofibular ligaments, or Tillaux-Chaput or

Wagstaffe avulsion fracture from the tibia or Ill

fibula, respeclively Short oblique fracture of the lateral malleolus

originating at the level of the ankle joint; on the lateral view, the fibular fracture appears transverse

Supinationeversion (external rotation) (Figure 10-26)

Disruption of the anterior-inferior tibiofibular

The talus externally

rotates about an axis comprised of the medial malleolus and deltoid ligament

II

ligament or avulsion fractures of Wagstaffe (fibula) or Chaput-lillauxtibia) Classic spiral fracture of the lateral malleolus, beginning at the joint line; the fracture line

runs laterally from superior-posterior

Ill

anterior-inferior to

Disruption of posterior-inferior tibiofibular

ligament or avulsion fracture of Volkmann's

IV Pronation-

External

eversion (external

rotation of

rotation)

about an axis

the talus

(Figure 10-27) consisting of the lateral malleolus and lateral collateral ligaments

II

posterior malleolus Rupture of deltoid ligaments or transverse fracture of medial malleolus Disruption of deltoid ligament or transverse avulsion fracture of medial malleolus rupture of anterior-inferior tibiofibular

ligament or Wagstaffe (fibula) or lillauxChaput (tibia) avulsion fracture Ill

Interosseous syndesmosis

membrane torn above and below fibular head,

followed by high fibular fracture at any level starting above joint line, all the way to the proximal neck of the fibula (Maisonneuve

fracture)

IV

Disruption of posterior-inferior tibiofibular ligaments or avulsion fracture of tibia

(Volkmann) or fibula

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275

Figure 10.25

Figure 10.24

Stage 4

Stage 1 4

Figure 10.26

Figure 10.27

The Danis Weber classification (Table 10-11) focuses on the level of the fibular fracture line relative to the ankle joint, and serves as a guide to repair of the fibula. The fibular fracture is considered dominant, and restoration of its anatomic length takes

precedence over repair of the inferior tibiofibular syndesmosis. The goals of ankle fracture repair are realignment of the ankle mortise, inspection of the talar dome and tibial plafond, and reapproximation of supporting soft tissue structures.

276

Ch. 10


TABLE 10-11. TilE DANIS WEBER CLASSIFICATION OF ANKlE FRACTURES. Type

Fracture pattern

Pathological anatomy

Corresponding lauge~Hansen

classification

A

Fibular fracture distal to the joint line

Transverse avulsion fracture of fibula at or distal to level of ankle joint

Supination-

adduction

Inferior tibiofibular ligaments remain intact

May see associated medial malleolar vertical fracture B

Fibular fracture at the joint line

c

Fibular fracture

above the joint line

Spiral or oblique fibularfracture beginning at inferior tibiofibular syndesmosis Tibiofibular ligaments are usually disrupted but interosseous membrane remains intact May have disruption of deltoid ligament or transverse medial malleolar fracture

Supinationeversion or pronationabduction

Fibular fracture above the level of the tibiofibular syndesmosis up to the fibular head Rupture of tibiofibular syndesmosis and interosseous membrane

Pronationeversion

Deltoid rupture or transverse medial malleolar fracture

Treatment in all cases begins with attempted closed reduction and immobilization, and certain fractures are amenable to closed reduction and immobilization as the mainstay of management Patients with minimal displacement, debilitated hosts, and patients with

limited ambulatory capacity may do best with closed reduction and immobilization, and supportive therapy for post-traumatic arthrosis afterwards. Conscious sedation usually aids closed reduction and immobilization. After closed reduction, immobilization in a curved plaster cast with 3-point pressure (minimal padding) is continued 6-8 weeks non-weight bearing. The radiographic criteria for adequate reduction of displaced ankle fractures include:

1. 2. 3. 4. 5.

No widening of medial clear space; No displacement of malleoli on AP view; <2 mm of posterior displacement at lateral malleolus on lateral view; No angular deformity ofthe ankle; and Posterior malleolar fracture involvement of less than 25-30% ofthe tibial plafond.

Open reduction and fixation is best performed as soon as possible after injury, before severe edema and hematoma form, as long as the patient is medically able to sustain operative intervention. After 6-8 hours, edema with hematoma may prevent wound closure, and fracture blisters may form. In such cases, therapy entails protection and rest, ice, compression and elevation (PRICE} with closed reduction and application of a Jones

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277

immobilizing dressing, and waiting 4-14 days until the skin barrier is intact and edema

reduced. Suggested techniques for OR IF of ankle fractures (there are other useful fixation methods, and the following are time honored guidelines) include: Supination-Adduction (Type A) 1. Use two 0.062 inch K-wires with 22-gauge tension band wire for transverse fibular fracture. 2. Use two 4.0 mm cancellous screws perpendicular to fracture line and parallel to each other to fix vertical medial malleolar fracture. Pronation-Abduction (Type B) 1. Fix the short oblique lateral malleolar fracture with a 5- or 6-hole 1/3tubular axial

compression plate with 3.5 mm cortical screws to secure the plate above the fracture line (through both fibular cortices) but not below the fracture line, as this could damage the talus. Only purchase the lateral fibular cortex. 2.

Repair inferior tibiofibular ligaments with 0-gauge non-absorbable suture. If

lillauxfracture is present, use 4.0 mm cancellous lag screw/s. 3.

Transverse medial malleolar fracture is fixed with two 4.0 mm cancellous screws perpendicular to fracture line and parallel to each other.

Supination-Eversion (Type B) 1. Spiral fracture of fibula is fixed with interfragmenta14.0 mm cancellous screws or 3.5 mm cortical screws. Supplement with 1/3 tubular 5-6-hole neutralization plate placed perpendicular to plane of the interfragmental screws. The plate is anchored with 3.5 mm cortical screws laterally, or a posterior anti-glide plate is used to both reduce and stabilize the lateral malleolar fragment. 2. Repair of anterior-inferior tibiofibular syndesmosis or avulsions, as noted above. 3. tf small posterior malleolar fracture fragment occurs, it should spontaneously reduce with reduction of the fibula since the posterior inferiortibiofibu!ar ligament is intact (vassal rule). 4. If there is a large tibia fragment posteriorly (greater than 25% of posterior malleolus) it must be reduced. Use 4.0 cancellous screws posterior to anterior. 5. Two 4.0 mm cancellous screws perpendicular to transverse avulsion medial malleolar fracture and parallel to each other. Pronation-Eversion (Type C) 1. For fibular fractures mid-diaphyseal level or lower, use interfragmental compression, with 4.0 mm cancellous or 3.5 mm cortical screws, then augment with 1/3 tubular neutralization plate. Use tibiofibular transfixing screw through or above the plate for fractured distal diaphysis. Alternatively, absorbable screws, or a nonabsorbable tension suture (TightRope®), could be used for tibiofibular transfixation. 2. In Maisonneuve fractures, do not open reduce due to potential complication with common peroneal nerve, and adequacy of tibiofibular transfixation. 3. First, fit distal fibula into fibular notch on tibia and temporarily transfix tibia and fibula with 5/64 Steinmann pins and X-rayto visualize mortise and length offibula.


