ORTHO NOTES BY JOACHIM & LIYANA (EDITED BY WAI WAI)
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TABLE OF CONTENTS NO. 1
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TITLE
INTRODUCTION TO ORTHOPAEDICS
• History-Taking • Analgesics Ladder (by WHO) • Post-Op Management (fever/oliguria/dyspnoea/shock) • Plaster Techniques FRACTURES – GENERAL PRINCIPLES*** • Definitive treatment • Open Fractures • Emergency Care • Irrigation & Debridement • Stabilisation of Fracture • Wound Coverage • Delayed Union & Non-Union • Management of Bone Loss • Fracture Healing • Compartment Syndrome • Avascular Necrosis • TipBits for Fractures SHOULDERS • Approach to Shoulder Problems • Rotator Cuff Impingement • Calcification of the Rotator Cuff • Biceps Tendonitis • Rupture of Biceps Tendon • Frozen Shoulder*** • Shoulder Joint Instability & Dislocations • Other Disorders of the GH Joint • Disorders of the Scapula • Fractures of the Clavicle • Fractures of the Scapula • AC Subluxation/Dislocations • SC Dislocations ARM • Fractures of the Proximal Humerus • Fractures of the Shaft of Humerus • Fractures Around the Elbow in Children • Fractures & Dislocations Around the Elbow in Adults
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ELBOWS & FOREARMS
• Cubitus Varus (Gunstalk Deformity) • Cubitus Valgus • Rheumatoid Arthritis • Osteoarthritis • Olecranon Bursitis • Tennis Elbow (Lateral Epicondylitis)** • Golfer’s Elbow (Medial Epicondylitis)** • Cubital Tunnel Syndrome** • Supracondylar Fractures • Elbow Dislocations • Medial Condylar Injury • Radial Head Fracture • Radial Neck Fracture • Forearm Fracture/Dislocations • Nightstick Injury • Causes of Tardy Ulnar Nerve Palsy HANDS & WRISTS • Types of Cases • DDx of Painful Elbow & Hand • Hands o Acute Infections o Skin o Muscle/Tendon Disorders o Lumps • Wrists o Joint Disorders o Lumps o Muscle/Tendon o Nerves • Hands & Wrists o Rheumatoid Arthritis o Osteoarthritis o Bone Disorders Colles’ Fracture Smith’s Fracture Scaphoid Fracture Complications of Wrist Fractures Lunate Dislocation Perilunate Dislodation Scaphoid Dislocation o Brachial Plexus Lesions o Zones of the Hand
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HIP
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51 Pelvic Fractures Approach to Hip Pain Congenital Dislocation of the Hip (CDH) / Developmental Dysplasia of the Hip (DDH) Hip Dislocation Perthes’ Disease (Coxa Plana) Slipped Capital Femoral Epiphysis (SCFE) Pyogenic Arthritis Transient Synovitis TB Hip RA Hip OA Hip AVN of the Hip*** Proximal Femoral Fractures – Summary
• • • • • • • • • • KNEE • Knee – DDx • Common Knee Symptoms • Meniscal Tears • Meniscal Cysts • Chronic Ligamentous Instability • Osgood-Schlatter Disease • Osteochondritis Dessecans • Patellar Fracture • Recurrent Dislocation of the Patella • Patellar/Quadriceps Tendon Rupture • Dislocated Knee • Chondromalacia Patellae • OA Knees*** • RA • Baker’s Cyst (Popliteal Cyst) • Housemaid’s Knee (Prepatellar Bursitis) • Clergyman’s Knee (Infrapatellar Bursitis) • Semimembranous Bursa • Charcot’s Joint TIBIA • Tibial Plateau Fracture • Tibial Diaphysis Fracture ANKLE • Evaluation of Ankle Complaints
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• • • • FOOT • • • • • • • • • • • • • SPINE • • • • • • • • • • • • • •
Danis Weber Classification Lauge Hansen Classification Ligamentous Injuries Recurrent Knee Subluxation Evaluation of Foot Complaints Congenital Talipes Equinovarus (Congenital Club Foot) Hallux Valgus Ruptured Tendo Archilles Hallux Rigidus Pes Planus Footballer’s Ankle Archilles Tendonitis Talar Fracture Calcaneal Fracture Plantar Fasciitis Bunions Metatarsal Fracture
Approach to Back Pain Prolapsed Intervertebral Disc (PID) Scoliosis Adolescent Idiopathic Scoliosis Lumbar Spondylosis Spinal Stenosis Spondylolisthesis Cauda Equina Syndrome PID vs. Spinal Stenosis Lumbar Spine Fractures Cervical Myelopathy Cervical Spondylosis Cervical Lesions Cervical Spine Trauma DM FOOT (ORTHO) POLYTRAUMA FRACTURES BONE & JOINT INFECTIONS • Acute Haematogenous Osteomyelitis • Subacute Haematogenous Osteomyelitis
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• Post-Traumatic / Operative Osteomyelitis • Chronic Osteomyelitis • Acute Suppurative Osteomyelitis • TB OSTEOPOROSIS*** RHEUMATOID ARTHRITIS*** ANKYLOSING SPONDYLITIS GOUT*** BONE TUMOURS & CYSTS (OSCES-ORIENTED) PAEDIATRIC ORTHOPAEDICS • Fractures o Ossification Centres o Ligamentous Laxaties • Congenital, Developmental & Physiological Conditions o Torticollis (wry neck) o Approach to Limping Child o DDH o Clubfoot (Congenital Talipes Equinovarus) o Flatfeet (Pes Cavus) o LL malalignment o Scoliosis o Cerebral Palsy (CP) IMPORTANT CLASSIFICATIONS FOR ORTHOPAEDICS DISEASE MNEMONICS
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INTRODUCTION TO ORTHOPAEDICS
HISTORY TAKING
PRESENTING COMPLAINT Pain - SOCRATES - For timing/frequency o Early morning pain – hallmark of inflammation o Relieved at night – often mechanical in nature o Night pain – indicates severity of pain, ?underlying malignancy - For relieving factors: include analgesics & TCM For upper limb Activity - Hand dominance Loss of function – for lower limb - Washing, dressing, combing, - Going to shops feeding, writing - Use of walking aids (community ambulant?) - Use of chopsticks (assess fine o Any lift landing? motor skills) - Walking distance - Use of stairs Also assess pre-morbid ADL status (dressing, eating, ambulating, toileting, hygiene) Specific to lumbar spine - History of injury - Radiation of pain (look for dermatomal distribution) - Associated neurological symptoms (numbness/paresthesia) & their distribution - Any sphincter disturbance (bladder & bowel symptoms secondary to cauda equina syndrome)
PAST MEDICAL HISTORY - Comorbidities (fitness for op) - Medication history - Any drug allergies SOCIAL HISTORY - Alcohol/smoking - See ‘activity’ - Any caregiver support SYSTEMIC REVIEW - Any recent history of trauma/falls - The usual systemic review questions (especially to rule out extra-articular manifestations of certain diseases such as rheumatoid arthritis) - Red flags for lower back pain o Metastasis: LOW, LOA, night sweats, history of malignancy, night pain o Infection: fever, history of TB / toe gangrene o Neurological deficits: BO, PU (continence), whether neuro deficits are progressive o History of trauma o Hairy patch / cafe-au-lait spots (especially in paediatric population)
ANALGESIC LADDER (BY WORLD HEALTH ORGANISATION) •
Mild pain: Step 1: Simple analgesics (non-opioid) o Initiate topical and/or simple oral non-opioid analgesics (e.g. paracetamol, NSAIDs) o + adjuvant e.g. tricyclic antidepressants, anticonvulsants (pregabalin or gabapentin) for neuropathic pain.
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Moderate pain: Step 2: Weak opioid o Weak opioid (e.g. tramadol, codeine phosphate or dextropropoxyphene) o + adjuvant e.g. tricyclic antidepressants, anticonvulsants
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Severe pain: Step 3: Strong opioid o Opioids (e.g. morphine, oxycodone) o + adjuvant e.g. tricyclics, anticonvulsants
Specific to the hip - Stiffness & pain arising from hip joint - Whether patient is able to care for their feet / pedicure Specific to the knee - Locking (due to jamming by torn meniscus or loose body) - Giving away (due to patellofemoral problem, loose bodies, torn flap of meniscus, ligamentous laxity) Specific to the feet - Back pain (referred pain) - Pins & needles (lumbar spine pathology/nerve entrapment/peripheral neuropathy) - Footwear
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POST-OPERATIVE MANAGEMENT 1. 2. 3. 4. 5. 6. 7.
then reabsorbed, with collapse of the supplied lung segments, usually the basal lobes. The collapsed lung may become secondarily infected by inhaled organisms.
Life Threatening – vital signs Limb Threatening – circulation Post op pain Post op urine output Post op nutrition Rehabilitation – independent, dependent in ADL, WB Discharge Days 3-5
Postoperative Management Related to Surgery 1. Postop consciousness – post sedation and anaesthesia, CVA, hypoxia, hypovolemia 2. Post op airway – aspiration, pneumonia 3. Post op circulation - Hypovolemic shock, PE/DVT 4. Local circulation - , vascular injury or compromise, Compartmental symptoms 5. Nerve compression 6. Post op GI 7. Postop urine 8. Postop fever 9. Post op wound infection
Post-Op Fever Days 0-2
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mild pyrexia o tissue damage and necrosis At the site of the operation o haematoma higher persistent pyrexia o postoperative atelectasis o specific infections related to the surgery biliary infection after biliary surgery urinary tract infection after urological surgery
Note that fever due to blood transfusion may occur in this initial post-op period. Postoperative atelectasis generally occurs within 48 hours. It is an extremely common post-operative complication with some degree of pulmonary collapse occurring after almost every abdominal or trans-thoracic procedure. Mucus is retained in the bronchial tree, blocking the finer bronchi; the alveolar air is
Predisposing factors • obesity • smoking • wound pain • opiates and drowsiness • pregnancy • muscular weakness • nasogastric tube • abdominal distension • bronchopneumonia • developing sepsis, which may be: o wound infection o drip site or drain infection o abscess formation, e.g. subphrenic or pelvic, depending on type of surgery performed. Indications for prophylactic antibiotics • patients at risk of subacute bacterial endocarditis, for example with mitral valve disease or prosthetic valves • patients undergoing prosthetic joint or vascular components • operations which involve contamination to some extent, for example colon or oesophageal resection • patients who have some other type of indwelling prosthesis, for example total hip replacement As a general rule prophylactic antibiotics should be given in the perioperative period and then discontinued. It is best if the first dose can be given on induction of anaesthesia. Prolonged administration of antibiotics is accompanied by undesirable side effects, such as the emergence of antibiotic resistant organisms, or the development of pseudomembranous colitis; it is for this reason that duration of therapy should be stated. Postoperative wound infection Postoperative wound infection is a potentially hazardous complication of surgery. It is important to consider the risk of it occurring, and to give prophylaxis if appropriate. Risk factors - senility, diabetes, ischaemia, malnutrition, vit C & Zn deficiency - steroids and cytotoxic drugs, radiotherapy - long preoperative hospital admission - shaving the operative site the night prior to surgery - rough handling of the tissue - poor blood supply, for example sutures too tight
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failure to debride devitalised tissues large dead space contamination of wound
Wound irrigation • removal of foreign bodies • reduction of pathogen numbers • removal of blood, clot and dead tissue • removal of free cancer cells • moistening of tissue
Days 5-7 >7 days
The solution used to irrigate may be: • physiological saline; its low osmolarity may aid in free tumour cell lysis • topical antiseptic, e.g. chlorhexidine and iodine; both may cause undesirable cell death of host tissue. Alternatives include spraying dry povidone-iodine spray onto the wound - this has been shown to reduce infection rates - or local injection of antibiotic peroperatively. • venous thrombosis, in the limbs or pelvis • causes related to specific op’s, e.g. failure of bowel anastomosis with fistula formation & leakage Causes are less likely to be directly related to the specific operation undertaken. Causes include:• wound sepsis • distant sites of sepsis eg cerebral or hepatic abscess • thrombotic disease • postoperative atelectasis • postoperative pneumonia • wound infection • intravenous phlebitis • urinary tract infection • prostitis • gout • central line sepsis • parotitis • drug reaction • transfusion reaction o non-haemolytic transfusion reactions o febrile transfusion reactions • complications of specific operations, for example pericarditis after cardiac surgery
IN SUMMARY • wind -- atelectasis within 48 hrs, aspiration, pneumonia • water -- UTI's, especially if catheterized • wound -- check for wound infection. • veins -- (OK, it's a "V") DVT, phlebitis from IV's • drugs -- drug reactions (uncommon) Fever within 48 hours is usually atelectasis. After 48 hours, atelectasis is less likely. After 5 days:
wound infection intraabdominal abscess (CT abdo and pelvis) DVT
Post-op Dyspnoea 1. Atelectasis -- usually within 48 hours, more likely in elderly, COPD, smokers, obese patients, and those with upper abdominal incisions. Treatment is to mobilize, encourage deep breathing and coughing, chest physiotherapy 2. Aspiration -- risk factors include GERD, food in the stomach, intestinal obstruction, and pregnancy (delayed gastric emptying). Prevent via preoperative fasting in elective patients, 'rapid sequence" induction in emergency patients, and those at high risk. 3. Pneumonia -- atelectasis, aspiration and copious secretions are predisposing factors. Often gram-negative, and or polymicrobial. 4. Heart failure -- caused by fluid overload in patients with limited myocardial reserve, post op MI, or dysrhythmias (most commonly a fib). 5. Pulmonary embolus -- most clinically significant pulmonary emboli arise from the iliac and femoral veins.
Post-Op Oliguria • Pre-renal -- COMMONEST CAUSE OF LOW URINE OUTPUT o external fluid loss (hemorrhage, dehydration, diarrhea) o internal, third space loss -- bowel obstruction, pancreatitis • Renal -- nephrotoxic medications o Untreated pre-renal causes leading to acute tubular necrosis • Post renal -- prostatic hypertrophy, blocked foley, stone in solitary kidney
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Post-Op Shock Basic haemodynamics: CO = SV x HR Recognising shock o Easy signs to find: Urine output • The best CVP is if you see pee • Think Foley Blood pressure Skin temperature Mental status Drain saturation o Lab investigations FBC • Serial FBC for any patient with bleeding risk Lactate BUN / Cr Coagulation profile Electrolytes (specifically bicarb) Resuscitation fluids o No evidence to show that one type of fluid is superior to another in resuscitation o Ensure that you use enough crystalloid. General principles o Resuscitation with appropriate and enough fluids o Give blood if bleeding or evidence of oxygen delivery problem o Pressors to mitigate hypotension o Stress dose steroids if indicated o Intensive insulin o Normothermia Hypovolaemic shock o Bleeding Think about the surgery and everything that could go wrong • Surgical bleeding vs. postoperative “oozing” Support with fluids and blood products. Treat hypothermia
Inadequate resuscitation Patients are NPO for several hours prior to surgery Patients with intraabdominal processes (especially infection and SBO) have tremendous fluid losses. The best prevention of postoperative resuscitation problems is preoperative resuscitation. Post-op septic shock o Utilize Rivers goal directed protocols (N Engl J Med 2001; 345:1368-1377, Nov 8, 2001 ) CVP 8-12 Urine output > 0.5 cc/kg/hr SvO2 > 70 • Hgb to 10, Dobutamine MAP>65 • Norepinephrine or Dopamine Post-op cardiogenic shock o Patient may not complain of chest pain although there may be clues on exam. o EKG/Echo/Swan/enzymes, etc. o Must weigh risk of bleeding (ASA, thrombolytics, cath) vs. benefit Usually benefit of treating heart outweighs risk o Inotropic support Abdominal compartment syndrome o Post op laparotomy patients can be at risk for this as well as cirrhotics o EASY to measure. Basically stick a foley catheter to a CVP monitor o Abnormal is over 20 cm water. Dangerous over 30. o Treatment is decompression o You only find it if you THINK about it. Summary o Resuscitation, resuscitation. o Think about hypovolemia o Think about bleeding. o Think about sepsis. o Think about abdominal compartment syndrome o Get an EKG in high risk patients. o And remember… The best treatment is PREVENTION o
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PLASTER TECHNIQUES Basic Principles 1. One joint above and below the fracture 2. Cast is well molded with no pressure points 3. Always place a backslab/U slab even if patient is just admitted for pain control. 4. All hand fractures have a standard functional hand position cast Indications • Fractures that can reduced and be stably maintained • No major soft tissue injury • No suspicion of compartment syndrome • No vascular compromise Types of Plaster Casting » Forearm U slab: Forearm fractures » Shoulder U and O slab: Proximal and midshaft humerus fractures » Intrinsic plus hand slab: Hand fractures » Above knee cylinder slab: Knee injuries » Above knee slab: Tibia/Fibula fractures » Below knee slab: Ankle fractures
FRACTURES—GENERAL PRINCIPLES Mechanism: remember the process leading to the fracture • Traumatic • Pathologic – remember O M I T: osteopenia/osteoporosis, metabolic bone disease (hyperparathyroidism, hyperthyroidism, osteogenesis imperfecta, rickets), infection, tumour • Stress – repetitive mechanical loading, periprosthetic CLINICAL FEATURES OF FRACTURES • Pain and tenderness • Loss of function • Deformity • Abnormal mobility and crepitus (avoid) • Altered neurovascular status (important to document)
INITIAL MANAGEMENT • ABCDEs • Limb - attend to neurovascular status (above and below) • Rule out other fractures/injuries (especially joint above and below) • Rule out open fracture • Take an AMPLE history - A llergies, M edications, P ast medical history, L ast meal, E vents surrounding injury • Analgesia • Splint fracture - makes patient more comfortable, decreases progression of soft tissue injury, decreases blood loss • Imaging RADIOGRAPHIC DESCRIPTION OF FRACTURES • Rule of 2s • 2 sides: bilateral • 2 views: AP and lateral • 2 joints: above and below the site of injury • 2 times: before and after reduction • Identify view + date + patient identification (“This is an AP X-ray view of the knee joint taken on 1/12/10 for Mdm. Gee”) • Anatomy • Which bone • If diaphyseal decribe by thirds : proximal/middle/distal • Type spiral # - rotational force, low energy (# line > 2x bone width) oblique # - angular and rotational force transverse # - direct force, high energy comminuted # (> 2 pieces) - direct force, high energy compression # avulsion # - strong muscle inserting into small bone e.g. quads to patella, triceps to olecranon, peroneus tertius to 5th metatarsal head butterfly # - 2 lines break out obliquely from point of contact of blow producing a free-floating ‘butterfly fragment’ • Articulation • Extra-articular: diaphysis/metaphysis • Intra-articular salter-harris classification (for children) • Apposition (% displacement) – any shortening? [i.e. bayonet #] • Angulation • Apex • Associated structures (aka soft tissue): calcification, gas, foreign bodies 8
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DEFINITIVE MANAGEMENT • Goals – “Obtain and Maintain Reduction” • reduce • stabilize • rehabilitate • Attempt closed reduction • if successful Then stabilize • if unsuccessful Open reduction Then stabilize-- usually internal fixation • Rehabilitate Reduction • Is reduction necessary? • may not be for clavicle, fibula, vertebral compression fractures • reduce when amount of displacement is unacceptable • imperfect apposition may be acceptable while imperfect alignment is rarely acceptable • Closed when possible • Closed reduction » Minimise damage to blood supply » Rely on soft tissue attachments » Rarely adequate for intraarticular # » Difficult in babies whose bones cannot see in X-ray • Open reduction: indications – remember NO CAST
N - N on-union O - O pen fracture C - neurovascular C ompromise A - intra- A rticular fractures (require anatomic reduction) S - S alter-Harris III, IV, V and/or special situations depending on site T - poly T rauma Others failure to reduce using closed reduction cannot cast or apply traction due to site (e.g. hip fracture) pathologic fractures fractures in paraplegics for nursing access potential for improved function with ORIF infection new fracture through screw holes implant failure
Stabilization Stabilize the fracture site but do not completely immobilize the limb if possible External stabilization 1. splints/tape 2. casts 3. traction 4. external fixator
Non-rigid fixation – risk of loss of reduction but stimulate rapid callus formation
Rigid fixation –
Internal fixation immediate loading but 1. percutaneous pinning (Kirschner or K-wires) does not stimulate callus formation 2. extramedullary fixation (screws, plates, wires) 3. intramedullary fixation (rods) - biomechanically advantageous Rehabilitation • To avoid joint stiffness • Isometric exercises to avoid muscle atrophy • Range of motion (ROM) for adjacent joints • Continuous Passive Motion (CPM) following rigid fixation of fracture allows joint motion to prevent stiffness for intra-articular fractures • After cast/splint removed and fracture healed resistive muscle strengthening • Evaluate bone healing (clinical, x-ray)
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OPEN FRACTURES EMERGENCY! • Definition: A fracture or its haematoma that communicates with the environment. • Gustilo-Anderson Classification of Open Fractures*****
Superficial to deep
Laceration <1cm long
Soft tissue Little damage, no crush
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1-10cm
IIIa
>10cm
Moderate crushing, no flap/avulsion Extensive damage to skin, muscle, neurovasculature
Fracture Usually transverse, short oblique, little comminution Moderate comminution
Contamination Clean puncture (compound from within)
Comments Simple # [5% chance of amputation]
Moderate contamination
Butterfly # [10% chance]
Extensive comminution & instability
Severe contamination
Adequate soft tissue coverage (NOT SKIN) despite extensive laceration/flaps - Segmental # (= # at 2 levels) - Farm injuries / any injury occurring in a highly-contaminated envt - GSW [20% chance] IIIb Extensive soft tissue injury/loss Periosteal stripping & exposure of bone [30% chance] IIIc Any open # a/w arterial injury that requires repair regardless of wound size/soft tissue injury Prophylactic fasciotomy always done to prevent post-op compartment syndrome [>40% chance] NB. can only differentiate Gr III into a, b and c ONLY AFTER SURGICAL INTERVENTION (i.e. debridement)
More energy, higher velocity trauma
Gr I
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EMERGENCY CARE
Sterile scrub: use scrubbing brush and scrub the site to debride all necrotic tissues (dead muscle/fat/other tissues) --- how to tell if muscle is dead or not? 4C’s Dead Live muscle muscle Consistency Mushy Turgid Colour Pale pink Pink/bright red Contraction (most important) Absent Present Capillary No bleed Bleeding
Repair vascular injury if present (i.e. re-anastomose the vessels) For crushed injuries involving both vascular & nerve injury amputate Remove comminuted fragments (anything that’s dead and without soft tissue attachments discard) Wash with 10L of saline (to dilute bacterial load) Take wound cultures at the end of the procedure THEN reduce THEN maintain • External fixation preferred – can be temporary (for 2/52 until you’re sure there’s no infection at site, then internal fixation) or permanent (for 3-6 months until # unites) • Disadvantage of internal fixation: must strip soft tissue :. Avoided for grade 2 & above • Disadvantage of intramedullary nail: may spread infection (even though in this case needn’t strip soft tissue) Wound usually left open to drain 48h later, • ‘relook operation’ – see if repeat I&D is necessary • Ensure soft tissue coverage over exposed area by 48th hour – exposed tendon will not survive for long... Need flap! 4-6 weeks later: bone graft/transport THEN skin graft (after swelling subsides; if not, compartment syndrome may occur after grafting)
Approx. 30% of patients with open fractures are polytrauma patients who have suffered damage to 2 or more systems. Manage according to ATLS. Only manage the fracture when the patient is stable. [In grey: for open #s] 1. ABCDE 2. Neurovascular status of the limbs (above & below) Control any haemorrhage with direct pressure. Set IV line & start IV fluids. Don’t reduce any # unless there is apparent neurovascular compromise from position of #. Dressings & splints that might have been put on at the accident site should be removed partially to assess soft tissue conditions and neuromuscular function. All sterile wound dressings should be left in place because redressing wounds in the emergency room increases the infection rate 3. Any other #/injuries (above & below) – remove gross debris, i.e. turf, rocks 4. Rule out open # 5. Take an AMPLE Hx 6. Analgesia – 75mg I/M pethidine 7. Start IV antibiotics [after wound c/s samples are taken] in all open # during the first 3-5 days (empirical NOT prophylactic!) Use broad spectrum antibiotic (e.g. 1st generation cephalosporins); in grade 3 #, add gentamicin +/- metronidazole, and monitor for toxicity. 8. Tetanus toxoid booster (TTB) – 0.5mL Human anti-tetanus immunoglobulin (HATI) – 250 units Simple wound Tetanus-prone wound Full course + booster within TTB 10y Full course + booster 10y ago TTB TTB + HATI Non-immunised / unknown TTB TTB + HATI 9. Splint – to decrease pain, progression of soft tissue injury, blood loss 10. Imaging (X-rays) 11. NBM and prepare for EOT Must get into OT within 6h (‘golden hours’) since risk of infection increases after this time Done under LA/GA
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Complications of open #s • Bone » Osteomyelitis » Mal-union (NB. healing will always take place, it’s only a matter of how good the healing is) » Non-union (healing has ceased, both pieces not united by 6 months) Certain bones are prone, e.g. tibia (due to poor muscle coverage), scaphoid, NOF (due to poor blood supply) Also depends on severity of injury Types • Hypertrophic: insecure fixation / premature wt bearing • Atrophic: poor blood supply, ends osteoporotic (e.g. in DM, vasculopathy, infection, sig tissue damage) --- Mx: open decortications & cancellous bone graft » AVN » Arthritis • Regional » Neurovascular injury » Soft tissue blisters Types: haemorrhagic and non-haemorrhagic Mechanisms of injury: shearing of skin (may become infected if operated on), ischaemia (can be due to compartment syndrome!) » Compartment syndrome***** » Complex regional pain syndrome 1 » Heterotopic ossification » Joint stiffness • Systemic » Hypovolaemic shock » Fat embolism » Venous thrombo-embolism (DVT/PE) from immobility » Multi-organ dysfunction syndrome » ARDS (especially in polytrauma patients)
Local
System -ic
Hemorrhagic shock Sepsis Fat embolism DVT / PE ARDS
Late Malunion Nonunion AVN Post-traumatic arthritis Osteomyelitis Heterotopic ossification Growth disturbance in children Joint instability Joint stiffness Nerve compression /entrapment Reflex sympathetic dystrophy (RSD) Multi-organ failure Renal failure Shocked lung PTSD, depression
IRRIGATION AND DEBRIDEMENT •
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NB. Can also be classified as early & late complications 1
Complex Regional Pain Syndrome (CRPS): a chronic pain state induced by Soft tissue / bone injury (CPRS I aka reflex sympathetic dystrophy aka Sudeck’s atrophy) Nerve injury (CPRS II aka causalgia) In which pain is a/w autonomic changes (e.g. sweating or vasomotor abnormalities), and/or trophic changes (e.g. skin/bone atrophy, skin loss, joint contractures). Aetiology unknown. Treatment: no cure; pain relief only.
Early Neurovascular injury Swelling Compartment syndrome Infection Implant failure Soft tissue blisters (infection)
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Irrigation and debridement (most important steps in treatment of open #) • To be done within 8h of the injury, otherwise wound is considered infected. • Done in the OT under LA/GA • Only now are all the splints and bandages removed • Reexamine thoroughly for neurovascular function. Fluids are delivered under pressure and under a pulsed system to remove any blood clots and foreign bodies. • Isotonic saline or water is used for irrigation. • Dilutes the degree of bacterial contamination. Repeat the irrigation at regular intervals once the wound is open as there is a higher chance of removing contaminated material. • Ensure that the whole wound is exposed to the fluids. • There is a debate as to the usefulness of adding antibiotics to the fluids. If proper debridement is done then only vascularised tissue should remain and adequate tissue levels can be achieved with systemic antibiotics. However, some studies have shown lower infection rates with added antibiotics. Ultimately, the effect of irrigation is still mechanical. Ensure wound incision is large enough to facilitate exposure and inspection of wound site, including the joint. 12
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Meticulous removal and resection of all foreign and dead material from the wound. • All non-viable, mutilated or macerated skin removed. Dead, frayed skin edges are excised. Skin colour is a good determinant of viability of skin. When a cut skin edge does not bleed then it is dead. • Fasciae are expendable so it can be safely removed without fear of functional deficit. • Difference between dead & live muscle (see ‘emergency care’) • Free fragments of bone are removed. Fractured bone ends must be exposed so that they can be cleaned with brushes or removed. Exposed tendon will not survive for long. Early skin coverage, skin grafting or a muscle/skin flap may be necessary to preserve its viability. Wound cultures should be taken at the end of the procedure.
STABILISATION OF FRACTURE •
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Immobilisation of the fracture is crucial for the healing of soft tissue and bone. • Stabilisation prevents further injury to the surrounding soft tissue, limits intensity and duration of inflammatory response, diminishes spread of bacteria, facilitates tissue perfusion and encourages early wound repair. • Should still provide free wound access for repeated debridement and placement of local or distant flaps and bone grafts. • Should not interfere with blood supply of fracture segments and should be sufficiently rigid to allow early joint motion and at least partial weight bearing. Slings, splints, casts and traction may be used as definite care of simple grade I and grade II injuries and as temporary methods for more complex fractures. Slings can be used in fractures of humeral shaft or to provide additional support for internally or externally stabilized forearm lesions. Splints can provide initial stabilization of fractures below the elbow and knee. Circular castshave no place in early Mx as they cannot accommodate swelling. • May prevent the detection of further soft tissue damage, circulatory impairment and/or increase in compartment pressures. Casts can be used as subsequent care of stable grade 1 and 2 tibial fractures after the wound is closed and swelling subsided. • Can also be used as a secondary method of immobilization after removal of an external fixator. Traction may be indicated for pelvic fractures, acetabular lesions and femoral fractures. But rarely used in the upper extremity. External fixation is indicated for most contaminated grade 3b and c fractures.
Advantages: 1) No foreign material in the wound. 2) Applied without any additional soft tissue dissection. 3) Provides easy access to the wound 4) Easily dismantled if further debridement needed. • Disadvantages: 1) Potential for pins to injure neurovascular structures and tie down muscle-tendon units interfering with joint motion and rehabilitation. 2) Possible interference of the pins in reconstructive procedures as well 3) Pin loosening 4) Secondary infection. • Usually removed or replaced by casts, braces or internal fixation as soon as soft tissue lesions have healed. Internal fixation provides excellent stabilization, allows early limb and patient mobilization and facilitates fracture consolidation while preventing malalignment. • However, procedure requires additional exposure and can cause partial loss of periosteal, cortical or intramedullary blood supply ↑es risk of infection. Screws are usually used in combination with a plate or external fixator for intraarticular and peri-articular fractures. Plates may be used in treatment of less severe diaphyseal, periarticular and intraarticular fractures of the upper limb. In the LL, plates are useful around joints. However, they must be covered well. Intramedullary nails are used for femoral fractures. They may be used as a secondary method after external fixation but carries a risk of infection. Therefore contraindicated if there is a history of local or pin track infection. Recent studies show that internal fixation for femoral shaft fractures and even tibial shaft fractures result in faster union times as well as decreased risks of reoperation, malunion and superficial infection. External fixation has also shown to be associated with severe pin track infection, longer union times and a higher number of surgical procedures to promote union. •
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WOUND COVERAGE •
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The timing of wound coverage is important. • Primary closure of wound associated with significant risk of infection. • Therefore, keep wounds open after initial debridement and decide again at the second inspection. Aim to close the wound within 3-5 days. • Keep moist meanwhile. • Once wound is clean and tissues are viable, delayed primary closure or skin grafts can be done. • Aims of wound coverage: 1) Achieve a safe early closure 2) Avoid nosocomial infection 3) Obliterate dead space 4) Facilitate future reconstruction. Direct closure done for fresh tidy wounds free from infection and contusion. 13
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Skin grafts are transplanted completely by detaching a portion of skin from a donor site and transferring it to a raw bed-- has to achieve a new blood supply within 2-3 days to ensure viability. • Often used as in intermediary measure before a flap. There are 2 kinds of skin grafts. • Partial/split-thickness skin graft consists of epidermis and part of the dermis. Can tolerate less ideal conditions and less vascularity than full thickness skin graft. The donor site must be able to heal spontaneously by epithelialisation and if necessary, more grafts may be taken from the same place. Good for covering large skin defects overlying viable tissue such as muscle, for large size wounds or those of questionable circulation. Grafts contract, have poor growth in children and have abnormal pigmentation. Partial thickness skin grafts are taken from inner thigh or lateral buttock. • Full thickness is composed of the full thickness of the skin. Generally used for fresh, non-contaminated wounds of small size. Full thickness skin grafts are taken from groin or postauricular area, supraclavicular area. Flaps contain a pedicle attachment to the body receiving it’s sustenance via a network of blood vessels. • Because of their own blood supply, they can be used to reconstruct skin and soft tissue defects irrespective of their vascularity. • Choice of flap coverage must take into account patient’s age & needs, location, size & condition of the defect, likelihood of subsequent reconstructive surgery & associated zone of injury, tissues available for the flap. Flaps can be classified as skin, fasciocutaneous, muscle and musculocutaneous. • Used for defects with poor vascular beds such as wounds overlying the tibia, exposed metal plates, bare bones and tendons, bone defects and open joints. Delayed bone or soft tissue reconstruction is proposed, especially if bone graft or tendon transfer is being planned. • An example of a local flap is the gastrocnemius. Used around the knee and proximal third of the tibia, one of the 2 heads of the gastocnemius is used and there must be a functional soleus. The soleus is sometimes used for mid-tibial defects or sometimes even the distal third of the tibia Free microvascular flap is used for large defect. • Helps prevent multiple reoperations. Provide durable coverage of the fracture site, diminishes the infection rate and shortens the healing time. E.g. latissimus dorsi and vertical rectus abdominis.
DELAYED UNION AND NON-UNION • •
•
Delayed union and non-union are common in open fractures. Delayed union is when healing has not advanced at the average rate for the location and type of fracture. I.e. reconstitution of mechanical stability but over a prolonged period of time and with associated morbidity. o Rx: adequate immobilization, internal fixation or even bone grafting. In non-union, there is evidence, clinically or radiologically that healing has ceased. I.e. failure of reconstitution of mechanical stability after appropriate time intervals. o MCQ: commonest site = junction of distal 1/3 and proximal 2/3 of tibia o Can be classified as hypervascular (elephant foot, horse hoof or oligotrophic pattern) or avascular (torsion wedge, comminuted, defect or strophic pattern). o Treated by stable internal fixation, bone grafting, bone transport or free composite tissue transfer.
MANAGEMENT OF BONE LOSS • •
Bone injury occurs during initial injury or from subsequent repeated debridement. Any bone replacement methods should only be done after adequate soft tissue coverage and revascularization.
Bone grafts • Work via 3 mechanisms: osteoconduction, osteoinduction and osteogenesis. • Osteoconduction is the process whereby transferred bone acts as a scaffold for new bone to grow. (+ neovascularisation) • Osteoinduction occurs when undeveloped tissue is transformed to bone by one or more inducing agents. • Osteogenesis is new bone formed from live osteoblasts in the transplanted autograft. Bone transport • Used for large gaps (Ilizarov’s principle of distraction osteogenesis: induction of new bone between bone surfaces that are pulled apart in a gradual, controlled manner. Distraction gives rise to neovascularisation hence stimulating new bone formation.) • A segment of bone is created by corticotomy or osteotomy through normal bone in one of the fragments of the fracture. This segment is transported by wires and new bone forms in the gap by gradual distraction. The segment is moved by 1mm a day. This technique of callostasis allows simultaneous restoration of a bony defect, correction of limb length and deformity, improvement in the condition of local soft tissues and the treatment of infection. 14
Free composite tissue transfer • Example: fibula, which is mainly a cortical bone that provides excellent strength and length for large segmental bony defects. It is used together with muscle and skin with its pedicle. FRACTURE HEALING Normal Healing 1 2
0h Within 8h
3
3-6 wks 6-12 wks
4 5
6-12 mths 1-2 yrs
Hematoma formation. Inflammatory reaction with proliferation of the cells under periosteum and within the medullary cana. Macrophages, undifferentiated stem cells and platelets surround fracture site. Osteoclasts remove sharp edges (thus # more visible on radiographs), Callus forms within hematoma Bone forms within the callus, bridging fragments. Forming woven bone. Consolidation—woven bone is replaced by lamellar bone Normal architecture is achieved through Remodelling
Evaluation of Healing - Tests of Union • Clinical - no longer tender to palpation or angulation stress • X-ray - trabeculae cross fracture site, visible callus bridging site COMPARTMENT SYNDROME
• • •
Venous obstruction Increased venous pressure Constrictive dressing, cast, splint
Diagnosis • Tibial compartments (common) and forearm flexor compartment • may lead to Volkmann’s ischemic contracture • Clinical signs and symptoms • Early Pain out of proportion to injury & not relieved by analgesics** Increases with Passive stretch of compartment muscles Paresthesias Pallor Palpable tense, swollen compartment • Late Paralysis (inability to move limb - late) Pulses are usually still present (CRT normal) •
Compartment pressure monitoring • In unresponsive or unreliable patients • Normal tissue pressure is about 0 mm Hg • Pressure increases markedly in compartment syndromes. • When intra-compartmental pressure rises to within 10-30mmHg of patient's diastolic blood pressure, inadequate perfusion and/or ischemia results • Fasciotomy usually indicated when the tissue pressure rises to 40-45mmHg in a patient who has any signs or symptoms of a compartment syndromeeven if distal pulses still present
Definition • Condition where pressure within an enclosed anatomical compartment rises sufficientto occlude the microvascular circulation causing tissue ischaemia and, if untreated, tissue necrosis. • Intracompartmental pressures over 30 mm Hg or over diastolic pressure requires intervention
Signs of Compartment Syndrome in Anterior Leg and Forearm Anterior leg Volar forearm Fracture Type Tibial fracture Supracondylar (humerus) Weakness Toe, foot extension Finger, wrist flexion Pain Toe, foot flexion Finger, wrist extension Sensory 1st dorsal web space Volar aspect of fingers
Etiology • Fracture, dislocation • Soft tissue damage & muscle swelling • Crush injury • Arterial compromise • Muscle anoxia
Treatment • Remove constrictive dressings • Bivalve casts down to skin and spread open • Place limb at level of heart • Emergency fasciotomy if difference between diastolic BP and compartment pressure is greater than 30 mmHg (treat within 4-6h of onset symptoms) 15
AVASCULAR NECROSIS
TIPBITS FOR #S
Aetiology • Steroid use --- NOT dose related – idiosyncratic • Alcohol • Post-traumatic fracture/dislocation • Septic arthritis • Sickle cell disease • Gaucher’s disease • Caisson’s disease – deep sea diving/the bends • Perthe’s disease • Idiopathic
1. Arm fractures: nerves affected by humerus fracture location ARM fracture: From superior to inferior: Axillary: head of humerus / Radial: mid shaft/ Median: supracondular
AVN Classification Stage Clinical Features X-ray Features 1 Preclinical phase of No plain x-ray abnormality; may be detectable on MRI ischemia and necrosis; no pain 2 Painful Early radiographic changes i.e. fragment appears dense, normal bone contour 3 4
Painful Very painful
Radiographic changes obvious, abnormal bone contour Collapse of articular surface and signs of arthritis on both sides of the joint
Mechanism • Occurs following disruption of blood supply to bone • Occurs especially in those bones extensively covered in cartilage which rely on intra-osseous blood supply and distal to proximal blood supply, e.g. head of femur, proximal pole of scaphoid, body of talus • Results in ischemia • Pathologic changes include resorption, subchondral fractures and loss of cartilage
2. Fractures: principles of management FRIAR: First aid, Reduction, Immobilisation, Active Rehabilitation 3. Forearm fractures: bone in Monteggia vs. Galeazzi "Break the forearm of the MUGR (mugger)": Monteggia=Ulna, Galeazzi=Radius 4. Salter Harris fracture classification Salter Harris, modified to SALTR: • type 1: Slipped epiphysis • type 2: Above the eiphyseal plat • type 3: Lower than the eiphyseal plate • type 4: Through both above and below eiphyseal plate • type 5: Raised epiphysis, as in a compression injury Salter Harris classification utilises visualising long bone distal portion with diaphysis superiorly placed and epiphysis inferiorly placed. 5. Bryant's traction: position BrYant's traction: Bent Y. Patient's body is the stem of the Y lying on the bed, and legs are the ends of the Y up in the air. 6. Differentials for non-union of #s --- you need a SPLINT: • Soft tissue interposition • Position of reduction (too much traction, immobilization, or movement) • Location (eg. lower third of tibia slow to heal) • Infection • Nutritional (damaged vessels or diseased bone) • Tumor (pathological fracture)
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IMPORTANT ORTHOPAEDIC CONDITIONS IN THE SHOULDERS
APPROACH TO SHOULDER PROBLEMS
CAUSES OF SHOULDER PAIN Tendon (rotator cuff disorders)
IMPORTANT HISTORY TO TAKE FOR SHOULDER PAIN - Duration (time course of frozen shoulder – pain and stiffness for first 6 months, less pain but persistent stiffness for next 6 to 12 months, and recovery of joint mobility 18 months after start of symptoms).