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Ch. 10

If satisfactory, suture interosseous membrane and then use final fixation with two 3.5 mm cortical screws. Goal is to stabilize the tibiofibular relationship

without compression ofthe mortise. 4.

Remove transfixing screws at 6-8 weeks and hardware at 4-6 months.

Tibial Pilon Fractures-the distal tibial metaphysis (pilon) can be seriously disrupted in a variety of injury patterns, and repair of this structure is difficult and requires considerable experience. Pilon fractures enter the ankle, and may be associated with fibular fracture as well. Repair entails anatomic reduction, autogenous corticocancel!ous bone grafting, and internal as well as external fixation. A high rate of post~traumatic arthrosis, osteomyelitis, delayed and nonunion, limb angular and length misalignment, and difficulty walking can ensue. Revisional surgery, bone transport, ankle and pantalar arthrodesis, and amputation are not uncommon. Although several classification systems are available, the most straightforward is that of Ruedi and Allgower (Table 10-12).

TABLE 10-12. THE RUEDI-AllGOWER CLASSIFICATION OF PILON FRACTURES. Type

Description of the pilon fracture

I

Pilon fracture with minimal displacement

II

Pilon fracture with significant displacement

Ill

Pilon fracture with significant displacement and loss of cancellous bone

Epiphyseal Plate Fractures--the epiphyseal complex consists of the epiphysis, physis, and the metaphysis. Epiphyses are either of the pressure or traction type. Pressure epiphyses are located at the end of a long bone and provide rapid longitudinal growth. Traction epiphyses are non-articular, and located where muscle or tendon attaches to bone, and do not contribute to axial growth. Anatomically the physis displays three distinct zones \Fig. 10-28). The zone of growth is closest to the epiphysis and contains resting chondrocytes that progress to dividing cells that arrange in columns. The next component is the zone of cartilage maturation, which is the weakest region due to loss of intracellular matrix. Finally,

Ossification Zone of Transformation

Figure 10.28

Figure 10.29

I'


Ch. 10

279

the zone of cartilage transformation displays cartilage converting to bone. Periosteum is

more vascularized, thicker, and stronger in the child. The cartilage is strongly attached to the metaphysis, and more loosely attached to the diaphysis. The periosteum also acts as a checkrein to resist fracture displacement. The vascular supply to the growth plate

complex is as follows: metaphysis-supplied by the nutrient artery of the diaphysis, vessels from periosteum and perichondrium, and these sources extend to the zone of

hypertrophied cells; epiphysis-supplied by nutrient epiphyseal vessels; physis-supplied by nutrient arteries from both the metaphysis and the epiphysis, as well as direct

perichondrial vessels to the physis.lfthe metaphyseal supply is compromised or lost, there is usually very little change in physeal perfusion. If, however, either the epiphyseal or perichondrial supply is lost, the physis may die and premature partial or total closure may ensue. The epiphyseal vessels supply the physeal zone of growth. Partial closure may cause angular deformity. The osseous ring of Lacroix is an extension of metaphyseal cortical bone that stabilizes the physis at the zone of Ranvier, where the physis interfaces with the metaphysis (Fig. 10-29). Evaluation of physeal injury requires at leastthree radiographic views and comparison with the uninjured extremity. Epiphyseal fractures are categorized by Salter-Harris (Table 10-13) and Aiken-Mueller (Table 10-14).

TABLE 10-13. SALTER-HARRIS ISH) CLASSIFICATION OF EPIPHYSEAL PLATE FRACTURES. Type I (Fig. 10-30)

II(Fig. 10-31)

Description 1. Separation of epiphysis· from metaphysis between layers of hypertrophy and calcification 2. Resting cells remain with the epiphysis 3. Minimal displacement usually due to strong periosteum 1. Most common acute physeal injury 2. Separation of epiphysis from metaphysis between layers of hypertrophy and calcification 3. Fracture line runs through physis then through metaphysis 4. Thurston-Holland sign-metaphyseal fragment where the periosteum is intact adjacentto the metaphyseal fragment 5. Werenskiold sign-small fragment of metaphyseal fragment on X-ray

III(Fig. 10-32)

1. Fracture begins in joint, runs up to the physis then makes a 90° turn through the layer of hypertrophied cells to periphery 2. Area of concern for blood supply to free fragment as well as congruity of joint surface 3. Most germinal cells remain intact

IV (Fig. 10-33)

1. Injury runs from joint, through epiphysis, through physis and out through metaphysis

v

1. Crushing injury that destroys all layers of physis 2. Premature closure usually ensues

VI(Fig. 10-34)

1. Injury associated with removal of bone loss at the zone of Ranvier, due to trauma such as a burn or degloving injury

VII(Fig. 10-35)

1. Avulsion fracture of the epiphysis, not involving the physis

Ch. 10


280

u Type lA fracture

Type IB fracture

Type IC fracture

Figure 10.30

g ~ g Type IIA fracture

Type liB fracture

Type IIC fracture

Type liD fracture

Figure 10.31

Type 1118 fracture

Type lilA fracture

Figure 10.32

it

~~ Type IVA fracture

Figure 10.33

Type IVB fracture

Type IVD fracture

Ch. 10


Type VJ fracture

Figure 10.34

281

Type VII fracture

Figure 10.35

A triplane fracture is special distal tibial epiphyseal fracture that usually occurs in older children, about 1 year prior to closure of the epiphysis, and results from external

rotation. The 2-part triplane fracture occurs when the medial part of the distal tibial epiphysis has already closed, and the lateral radiograph displays a SH IV fracture, and the posterior tibial plafond fragment extends to the metaphysis, and may be comminuted. The 3-part triplane fracture consists of a combination of a SH II and a SH Ill fracture, and

occurs when the middle portion of the distal tibial epiphysis has closed. The lateral radiograph displays aSH II fracture, while the mortise view shows aSH Ill fracture. The tibia displays a large posterior fragment consisting of a large posterior fragment of posterior and medial portions of the metaphysis, while the mediall/3·1/4 of the tibial plafond and medial malleolus remains intact. The fibula is also usua!!yfractured. Treatment recommendations for epiphyseal plate fractures entail the fo!!owing guidelines: Types I and II 1. Usua!!y respond well to closed reduction, especia!!y if seen early. 2. If seen 7 days after injury, the attempt at closed reduction may do more harm than good due to fast healing that occurs at this site. Types Ill, IV, V, and VI 1. Should attempt closed reduction first, but usually requires ORIF. 2. Must anatomica!!y reduce the physis and preserve joint congruity. 3. Try to keep threaded K-wires or screws out of physis. 4. Try and maintain fixation devlces in metaphysis.

TABLE 10-14. THE AIKEN-MUELLER EPIPHYSEAL PLATE FRACTURE CLASSIFICATION SYSTEMS. Aiken 1 ~Salter II

Mueller A~

Salter I, II

2 ~Salter Ill

B ~Salter Ill, IV, VI

3 ~Salter IV

C~ SalterV

Foot and Ankle Disability and Rehabilitation

232

Ch. 11

FOOT AND ANKLE DISABILITY AND REHABILITATION WORKABiliTY, DISABiliTY, AND REHABiliTATION Rehabilitation ott.he foot and ankle following injury or surgery, or as a part of the treatment of disease, ranges from straightfmward and simple intervention such as walking and range of

motion (ROM) exercises, to complicated diagnostic and therapeutic regimens that require specialized training and equipment Specialization has developed due to an ever-increasing number of woriHelated injuries, workers' compensation and disability lawsuits, costs, and regulatory agencies and the Americans with Disabilities Act. Occupational therapy or industrial medicine consultation and referral can be helpful, in such cases. Work is defined as any and all forms of productive activity, regardless of whether or not there is reimbursement. Work levels, as defined by the US Department of Labor, are depicted in Table 11-1. Cumulative trauma disorders often develop secondary to repetitive strain, vibration or cold exposure, and include plantarfasclitis and heel spur syndrome, tarsal tunnel syndrome, stress fracture, and chronic tendonitis and/or capuslitis. Physical therapy entails exercise and other physical modalities used in primarily the acute and subacute phases oftreatment. WorkabHITy may be determined using a functional capacity assessment (FCA), which entails a standardized questionnaire to assess appropriate behavior and symptom magnification; direct measurements of strength, power, endurance, coordination, balance and mobility; and job simulation. Patients who have been out of work or incapacitated for greater than 3-6 months, despite accurate diagnosis and treatment including physical therapy, may benefit from functional capacity assessment.lndividuals incapacitated >6 months may require work conditioning in an effort to reestablish strength, flexibility, and aerobic capacity, with outwork simulation. Work hardening involves real and simulated conditioning tasks, designed to enable productive, safe, and tolerable re~entryto the work place after temporary Incapacitation. Job modification may be recommended based on the functional capacity assessment and efforts at work hardening, and may entail work aids (a stool to sit upon, a cushioned floor mat, special shoes, etcl alteration of labor category (job description), and measures to assure safety and prevent rein jury. Not all physical therapists are equipped to pertorm a FCA, or to undertake work conditioning or work hardening programs.

TABLE 11-1. WORK lEVElS DEFINED BY THE US DEPARTMENT OF LABOR* Work level Sedentary Light work Medium work Heavy work Very heavy work

Maximum lift

Frequently lilts

10 lb. 201b 50 lb. 1001b. >100 lb.

None 10 lbs. 251bs. 50 lbs. >50 lbs.

Ambulation Infrequent walkin or standing Frequent walking and/or standing Frequent walking and/or standing Frequent walking and/or standing Frequent lifting and carrying

* http://www.d ol.gov/esa/regs/compliance/whd/fa irpay!fs17a_ overview. htm, website last visited 10/27/2007.

Such reports may also be useful in legal matters where disability determination is in question. Occupational therapy and social service intervention will often enhance the patient's progress and lifestyle. For patients with chronic pain, or suspected RSDS/CRPS, referral to the pain clinic can also be helpful. Categories for the industrial rehabilitation prescription are depicted in Table 11-2.

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283

TABLE 11-2. INDUSTRIAL REHABILITATION PRESCRIPTIONS. Phase acute and subacute (<3 months)

Prescription Accurate diagnosis, protection of the injured part, rest. ice, compression and elevation, medications and physical therapy

;:;::3 months

FCA and work hardening

Prolonged rehabilitation (>6 months)

FCA, work conditioning, work hardening

An example of a prescription for physical therapy following an ankle sprain follows:

Rx Physical therapy for: 1) strengthening, 2) flexibility/range of motion, and 3) proprioception, right ankle; 6-8 sessions over 3-4 weeks, evaluate and treat. Diagnosis: status-post ankle sprain (ICD9 xxx.xx) An example of a prescription for work hardening following an ankle fracture follows: Rx Work hardening status-post OR IF ankle fracture (ICD9 xxx.xx), please

send report Activities of daily living (ADLs) include feeding, grooming, dressing, toileting, bathing, continence, transfers, and communication. Some examples of complex ADLs include: cooking, cleaning, laundering, shopping, housekeeping, telephone, money management, care giving, traveling, and taking medications. Functional capabilities include self~care (fundamental and complex activities of daily living), work, play and leisure. Disability status can be categorized using the Karnofsky scale (Table 11-3). TABLE 11-3. DISABILITY STATUS ACCORDING TO THE KAMOFSKY SCALE OF PERFORMANCE. Score 100 90 80 70

Disability Normal, no complaint or apparent disease Normal, minor signs and symptoms of disease Normal with extra effort, moderate signs and symptoms of disease Unable to carry on normal activities or actively work, can care for self; marked signs and symptoms of disease 60 Requires ·occasional assistance, primarily cares for self; marked signs and symptoms of disease 50 Requires considerable assistance and frequent medical care; marked signs and symptoms of disease 40 Disabled, requires special care and assistance; marked signs and symptoms of disease 30 Severe disability, hospitalized or institutional care indicated; marked signs and symptoms of disease 20 Very sick, hospitalization with active supportive care is necessary 10 Moribund, fatal processes progressing 0 Death

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Ch. 11

Range 100-80--the patient is able to carry on normal activity, and no special care is needed.