Tendinitis Rupture Frozen shoulder
Joint disorders
Glenohumeral arthritis Acromioclavicular arthritis
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Any preceding trauma (frozen shoulder and rotator cuff tear often follow minor precending injury).
Referred pain
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Neck pain – shoulder pain may be due to cervical pathology; shoulder pain is typically located over the deltoid insertion and tip of shoulder, not along the trapezius or neck.
Cervical spondylosis Cardiac ischaemia Mediastinal pathology
Instability
Dislocation Subluxation
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Shooting pains travelling down arm, numbness and/or weakness of hand – indicative of cervical spine pathology or nerve problem.
Bone lesions
Infection Neoplasm
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Pain on lying on shoulder while sleeping.
Nerve lesions
Suprascapular nerve entrapment
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Function of shoulder (see below).
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Diabetes (very important as diabetes is a cause of idiopathic frozen shoulder).
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Heart disease – may result in referred pain to shoulder.
FUNCTIONAL ASSESSMENT IN SHOULDER PROBLEMS - Ability to reach for objects placed in overhead positions - Ability to comb hair - Ability to touch opposite shoulder and back (for personal hygiene)*** - Ability to wear top e.g. shirt, T-shirt, blouse
Think 4 Ss for Shoulder: Stiffness, Stability, Strength, Smoothness Stiffness: Frozen Shoulder, Post-traumatic/post-surgical stiff shoulder. Strength: Rotator cuff tears Stability: TUBS vs AMBRII Smoothness: Subacromial abrasion, primary degenerative joint disease, AVNs, Recurrent dislocations, post-surgery arthritis, RA.
INVESTIGATIONS: No blood investigations are required usually; shoulder X-ray is the most useful invx Important features to look out for on shoulder X-ray: - Narrowing of subacromial space - Bony spur on inferior aspect of acromion or acromioclavicular joint - Calcification of supraspinatus tendon (acute calcific tendinitis) - Narrowing of joint spaces esp. glenohumeral joint - Osseous lesion(s) if any
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SHOULDER PAIN – likely OSCEs scenarios Young
Instability AC joint injuries Impingement syndrome Frozen shoulder (women) – primary cause Rotator cuff tears Degenerative arthritis Frozen shoulder – primary/secondary cause
Middle-aged Old
Rotator cuff Elderly gentleman S: shoulder +/- lateral aspect of arm (confused w radiculopathy) O: insidious/sudden after freq use C: R: none A: T: worse at night E: cannot lie on affected arm S:
Stem Pain
Any preceding trauma
Past medical history + any drug allergies Rule out cervical pathology
Functional assessment
Frozen shoulder Old gentleman / middle-aged lady S: shoulder O: <18months ago C: R: none A: T: E: lying on shoulder while sleeping / night pain because ‘I’m not conscious of where my hands & arms go when I’m asleep’ S:
Shoulder instability Young gentleman S: shoulder O: C: R: none A: T: E: S:
TUBS vs. AMBRII a/w weakness a/w shoulder stiffness a/w stiffness if post-traumatic If yes, check if patient had dislocated shoulder back then any pain before the trauma (patient may already have rotator cuff tear of which the pain was accentuated by the trauma – in which case, surgical outcome may be poorer [attaching fat to bone instead of muscle to bone, hence no function!]) Diabetes Have you been told by (cause of idiopathic frozen shoulder) doctors previously that you have ligamentous laxities? - Shoulder pain typically located over the deltoid insertion and tip of shoulder, not along trapezius or neck - Shooting pains travelling down arm, numbness and/or weakness of hand – indicative of cervical spine pathology or nerve problem Ability to reach for objects placed in overhead positions Ability to comb hair Ability to touch opposite shoulder and back (for personal hygiene) Ability to wear top e.g. shirt, T-shirt, blouse -
Occupation & hobbies, whether those are affected
OTHER DIFFERENTIALS FOR SHOULDER PAIN Tendon (rotator cuff disorders), Joint disorders, Referred pain, Instability, Bony lesions, Nerve lesions What are the important steps in the shoulder exam that you would like to elicit? I would still follow the LOOK, FEEL, MOVE sequence. Rotator cuff Any post-traumatic/post-surgical scars Tenderness Painful arc (tendinitis) Drop arm sign (tear) Difficulty initiating abduction (tear)
LOOK FEEL MOVE
SPECIAL TESTS
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For supraspinatus tendinitis: Jobe’s, Hawkin’s, Neer’s
Frozen shoulder
Shoulder instability
Decreased active AND passive ROM in ALL directions but NO muscle wasting
Apprehension tests for shoulder instability
Describe what you mean by impingement syndrome / frozen shoulder / shoulder instability. Definition
Impingement syndrome “impingement position” where the glenohumeral joint is in abduction, slight flexion and internal rotation -
Site of impingement is usually the “critical area” of decreased vascularity in the supraspinatus tendon 1cm proximal to its insertion into the greater tuberosity
Frozen shoulder Known also as adhesive capsulitis, it is a well-defined disorder characterised by progressive pain and stiffness which usually resolves spontaneously after 18 months.
‘Freezing’ 6-12 weeks ‘Frozen’ 3-4 months ‘Thawing’ up to 18 months
Shoulder instability Shallowness of the glenoid fossa of the scapula & lack of support provided by weak lig (3 GH ligaments—Medial, Inferior, Superior; transverse humeral lig; coracohumeral lig) make the GH joint unstable strength mainly depends on the rotator cuff muscles
Aetiology +/risk factors
Investigations: X-ray
Management
Repetitive rubbing of rotator cuff tendons under coracoacromial arch (coracoacromial ligament forms the roof, runs between coracoid process & acromion) Bone: OA (osteophytes) Tendon: rotator cuff tendinitis (in inflammatory conditions, e.g. RA, gout) Bursa: subacromial bursitis (also in inflamm. conditions)
PRIMARY ADHESIVE CAPSULITIS Idiopathic in cause a/w DM, Dupuytren’s contracture, hyperlipidaemia, hyperthyroidism, cardiac disease Global contracture of the shoulder joint, but maximally in the rotator interval area and around the coracohumeral ligament
Pathogenesis SECONDARY ADHESIVE CAPSULITIS Friction leads to localised oedema and Intrinsic causes Chronic rotator cuff injuries swelling (tendinitis) – “wear” Post-traumatic scarring following Tendinitis is usually self-limiting but injuries at the shoulder e.g. fracture of with prolonged or repetitive the surgical neck, greater tuberosity. impingement minute tears can occur, especially in elderly – “tear” Extrinsic causes Painful disorders resulting in Tears can be complicated by scarring, decreased movements of the shoulder: fibrocartilaginous metaplasia or referred pain from cervical calcification in the tendon Vascular reaction occurs in an attempt radiculopathy, post-hand, wrist or to repair a torn tendon or to elbow surgery, post-MI revascularize a degenerate area. New BVs grow in & calcium deposits are resorbed. This vascular reaction causes congestion & pain. Pain is caused by wear, tear & repair of the tendons! All 3 happen in varying levels across the ages. Usually normal in early impingement X-rays usually normal – useful in +/- erosion, sclerosis or cyst formation excluding other causes of painful shoulder, at the greater tuberosity (insertion of such as infection, post-traumatic stiffness, the supraspinatus tendon) in chronic diffuse stiffness and reflex sympathetic tendinitis dystrophy when patient 1st presents May see calcification of the supraspinatus tendon (incidental and not the cause of pain) May see narrowing of the space between AC joint & humeral head May see signs of AC joint arthritis – osteophytes Aim of conservative treatment is to relieve TENDINITIS pain and prevent further stiffening while Conservative: Eliminate aggravating activity, and waiting for recovery (since natural course avoid “impingement position” is recovery in 12-18 months) Physiotherapy Short courses of analgesia e.g. NSAIDs Analgesia (NSAIDs), H&L (at shoulder Subacromial Hydrocortisone & joint), local heat. Lignocaine / Triamcinolone & Xylocaine injections at subacromial Physiotherapy: joint for pain relief (LA takes effect Repeated circular movement of immediately, lasts 1 day; corticosteroid shoulder Assisted abduction – use towel or takes effect 3-5 days later) rope, loop it over an overhead bar like Surgical Open or arthroscopic subacromial a pulley system, and hold on to each decompression (acromioplasty) end with one hand. Patient uses o Excise coracoacromial downward pull of normal arm to ligament & anteroinferior part passively abduct painful arm of acromion overhead. o Remove acromioclavicular Assisted internal rotation – both hands osteophytes if present gripping either end of a towel slung across the patient’s back diagonally; TEAR the hand on the painful side holds the Conservative Physiotherapy to improve strength lower end while the hand on the Heat therapy normal side holds the end above the shoulder. Patient uses hand on normal Local anaesthesia if necessary side to pull upwards on towel, Surgical If amenable to repair, open or passively internally rotating the arthroscopic cuff repair followed by painful shoulder. subacromial decompression. Especially Wall-crawling – patient uses fingers for young active individuals. With to “crawl” up a wall slowly, complete tears. Partial tears do not increasing flexion movement.
Classification of patients with recurrent shoulder instability: TUBS: Traumatic, Unidirectional (unilateral), Bankart lesion, Surgery. AMBRII: Atraumatic, Multi-directional, Bilateral, Rehabilitation, Inferior Capsular Shift, Interval Closure
To see if dislocation is present upon visit & to see if there is Bankart lesion / Hill Sacks lesion.
Anterior instability For acute dislocations: Manipulation and reduction followed by immobilisation in a bandage or sling for several wks Recurrent dislocations: Indications for surgery include frequent painful dislocation and recurrent subluxation Posterior instability M. strengthening exercises Surgery considered when condition is disabling & there is no gross joint laxity Anterior dislocation M & R with sedation / GA Hippocratic method: increasing traction applied to the arm with the shoulder in slight abduction while an assistant applies firm counter traction to the
19
-
require surgery unless persistent pain or considerable instability. If not amenable to repair, open or arthroscopic debridement of degenerate cuff tissue and subacromial decompression.
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-
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body; e.g. using a towel slung around the chest under the axilla X-ray post-reduction to check position and exclude fracture. Exclude an axillary nerve injury, rotator cuff tear, median, radial, ulnar and musculocutaneous nerve injuries after reduction Rest the arm in a sling for 3 wks, 1 wk for those>30yrs old due to risk of stiffness Avoid abduction and lateral rotation for 3 wks Elbow and finger movements
Posterior dislocation M & R by pulling on the arm with shoulder in adduction followed by lateral rotation while humeral head is pushed forwards. Immobilisation in a sling
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ROTATOR CUFF IMPINGEMENT AETIOLOGY - The cuff is made of subscapularis in front, supraspinatus above and infraspinatus and teres minor behind. - Repeated rubbing of the rotator cuff tendons under the coracoacromial arch (the roof of which is formed by the coracoacromial ligament running between the coracoid tubercle anteriorly to the anterior third of the acromion posteriorly) -
The greatest amount of wear occurs in the “impingement position” where the glenohumeral joint is in abduction, slight flexion and internal rotation
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Site of impingement is usually the “critical area” of decreased vascularity in the supraspinatus tendon 1cm proximal to its insertion into the greater tuberosity
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Vascular reaction occurs in an attempt to repair a torn tendon or to revascularize a degenerate area. New blood vessels grow in and calcium deposits are resorbed. This vascular reaction causes congestion and pain. Pain is caused by wear, tear and repair of the tendons! All 3 happen in varying levels across the ages.
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Contributing factors to impingement Bone: OA thickening of AC joint, osteophytes along anterior edge of acromion Tendon: rotator cuff swelling (in inflammatory disorders such as RA & gout) Bursa: subacromial bursitis (in inflammatory disorders)
PATHOPHYSIOLOGY - Pathological processes can be summed up into “wear, tear and repair” - Friction leads to localised oedema and swelling (tendinitis) – “wear” - Tendinitis is usually self-limiting but with prolonged or repetitive impingement minute tears can occur, especially in elderly – “tear” - Tears can be complicated by scarring, fibrocartilaginous metaplasia or calcification in the tendon - Healing is accompanied by a vascular reaction and local congestion which is painful, and this may contribute to further impingement - Healing is more rapid in younger patients (but also more painful) and less vigorous in the elderly (less pain, chronic tendinitis that doesn’t heal completely). - Deposits of calcium hydroxyapatite appear in the supraspinatus tendon in acute (calcific) tendinitis. Although these calcifications are not painful, the florid vascular reaction which produces swelling and tension causes severe symptoms. The calcium usually resorbs quickly and disappears in a few months. HISTORY (SUB)ACUTE TENDINITIS - Patient <40 years old
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Shoulder pain occurs after a bout of vigorous unaccustomed activity Patient complains of a “painful arc” (60-120 deg) on abducting the arm Complains of pain of increasing severity, reaching a climax after a few days. After which, the pain subsides and shoulder returns to normal.
CHRONIC TENDINITIS - Patient 40-50 years old - Patient has a history of recurrent attacks of subacute tendinitis - Pain settles with medications (NSAIDs) or rest but recurs when doing more demanding activities - Pain characteristically worse at night, and patient cannot lie on affected side - Pain and stiffness restrict daily activities CUFF TEAR - Partial or full thickness tear occurs with progressive fibrosis & disruption of the rotator cuff - Usually >45yo with refractory shoulder pain with increasing stiffness and weakness - Partial tears are hard to detect as they present with painful arc but still normal motion of the shoulder. Patient can abduct the shoulder upon giving LA because pain is the limiting factor usually. Intact tendon fibres provide continuity for vascular ingrowth and repair. - Complete tears occur spontaneously after a sprain or jerking injury of the shoulder, and the patient complains of acute pain and inability to abduct the arm. To distinguish from partial tear: No abduction despite LA. There is little or no reaction and no repair; proxial fibres may retract and become stuck down. PHYSICAL EXAMINATION SIGNS OF SUPRASPINATUS TENDINITIS - Pain at the point of insertion of the supraspinatus along the anterior border of the acromion, best felt with the arm held in extension - Painful arc: Pain on active abduction between 60 and 120 degrees of motion, with disruption of scapulohumeral rhythm. - Impingement sign: Pain elicited when affected arm is passively flexed, abducted and internally rotated (the greater tuberosity is brought under the coracoacromial arch impinging the supraspinatus) - Impingement test: Pain on doing the above procedure is reduced after injection of H&L into the subacromial space SUPRASPINATUS TEAR - Difficulty in initiating abduction
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Ability to actively abduct the arm after passively abducting it above 90 degrees – the abduction paradox, as supraspinatus initiates abduction but deltoid can abduct the shoulder the rest of the way “Drop sign”: the abducted arm suddenly drops to the side when it is lowered past a certain angle of abduction
INVESTIGATIONS
TEAR Conservative
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Surgical
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1. X-ray
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Usually normal in early impingement May be erosion, sclerosis or cyst formation at the greater tuberosity (insertion of the supraspinatus tendon) in chronic tendinitis May see calcification of the supraspinatus tendon (incidental and not the cause of pain) May see narrowing of the space between the acromioclavicular joint and the humeral head May see signs of acromiclavicular joint arthritis – osteophytes
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May detect large tears, but operator-dependent
3. MRI
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Accurate delineation of anatomy Can help determine site and size of a tear if present
If amenable to repair, open or arthroscopic cuff repair followed by subacromial decompression. Especially for young active individuals with complete tears. Partial tears do not require surgery unless persistent pain or considerable instability. If not amenable to repair, open or arthroscopic debridement of degenerate cuff tissue and subacromial decompression.
CALCIFICATION OF THE ROTATOR CUFF (i) -
2. Ultrasound
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Physiotherapy to improve strength Heat therapy Local anaesthesia if necessary
(ii)
Acute calcific tendinitis Acute shoulder pain due to deposition of calcium hydroxyapatite crystals in the critical zone of the supraspinatus tendon just medial to its insertion Usually affects those btw 30-50yrs old Investigations – X-ray shoulder jt: calcification seen just above greater tuberosity Treatment – rest arm in a sling, NSAIDs, H&L and LA injection if necessary Chronic calcification
MANAGEMENT
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TENDINITIS
BICEPS TENDONITIS - Impingement syndrome. - Pain and tenderness sharply localised to the bicipital groove. - Rest, local heat and deep transverse frictions. Consider a local corticosteroid
Conservative:
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Eliminate aggravating activity, and avoid “impingement position” Physiotherapy Short courses of analgesia e.g. NSAIDs Subacromial Hydrocortisone & Lignocaine / Triamcinolone & Xylocaine injections for pain relief (LA takes effect immediately, lasts 1 day; corticosteroid takes effect 3-5 days later)
Surgical
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Open or arthroscopic subacromial decompression (acromioplasty) o Excise coracoacromial ligament & anteroinferior part of acromion o Remove acromioclavicular osteophytes if present
common, usually asymptomatic
injection if healing is delayed.
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RUPTURE OF BICEPS TENDON -
Patient usu >50yo, can be part of rotator cuff lesion Presentation: upper arm becomes painful and bruised after patient lifted something and he/she feels something snap in the shoulder Signs: prominent lump in the lower part of the arm (detached belly of the long head of biceps) upon flexion of the elbow 22
Treatment: - No treatment in the elderly if isolated lesion. - If part of a rotator cuff lesion esp if patient is young, may need anterior acromioplasty with reattachment of the tendon (splint the arm with the elbow flexed for 4 wks) Biceps: Origin - long head from the supraglenoid tubercle and lies in the bicipital groove, short head is from the tip of the coracoid process of the scapula; Insertion - posterior part of the tuberosity of the radius and deep fascia on medial aspect of forearm via bicipital aponeurosis Action- supinator of the forearm, flexor of the elbow jt and weak flexor of the shoulder jt]
FROZEN SHOULDER (ADHESIVE CAPSULITIS)
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INVESTIGATIONS - X-rays usually normal – useful in excluding other causes of painful shoulder, such as infection, post-traumatic stiffness, diffuse stiffness and reflex sympathetic dystrophy when patient 1st presents MANAGEMENT Conservative
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AETIOLOGY The term frozen shoulder should be reserved for a well-defined disorder characterised by progressive pain and stiffness which usually resolves spontaneously after 18 months. PRIMARY ADHESIVE CAPSULITIS - Idiopathic in cause - Associated with DM, Dupuytren’s contracture, hyperlipidaemia, hyperthyroidism, cardiac disease - Global contracture of the shoulder joint, but maximally in the rotator interval area and around the coracohumeral ligament SECONDARY ADHESIVE CAPSULITIS -
Intrinsic causes
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Extrinsic causes
Chronic rotator cuff injuries Post-traumatic scarring following injuries at the shoulder e.g. fracture of the surgical neck, greater tuberosity. Painful disorders resulting in decreased movements of the shoulder: referred pain from cervical radiculopathy, post-hand, wrist or elbow surgery, post-MI
CLINICAL FEATURES - Patient aged 40-60 years - Aching in the arms and shoulder after trauma, often trivial - Pain gradually increases in severity and prevents sleeping on the affected side - Subsides after several months with increasing stiffness that continues for 6-12mths - Movement is regained gradually but may not return to normal
Physical findings: shoulder appears normal with no wasting; most marked feature is decreased active and passive movement in all directions
Aim of conservative treatment is to relieve pain and prevent further stiffening while waiting for recovery (since natural course is recovery in 12-18 months) Analgesia (NSAIDs), corticosteroid injections, local heat. Physiotherapy: o Repeated circular movement of shoulder o Assisted abduction – use towel or rope, loop it over an overhead bar like a pulley system, and hold on to each end with one hand. Patient uses downward pull of normal arm to passively abduct painful arm overhead. o Assisted internal rotation – both hands gripping either end of a towel slung across the patient’s back diagonally; the hand on the painful side holds the lower end while the hand on the normal side holds the end above the shoulder. Patient uses hand on normal side to pull upwards on towel, passively internally rotating the painful shoulder. o Wall-crawling – patient uses fingers to “crawl” up a wall slowly, increasing flexion movement.
Surgical
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Poorly defined role, only for patients who fail conservative management Manipulation under anaesthesia (least invasive) – passive stretching of the capsule while patient is under anaesthesia, but be careful of causing fractures especially in the elderly. Distend the joint by injecting a large volume of sterile saline under pressure Fibrolysis/ division (open or arthroscopic) of the supraspinatus and infraspinatus may dramatically improve ROM. Must be followed by aggressive physiotherapy post-op.
PROGNOSIS - Better in younger patients with post-traumatic frozen shoulder; the idiopathic frozen shoulders that occur in diabetics tend to recur and not improve.
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SHOULDER JOINT INSTABILITY AND DISLOCATIONS ANATOMY OF THE SHOULDER JOINT - Articulation: occurs btw the rounded head of the humerus and the shallow pearshaped glenoid cavity of the scapula - Movements: flexion, extension, abduction, adduction, lateral/medial rotation, circumduction - Relations: Ant: subscapularis, axillary vessels, brachial vessels Post: infraspinatus, teres minor Sup: supraspinatus, subacromial bursa, coracoacromial lig, deltoid Inf: long head of triceps, axillary nerve, posterior circumflex humeral vessels - Shallowness of the glenoid fossa of the scapula and lack of support provided by weak ligaments(3 glenohumeral ligaments—Medial, Inferior, Superior; transverse humeral ligament; coracohumeral ligament) make the shoulder joint an unstable structure - Strength mainly depends on the rotator cuff muscles - Least supported part of the jt lies in the inferior location where it is unprotected by the muscles - Shoulder laxity is not equivalent to instability!!!
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Bilaterally, and the instability usually responds to a Rehabilitation program. Surgery rarely indicated. When surgery is necessary, it involves tightening of the Inferior capsule – inferior capsular shift, or Interval Closure.
1. ANTERIOR DISLOCATION OF THE SHOULDER MECHANISM OF INJURY Fall on the hand, driving humerus forwards, tearing the capsule or avulsing the glenoid labrum CLINICAL FEATURES Severe pain, shoulder deformity Lateral outline of the shoulder may be flattened; bulge may be felt just below the clavicle
X-RAY FEATURES ANTERIOR SHOULDER DISLOCATION – TYPES OF X-RAY VIEWS Y-SCAPULAR (LATERAL AP VIEW AXILLARY VIEW SCAPULAR) VIEW
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Classification of patients with recurrent shoulder instability: a. TUBS: Traumatic, Uni-directional (unilateral), Bankart lesion, Surgery. - instability related to a clear Traumatic event that presents as Unidirectional instability, usually involves a Bankart lesion (tear in the glenoid labrum), and frequently requires Surgery b. AMBRII: Atraumatic, Multi-directional, Bilateral, Rehabilitation, Inferior Capsular Shift, Interval Closure - Instability that arises Atraumatically, occurring in patients prone to Multidirectional instability who have excessive shoulder laxity 24
AP-overlapping shadows of the humeral head and glenoid fossa with the head lying below and medial to the socket. Look out for Hill-sachs lesion which may indicate recurrent anterior dislocations
Normal shoulder jt
Anterior dislocation of the shoulder
COMPLICATIONS Early (i) Rotator cuff tear: occurs usu in older people, difficulty in abducting the arm after reduction (ii) Axillary nerve injury: patient unable to contract the deltoid (can inititate abduction but difficulty in abduction beyond a certain angle) and small patch of anaesthesia over the muscle (regimental badge area); usu a neuropraxia [course of axillary n.: arises from posterior cord of the brachial plexus (C5,6) in the axilla, passes through quadrangular space then comes into close relationship with the inf aspect of the capsule of the shoulder jt and medial side of the surgical neck of the humerus] Radial n., median n., ulnar n, musculocutaneous n. may be injured sometimes (iii) Axillary artery injury: examine for ischaemia before and after reduction (iv) Fracture-dislocation: associated fracture of the humerus-ORIF. Greater tuberosity may be sheared off Late (i) (ii) (iii)
Shoulder stiffness Unreduced dislocation: closed reduction can be attempted up to 6wks after injury Recurrent dislocation: common if the glenoid labrum is detached or the capsule is stripped off the front of the neck of the glenoid; more common in younger patients – 90%, 50% in older patients
TREATMENT M & R with sedation or sometimes GA (i) Kocher’s method: not recommended due to risk of nerve, vessel & bone injury (ii) Stimson’s technique: patient lies prone with arm hanging over side of bed;
(iii)
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shoulder may reduce after 15-20mins Hippocratic method: increasing traction applied to the arm with the shoulder in slight abduction while an assistant applies firm counter traction to the body; e.g. using a towel slung ard the chest under the axilla – know at least this one!
X-ray post-reduction to check position and exclude fracture. Exclude an axillary nerve injury, rotator cuff tear, median, radial, ulnar and musculocutaneous nerve injuries after reduction Rest the arm in a sling for 3 wks, 1 wk for those >30yrs old due to risk of stiffness Avoid abduction and lateral rotation for 3 wks Elbow and finger movements
ANTERIOR INSTABILITY most common type, accounts for 95% of instability Mechanism of injury: arm is forced into abduction, external rotation and extension In recurrent dislocations: labrum and capsule often detached from the anterior rim of the glenoid(Bankart lesion) and there is the presence of an indentation on the posterolateral aspect of the humeral head (Hill-Sachs lesion)
CLINICAL FEATURES - Patient may describe his shoulder as ‘coming out’ after a sporting event in an acute dislocation - Complain that shoulder dislocates with relatively trivial actions and often he/she can reduce the dislocation himself - In recurrent subluxation: patient may describe a catching sensation followed by numbness or weakness - ROM full btw episodes of dislocation - Apprehension test: examiner lifts the arm into abduction, external rotation and then extension, patient’s body tautens in apprehension when he senses that the humeral head is abt to slip anteriorly. Repeat test by applying pressure to the front of the shoulder at the same time, patient will feel more secure now - Drawer test: scapula is stabilised with one hand while examiner grasps the upper arm with the other hand to manipulate the head of the humerus forwards and backwards with the patient supine 25
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Fulcrum test: patient lies supine and examiner places one hand behind the patient’s shoulder to lever the humeral head forward by extending and laterally rotating the arm, patient becomes apprehensive.
INVESTIGATIONS - X-ray shoulder jt: AP, lateral and axillary views: Hill Sachs lesion best shown on AP with arm internally rotated
X-RAY FEATURES - AP view –humeral head looks abnormal in shape as it is medially rotated(light bulb sign); humeral head stands somewhat away from the glenoid fossa (empty glenoid sign)
AP view transcapular view axillary view Lat view- posterior subluxation, dislocation and sometimes deep indentation on the ant aspect of humeral head, may have accompanying fractures of the humeral neck, posterior glenoid rim or lesser tuberosity -
CT shoulder Arthroscopy Examination under anaesthesia (EUA) to determine direction of instability
TREATMENT - For acute dislocations: Manipulation and reduction followed by immobilisation in a bandage or sling for several wks - Recurrent dislocations: Indications for surgery include frequent painful dislocation and recurrent subluxation
3. POSTERIOR DISLOCATION OF THE SHOULDER - rare, <2% of shoulder dislocations MECHANISM OF INJURY - Indirect force producing internal rotation and adduction; occurs most commonly during a epileptic fit or electric shock; can also be due to a fall on to the flexed, adducted arm, direct blow to the front or fall on the outstretched hand. CLINICAL FEATURES - Arm is held in medial rotation, front of shoulder looks flat with a prominent coracoid
COMPLICATIONS (i) unreduced dislocations (ii) recurrent dislocations TREATMENT - M & R by pulling on the arm with shoulder in adduction followed by lateral rotation while humeral head is pushed forwards. - Immobilisation in a sling
4. POSTERIOR INSTABILITY - Recurrent instability almost always a posterior subluxation with the humeral head riding back on the posterior lip of the glenoid - Subluxation when the arm is in flexion and internal rotation - Posterior drawer test positive: humeral head pushed backwards while the scapular spine and coracoid process are held by the other hand - Posterior apprehension test positive: forward flexion and internal rotation of the shoulder with a posterior force on the elbow - Treatment: muscle strengthening exercises, surgery considered when condition is disabling and there is no gross joint laxity
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INFERIOR DISLOCATION OF THE SHOULDER Occurs when the arm is hyperabducted Humeral head is levered out of its socket and pokes into the axilla May have severe soft tissue injury with avulsion of the capsule and surrounding tendons, rupture of muscles, fractures of the glenoid or proximal humerus and damage to the brachial plexus and axillary artery Patient’s arm will be locked in abduction and head of the humerus may be felt in or below the axilla
6. MULTI DIRECTIONAL INSTABILITY - Same as AMBRII X-RAY FEATURES - Humeral shaft points upwards with the head sitting below the glenoid TREATMENT - M&R: Pull upwards in the line of the abducted arm with counter-traction downwards over the top of the shoulder. Examine for neurovascular damage post-reduction. Rest arm in sling for 3 wks. - If this doesn’t work then open reduction may be needed.
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DISORDERS OF THE SCAPULA -
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OTHER DISORDERS OF THE GLENOHUMERAL JOINT -
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Tuberculosis - Uncommon - Starts as osteitis, rarely diagnosed till arthritis supervenes. - May proceed to abscess and sinus formation, and possibly fibrosis ankylosis. - X-ray shows generalized rarefraction of bone in early stages with erosion of joint surfaces. Late cases may have cystic destruction of the joint. - Treatment: Anti-TB meds and rest the joint until acute symptoms settle. Rheumatoid Arthritis - AC joint, shoulder joint and various synovial pouches usually involved. - X-ray shows progressive loss of articular space and peri-articular erosions - Treatment: Methylprednisolone may be injected into joint & subacromial bursa. Osteoarthritis - Usually secondary to other fairly obvious disorders: congenital dysplasia, local trauma, long-standing rotator cuff lesions, RA or AVN of head of humerus. - X-rays show characteristic OA picture. Milwaukee Shoulder
Patient presents with swelling of the shoulder and x-rays show a bizarrely destructive form of arthritis. Similar conditions are encountered in other joints. Largely crystal-induced rapidly progressive arthropathy; sometimes associated with massive rotator cuff tears. No satisfactory treatment
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Congenital Elevation of the Scapula (Sprengel’s Shoulder) o Scapula normally descends from neck by third month of fetal life. One remains high in this case. o Affected side is elevated, smaller and somewhat prominent. o Usually painless but associated with other abnormalities like fusion of cervical vertebrae, kyphosis/scoliosis. Klippel-Feil Syndrome o Bilateral failure of scapular descent and fusion of several cervical vertebrae. Neck usually short and may be webbed, cervical mobility restricted o Usually left untreated. Winged Scapula o Due to weakness of serratus anterior---which stabilizes the scapula on the thoracic cage. Usually not apparent unless contracting the serratus anterior against resistance. Ie push against a wall. o Causes: Damage to Long thoracic nerve, injury or viral infxn to 5th, 6th and 7th cervical roots, certain types of muscular dystrophy Acromioclavicular Instability o Common condition resulting from dislocation of AC joint and rupture of ligaments which tether the outer end of the clavicle. \ o Fairly obvious bump/step over the AC joint. If X-ray not obvious, ask patient to carry weight on the affected arm and re-shoot the X-ray. OA of AC joint o Common in old people. o Relieved by H&L injections or excision of the lateral end of the clavicle.