Range 70-50-the patient is unable to work, but is able to live at home and care for most personal needs, with a varying amount of assistance as needed. Range 40-10--the patient is unable to care for self and requires equivalent of institutional, or hospital care, and disease may be progressing rapidly.

Evidence-Based Medicine (EBM) and Documentation

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285

EVIDENCE-BASED MEDICINE (EBM) AND llllCUMENTATION EVIDENCE-BASED MEDICINE (EBM) Evidence-based medicine (EBM) entails the application of 3 elements of information used to make clinical decisions. The 3 components of EBM are: 1) the clinician's experience, 2) the individual patient's needs, and 3) the scientific evidence related to the clinical question at hand. There is a hierarchy of evidence related to human clinical scientific knowledge (Table 12-1).

TABLE 12-1. lEVELS OF HUMAN CLINICAl EVIDENCE. ACFAS* Score 1a

level of Clinical Evidence Systematic review of homogenous RCTst Individual RCT with narrow confidence intervals

1b 1c

"Ali-or-none" observational stUdy

2a

Systematic review of homogenous cohort studies

2b

Single cohort study, or poor quality RCT

2c

Outcomes research or ecological study

3a

Systematic review of homogenous case-control studies

3b 4

Case report or series, or poor quality case-control study

5

Expert opinion, animal physiology, bench study

Single case-control study

* ACFAS- American College of Foot and Ankle Surgeons (http://VIIWW.acfas.org) t RCT =randomized controlled trial

Furthermore, human clinical research follows a hierarchy of research design options (Table 12-2).

TABLE 12-2. HUMAN CLINICAL RESEARCH DESIGN OPTIONS. Research Design Options* Analytical hypothesistesting

RCTt (interventional experiment) Prospective cohort study (observational) Retrospective cohort study (observational) Case-control study (observational)

Descriptive hypothesisforming

Analysis of secular trends (group correlational) Cross sectional (individual point-in-time) Case series Case report (rare disease, novel treatment) Animal physiology, cadaver, synthetic or computer model study

*The table is arranged from top to bottom, beginning with the research design that is most likely to produce valid results (and conclusions), that being the randomized controlled trial, to the research design that is considered to be least likely to produce valid results in regard to human clinical outcomes, that being the animal or berJCh-top investigation. tRCT =randomized controlled trial

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The elements of a scientific investigation that contribute to the validity of the conclusions gleaned from the study are depicted in Table 12-3.

TABLE 12-3. THE BUILDING BLOCKS OF GOOD CliNICAl EVIDENCE. 1.

Building Blocks of Clinical Evidence* Explicitly defined research question, population, and end points

2. 3.

Randomized treatment allocation and intention-to-treat analysis Participants and outcomes assessors blind to treatment allocation

4. 5. 6.

Use of a valid health measurement (quality of life) instrument Power and sample size determined a priori Statistical analyses compatible with type and distribution ofthe data

7.

Point estimate and 95% confidence interval reported

~Turlick

MA, Kushner 0, Stock 0. JAm Podiatri Med Assoc 93:392-8,2003.

FUNDAMENTAL ElEMENTS OF SCIENTIFIC PUBliCATION When reporting scientific information, or submitting a manuscript to a peer-reviewed journal, the fo!!owing information can be used to develop the report. Abstract: Submit an abstract of:::; 250 words summarizing the contents of the article. The Abstract canbe no longer than 250 words, since the National library of Medicine (via Pubmed) truncates longer abstracts at 250 words, resulting in loss of information. The Abstract can be written as continuous prose, or with subheadings for each section of the manuscript, depending on the specific journal's preference. The Abstract for a report of research should reflect the format ofthe manuscript itself, describing pertinent information for each section of the manuscript It should briefly introduce the research problem, explain methods, summarize results, and provide a conclusion. The Abstract for a case study should state the condition of interest, and include a brief summary of the specific clinical situation, the uniqueness or rarity of the diagnosis or the novelty of the intervention, and a statement regarding the clinical significance of the case. Do not use any abbreviations or bibliographic reference citations in the Abstract, since electronic searching rnay limit the space not all abbreviations will be recognizable to all readers. If necessary, parts of the Abstract may be written as phrases, rather than as complete sentences. The level of clinical evidence (Table 12-1) should be noted in the last sentence of the Abstract Key Words: Provide 3-5 key words or phrases for electronic indexing purposes. Keep in mind that electronic searches of the biomedical literature depend to a large degree on key words. Refer to the National Library of Medicine's (via Pubmed) Medical Subject Heading IMeSH) webpage (http.//www.ncbi.nlm.nih.gov) lor help selecting key words. Key words are to be spelled in small case letters, unless representative of a proper name, and listed in alphabetical order separated by a comma between each word/term. Avoid abbreviations in the keywords, unless a proprietary name uses an abbreviation. In general, proper names are not used as key words. Introduction: This section should provide a concise overview of the state of knowledge regarding the specific problem being studied. It should begin with a statement of the

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problem and its clinical/social importance, followed by an explanation of recent and important research related to the topic, supported by reference citations. The importance of the topic is best t;:onveyed by means of statistics that indicate the prevalence and/or

economic impact of the condition in the population/society. After an explanation of what is known, and what remains unknown in regard to the focus of the study, the author should concisely state the specific research question or hypothesis for the current investigation. Generally, the last sentence of the introduction should include a statement that describes the specific study design I see Table 12-2) and reiterates the research question. Patients/Materials and Methods: If the study is a clinical investigation involving living, human participants !patients, subjects), then the heading for this section should be "Patients and Methods." ltthe investigation involves animals, cadavers, or in vitro models of any sort, including computer models, then this section should be termed "Materials and Methods." In general, the methods section should describe the following elements of the investigation: aims, assessors and other members ofthe investigational team, population or sample, intervention, endpoints \measured variables), and the statistical methods used to determine the meaning o_f the results (see details below). Ideally, this section should provide enough detail to allow subsequent researchers to replicate the study. When reporting randomized controlled trials, a study flow diagram in CONSORT format, as well as all of the information required by the CONSORT checklist, should be provided. The CONSORT statement, checklist, and study flow diagram are available at http.//\IIILIIIVv.consort-statement.org. For observational investigations, the STROBE statement (http//wiiVWstrobe-statementorg) guidlelines and checklist can be used.

Aims: The primary aim of the investigation, as well as any secondary aims, should also be clearly stated. A distinction should be made between primary and secondary aims. As a rule, the sample size should be adequate to identify. a statistically significant difference in regard to the primaJY aim, if such a difference exists. Power and sample size calculations can be determined using any of a number of software programs, such as that found at: http//biostatmc.vanderbiltedu/twiki/bin/view/Main/PowerSampleSize. In describing the primary aim, many authors will restate, in some fashion, their hypothesis and research question, emphasizing that they undertook to answer the question.

Assessors: Members of the investigational team should be described in regard to their participation in the study; namely, ifthey served as outcome assessors or if they performed an intervention or, in the case of a retrospective study, if they abstracted data from medical records. For studies in which subjective measurements are determined, such as measurements of radiographic angles, a method should be described for breaking ties and determining an outcome when indecision or uncertainty exists. If outcomes assessors were blind to treatment allocation, this must be stated. If outcomes assessors were participants in the intervention, such as members of the surgical team or treating clinicians, this must also be stated.

Study population: The methods section should provide readers with an explicit description of the participant/patient population and the time period from which they were selected. The time period should delineate the day, month and year that the period started; and the day, month and yearthatthe period ended IMM/DD!YYYY-MM/DD!YYYY.Ifthe daythatthe time period started is not known, then it is acceptable to state just the month and year that

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initiated and ended the period (MM!YYYY-MM!YYYY). It is also important for the author to

state whether or nottreatment allocation was determined in a random fashion, and whether or not participants in a clinical trial were blind to treatment allocation. The method of randomization should be described {random number table, electronic random number generator, sealed envelopes, other). For case series and cohort studies, the author should state whether or not the participants were enrolled consecutively. The inclusion and

exclusion criteria must be clearly stated, and it is best to simply list these.

Intervention: In any investigation, the intervention needs to be explicitly described. If participants were randomized to an active therapy that was compared to standard therapy, or placebo, each treatment arm needs to be described. Authors are encouraged to avoid presenting a detailed narrative report of an operative intervention for a standard procedure that can be referenced in any of a number of textbooks. Reference can be made, with an appropriate citation, to a standard procedure as it is described in a textbook; and variations on the procedure should be described in detail. Nov.el interventions, notable variations on standard procedures, decision points related to an intervention, and adjunct procedures should be thoroughly described. Endpoints (outcomes): Outcome measures should be explicitly defined in terms of how the variable was measured, who made the measurement, and whether or notthe assessor was blind to the intervention (for an intervention trial). Authors should clearly state if outcomes were based on physical examination, chart review, telephone interview, questionnaire or radiographic films. As a rule, any variable that a reasonable clinician would consider important in regard the treatment of a patient, as it pertains to the investigation, should be considered in the analysis. In addition to the intervention/s or outcome/s of interest, typical independent variables include such things as age and age category, gender, activity level, body mass index (BMI) or BMI category, comorbidities, medications, duration of treatment, surgeon or clinical site, adjunct therapies, frequency and duration of follow-up, and post-intervention management procedures (immobilization, physical therapy, etc.). ltems such as those just listed above should be referred to as "variables" and not as "parameters," since the term "parameter" should be reserved for statistical expressions that describe the data, such as the mean and standard deviation, or beta coefficients derived from a regression analysis. Whenever possible, it is preferable that "hard" endpoints be used, such as analytical measurements, clinical or microbiology laboratory results, and the like. Whenever "soft" endpoints, such as quality of life (QQL), are considered, it is preferable to use health measurement instruments that have previously been shown to be reliable and valid. QOL instruments should be specific to the foot and ankle (ACFAS, AOFAS, Bristol Foot Score, Foot Function Index, etc.), as well as measures of general health (SF-36, etc). Investigator derived questionnaires should be described in terms of reliability and validity, if such testing was undertaken. For scales that rank categories (mild, moderate, severe, for example) an aggregate score should be used. For measurements of pain, the 10-cm Visual Analog Scale (VAS) is recommended. Statistical Methods: The statistical plan should be clearly described, and every investigation should include at least descriptive and inferential, as well as univariate and multiple variable, statistical analyses. The descriptive statistical analysis should define parameters such as the measure of central tendency (mean or median average), and measures of dispersion \standard deviation or range). The parameter, as well as the statistical test, should be selected

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based on the type and distribution of the data. In short, continuous numeric data that are normally distributed are suitable for representation using the mean and standard deviation, and may be analyzed using mean-based statistical tests (such as Student's

Hest). Categorical data, and data that are non-normally distributed, are suitable for representation. using the median and range, and may be analyzed using median-based

methods such as the Wilcoxon matched-pairs signed-ranks test, sign test, Wilcoxon rank-sum test, and the Kruskai-Wallis equality-of-populations rank test, and other null hypothesis tests and methods of estimation. For categorical data, Fisher's exact method should be used as much as possible. Univariate analyses should describe the association of independent variables with the outcome of interest (dependent variable), whereas multiple variable analyses should describe the association of all of the clinically important variables with the outcome of interest. Results should be presented with only as much precision as is of scientific value. For example, measures of association (odds ratios, relative risks, risk differences, etc.) should typically be reported to two significant digits. As a rule, the terms "significant" and "significantly" should be reserved for use when describing statistical differences. The statement "no significant difference was found" between two groups should not be made unless a power analysis was done and the value of alpha (level of significance, typically 5%) or beta (the power to detect a statistically significant difference, usually 80% or 90%) is reported. Use of the word "significant" requires reporting of a P-value (probability), or the 95% confidence interval about a point estimate. It is preferable to report the 95% confidence interval (CI) rather than the P-value, since the 95%CI describes whether or not the result was statistically significant, while also showing just how precise the estimate was. Except when 1-sided tests are required by study methodology, such as in noninferiority trials, 2-sided P-values should be reported. By convention, P-values larger than O.Ot should be reported to two decimal places, those between 0.01 and 0.001 to three decimal places, and P-values smaller than 0.001 should be reported asP< 0.001. P-values should not be reported as "P::::: O."Furthermore, use of the word "correlation" or the term "correlates with" requires that a correlation coefficient (Cronbach's alpha) be calculated and reported. The results of a sensitivity analysis, such as that described by Greenland (Maldonado G, Greenland S: Simulation study of confounder-selection strategies. Amer J Epidemiol. 1993; 138: 923-936.1, or that described by Rosenbaum (Rosenbaum PR. Sensitivity analysis for matched case-control studies. Biometrics. 1991 Mar; 47(1): 87-100; and, Rosenbaum PR Discussing hidden bias in observational studies. Ann Intern Med.1991 Dec 1; 115(11): 901-5.1, should be presented for retrospective studies where unmeasured independent variables may have potentially influenced the results. Additional references that may be useful in regard to the description of the methods and the presentation of a statistical plan include: Bailar JC Ill, Mosteller F. Guidelines for statistical reporting in articles for medical journals: amplifications and explanations. Ann Intern Med 1988; 108: 266-73. Altman DG, Machin D, Bryant TN, Gardner MJ (eds). Statistics with Confidence. second edition. London: BMJ Books, 2000. Malay OS. Some thoughts about data type, distribution, and statistical significance. J Foot Ankle Surg 45: 57-9, 2006. Malay OS. Levels of clinical evidence. J Foot Ankle Surg 46: 63-4, 2007.