FRACTURES OF THE CLAVICLE -
[MCQ] Embryology of clavicle: membranous ossification Mechanism of injury: fall on the shoulder or outstretched hand (FOOSH) May have a subcutaneous lump Note: in children, clavicle fractures easily but unites rapidly w/o complications too. X-ray features: 27
Most commonly involve the middle 1/3 of the clavicle, outer fragment will be pulled down by the weight of the arm while inner half held up by SCM • Displacement may be severe in outer 1/3 fractures when the coracoclavicular ligaments are torn Complications: • Early 1. Pneumothorax 2. Damage to subclavian vessels 3. Brachial plexus injury • Late 1. Non-union, esp displaced outer 1/3 fractures 2. Malunion (healed #leaves a lump, most common Cx) 3. Shoulder stiffness Treatment: • Middle 1/3#:Support arm in a sling for 2-3wks followed by physio; internal fixation rarely required • Displaced outer 1/3 #: ORIF •
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FRACTURES OF THE SCAPULA -
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Mechanism of injury: body is fractured by a crushing force, a/w rib fractures, lung contusion and haemo/pneumothorax, neck is fractured due to a blow or a fall on the shoulder Fractures of the scapula (high energy fracture) can be a/w injuries to the chest, brachial plexus, spine, abdomen and head Treatment: • Sling and physio for body and neck# • ORIF for fracture-dislocation(glenoid #) Complications: • Malunion (+ crepitus)
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X-ray: • Stress view may be needed to differentiate AC subluxation from dislocation (patient is standing and holding a 5kg wt on each hand; diff in the distance btw the coracoid process and inf border of the clavicle >50% diagnostic of AC dislocation)
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Complications: (i) Supraspinatus tendinitis (ii) Unreduced dislocation (iii) Ossification of the ligaments (iv) secondary OA Treatment: • AC subluxation- Rest arm in a sling+physio • AC dislocation: fixation with a screw for 8wks, rest the arm for 2 wks followed by physio; considered only for young and active patients
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STERNOCLAVICULAR DISLOCATIONS -
ACROMIOCLAVICULAR SUBLUXATION/DISLOCATIONS -
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Definitions • AC subluxation- acromioclavicular ligaments are torn with upwards subluxation of clavicle • AC dislocation- both the acromioclavicular ligaments and coracoclavicular ligaments may be torn, clavicle is elevated, causing a visible and palpable step Mechanism of injury: fall on point of shoulder with arm adducted (sports injury) Clinical manifestations: pain & swelling over AC joint; inability to ab/adduct arm
Mechanism of injury: lateral compression of the shoulders Anterior(prominent lump over SC jt) more common than posterior dislocation Posterior dislocation more serious as there can be pressure on the trachea and large vessels, causing venous congestion of the neck and arm Treatment: • Anterior dislocations: Conservative mx ( IF dangerous as large vessels are behind the sternum) • Posterior dislocations 1. Closed reduction (sedate patient first, then pull at the shoulder) 2. If unreduced ORIF or acceptance of some degree of permanent instability (depending on patient characteristics and functionality)
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IMPORTANT ORTHOPAEDIC CONDITIONS IN THE ARM
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4 major segments involved: head of humerus, lesser tuberosity, greater tuberosity, shaft
One part
Two part
No matter how many fracture lines there are, as long as they are undisplaced, considered as one part 1fragment is displaced
FRACTURES OF THE PROXIMAL HUMERUS -
Epidemiology: occurs after middle age. Most common in osteoporotic postmenopausal women Mechanism of injury: fall on the outstretched arm (causes # in older patients, dislocation in younger patients) Clinical features: large bruise on upper part of arm, may have associated axillary n. and brachial plexus injury X- ray: • single impacted fracture extending across surgical neck in elderly, fragments more clearly separated in younger patients • Obtain axillary and scapular lateral views to exclude shoulder dislocation • Inf subluxation of the humeral head as fracture heals
Three part Four part
2 fragments are displaced, usu head (# along surgical neck) and greater tuberosity All the major parts are displaced
Collar & cuff for 1-2 wks Active exercises once fracture unites (usu aft 6wks) Cause few problems Closed reduction, collar & cuff for 4wks IF if reduction fails or fracture unstable after reduction For fractures of the anatomical neck in elderly may need prosthesis due to high risk of AVN of humeral head(rare); fixation in younger patients For 2-part fracture dislocations, closed reduction usu possible Fracture of the greater tuberosity may be a/w ant dislocation of shoulder while fracture of the lesser tuberosity a/w post dislocation ORIF 3 part fracture dislocation requires ORIF, at risk of brachial plexus injury A/w poor outcome, high risk of vascular injury, brachial plexus damage, injuries of chest wall and AVN of humeral head Usu needs prosthetic replacement (reserved for the elderly)
- Complications: One part fracture involving surgical neck 1. Vascular and nerve injuries esp axillary nerve 2. Stiffness of the shoulder maximal at the outset 3. Malunion with loss of rotation 4. Avascular necrosis of the head of humerus: 10% of 3-part fractures, 20% of 4-part fractures -
Treatment • Neer’s classification: distinguishes btw no of displaced fragments(defined as >45o angulation or >1cm separation)
Proximal humerus fractures in children - In children, the physis can separate or there can be metaphyseal fractures, considerable displacement and angulation is acceptable
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Fractures may be pathological as proximal humerus is a common site of bone cysts and tumors in children Fractures due to bone cyst: rest the arm in a sling for 4-6 wks
FRACTURES OF THE SHAFT OF HUMERUS Mechanism of injury: • RTA / FOOSH (fall on oustretched hand) • Fall on the hand causes a spiral fracture. • Fall on the elbow with the arm abducted causes a oblique or transverse # • Direct blow to the arm causes a transverse or comminuted fracture • Note: In the elderly, fracture may be due to mets Clinical features: o Painful, bruised and swollen arm o Displacement of fragments depends on relation of the site of fracture to the insertion of the deltoid. - If fracture line proximal to deltoid insertion, proximal fragment adducted by pectoralis major, lat dorsi and teres major while distal fragment abducted by deltoid - When fracture is distal to delotoid insertion, proximal fragment is abducted by deltoid and distal fragment pulled proximally by biceps and triceps
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May have radial n. injury (radial nerve lies in the spiral grove on the posterior surface of the humerus under to cover of the triceps). Test radial n. function before and after treatment by assessing active extension at MCP jt X-ray: Look for tumors in elderly as fracture may be pathological
Complications: Early 1. Brachial artery injury (dx with arteriography) 2. Radial nerve injury- patient presents with wrist drop and paralysis of the MCP extensors; common with oblique #s at the junction of the middle and distal 1/3 of bones Late 1. Delayed union, malunion and non-union (common in conservatively managed patients) 2. Joint stiffness Treatment: - U slab Cast Brace, or - ORIF - Most heal readily; weight of arm with external cast enough to pull fragments together. Hanging cast is applied from shoulder to wrist with elbow flexed and forearm is suspended by a sling around patient’s neck - Spiral fractures unite in about 6wks while other fractures take 4-6wks longer - Cx rate after IF of humerus high (compression plate, screws, intramedullary nail, external fixation) Indications for surgery: Radial n palsy Segmental # Open # Pathological # Intra-articular extension Floating elbow (humeral + forearm #) Non-union
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ANATOMY OF THE ELBOW JOINT Type of jt: Hinge jt, Stability due to the shape and fit of the bones that make up the jt and the capsular and collateral ligaments Articulation: Btw the trochlea and capitulum of the humerus and the trochlea notch of the ulna and head of the radius Ligaments: Lateral collateral lig attached by apex to the lateral epicondyle and base to annular ligament of radius Medial collateral lig attached to the medial epicondyle to medial margins of olecranon and coronoid process Nerve supply: branch from median, ulnar, musculocutaneous, radial n. Movements: Flexionbrachialis, biceps brachii,, brachioradialis, pronator teres; in flexion, the bony points form the boundaries of an equilateral triangle Extension triceps, anconeus; in extension, the med and lat epicodyles and top of the olecranon are in a straight line Relations: Ant brachialis, biceps tendon, median n., brachial artery Post triceps, small bursa Medulnar n. passes behind the med epicondyle and crosses medial ligament of the jt Lat common extensor tendon, supinator Forearm normally slightly in valgus in relation to the upper arm, average carrying angle in children being abt 15 degrees. In children, the secondary ossification centres can be seen on x-rays. The average ages at which the ossific centres appear are ‘CRITOE’ C apitulum-2yrs R adial head- 4yrs I nternal (medial) epicondyle-6yrs Trochlea-8yrs O lecranon-10yrs E xternal (lateral) epicondyle-12yrs
FRACTURES AROUND THE ELBOW IN CHILDREN 1. SUPRACONDYLAR FRACTURES One of the commonest # in children
Mechanism of injury: Posterior displacement due to fall on outstretched hand (hyperextension injury), distal fragment pushed backwards and twisted inwards while proximal fragment can poke into the soft tissue anteriorly, injuring the brachial artery or median nerve. Anterior displacement use due to direct trauma (rare) with jt in flexion Clinical features: ‘S’ deformity in posteriorly displaced #. Examine for vascular (check pulse and capillary return) and nerve injury. X-ray: Fracture best seen on lat view Fat pad sign in undisplaced # : triangular lucency in front of distal humerus due to fat pad being pushed forwards by a haematoma
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cortex still in continuity
Type III #, distal fragment tilted Both anterior and posterior fat pads backwards visible, sail sign configuration
Baumann’s angle: assess degree of medial angulation (angle is subtended by longitudinal axis of humeral shaft and a line through coronal axis of capitellar physis; usually <80 degrees)
Increase in Baumann’s angle occur in residual varus and internal rotation deformities
Complications: Early 1. Brachial artery injury, can cause Volkman’s ischaemia 2. Compartment syndrome pain + 1 positive sign [pain on passive extension of the fingers, tnese and tender forearn, pulseness, blunted sensation, increased capillary refill time], KIV angiography, vessel graft, forearm fasciotomy 3. Median n., esp anterior interosseous branch, recovery usu in 6-8wks 4. Ulnar n. damaged by careless pinning Late 1. Malunion, causing varus deformity of the elbow（gunstock deformity,） rarely valgus(may cause late ulnar n. palsy), may need correction by supracondylar osteotomy 2. Elbow stiffness 3. Myositis ossificans Treatment Type I
Undisplaced fracture
Type II
Angulated fracture with the posterior
Immobilize in 90o, sling x 3wks Check x-ray 5-7days later to ensure no displacement Reduce under GAtraction in the
Type IIa
Less severe and merely angulated
Type IIb
More severe, both angulated and malrotated Increased risk of neurovascular injury or circulatory compromise due to swelling Completely displaced fracture Increased risk of neurovascular injury or circulatory compromise due to swelling
Type III
length of the arm with counter-traction above elbow correct lateral shift and tilt correct rotationcorrect backwards shift and tilt. Check pulse! Collar and cuff x 3wks Reduce under GA, hold with wires
Reduce under GA, hold with wires Open reduction if (i) closed reduction fails (ii) open fracture (iii) vascular damage present Continuous traction through a screw in the olecranon or skin traction with the elbow almost straight and the arm in a small Thomas splint (Dunlop traction)
2. FRACTURES OF THE LATERAL CONDYLE Mechanism of injury: Fall on outstretched hand with elbow extended and forced into varus. Fragment “capsized” by extensor tendons. Fracture always involves joint; fracture line usu runs along the physis and into the trochlea; fracture may damage the growth plate Clinical features: swollen and deformed elbow, passive flexion of the wrist (pulling on the extensors) may be painful. X-ray: Oblique view should be taken Usu there is a fracture through the middle of the trochlea and the elbow is unstable and may dislocate (Salter Harris Type II) Less commonly, the fracture runs through lateral condyle into the trochlea, stable fracture with no involvement of the humero-ulnar jt (Salter Harris Type IV) Complications: 1. Non-union and malunion, causing cubitus valgus and tardy ulnar n. palsy 2. Recurrent posterolateral dislocation of elbow Treatment: • Minimal displacement – backslab with elbow flexed & wrist extended 32
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(relaxes extensor mechanism) for 2/52 Displaced # (gap of >2mm) – ORIF, immobilize arm in a cast for 3-4/52
Treatment: • Displacement <30deg- collar and cuff • Displacement>30 deg- closed or open reduction. IF not necessary • Never remove radial head as it interferes with growth of the radius
3. FRACTURES OF THE MEDIAL CONDYLE Mechanism of injury: Fall on outstretched hand, elbow forced into valgus or fall from ht with direct blow to the elbow, medial fragment may be displaced by pull of the flexor muscles
FRACTURES AND DISLOCATIONS AROUND THE ELBOW IN ADULTS
Clinical features: pain and swelling
1. FRACTURES OF THE DISTAL HUMERUS
X-ray: intra-articular #; in younger children, much of the medial condylar epiphysis is cartilaginous and may not be visible on x-ray, an arthrogram may be useful in some cases Complications: Early 1. Ulnar n. damage
Late 1. Stiffness of the elbow 2. Late ulnar n. palsy due to friction in roughened bony groove
Treatment: Undisplaced-splint and repeat x-ray Displaced- closed reduction with percutaneous pinning or ORIF 4. PULLED ELBOW Mechanism of injury: pull on the arm with forearm pronated, causing subluxation of annular ligament over head of radius into radiocapitellar joint. - Usually affects a child between 2-3yo No x-ray findings
Type A Extra-articular supracondylar # - rare in adults - usu displaced and unstable ORIF
Type B
Type C Intra-articular bicondylar# with Intra-articular unicondylar # varying degrees of comminution - high energy # with soft tissue damage - examine for vascular or nerve injury Undisplaced # • Posterior slab with elbow flexed almost 90 deg • Check x-rays 1/52 after injury Displaced# • ORIF, elbow held at 90 deg with arm in a sling, healing occurs by 12wks • Skeletal traction may be considered for severely comminuted # • Elbow replacement in the elderly Complications Early 1.Vascular injury 2.Median n. or ulnar n. damage Late 1. Elbow stiffness 2. Heterotopic ossification
Treatment: Supinate then flex the elbow, ligament pops back in place 5. FRACTURED NECK OF RADIUS Mechanism of injury: Fall on outstretched hand, forcing elbow into valgus and pushing radial head against capitulum; same injury in adult usu causes radial head # Clinical features: pain on rotating forearm X-ray: may have a Salter Harris II injury; proximal fragment is tilted distally, forwards and outwards
2. FRACTURED HEAD OF RADIUS Common in adults but rare in children Mechanism of injury: Fall on outstretched hand with elbow extended and forearm pronated articular cartilage of the capitulum may be bruised or chipped Clinical features: tenderness over radial head, pain on pronation and supination X-ray: to exclude concomitant injury of distal RUJ i.e. damage to interosseous memb.
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Complications: 1. Joint stiffness of the elbow and radioulnar jt 2. Myositis ossificans 3. Recurrent instability of the elbow if injury to the medial collateral lig and if there is excision of the radial head Mason classification
Type I Vertical split in the radial head LA injection and aspiration of haematoma Collar and cuff for 3/52
X-ray: lateral view needed, check position of radial head as it may be dislocated Complications: 1. Stiffness 2. Non-union
3. Transient ulnar n. palsy 4. OA
Treatment: - Comminuted # with triceps intacttreat as a bruise and rest in sling for 1/52 as immobilization can lead to stiffness in the elderly; obtain check x-ray - Undisplaced transverse# immoblise at 60 deg in a cast for 2-3/52 - Displaced transverse # ORIF with tension band wiring Type II Single fragment of lateral portion of the head broken off and usu displaced distally Reduction and fixation with a small screw
Type III Head is comminuted Excision of radial head
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DISLOCATION OF THE ELBOW Posterior or posterolateral dislocation in 90% of cases; lateral shift may occur Reduction usu stable and recurrent dislocation unlikely if there are no associated # If there is # of the radial head, coronoid process or olecranon process, joint is more unstable and more prone to redislocation unless # are fixed Considerable soft tissue disruption and possible vascular and nerve injuries
Reconstruction of radial head if there are forearm injuries, disruption of the distal RUJ which increases risk of proximal migration of the radius and instability
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Fracture dislocation: reduction and fixation, need to restore radial pillar
Clinical features: obvious deformity, patient supports forearm with elbow - Examine for vascular or nerve damage
**TERRIBLE TRIAD = Radial head # + coronoid process # + MCL injury **
Mechanism of injury: - FOOSH with elbow in extension causes posterior dislocation - Side swipe injury (driver with elbow out of the window) causes forward dislocations usu a/w # and severe soft tissue damage
X-ray: confirms dislocation and identify associated #
3. FRACTURES OF THE OLECRANON Mechanism of injury: - Direct blow or fall on the elbow causing a comminuted # - Traction when patient falls on hand with triceps contracted, causing a clean transverse break Clinical features: - Bruise over the elbow in comminuted #, intact triceps - Palpable gap and patient unable to extend elbow against resistance in transverse # 34
Complications: Early 1. Brachial artery injury 2. Median or ulnar n. injury Late 1. Stiffness 2. Heterotopic ossification, myositis ossificans; if bone mass restricts elbow function, excise when mature 3. Unreduced dislocation 4. Recurrent dislocation if there is a large coronoid# or radial head # 5. Secondary OA
Line drawn down the long axis of the radius does not intersect the capitulum, indicating radial head dislocation
Treatment: Uncomplicated dislocation: reduce under anaesthesia Slight flexion of elbow and traction on forearm correct lateral displacement further flexion of elbow while pushing olecranon forwards check nerves and circulation + check x-raycollar and cuff for 3/52 with elbow flexed>90deg Dislocation with associated #: fix the # Side swipe injuries — repair vascular damage, skeletal stabilization Persistent instability — temporary external fixation 5. -
RADIAL HEAD DISLOCATION Isolated dislocation are rare Usually a/w ulna # (Monteggia injury) Common in children; rule out NAI • Another mechanism of injury: parents pulling kids by the hands (yanking) Important to identify ulnar # in children as if a minor deformity allowed to persist, may prevent full reduction of dislocation Look for posterior interosseous nerve injury Treatment: manipulation under anaesthesia (supination, direct pressure), cast 6/52
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IMPORTANT ORTHOPAEDIC CONDITIONS IN ELBOWS & FOREARMS
TENNIS ELBOW (LATERAL EPICONDYLITIS)
Cause: Malunion of supracondylar #
Cause: minor trauma to origin of wrist extensors / fibrosis of extensor carpi radialis brevis (ECRB) e.g. painting, carpenter
CUBITUS VARUS (GUNSTALK DEFORMITY) Rx: wedge osteotomy of lower humerus Cx: median nerve palsy
CUBITUS VALGUS Cause: non-union of # lateral condyle (a/w bony knob on medial elbow) Mx: Undisplaced – backslab Moderate displacement – closed reduction and backslab Unstable – K-wire and cast Rotated – Open reduction and K-wire
X-ray weekly to detect slipping
Cx: Tardy ulnar nerve palsy – manage by transposing ulnar nerve anterior to elbow
RHEUMATOID ARTHRITIS Features: pain, tenderness, swelling, stiffness, usually bilateral X-ray: bone erosion, radial head destruction, widened trochlear notch of the ulna Rx: splint, radial head resection, partial synovectomy, arthroplasty
OSTEOARTHRITIS Cause: intraarticular #s, loose bodies, crystal deposition dz Features: pain, stiffness, ↓ROM, ± ulnar n palsy X-ray: ↓ Jt space, bone sclerosis, osteophytes, loose bodies
OLECRANON BURSITIS Causes: pressure, friction, infxn, gout (a/w tophi), RA (a/w polyarthritis & subcutaneous nodules over the olecranon)
Features: o Lateral epicondylar pain, aggravated by shaking hands & opening doors. o Pain on active wrist extension with a straight elbow. Normal ROM. o Pain reproduced by extending wrist against resistance or by passively flexing in thus extending the tendons Rx: rest, lifestyle modification, H&L injection, extra-corporal shockwave, excision of fibrous mass, lengthen tendon (ECRB)
GOLFER’S ELBOW (MEDIAL EPICONDYLITIS) Similar to tennis elbow, but affecting flexor origin at medial epicondyle Memory aid: Golfer’s already has ‘L’ hence Medial Epicondylitis
CUBITAL TUNNEL SYNDROME Compressive ulnar neuropathy at the elbow, in the retrocondylar groove or as ulnar nerve passes between the 2 heads of the flexor carpi ulnaris Caused by constriction of fascial bands, subluxation of ulnar nerve over medial epicondyle, cubitus valgus, bony spurs, tumours, ganglions, repetitive elbow flexion & extension Features: paraesthesia along ulnar 1.5 fingers; weak grip strength especially when patient rest upon or flexes the elbow; +/- nocturnal symptoms; loss of fine dexterity; rarely, wasting of intrinsic muscles & clawing/abduction of little finger. Male> Female. DDx: cervical spondylosis, ulnar tunnel syndrome (compression at canal of Guyon at the wrist) – preserved strength of wrist and 4th & 5th digit flexors McGowan Grading system 1) Parasthesia in distribution, clumsiness in hand, 2) Weak interossei & muscle wasting, 3) Paralysis of interossei, marked weakeness. Rx: Simple decompression, medial epicondylectomy if a/w non-union of epicondyle #, anterior transposition of the ulnar nerve, injection of steroids in the cubital tunnel
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SUPRACONDYLAR FRACTURES Fractures in distal 1/3 of humerus proximal to the trochlea & capitulum Epidemiology: common childhood #. Adults: More proximal, commonly with comminution, spiraling & angulation Mechanism of injury: FOOSH Features: pain over elbow, swelling, deformity Important complication: Volkmann’s ischaemic contracture – df: irreversible contracture of flexor muscles of the hand due to ischaemic processes in the forearm DDx: dislocation of elbow (equilateral Δ by epicondyles & olecranon is disrupted)
Support
Collar & cuff for 3 wks Sling for another 3 wks to avoid extension, but flexion is allowed.
Cx: 1. Arterial obstruction: Brachial arterial kinking by proximal fragment. Arterial wall damage results in Volkmann’s ischaemic contracture. Symptoms = Pain, Pallor, Paraesthesia, Paralysis, Perishing cold, swelling & bruising) 2. Median nerve injury 3. Malunion – cubitus varus (may cause ulnar tunnel syndrome)
X-ray: # line across distal humerus, posterior tilt/displacement of distal fragment, ± medial or lateral displacement.
ELBOW DISLOCATIONS
Mx:
Mechanism: fall on outstretched hand Assoc injuries routinely checked for: #s of epicondyles (usually medial), lateral condyle, coronoid & radial head & neck
Indications for reduction
Manipulation technique
Fixation
X-rays Remanipulation if reduction is poor Observation
Arterial obstruction # displacement &/or angulation <50% bony contact Backward tilt ≥15% Medial or lat tilting of ≥10% (may cause tardy ulnar n palsy) Severe torsional deformity Manipulation under GA 1. Disimpaction: Traction applied at 20o flexion with countertraction applied to arm 2. Reduce post tilt/displacement: Flex elbow to 80o while maintaining traction 3. Correct lat displacement/torsional deformity: manipulate epiphyseal complex Fix with elbow at greatest angle of flexion possible w/o compromising circulation (check radial pulse) Never apply a complete plaster due to risk of swelling AP & lateral No more than 2 remanipulations due to risk of swelling. Employ continuous traction instead (e.g. Dunlop traction) K-wires & plaster backslab may be used for unstable # Overnight, esp for complications of vascular compromise
X-ray: posterolateral dislocation of elbow Rx: o Apply strong traction in the line of the limb under GA. Slight flexion might be required. o Alternative: clasp humerus from behind & push olecranon fwd & medially while asstant applies traction in moderate flexion o Support with sling for 3 wks. Cx: exclude ulnar n, median n & brachial arterial injuries; elbow stiffness, myositis ossificans.
MEDIAL CONDYLAR INJURY Mechanism: direct violence or avulsion by ulnar collateral ligament on forceful abduction Mx: immobilize in plaster cast for 2-3 wks Cx: 1. Tardy ulnar n. palsy 2. Trapping of medial epicondyle in the elbow joint
37
RADIAL HEAD FRACTURE
Monteggia
Mechanism: direct violence, or FOOSH Features: elbow pain, swelling, bruising, restricted elbow extension Galeazzi
X-ray: # radial head, ± subluxation of distal end of ulna. (+) AP projections in mid-prone & full pronation required. Assess type of #. Mx: Fracture
Hairline Undisplaced (marginal or segmental) Displaced (marginal or segmental) Comminuted
Rx
Light compression bandage & sling for 3 wks, + backslab if pain is severe. Excellent outcome Conservative Rx, r/v in 3 mths. Late excision of radial head if movts are severely restricted Radial head excision w/in 48hrs ± silastic prosthetic replacement, splint for 3 wks
Mx: o o o Cx: o o o o o o
RADIAL NECK FRACTURE Mechanism & Dx: Similar to radial head # Mx: Conservative
Minimal tilting o
Marked tilting (>20 o adults, >30 children)
Manipulate – apply traction, pronate & supinate, apply pressure when prominent part of radial head presents, + K-wire if unstable
Fracture of upper ulnar (shortening & angulation) + radial head dislocation (MUF: Monteggia Ulnar Fracture) Mechanism: direct violence on forearm or forced pronation (eg fall on outstretched hand with trunk rotation) Fracture lower radius + inferior radioulnar joint dislocation with ulnar displacement (GUD: Galeazzi Ulnar Dislocation) More common than Monteggia.
Principle: Restore length of fractured bone, then reduce dislocation Children: manipulation + plaster fixation Adults or children w displaced #s: ORIF (plate & screw), plaster fixation in 90 degrees flexion with supination Cross union – radius malunites with ulnar Loss of pronation/supination Loss of extension of elbow Difficult to reduce and maintain closed. Usually requires ORIF Shoulder to hand syndrome (frozen shoulder) If due to persistent unreduced dislocation or late Dx:
Monteggia
•
Galeazzi
• • •
Anterior protrusion of radial head :. ↓ elbow ROM – Rx: excise radial head Tardy ulnar n palsy – Rx: transposition of ulnar nerve Prominent ulna & chronic wrist pain – Rx: excise distal ulna Ligaments potentially torn :. Instability at DRUJ – Rx: put in cast, arm in supination OR use K-wires
NIGHTSTICK INJURY FOREARM FRACTURE-DISLOCATIONS • • •
More commonly fracture of both bones of the forearam, usually displaced. If only one bone fractured, look for dislocation of the other. Displaced fractures of the forearm usually treated by ORIF as non-surgical means often result in limitation of pronation/supination.
Types: Remember, “Big bone #s, small bone dislocates”
• • • •
Isolated fracture of the ulnar with minimal displacement. MOI: Holding up arm to protect face from blow Rule out fracture clinically and radiographically Rx: Below elbow cast for 6 wks for distal one-third #. If angulation of proximal two-thirds severe, consider ORIF.
CAUSES OF TARDY ULNAR NERVE PALSY • •
Medial / Lateral condylar fracture Monteggia fracture 38
IMPORTANT ORTHOPAEDIC CONDITIONS IN THE HANDS & WRISTS
TYPES OF CASES
Ganglion Pigmented villonodular synovitis (PVNS) Implantation dermoid cyst OA – Heberden’s & Bouchard’s nodes
Haemangiomas Pseudoaneurysms SCC Glomus tumours
Joint
RA hands
OA hands
Vascular Nerve
Haemangiomas Ulnar n palsy Median n palsy Radial n palsy Carpal tunnel syndrome
Lumps
Muscle / tendon
Bones
DDX OF PAINFUL WRIST & HAND Referred
Joint
Periarticular
Radiculopathies Erb’s palsy (C5-6) Klumpke palsy (C8-T1)
de Quervain’s dz Tenosynovitis RA – Swan neck & Boutonniere deformities, tendon rupture
Trigger finger Dupuytren’s contracture Mallet finger
Colles’ # Smith’s # Scaphoid # Bennett’s #
Boxer’s # Gamekeeper’s thumb Scaphoid dislocation Lunate dislocation
RA OA Infection De Quervain Tenosynovitis Instability
Painful Hand Neck Shoulder Mediastinum RA OA Carpal tunnel Tenosynovitis Infection
NB. CTS, De Quervain’s disease and trigger finger are all tenosynovitis (i.e. same Mx)
I. HANDS ACUTE INFECTIONS GENERAL -
PATHOLOGIES 1. Trauma 2. Tumour 3. Infection 4. Inflammation 5. Degeneration
Painful Wrist Cervical spondylosis
-
Frequently limited to 1) Nail Fold, 2) Pulp space, 3) Subcutaneous tissues, 4) Tendon sheath, 5) Deep Fascial spaces or joint Cause: Almost invariably implanted Staphylococcus Pathophysiology: Acute inflammation and suppuration in a small compartment will result in increase in pressure leading to threatened local blood supply tissue necrosis or a stiff and useless hand Clinical features: Usually a hx of trauma, may be unnoticed. Painful and swollen hand. Throbbing pain. May be a/w with fever. Exquisite tenderness, red and tense tissues with decreased ROM. Principals of Rx: 1) Antibiotics—usually flucloxacillin, and in severe cases, fusidic acid or a cephalosporin as well. 2) Rest and elevation. 3) Analgesics 4) Drainage only if there’s sign(s) of abscess (throbbing pain, marked tenderness and toxaemia. 5) Splintage in a the position of safe immobilisation (wrist slightly extended, MCP in full flexion, IP joints extended and thumb abducted—ligaments are at greatest length. 6) Physiotherapy
SPECIFIC TYPES PARONYCHIA Infection under nailfold. 39
PULP SPACE INFECTION Usually prick or splinter of the finger tip
MUSCLE / TENDON DISORDERS
TENDON SHEATH INFECTIONS • Uncommon but dangerous. Risk of tendon necrosis and pt may end up with useless hand. Present with painful, tender swollen hand with zero ROM (active and passive not permitted) • Rx: As above. May require surgical drainage if no improvement over 24 hrs.
DEEP FASCIAL SPACE INFECTION • Usually infection from a web space or tendon sheath. The palm is ballooned. Loss of normal concavity, with whole hand held still. • Rx: Incision and drainage. JOINT INFECTION • Can be infected directly or indirectly. Clinically hard to distinguish from acute gout. So aspirate joint. • Rx: IV antibiotics and splint. If no improvement in 24 hrs open drainage. BITES • Animal Bites: Usual organisms — Staph and strep Human Bites: Organisms more varied and includes Anaerobes. • X-ray done to exclude fracture or foreign body. • Mx: o Fresh wound: Examined in OT. Swab for c/s. Explore for foreign bodies such as tooth. Splint elevate and start prophylactic antibiotics o Infected Bites: debridement and washout. Start IV antibiotics—Broad sprectrum penicillin and cephalosporin. Consider Rabies. o Post op: Physiotherapy. Deal with tendon lacerations when tissues are completely healed. SKIN SKIN CONTRACTURES - Cuts and burns are liable to heal with contractures, causing puckering of the palm or fixed flexion deformities. Surgery incisions should never cross flexor creases. - Rx: Established contractures may require excision of the scar and Z–plasty of the overlying skin.
DUPUYTREN’S CONTRACTURE Definition: nodular hypertrophy & contracture of palmar aponeurosis. Pathogenesis: local microvessel ischaemia increased xanthine oxidase activity superoxide free radical production stimulate myofibroblast proliferation & type III collagen formation. Specific platelet-derived and fibroblast growth factors also play a role in the aetiology. o Allopurinol may help to reduce symptoms (XO inhibitor) o The process of chronic inflammation is thought to be essential to the subsequent fibrosis Features: Middle-aged man. LOOK o Appearance of any visible cords, any pitting/tethering of skin on palmar aspect of hand o Scars from previous surgery o Flexion deformities at MCPJ and PIPJ of the involved fingers o Involvement of thumb & 1st web space (a sign of more aggressive dz) o Garrod’s pads at PIPJs on dorsum of hand (thickening of s/c tissues) FEEL o Palpate swelling, note fixation to skin o Compare with other palm! MOVE o ROM of involved fingers o Passively move the joints with fixed deformities OFFER o To enquire about causes & associations o Assess patient’s function, e.g. writing & dressing o Look for other features of diffuse fibromatosis
DDx: o Skin contracture (look for scar from previous wound) o Tendon contracture (thickened area or ‘cord’ moves on passive flexion of involved finger) o Congenital contracture of little finger (affects PIPJ) o Ulnar nerve palsy (claw hand deformity) Conditions associated with Dupuytren’s contracture (DEAFEST PAIL) o DM o Epilepsy o Age o Family history (AD) / fibromatoses o Epileptic medication (e.g. phenobarbitone) o Smoking o Trauma & heavy manual labour
40
Peyronie’s disease (fibrosis of the corpus cavernosum – seen in 3% of patients with Dupuytren’s contracture) o AIDS o Idiopathic o Liver disease (secondary to alcohol) Treatment: Indicated when deformity is progressive and interferes with function (i.e. when MCPJ or PIPJ contracture exceeds 30deg). o Fasciotomy – for prominent bands o Partial fasciectomy (with Z-plasty to lengthen wound) – in conjunction with post-op physiotherapy (early active flexion ROM exercises for grip strength) and night-time splintage in extension o Dermofasciectomy (with full-thickness skin grafting) – a/w lowest risk of recurrence o Arthrodesis/amputation – for late presentations & repeated recurrences
Bone (avulsion #) Extra-articular or involving <2/3 of joint conservative Rx Intra-articular or involving ≥2/3 of joint surgical reduction
o
MUSCLE CONTRACTURE Forearm
Intrinsic muscles
Ischaemic contracture of forearm muscles, commonly caused by: o Volkmann’s ischaemic contracture: # causing compartment syndrome resulting in muscle ischaemia & necrosis. Infarcted muscles replaced by fibrous tissues. Usually follows circulatory insufficiency due to injuries at or below the elbow. o Tight plaster cast & limb swelling Shortening of long flexors causing flexion deformity of fingers which is only correctable on wrist flexion (tendodesis effect) May be a/w ulnar and/or median nerve palsies Treatment: If marked disability: muscle release, Excise dead muscle or tendon transfer MCPJ flexion, IPJ extension & thumb adduction Causes: spasticity (eg CP), scarring (trauma and infection) Treatment: muscle release Aka intrinsic plus. Intinsic minus is used to describe Ulnar claw due to paralysis of the intrinsic muscles.
MALLET FINGER
Injury to extensor tendon of terminal phalanx Clinical features: loss of active DIPJ extension, normal passive DIPJ extension Types & Rx
Muscle (imbalance) Treat with mallet splint (conservative)
RUPTURED EXTENSOR POLICIS LONGUS
Injury to long thumb extensor after fraying Secondary to colle’s fracture, rheumatoid arthritis Rx: Tendon transfer usually required
DROPPED FINGER
Rupture of extensor tendon Patient unable to hold finger at extension at MCP joint Rx: (1) direct repair (2) distal portion of the tendon attached to adjacent finger extensor
BOUTONNIERE
Flexion deformity of PIP joint due to interruption of central slip of extensor tendon Lateral slips separate and head of proximal phalanx pops up in between Rx: post traumatic usually repairable. Chronic deformity (in RA) usually cannot be repaired
SWAN NECK DEFORMITY
Reverse of Boutonniere – PIP hyperextended, DIP flexed Due to imbalance of extensor vs flexor action in finger (commonly in RA) Rx: tendon rebalancing and joint stabilisation
TRIGGER FINGER (STENOSING TENOVAGINITIS)
Epidemiology: 55- 60 years old, women > men Causes: o Idiopathic o Congenital o Overuse / Local trauma causing sheath thickening o RA Clinical features: 41
LOOK FEEL MOVE
Flexion of ≥1 finger; commonly affecting middle & ring fingers of dominant hand (NB. finger doesn’t need to be in fixed flexion the whole time for it to be triggering) Ask if there’s any pain. Palpate for small nodule overlying the tendon sheath (usually approx. at the level of proximal transverse palmar crease). Triggering on extension, snapping sensation, tenderness over A1 pulley
Pathology: » Most often due to formation of nodule in FDS tendon where it glides under the A1 pulley in the region of the metacarpal head. » Flexor tendon trapped at entrance of tendon sheath; forced extension causes opening snap. Tender nodule may be felt in front of sheath at the MCPJ
DDx: » RA » Septic arthritis » Suppurative tenosynovitis » Tumour of tendon sheath » Dislocation » Dupuytren’s contracture
Staging & Mx (Green’s Classification): Stage
Pre-triggering Triggering Triggering & Locking Contracture
Features Hx of triggering not demonstratable on PE; tenderness Demonstrable catching, but patient can actively extend the digit Demonstrable locking, requiring passive extension (IIIa) or inability to actively flex (IIIb) Fixed flexion contracture of PIP joint
Mx: » Splinting (MCP joint flexed 15˚; not that efficacious) » Activity modification (i.e. reduce local trauma) » H&L into tendon sheath: high rate of success in female patients, with short duration of symptoms (<4mths), for discrete palpable nodule, single digit involvement, no associated conditions (e.g. RA, DM) » Surgical release o If injection therapy failed or if patient has other pathologies (e.g. RA) which is suspected to cause triggering & cannot be treated conservatively
o
o
Divide entire A1 pulley (tendon sheath) in the midline under vision, then ask patient to actively move the digit to confirm full release (motion encouraged immediately following the procedure) Complications: incising too distally cut the A2 pulley bowstringing
LUMPS PIGMENTED VILLONODULAR SYNOVITIS (PVNS) Definition: benign proliferative disorder of synovial lining of joint, bursa & tendon sheaths. Produces localised/diffused nodular thickening of the synovial membrane.
Epidemiology: commonest hand lump disorder, occurs in patients 20-50yo
2 types (+ sites) i) Diffuse form o Affects entire synovial lining of a joint, bursa or tendon sheath; affects large joints o More commonly in the knee, followed by the hip; ankle; shoulder joints ii) Localized/nodular form o Appears in the form of a localized nodule or mass in a synovium, and the surrounding synovium is generally normal o Affects tendon sheaths around small jts of hands & feet (termed nodular tenosynovitis)
Presentation: solitary, well circumscribed, tan colored, and sometimes has pale
X-ray: joint swelling, periarticular erosions, joint space narrowing, sub chondral cyst, osteophytes formation (secondary OA changes)
Treatment: Surgical Excision. However, diffuse lesions have a high rate of
yellow regions of lipid deposition. Insidious onset, dull aching jt pain, nodular or diffused jt swelling, ↓ROM, locking of joint.
recurrence (>50%) If refractory to repeated surgery, may be managed with lowdose radiotherapy
IMPLANTATION DERMOID CYSTS Usually sited along the volar surfaces of the fingers & palms Associated with trauma to the overlying skin – look for scars GOUTY TOPHI • Relatively mobile, stuck to tendon/joint, firm, can be soft, whitish, not transillumnant, tender in acute cases • Where: ear, ankle, elbow, finger 42
• •
Complications: skin ulceration DDx: PVNS
SQUAMOUS CELL CARCINOMAS Due to burns, sunburn, Arsenic Spread by lymphatics
ENCHONDROMA • Commonest primary bone tumor of hand • Hard, irregular, fixed swelling MALIGNANT MELANOMA NEUROMA
NEUROFIBROMA • Localised to digit and part of hand • 4-5cm, irregular and wrinkled skin, soft, mobile with skin, a/w cafe au lait spots
GIANT CELL TUMOUR LIPOMA
GLOMUS TUMOURS
AKA glomangioma, or nonchromaffin paraganglioma): a rare benign neoplasm, specialized arteriovenous anastamosis and usually found in the skin of the extremities. It arises from the glomus body (Component of the dermis layer of skin, involved in body temperature regulation. The glomus body consists of an AV shunt surrounded by a capsule of connective tissue. Glomus bodies are most numerous in the fingers and toes. The role of the glomus body is to shunt blood away from skin surface when exposed to cold temperature, thus preventing heat loss, and allowing maximum heat flow to the skin in warm weather to allow heat to dissipate.) Small, vascular & tender swelling, usually occuring at the region of the nail beds. Treatment: Radiotherapy and surgery
VASCULAR TUMOURS May have thrills and bruits PYOGENIC GRANULOMA Relatively common benign vascular lesion of skin and mucosa. Exact cause unknown Usually occurs in children and young adults as a solitary, glistening, friable, polypoid bright red papule or nodule. Prone to bleeding and ulceration. Ranges from few mm to several cm in size. Regressing lesions: Appear as soft fibroma. Normally occurs at head & neck, and distal extremities. Typically evolves rapidly over a period of a few weeks. Usually Hx of trauma preceding the onset of lesion may be elicited Untreated lesions eventually atrophy, fibrose and slowly regress.
OSTEOCHONDROMA
II. WRISTS Carpal Bones (lateral to medial): “Some Lovers Try Positions That They Cannot Handle” Scaphoid, Lunate, Triquetrium, Pisiform, Trapezium, Trapezoid, Capitate and Hamate Alignment in Gilula’s Arc (Carpal Arc)
JOINT DISORDERS CHRONIC CARPAL INSTABILITY Causes:
Injury Arthritis Kienböck’s disease (patchy lunate AVN after trauma)
Features:
Pain Weakness Clicking on movement Commonest type: Scapholunate dissociation – X-ray shows Terry Thomas sign (abnormal gap between scaphoid & lunate) 43
Rx:
Acute: reduction & fixation with plaster or K-wires Chronic: splintage, analgesics, H&L injections, arthrodesis
3. Occult 4. Interosseous Treatment:
KIENBOCK’S DISEASE
Patchy AVN secondary to post-stress/injury of the lunate. Predisposing factor: relative shortening of ulna excessive stress on lunate Presentation: ache and stiffness, localised to centre of dorsal wrist. Possible limitation of wrist extension Imaging: Earliest signs of osteonecrosis only detected by MRI. X-ray: increased density, later irregularity and flattening of bone. Eventually OA features. Treatment: (1) Osteotomy of distal end of radius (reduce pressure on lunate) (2) Microrevascularisation of bone if expertise available. (3) Partial arthodesis in late cases.
MUSCLE / TENDON TENOSYNOVITIS/TENOVAGINITIS -
TEARS OF TRIANGULAR FIBROCARTILAGE COMPLEX (TFCC)
TFCC fans out from the base of ulnar styloid process to medial edge of distal radius. S/S: chronic pain, clicking on supination and loss of grip strength Dx: Arthroscopy Rx: Arthroscopy—repair and remove fragments
Usually disappears after some months. So there’s no haste to Rx Aspiration (recurs 6-12 mths later) Excision if recurrence: Cosmesis or if ganglion is causing pain (recurs in 20-30%)
-
Extensor retinaculum contains 6 compartments which transmit tendons lined with synovium Causes: Unaccustomed movement, overuse, repetitive minor trauma. Sometimes spontaneous occurrence. Pathophysiology: resulting synovial inflammation secondary thickening of the sheath & stenosis of compartment further compresses the tendon 1st dorsal compartment (APL and EPB), and 2nd dorsal compartment (ECRL, ECRB) most commonly affected. 3rd compartment: extensor pollicis longus 4th compartment: extensor digitorum comunis (four tendons) and extensor indicis 5th compartment: extensor digiti minimi 6th compartment: extensor carpi ulnaris
LUMPS
DE QUERVAIN’S DISEASE (STENOSING TENOSYNOVITIS)
GANGLION
Definition:
Cystic degeneration of joint capsule or tendon sheath. Locations (from most to least common): o Dorsum of wrist (at scapholunate joint) o Volar aspect of wrist o Volar aspect of MCP joint o Dorsal aspect of DIPJs (termed mucous cysts) Well defined, cystic, non-tender, positive transillumination. Contains glairy fluid (i.e. uncooked egg-white colour & consistency). May be attached to tendon.
Entrapment tendinitis of the tendons contained within the first dorsal compartment at the wrist (MCQs: APL & EPB); causing pain with tendon movement Pathology
Features:
Types:
1. Simple 2. Compound – chronic inflammation distends tendon sheath above & below the flexor retinaculum ( a/w TB, RA)
Inflammation causes thickening & stenosis of synovial sheath of the 1st dorsal compartment containing the EPB & APL Cause: wringing out clothes, pruning roses, cutting with scissors, cradling baby
Women 30-50 YO Pain over radial styloid process, swelling & palpable thickening of fibrous sheath along course of tendons Finkelstein’s test +ve (exquisite pain in region of radial styloid on forced ulnar deviation of wrist with thumb in fist); NB. This test may also be positive in CMC degenerative joint disease, e.g. OA 44
DDx:
Arthritis thumb MCP jt, scaphoid fracture, scapholunate instability Radiograph:
Aetiology
o o
If diagnosis is still in doubt, obtain Robert’s view in order to profile CMC joint Treatment
Conservative NSAIDs Cold compression H&L injection: inject in sheath AND/OR Thumb spica splint for 1 month
Surgical Decompression of 1st compartment sheath (tendon sheath release) - Determine if there is any instability of the wrist joint & correct it if present
o
Pathophysiology
o
Complications of surgical release:
Infection Radial n palsy (+ve Tinel’s) Snapping of extensor tendon (due to extreme radial release of extensor retinaculum) APL & EPB tendon adherence (will limit thumb movements)
o
-
Extensor Carpi Radialis Brevis (most power extensor of the wrist— Second Compartment o Pain and point of tenderness just medial to anatomical snuff box th Extensor Carpi Ulnaris – 6 compartment o Pain and point of tenderness immediately distal to head of ulnar Treatment: Splintage and H&L injections usually effective.
NERVES CARPAL TUNNEL SYNDROME
Pressure on nerve blood flow obstruction in vasa nervorum venous congestion & oedema With time, fibroblast proliferation occurs in the nerve inefficiency of cell transport mechanisms and the sodium pump n. conduction impairment
Features
OTHER SITES OF EXTENSOR TENOSYNOVITIS -
Most common cause is IDIOPATHIC! Others include Anatomical abnormalities Bone: previous wrist #s (e.g. Colles’ #), acromegaly Soft tissues: lipomas, ganglia Physiological abnormalities Fluid balance alterations: pregnancy, menopause, hypothyroidism, obesity, amyloidosis, cardiac/renal failure Inflammatory conditions: RA, GA Neuropathic conditions: DM, alcoholism
Symptoms may present at night or with certain activities e.g. driving, reading newspaper. Pain, paraesthesia numbness over lateral 3.5 fingers. Burning pain & paraesthesia over median n distribution. Usually occurs at night, waking the patient up, relieved by shaking arm and/or hanging arm over side of bed. Late symptoms: Wasting of thenar eminence, weak thumb abduction (autonomic innervations by median n.), decreased sensation of lateral 3.5 fingers Tinel’s & Phalen’s tests positive DDx:
o o o
Definition
Compression ischaemia of median nerve Epidemiology
40-50YO Women > men
o
Cervical n. root lesions (e.g. cervical spondylosis of C6-7 level, or secondary to a cervical disc herniation) Thoracic outlet syndrome AIN syndrome: entrapment usually at the origin of the deep head of pronator teres; supplies FPL, pronator quadratus and radial side of FDP inability to make OK sign but sensory INTACT Pronator syndrome: compression of median n. by ligament of Struthers (fibrous band arising from medial epicondyle of humerus, attaches to supratrochlear spur on the lower anterior humerus), pronator teres muscle or proximal arch of FDS
Investigations
Anatomical boundaries
Radial side: scaphoid & trapezium Ulnar side: pisiform & hook of hamate Volar aspect: trasverse carpal ligament
Nerve conduction studies (to rule out other differentials)
45
Treatment
Non-surgical NSAIDs Splinting of wrist in a neutral position (especially at night) H&L injections just proximal to the carpal tunnel Surgical Carpal tunnel decompression (division of flexor retinaculum under tourniquet control) – either as open or endoscopic procedure Potential complications to be explained to patient o Scar formation (keloid/hypertrophic scars) o Scar tenderness post-op o Failure to relieve symptoms due to incomplete division of flexor retinaculum o Nerve injury – palmar cutaneous n. (lies supf to flexor retinaculum) and motor branch of thenar muscles (usually leaves the radial side of median n. towards distal extent of the standard incision) – risk of n. injury can be decreased by making the skin incision on the ulnar side of the palmar crease
X-ray: Narrowing of joint spaces, osteophytes, bone sclerosis, irregularity of carpal
bones, signs of old injuries. Management: For CMC joint: Corticosteroid injection may help to relieve the pain and ↓ ROM. Everything: Rest, splint, surgery if fracture or if necessary (e.g. arthrodesis) o
TRUE [MCQ]
OA of CMC joint of thumb can be treated conservatively / by excision arthroplasty / by replacement arthroplasty OA of DIPJ can be treated by arthrodesis
IV. BONE DISORDERS OF WRIST & HANDS MCQ Commonest complication of injury in hand fractures is tendon adhesion But deformity in hand fractures is due to malunion! COLLES’ FRACTURE
ULNAR TUNNEL SYNDROME
Compression of ulnar n. as it passes between pisiform & hook of hamate (Guyon’s canal) Clinical features: small muscle wasting, weakness of hand, sensory disturbance on volar aspect of little finger. Causes: ganglions, trauma, ulnar artery disease, old carpal or metacarpal #s DDx: Cubital tunnel syndrome, cervical spondylosis
III. JOINT DISORDERS OF WRIST & HANDS RHEUMATOID ARTHRITIS OSTEOARTHRITIS Primary OA: usually in DIPJ (most common) and Carpometacarpal joint of the thumb in postmenopausal women. Usually a presentation of polyarticular disease. Secondary OA: history of trauma or # e.g. scaphoid #, Kienbock’s disease Features: bilateral pain, swelling & tenderness. Usually starts with 1 or 2 fingers, which usually spreads to all fingers and both hands. Bony thickening around the DIPJ (Heberden’s nodes), PIPJ (Bouchard’s nodes) & carpometacarpal joint of thumb. Square hand. ↓ ROM & crepitus. In CMCJ OA, tenderness localised to 1 cm distal to radial styloid.
Fracture of radius within 2.5 cm of wrist (deformity) – extra-articular #! ‘Dinner-fork’ deformity: palmar & ulnar angulation (AUA), dorsal & radial displacement (DRD) of distal fragment, torsional deformity, DRUJ disruption (ulnar styloid avulsion or tearing of fibrocartilage)
Mechanism: FOOSH, commonly in elderly osteoporotic women
S/S: wrist pain & tenderness over distal radius, characteristic deformity
X-ray: distal fragment is
o o o o o o
Dorsally displaced with dorsal comminution Dorsally tilted fragment with apex of fracture volar Supinated Radially deviated Shortened Extra-articular features:
46
Radial height from scaphoid
From head of ulna to tip of radial styloid
Normal: 11mm If #: <11mm
Volar tilt
Seen on lateral view
Carpal tunnel syndrome Delayed rupture
Normal: 22˚ If #: <20˚
Reduction method
Backslab
External fixation Post reduction
Radioulnar joint subluxation Associated scaphoid # Comminution of radial fragment Persisting stiffness
Normal: 11˚ If #: <11˚
Management: Manipulation
Radial Inclination
Indicated if displaced, deformity or angulation present, joint line in lateral X-ray tilted ≥10o posteriorly 1. Bier’s block (IV lignocaine), haematoma block (intraosseous) or GA 2. Disimpaction (distraction): apply traction in line of forearm with countertraction applied by assistant to flexed elbow 3. Maintain traction with elbow extended 4. Correct anterior angulation & post displacement: apply pressure anteriorly 5. Correct radial displacement: push distal fragment ulnarwards 6. Correct ulnar angulation by putting wrist in full ulnar deviation Apply backslab w wrist in full pronation, full ulnar deviation & slight palmar flexion Plaster should extend from olecranon to metacarpal heads Final moulding with pressure over post-lat aspect of distal fragment If # is unstable
sweaty skin Mx: physioRx, rest & splintage for pain, chemical sympathetic blockade if severe Most common complication Of the extensor pollicis longus. Mx: tendon transfer TFCC tear Shoulders & fingers
SMITH’S FRACTURE (AKA REVERSED COLLES’ #) Ant displacement & post angulation of distal fragments due to fall on back of hand Mx: M&R, splintage with wrist extended, above elbow cast for 6 wks BARTON’S FRACTURE Distal radial # with fracture line running into the wrist joint; anterior displacement of distal fragment carrying the carpus with it; a/w joint subluxation (volar/dorsal)
Mx: inherently unstable, therefore require ORIF
SCAPHOID FRACTURE Accounts for 75% of wrist # Mechanism of injury: FOOSH with wrist extended. Combination of dorsiflexion & radial deviation Blood supply of scaphoid diminishes proximally [supply by dorsal and volar branches of radial artery] NB. Rare in the elderly osteoporotic patient [MCQ]
X-ray: Repeat to ensure adequate reduction F/U: check circulation & assess swelling, complete plaster if swelling is minimal Finger, elbow & shoulder exercises
Complications
Malunion / persistent deformity
Radial drift of distal fragment
Sudeck’s atrophy
Pain, trophic skin changes, vasomotor instability & osteoporosis due to sympathetic overactivity - swelling, erythema, warmth, changing to cyanosis with blotchy, cold &
Clinical Features:
o
Pain in anatomical snuffbox*** 47
o o o
Pain over scaphoid tubercle (following course of FCR) Restriction of thumb movement (not so much the wrist movement) Axial loading along 1st metacarpal bone also increases the pain
X-ray: often hard to see, 4 views required (AP, lat & 2 oblique), repeat in 14 days if unsure (# may not be seen in first few days). Usually # is through narrowest part of bone (i.e. waist); other potential # sites include tubercle and proximal pole #.
COMPLICATIONS OF WRIST FRACTURES • • •
•
Type a
Type b
Type c
Mx: Initial Mx
Scaphoid plaster & sling, repeat X-rays in 2 wks
Scaphoid plaster for 6 wks: Fix hand in full pronation, radial deviation & moderate dorsiflexion. “Glass holding position” Plaster to extend from below elbow to just below MCP & IPJ of thumb. Incorporate proximal phalanx of thumb. » 90% should heal. » If still tender and X Ray shows no healing at 6 wks, continue plaster cast for another 6 wks » Consider internal fixation and bone graft if non-union found at f/u at 12 wks Displaced # ORIF (with compression screw) Scaphoid tubercle # needs no splintage; treat it as wrist sprain. Undisplaced #
Cx:
o
o
o
»
AVN of proximal pole causing secondary radiocarpal OA (X Ray at 2-3 months shows density of proximal fragment) – excise scaphoid, consider arthrodesis of carpal bones Non-union – plaster fixation, internal fixation & bone grafting. Excise radial styloid if OA threatens Poor blood supply at proximal part of scaphoid, hence union may take several months. Osteoarthritis
Most common complications are poor grip strength, stiffness and radial shortening 80% have normal function in 6-12 months Early Cx: O Difficult reduction +/- Loss of reduction O Compartment syndrome O EPL tendon rupture O Acute carpal tunnel syndrome O Finger swelling with venous or lymphatic block Late Cx: O Malunion, radial shortening O Painful wrist secondary to ulnar prominence O Frozen shoulder (shoulder-hand syndrome; aetiology unknown) O Post-traumatic arthritis O Carpal Tunnel Syndrome O Reflex sympathetic dystrophy
LUNATE DISLOCATION Rotation & anterior displacement of lunate X-ray: crescent moon shape of bone becomes obvious on AP view Cx: median n. palsy, Sudeck’s atrophy, AVN (& secondary OA) Rx: closed reduction under GA + plaster fixation, open reduction if closed reduction fails PERILUNATE DISLOCATION More common than Lunate dislocation Rest of Carpus displaced backwards Lunate vs. perilunate dislocation The key to differentiation between both is what is centered over the radius. If the capitate is centered over the radius and the lunate is tilted out, it is a lunate dislocation (left). If however the lunate centers over the distal radius and the capitate is dorsal, we are dealing with a perilunate dislocation (right). Radiology Assistant, Wrist – Carpal Instability
48
SCAPHOID DISLOCATION Displacement is usually anterior Rx: closed reduction + plaster fixation in stable position. If instability is present, fix with K-wires BENNETT’S FRACTURE Fracture of 1st metacarpal bone with fracture line extending to the CMC joint Small medial fragment of bone seen on X-ray. Proximal & lateral subluxation of 1st metacarpal present. Rx: closed reduction & plaster fixation GAMEKEEPER’S THUMB Rupture of ulnar collateral ligament. Also equals to skiier’s thumb Mechanism: forced abduction of thumb (FOOSH, killing of game animals by breaking their neck in between thumb and finger) Progressive MCPJ subluxation and impaired grasp results, with tenderness over medial side of MCPJ. May be a/w avulsion fracture Rx: Scaphoid cast for 6 wks if minimally displaced. Internal fixation, Sx repair, MCPJ fusion depending on severity of displacement / tear. BOXER’S FRACTURE At 5th metacarpal (picture on the right) 60 degree flexion at fracture site acceptable. Dropped knuckle deformity permanent. METACARPAL SHAFT FRACTURE Mostly stable and undisplaced. If displaced, need ORIF with plates or K-wire. Make sure that there is no rotational deformity. Otherwise will have scissoring of fingers on flexion. RUGGER JERSEY FINGER Results from forceful hyperextension of DIPJ with FDP in maximal contraction (e.g. player grasping the jersey of his opponent during tackling) – opposite MOI from mallet finger Tendon may rupture directly from its insertion into the bone, or it may avulse bone fragment from the base of distal phalanx
Patient usually presents late Ring finger most often involved (75%) Pain & tenderness over volar distal finger, finger lies in slight extension relative to other fingers in resting position
Acronym: ReaCTeD H & L INJECTIONS Common hand indications: Trigger finger, De Quervain’s tendosynovitis, CTS, RA Up to 2 injections on the same digit (interval of at least 3 months) Complications: tendon rupture BRACHIAL PLEXUS LESIONS Types • Lesions in continuity – more than half of plexus injuries. Traction commonest cause. Nerve roots affected postganglionic. Treatment is expectant. • Lesions with ruptured nerve roots – only surgical intervention can offer any hope of recovery • Complete avulsion lesions – nerve avulsed from cord (both dorsal n ventral roots ruptured) as opposed to brachial plexus injuries where dorsal roots are spared. • Partial avulsion – dorsal roots spared thus muscle paralysis with preservation of sensation Long standing plexus lesions • Erbs’s palsy (C5 C6, sometimes c7) – overweight babies with shoulder dystocia at delivery (upper obstetrical palsy); waiter’s tip deformity – shoulder internally rotated, elbow extended, wrist flexed n pronated. N to rhomboids and long thoracic N spared. • Klumpke’s palsy (C8, T1) – lower obstetrical palsy; intrinsic muscles wasted, clawhand, sensory loss on medial side of forearm n wrist, commonly a/w Horner’s syndrome because T1 is affected. • T1 root only – wasted intrinsic muscles, sensory loss on medial side of hand, (incomplete lower obstetrical palsy, cervical spondylosis, neurofibromatosis, CA) • Acute traumatic lesions – commonest mechanisms - depression of shoulder with lat flexion of the neck to opposite side or traction of arm will find bruise on lateral jaw, inferior jaw and on shoulder. o Might have subclavian artery trauma
49
SEDDON’S CLASSIFICATION 1.
2.
3.
Axonotmesis: loss of the relative continuity of the axon and its covering of myelin, but preservation of the connective tissue framework of the nerve • Distal wallerian degeneration occurs. • Loss in both motor and sensory fnx is more complete with axonotmesis than with neuropraxia, • Usually the result of a more severe crush or contusion than neuropraxia. • Regeneration requires a number of weeks.
Neurotmesis: • Occurs on severe contusion, stretch, lacerations. • Surgical repair essential and quality of recovery always imperfect. For neurotmesis is better to use a new, more complete classification, , called Sunderland System
Wallerian Degeneration: degeneration of axons distal to sight of transection (resorbed by phagocytes)
SUNDERLAND SYSTEM
Neuropraxia: mildest for nerve injury. an interruption in conduction of the impulse 1. down the nerve fiber with axonal continuity conserved 2. • Likely a biochemical lesion caused by concussion /shock-like injuries to the fibres. 3. • Recovery takes place without wallerian degeneration. • Temporary loss of function reversible within hours to months of the injury (the average is 6-8 weeks). (not the ‘1mm/day’ rule). Nerve • Frequently greater involvement of motor than sensory function with autonomic function being retained. Brachial plexus
First-degree: "Seddon’s neuropraxia" Second-degree: "Seddon’s axonotmesis" Third-degree: endoneurium disruptured, epineurium & perineurium intact • Thus, when the axons regenerate, they may enter an incorrect nerve sheath, resulting in abnormal regeneration. Site of Entrapment
Provocative Test
Supra/infraclavicular
Arm elevation Pressure between the scalene muscles
Radial nerve
Distal forearm
Forearm pronation + wrist ulnar deviation Pressure over tendinous junction of ECR and brachioradialis
Ulnar nerve
Median nerve
Cubital tunnel
Elbow flexion + pressure on cubital tunnel region
Guyon's canal
Pressure at Guyon's canal
Proximal forearm
Forearm supination + pressure on pronator teres
Carpal tunnel
Wrist flexion and/or extension with pressure proximal to carpal tunnel
Accompanying the loss of the nerve sheath is intraneural scarring, which further obstructs axonal regrowth through the site of injury. • Recovery may range from poor to complete and depends on degree of intrafascicular fibrosis; Fourth-degree: interruption of all neural and supporting elements; epineurium intact; the nerve is usually enlarged. Fifth-degree: complete transection with loss of continuity. Grade V corresponds to Seddon's classification of a neurotmesis lesion
•
MCQ: Worst nerve injury (after surgical intervention) – traction injury 4. 5.
ZONES OF THE HAND
Zone 2 is no man’s land. Return of function is difficult in Zone I because of short stump of FDP
50
IMPORTANT ORTHOPAEDIC CONDITIONS IN THE HIP
PELVIC FRACTURES
Most common fracture involves pubic rami, followed by ilial, ischial, acetabular,
coccygeal and sacral bones
Tile Classification
Type A
• • •
Type B
Type C
Type A: stable, minimally displaced, includes avulsion fractures and fractures not involving pelvic ring, e.g. rami fracture Type B: partially unstable, rotationally unstable, but vertically stable, e.g. “open book” fracture from external rotational force to pelvis Type C: unstable, rotationally and vertically unstable, associated with rupture of ipsilateral ligaments, e.g. vertical shear fracture
Treatment • ABCs • Assess genitourinary injury (rectal exam/vaginal exam mandatory) • Type A - bedrest and mobilization w walking aids • Type B/C - external or internal fixation Complications • Hemorrhage - life threatening • Fat embolism • Bladder/bowel injuries • Neurological damage • Obstetrical difficulties • Persistent sacro-iliac (SI) joint pain • Post-traumatic arthritis of the hip with acetabular fractures [MCQ] Trendelenburg test is a test of stability of pelvis on femur
APPROACH TO HIP PAIN
Diagnosis • History of injury, high energy trauma • Examination reveals local swelling, tenderness; if unstable, may have • Deformity of the hips and instability of pelvis with palpation • X-rays (i.e. AP, inlet, and outlet views) judet view for acetabular fractures
CAUSES OF PAINFUL HIP
6 lines to look for in a pelvic X-ray specifically looking for acetabular fracture 1. Iliopectineal line – anterior column of pelvis 2. Ilioischial line – posterior column 3. Acetabular teardrop – should in line with ilioischial line 4. Dome – superior weight bearing area costing of both ant and post column 5. Ant wall of acetabulum 6. Post wall of acetabulum
1. Site of pathology
Referred pain Joint disorders
Periarticular disorders
Discogenic dz Infection Perthes’ dz OA Osteonecrosis RA Hernia Tendinitis
Slipped capital femoral epiphysis Bursitis / synovitis
HISTORY AND PHYSICAL EXAMINATION: - Hip pain (anterior) — usually at groin - Pain at gluteal region (posterior) — usually lumbar pathology
2. Cause of pathology
-
Vascular: Infection: Trauma: Autoimmune: M I
Perthes’ disease, AVN OM, TB, Transient synovitis OA, dislocation, fracture RA
51
- N - Congenital:
SCFE, CDH
3. Look for predisposing factors e.g. Osteoporosis and fall risk 4. Look for complications of pathology 5. Assess premorbid status (goal for mgmt is to regain premorbid status)
» Medial gap – the greater the gap, the greater the possibility of dislocation » Neck/shaft angle (normal 120-135˚; <120˚ coxa varus, >135˚ coxa valgus) 4. Other neighbouring structures » Acetabular margins » Sacroiliac joint » Joint space » Ischium
6. Assess carer support
COMMON HIP DISORDERS BY AGE <1YO 1-5YO 5-10YO 10-20YO Adults
CDH Transient synovitis (commonest cause of hip pain in child) Septic arthritis Perthes’ disease Juvenile Chronic Arthritis SCFE OA, AVN, RA
FEATURES OF AP HIP X-RAY TO NOTE 1. Any fractures » Neck of femur (subcapital, transcervical, base of neck) » Intertrochanteric » Subtrochanteric 2. Quality of bone » Bone texture » Density of femoral head 3. Lines » Shenton’s line – broken in • Congenital dislocation of hip • Posterior dislocation of hip • Pathological dislocation of hip • Tom-Smith arthritis (septic arthritis of the hip in infants which destroys the whole head of femur) Not broken in impacted NOF # » Perkin’s line (line drawn along lateralmost aspect of acetabular roof) & Hilgrenreihner’s line (line drawn horizontally through superior aspect of the triradiate cartilages) – both lines are perpendicular to one another. Femoral head should be in the inner lower quadrant of both these lines. » Acetabular index – should be low (want acetabulum to hug femoral head)
GAIT ANALYSIS Normal Gait 1. Stance phase = heel strike + mid stance + push off 2. Swing phase = acceleration + initial swing + midswing + deceleration Type of gait Antalgic Trendelenburg
Notes Short stance phase ‘Sound side sags’
Short leg
Ipsilateral hip drops when weight is on short leg
Adductor lurch Toe to heel High steppage Broad based Parkinsonian / festinant Spastic (scissoring)
Foot lands flat or on ball instead Small shuffling steps Jerky, feet in quinus, hips adducted
Causes Pain (infxn, inflammation, transient synovitis) Contralateral abductor weakness, hip dislocation/ subluxation, short NOF, hip pain Previous # or congenital shortening Hip dysplasia, CP CP, club foot, idiopathic Proprioception loss, foot drop (damage to L5; common peroneal n. palsy) Ataxia (cerebellar lesions) Parkinson’s disease UMN lesion e.g. cord compression, multiple sclerosis or CP
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CONGENITAL DISLOCATION OF DYSPLASIA OF THE HIP (DDH)
THE
HIP (CDH) / DEVELOPMENTAL
Features
Easily dislocatable hip secondary to shallow acetabulum – usually posterior & superior dislocation 1 per 1000 live births (common enough for it to be screened by neonatologists) Girls > boys Bilateral in 30% Risk factors o 1st female child o Family history o Breech delivery o Condition predisposing to crowding of uterus (multiple pregnancies, oligohydramnios, fibroids, baby too big, mother too small)
U/S not done at birth because laxity of hip joint, may get spurious reading at birth (in order for baby to come out of birth canal) – hence earliest U/S is at 6 weeks When to do U/S – For high-risk cases (e.g. positive family history / extended breech delivery) / hip laxity / hip clicks – To ensure concentric stable reduction after treatment » Weekly after with splint to ensure reduction and correct application of splints » Every 6 weeks after once hip reduced » Most effective <3 months old (3 months onwards: X-rays; must ensure concentric reduction with good acetabular cover, if not mechanical forces of hip not evenly distributed may get OA) –
•
Mx
1. Watch
Possible causes:
Intrauterine malposition (a/w breech presentatn) Tight iliopsoas
Postnatal posture (hip extension) Hypertrophic lig teres Hourglass capsule
Shallow acetabulum (acetabular dysplasia) Fibrous tissue in acetabulum
Repeat U/S at 4-6 weeks – If hips reduced and stable, no further Rx – Otherwise treat as DDH
Physical examination:
Assymetrical skin creases, short limb, internally rotated, ↓ hip abduction ROM Ortolani’s test (tests reducibility) – impeded hip abduction + clunk as dislocation reduces Barlow’s test (tests dislocatability) – dislocate the hip by flexing the hip joint and adducting it followed by posterior force in the line of the shaft of femur. Trendelenburg’s test – positive Ix
• •
U/S Hip
Abnormal acetabular shape and femoral head position
X-ray
Abnormal sloping of acetabular roof shallow acetabulum small underdevted femoral head femoral head displaced upwards & outwards
Diagnosis is CLINICAL U/S or X-rays can be used but both are NOT used to diagnose at birth – X-ray: radiation + hip is not ossified
Observe if – Hip laxity only – Hip clicks
2. Abduction splint / Pavlik harness
When to watch instead of intervening for DDH? When you are not sure of the diagnosis. 0 to 6 months – Abduction splint (old mtd) or Pavlik Harness – Repeat U/S in harness after 1/52 and out of harness at 6/52 – Worn for at least 3 months until 1st X-rays – If X-rays show concentric hips with good acetabular cover, then wean off splints
For Pavlik harness: - Human position: 50deg of abduction of each side and 100deg of flexion (preferred position) - Frog position: entire hip down at 90deg, can cause AVN (femoral head very sensitive to tension) 53
3. Close reduction & hip spica
0 to 6 months If unable to achieve stable reduction with splints then closed reduction and hip spica attempted –
BEFORE
4. Open reduction & hip spica
Acetabular surgery (Salter osteotomy) - Done at 2yo - In Salter’s osteotomy the entire acetabulum, together with the pubis and ischium, is rotated anteriorly and laterally as a unit, with the symphysis pubis acting as a hinge. The osteotomy is held open anterolaterally by a wedge of full thickness bone graft, usually taken from the anterior part of the iliac crest - Osteotomy redirects entire acetabulum so that its roof covers femoral head both anteriorly and superiorly - In young children, the acetabular deficiency is usually anterior, and therfore the Salter Osteotomy is designed to provide coverage anteriorly at the expense of posterior coverage; - Success of procedure depends to some extent on the flexibility of the symphysis pubis (which decreases w/ age) - Importance of screening so as to intervene earlier
AFTER
Decreased joint space after reduction
6 to 12 months – Closed reduction can still be attempted but more difficult to achieve stability – Open reduction then done 12 to 18 months – Child is already weight bearing – Open reduction usually involves femoral derotation and shortening – Acceptable is thought to remodel accordingly Above 18 months – Potential for acetabular remodeling is less – Both acetabular and proximal femoral surgery will be required.
Prognosis
Good results if treated <6yo For chronic neglected dislocations: reductions usually not attempted if o >8yo for unilateral (no more remodelling past 8yo :. reduction may cause OA) o >5yo for bilateral Consequences of not reducing o Partially dislocated (formation of false joint) – progressive deformity, disability & secondary OA hip o Completely dislocated – will have Trendelenburg gait, cost of energy to walk will be high hence not ideal (have to sit on side back pain, will get scoliosis o Bilateral: waddling gait, hips dislocated behind so nothing to hold pelvis in between, would get lordosis o ALL will walk assuming muscles and nerves are functional 54
DISLOCATION OF THE HIP Mainly seen in artificial hips Cause
Pyogenic arthritis
X-ray
Absent femoral head
Management
Traction, open reduction, varus osteotomy of femur
Muscle imbalance
Valgus femoral head
As for CDH + muscle rebalancing operation
Trauma
Look for associated acetabular rim #
Reduction, ORIF if rim # present
Myositis ossificans Knee injury Coxa magna (occurs in up to 50% of children after a hip dislocation)
PERTHES’ DISEASE (COXA PLANA) Features
Femoral head necrosis secondary to disturbance in blood supply 4-8YO, boys:girls = 4:1, 5-10% bilat DDx: non-specific transient synovitis Precipitant: effusion, trauma or synovitis occluding blood supply to femoral head
Dislocation after Total Hip Arthroplasty (THA)
Stages (similar to AVN classification)
•
Posture
Stage 2: revascularisation & repair. X-ray shows ↑ bone density Stage 3: distortion & remodelling. Epiphyseal collapse, flattening or enlargement may result.