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Results: The results section should presents quantitative information on the data collected, in the form of descriptive and inferential statistics. Relevant information on the study population includes demographic information for each subgroup (control group and study groupsL exclusions and attrition. Inferential statistics should be used to compare groups using appropriate statistical tests based on the size of the study population, type of variables under study {discrete vs. continuous), and the distribution of the data collected. Quantitative information should be summarized in the text, and readers should be referred to relevant tables for more detailed information. As a rule, three results tables should be presented, and designated Tables 1, 2, and 3. Table 1 typically depicts the baseline demographic characteristics of the sample population, often categorizing the patients/ participants by intervention or outcome, and showing whether or not statistically significant differences existed between the groups. For randomized controlled trials, it is not necessary to depict statistically significant differences at baseline, since randomization distributes the characteristics by chance. Table 2 generally depicts the results of the univariate analyses, and Table 3 generally depicts the results of the multiple variable analyses. Additional tables can be helpful when the data warrant such detail. Discussion: The discussion section should offer the authors' interpretation of the results of their investigation, Authors should consider how their results fit into the general state of knowledge on the subject, as well as their clinical relevance. In addition, authors should acknowledge the limitations of their investigation that may have introduced bias, and they should discuss how the results may have been affected by bias. It is advise able that authors tell the readers all of the shortcomings that they (the authors) understand to have influenced their results and conclusions, rather than leave this criticism solely up to the readers. Investigations that show a statistically significant difference betvveen treatment groups should not be ·criticized for having too small a sample, Finally, suggestions for clinical applications and/or further research may be appropriate. Do not include a separate "Conclusion" subsection, as the final paragraph of the discussion should describe the authors' conclusions. Acknowledgement: In genera!, acknowledgments should be made to those who have informally contributed their expertise or assisted in the investigation, ratherthan to those who have contributed to the manuscript while performing the role of their regular occupation. References: References are cited in the body of the text by means of numeric citations listed parenthetically in the appropriate sentence, prior to the end of the sentence (usually just before the period ending the sentence). Reference citations are to appear in sequential numeric order, beginning with the number 'T' and continuing in sequential numeric order the first time that a particular reference is cited, until the last citation is noted. In other words, supply references numbered in the exact order they appear in the text (not alphabetically). Sources not identified in the text should be listed as Additional References. Unpublished sources must be included in parentheses within the body of the text, not in the Reference Section. Abbreviations for journal titles should conform to those used by Medline (www.ncbi.nfm.nih.gov/sites/entrez?db=pubmed). If Medline does not index a journal, then spell out the entire journal name in addition to listing the author name/s, title of the article, volume number, page numbers, and year of publication. Always list all authors, and do not use "eta!" when listing your references. The term "eta!" may be used in the body of the text; however, it is generally reserved for mentioning papers written by

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more than 3 authors. Whenever a textbook is referenced, it is necessary to include the specific page or pages used. Whenever a web reference is cited, it is necessary to include the date when the site was last accessed. Examples of reference citations include: Journal article: 1. Mendicino RW, Orsini RC, Whitman SE, Cantanzariti AR. Fibular grove deepening for recurrent peroneal subluxation. J Foot Ankle Surg 40:252-263, 2001. Textbook: 2. Trevino SG. Disorders of the hallucal sesamoids. In Foot and Ankle Disorders, pp 379-398, edited by MS Myerson, WB Saunders, Philadelphia, 2000. Electronic version of a print journal: 3. Gardner MJ, Boraiah S, Hentel KD, Helfet DL, Lorich DG. The hyperplantarflexion ankle fracture variant. J Foot Ankle Surg [serial on the lnternet]46:256-60, 2007.Mvailable at http://www.jfas.org/issues/contents.

Web page: 4. Clinical Practice Guideline Heel Pain Panel. Diagnosis and Treatment of Heel Pain. American College of Foot and Ankle Surgeons Web site. September/ October 2001. Available at: http://www.acfas.org/pubresearch/c pg/heelpain-cpg.htm. Accessed mm/dd/yyyy.

Figures: Photographs and illustrations should be clear and support the specific points mentioned in the text. Figures and their accompanying legends should be able to stand alone, communicating the meaning of the information without reference to the main text. In the text, figures should be cited using parentheses about the figure-reference being cited. For example: "[Agure 1)". Each figure should be titled, and accompanied by a figure legend. The figure title should be formatted as in the following example: "Figure 1. The gastrocnemius recession." Do not use abbreviations in either the figure title or the figure legend, unless the abbreviation is defined in the legend. Abbreviations or footnotes shou!d be explained in lower case alphabetical superscripts beneath the figure.lfthe figure reports a statistical result, such asaP-value, then the statistical test used to determine the P-va!ue needs to be described in the legend or elsewhere in the figure. Rgure titles and legends must be submitted for each figure, and should be typed in consecutive order, double-spaced, on a separate page from the text. Each figure must be submitted as a separate page [electronic file). Images should be provided in TIF, GIF or EPS format, per the specific journal's instructions. Manuscripts that describe a pathological entity should be accompanied by a photomicrograph, with the type of stain and magnification indicated. Radographic images should be submitted in grayscale format. Black and white line drawings are acceptable only it they are of professional-quality. All figures must be original, unless indicated otherwise. A Jetter should accompany figures that have already been published in other sources, indicating that the previous publisher and author have granted permission for their use. Keep in mind that hardcopy llustrations and figures are usually not returned to authors. Tables: Tables should be clear and support the specific points mentioned in the text Black and white lines and text are preferred, and the "inserttable" function ofthetoolbar of most

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word processors works well for this. Tables and their accompanying legends should be

able to stand alone, communicating the meaning of the information without reference to the main text. In the text, tables are cited using parentheses about the table-reference being cited. For example: "(Table 1)." Each table should be titled, and accompanied by a table legend. The table title should be formatted as in the following example: "Table 1. The dataset." Do not use abbreviations in either the title or the table legend, unless the abbreviation is defined in the legend. Abbreviations or footnotes should be explained in lower case alphabetical superscripts beneath the table. If the table reports a statistical

result, such asaP-value, then the statistical test used to determine the P-value needs to be described in the legend or elsewhere in the table. Table titles and legends must be submitted for each figure, and should be typed in consecutive order, double-spaced, on a separate page from the text Each table must be submitted as a separate page (electronic file). Tables should be provided in either .doc, TIF, GIF or EPS format, per the journal's instructions for online submission. All tables must be original, unless indicated otherwise. A letter should accompany tables that have already been published in other sources, indicating that the previous publisher and author have granted permission for their use. Registered trademarks and copyrights: As a rule, generic terminology is preferred. Any and every time that a proprietary substance (such as a medication), device, equipment, or softvvare program is mentioned in the manuscript it must be accompanied by either of the following symbols: "®" or "'""', indicating that the substance or device is a registered trademark; and the following information must be provided in parentheses, immediately following mention ofthe proprietary item: proprietor's name (the name of the company that owns the registered trademark), city and state wherein the proprietor's headquarters are located, and the country if other than the United States. If copyrighted material is mentioned, then the "©" symbol should accompany the item. Furthermore, the use of copyrighted material requires that the author obtain explicit permission from the owner of the copyright (publisher). and the author, for such use. As a rule, proprietary names should not be used in the manuscript's title, and once a proprietary name is used to describe an intervention or diagnostic test, generic terminology should be used thereafter. In an effort to remain scientific, and to avoid the appearance of proprietary bias, generic terminology is generally preferred by peer reviewers and editors. Abbreviations: Do not use abbreviations in the litle, Abstract, or Key Words section of the manuscript, because information from these portions of the paper is used in the process of electronically indexing biomedical literature. If a proper or proprietary name entails the use of an abbreviation, only then can it be used in the Title, Abstract or Key Words sections. Abbreviations can be used in the Introduction, as well as any area of the manuscript thereafter. Abbreviations are not to be used unless the term has first been spelled in full, and the abbreviation noted in parentheses immediately following the full term. For example: " ... deep peroneal nerve \DPN)." Abbreviations that are part of a proprietary name are to be used in accordance with the guidelines noted for registered trademarks and copyrights. EBM websites: Much of the information described above can be found in greater detail at a number of evidence-based medicine websites, such as the Centre for Health Evidence (http://www.cche.net/), the Centre for Evidence-based Medicine (http://www.cebm.utoronto.ca/!, and the Oxford Centre for Evidence-based Medicine

(http://www.cebm.net/).

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APPENDICES ORAL EXAM TEST- TAKING AlGORITHM Do not deviate from this algorithm unless prompted by the examiner. You may ask if a specific segment has been adequately covered, however do not assume anything unless the proctor indicates so. Start with the history and physicai(H&P) examination, then make a diagnosis and describe a treatment plan and fotlow~up. History and Physical Chief complaint Nature of sign and/ or symptom Location of sign and/or symptom Duration of sign and/or symptom Onset of sign and/or symptom Course of sign and/or symptom Aggravated by (activities or circumstances) Treatment (what has been tried, helpful or not)

Previous Medical History, Medications, Allergies Surgical History Social History, Occupation/Avocation, Fami!y History Physical Exam Vital Signs (Temp, Pulse, Respiration, BPI

Vascular Neurological Dermatological Orthopedic Biomechanical X~ray, and other clinical or diagnostic testing Differential diagnosis Consider confirmatory consultation or other testing Diagnosis Treatment Options and Plan Non-surgical treatment Pharmacological Biomechanical Physical therapy Surgical treatment Preoperative preparation Intra-operative plan Postoperative plan Altercare in accordance with clinical response

Appendices

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INFORMED CONSENT Informed consent is a crucial part of adequate patient preparation for any procedure or operation, and should be written, signed by the surgeon or person explaining the case, witnessed, dated, and timed. The components of informed consent include, but are not limited to, an explanation, in layman's terms, of the following points: 1. 2. 3. 4.

5. 6. 7.

8.

9.

Goals and objectives of the planned procedure or operation. Diagnosis (what you are treating). Planned procedure and anesthesia. Potential risks and complications (such as infection, recurrence of pain &/or deformity, new and/or permanent pain &/or deformity, overcorrection, stiffness, weakness, instability, scar pain or disfigurement, nerve &/or tendon injury, hematoma, phlebitis and pulmonary embolism, bone or hardware breakage, prolonged swelling or slow wound healing, difficulty walking, and other concerns pertinentto the individual's specific case (cardiac arrest, severe blood loss, etc.). Postoperative course and rehabilitation \ambulatory status, bandages, casts, shoes, time off from work or school, or driving). Therapeutic alternatives and surgical options. No guarantees are given regarding an outcome. Other points may be made depending upon the specific merits of the case. When using a new or experimental drug or technique {not FDA labeled for the application), this fact should be noted in the written consent. lntentto have observers in the operating room, or to image the case (photo, video) should be noted.

HOSPITAL ADMISSION ORDERS Standard admission orders may include: 1. AdmittoserviceofDr. 2. Dr. __ for medical management (admission to a specific service may vary depending upon hospital bylaws, rules and regulations, and staff privilege delineation). 3. Diagnosis: _ _. 4. Condition:_ (stable, guarded, critical or urgent emergent). 5. Resuscitation status: _ _ {full, or otherwise). 6. IV access and fluids ("IV 05LR at KVO [keep vein open] via 18 gauge venous catheter [specify preferences]." 7. Shave and prep [specify] preop. 8. Activity and WB status [specify]. 9. Diet [specify]. 10. NPO after 2400 preop [coordinate with dietary]. 11. Labs and ancillary testing [specify]. 12. Medications [specify]. 13. Consultations [specify]. 14. Supplies to bedside [specify]. 15. Social services for discharge planning [specify]. 16. Other items specific to the case at hand [wound and skin isolation, etc.].