Anterior dislocation: hip flexion, abduction and external rotation [MCQ] Posterior dislocation: hip flexion, abduction & internal rotation, shortened leg. X-ray shows smaller femoral head and less prominent trochanter because leg adducted and internally rotated. [MCQ: AVN is a distinct possibility]
Hip pain & irritation Limp, shortened leg Decreased abduction & internal rotation
Treatment
X-ray:
• •
Occurs in 1-4% of primary THA and 16% in revision cases About 74% are posterior dislocations, 16% anterior and 8% central THA are unstable in the position of flexion and internal rotation
1. Muscle relaxtion is key—conscious sedation (IV fentanyl) or spinal or GA 2. Assistant applies downward pressure to pelvis 3. Reduction for posterior dislocation — Fully flex hip, abduct and externally rotate hip, apply upward traction on femur (i) Known as Bigelow’s manoeuvre (ii) Maintained until patient is pain-free (approx. 2 weeks) 4. Reduction for anterior dislocation – Fully flex hip, adduct and internally rotate hip, apply downward pressure on femur (Barlow’s equivalent) Complications
Post-traumatic arthritis due to cartilage injury or intra-articular loose bodies # femoral head, NOF, femoral shaft Slipped upper femoral epiphysis AVN femoral head Sciatic nerve palsy (esp when rim # is present) Femoral vein compression – causing thrombosis & embolism Secondary OA hip Recurrent dislocation
Stage 1: ischaemia causing femoral head bone death. Normal X-ray
Clinical features:
Apparent widening of joint space ↑ epiphyseal density – healing & reossification Flattening, fragmentation & lat displacement of epiphysis Subchondral fracture Metaphyseal rarefaction & broadening
Small dense capital epiphysis
Catterall grading
According to degree of femoral head involvement Grade
Severity
Prognosis
2
≤ 50 % involvement with a sequestrum
Bony collapse inevitable
3
~75% involved, with collapse & sequestrum
4
whole epiphysis involved
Bony collapse inevitable. Poor prognosis
1
Involves anterior portion of epiphysis only. No collapse or sequestrum
Revascularisation may be complete w/o bone collapse
55
Mx: Initial
Skin traction until pain resolves
Definitive
Good prognosis: Onset <6YO Partial fem head involvement No metaphyseal rarefaction Normal fem head shape
No Rx needed
Poor prognosis: Onset >6YO Complete fem head involvement Severe metaphyseal rarefaction Lateral fem head displacement
Containment of femoral head Abduction splint OR varus osteotomy of femur OR innominate osteotomy of pelvis
AVN Coxa vara – Rx: osteotomy to prevent secondary OA Secondary OA Bilat SCFE: 1/3 of cases
Mx
Manipulation is contraindicated!!! Displacement <1/3 of epiphyseal width
Accept position Epiphyseal fixation with pins
Displacement 1/3 to half of epiphyseal width
Epiphyseal fixation with pins Osteotomy: if residual deformity is present even after remodelling
Displacement >half of epiphyseal width
Epiphyseal fixation with pins +/- osteotomy OR Epiphyseal replacement & fixation with pins
SLIPPED CAPITAL FEMORAL EPIPHYSIS (SCFE) Epidemiology:
Usually occurs in very tall, fat pubertal (11-15yo) boys with delayed gonadal development. Boys > girls History:
Pain in groin ± radiation to anterior thigh or knee (referred) Limp Hx of trauma Physical Examination:
Coxa vara deformity Externally rotated short leg Decreased abduction & internal rotation Pain on movement
X-ray:
Wide & “woolly” epiphyseal plate Trethowan’s sign: femoral head falls below line drawn along superior surface of femoral neck (normally cuts through fem head) – “ice-cream falling off cone” Complications
PYOGENIC/SEPTIC ARTHRITIS Epidemiology:
Children <2yo, usually Staph by haematogenous or local spread (from femoral OM) *** True clinical emergency; if undiagnosed, may result in complications such as complete destruction of the articular cartilage and the underlying epiphysis, loss of the adjacent growth plate, and dislocation of the joint *** Investigations:
» »
Culture blood & joint aspirates Choice of ABx depending on Gram stain results & culture sensitivities
Management:
Medical o IV antibiotics (penicillin – for strep; and cloxacillin – for staph) o ESR and CRP levels are valuable indicators of clinical response. The CRP is generally more sensitive than the ESR, and antibiotics should be continued at least until this measure has normalized. o Switching to oral antibiotics is also acceptable, provided that adequate blood levels of the antibiotic are demonstrated, the patient’s parents are reliable, and the antibiotic does not cause a gastrointestinal disturbance that would interfere with its absorption. Surgical o Consider septic joint to be a closed abscess :. Don’t expect ABx alone to work 56
Perform repeated percutaneous joint aspirations in cases of involvement of an easily accessible peripheral joint; a clinical course shorter than 6 days; and no evidence of an associated OM, immune deficiency, or other chronic illness o If the patient's condition fails to improve, perform open drainage in OT Definitely indicated in the hip and the shoulder and in peripheral joints that do not respond to percutaneous aspiration. Indicated in patients who are systemically ill, and it should be given greater consideration when the suspected organism is S aureus or a gram-negative bacterium that produces cartilage-damaging enzymes. (Gonococcal arthritis less likely to rapidly damage a joint :. may be managed with repeated aspirations if the joints involved are peripheral. Open drainage should still be performed in cases of gonococcal arthritis of the hip.) o If treatment was significantly delayed, substantial capsular damage may have occurred. If instability is suspected, immobilize the patient for a longer period. A neglected septic hip with radiographic instability requires a spica cast, and an unstable shoulder requires a sling and swathe. Follow-up (at least up to 1 year after surgery) o Whether joint function has returned to normal o No radiographic evidence suggestive of loss of joint space, AVN of the epiphysis, joint instability, or damage to the growth plate o
TB HIP Groin / thigh pain, limp, muscle wasting, limb shortening, hip deformity, ↓ROM X-ray:
General rarefaction Femoral epiphyseal enlargement Bone abscess Articular destruction Healing by fibrous ankylosis
Management:
Anti-TB drugs Skin traction Evacuate abscess, joint debridement Arthrodesis or joint replacement if joint is destroyed
RA HIP Multiple joint involvement, groin pain, limp, ↓ & painful movement X-ray:
TRANSIENT SYNOVITIS Epidemiology: boys 2x more than girls, 3-10yo; commonest cause of irritable hip History o Unilateral groin/hip pain o Very young children: no other symptoms except crying at night o Recent Hx of URTI, pharyngitis, bronchitis or otitis media (in >50% of cases) o No definitive cause known Physical examination o Antalgic gait o Tenderness during palpation even during passive movement o Mild restriction of motion (in 2/3 of patients) o Log roll (most sensitive test): detect involuntary muscle guarding of one side compared to the other Treatment o Apply heat & massage o Bed rest for 7-10 days in a position of comfort o Medications: NSAIDs (naproxen/ibuprofen)
Osteoporosis Decreased joint space Periarticular erosion and bone destruction Management:
Total hip replacement
OA HIP Causes:
Young adults
Congenital subluxation Perthes’ disease SCFE Coxa vara, Acetabular deformities / injury
Older adults
RA, AVN, Paget’s dz, Primary OA 57
Clinical features:
More common in Caucasians (in Caucasians, OA hip > OA knee; in Asians, OA knee > OA hip) Groin pain ± radiation to knee Joint stiffness due to synovial hypertrophy & capsular fibrosis Limp, Trendelenburg positive Fixed flexion deformity Leg in ext rotation & adduction posture Decreased ROM X-ray:
Decreased joint space Subarticular sclerosis Cyst formation Osteophytes (‘elephant trunk’ osteophytes)
Management:
Analgesics Physiotherapy Walking aids Surgery: Osteotomy, arthroplasty
AVASCULAR NECROSIS OF THE HIP AETIOLOGY / PREDISPOSING FACTORS: Traumatic Atraumatic
Neck of femur fracture Fracture-dislocation or dislocation of the hip joint Iatrogenic Glucocorticoid use, including TCM (causes two things: 1) changes in circulating lipids microemboli; 2) changes in venous endothelium stasis increased intraosseous pressure necrosis) Alcohol Congenital Perthes’ disease SCFE-associated AVN Inherited thrombophilia e.g. Factor V Leiden Immunocompromised states Systemic lupus erythematosus (3-30% of SLE patients get AVN; SLE+steroids highest risk) HIV
Transplant surgery Others Antiphospholipid antibodies Gaucher disease (hereditary, autosomal recessive disease of glucocerebroside metabolism, results in accumulation of cerebrosidefilled cells in bone marrow) Decompression disease (Caisson disease) nitrogen bubbles Sickle cell disease
PATHOGENESIS Multifactorial, involving (a) Metabolic factors (b) Local factors affecting blood supply to bone - Vascular damage - Increased intraosseous pressure - Mechanical stresses Summary of various pathogenetic mechanisms 1) Arterial supply interruption: - Fracture - Dislocation - Infection 2) Arterial occlusion: (intra-vascular occlusion / venous stasis & regrograde arteriolar stoppage) - Sickle cell disease - Vasculitis - Caisson disease 3) Capillary compression: (by marrow swelling) - Steroids - Gaucher’s disease Begins with interruption of blood supply hyperaemia of surrounding area demineralisation, trabecular thinning collapse of bone with mild stress CLINICAL FEATURES Usually affects anterolateral femoral head Other bones that can be affected: humeral head, femoral condyles, proximal tibia, vertebrae, small bones of hands and feet – scaphoid, talus Commonly presents with pain - Weight-bearing and motion-induced pain in most cases - Rest pain occurs in two-thirds of patients, and night pain in one-third 58
Surgery
IMAGING (a) Plain films
Earliest findings are mild density changes (plain XR may be normal for months after symptoms begin) Sclerosis, cysts in subsequent part of disease Pathognomonic crescent sign – subchondral lucency (evidence of subchondral collapse) Later stages: Loss of sphericity or collapse of femoral head Ultimately joint space narrowing, degenerative changes in the acetabulum result
(b) MRI
98% sensitivity for diagnosis Changes can be seen early in the disease when other investigations are negative Earliest finding is a single low-density line on T1 weighted scan that represents the separation between normal and ischaemic bone A high-intensity line on T2 weighted images represents hypervascular granulation tissue pathognomonic double-line sign (low-density line plus high-density line)
DIAGNOSIS Clinical, based on typical symptoms with compatible findings on imaging Rule out other causes of pain and bony abnormalities FICAT-ARLET STAGING Stage 0 Stage 1 Stage 2 Stage 3 Stage 4
Hip-at-risk CT scan and XR normal Positive findings on MRI or biopsy XR changes seen but no collapse Early flattening of dome – crescent sign Flattening of femoral head with joint space narrowing Signs of early OA
TREATMENT Conservative (ineffective at halting progression)
Bed rest Partial weightbearing with crutches NSAIDs or other analgesics Bisphosphanates – slows resorption of necrotic bone
(a) Core decompression with or without bone grafting Centre of head of femur is excavated Fibular graft or other formed graft is used to fill up the cavity Used in stage 0 to 2 disease in young and active patients – best chance of preserving femoral head (b) Osteotomy Joint-sparing – redistributes weight-bearing forces to articular cartilage which is supported by healthy bone For late stage 2 disease with cyst formation, and stage 3 disease (c) Resurfacing arthroplasty (d) Total hip replacement For stage 4 disease and in older sedentary patients with not so severe disease
PROXIMAL FEMORAL FRACTURES SUMMARY DDX OF HIP FRACTURES: Pubic ramus fracture Acetabular fracture Isolated fracture of greater trochanter Trochanteric bursitis/ contusion BLOOD SUPPLY OF FEMORAL NECK***
Extent of dz: A: <15% B: 15-30% C: >30%
Nutrient artery of femur Retinacular Arteries (from medial and lateral circumflex arteries) Artery through ligamentum teres (from obturator artery) In NOF fracture - Nutrient artery severed - If significant displacement, retinacular vessels severed AVN - Only ligamentum teres vessels remain
PREDISPOSING FACTORS Nonmodifiable
Old Age Early menopause Female Sex Nulliparity Caucasian Family/Personal History of fractures 59
Modifiable
Anything that causes increased risk of falls, e.g. Poor vision, vestibular dysfunction LL weakness Hazards at home Significant co-morbitidies e.g. CCF, CVA Reduction of bone strength Osteoporosis, low Ca intake Steroids, alcohol, smoking, thyroxine, increased/decreased T4 Physical immobility Pathological bone conditions Chronic liver and renal failure
HISTORY Fall
How pt fell – e.g. landed on bum Pain, tenderness, deformity Can walk? (If yes impacted [Garden 1] fracture, which
is undisplaced need to admit to prevent progression to displaced fracture which has poorer prognosis)
What happened before fall
[hazards at home]
Predisposing factors to fracture
Modifiable Non-modifiable
Comorbidities Premorbid functional status Osetoporotic Risk Factors
Radiological Preop
Analgesia Antibiotics if infection suspected Pre-op traction for pain relief and to ensure union takes place in a good position Thromboembolism prophylaxis (SC heparin 5000 units BD)
TYPES OF FRACTURES ACCORDING TO SITE Intracapsular
NOF Other
Extracapsular
INVESTIGATIONS Confirm diagnosis, determine severity Pre-operative investigations
Subcapital Transcervical Basal Intertrochanteric Pertrochanteric Involves the trochanter(s) which are themselves fractured
GARDEN CLASSIFICATION OF NOF FRACTURES Undisplaced
PHYSICAL EXAMINATION Shortened Externally rotated [MCQ] # of proximal half: flexion & abduction Bruising (suggest extra capsular #) Tenderness over femoral neck Painful limited hip movements
AP Pelvis (not hip) Lateral XR of affected hip joint FBC U/E/Cr PT/aPTT urinalysis GXM CXR ECG
INITIAL MANAGEMENT
1
2 3
4
Displaced
Inferior cortex not completely broken Fracture line not complete May have some angulation of trabeculae Inferior cortex completely broken Fracture line complete Minimal displacement Inferior cortex completely broken Fracture line complete Significant displacement Head internally rotated, abducted (distal fragment externally rotated) Inferior cortex completely broken Fracture line complete Complete displacement Head retains neutral position in acetabulum 60
WHO FRACTURE RISK ASSESSMENT TOOL (FRAX) -
-
-
Developed by WHO to evaluate fracture risk for patients Gives 10-year probability of hip fracture and the 10-year probability of a major osteoporotic fracture (clinical spine, forearm, hip or shoulder fracture). o For local Chinese: use Hong Kong Chinese o For local Indians: use US (Asian) Disadvantages o Cannot calculate for patients <40yo o Does not take into account type of fractures, number of fractures o Does not tell you who to treat – still rely on clinical judgement Website: http://www.shef.ac.uk/FRAX/faq.jsp Risk factors used:
MANAGEMENT -
Conservative: if undisplaced, clinically stable & ROM is full and painless Total hip replacement: for OA hips, pathological #, acetabular involvement, or revision hip
For NOF #:
<60yo >60yo
Gardens 1, 2 Gardens 3, 4 Cancellous bone screw [PRESERVE HEAD] Cancellous bone screw (~65yo) Hemiarthroplasty Hemiarthroplasty (uni/bipolar) (~90yo) Total hip replacement
Ultimately depends on patient’s pre-morbid ADL status & his/her aims, probability of successful op & risks of requiring a 2nd operation -
Sample of questionnaire:
For Intertrochanteric / Pertrochanteric
Internal fixation with a dynamic hip screw will suffice usually. Unless it is a reverse oblique fracture. [MCQ] If treated conservatively, will result in MALUNION
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NOTE: Total Hip Replacement involves replacement of the acetabulum also, usually reserved for patients with OA, pathological fracture, revision of implant – will see on X-ray that acetabulum is metal as well, with screws going into hip bone
Physiotherapy
Preserve joint movement Restore muscle power Assess what type of mobility aids needed
Treat osteoporosis and comorbidities Thompson (has neck, no holes, needs cement)
DHS Plate and Screw
Austin Moore (has 2 holes, no neck, doesn’t need cement)
Moore’s has a short neck, thus used for subcapital and mid-neck fractures; Thompson has longer neck, used for fractures near base of NOF Thompson better for osteoporotic patients Lifespan: about 10 yrs [must explain to patients before and after op that lifespan varies between patients – if you have no symptoms past 10 years, you need not replace it immediately] Material: ultra high molecular wt polyethylene and surgical grade stainless steel HIP ARTHROPLASTY Hip Arthoplasty
Hemi arthroplasty (Only femoral component) Total Hip replacement (THR) (Femoral & acetabular component)
COMPLICATIONS OF TOTAL HIP REPLACEMENT Intraoperative Immediate (within 24h) Early (within 30 days)
Bipolar arthroplasty Unipolar arthroplasty (Moore’s & Thompson)
AFTER-CARE: Weight bearing
COMPLICATIONS OF FEMORAL FRACTURES Non-union in 30% Redisplacement AVN in intracapsular NOF #, rarely occurs in intertrochanteric - Undisplaced – 10-30% - Displaced – 50-80% - Rx: total hip replacement Erosion of femoral head in unstable IT fractures causing coxa vara Complications: delayed union, non-union, malunion (coxa vara), OA
Implant Try and get pt to sit up by 24h, walk by 72h Internal fixation Sit up by 24h Encourage mobility with non-wtbearing (wheelchair)by 72h Do not weight bear until healing of # occurs, if not high risk of cutout
Late (>30 days)
Perforation/# of the acetabulum or femur Dislocation (due to incorrect placement of the prosthetic components) Infection DVT (most common complication) / PE Fat embolism Sciatic n. palsy (more common in the posterior surgical approach to the hip joint) Infection Heterotopic ossification Disuse osteoporosis Tissue atrophy Implant failure Wearing of articular surfaces (esp acetabulum for unipolar’s) Loosening Erosion, cut-out etc Peri-prosthetic #
POST-OP MANAGEMENT Use GS principles Ask about relevant social history & family support Management of post-op DVT 62
o o o
Pre-op: thromboembolic deterrent (TED) stockings fitted pre-op Peri-op: TED stockings, minimize duration of surgery, use compression boots & foot pumps Post-op: low dose of LMWH, early mobilization of patients with the help of physiotherapists
OUTCOME OF NOF FRACTURES 25% mortality at one year 10% bedbound 33% wheelchair bound 33% ambulating + walking aid Union takes about 3 months
SUBTRONCHANTERIC FRACTURES • least common hip fracture, seen in younger population with high energy injuries • highly unstable • transverse, spiral or oblique fracture passes below lesser trochanter • x-rays show flexed and abducted proximal fragment, from pull of iliopsoas on lesser trochanter, gluteus medius and minimus on greater trochanter • Treatment a. obtain a good closed reduction under fluoroscopy on the fracture table b. internal fixation with intramedullary nail FEMORAL DIAPHYSIS FRACTURES • high energy (MVA, fall from height, gunshot wounds) • low energy (spiral fracture in children) • high morbidity/mortality (hemorrhage, fat embolism, ARDS, MODS) • blood replacement often required • frequently comminuted with soft tissue trauma • Clinical a. leg is shortened, externally rotated b. unable to weight bear c. assess neurovascular status d. r/o: open fracture, soft tissue compromise e. r/o: child abuse with spiral fractures in children • Treatment o ABCs of trauma are essential
o o o o
Immobilize leg with Thomas Splint Adequate analgesia Surgical fixation (intramedullary nail) within 24 hours high rate of surgical union after 6 to 12 weeks Early mobilization of hip and knee
SUPRACONDYLAR FEMORAL FRACTURE • high energy, multiple trauma • knee joint is disrupted severely with bicondylar fracture • distal fragment moves posteriorly due to pull of gastrocnemius • poor prognosis with comminuted fractures • can be intra or extra articular • high incidence of post-traumatic arthritis • Treatment o internal fixation and early knee ROM o if conservative treatment need pearson knee piece to allow flexion and thus decrease pull and prevent flexion deformity. o quadriceps strengthening INTERTROCHANTERIC FRACTURE OF THE FEMUR Evans- Jensen Classification I 2 fragments, undisplaced II 2 fragments, displaced III 3 fragments w/o posterolateral support (ie # of the greater trochanters) IV 3 fragments w/o medial support (ie # of the lesser trochanter) V 4 fragments R Reversed oblique # (prone to displacement) *Alternative classification: according to number of fragments + reversed oblique #
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IMPORTANT ORTHOPAEDIC CONDITIONS IN THE KNEE KNEE – DDX Lump
Pain Generalised OA RA
Deformity
Instability
Anterior Posterior Lateral Osgood-Schlatter dz Baker’s cyst Meniscal cyst Housemaid’s knee Popliteal cyst Clergyman’s knee Popliteal aneurysm Chondromalacia Meniscal tear patellae (CMP) (med & lat) Patellofemoral OA Osteochondritis dissecans (OCD) Meniscal disorders Tendinitis Bursitis Osgood-Schlatter’s dz RA TB Recurrent dislocation of patella Genu varum / valgum Charcot jt: DM, perineuropathy, tertiary syphilis, tabes dorsalis, syringomyelia, myelomeningocele Ligamentous instability (ACL, PCL, med & lat collateral ligs) Recurrent dislocation of patella Osteochondritis dissecans RA
DIFFERENTIALS FOR POPLITEAL FOSSA SWELLINGS (OSCES) Tissue type Skin & subcutaneous tissues
Pathology Lipoma
Sebaceous cyst
Artery
Popliteal artery aneurysm
PE & Comments - Soft to firm; smooth/lobulated surface - If large & soft elicit fluctuation - ‘slip sign’ - Elicit which layer lipoma is in e.g. S/C or I/M (in the latter, the lipoma disappears on m. contraction) - Soft to firm; smooth surface - +/- punctum (present in 50%) - Attached to the skin, hence does not move independently from the skin - 50% bilateral; expansile pulsation - Comment on diameter (≥2cm diameter) - Palpate all LL pulses (distal pulses may not be palpable if aneurysm is thrombosed)
Vein
Nerve Enlarged bursae
Cysts
Saphena varix (@ saphenopopliteal junction)
DVT Neuroma
Baker’s cyst Popliteal cyst
Gaiter area: look for complications of varicose v. - Venous eczema - Lipodermatosclerosis - Ulceration: active & healed (latter causes white patch called atrophie blanche) - Peripheral oedema Look for varicosities along long saphenous v. Tourniquet test, Trendelenburg test, Perthes test E.g. tibial n. - Above the joint line - a/w semimembranosus and medial head of gastrocnemius medially & with popliteus and lateral head of gastrocnemius laterally - Below the joint line & deep to gastrocnemius - a/w degenerative changes in knee joint Enlargement of popliteal bursa Knee joint is normal
COMMON KNEE SYMPTOMS -
-
locking = spontaneous block to extension • torn meniscus, loose body pseudo-locking = restricted ROM without mechanical block • arthritis (effusion, pain), muscle spasm following injury instability = “giving out” • torn ACL, patellar subluxation, torn meniscus, loose body traumatic knee swelling • effusion, usually represents hemarthrosis • ligamentous injury with hemarthrosis • meniscal injury • traumatic synovitis non-traumatic knee swelling without trauma • septic or crystal-induced arthritis • seronegative arthritis (P-A-I-R: Psoriatic, AS, IBD, Reiter's) • seropositive arthritis (RA, SLE) • avascular necrosis (rare) • sickle cell disease
History - ligamentous injuries require high energy force - meniscal injury in young & old person requires moderate & mild force respectively 64
X-Rays of the Knee AP, lateral weight-bearing Skyline view • with knees in flexion, beam is aimed from anterior tibia to anterior femur • allows for view of patellofemoral joint Tunnel view Knee bent, can see the hollow between 2 articular surfaces Oblique For intra-articular fractures Erect-leg full- • radiograph from hip to foot with patient in standing position length view • useful in evaluating limb length discrepancies and genu varus / valgus Rosemberg • 30-40 deg flexed weight bearing view with the x-ray beam view tilted caudal to profile the joint line • Best view to visualise loss of medial joint space MENISCAL TEARS History & PE: Mechanism: twisting injury, usually during sports (esp football) Locking of knee in partial flexion: torn portion of menisci jammed between femur & tibia, blocking extension. Unlocks with flexion. Suggestive of bucket-handle type meniscal tear. Pain, swelling, effusion. Tenderness: medial meniscal tear (well localized med joint line tenderness); lateral meniscal tear (ill-defined joint line tenderness) Course: Symptoms resolves, recurs periodically w twists/strains. Sometimes, knee gives way spontaneously. McMurray’s & Apley’s grinding test positive Ix: Arthrography MRI Prognosis & Mx: Outer 1/3 Good vascular supply, good healing. Attempt operative repair Mid 1/3 Intermediate vascular supply & healing Inner 1/3 Avascular, poor healing. Excision required
Cx: Recurrent synovial effusion & articular cartilage damage due to loose meniscal tag swelling, OA MENISCAL CYSTS Tender & tense swelling arising from outer part of meniscus along the joint line (usu lateral) Hx of joint injury may be present Rx: if symptomatic, arthroscopic decompression or removal CHRONIC LIGAMENTOUS INSTABILITY Chronic instability – sense of joint wanting to or actually giving way ± pain & recurrent swelling O’Donahue’s triad (aka unhappy triad): ACL tear + med meniscus tear + med collateral lig tear ACL injury more common than PCL injury History
PE Rx
Post-op physio impt in all cases
ACL Tear PCL Tear o indirect varus blow to knee o fall onto flexed knee o hyperextended knee + internal rotation with plantar flexed foot o hit anterior tibia on o audible pop, knee instability o “giving way” dashboard in MVA o immediate swelling (dashboard injury) o hyperflexion or o inability to continue activity o patients with greater Q-angle got hyperextension with greater chance of ACL tear anterior tibial force Anterior drawer + Sag sign + Lachman’s + (falsely +ve in PCL tears) Posterior drawer + Apley’s distraction test + Apley’s distraction test + Conservative – hamstring & quadriceps ex., physio, external brace Stabilization / Reconstruction – o Reattachment (tightening of loose lig / capsule), o Reinforcement (diversion of healthy muscles or tendons to strengthen weak structures), using hamstrings, patellar, quadriceps o Replacement (rerouting living structures or inserting synthetic material)
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History
PE
MCL Tear o valgus force to knee o +/– "pop" heard o severe pain with partial tears o complete tear may be painless • • • •
Rx
• • •
LCL Tear o varus force to knee o similar history to MCL o rule out common peroneal n. injury (difficult dorsiflexion and decreased sensation at the top of the foot)
swelling tender above and below medial joint line Medial & Lateral collateral ligament tears: Valgus & Varus stress tests + respectively assess joint space opening with valgus force o pain o Laxity with end point - partial tear o absence of end point - complete tear o rule out ACL and medial meniscus tear minor o immobilize briefly, early ROM and strengthening moderate o knee immobilizer or cast (NB. Ligaments take 3/52 to heal) o early physiotherapy with ROM and strengthening severe or combined o surgical repair of associated injuries o surgical repair of isolated MCL/LCL tear is controversial
OSGOOD-SCHLATTER DISEASE Traction injury of apophysis which patellar ligament inserts into (partial avulsion of tibial tuberosity cos of unequal growth rate between patellar ligament and bone) Tender lump over tibial tuberosity Pain after activity, usually on active knee extension Usually young adolescent X-ray: fragmentation/displacement of tibial apophysis Rx: Restrict activities especially sports. Spontaneous recovery. [MCQ] patient doesn’t present with loose bodies in knee joint because it is extraarticular! OSTEOCHONDRITIS DESSECANS Separation of small osteocartilaginous fragment of condyle articular usually a/w hx of trauma
PATELLAR FRACTURE History • Direct - blow to patella (Usually comminuted) • Indirect - sudden strong contraction of the quadriceps femoris against resistance (Usually a transverse #) • Immediate pain Physical • Swelling & bruising of knee joint +/- abrasions • Marked tenderness at knee joint • Patellar deformity (+/- palpable gap) • Inability to extend knee • Proximal displacement of patella X-Ray • AP, lateral (need to exclude bipartite patella - common congenital fragmentation of the patella) Treatment • Isolated vertical fractures - non-operative treatment - plaster cast 6/52, early ROM • Transverse displaced fracture – ORIF with wires. • Comminuted fracture - ORIF; may require complete or partial patellectomy • Indications for surgical tx o sig articular step-off > 2mm o loss of extensor mechanism with displacement > 3mm o open # RECURRENT DISLOCATION OF THE PATELLA
surface,
Intermittent ache or swelling, locking, giving way, effusion 15-20yo, Bilateral in 50%, male > female X-ray – tunnel view: Loose fragment in joint, crater on the medial femoral condyle Rx: removal of small fragments, fixation of larger fragments, cast for 6 wks.
Girls > Boys Usually bilateral Apprehension test +: Lateral dislocation of patella if quadriceps contract when knee is in flexion. Results in pain and inability to extend knee. Predisposing factors: lax ligaments, abnormalities of patella (high, low or lateral) or lat fem condyle, genu valgus, tibial tubercle mal-alignment
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Mx Reduction & backslab Quadriceps strengthening exercise Operation: repair of torn medial structures / soft-tissue realignment / transposing patellar ligament medially (realignment procedure) PATELLAR/QUADRICEPS TENDON RUPTURE • • • • • • •
Low energy injury, sudden forceful contraction during attempt to stop fall Partial or complete More common in patients with DM, SLE, RA, steroid use History o fall onto flexed knee o inability to extend knee Physical o palpable gap between patella and quadriceps o may have hemarthrosis / effusion of knee Investigations o knee radiographs to rule out patellar fracture o joint aspirate may show hemarthrosis Treatment o surgical repair of tendon
DISLOCATED KNEE • • •
• •
•
Bad high energy injury Can be anterior (most common), posterior, rotatory or lateral Associated injuries o popliteal artery (immobile due to geniculate arteries and the anterior tibial artery going thru hiatus in interosseous membrane) intimal tear or disruption in 35-50% o capsular, ligamentous and common peroneal nerve injury Investigations o Angiogram, doppler Treatment o closed reduction, above knee cast x 4 weeks o alternately, external fixation especially if vascular repair o surgical repair of all ligaments if high demand patient Cx : ischemia, peroneal nerve injury, compartment syndrome, reperfusion injury, stiffness
CHONDROMALACIA PATELLAE Anterior knee pain in adolescent girls – worse on climbing stairs Retropatellar tenderness, friction test +, effusion Chronic / recurrent overload of patellar articular surface due to malcongruence of patellofemoral surfaces OR abnormal tracking of patella during flexion/extension. A/w development of OA Ix: skyline views of patella, CT, arthroscopy Rx: Conservative: analgesics, reduce activities, physioRx, quadriceps-strengthening exercises Operative: shaving of articular cartilage, arthroscopy lavage, realignment of patella, patellectomy RHEUMATOID ARTHRITIS Stage 1 (synovitis) – pain, chronic swelling, large effusion, thickened synovium Stage 2 (articular erosion) – joint instability, ↓ROM. X-ray: loss of jt space & marginal erosion, but lack of osteophytes c.f. OA Stage 3 (deformity) – pain, deformity, instability & disability. X-ray: bone destruction Rx: Conservative – splintage, intraarticular steroid injection Operative – osteotomy, TKR BAKER’S CYST Definition o Posterior herniation of knee joint capsule o Leading to escape of synovial fluid into the posterior bursae, stiffness & knee swelling (fluid distention of the gastrocnemio-semimembranous bursa) o Common in children, occurring more often in boys o Often a/w OA and Charcot’s joints o Important to rule out DVT, but the two can co-exist Diagnosis o PE: swelling usually below the joint Fluctuant Transillumination possible Non-tender Positive slip sign – it is a deep structure. 67
-
-
Reducible only if connected to knee joints which not all baker’s cysts are – especially in children. o U/S: fluid between semimenbranosus & medial gastronemius tendons in communication with posterior knee cyst (100% accuracy) Because of their anatomic location, Baker’s cysts can increase risk of DVT o Most commonly, the Baker cyst is located between tendons of the medial head of the gastrocnemius and the semimembranous bursa. Occasionally, the Baker cyst can be found between the heads of the gastrocnemius muscles. This can result in a lateral deviation of the popliteal vein, and a compression of the popliteal vein-predisposing to venous stasis and DVT Treatment o In children, surgical excision of popliteal cysts is rarely indicated Usually spontaneous resolution of cysts in 10-20 months; A prolonged period of observation is strongly recommended before surgical excision is considered. In protracted cases, cysts may respond to aspiration and steroid injection, (note that unlike adults, the cyst may not be intra-articular and therefore may respond to aspiration o In adults: reoccurrence is common, even following surgical removal, and therefore treatment is directed toward intra-articular pathology;
POPLITEAL CYST Definition o Cyst located on the medial side of popliteal fossa, just distal to flexion crease of the knee, under medial head of gastrocnemius Epidemiology o Found in children & young adults o 2x more common in boys o Usually unilateral Diagnosis o More prominent during knee extension & vice versa o If cyst is not found in medial part of popliteal fossa or has a solid component (on U/S), rule out tumour with CT/MRI scan Treatment o Asymptomatic ones can be treated non-surgically with good results o Though spontaneous remission is not to be expected in all cases
CLERGYMAN’S KNEE (INFRAPATELLAR BURSITIS) Swelling superficial to patellar ligament & distal to the patella Rx: firm bandaging, avoid kneeling, aspiration, excision if chronic SEMIMEMBRANOUSUS BURSA Painless fluctuant swelling in medial part of popliteal fossa Enlargement of bursa between semimembranousus & medial head of gastrocnemius Rx: excision if symptomatic (pain) CHARCOT’S JOINT Causes: - Peripheral neuropathy - DM - Tertiary syphilis - Tabes dorsalis - Syringomyelia - Myelomeningocele - Cauda equina lesion Rapidly progressive OA Gross jt deformity, but painless Unstable jt, effusion, no warmth Mx: Rest, immobilize Stabilize with cast/ calipers Surgical arthrodesis
Popliteal Fossa Boundaries (right) - roof: fascia lata - floor: (prox to distal) popliteal surface of femur, capsule of knee joint, popliteus m. covered by its fascia
HOUSEMAID’S KNEE (PREPATELLAR BURSITIS) Swelling over patella due to friction between skin & patella Rx: firm bandaging; avoid kneeling; aspiration; excision if chronic 68
Osteoarthritis (Knees)
Most common joint disease in the world Degenerative joint disease Morphological changes Cartilage degeneration o Fissuring o Pitting o Eburnation as joint motion polishes surface Bone Hypertrophy o Osteophyte formation Mild synovitis Two types Primary - Senile (old-age) - Post-menopausal
Secondary Trauma – acute or chronic Rheumato – RA Infections – Syphilis Metabolic – Hyper PTH
Joints affected: PIPJs of hands (Bouchard’s nodes) DIPJs of hands (Heberden’s nodes) Thumb joints MTPJ of big toe Cervical and lumbar spine Hip Knee * frequency of OA: Asians: knees > hips; Caucasians: hip > kness OA of knees and hands – F>M ; OA hip- M> F Other risk factors Hereditary Obesity Competitive contact sport Deformities – e..g genu valgus/varum Recreational running is NOT a risk factor
Differentials – need to exclude other DDx of hip/knee pain from history Referred pain from hip, back VITAMIN » Vascular – AVN » Infections – warmth, fever, inoculation e.g. intra-articular injection by GP » Traumatic » Autoimmune/ inflammatory – PMHx » Metabolic – Gout, tophi » Neoplastic – LOW/LOA, SOB, goiter, urinary, GIT History NO systemic involvement Joint pain o The usual 6 points about pain o Which joints? o Insidious onset o Morning stiffness not prominent (<30mins) o Worsened by activity o Alleviated by rest ASK ABOUT BACK PAIN, HIP PAIN WHICH CAN BE REFERRED TO THE KNEE Precipitating causes o Trauma o History of contact sports / occupation o Associated conditions – RA, syphilis o BMI of patient Functional Loss o Job scope o Recreational activity restriction o Premorbid status: function & mobility Social hx – ask about housing (floor, lift landing) Treatments tried (TCM?) GI bleed risk o History of ulcer disease and/or GI bleeding
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o o o
High dose or multiple NSAIDs Concomitant use of corticosteroids and/or warfarin Age >60 yrs
Physical Examination Genu varum/valgus predisposes to OA – usually genu varum Fixed flexion deformity Externally rotated If joint swelling, is MILD Joint line tenderness Crepitus Decreased ROM Patellofemoral OA (5%) Examine other joints as well Note absence of rheumatoid nodules / tophi / rashes / Sjogren’s Examine HIP, BACK Neuro exam – SMART – sensory, motor, autonomic, reflexes, trophic changes Investigations To confirm diagnosis and exclude differentials To look for causes (not applicable usually) To look for complications (not applicable usually) Radiological
AP weight bearing (so that even small degrees of articular cartilage thinning can be seen) Lateral Skyline (tangential) view Long film (to see degree of varus/valgus)
To view all 3 compartments – medial, lateral, patellofemoral compartment Mechanical axis – centre of hip to centre of ankle Anatomical axis – line of femur to line of tibia (normally 4°-6° valgus)
L-O-S-S findings Loss of joint space Loose bodies Osteophytes Subchondral sclerosis Subchondral cyst
Management Nonpharmacological Physiotherapy Preservation and improvement of joint mobility Exercise Range of motion and muscle strengthening exercises Load reduction Body weight reduction if obese Use of walking aids Avoid kneeling and squatting. Pharmacological Paracetamol NSAIDs
Should be first line drug; effective in a proportion of patients Must be used with special care in >60y previous history of GI bleed concurrent warfarin/ steroid medications renal dysfunction
COX-2 inhibitors acorxia Glucosamine with chondroitin Tramadol Intraarticular injections of corticosteroids Intraarticular hyaluronic acid injections (e.g. Synvisc) Surgical Minimally invasive (Arthroscopic)
Prescribe with PPI/H2RA in patients with increased likelihood of GI bleeding Vioxx a/w increased risk of stroke and cardiac events. Glucosamine has anti-inflammatory properties Chondroitin inhibits cartilage breakdown and stimulate cartilage repair Have been found to be at least as effective as NSAIDS, with the added advantage of fewer side effects Consider in patients with highly-resistant pain Consider is patients with highly resistant pain. It is recommended that no more than 4 glucocorticoid injections be administered to a single joint per year because of the concerns with long-term damage to cartilage Marketed as ‘joint replacement’ substances; expensive, no evidence to support its efficacy
For early degenerative arthritis Alternative to osteotomy and TKR if the patient is reluctant to have more aggressive surgery Techniques include Washout and debridement Cartilage regeneration procedures o Chondrocyte transplant o Microfracture of subchondral bone o Mosaicplasty Arthroscopic surgery may defer definitive operation by up to 5 years
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High tibial osteotomy
Knee replacement
Only in certain cases e.g. unicompartmental involvement. Osteotomy permits redistribution of weight Contraindications Inflammatory arthritis Severe flexion deformity >15o Varus/ valgus >15o >5mm loss of subchondral bone lateral thrust while walking When symptoms are severe Try to avoid doing in patients <60 as TKRs usu last only ~10y Types o Unicompartmental o Total +/- preservation of PCL; PCL preservation preserves proprioception function but ↑ wear of prosthesis
For PFOA
Complications Intraop – GA, # of tibia or femur Immediate – vascular injury to superficial femoral, popliteal and genicular vessel Early – DVT/PE, fat embolism, infection, peroneal nerve palsy (1%) Late –loosening, patellar instability, #, disruptn of extensor mechanism, periprosthetic #, wear of polythene surfaces Arthroscopy to confirm diagnosis Rx - Realignment procedures - Cartilage transplantation (still under research) - Patellectomy (problems a/w it include loss of normal knee power and function, quadriceps weakness, and failure to resolve anterior knee pain, may eventually require total knee arthroplasty for knee arthritis) - Patellofemoral arthroplasty - Total knee arthroplasty
Cartilage regeneration procedures Chondrocyte transplant Harvest condrocytes from non weight-bearing sites, e.g. patellofemoral surface, culture, reimplant Microfracture Subchondral penetration of bone, inducing regrowth of fibrocartilage Mosaicplasty Cylindrical cartilage taken from non-weight bearing areas, implanted on knee joint surface to form a new layer of cartilage, comprised of the intact original cartilage and the transplanted grafts Post-surgical Physiotherapy Continuous Passive Movement (CPM)
To maintain joint ROM & muscle power
Approach to OA knee 1) Confirm Dx of OA knee: pain and its characteristics 2) Exclude other sites of pathology a) back – pain, PU claudication b) hip c) ischaemic pain or neuropathic pain Ischaemic pain Neuropathic pain Fixed claudication distance Variable claudication distance Better walking downslope Better walking upslope Recovers quickly with rest Recovers slowly with rest Pain present at night Pt usu sleep in kyphosed position with no pain 3) Exclude DDx a) malignancy – other bone pain, LOW, LOA etc. b) septic arthritis – fever, tenderness, swelling, trauma, intraarticular injectn c) RA – other jts, morning stiffness, pain d) gout – precipitant, inflammation
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IMPORTANT ORTHOPAEDIC CONDITIONS IN TIBIA TIBIAL PLATEAU FRACTURE • Results from femoral condyle(s) being driven into the proximal tibia often due to a valgus (eg. Bumper # from getting hit by a car from the side) or varus force • Lateral > medial • Associated injuries / complications: popliteal artery injury, compartment syndrome, ligament tear, meniscal tear, malunion Schatzker classification • I – lateral split • II – lateral split with depression (the force may have been greater or underlying bone may be osteoporotic & unable to resist depression) • III – pure lateral depression • IV – pure medial depression • V – bicondylar • VI – split extends to metadiaphysis Treatment Fracture displacement ranging from 4-10 mm can be treated nonoperatively • if depression is < 3 mm o Sarmiento program of functional cast bracing, NWB x 2 months • if depression > 3 mm, displaced or comminuted o ORIF +/- bone graft to elevate fragment Absolute indications for surgery: • Open plateau fractures • Fractures with an associated compartment syndrome • Fractures associated with a vascular injury Relative indications for surgery: • Most displaced bicondylar fractures • Displaced medial condylar fractures • Lateral plateau fractures that result in joint instability Contraindications for surgery 1. Presence of a compromised soft-tissue envelope (for immediate open reduction)
2. Fractures that do not result in joint instability or deformity and can therefore be treated with nonoperative modalities. TIBIAL DIAPHYSIS FRACTURE • Most common long bone #. • Commonly open # • High intensity injury o associated with crush injuries and MVAs • Soft tissue, nerve and vessel injury common o assess neurovascular status o rule out open fracture • Displacement is difficult to control • Good reduction is required o minimal shortening and angulation • Healing time: 16 weeks on average Treatment • ATLS principles first • Conservative managemenet o For closed injuries (= closed reduction) o Long leg cast x 4-6/52 o Followed by below-knee cast until healed • Surgical management o For open injuries • ORIF with external fixator • wounds on anterior surface heal poorly and may necrose o For unstable injuries or failed closed reduction require IM nail o For patients with high risk of compartment syndrome Closed reduction and cast; admit and observe for compartment syndrome; prophylactic fasciotomy if operating on tibia fracture Indications for surgery Associated intra-articular and shaft fractures, open fractures, Definitive indications Relative indications
Delayed indications
major bone loss, neurovascular injury, limb reimplantation, compartment syndrome, and a floating knee. Associated intra-articular and shaft fractures, unstable fractures, an inability to maintain reduction, relative shortening of segmental fractures, a tibial fracture with an intact fibula, a transition zone fracture, and polytrauma. Failure to maintain reduction, unacceptable reduction, complications 72
PILON FRACTURE OF DISTAL TIBIA • • • •
•
•
Combination of talar # & distal tibial metaphyseal #, usually with intra-articular comminution Vertical loading drives talus into tibial plafond. The cortical bone shatters; the softer metaphyseal bone can also be affected. 20-25% of these will be open # Associated injuries / complications: 30% will have ipsilateral injuries and 5-10% will have bilateral injuries; - compartment syndrome - compression # of vertebral column, particularly L1; - contralateral # of: os calcis, tibial plateau, pelvis, or acetabulum (vertical shear injuries) - vascular injuries Treatment o Conservative Pain relief Antibiotic prophylaxis (open # / internal fixations) Splint cast immobilisation if # is undisplaced o Surgical Preliminary stabilisation with external fixator +/- fibular # fixation Definitive surgery after condition of soft tissues is optimised (blisters have epithelised, skin is wrinkled) Types: ORIF, external fixation, limited internal fixation with external fixation, percutaneous pinning Indications for surgery include the following: o Open fracture o Displaced fracture Articular fragments with a gap of >2 mm or step of >1 mm Rotational malalignment o Vascular compromise o Compartment syndrome
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IMPORTANT ORTHOPAEDIC CONDITIONS IN THE ANKLE EVALUATION OF ANKLE COMPLAINTS Most common dislocation of ankle joint is subtalar joint – must reduce before X-ray! History Ask about pain, swelling, mechanism of injury, effect on standing/walking PE • • • •
• avulsion fractures are transverse • shear fractures are oblique if pure inversion / eversion • shear fractures are spiral if rotational force DANIS WEBER CLASSIFICATION Based on level of fibular fracture relative to syndesmosis
neurovascular status look, feel, move (dorsiflexion, plantarflexion) assess for tenderness at knee (Maisonneuve), lateral and medial malleoli special test: anterior draw (for ankle), talar tilt, squeeze test, Thompson test
X-ray • views o AP, Lateral and Mortise (15 degrees internal rotation) o Mortise gives true view of talus in tibiotalar joint o space between talus ––> tibia and talus ––> fibula o space should be symmetric and < 4 mm with no talar tilt o disrupted space signifies ligamentous or bony injury • When to x-ray - Ottawa ankle rules • Ankle x-ray is only required with o pain in malleolar zone AND o bony tenderness over posterior aspect of the distal 6 cm of medial or lateral malleolus OR inability to weight bear both immediately and in E.R. • Foot x-ray series is only required with o pain in midfoot zone AND o bony tenderness over navicular or base of fifth metatarsal OR inability to weight bear both immediately and in E.R. Ring Principle of the Ankle The ankle can be thought of as a ring comprising of • a: lateral malleolus • d: deltoid ligament • b: medial malleolus • e: syndesmotic ligament • c: posterior (medial) malleolus (syndesmosis) • f: calcaneofibular ligament Fractures of the ankle involve • ipsilateral ligamentous tears or bony avulsion • contralateral shear fractures
(Types A C = increased risk of syndesmotic injury) Type A (infra-syndesmotic) • avulsion of lateral malleolus below plafond or torn calcaneofibular ligament • +/– shear fracture of medial malleolus Type B (trans-syndesmotic) • avulsion of medial malleolus or rupture of deltoid ligament • spiral fracture of lateral malleolus starting at plafond Type C (supra-syndesmotic) • avulsion of medial malleolus or torn deltoid ligament • fibular fracture is above plafond • frequently tears syndesmosis • Maisonneuve fracture if at proximal fibula • posterior malleolus avulsed with posterior tibio-fibular ligament LAUGE HANSEN CLASSIFICATION Based on mechanism of injury; First word= position of foot, Second word = direction of movement of the talus in relation to the leg NB. supination = inversion, pronation = eversion of the foot Supination-External Rotation (Weber B) • most common (45-65%) • supination and external rotation oblique fracture at level of the sydesmosis
Pattern of fracture • determined by mechanism of injury 74
Pronation-Abduction (Weber B/C) • sequence of injury: 1) avulsion fracture of medial malleolus or rupture of deltoid ligament; 2) abduction force then either ruptures the syndesmosis or avulses its bony attachment sites; 3) lateral force from talus impacts and fractures fibula at or above level of syndesmosis and ruptures interosseous membrane
Lauge Hansen classification SA SE PA PE
In Summary... Corresponds to Danis Weber type... A B C
Pronation-External Rotation (Weber C) • sequence of injury: 1. transverse fracture of the medial malleolus or disruption of deltoid ligament; 2. external rotation then results in rupture of the anterior tibiofibular ligament or its bony insertion; 3. oblique or spiral fracture of fibula above the level of the joint; 4. posterior injury with tibiofibular ligament rupture or avulsion of posterior malleolus • fibular fracture may be proximal (i.e., Maisonneuve fracture 2) 1F
Supination-Adduction (Weber A) • sequence of injury: 1. supination force may rupture portions of lateral collateral ligaments or may avulse distal fibula, resulting in transverse fracture below the level of intact syndesmosis; 2. adduction forces talus against the medial side of the joint, resulting in vertical fracture of the medial malleolus Treatment • Undisplaced fractures: NWB BK cast • Displaced fractures: reduce ASAP • Indications for ORlF • all fracture-dislocations • all type C fractures • trimalleolar (lateral, medial, posterior) fractures • talar shift or tilt • failure to achieve or maintain closed reduction • Prognosis dependent upon anatomic reduction • high incidence of post-traumatic arthritis 2
Maisonneuve fracture: spiral fracture of the proximal third of the fibula associated with a tear of the distal tibiofibular syndesmosis and the interosseous membrane
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- Crutches are only necessary for a few days. - Physiotherapy - Usually return to play within 2-3 weeks
LIGAMENTOUS INJURIES Medial Ligament Complex (deltoid ligament) • Responsible for medial stability • Usually avulses medial or posterior malleolus • usually a/w syndesmotic or lateral ankle sprain Lateral Ligament Complex (ATFL, CFL, PTFL) • Responsible for lateral stability • Makes up for >90% of ankle ligament injuries • Clinical: swelling and discoloration, ‘pop’ sound, giving way • Diagnosis: stress x-rays and mortise view o talar inversion produces joint separation exceeding the unaffected side by six degrees (talar tilt test) • Frequncy of injury: ATFL > CFL > PTFL Anterior Talofibular Ligament (ATFL) • Most common ligamentous ankle injury • Sprained by inversion and while ankle is in plantar flexion • Swelling and tenderness anterior to lateral malleolus, ++ ecchymoses • Anterior draw test for ankle positive with Grade III ATFL injury • attempt to sublux talus anteriorly • if positive then stress other lateral ligaments • Talar tilt test for integrity of other ligaments Grading and Treatment of Ligamentous Ankle Injuries Initial treatment of all sprains follows the RICE protocol (Rest, Ice, Compression, Elevation). Protective weight-bearing is instituted with crutches. This is continued until normal gait is restored.
Grade III sprains are treated non-operatively nowadays - Bracing with a hinged knee orthosis (in the past: BK walking cast for 3 weeks) - Crutches for 1-2 weeks - Physiotherapy - Usually return to play after ≥6 weeks Focus of rehabilitation (NB. Allow sufficient healing of ligament first = 3wks) » Restore full ROM at the knee » Controlled strengthening. Often in the knee, the functional strength of the quadriceps muscle, especially the medial VMO muscle, is weak and atrophied. » Sport-specific or function-based training. Upon achieving full strength and pain-free ROM in the lower extremity, the athlete can be cleared to return to their sport, most often without any brace or external support. RECURRENT ANKLE SUBLUXATION • • • •
Aetiology • ligamentous laxity Joint (loss of normal proprioception) • internal derangement of anatomy • intra-articular loose body Treatment depends on cause Strengthening and balance training for neuropathic joint • ligament reconstruction for lateral laxity and talar tilt • arthroscopy / arthrotomy for internal derangement
Goal of therapy: decrease pain, restore ROM & regain strength Grade I – microscopic stretch/tear (pain) Grade II – macroscopic tear (pain on motion) Grade III – complete tear (unstable ankle, talar tilt apparent on mortise view) Grade I and II sprains are routinely treated nonoperatively. - Ankle brace, usually in dorsiflexion & eversion (individualized to the patient's discomfort). 76
IMPORTANT ORTHOPAEDIC CONDITIONS IN THE FOOT EVALUATION OF FOOT COMPLAINTS History
•
Physical
• • •
X-rays
pain, swelling, loss of function, sensory changes, deformity, mechanism of injury, activity level of patient inspection, palpation, active and passive ROM, weight bearing status neurovascular status AP, lateral, oblique (as a minimum)
LOOK
FEEL MOVE OFFER Non-surg Rx Surgical Rx
Hammer toe Mallet toe Claw toe More common in Females, Elderly, with RA Imbalance between intrinsic (lumbricals & interossei) and extrinsic (long flexors & extensors) muscles of the lesser toes For claw toe: may be 2˚ to neurological disorders e.g. peripheral neuropathy (Charcot-Marie-Tooth disease, DM), LMN disease (polio), UMN disease (CP, stroke, multiple sclerosis) Affects lesser toes, most commonly 2nd toe Usu all 4 lesser toes involved; may be B/L Flexion deformity at Flexion deformity Flexion deformity PIPJ at DIPJ at PIPJ and DIPJ +/- DIPJ extension NO MTPJ/PIPJ + hyperextension of +/- MTPJ extension involvement MTPJ Any callosities Any tenderness Is the deformity fixed or mobile Watch the patient walk Examine patient’s shoes Ask questions to assess effect of the condition on his/her life Appropriate footwear (usually unhelpful for mallet toe) Mobile deformity Mobile deformity Mobile deformity Flexor-to-extensor Flexor digitorum Flexor-to-extensor tendon transfer longus tenotomy tendon transfer Fixed deformity Resection of proximal phalangeal H&N +/- flexor & extensor release Proximal phalangectomy PIPJ arthrodesis
Fixed deformity Resection of middle phalangeal H&N +/- flexor tenotomy DIPJ arthrodesis Amputation of distal ½ of distal
Fixed deformity Resection of proximal phalangeal H&N +/- flexor & extensor release Extensor tenotomy for MTPJ
phalanx (to include nail & matrix)
contractures Resection of metatarsal heads of the lesser toes
Hammer toe
Mallet toe
HAMMER/MALLET/CLAW TOE Epidemiology Aetiology
Painful callosities: Terminal phalangectomy
Claw toe
HALLUX VALGUS Definition: valgus angulation of 1st metatarsal (i.e. lateral angulation of big toe) Epidemiology: most common disorder involving the 1st MTP joint Causes: idiopathic; hereditary, loss of muscle tone, RA; increased incidence in those who wear enclosed footwear Associated deformities: inflamed bunion, hammer toe, metatarsalgia, secondary OA of 1st MTP jt Ix: do a plain weight-bearing X-ray to assess 1) degree of valgus deformity 2) presence of OA of the first MTPJ Rx: - Non-surgical: appropriate footwear & physiotherapy - Surgical: depending on patient’s wishes, level of activity & state of peripheral vascular system • Bunionectomy • 1st metatarsal realignment osteotomy • Excision arthroplasty (Keller’s procedure) – essentially a proximal hemiphalangectomy • Fusion – for degenerative joint disease
77
HALLUX RIDGDUS • • • •
•
Definition: literally means “stiff great toe”; however, limited ROM is only one of the symptoms that constitute this diagnosis Epidemiology: second most common disorder involving the 1st MTP joint (the first being hallux valgus). Seen in adolescents & in adults. Causes: Primary OA of MPJ of great toe. Diagnosis • Symptoms: pain on top of great toe +/- diffuse, lateral forefoot pain resulting from increased weight-bearing on lateral foot to offload the hallux. Pain is worse with certain activities and with certain footwear. • Signs: tender dorsal osteophyte at 1st MTP joint (usually confirms this dx); slightly antalgic gait; limited plantarflexion & dorsiflexion a/w pain especially at the end of ROM Treatment • Conservative - Activity modification: use of in-sole orthotics, avoid extreme DF of great toe (e.g. kneeling/squatting with toes in great extension) - Pharmacological: paracetamol, NSAIDs • Surgical - Cheilectomy: excision of all irregular bony spurs that limit motion - MT osteotomy: based on the premise that metatarsus elevatus or a long first MT are the underlying causes of hallux rigidus - Joint arthroplasty (commonly known as Keller technique): involves the excision of the base of the proximal phalanx; indicated in moderate to severe cases of hallux rigidus in individuals with low functional demands who desire the maintenance of joint motion; however, complications are common such as hallux weakness, elevation, floppiness, a short hallux, and development of transfer lesions under the second MTP joint - Arthrodesis: salvage procedure should other surgical interventions fail & hallux rigidius is severe enough
RUPTURED TENDO ARCHILLES Degenerate tendon ruptures during pushing off (jumping/ running) >40 years old (i.e. middle-aged), a/w long term steroid use Rupture at musculous tendinous junction occurs most often in young people, but ruptures near the calcaneus also occur Mechanism usually involves eccentric loading on a dorsiflexed ankle with the knee extended (soleus and gastroc on maximal stretch)
Unable to tip toe Gap felt 5cm above insertion of tendon Weak plantar flexion, not a/w tautening of tendon Thompson aka Simmond’s test: lack of plantar flexion on squeezing calf Mx: Acute – plaster cast with foot in equines to approximate tendon ends + shoes with raised heels for 6 wks Operative – repair to equinus, plaster and raised heels for 8 wks
PES PLANUS (AKA FLATFOOT) Definition:
= flat foot Condition whereby the arch of the foot collapses with the entire sole of the foot coming into complete / near complete contact with the ground.
Epidemiology: very common
Aetiology: Young Flexible • Functional • Hypermobile – lig laxity • Tibialis post tendon dysfunction
Rigid • Tarsal coalition • Inflammatory jt dz • Neurogenic disorders
Adult Acquired
Diagnosis: • Physical Examination (see picture) o Abducted forefoot o Valgus hindfoot o Flexible flatfoot: arch appears when patient dorsiflexes (not a true collapsed arch because medial longitudinal arch is still present) Treatment: • When to treat: (1) if patient has rigid flatfeet, (2) if there is associated foot or lower leg pain, or if the condition affects the knees or the lower back • Use of orthotics (arch support – to be used for the rest of patient’s life; exercises recommended by podiatrist) • Surgery as last resort (usually time-consuming & costly) 78
• FOOTBALLER’S ANKLE Anterior ankle impingement syndrome - Definition of ankle impingement syndrome: painful mechanical limitation of full ankle ROM secondary to an osseous or soft-tissue abnormality Repeated forced dorsiflexion tearing of anterior capsule of ankle joint subsequent bone spur formation (osteophytes) aka anterior exostoses of the tibia subsequent pain + limited ROM Treatment: Acute phase • Conservative: NSAIDs, physiotherapy, orthotics, bracing • Surgical: arthroscopic excision & debridement Recovery phase • Posterior splinting for 1/52 with supportive brace & compression stocking • Physiotherapy for 2/52 for strengthening, ROM, proprioception and sportsspecific rehabilitation
• • • •
CALCANEAL FRACTURE • •
ACHILLES TENDONITIS -
Chronic inflammation from running and shoe-wear (high heels) May develop heel bumps (Haglund’s deformity: prominence of the posterior superior calcaneus where the Achilles tendon laterally inserts into calcaneus)
Diagnosis pain, aggravated by passive stretching tenderness, swelling crepitus on plantar flexion Treatment rest, gentle stretching, NSAIDs proper footwear +/- orthotics do NOT inject steroids (prone to rupture) TALAR FRACTURE (RARE) •
60% of talus covered by articular surface (7 articular facets!) • Decreased surface area for vascular perforation • Blood supply to talus: distal to proximal • Fractures of the neck at risk of AVN
Mechanism: MVA or fall from height • axial loading or hyper-plantar flexion injury • talar neck driven into tibial margin Rule out potential associated injuries • spinal injuries, femoral neck fractures, tibial plateau fractures X-Rays • AP/lateral films with CT scan of talus Treatment (aims: revsacularisation & fracture healing) • BK cast, NWB x 6 months • ORIF: to reduce displacement and prevent AVN or non-union Complications • undisplaced: 0-10% risk of AVN • displaced: 100% risk of AVN
•
• •
•
Mechanism: axial loading (fall from a height onto heels) Rule out potential associated injuries • Spinal injuries (10%) • Femoral neck fractures • Tibial plateau fractures • Knee ligamentous injuries Physical • Heel viewed from behind is wider, shorter, flatter, varus tilt • May be swollen, with bruising on soles X-Rays • Broden’s views (oblique views of subtalar joint) • Bohler's Angle decreased (normal: 20 - 40 degrees) Bohler's Angle Treatment • Goal is to prevent widened heel and maintain subtalar joint congruency • NWB, early ROM • ORIF if depressed centrally or tongue-type fracture • Closed vs. open treatment is controversial (open: potential vascular complications) • Primary arthrodesis if severe Cx : malunion, subtalar arthritis, chronic heel pad pain, calcaneal widening ( increase in shoe size)
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PLANTAR FASCIITIS • • • • •
•
•
•
Repetitive strain injury of plantar fascia Most common cause of heel pain [MCQ] Epidemiology: common in runners, jumpers, ballet dancers, obese individuals Pathogenesis: chronic inflammation due to microtears of plantar fascia History • Intense pain on waking or after rest • Subsides as patient walks • May be associated with systemic diseases Diabetes mellitus Enthesopathies including seronegative and seropositive arthritis Physical • Swelling, local tenderness over plantar fascia mostly at medial calcaneal tubercle • Pain with toe dorsiflexion (stretches plantar fascia) X-Ray • Sometimes show heel spur at insertion of fascia into medial calcaneal tubercle • Note: spur is reactive, not the cause of pain Treatment • Non-operative (90% resolve) Rest and NSAIDs x 4-6 months Stretching exercises Supportive shoes with heel cup Steroid injection • Surgical in refractory cases (rule out nerve entrapment as cause of pain first) Release of plantar fascia--50% effective at pain relief Spur removal not required Can be done endoscopically
BUNIONS •
• • •
Definition: localised painful swelling at the base of the big toe • Joint is enlarged, toe is often malaligned • Frequenly associated with inflammation • Can be a/w degenerative joint disease (OA) or bursitis Epidemiology: 10x more frequent in women Two primary causes: heriditary, shoewear Diagnosis & pathogenesis: a/w hallux valgus deformity • valgus alignment of MTP joint is aggravated by eccentric pull of EHL and
•
intrinsics • secondary exostosis forms with bursa and thick skin creating the bunion Treatment: (1) cosmetic reasons, (2) for pain with shoes • Conservative: properly fitted shoes and toe spacer • Surgical: removal of bunion with realignment of 1st MTP joint
METATARSAL FRACTURE As with the hand, 1st, 4th, 5th metatarsals (MT) are relatively mobile, while the 2nd and 3rd are fixed Types of Metatarsal #s
Fracture
Avulsion of base of 5th MT Jones Fracture midshaft 5th MT
March Fracture shaft 2nd, 3rd MT
Mechanism
Sudden inversion followed by contraction of peroneus brevis Stress injury
Stress injury
Clinical
Treatment
Tenderness along shaft of 5th MT Tends to displace b/c of peroneus brevis and tilting Painful shaft of 2nd or 3rd MT
NWB BK cast x 6/52 ORIF if athlete
Tenderness at base of 5th MT X-ray foot
Requires ORIF if displaced
Symptomatic
80
1st MT Fracture
Trauma
Painful 1st MT
Lisfranc Fracture 2nd Tarso-MT fracture- dislocation
Fall onto plantar flexed foot or direct crush injury
Shortened forefoot prominent base
ORIF if displaced otherwise NWB BK cast x 3 weeks then walking cast x 2 weeks ORIF
Kohler’s disease – AVN of navicular bone
MCQ --- Stress fractures: common sites a. head of femur b. 2nd metatarsal c. distal end of femur d. tibia
81
IMPORTANT ORTHOPAEDIC CONDITIONS IN THE SPINE
APPROACH TO LOWER BACK PAIN
Axial
Diagnosis
Hx
Tx
Facet Spondylosis (OA)
Epidemiology Pain dominance Worse with Onset Duration
Old Back
Other aspects of history
NB. Patient is usually asymptomatic. Lumbar spondylosis is hence not found unless a complication ensues, e.g. nerve root compression from posterior osteophytes with superimposed spinal stenosis
PE
Normal
Ix Conservative
MRI NSAIDs Activity modification Exercise/physiotherapy Lumbar corset
Surgical (all under GA)
Fuse
Extension Short (days to weeks)
LOWER BACK PAIN Discogenic Degenerative disc disease Back Flexion Gradual Long (weeks to months)
Leg Pain Radicular PID (commonly L5, S1 S1 affected) Young Old Leg Leg
Claudication Spinal stenosis
Flexion
Extension Congenital/acquired Short episode attacks (minutes) Acute or chronic (weeks to months) Symptoms of radiculopathy Neurogenic claudication • Sciatica (+/- cross sciatica) • Pain, weakness and/or numbness in the legs • Shooting pain down calf while walking (ask for • a/w m. weakness, tingling / segmental sensory numbness deficits) • Cough impulse positive Rule out cauda equina syndrome • Variable claudication distance (impt complication) • Pain even on standing • Urinary retention • ‘Park bench to park • Saddle anaesthesia (loss of bench’ – relieved with sensation over the buttocks flexion & the perineum) • No pain at night (patient • LL weakness sleeps on lateral decubitus foetal position) Rule out vascular claudn 1. Listing (to relieve n. root Same as radicular compression), paravertebral (+) 4. Pulses m. spasm, restricted ROM 2. SLR, Bowstringing, Laseague tests +ve 3. Tone, Reflex, Power 4. Sensation X-ray (to exclude bone disease) & MRI NSAIDs Back care education Bed rest Epidural steroid injection Physiotherapy Back care education Discectomy Nerve decompression Indication: failure of 3 months of conservative mx, cauda equina syndrome Usually only alleviate symptoms of radiculopathy, not of LBP & fuse (Transforaminal Lumbar Interbody Fusion, or TLIF)
Caveats Sciatica (df): leg pain localised in the distribution of one/more lumbosacral nerve roots, typically L4-S2, with or without neurological deficit. [when the dermatomal distribution is unclear, please describe it as ‘non-specific radicular pattern’] Both spondylosis and degenerative disc disease may occur at the same time (chicken & egg phenomenon) Can have 2 or more concurrent pathologies, e.g. lumbar spondylosis with spinal stenosis (spinal stenosis increases with age but the symptoms may be exacerbated by further compression due to spondylosis) Causes of spinal stenosis can also cause radiculopathy as well Give the other as differential, e.g. PID – ddx spinal stenosis
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Other differentials Cauda Equina syndrome Neoplastic (primary, metastatic) Trauma - fracture (compression, distraction, translation, rotation) Spondyloarthropathies (e.g. ankylosing spondylitis) Referred pain - aorta, renal, ureter, pancreas Important Red flags (rule out malignancy, infection, trauma) - Age (<20 or >50 increased risk of conditions listed above) - LOW, LOA - Hx of malignancy - Night pain - Fever, chills, rigors - Hx of trauma - Any bladder/bowel symptoms
How to read Spine X-rays Lateral view
Lateral view of spine 1) anterior vertebral line 2) posterior vertebral line 3) spinolaminar line 4) interspinous line • Also look out for soft tissue (prevertebral fat stripe) should be – <6mm at C2 – <2mm at C6
X-Ray Oblique views: look for "Scottie Dog" sign (= spondylolysis) S – superior facet N – transverse process I – inferior facet P – pars interarticularis
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PROLAPSED INTERVERTEBRAL DISC (USUALLY YOUNGER PTS)
- Fenestration & discectomy OR microdiscectomy - Usually only alleviate symptoms of radiculopathy, but not of LBP
Surgical
- Acute posterior or post-lateral herniation of nucleus pulposus causing pressure on nerve root (traversing nerve root, not exiting nerve root) - Young adult - DDx: AS, TB spine, vertebral tumours, nerve tumours - L4/5 commonest (a/w L5 radiculopathy) followed by L5/S1(a/w S1 radiculopathy) Symptoms
- Backache (pressure on post longitudinal ligaments) - Sciatica (pressure on dural envelope or nerve root) - Radiculopathy (usu L5 or S1): Numbness, paraesthesia & muscle weakness in leg or foot (compression of nerve root) relieved by flexion to 1 side (listing) - Aggravated by coughing, straining, lifting, flexion of spine
- Indications: failure of 3 months of conservative management (i.e. progressive neurological deficit, persistent pain), cauda equina syndrome
SCOLIOSIS Causes Nonstructural Structural
Signs
- Listing (to relieve compression on nerve root), paravertebral muscle spasm, protective scoliosis, loss of lumbar lordosis - Restricted ROM - SLR limited, + bowstringing / sciatic nerve stretch test - Cross sciatic tension + - Segmental myotomal/ dermatomal deficits – sensory deficits, ↓power, ↓reflexes Lumbar Radiculopathy/Neuropathy Root L4 Quadriceps, tibialis anterior motor sensory reflex test
posteromedial knee reflex limitation of femoral stretch
L5 ankle dorsiflexion, great toe extensor, hip abductor lateral calf or 1st web space hamstring reflex limitation of SLR
Complications:
S1 ankle plantar flexion lateral aspect of foot ankle reflex limitation bowstring
- Cauda equina syndrome – urinary retention, saddle anaesthesia, lower limb weakness Investigations:
- X-rays: AP, lat, oblique to exclude bone disease - CT/MRI/myelogram Management
Conservative
-
Bed rest NSAID Epidural steroid injection Physiotherapy Back care education
- Limb length discrepancy (apparent or true shortening of one leg) - Hip contracture - Muscle spasm – eg 2o to PID -
Adolescent idiopathic (commonest, 80%) Infantile idiopathic – may resolve or progress Osteopathic – due to congenital vertebral anomalies Neuropathic – eg 2o to polio or CP. Causing asymmetrical muscle weakness - Myopathic – due to muscular dystrophies - Neurofibromatosis
ADOLESCENT IDIOPATHIC SCOLIOSIS - Progression: greatest during pubertal growth spurt, minimal progress post-puberty. - Deformity: Fixed 1o curve may be in thoracic or lumbar spine. Vertebrae are rotated w spinous processes pointing to the concavity of the curve. Ribs on the convex side are carried around to form a prominent hump Shoulder is elevated on side of convexity, hip sticks out on side of concavity Mobile 2o curves may develop above &/or below 1o curve to maintain normal head & pelvic position X-ray:
- full length AP spine X-ray (measure Cobb’s angle – sup & inf extent of scoliosis is where both sides of the intervertebral space is of equal height) - lateral flexion X-rays, - X-ray pelvis (look for Risser sign)
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Definition: Risser sign is defined by the amount of calcification present in the iliac apophysis and measures the progressive ossification from anterolaterally to posteromedially. Measure of skeletal maturity (Risser III patient has past peak of growth spurt, a period of rapid spinal growth during which scoliosis curvatures can increase rapidly) Grade I: 25% ossification action of the iliac apophysis Grade II: 50% Grade III: 75% Grade IV: 100% Grade V: means the iliac apophysis has fused to the iliac crest after 100% ossification Complications:
-
Pulmonary – ↓TLC & ↓FVC due to thoracic lordosis deformity (Cobb’s angle >70o) Cardiac – Right heart dz causing pulm HPT. ( Cobb’s angle >80o) Listing Limb length discrepancy Backache Radiculopathies
Mx: Age Prepubertal/ Pubertal Postpubertal
Cobb’s Angle
<20
o
20-40o >40o >50o
S/S
- Backache – intermittent; aggravated by standing, walking & prolonged sitting; relieved by lying down - Pain referred to buttocks and sometimes extends down leg - Acute incidents of pain, locking or giving way - Reduced lumbar ROM X-rays – narrowed disc space, osteophytes Mx:
- Conservative – modify activities, exercise, manipulation, NSAIDs, lumbar corset - Surgical – spinal fusion
SPINAL STENOSIS (USU OLDER PTS) - Causes: disc degeneration, OA & hypertrophy of post disc margin & facet joint, degenerative spondylolisthesis (usually L4/5 level), spondylolytic spondylolisthesis (usually L4/5 or L5/S1) - Causes of spinal stenosis can cause radiculopathy as well S/S:
- Neurogenic claudication: Thigh aches, numbness, paraesthesia after standing upright / walking. Claudication distance is variable - Relieved by spine flexion / sitting Patient stands in slight flexion - Limited spinal extension - Segmental sensory deficits, ↓power, ↓reflexes
Mx Neurogenic claudication
4mthly F/U & full length spine X-ray to check for progression of scoliosis Supports (e.g. Milwaukee brace) Spinal fusion + supports post-op to prevent recurrence Spinal fusion
LUMBAR SPONDYLOSIS Definition:
Flattening of disc & displacement of posterior facet joints, due to 2o OA facet joint
- Variable claudication distance - Better walking uphill due to spine flexion. Worse on walking downhill - Pain even on standing - ‘park bench to park bench’ – pain requires spine flexion to be relieved. - No pain at night – PT sleeps on lateral decubitus fetal position
Vascular claudication
- Constant claudication distance - Better walking downhill as effort is less. Worse on walking uphill - ‘Shop window to shop window’ – pain relieve simply by resting, even if standing up - Pain at night Also ask for PMHx of peripheral vascular disease, hx of smoking...
Invx: lat X-ray, CT myelogram (waisting of dye column, posterior indentation, partial
or complete block)
Epidemiology:
Usually >40YO, males > females 85
CAUDA EQUINA SYNDROME
Mx: Conservative
Education on spinal posture
Surgical
Nerve root compression
Decompression
Nerve root compression & spinal instability
Decompression & spinal fusion
SPONDYLOLISTHESIS Forward translation of upper vertebral body over the lower vertebral body, usually at L4/5 or L5/S1 level Causes
1. 2. 3. 4. 5. 6.
Dysplasia – congenital lumbosacral facet jt dysplasia Isthmic (spondylolytic) – break in the pars interarticularis Elderly (degenerative) – OA degeneration of facet joints Trauma Suspicious (pathological) – neoplasm Post-op – due to laminectomy for decompression
Spondylolytic Pathological Operative Trauma Elderly Dysplastic
S/S
- Backache – intermittent, worse on exercise or straining - ‘Stepping’ of spine - Stiffness (for degenerative type) X-ray:
- Fwd shift of upper spinal column - Elongation of the archs / defective facets - Gap in the pars interarticularis on oblique view (Scotty dog sign) Meyerding classification Grade % translation of VB
I II III IV
0-25 25-50 50-75 75-100
Mx
Conservative – bed rest & supporting corset Operative – spinal fusion
Old patients, non-disabling symptoms Disabling symptoms, young adult, neurological compression
Definition Cauda equina syndrome (CES) has been defined as low back pain, unilateral or usually bilateral sciatica, saddle sensory disturbances, bladder and bowel dysfunction, and variable lower extremity motor and sensory loss usually due to mechanical compression of the cauda equina. Aetiology V Spinal epidural hematoma Spinal anaesthesia IVC thrombosis I Abscess T Traumatic injury A M I Idiopathic N Tumour (primary/metastatic) Lymphoma Others • Spinal anaesthesia • Lumbar disk herniation • Late-stage ankylosing spondylitis History • Low back pain - This pain may have some characteristic that suggests something different from the far more common lumbar strain. Patients may report severity or a trigger, such as head turning that seem unusual. • Radiating pain o Acute or chronic • Unilateral or bilateral lower extremity motor and/or sensory abnormality • Bowel and/or bladder dysfunction o Initial presentation may be of difficulty starting or stopping a stream of urine that may be followed by frank incontinence first of urine then of stool. Urinary incontinence is on the basis of overflow. o Usually with associated saddle (perineal) anaesthesia (Examiner can ask if toilet paper feels different when wiping.)
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Physical Examination • Local tenderness to palpation over the lower back • Pain radiating to the legs • Loss or decreased reflexes o Hyperactive reflexes may signal cord involvement, hence ruling out CES o Similarly, Babinski sign / other signs of UMN involvement rule out CES • Sensory loss/abnormality in perineal area or lower extremities o Test light touch o Anaesthetic areas may show skin breakdown • Muscle weakness o +/- muscle wasting (if chronic) • Alteration in bladder function may be assessed empirically by obtaining urine via catheterization. A significant volume with little or no urge to void, or as a post-void residual, may indicate bladder dysfunction. Bedside ultrasonography may be also used to estimate or measure post-void residual bladder volume.
Management
Other Problems to Be Considered • Conus medullaris syndrome • Spinal cord compression • Lumbosacral plexopathy • Peripheral nerve disorder
Remember, it is a SURGICAL EMERGENCY! It will cause permanent urinary/bowel incontinence if untreated. Must operate on patient within 48h.
Investigations • Imaging o Plain radiography - Unlikely to be helpful in cauda equina syndrome but may be performed in cases of traumatic injury or in search of destructive changes, disk-space narrowing, or spondylolysis o CT with and/or without contrast - Lumbar myelogram followed by CT o MRI - Superiority of MRI over CT only suggested by case reports (Early consultation with the appropriate subspecialty is encouraged to guide imaging studies.)7 o Ultrasonography may be used to estimate or measure post-void residual volume. • Other Tests o Catheterization for residual urine volume may reveal urinary retention suggesting a neurogenic bladder.
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-
-
Prehospital care should focus on associated symptoms related to the pain (ie, what besides the pain is different). • Stabilize acute life-threatening conditions. • Immobilize the spine if traumatic. Emergency Department Care • No proven medical treatment exists, and therapy generally is directed at the underlying cause of cauda equina syndrome (CES). • For mechanical compression of the cauda due to disk herniation, surgical intervention may be indicated. Admit patients to appropriate service (usually neurology, neurosurgery, or orthopedic surgery) with frequent neurologic checks. Complications: Residual weakness, incontinence, impotence, and/or sensory abnormalities are potential problems if therapy is delayed
LUMBAR SPINE FRACTURES Elements of 3 Column Spine*** Anterior Column Ant longitudinal ligament Ant annulus fibrosis Ant 1/2 of vertebral body
Middle Column Post longitudinal ligament Post annulus fibrosis Post 1/2 of vertebral body
Posterior Column Post body elements Supra- & intraspinous lig. Facet joints Ligamentum flavum
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Basic Types of Spine Fractures and their Mechanisms Type Mechanism Compression Flexion • Anterior Anterior flexion • Lateral Lateral flexion Burst Axial load +/- flexion/rotation Flexion Flexion, distraction, common in lap-belted motor vehicle Distraction collision (Chance) Fracture Flexion-Rotation, Shear, Flexion Distraction dislocation Chance Fracture of the Spine - Hyperflexion injury - Fracture extends through all 3 columns! - Most commonly seen in MVC lap-belted passenger - CT scan to assist with diagnosis
Relieved by Neuro symptoms Inspection Straight leg raise
Neurological signs
Younger - Increase in abdominal pressure (laughing, coughing, lifting, straining) - Spine flexion, prolonged sitting Listing to 1 side Pain, numbness, paraesthesia, weakness Listing, scoliosis, loss of lumbar lordosis, paravertebral spasm - SLR elicits nerve root compression (i.e. radiculopathy) - SLR, SNST, Bowstring and cross SLR positive Radiculopathy (usu L5 &/or S1)
(NEUROLOGICAL DISEASE WITH POSSIBLE ORTHO CAUSE) Site
- C5-6 > C4-5 > C3-4 > C6-7 -
Cervical spondylosis – due to bony spurs & thickened ligament Infection Vascular disease Trauma Degenerative conditions - Demyelinating disorders - Tumours
PID VS SPINAL STENOSIS*** PID
CERVICAL MYELOPATHY
Causes of cervical myelopathy
Insert notes from Spine Trauma slides from CGH
Patient age LBP aggravating factors
variable depending on severity of stenosis) - Radiculopathy(if n. root is compressed by underlying spinal stenosis)
Spinal stenosis
Causes of compression
Older (unless cause is PID) Neurogenic claudication symptoms
-
Spine flexion
Symptoms
Pain, numbness, paraesthesia, weakness Pt stands in flexion SLR, SNST, Bowstring and cross SLR may or may not be positive (depending on whether nerve root is compressed by underlying cause of spinal stenosis) - Spinal stenosis: LMN signs at level of compression, UMN signs downwards (but signs are
-
Anterior: protruding disc or posterior osteophytes Anterolateral: jts of Luschka (uncovertebral jt) Lateral: cervical facets (thickening / bony spurs) Posterior: ligamentum flavum Weakness and clumsiness of the hands, paraesthesias in the hand Tightness, hot or cold sensations in the trunk Tingling in the legs Gait disturbances (ataxic, broad based, clumsy, shuffling) May have symptoms associated with malignancy – LOA, LOW, malaise, etc.
Signs
- Lower motor neuron findings at the level of the lesion - Upper motor neuron findings below the level of the lesion/cord compression - Upper limbs usually show a mix of UMN & LMN signs, while lower limbs usually show UMN signs only - Skipping of the face & head - ± Clonus, Lhermitte's sign (electric shock-like, radiating down body on neck flexion), Babinski and Hoffman's pathologic reflexes 88
- ± "Finger escape sign" (the patient is asked to hold out their hand with fingers extended and the medial fingers drift into flexion) - ± Urinary retention (rare) Investigations
-
Exclude tumour! Plain X-rays CT (bony spurs & ligament ossification) MRI (disc prolapse & cord compression) Pavlov's Ratio: ratio of the distance from the posterior aspect of the vertebral body to the anterior aspect of the lamina (i.e. space allowed for the cord at the same level) to the AP width of the vertebral body. Normal: ≥ 1 Abnormal: ≤0.85
Management
- As for cervical spondylosis
CERVICAL SPONDYLOSIS (ORTHOPAEDIC DEGENERATIVE DISEASE OF THE C-SPINE) Features
- IV disc degenerate & flatten + bony spurs on ant & post margins of vertebral bodies - Posterior spurs may encroach upon the IV foramina compressing nerve roots - >40YO, male > female, usually C5/6 DDx
- Thoracic outlet syndrome (look for signs of limb ischaemia; perform Roos test and Adson’s manoeuvre) (a/w ulnar n. palsy) - Carpal tunnel syndrome - Rotator cuff lesions (abnormal shoulder movements, no neurological signs) - Cervical tumour (symptoms are constant) Risk factors
- Smoking - Drinking - Excessive driving
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Radiation: occiput (‘headache’), scapular muscles, down one or both arms. Paraesthesia, weakness, clumsiness Periods of exacerbation & quiescence Posterior neck & scapular tenderness ↓ neck ROM throughout with pain Limb numbness, weakness, ↓ reflexes
Investigations
- X-ray: narrowed IV disc space, bony spurs (‘osteophytes’), encroachment of IV foramina in oblique view Management
Conservative: - Heat & massage, NSAIDs, cervical collar, physioRx Surgical: - Discectomy ± anterior fusion - Corpectomy (removing part of vertebral body; latin corpus vertebrae) - Laminoplasty - Laminectomy ± foraminectomy. - Indications: progressive neurological deficits, multiple levels of cord compression
CERVICAL LESIONS TORTICOLLIS Causes
Acquired • Acute - muscular damage caused by inflammatory diseases, such as myositis, lymphadenitis, or tuberculosis (TB); from cervical spinal injuries that produce scar tissue contracture; and, less commonly, from tumor or medication • Spasmodic - organic central nervous system disorder, probably due to irritation of the nerve root by arthritis or osteomyelitis. Benign paroxysmal torticollis – might be migraine variant. • Ocular torticollis - compensatory mechanism enacted by patients with trochlear nerve palsy or superior oblique muscle weakness • Hysterical
Presentation
- Neck pain & stiffness, worse in the morning 89
Congenital • Traumatic – infants after difficult delivery - breech presentation (delivery buttocks first instead of heads first) • Skeletal anomalies, atlantoaxial instability • Klippel-Feil syndrome
• • •
The presence of craniofacial asymmetry (e.g. hypoplasia of the face including the small left eye) indicates congenital or long-standing torticollis. Management
- Pre-hospital care: ensure patent airway, perform C-spine immobilisation / precaution for patients with history of trauma - A&E: ABCDEs, give antibiotics if infection suspected - Definitive treatment » Generally supportive; includes analgesics, benzodiazepines, anti-cholinergics, heat, massage, stretching exercises » Drug-induced torticollis: treated with diphenhyrdramine, benztropine, or benzodiazepines » Surgical Rx: SCM release (>1yo: don’t need to wait or try conservative Rx)
THORACIC OUTLET SYNDROME
1. Lower trunk of brachial plexus n subclavian artery pass btw the ant n middle scalene muscles and over the 1st rib. 2. Compression maybe due to cervical rib (rare), fibrous bands or abnormalities of scalene attachments, or by a pancoast tumour 3. Symptoms increase with increasing age as shoulders sag 4. Typically woman in her 30s complains of pain n paraesthesia extending down from her shoulder down the ulnar aspect of her arm to the medial two fingers 5. Worse at night, agg by bracing shoulders or raising arms above shoulder height
ACUTE PROLAPSED INTERVETEBRAL DISC (PID) • •
Precipitated by local sprain or injury, usually underlying pathology already present e.g. ↑ intervertebral disc pressure Leads to compression of o Post intervertebral lig – pain, stiffness, from back of neck to scapula, occiput
N root – pain, paraesthesia in one / both (rare) arms. Radiating to outer elbow, dorsum of wrist, middle n index finger. Weakness is rare. Prolapse usually above/below C6 vertebrae so C6 & C7 N roots commonly affected Acute torticollis may be present X-ray shows ↓ disc space. MRI to confirm. Ddx o Soft tissue sprain – neurological S&S absent. o Neurological amyotrophy (acute brachial neuritis) – sudden, severe pain @ back or shoulder. Multiple neurological sites affected & might have winging of scapula. Pain followed by flaccid paralysis a few days later. o Cervical spine infection – unrelenting & local spasm with severe pain. X-ray: erosion of bone o Cervical tumors – neurological signs progressive. X-ray/MRI shows bone destruction. Primary tumors rare, secondary more common. Of primary, sarcoma & multiple myeloma most common. Treatment o Heat, analgesics o Rest with collar (in 75% of patients symptoms will resolve with non-operative measures) o Reduce: traction intermittently placed for 30 mins @ a time. Up to 8kg o Remove: anterior approach discectomy – fuse affected area / maintain height using bone grafts. o
•
CERVICAL SPINE TRAUMA Neuro examination by levels (check dermatome for each of them) • C4 – spontaneous respiration • C5 – biceps reflex, deltoid strength • C6 – wrist extension, brachioradialis reflex • C7 - wrist flexion, triceps reflex • C8 – finger flexion • T1 – interossei • L1, L2 – hip flexion (femoral n.) • L2, L3 – hip adduction (obturator n.) • L3, L4 – knee extension (femoral n.) – knee jerk • L4 – dorsiflexion (deep peroneal n.) • L4, L5 – hip abduction (superior gluteal n.) • L5, S1 – hip extension (inferior gluteal n.) • S1 – knee flexion (sciatic n.) • S1, S2 – plantarflexion (tibial n.) – ankle jerk (S1) 90
Pathologic reflexes (UMNL) – Hoffman’s sign, Babinski’s reflex, Oppenheim’s sign (dorsiflexion of big toe elicited by downward irritation of medial side of tibia) Sacral sparing: incomplete injury - perianal sensation, rectal motor function, great toe flexor activity • Frankel Score A Complete Motor / Sensory B Complete Motor / Incomplete Sensory C Incomplete Motor < 3 / Incomplete Sensory D Incomplete Motor > 3 / Incomplete Sensory E Normal Spinal shock - state of complete spinal areflexia. • over in 24-48 hours - Bulbocavernosus reflex signifies the end of spinal shock • Treatment of Spinal Cord Injury o attributed to contusion and/or compression - Microvasculature disruption o Treatment: Methylprednisolone- bolus 30mg/kg followed by 5.4 mg/kg/hr over 23 hours. Patients treated within 8 hours respond best.