Appendices

295

HOSPITAL POSTOPERATIVE ORDERS Standard initial postoperative orders may include: 1. Vital signs ("VS q shift after return to floor"). 2. Activity ("CBR (complete bed rest) with side rails up"; "absolute Non-weight bearing operated foot at all times";" BRP Non-weight bearing operated foot with assistance" ; " PT for gait and transfer training Non-weight bearing operated foot"; "Assist with first OOB (out of bed) activity"; Dangle feet over bedside while seated 3-5 minutes before first OOB activity"). 3. IV fluids ("maintain IV 05LR [or other IV fluid as indicated] at KVO [or faster rate as indicated] until fully reactive/stable"; "convert to heparin lock after 0/C IV"). 4. Medications, considerations include antibiotics, analgesics for moderate and severe pain, anti-inflammatory, muscle relaxant, anti-emetic, stool softener/bowel stimulant, sedative/hypnotic, other indicated meds. as well as the patient's regular meds. 5. Respiratory therapy ("Triflow incentive spirometry q 1 hour while awake, instruct and encourage"). 6. Drain management ("monitor drain/s [TLS, Hemovac or Jackson-Pratt] and record output, change when '}j3 full or at least q shift"). 7. Diet (regular, diabetic, restricted calorie, low sodium, as indicated). 8. Discharge planning ("social services for home antibiotic [specify], lab testing [specify], PT. [specify], and wound care [specify]"). 9. Radiographs {specify views, weight bearing status and any special attention items). 10. Other orders, such as supplies to bedside, consultations, physical therapy, notification of the attending internist or general practitioner of the patient's postoperative status, and any other items that are specific to the case at hand.

HOSPITAL DISCHARGE ORDERS Standard discharge orders may include: 1. 2.

3. 4. 5.

Discharge _ _ (specify when, or "at-the discretion of" whomever). Dispense written and oral postoperative instructions (separate form detailing activities, medications, home or special care, problems to be aware of or on the look out for, follow-up appointments, home health care, etc.). Dispense prescriptions (specify). Ambulatory status (specify). Other pertinent items.[AEDl]

296

Index

A Abdomen 120,127

Abduct 234 Abduction 70, 106-9, 112, 176, 214,217,232, 234-5,174,276-7 Abductor digiti quinti 6, 13 hallocis 6, 13, 16, 18,130,191,208-9,231-2,

234-5, 237-8,255 Abductor hallucis muscle belly 208 recession 231-2,235,238 Abductorha!lucis Medial 13 Abductus 106,114,171,176,189,192,217,

225-7,232,234, 259 pes 225-7

ABIIANKLE-BRACHIAL INDEX) 53-4 Ablation 60, 72, 138 Absorbable fixation 148,170

Absorbable suture 123, 177,207, 209,246,277 Absorption, primary bone callus 25 Accommodative foot orthoses 161, 223 Achilles 11,102,202-4,207,209,237,241,255 tendon 11, 13,113,129-30,135,154,198,

201-5,207, 213, 238,241,254-5, 272 Acid fast 41,100-1 uric acid 63-4,97,99

Acidosis 60, 85, 95, 99 ACLS (Advanced Cardiac Life Support) 82,

85-7 Acral lentiginous melanoma 75 Acrallentiginous melanoma (ALM) 75 Acromegaly 39, 99

Actinic 39 Activities of daily living (ADLs) 283 Acute adrenal crisis 83 Acute gouty arthritis 63-4,99 Acute metatarsal fracture 258 Addison's disease 83, 99 Adduct 196 Adduction 70,106-9,161,166,172,191,193,

214-9,232, 235, 237, 239-40, 274,276-7 Adductor canal 17,32 halluc is 6, 8, 13, 17, 175,255 tendon 175 Adductovarus 112~3, 166,196 Add actus 106,112,114,172,179,183,191,215,

217, 225, 232, 234-7, 240, 242 Adenopathy 38, 59, 76, 81 Adherent 12,58 Adhesion 67,111,127,141,185 Adhesive skin strips 124-5 Adjacent metatarsal fracture 262

Adjunct procedures 176-7,192,195-6,220,288 radiation 72, 74, 79 ADLs (Activities of daily living) 283 Administration 31, 45, 55, 58, 60, 81-6, 88, 93,

118, 122, 160, 244, 248, 256 Admission 46,294 Adnexae 33 Adrenal 83-4,158 Adrenergic 31,53 Advanced cardiac life support (ACLS) 86-7 Aerobic 40-1,46,67,100,116,282 Aerosol bronchodilator 82 Aftercare 139, 142, 144, 146, 225 Age 37-8,42-3,56, 65-6,69,72,74-5,80, 107,

112,131,158,165,171,202,205,214-5,213, 232-3, 235, 237, 239-43, 254, 261' 272, 288 Agents 31,47-9,54, 82,157-60 Agglutination 62-3, 96 Agranulocytosis 159 AHO (Acute Hematogenous Osteomyelitis) 42 AIDS (Acquired Immunodeficiency Syndrome)

51-2, 74 Aigner's syndrome 35 Aiken-Mueller Epiphyseal Plate Fracture Classification Systems 281 Ainhum 34,38 Airway 81-2,84-7,118,244,248 obstruction 84-5 Akin osteotomy 176-7, 187, 232 procedure 176 Albumin 63, 100 Alcohol withdrawal 84 Alcoholic keratosis 34 Alkaline phosphatase 79,80, 99,100 Allergen 36,81-2 Allergic 35-6,38, 81 Allergy 95,157,189,258 Allodynia 70, 255 Allogeneic 127,131-3,217-8,227,273 Allograft 131,133 Alloimplant 131 Alloimplants 131,133 Allopurinol 37,64 ALM (Acrallentiginous melanoma) 75 Alopecia 36 Ambu bag 87 Ambulation, early 57 American College of Foot and Ankle Surgeons

285, 291 Amide 85,157-8 Aminophylline 82 Amphotericin-8 48 Ampicillin 49-51 Amputation, transmetatarsal 211,213

Podiatry Institute Manual

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