TRAUMA C-SPINE SERIES – AP, lateral, open mouth odontoid Who needs C-spine X-ray? • Midline cervical tenderness • History of neck/distracting injury • Have focal neurological deficits • Intoxicated / not response to person, time, place and event
NB. Pure dislocation of the spine is commonest in the cervical region Lateral • adequate exposure - must see occiput to T1, need to be able to see soft tissue shadows, Swimmers view or CT if unable to see to T1 • Specific things to look for 1. anatomic lines -> 4 parallel lines
1) 2) 3) 4)
Anterior vertebral line Posterior vertebral line Spinolaminal line Interspinous line
Also look for soft tissue swelling (prevertebral fat stripe) which should be - <6mm at C2 level - <2mm at C6 level
2. Step deformity of >3.5mm anywhere Anterior subluxation of 1 vertebra on another indicates facet dislocation Less than 50% of the width of a vertebral body implies unifacet dislocation Greater than 50% implies bilateral facet dislocation This is usually accompanied by widening of the interspinous and interlaminar spaces 3. Atlantodens interval (ADI) – distance between odontoid process and posterior border of arch anterior of atlas – atlantoaxial instability (AAI) present if >3mm in adults >5mm in children 4. Uniformity of shape & height of IV disc (all the same except C1 & C2) Compression #: anterior wedging of vertebral body or teardrop fractures of antero-inferior portion of body Burst #: anterior compression of greater than 40% of normal vertebral body height (with retropulsion of fragments of the vertebral body into the spinal canal) Loss of height disc herniation 5. Angulation 11° greater than contiguous segments (Disruption of the PLL, Subluxation of C3 on C4) 6. Anterior Occipitoatlantal Dislocation (Powers Ratio)
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Odontoid view Shows C1 burst fractures, C1-2 alignment, Dens fractures C1 Ring Fracture Classification - Posterior Arch - 28%, Jefferson Burst Fx, Anterior Arch “Blow Out”, Lateral Mass Fx, Transverse Process Fx Jefferson Fracture - Axial loading. Open Mouth View - Lateral Mass Spreading, > 6.9 mm = Transverse Lig Avulsion. C1 Burst Fracture Treatment 1. Stable (Intact Transverse Ligament) - Rx - Halo 10 - 12 wks. 2. Unstable - Traction Reduction, Halo 12 - 16 wks, Late Instability: C1-2 Fusion Odontoid Fracture Classification 1. Type 1 - Tip Avulsion, Type 2 – Waist (worst), Type 3 – Body 2. Type 2 – Unstable, Easily Missed, 10% Spinal Cord Injury due to translation, Poor Prognosis, Assoc Fx 20 - 30% 3. Type 3 - Good prognosis, Reduction, Brace (halo device) vs fixation, heals easily AP view Spinous processes should line up and have equal gaps sagital plane fractures lateral mass fractures facet fractures / dislocations (below)
Complete the exam – If films negative remove collar and complete exam. Palpation- one person supports the head with axial traction while the other palpates from occiput to T1. Check for tenderness, swelling, stepoff. cannot rely on clinical exam if decreased mental status or distracting injury. If symptomatic replace collar. If negative then proceed to ROM. Active ROM only. Should be full and pain free. If exam completely negative and films negative at this point may remove collar. Write order that C-spine is clear If unable to perform ROM but the rest of exam is negative: replace collar and have patient return in 10-14 days for flexion and extension views. If done acutely muscle spasm or guarding may hide a ligamentous injury. Obtunded patient with normal films - Leave the collar on. Dynamic Fluoroscopy. MRI Hangman’s Fracture of C2 Flexion Tear drop fracture of ant-inf part of vertebral body. Unstable fracture. Treatment – gardner-wells traction tongs, halo device
LEFT: Unilateral facet dislocation. (A) Lateral view of this fracture caused by a flexion-rotation mechanism shows that it is stable. Anterior displacement of spine is less than one half of the diameter of a vertebral body. (B) Anteroposterior view shows disruption of a line connecting spinous processes at the level of the dislocation. (C) Oblique view shows that the expected tiling of the laminae is disrupted, and the dislocated superior articulating facet of the lower vertebra is seen projecting within the neural foramina.
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DM FOOT (ORTHO) EPIDEMIOLOGY - Prevalence of DM is 8.2% (28.4% in 60-69 age group) - 5% of all Diabetics develop foot ulcers - In S’pore, 2 amputations done daily o Foot ulcers commonly become infected gangrene result in Major Lower Limb Amputation - Mortality: 10% at time of amputation, 30% within a year, 70% within 5 years
• • • •
Osteomyelitis / septic arthritis Gangrene (dry/wet) Charcot’s osteoarthropathy Necrotising fasciitis
HISTORY: PATIENT PROFILE (include OCCUPATION! – nature of job)
2. VASCULOPATHY: o Microangiopathy: terminal arterioles thickening of basement membrance of endothelium o Atherosclerosis: middle-sized and large arteries
PRESENTING COMPLAINT: ulcer/abscess/gangrene, pain/swollen/infection When did you sustain the injury? How was it sustained? What were you doing at that time? Footwear at point of injury? When did you discover it? How did you realize it? If not discovered at point of injury reason? Numbness/weakness Precipitating injuries: trauma, rusty nails, pressure Type of wound: open/closed, bleeding? Progression of injury: grew bigger, more painful, discharge, gangrene 1st episode? Any previous injuries of similar nature? • Ask for poor wound healing
3. IMMUNOPATHY o Defects in leukocyte function (phagocytosis, chemotaxis, adherence, neutrophil dysfxn)
PAIN: SOCRATES Localised to toe/heel?
PATHOGENESIS OF DM FOOT 1. NEUROPATHY (20-40% of all diabetics) o Sensory o Motor o Autonomic
o
Inherent susceptibility to infections Mild – monomicrobial Severe – polymicrobial, a/w ostemyelitis Prior use of ABx predisposes to MRSA & Pseudomonas
Vascular claudication 1) Pain in muscle (usu described as cramp) 2) Only on exercise (ask abt claudication distance: quantify in eg. no. of bus stops) 3) Disappears on rest
o
Predominantly Gm positive cocci (Staph aureus, coagulase –ve staph eg. epidermidis, Group B Strep, Enterococci, Corynebacterium) All forms of Staphylocci a/w increased risk of mortality
o
Followed by Gram negative rods (eg. Pseudomonas (rotten fruit smell, green discharge), Proteus, E. coli) and anaerobes eg. Bacteroides (faecal smell)
Rest pain (present at rest throughout day and night) – o Continuous severe aching pain bad enough to stop sleep and use of limb; o Usu in most distal part of limb (toes and forefoot) o A/w gangrene pain at border of living and dead tissue o Relieved by hanging leg over side of bed; prefer to sleep sitting in chair o May be so bad (unremitting, progressively worse) that beg for amputation • NB: Critical limb ischaemia (rest pain and ulceration/gangrene) o ? Night pain
MODES OF PRESENTATION: • • •
Cellulitis Abscess (supf/deep) Ulcer (decubitus / vascular / neuropathic) 93
ULCER: Site: • Plantar (sole) – neuropathic • Heel/toes – vascular (ischaemic) Size Any discharge? Colour? (green – Pseudomonas) Foul-smelling? (eg. fish, rotten fruit smell) Pain? Recent trauma / foreign body penetration eg. rusty nail (even seemingly insignificant) Footwear (ill-fitting shoes, slippers, barefeet) SWELLING: Acute onset Pain Erythematous, warmth Discharge? – colour, odour, pus Fever chills rigors SWOLLEN JOINT Symptoms of inflammation – red, hot, swollen, pain, loss of function think septic arthritis Weakness, difficulty walking, deformity think Charcot’s arthropathy GANGRENE: Toe/ heel/ foot Dry/ wet? Other symptoms of ischaemia – claudication, rest pain, cold extremities, discolouration HISTORY OF SELF-MEDICATION Seek medical help from doctors? Sinseh : skin burns ulceration sepsis Self-medicate : nail digging, self cutting callosity DIABETES HISTORY (DETERMINE TYPE 1 OR 2): How long? How was it diagnosed? Treatment: Diet/OHGAs/Insulin/Combination? Dosage/med changes, compliance Control: Symptoms of poor control to ask: 1) polyuria, 2) polydipsia, 3) polyphagia
Monitoring of DM: hypocount, HbA1c; what are the usual values? How often follow-up? Did doctor say good control? Previous hospitalizations for DM, any surgery done? – DKA, HHNK, abscess, ulcer, gangrene etc Complications: o Microvascular Retinopathy – blurring of vision, cataracts, previous laser PRP Nephropathy – bubbly urine (?microalbuminuria), 24hr urine test CCT, UTP Neuropathy – Sensory: numbness, paraesthesia, loss of proprioception Motor: weakness Autonomic: postural hypotension, gastroparesis, diarrhoea, impotence o Macrovascular CAD – IHD (CP, SOB), h/o AMI, cardiomyopathy CVA – TIA, major stroke PVD – paraesthesia, intermittent claudication, pallor, poor wound healing Co-morbidities – HTN, IHD, CVA, CRF (worst combination with DM), Other risk factors – smoking, HTN, HCL (aggravates atherosclerosis) Functional status – community walker / housebound / unable to walk (stroke), can do household chores? ADL independent? How does the current orthopaedic problem affect the pt’s function in general? Care-giver? Family history of DM
Determine if Foot ulcer is: Vascular - punched out - gangrene - ischemic limb sympts
Neurogenic - painless - deformed joints - loss of sensation (vibration, proprioception)
PHYSICAL EXAMINATION: GENERAL: Well / ill / toxic Acidotic breathing (Kussmaul) Alert, oriented / drowsy (hypoglycaemia) Pallor / sallow appearance (renal failure) Dehydration: furred tongue, dry mucosa, sunken eyes Fundoscopy – diabetic retinopathy 94
VITALS BP (both sides, postural) Palpate ALL pulses – carotids (thrill, bruit), UL, LL SYSTEMIC REVIEW: Heart, lungs, abdomen LOCAL EXAMINATION: Inspection: Skin: o Scars, Sinus, Healed wounds Signs of PVD (chronic ischaemia): • Shiny • Loss of hair • Dusky discolouration, pale • Trophic nail changes • Pigmented skin • NO varicose veins (good negative to mention) o Signs of DM neuropathy • Sensory: Joint deformity (charcot’s jt, claw toe, hammer toe) • Motor: Muscle wasting • Autonomic: Dry skin, Fissuring, Callosity Ulcer: o Site – interdigital web space, dorsum, sole, heel o Size o Shape o Floor: pus, slough, necrotic tissue, granulation tissue o Edge: punched-out vascular; irregular o Any foreign body in ulcer? o Surrounding skin : erythematous, necrotic, warm, tender Swelling Cellulitis Gangrene – dry / wet?
o
Popliteal pulse Femoral pulse o NB: Vasculopathy assessment: (prognostic significance for distal amputation) 2 pulses palpable – v good chance of success 1 pulse – fairly good 0 pulses – NO chance Ulcer: o Tenderness, bogginess around ulcer o Squeeze surrounding skin for discharge – quantity, colour, odour Tenderness of each individual metatarsal bone / joint (OM, SA): o dorsal surface o deep palpation of SOLE (pus tends to be dependent) Sensation: o Semmes-Weinstein monofilament (5.07 gauge applies 10g of force – test 9 points on sole and 1 point in 1st web space – if pt cannot feel means high risk!!! o Vibration o Propioception o Pin prick o Light touch Motor (usually not required): test ankle reflexes. Test upper limb for glove and stocking distribution too!
Move:
Palpation:
Temp – warm (normal?) / hot (infected) / cold (ischaemia) Capillary refill time (<2sec) Pulses – DP (midpt of 2 malleoli, 1/3 way down to 1st digital cleft) PT (hip in ER, knee flexed, foot dorsiflexed, 1/3 way down line from med malleolus to TA) 95
Buerger’s test (2 components): o Pt supine, raise LL, look for pallor of sole and toes, record vascular angle • Normal: 90deg pink • Ischaemia: 15-30deg pallor • Critical Ischemia: <20deg o Pt sitting with legs hanging over side of bed, note time of reactive hyperemia • Normal: remain pink • Ischaemia: white to pink • CAPILLARY FILLING TIME >15-30 secs = severe ischaemia ABI: o Doppler ultrasound probe used to measure ankle systolic pressure (should have 3 waveforms – systolic, diastolic, recoil. If only 2 means already partial obstruction.) o ABI = Ankle systolic press/Brachial systolic press • Normal > 1.0 • Ischaemia <0.8 • Min to mod dz 0.5 – 0.9 • Severe dz <0.5 • Critical ischemia <0.3 o Digital pressure index • Normal >0.7 • Abnormal <0.7
INVESTIGATIONS: BLOODS FBC – anaemia, TWC with differential count for infx ( leukocytosis, ↑ polymorphic neutrophils) ESR, CRP (acute phase reactants) U/E/Cr – nephropathy Venous bld glucose (fasting >8mmol/l, random> 11mmol/L) Hypocount (TDS including 10pm) HBA1c – normal 4-7% Urinalysis – glycosuria, ketonuria (DKA), proteinuria (nephropathy) Blood c/s if septic (For medical case, please include urine dipstix, lipid profile)
CULTURES Wound swab of ulcer – take pus and from deepest possible part to increase yield o Gram stain o C/s (aerobic and anaerobic) IMAGING ECG – cardiac status
CXR – anaesthesia fitness
X-ray foot (AP, Lat): 1. Osteomyelitis – rarefaction / osteopaenic, erosions, periosteal reaction (early), cortical sclerosis (chronic) 2. Septic arthritis – widening of jt space, periarticular osteoporosis (early), jt space narrowed (+/- erosions) (late) 3. GAS gangrene – Clostridium, Strep. Microaerophiles – excl NECROTISING FASCIITIS if there’s gas present 4. Bony destruction (Charcot’s/ LisFranc jt) – neuropathic changes 5. Calcification of vessels 6. Foreign body
Duplex scan – arterial insufficiency
Angiogram, femoral (if vascular reconstruction needed) – localize areas of occlusion amenable to bypass Sx or angioplasty
MANAGEMENT: WAGNER CLASSIFICATION of DM foot ulcers: This determines management. In general, lower grades respond to ABs and debridement. Higher grades (2-5) require amputation. Grade
Description
1
Superficial ulcer, no penetration into deeper tissue, no infection Deep ulcer extending to muscle, tendon, bone, ligament
0
2
3
Foot at risk, No open wound
Infection of deep tissue with pus,
Treatment
Patient education Accommodative footwear Regular clinical, podiatry exam Offloading with total contact cast Walking brace/special footwear Surgical debridement Wound care Offloading Culture-specific Antibiotics Debridement or partial amputation 96
4
gangrene (e.g. tendinitis, osteomyelitis, deep abscess) Forefoot gangrene
5
Whole foot gangrene
Offloading Culture-specific antibiotics Lower extremity amputation Vascular consultation Major extremity amputation Vascular consultation o
KING’S CLASSIFICATION Clinical Condition Normal High-risk Ulcerated Cellulitic Necrotic Major Amputation
Stage 1 2 3 4 5 6
o
o
General measures:
o
IV Line for DS/NS at least 1.5L/day to prevent DEHYDRATION Intake/output charts – urine output monitoring Diabetic chart – Hypocount TDS including 10pm (watch out for HYPOGLYCAEMIA) IV antibiotics (broad spectrum: Augmentin (Gm positive cocci, Gm negative rods, anaerobes) or Clindamycin (Gm positive, anaerobes, esp for necrotising fasciitis) + Ciprofloxacin (Gm negative), ONCE c/s results obtained change to culture-specific antibiotics Daily wound dressing – Chlorhexidine, flush with H202, saline then Chlorhexidine dressing Elevate leg if swollen Topical antibiotics: • BNP (bacitracin, neomycin, polymycin) powder for Pseudomonas • Bactroban cream for MRSA
Surgery:
I&D for ABSCESS Radical debridement for ULCER – all slough excised, exposed tendons excised (or else become necrotic), in heel whole part of TA exposed must be excised (desloughing) • Heel ulcer / gangrene unless successfully resurfaced = BKA
Dry gangrene:
Gangrene – dry / wet determines management options If vascular cause consider whether amenable to bypass or not
Pulses usually v bad Clean with ethanol, splint and dressing Prophylactic antibiotics (sides usually get infected) Toe may auto-amputate Ray amputation can be considered in young pt (in older pts better to leave it alone after all it’s quite easy to care for dry gangrene) +/- Hyperbaric Oxygen Therapy (HBOT)
Wet gangrene: AMPUTATE
o
Ray amputation (open/closed) • Amputation of digit through metatarsal removing large part of 1 ray • Open ray – for adequate drainage of pus involving 1 ray, upon healing with health granulation tissue, split skin graft is used • Closed ray – if after debridement all infectious tissue has been removed, close wound by tagging
Disarticulation at joint (PIP, DIP) Ray amputation (through metatarsal) Forefoot Lisfranc (Tarsometatarsal) Chopard’s (Midtarsal) Syme’s (through ankle) – rare, requires good PT pulse [MCQ] BKA – require 30% more energy to walk; bilateral BKA – 40% Through knee (Stokes-Gritti) AKA – require 40% more energy to walk Hip disarticulation Hindquarter amputation (hemipelvectomy)
Multidisciplinary approach
Orthopaedic surgeon, vascular surgeon Endocrinologist Infectious Disease Specialist Podiatrist Diabetic Nurses, Wound-Care Nurses Dietician PT/OT MSW Amputation support group 97
POLYTRAUMA Definition of polytrauma Injury to several (>1) physical regions or organ systems where at least 1 injury or a combination of several injuries is life threatening Different from multiple injuries – not life threatening – or a severe life-threatening single injury (barytrauma) Trimodal peak of trauma mortality: - 1st hour after injury: most patients die - 1-4 hours after injury: “golden hour” Death usually caused by hypovolemic shock - Several weeks later: late complications & multiple organ failure Mechanism of accident Deceleration trauma Fall trauma Trauma resulting from being run over Crush trauma Avulsion trauma Penetrating injury Explosion injury Thermal injury Chemical injury Radiation injury
Important to break the figure down into its components, such as E3V3M5 = GCS 11. A Coma Score of 13 or higher correlates with a mild brain injury, 9 to 12 is a moderate injury and 8 or less a severe brain injury. Abbreviated Injury Scale • An anatomical scoring system. • Injuries are ranked on a scale of 1 to 6, with 1 being minor, 5 severe and 6 an unsurvivable injury.
Suspect Polytrauma when: - Fall from height > 3m - Ejection from vehicle - Death of fellow passenger - Pedestrian/Motorcyclist and car - High speed accident - Entrapment, Pinning or Burial - Explosion
Glasgow Coma Scale Eye Response (4) Eyes open spontaneously – 4 Eyes open on verbal command – 3 Eyes open to pain – 2 No eye opening – 1
Motor Response (6) Obeys commands – 6 Localising to pain – 5 Withdrawing from pain – 4 Flexion to pain – 3 Extension to pain – 2 No motor response – 1
Verbal Response (5) Oriented – 5 Confused – 4 Inappropriate words – 3 Incomprehensible sounds – 2 No verbal response – 1
AIS Score Injury Injury Severity Score • Each injury is assigned an AIS score and is 1 Minor allocated to one of six body regions (Head, 2 Moderate Face, Chest, Abdomen, Extremities (including 3 Serious Pelvis), External). Only the highest AIS score 4 Severe in each body region is used. The 3 most Critical severely injured body regions have their score 5 squared and added together to produce the ISS 6 Unsurvivable score. • The ISS score takes values from 0 to 75. If an injury is assigned an AIS of 6 (unsurvivable injury), the ISS score is automatically assigned to 75. • The only anatomical scoring system in use and correlates slinearly with mortality, morbidity, hospital stay and other measures of severity. • weaknesses o any error in AIS scoring increases the ISS error, o many different injury patterns can yield the same ISS score and injuries to different body regions are not weighted. o the ISS (along with other anatomical scoring systems) is not useful as a triage tool.
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Example
o
Region
Injury Description
AIS
Square Top Three
Chest
Cerebral Contusion
3
9
Head & Neck
No Injury
0
Face
Flail Chest
4
16
Abdomen
Minor Contusion of Liver Complex Rupture Spleen
2 5
25
Extremity
Fractured femur
3
External
No Injury
0
Injury severity
o
o
o 50
Physiological response to polytrauma Mediated mainly by: Tissue damage Hypovolaemia Manifested by Changes in cardiovascular system Inflammatory reaction → SIRS → ARDS → MOF → immune suppresion Changes in metabolic status Closely interlinked by the neuroendocrine system. Hypovolaemia 1 Systemic compensation by sympathetic activation Renin-angiotensin-aldosterone activation Anti-diuretic hormone secretion o Reduced right heart filling pressure → reduced oxygen uptake o Reduced left heart filling pressure 2° reduced pulmonary venous return → reduced cardiac output
Less inhibitory stimulation of baroceptors in aortic arch & carotid sinus → reflex inhibition of vagal activity + ↑sympathetic stimulation to heart & vessels → ↑ CO & SVR o (cerebral & myocardial vessels not involved; peripheral vasoconstriction in cutaneous, skeletal & visceral tissue, preserving circulation to important organs (brain, heart & kidneys) Further intravascular loss → distortion of incompletely filled chambers stimulates cardiac C fibres → reflex vagal slowing of heart rate + vasodilation → circulatory collapse Chemoceptors of carotid sinus & aortic arch becomes more sensitive to ↓PaO2 at ↑PaCO2 (↓pH) → tachypnea, vagal slowing of HR, sympathetic vasoconstriction in skeletal muscles High sympathetic drive causes catecholamine release from adrenals → activation of renin-angiotensin-aldosterone system → further release of corticosteriod, antidiuretic hormone, glucagon, insulin & human growth hormone → Na & water retention to incr circulating blood volume & maintain BP Cellular compensation by anaerobic respiration o compensatory anaerobic metabolism → lactic acidosis
Classification of shock (% of blood Class I loss) <15% Pulse pressure ↑ Resp Rate 14-20 Urine outpt >30 Mental status -
Class II 15-30% ↓ 20-30 20-30 Mild anxiety
Class III 30-40% ↓(SPB↓) 30-35 5-15 Confused
Class IV >40% ↓ >35 Neg Lethargic/ obtunded
Inflammatory response 1,2 Any tissue injury generates a local inflammatory response (with/without pre-existing infection) → directed at elimination of dead tissue, foreign invaders & healing Greater trauma causes more inflammatory reaction
Cellular mediators: PMNs, macrophages & fibroblasts Cytokines: esp IL-1 & TNF-α Complement system: esp C3 (anaphylactoid reaction) & C5 (PMN stimulator) Prostaglandins: thromboxane, prostacyclins etc 99
Acute-phase reactants Liver synthesis of acute phase reactants such as opsonins (CRP), protease inhibitor, haemostatic agents (fibrinogen) & transporters (transferin) Stress hormones: adrenaline, cortisol release Insulin secretion suppressed, glucagon enhances glycogenolysis → overall hyperglycaemia
Overwhelming inflammatory response Both pro-inflammatory + anti-inflammatory cytokines are generated in an inflammatory response Major trauma causes systemic release of inflammatory agents Spillover of such inflammatory agents systemically can occur with major trauma → Systemic inflammatory response syndrome (SIRS) → ARDS /MOF • In severe states, SIRS can evolve into acute respiratory distress syndrome (ARDS) or multi-organ failure (MOF) • SIRS can occur in a non-septic state • ARDS or lung failure is usually the first to occur followed by other organ systems damage with hypoxia(MOF). • MOF can occur in without SIRS • SIRS can be precipitated by a 2nd time injurious event (eg: surgery or secondary infection) after the initial trauma → “2-hit” theory of SIRS
• Liver → Glycogenolysis & gluconeogenesis • Anaerobic metabolism → lactic acidosis Skeletal muscle catabolism (-ve nitrogen balance) substrate for liver gluconeogenesis (negative nitrogen balance) Lipolysis → release of FFA & glycerol (↑TG & LDL) High resting energy expenditure - General catabolic state ↑ body temperature Convalescent state Insulin secretion resumes, insulin resistance decreases Aerobic respiration reestablished
Clinical manifestation of SIRS Defined as presence of ≥2 of the following signs: Hyperthermia >38C or hypothermia <36C Tachycardia >90bpm Tachypnea >20breaths/min or PaCO2<32mmHg Elevated/depressed white cell count [>12,000/uL or <4000/uL] or 10% immature band forms Initial hypermetabolism
Early hyperglycaemia •
• • •
Plasma cortisol increases in proportion to injury with corresponding sympathoadrenal response (until adrenal perfusion fails) Early hyperglycaemia occurs with increased sympatho-adrenal activity Peripheral insulin resistance & depressed insulin secretion with high circulating catecholamines & glucagon release Skeletal glycogenolysis 100
Life and Limb Threatening Conditions Life Threatening Conditions: Airway 1. Facial fractures a. major fractures of maxilla and mandible b. nasal intubation not recommended 2. Larynx injuries a. presents with stridor, hoarseness, crepitus in the neck and rapid respiratory obstruction b. do tracheostomy to secure airway Breathing 1. Spinal injury a) always assume cervical injury until proven otherwise b) high cervical cord transection paralyses intercostal muscles and diaphragm, c) resulting in apnoea in minutes to hours d) steroids useful if administered within first 8 hrs 2. Chest injuries a) Rib fracture: presents with tenderness and crepitus b) Tension pneumothorax: accumulation of air under pressure in the pleural space. This develops when the injured tissue forms a one-way valve, allowing air to enter the pleural space & preventing the air from escaping naturally. i. Air trapped pushes heart and mediastinal structures to the contralateral side, impinging on the contralateral lung. ii. Hypoxia decreases venous return and cardiac output, causing hypotension. iii. Haemodynamic collapse leads to death. c) Haemothorax d) Pulmonary contusion: parenchymal damage leads to impaired gaseous exchange. e) Flail chest: paradoxical movement of a segment of chest wall, usually caused by fracture of 3 or more ribs, resulting in injury to heart and lungs, leading to pulmonary contusion, VQ mismatch and respiratory distress. 3. Fat embolism - Results when embolic marrow fat macroglobules damage small vessel perfusion leading to endothelial damage in pulmonary capillary beds - Risk factors Long bone # [note that the risk is especially high with femoral shaft fracture and concomitant head injury]
Risk is higher w/ non-operative therapy but is also higher w/ overzealous reaming of femoral canal Multiple trauma w/ major visceral injuries and blood loss (incidence may be as high as 5-10%) - Cause of death on 3rd day after pelvic fracture is due to fat embolism - NB. Complications of skeletal traction do not include fat embolism - Clinical manifestations Symptoms usually begin 24-48 hours after injury Major criteria • Hypoxia • Altered mental status • Petechial rash Minor criteria • Tachycardia (>110/min) • Tachypnoea • Hypotention • Fever (>38.5 º C) • Retinal changes of fat globules or petechiae • Renal dysfunction • Jaundice • Acute drop in hemoglobin and/or platelets • Elevated ESR 1 major and 4 minor criteria, plus fat microglobulinemia, must be present to formally diagnose fat embolism syndrome - Treat the hypoxaemia 4. Thromboembolism (DVT) - develops 5-7 days later, worried about pulmonary embolism 5. Tetanus - develops 7 days later - administer tetanus toxoid as prophylaxis, especially with lacerations, abrasions, dirty wounds and open fractures Circulation 1. Posterior dislocation of sternoclavicular joint 2. Abdominal injuries: liver injuries and splenic rupture 3. Pelvic ring fracture 4. Hip injuries: may sustain internal bleeding and neuropathies as well. Usually caused by dislocations and fractures. 5. Femoral shaft fractures: femoral artery involved
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Limb Threatening Conditions: Vascular Impairment - Haemorrahge: visible or occult - Ischaemia: acute interruption of flow of blood to a limb or organ. Anaerobic respiration predominates, leading to lactic acidosis and eventually cell death. - Causes: Dislocations or fractures - Arteries involved: Axillary, brachial, femoral, popliteal
-
Mangled Extremity - High energy transfer or crush resulting in some combination of injuries to arteries, bones, tendons, nerves and/or soft tissue - Scored using MESS (Mangled Extremity Severity Score) A) Skeletal/ Soft Tissue Injury • Low energy (stab: simple fracture; pistol/ gunshot wound) • Medium energy (open or multiple fractures; dislocation) • High energy (high speed MVA or rifle GSW) • Very high energy (high speed trauma + gross contamination) B) Limb Ischemia • Pulse reduced or absent but perfusion normal • Pulseless; paresthesia, diminished capillary refill • Cool, paralysed, insensate, numb C) Shock • Systolic BP always > 90mmHg • Hypotensive transiently • Persistent hypotension D) Age (years) • <30 • 30-50 • >50 * Score doubled for ischaemia > 6hrs - Acutely differentiates salvageable and unsalvageable limbs - MESS ≥ 7 carries a 100% predictive value for amputation Acute Compartment Syndrome - pressure within a closed muscle compartment exceeds the perfusion pressure - tissue pressure exceeds venous pressure and impairs blood outflow
1 2 3 4 1* 2 3* 0 1 2 0 1 2
lack of oxygenated blood and lack of waste product removal results in pain and decreased peripheral sensation secondary to nerve irritation caused by either external restriction of compartment (eg. tight splints, casts, dressings) or internal increase in compartment volume (eg. haemorrhage, post-ischaemic swelling) 5Ps: Pain, paresthesia, pallor, paralysis, pulselessness Complications: muscle necrosis, Volkmann contracture Treatment: Fasciotomy
Necrotizing Fasciitis - insidious soft tissue infection characterized by tissue necrosis - organisms spread from subcutaneous tissue along superficial and deep tissue planes, of which the latter causes vascular occlusion, ischaemia and tissue necrosis. - less seen in multiple trauma - 3 types of NF: Type 1 – Polymicrobial NF Type 2 – Grp A Strep NF (Flesh-eating bacterial infection) Type 3 – Gas gangrene - presents with fever, chills, erythema and painless bullae formation - treatment: antibiotics and surgical debridement Gas Gangrene - onset: 12-24hrs after injury - commonly Clostridial infection, but may be caused by other organisms - decreased oxidation reduction potential promotes advance of a highly lethal condition - less seen in multiple trauma - present with intense pain and swelling around the wound - associated with a brownish discharge and bronze discolouration of wound - gas (with a musty odour) formation usually not marked - important to distinguish from anaerobic cellulitis, which presents with abundant gas formation that is foul smelling in nature - distinction between the 2 made by doing a Gram stain of the exudate - management: fluid & electrolyte replacement, antibiotics, multiple incisions & fasciotomy, hyperbaric oxygen Osteomyelitis - infection of bone and bone marrow - difficult to treat, can be life threatening as well due to septicaemia - routes of spread: haematogenous, contiguous from a focus of infection - bacteria can be inoculated at the time of trauma 102
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present with fever, headache, vomiting, severe bone pain treatment: antibiotics and extensive debridement of necrotic tissue
Principles in management of orthopaedic injuries in polytrauma Polytrauma is defined as the presence of 2 long bones# plus 1 visceral injury OR 2 visceral injuries OR ≥ 3 # In polytrauma patients, limb injuries are the commonest and this can take the form of long bone # or soft tissue injuries. However it is the head and visceral injuries that are most lethal. Management
• •
Primary survey
• • • • •
Acute or resuscitation period (1-3 hrs after trauma) Primary or stabilization period (<24hrs) Secondary or re generation period (3-8 days) Tertiary or rehabilitation period (>8 days)
Continued haemodynamic and resp stability Debridement of soft tissue necrosis Eliminate septic foci Wound closure Joint reconstruction
Tertiary period
• • •
Secondary survey
4 different periods in orthopaedic management of trauma injuries
• • • •
Secondary period (3-8 days)
Patient weaned off intensive care Physiotherapy initiated If patient has developed multiple organ failure, no further operative procedures can be considered at this stage.
Optimal timing of long bone # stabilization in trauma patients in the primary period – divided into 3 groups of patients: * Early stabilisation (within 48h) does not improve Polytrauma survival but it will benefit some patients, e.g. reduces without brain the number of days of mechanical ventilation and chest injury (? Improves morbidity) * Hence it is preferable to perform long bone stabilisation in polytrauma patients * No evidence that early stabilisation (within 48h) Brain injury improves survival compared to late stabilisation Chest injury 0B
1B
2B
Acute period
• • •
Decompression of organ cavities (tension pnemothorax, cardiac tamponade) Haemorrhage control
Decision on temporary and definitive fixation of fractures
– articular congruity – stable fixation – axial alignment with the rest of the extremity – restoration of full range of motion
Limb salvage v.s. amputation (many scoring systems i.e. mangled extremity scores/Hannover fracture scale)
Special considerations
If pelvis is fractured, early stabilisation with pelvic clamp is crucial
Primary period(<24 hrs): stabilization of fractures
• •
In definitive treatment of #, in order to preserve normal function, there should be
• •
Pelvis Spine 103
•
Long bones
Pelvic # • Ensure that there’s no need for general surgical intervention e.g. intra-abdominal or retroperitoneal haemorrhage • Haemorrhage control with pelvic packing and temporary stabilisation with external fixators and pelvic clamps Spine # •
Urgent spinal stabilisation required (urgent = within 24h of injury)
Long bones # • Pts with # shaft of femur can lose up to 1L of blood. Femoral shaft fractures should undergo immediate stabilization of the fracture within 24h of injury • Immediate stabilization of long bone fractures has many advantages in the multiply injured patient, such as improved long-term function, prevention of deep venous thrombosis and decubitus ulcer, decreased need for analgesia, and reduction in the incidence of adult respiratory distress syndrome and fat emboli19 Recommendations for staged treatment of femoral shaft fractures
FRACTURES General Mx of # ABCDE - Assess neurovascular status, beware of compartment syndrome - If hypovolaemic IV fluids, packed cells, whole blood Analgesics Preliminary skin traction to relieve pain, minimize further displacement How to determine if # is displaced or not: compare continuity of trabeculae lines Traction: things to note Traction can be skin or skeletal Skeletal traction can be with Thomas’s splint or pulley frame or both Traction care Ring pressure (Thomas’s splint) Pressure sores: Buttocks, Tendo Achilles, under heel Common peroneal palsy weakness of dorsi flexion Loosening of Steinmann pin Upper limb fractures dislocations by Lee Yizhi Fracture Clavicle
Method
Remarks Malunion in adults Excellent remodeling in children
Sling 3/52 Scapula body: Scapula neck:
Physio
Sling & physio
ORIF if # dislocat n
AC subluxat : n AC dislocat :
n
Sling ~1/52 & physio
young and active : Arthrodesis, 3/52 rest, physio Inactive: Sling & physio Late OA: excision outer 1/3 clavicle Sternoclavicular n dislocat n Anterior dislocat :
Anterior: conservative Posterior: ORIF Reduction under GA Hippocrates/Kocher’s
Associated with 1)rib # 2)lung contusion 3)hemo/pneumothorax Body # by crushing force n Partial dislocat : AC ligaments torn Complete dislocation: CC ligaments torn (conoid & trapezoid) Tenting of skin may cause necrosis n Post dislocat : Tracheal and n vascular compress X-ray to exclude # Axillary n often damaged n 95% of shoulder dislocat s
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Sling 3/52
dislocation Pulled elbow
pressure), cast 6/52 Sling 3/7 or Supinate + flex elbow
Radius and ulnar in adults: in children: Single forearm bone Monteggia’s:
ORIF (plates/screws/rods) Long arm cast 6/52, check x-ray at 2/52
Physio Posterior n dislocat : Prox humerus:
# prox humerus: ORIF Recurrent: Surgery n GA Reduct Same as ant dislocatn
Neers 1: Sling 6/52 Neers 2: Collar cuff 6/52 Neers 3: ORIF/HemiA Neers 4: HemiA All followed by physio
Shaft of humerus
Supracondylar
U-slab 3-6/52 + sling
If very unstable, plate/nail n Closed reduct ASAP C&C 3/52 then sling 3/52 ORIF (dbl plating) in adult for early f(x) GENTLE physio
Lateral condyle Proximal radius in adults:
In children: Olecranon
Elbow dislocation
Radial head
Undisplaced: C&C 3/52 Displaced: ORIF (Kwire) Mason 1: C&C 3/52, gentle physio Mason 2: ORIF plate & screw Mason 3: Excision in 48hrs Mason 3 with Essex L: Prosthesis, splint 2/52, physio o <20 : C&C 2/52 o >20 : MUA, if fail OR. If unstable, IF (Kwire) Stable & undisplaced (<2mm + no change in flexion + extend against grav): C&C 3/52 Displaced: tension band wiring Displaced + comminuted: plate & screw n MUA (tract , flexion, push olecranon) then C&C 3/52 or above elbow backslab
trauma: MUA (supination, direct
Commonly missed! 4% of shoulder dislocatns Usually seen in osteoporotic pple >50yrs Try to conserve head in young pts even with Neers 3/4 Suspect mets in elderly!
Galeazzi’s: Cx: Shortening, angular deformity (gunstock), decreased ROM Acute: Brachial A inj, compartment sx, volkmann’s ischaemia Myositis ossificans Cubitus valgus, tardy ulnar palsy: corrective osteotomy
Posterolateral most common Cx= brachial A, median (AIN)/ulnar, stiffness, myositis ossificans, associated #s Monteggia #, PI Nerve inj
Both in children: Colles’
ORIF or long arm cast 12/52 ORIF (ulnar plating, reduce radial head), o n long arm cast 90 flexion, partial supinat ORIF (radial plating, reduce ulnar head), long arm cast in supination 6-8/52 Reduction under GA, immobilisatn 6/52
Undisplaced: Splintage in plaster slab Displaced: MUA (Bier’s/ hematoma block), below elbow backslab 6/52 in neutral or slight flexion, xray @ 2/52
Smith’s (reverse Colles’) Barton’s Radial styloid/ Chauffeur’s Undisplaced scaphoid Displaced scaphoid Trans-scaphoid perilunate dislocation
As for Colles’ but with wrist extension
Peri-lunate dislocation
Closed reduction, cast 6/52 If irreducible, OR with IF of scaphoid # if present, CTR and ligamental + capsular repair Undisplaced: Crepe bandage 3/52 and finger exercises Displaced: Closed reduction, plaster slab 3/52, finger exercises Displaced + unstable: ORIF with K-wire
Metacarpal
ORIF with buttress plate Percut K-wire/ lag screw Below elbow cast (exclude PIPJ) 10/52
Pain, lateral tenderness, refusal to move arm 9m-6yrs No X-ray findings Radial head slips out of annular lig Compartment sx, PIN/ AIN inj, delayed/non/mal-union, PIN Non-union! Cross-union Radial/ PIN palsy (Mont), ECU & EDM inj (Gal) myositis Ossificans, nonunion, missed dislocation
EPL rupture, malunion, median n compression, Sudeck’s atrophy, DRUJ n subluxat , hand shoulder stiffness
n
A/w lunate dislocat
AVN, non-union, scaphoid collapse, OA
ORIF, cast 3/52 Chronic carpal instability
Median n compression Lunate AVN leading to OA
Rotational malunion, stiffness
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Bennet’s (intraart # dislocation @ base of CMCJ of thumb) Phalangeal
Mallet finger Game-keeper’s thumb
CRIF with precut kwires
Undisplaced: buddy splintage 3/52 Displaced: MUA, plasterslab 3/52 or IF with Kwires Splinting in extension 6/52 Partial tear: short arm cast w thumb spica Gross instability: ligamental repair
Treat open wounds first!!
Impt Hip & Lower Limb #s and Ds (plus impt tendon ruptures) Type Acetabulum, #
Hip, post. D -- Hip is flexed, add & int rot
Hip, ant. D -- Hip is abd, ext rot
Fem epiphysis, slipped -- fem shaft move up & ext rot on epiphysis Neck of Fem (intracap) # -- shortened, ext rot -- 1. subcapital, 2. transcervical -- osteoporosis impt factor Garden Classification o Typ 1: incomplete #, trabeculae angulated o Typ 2: complete #, trabeculae disrupted but NOT angulated o Typ 3: complete #, fem head rotated, trabeculae disturbed,
Treatment o minimal displc/ highly frag Traction, Hamilton-Russell o main part intact, fem head displc ORIF w cancellous screws & plates o Muscle relaxant + Reduce, flex knee, hip 900, correct add & int rot, lift fem head into acetabulum o OR if irreducible o ORIF if a/w #s elsewhere o Muscle relaxant + Reduce, flex knee, hip 900, correct abd & ext rot, push down, convert to post. D, lift fem head into acetabulum o IF w screws + Manipulate if slip > 30% + epiphyseal closure o Subtroch Osteotomy if epiphysis closed (chronic) o Undisplc --> CRIF o Displc --> Arthroplasty o unfit for multiple Sx or badly displc, typ 4, avn & non-union likely --> Hemiarthroplasty/ Total hip replacement w/o tryring CRIF
Remarks & specific Cxs Cxs o Hemorrhage > 5L o Ruptured urethra, bladder o Bowel injury Cxs o Irreducible due to in-turned labrum or bony frags in acetabulum o # (fem head, NOF, patellar, fem shaft) o Sciatic nerve palsy o AVN due to tearing of capsule o 20 OA o Recurrent D o Myositis Ossifcans (post exploration or D a/w head injury)
displc o Typ 4: complete #, totally displc Neck of fem, basal (extracap) # -- shortened, ext rot Intertroch # -- shortened, ext rot Types: 1) # line thru mass of Great Troch, 2) (1) + separation of Less Troch, 3) separation of Great & Less Troch, 4) 4. w a spiral # down prox fem shaft Fem shaft # -- leg is shortened, ext rot, abd due to pull of quds & hams
o AVN o Involvement of Other Hip Tx principles o Young (< 50 y.o.) CRIF o Elderly --> arthroplasty Cxs o AVN disruption of arterial ring @ base of neck o Non-union typ 3 & 4, bone graft (young), arthroplasty (elderly)
Fem Supra, Uni, T & Y condylar #
Patellar D
o Displc/ Undisplc --> ORIF w DHS or Gamma Nail, fixation not removed unless pat < 45 y.o or pain o Stable, little frag DHS w long plate o Unstable DHS w long plate or Gamma Nail, then nonweight bear crutches after 48 hrs to 16 weeks o Alt -->Traction +/- Thomas’s splint
Cxs o AVN & non-union NOT common
Cxs o Failure of fixation (cutting out of fixation device) coxa vara* *if early, bedrest & skeletal traction
o Traction to overcome pull of quads & hams o Intramed Nail o Alt --> Traction, EF (Ilizarov), Plating o Fem & Tib # Cx rate high, early mobilisation by Intramed Nail o Metastatic # Intramed Nail + packed cement to relieve pain & give support o Fem shaft # w nerve palsy exploration w repair + IF o Fem neck & prox shaft # DHS + long Plate o Fem shaft & patellar # close nailing for both, mobilise knee early o Open # deribement + IF o Open #, IIIB,C conservative or EF o Child supracondylar plaster o Others IF for good reduction & permit early mobilisation o If displc, grossly comminuted conservative w traction o CR, plaster backslab x 3/52, knee exercise
Cxs o Hypovolemic shock o Fat embolism o Delayed Union, Non-union esp. conservative o Mal-union lat. Angulation Tx = osteotomy o Limb Shortening o Knee stiffness due to quads tethering, knee jt invovlement or prolonged immobilisation o Infection
Remarks
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Patellar #
Tibial tubercle, avulsion Quads tendon, rupture
Patellar ligament, rupture Tibial plateau, # o all involve articular surface o key is to get knee f(x) vs pretty x-ray o knee exercises ASAP o “bumper #” o commonly lat. tibial condyle
Tibia & Fibula, # o Usu. # both, esp. adult o commonly open o usu. spiral #
o vertical # --> cylinder cast 6/52 w crutches during first 2/52, physio after cast removal o horizontal, undisplc # --> as of above o horizontal, displc # --> 1. sight communition: ORIF, 2. limited damage to patellar: partial patellectomy, 3. major damage: patellectomy, repair quads insertion & lateral expansions o CRIF (w screw) o ORIF (risk of premature epiphyseal fusion in child) o Tendon reattachment, plaster cast, quads exercises at 2nd week, weight bear at 4th week, felxion at 6th week o As of above o minimally displc --> aspirate hemarthrosis, compression bandage, CPM & active exercise, weight bear after 6/52 o comminuted--> aspirate, compression bandage, sk traction, CPM & exercise crutches after 6/52 o depressed # --> CR or ORIF, active exercises ASAP, castbrace after 2/52 o closed, minimally displc --> full cast x 12/52 (upper thigh to MT necks, knee slight flexion, ankle at 900), exercise foot, ankle, knee ASAP o closed, displc --> MUA (IF when CR fails), full cast x 12/52, exercise ASAP o comminuted --> EF x 6/52 + partial weight-bear, then f(x)al brace o open --> Ab ASAP, debride, clean, leave open (above grd II), EF to stabilise, WI, suture or graft when granulate
Injuries to patellar & extensor apparatus of knee (patellar #, rupture of quads tendon, rupture of patellar ligament, avulsion of tibial tubercle) due to: 1) direct force on knee 2) violent contraction of quads Every knee injury, exclude: o damage to extensor apparatus o lateral D of patellar w spontaneous reduction o torn ligaments o torn mensici
Cxs o Compartment syndrome o Valgus deformity o Joint stiffness
Cxs o Infection o Vascular injury (prox # damage pop artery) o Compartment Syndrome o Delayed, Non-union --> Intramed Nail + bone graft indicated o Malunion --> angulated --> osteotomy
Ankle, ligament injury o partial/ complete tear of lateral ligament o bruising, swelling, tenderness o painful passive inversion o complete tear --> excessive movement Ankle # o normally talus seated in mortise o one or both mall can be # o eversion + ext rot = oblique # of lat mall (pushed off), transverse # of med mall (pulled off); vice-versa for inversion Distal tibial & fibular epiphyses, #-separation o physeal injury
Calcaneum # o fall from height o calcaneum driven up against talus o flattened Bohler’s angle o check hip, pelvis, spine for # o extra-art --> involve posterior part, calcaneal processes o intra-art --> oblique # line, run to superior articular surface
o partial --> crepe bandage, activity ASAP o complete --> plaster immobilisation or operative repair o 1 mall # --> reduce, cast x 6/52 (below knee), IF with screw if frag large o 2 mall #, below tibiofibular jt -> CR, +/- IF ,cast o 2 mall #, above tibiofibular jt --> unstable, IF with screw for frag & plate for fibula, +/- transverse screws between tibia & fibula o Salter-Harris 1,2 --> MUA, full cast x 3/52, below knee cast x next 3/52 o Salter-Harris 3,4 (undisplc) --> as above, re x-ray 5d after to ensure good reduction o Salter-Harris 3,4 (displc) --> ORIF, below knee cast x 6/52 o undisplc --> exercise ASAP, bandage after swell subside, nwb crutches x 6/52 o displc, avulsed tuberosity --> CRIF, immobilise in equinus (relieve tension of tendon Ach), wb after 6/52 o displc, intra-art --> ORIF + bone grafts, splint & elevate, exercises ASAP, nwb crutches after 3/52, wb after 12/52
Cxs o Adhesions o Recurrent subluxation
Tx principles o reduce to restore shape of mortise o plaster x 8/52 Cxs o Joint stiffness o OA (not common) Cxs o Mal-union (valgus) o Asymmetrical growth (# thru epiphysis may cause fusion of physis) o Shortening of leg Tx principles o elevate leg + ice packs --> decrease swelling o x-rays, CT scans (better views) Cxs o Broadening of foot o Talocalcaneal stiffness --> subtalar arthrodesis or triple arthrodesis
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Chronic OM: pus discharges through cloacae (perforations) in the involucrum
BONE & JOINT INFECTIONS
Types:
Clinical features
1. 2. 3. 4. 5. 6.
Acute haematogenous osteomyelitis Subacute haematogenous osteomyelitis Post-traumatic/operative osteomyelitis Chronic osteomyelitis Acute suppurative arthritis TB infxns of bone & joints
Investigations
Waldvagel Classification:
A – haematological spread B – a/w wound C – contiguous spread from local infection 1) type of organism 2) site of infection 3) host response (immunocompromised?) Principles of treatment
Rest affected part Provide analgesia & general supportive measures Initiate antibiotic treatment Surgical debridement (of pus & necrotic tissue)
A = sound bone B = new bone C = involucrum D = cloaca E = sequestrum
ACUTE HAEMATOGENOUS OSTEOMYELITIS Common organisms:
Adults: Staph. Aureus Children <4YO: H. influenzae Hx of sickle cell anaemia: salm onella
<1YO: GBS, Staph A, E Coli 1-16YO: Hib, Staph A, Strep, Enterobacter Adults: Staph, Strep, Pseudomonas, E Coli
Site:
X-ray: normal in first 10 days. Later, rarefaction of metaphysis & periosteal new bone formation. Sclerosis when healing occurs FBC: leukocytosis ESR ↑ Blood C/S Bone scan (usu. technetium or gallium radioisotopes used): turns + before x-ray changes appear. For doubtful cases.
Complications
3 things to consider:
5. 6. 7. 8.
Pain, malaise, fever, toxaemia Cellulitis, swelling, oedema, erythema, warmth, tenderness, ↓ROM
Adults: anywhere, esp thoracolumbar spine. Adults are usu immunocompromised Children: usu. metaphysis of growing long bone. Growth plate limits spread towards epiphysis. Infants: risk of epiphyseal extension, jt involvement & growth disturbance.
Spread – septic arthritis, metastatic OM (i.e. to other bones) Growth disturbance – shortening / deformity if physis is damaged Chronic OM
Management
Empirical antibiotics first, changing when C/S returns Adults/older children – flucloxacillin & fusidic acid (IV 3/7, PO 3-6/52) Children <4YO or G negative organisms cultured – Cephalosporin Analgesia CRIB & splintage (+ traction in upper femur OM to prevent hip dislocation) Drainage for subperiosteal abscess or persistent pyrexia & local tenderness of >24h
-
SUBACUTE HAEMATOGENOUS OSTEOMYELITIS • • • • •
Milder form of acute OM – less virulent organism or better patient resistance Common sites: distal femur, prox & distal tibia PT: child/adolescent X-ray: Brodie’s abscess (small oval cavity surrounded by sclerotic bone) (DDx: osteoid osteoma) Management: drainage & ABx cover
Pathology
Infection spreads to form subperiosteal abscess Bone dies, forming a sequestra encased by the involucrum (periosteal new bone) 108
POST-TRAUMATIC / OPERATIVE OSTEOMYELITIS •
Risk factors: DM, old age, immunosuppressed, steroid Rx, chronic disease, obese,
•
Organism: Staph. Aureus
•
Opley classification: A Early – 1 mth B Intermediate – 1mth to 1 yr C Late – >1 yr
•
multiple ops at same site, difficult / long ops, haematoma formation, tight dressings, wound tension
Management:
Clean surgical technique Thorough debridement Drainage Antibiotic cover External fixation of unstable/unfixed #
CHRONIC OSTEOMYELITIS • •
Sequelae of acute haematogenous, post-traumatic & post-op OM Recurrent flares of acute infxns – pain, pyrexia, erythema, tenderness, discharging sinus, non-healing ulcer
Investigations:
X-ray: bone rarefaction surrounded by sclerosis ± sequestra Bone scan: to reveal hidden foci of infxn
Management:
Incise abscess, remove necrotic bone, fill with bone chips Antibiotics – fusidic acid or cephalosporins Sequestrectomy
Investigations
Blood C/S Joint aspiration, pus microscopy & C/S X-ray: widened joint space & soft tissue swelling; subarticular bone destruction if late stage U/S: joint effusion
Complications:
Dislocation Epiphyseal destruction & pseudoarthrosis Growth disturbance – shortening or deformity if physis is damaged Ankylosis – if articular cartilage is eroded Sepsis – 25% if untreated
Management:
Joint aspiration Systemic antibiotics Splintage Drainage and joint washout Rehab: increasing movement when joint is not inflamed. If cartilage has been destroyed, keep immobile to allow ankylosis to occur
TUBERCULOSIS Main TB entities in orthopaedics
Common sites (wt bearing joints)
TB spondylitis TB osteomyelitis TB arthritis TB tenosynovitis TB myositis
Pathology
Spreads to skeleton by haematogenous seeding May spread to articular surfaces causing jt destruction and fibrosing ankylosis May spread to soft tissue to form subacute abscess, which may form a chronic discharging sinus
Common organisms:
Clinical features
ACUTE SUPPURATIVE ARTHRITIS Adults: Staph. Aureus Children <4YO: H. influenzae
Clinical features
Acute monoarthropathy – usu. hip in children & knee in adults Swelling, erythema, warmth, tenderness, fluctuation, ↓ROM, pain, spasm
Spine (50%) Hip Knees
TB symptoms: fever, wt loss, night sweats etc Joint symptoms: chronic course, pain, swelling, wasting, synovial thickening, ↓ROM, joint stiffness and deformity 109
Spine: vertebrae may collapse causing a Pott’s gibbus (usu. thoracic)
Investigations:
X-ray: soft tissue swelling, rarefaction of bone, joint space narrowing & irregularities w bone erosion on both sides of joint, periarticular osteoperosis Synovial biopsy ESR ↑, Mantoux test +
Management:
Anti-TB drugs – as for pulmonary TB (isoniazid, rifampicin, pyrazinamide - RHZ) Rest, traction, splintage, operation If articular surfaces are destroyed – Immobilize joint Long term – Joint arthrodesis or replacement
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OSTEOPOROSIS
If both Z & T-scores are abnormal, it means patient has secondary osteoporosis
DEFINITION A bone disease characterized by
o Decreased bone mass o Weakening of microarchitectural structure of bone Leading to o Increase in bone fragility and hence fractures, commonly at 1. Distal radius (Colles’) 2. Spine (compression fracture) 3. Hip fracture (NOF or intertrochanteric) 4. Head of humerus 5. Pubic rami “Little of normal bone” – Prof S Das De PATHOGENESIS Loss of balance between bone resorption and bone formation. Bone matrix manufactured by osteoblasts. Bone resorption by osteoclasts. Each cyle of remodelling takes abt 4-6 months. Annual rate of turnover is abt 4% for
cortical and 25% for trabecular bone. [bone loss occurs within 2wks; bone formation takes 3 mths] Bone size increases from childhood to adolescence and peaks at ard 35 yrs. From then on, decrease at 0.3%/yr for men and 0.5%/yr for women till 50 yrs old. Menopause for women (50-60 yr old) causes decrease at 3%/year due to decrease in oestrogen; it subsequently normalises again at 0.5%/yr. Wolff’s law - Bone is deposited and resorbed in accordance with the stresses placed upon it.
INDICATIONS FOR BMD SCREENING OF OSTEOPOROSIS:
Previous fragility fracture Patients with strong risk factors High risk postmenopausal women as categorized by OSTA Radiological evidence of osteopaenia / vertebral deformity Women who are considering prevention therapy for osteoporosis Monitoring of treatment
RISK FACTORS Osteoporosis Selfassessment Tool for Asians (OSTA)
Nonmodifiable Modifiable
Use age – weight = x If x >20, measure BMD If x = 0-20, measure if other risk factors present If x <-20, low risk, no need to measure unless positive history of fragility fracture Previous adult fracture history Previous family history fracture Weight (lean people predisposed to osteoporosis) Drugs – smoking, alcohol (both a/w nutritional def), steroids, thyroxine, anticonvulsts Early menopause (<45YO) Comorbidities – hyperthyroidism, hyperPTHism, Cushing syndrome, liver disease, COPD, CRF, RA, organ transplant etc. Immobilization Lack of physical exercise
LAB DEFINITION, BY BONE MARROW DENSITY AT THE HIP BMD T-score >-1 -1 to -2.5 <-2.5 <-2.5 + fragility fracture
Definition Normal Osteopaenia Osteoporosis Severe osteoporosis
T-score is the number of s.d. below the average for a young adult at peak bone density (based on BMD of 25yo Caucasian females) Z-score is the number of s.d. below an average person of the same age. If Z-score is normal but T-score is not, it means patient has primary osteoporosis (i.e. senile or post-menopausal osteoporosis)
INVESTIGATIONS X-Ray if applicable
Vertical trabeculae bears the most weight of stress hence disappear last. Osteoporosis got prominent vertical trabeculae but no horizontal. o Picture-framing of vertebrae – accentuation of cortical outline o Codfish appearnace of vertebrae due to concave end-plates o Pathologic fractures –vertebral compression fracture (ant height of vertebrae is 80% or less of the posterior height) if multiple of spine -> Dowager’s hump o Singh’s index for trabeculae at hip jnt – grade I (only one present) to grade VI (all present) Ca/ PO4 to exclude osteomalacia (normal in osteoporosis, low in osteomalacia) o
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FBC, ESR, U/E/Cr, Vit D Others if suspect underlying associated disease
TFT; LFT; tumor markers and myeloma screen (FBC, ESR, bone marrow aspiration, urine electrophoresis, skull X-ray) Measurement of BMD o Dual energy X Ray absorptiometry (DEXA) of hip for diagnosis, spine for monitoring of treatment is the investigation of choice Rationale for dual energy: to take X-ray of soft tissues and of bone at different penetrance levels o Other rarely done investigations include U/S heel/ tibia, quantitative CT scan o
Selective Estrogen Receptor Modulators (SERMs)
Synthetic Steroid
Others
Raloxifene (EVista)
Agonist in bone; antagonist in breast & uterine cells Induces osteoclast apoptosis Hot flushes, sweating, leg cramps oral Increased risk of clots e.g. DVT, PE Teratogenic Has also been shown to be protective against breast ca Tibolone Has progestogenic and some androgenic properties as (Livial) well as oestrogenic effects Also has value in controlling hot flushes Calcitonin Intermittent PTH Rx Calcium & Vit D Cyclical etidronate
MANAGEMENT:
BMD T-score >+1 1 to -1 -1 to -2.5 < -2.5 + fragility fracture
Action Re-BMD in 5y Re-BMD in 2y Medical prevention, F/U BMD @ >1yr Medical treatment, F/U BMD @ >1yr
Lifestyle measures, to be encouraged in everyone Nutrition Age Calcium Vitamin D 11-18 1000mg 400IU 18-65 800mg 400IU >65 800mg 800IU Exercise Weight bearing exercises (3x30min/wk) Smoking, alcohol cessation Fall prevention
Remove hazards (+ install bars, anti-slippery mats etc.) Treat comorbidities predisposing to fall e.g. cataracts Correct postural hypotension
Medications available HRT
Bisphosphonates
Aledronate (Fosamax)
Not to be used if osteoporosis is the only problem Use only if other indications e.g. unbearable hot flushes Switch to other treatments when symptoms abate Similar in structure to pyrophosphate; osteoclasts ingest it apoptosis Hypersensitivity Oesophageal reaction e.g. heartburn Take medicine sitting up, keep upright for 30min after swallowing, wkly dosing Overuse will result in SSBT (severe suppression of bone turnover) --- bone would hence be brittle
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RHEUMATOID ARTHRITIS DEFINITION
PATHOLOGY
Systemic chronic inflammatory disorder of unknown cause that affects the
-
3 stages: Synovitis, Destruction, Deformity
peripheral joints in a symmetrical fashion EPIDEMIOLOGY -
Prevalence: Gender: Age of onset: Morbidity: Mortality:
0.8% of adult population 3x more common in females 80% of patients develop it b/w 35 to 50 years old High level of functional impairment If untreated, 20-30% will become permanently work-disabled within 3 yrs Related mainly to extra-articular manifestations
- Synovial cell hyperplasia & proliferation - Dense perivascular inflammatory infiltrates - ↑ vascularity (angiogenesis) - Neutrophils & aggregates of organizing fibrin on synovial surface - P/E: Fusiform swelling @ PIP jts
PATHOGENESIS -
- Erosion of articular cartilage and subarticular bone o Direct invasion by pannus o Degradative enzymes secreted by neutrophils o ↑ osteoclastic activity in underlying bone - Tendons, ligaments, jt capsule also destroyed
- Deformity and loss of function o Fibrosis/Ca2+ of pannus o Fibrous/Bony Ankylosis o Destruction of articular cartilage, subarticular bone, tendon, ligaments, capsule - P/E: o Z-deformity of thumb o Swan-neck deformity o Boutonneire’s deformity o Ulnar deviation @ MCP jts
Cause unknown Postulated to be response of a genetically susceptible host to an infectious agent CLINICAL PRESENTATION SYMPTOMS / HISTORY TAKING - HLA-DR4, HLA-DR1 - Twin studies o Monozygotic twins: 30% concordance rate o Dizygotic twins: 3%
- Persistent infection of articular structures/retention of microbial pdts in synovial tissues - Alterations of jt components by microorganism/response to microorganism - Molecular mimicry
1. Joint involvement: typically affects PIP, MCP, wrist, elbow, shoulders, knees,
ankles, feet - Pain - Stiffness: - Swelling - Deformity - ↓ ROM •
Insidious onset Early morning stiffness at jt, last for >1hr before improvement Symmetrical, Red inflamed, warm to touch Progressive in nature
Usually periods of relative quiescence with periods of flare
2. Extra-articular manifestations (occurs later in the course of the disease) 3. Constitutional symptoms
-
Fever Fatigue, malaise Weight Loss
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4. Associated with
-
Sjogren’s Syndrome: Felty’s Syndrome:
Palm Palmar erythema Dorsum Wasting of the interossei, best seen in 1st dorsal web space
Dry eyes, Dry mouth, Recurrent chest infection Splenomegaly, Leg ulcers, Recurrent infections, LN, Wt loss
5. Loss of function
-
Class 1: Normal functional ability Class 2: Normal functional ability despite discomfort Class 3: can only perform a few tasks of work/self care Class 4: Complete/ Almost complete incapacity
FEEL
6. Previous treatment history
-
Medications: Anti-inflammatory drugs, Steroids (assess for adverse SEs) Intraarticular injections Previous operations
MOVE
7. Family history 8. Social History
-
OFFER
Occupation Family setup Caregiver
PHYSICAL EXAMINATION LOOK
Wrist -
Volar subluxation Radial deviation Piano key sign – subluxation of DRUJ causing head of ulna to pop up on dorsum of the wrist where it can be jogged up & down
Thumb Z-thumb deformity (flexion of IPJ and hyperextension of MCPJ)
Fingers Ulnar deviation of the fingers, involving the more lateral digits in the more advanced cases Volar subluxation at MCPJ, most commonly over index & middle fingers Swelling of PIPJ Swan-neck deformity (flexion of DIPJ, hyperextension of PIPJ) Boutonniere deformity (hyperextension of DIPJ, flexion of PIPJ)
Palpate over swollen joints to detect warmth & tenderness of acutely inflamed joints Palpate the elbows for rheumatoid nodules (present in 25% of patients). You may also find rheumatoid nodules at other pressure areas, e.g. pulp of the fingers & radial side of index finger Functional assessment Unbutton a shirt Write with a pen Hand exam (median n. for any carpal tunnel syndrome**) Examine other joints in the body that are affected by RA MCPJ,PIP,thumb, wrist, elbow, knee, ankle, mtpj [CERVICAL NECK] Examine the rest of the patient for extra-articular manifestations of RA Ask patient how the condition affects his/her life -
Extra-articular manifestations: Ophthalmic Sleritis Episcleritis Keroconjunctivitis sicca Respiratory Pulmonary effusion Pulmonary fibrosis Cardiac Pericarditis Vascular Vasculitis Reticulo-endothelial Lymphadenopathy Splenomegaly Felty’s syndrome Neurological Multifocal neuropathies Carpal tunnel syndrome
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American College of Rheumatology Diagnostic Criteria (fulfill 5 out of 7 criteria) 1. Morning stiffness >1 hr 2. Affects at least 3 out of 14 joints with soft tissue swelling or fluid (PIP, MCP, Wrist, Elbow, Knees, ankles, MTP) 3. Arthritis of hand joints 4. Symmetrical joint swelling 5. Subcutaneous nodules 6. Positive Rheumatoid factor test 7. Radiological changes consistent with RA
First 4 must be present continuously for 6 weeks
INVESTIGATIONS BLOODS 1. FBC
Anemia, Thrombocytosis, WBC & D/C: eosinophilia, exclude infection
2. U/E/Cr
Assess renal function before starting treatment
3. LFT
Assess liver function before starting treatment
4. ESR,CRP Inflammatory markers = indicate active disease
-
Used for disease progression monitoring, treatment response
5. RF
Anti-IgG autoantibodies (65-85% of patients) - Not diagnostic (present in healthy pple, SBE, TB, Viral infections) - Prognostic: high titre = poor prognosis
6. ANA
Positive in autoimmune disease - Not diagnostic (present in SLE, Scleroderma, Sjogren’s, Raynaud’s disease)
JOINT ASPIRATION 1. Analysis of synovial fluid: Straw coloured, cloudy, flecks of fibrin
Large numbers of WBCs , esp neutrophils
2. Biopsy: Histological features non-specific and not diagnostic
IMAGING X-rays: disease monitoring, treatment response
Early: Periarticular osteopenia Later: Marginal bone erosions Advanced: Articular destruction, Joint deformities
C-spine: Atlanto-axial subluxation
MANAGEMENT
Goals:
Control disease activity Prevent/ control joint damage Prevent Loss of function Control Pain Maximise quality of life
CONSERVATIVE MANAGEMENT 1. Non-pharmacological:
Rest Patient education Physiotherapy Occupational therapy
2. Pharmacological: (early aggressive treatment, Esp those w poor prognostic
factors) NSAIDs: Indomethacin, Diclofenac, Naproxen o Symptomatic treatment: anti-inflammatory, analgesia o Does not alter disease progression o ADRs: PUD o Contraindication: Renal impairment Steroids: Prednisolone o Symptomatic treatment: anti-inflammatory o May help slow disease progression/joint damage Disease modifying anti-rheumatic drugs (DMARDs): Methotrexate, Gold, Hydroxychloroquine (See Table) o Slow down disease progression of bone & cartilage destruction o Take 1-6 months to be effective o Monotherapy/Combination Anti-TNF α: Etanercept, Abcliximab, Infliximab
SURGICAL MANAGEMENT 1. Surgical Release for nerve entrapment syndromes (eg. Trigger finger, CTS, De Quervain’s) 2. Synovectomy For persistent synovitis > 6 mths 115
Symptomatic relief of pain and swelling Restore ROM 3. Arthroplasty Mainly for knees, can also be done for hip, shoulder, elbow Pain relief, correction of deformity, Stability and alignment, Preserve ROM 4. Others: Tendon repair Osteotomy: genu valgum Arthrodesis: mainly triple arthodesis of ankle o surgical fusion of joint to give stability, pain relief, deformity correction DMARDS SUMMARY TABLE DMARDs
Methotrexate
Pharmacology
- Recommended as initial DMARD - Rapid onset of action (12mths) - Retards progression of radiological erosions
Hydroxychloroquine
Toxicity
Investigations
- Rash - Abdominal cramps - Diarrhoea - Retinal pigmentation
- Eye examination (612 mthly)
- N+V - Mucosal ulcers - Liver cirrhosis, ↑ LFTs - Interstitial pneumonitis - Severe BM suppression
- Baseline FBCs, U/E/Cr - LFTs, Hep B/C status - CXR
Sulfasalazine
- Faster onset (1-3 mths) - Retard Radiographic progression
- N+V - Headache - Rash - BM suppression
- FBC, LFTs
Gold
- Oral: Slow onset (6mths) - IM: Faster onset (weekly injection of 22 wks)
- Rash - Ulceration, mucositis - Nephrotic syndrome - Pancytopenia
- FBC - UFEME, U/E/Cr (at every injection)
Leflunomide
- Alternative to MTX - Slows radiographic progression
- Diarrhoea - Alopecia - Headache - Immunosuppression - ↑ LFTs
- FBC, U/E/Cr
*Blue boxes: teratogenic
- LFTs, Hep B/C status
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ANKYLOSING SPONDYLITIS Definition: chronic, multi-systemic inflammatory disorder of the sacroiliac joints and axial skeleton (characterised as a seronegative spondyloarthropathy) •
Predilection for SI joints & spine progressive stiffening & fusion of axial skeleton
EPIDEMIOLOGY • 15-25 YO • Male : Female = 4:1 Mnemonic: P-A-I-R • HLA-B27 • First degree relatives at risk of psoriatic arthritis, IBD & Reiter’s syndrome PATHOLOGY • Enthesitis: subchondral granulation tissue that erodes the joint & is replaced gradually by fibrocartilage and then ossification (occurs in ligamentous capsular attachment sites to bone) • In the spine, this occurs at junction between vertebral bodies and annulus fibrosus of IV discs. Outer fibres of the discs eventually undergo ossification syndesmophyte is formed progresses to the characteristic bamboo spine SIGNS • Decreased lumbar lordosis • Kyphosis • Restricted lumbar spine movement in all planes • Restricted chest expansion : <5cm at 4th intercostal space • Extra-articular manifestations – Iritis, uveitis, myelopathy, AR, arrhythmia, pulmonary fibrosis SYMPTOMS • Recurrent lower back pain o Insiduous onset o For >3 months o Often begins unilaterally & intermittently As the disease persists, it becomes more persistent & bilateral & progresses more proximally o Dull character o Poorly localised to the buttock/thighs o Symptoms worse in the morning & after periods of inactivity, relieved with exercise
• • •
o a/w loss of spine extension Costovertebral & costotransverse joint involvement: difficulty breathing / chest tightness Temporomandibular joint involvement: decreased ROM / jaw pain Extra-articular manifestations Eye
Acute anterior uveitis Iritis
2C
Cauda equina syndrome Cardiac conduction defects
Spinal cord
Myelopathy due to atlantoaxial subluxation Cauda euina syndrome
6A
Heart
Aortic regurgitation Cardiac conduction defects
Lung
Apical pulmonary fibrosis
Anterior uveitis Atlantoaxial subluxation Aortic regurgitation Apical lung fibrosis Amyloidosis Archilles tendonitis
Systemic
Amyloidosis Osteoporosis
INVESTIGATIONS ESR Rh factor FBC ECG
Raised Negative Normochromic anaemia Conduction defects
Synovial fluid complement X-ray
Not depressed, decreased viscosity, leukocytosis
Bone scan
Squaring of vertebrae Vertebral fusion Romanus lesion: shiny corners of vertebrae due to sclerosis Bamboo spine – due to syndesmophyte formation Erosion & sclerosis at anterior corners of vertebrae Facet joint fusion Atlantoaxial dislocation SI joint – bony erosion, marginal sclerosis, +/- fusion Whiskering – calcification of tendons attached to ischial tuberosity Osteoporosis / OA changes (↓ jt space, sclerosis, ossified bone cysts) • Apical lung fibrosis • Costovertebral jt involvement Sacroilitis & spinal involvement
• • • • • • • • • •
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GOUT
GRADES OF SACROILITIS I II III IV
Widening of joint Joint erosion Sclerosis on both sides Ankylosis
Inflammatory arthritis caused by cellular reaction to uric acid crystal deposition (monosodium urate)
Rome criteria
Bilateral sacrolitis > grade I + any of the following: • LBP + stiffness > 3 mths not relieved by rest • Thoracic pain or stiffness • ↓ lumbar spine ROM • ↓ chest expansion • Hx of uveitis
NY criteria
Bilat Sacroilitis > grade I OR Unilat Sacroilitis > grade II AND any of the following: • LBP of inflammatory nature • ↓ lumbar spine movt in sagittal & frontal planes • ↓ chest expansion
MANAGEMENT Aims:
• • •
Relieve pain & stiffness Maximise skeletal mobility Avoid development of deformities
CONSERVATIVE Lifestyle modification Pharmacotherapy - NSAIDs (usually indomethacin) - Sulphasalazine Radiotherapy Local corticosteroid injection Systemic steroids SURGICAL Hip stiffness Spine flexion deformity
Exercise, ensure good posture Pain relief (ask abt renal function, hx of GI bld, coagulant Rx) For persistent peripheral arthritis. Not useful for axial disease If drug therapy is ineffective For plantar fasciitis & enthesopathy For acute iritis Total hip replacement Vertebral osteotomy
Pathophysiology – accumulation of uric acid/urate in blood and tissues. Supersaturation of tissues urate crystals precipitate into crystals. • Causes – Hyperuricemia (incl renal impairment) Alcohol ingestion. Dietary excess (especially sardines, kidney, liver, meat extracts). Thiazide diuretics. Salicylates. Lead poisoning. • Acute changes in the level of uric acid cause gout (not high levels) • Hyperuricemia is found in 90% in individuals with gout, but also found in patients taking diuretics and even in those taking low doses of aspirin • Most individuals with hyperuricemia do not have gout, but if high uric acid are not treated, 90% develop gout in 30 yrs Epidemiology – 90% male predominance; men > 20yo & post-menopausal women Presentation – • Redness, swelling, heat, tenderness and interference with range of movement typically most intense in 24 hrs, tenderness exquisite. • Monoarticular, 1st MTP jnt most commonly affected – podagra. Knee and ankle jnts next most commonly affected. • Tophus deposit may exist in the antihelix of the ear or subcut regions e.g. olecranon, archilles tendon, fingertips, cornea • Other findings – fever, chills, carpal tunnel syndrome • May progress to chronic arthritis or even present as chronic arthritis DDx: septic arthritis, pseudogout (tends to affect larger jnts and women more), bursitis, RA if polyarticular gout affecting finger, haemarthrosis Lab studies• Identification of causative crystals or classic radiographic findings • Joint Aspiration: Negatively birefringent needle shaped urate crystals on polarising examination. Synovial fluid WBC count usually elevated. (pseudogout – rhomboid shaped crystals) • Blood Investigations: o FBC: WCC often elevated, with left shift during acute attacks o ESR elevated during acute attacks. o Hyperuricemia present in 95% of cases but not diagnostic. • Once acute gout episode controlled, 24-hr urine uric acid lvl also assessed for choosing medication to control the associated hyperuricemia
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•
Imaging o Punched out lesions / rat-bitten / lytic areas with overhanging edges(after 1st year of disease) o Erosion with joint space preservation is typical.
Treatment – to relieve pain, prevent disease progression and prevent tissue deposition of uric acid •
•
Treatment of the acute attack o NSAID (e.g. naproxen 500mg twice daily or indomethacin 50mg three times daily) at full dosage (2-5 days), reduce to1/2 or 1/4 once attack controlled o Low dose NSAIDs for the 1st 6-18 mnts Mx of underlying hyperuricemia - ppt gouts in up to 50% of patients o Avoid aspirin – paradoxical(increases urate absorption) o Oral colchicine (anti-inflammatory) frequently causes unpleasant side-effects Treatment of underlying hyperuricemia – most untreated pts with gout will experience a recurrent episode in 2 yrs o Pharmacologial Allopurinol (antihyperuricaemic) – once daily Frequent and disabling attacks,Signs of chronic gouty joint disease, Tophi, Renal insufficiency, Recurrent nephrolithiasis, or Urinary uric acid excretion > 1100 mg/day Probenicid, Sulphinpyrazone (urocosuric) – multiple times daily Initial therapy < 60 who excrete <800 mg of uricacid perday, no renal insufficiency, hx of urolithiasis or tophi Colchicine Low dose prophylaxis during the initiation of anti hyperuricemic therapy. NSAIDs if cannot tolerate colchicine. o Non-pharmacological Dietary: caloric restriction (↑ protein – low fat dairy not meat/fish, replace refined with complex carbos, ↓saturated fat) Limit intake of alcohol. Surgery: Complications of trophaceous disease – infection, nerve compression, jnt deformity and intractable pain, cosmetic reasons
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c.
As little as possible of the tumour is exposed; block of tissue is removed – ideally in the boundary zone, so as to include normal tissue, pseudocapsule and abnormal tissue d. Frozen section examined; several samples taken if necessary e. If bone removed, the raw area is covered with bone wax or methylmethacrylate cement f. Drains should be avoided to minimise risk of tumour seeding g. For tumours that are almost certainly benign: excisional biopsy can be done (remove entire lesion) h. For cysts: careful curettage to remove representative tissue
BONE TUMOURS & CYSTS (OSCE ORIENTED) DX OF BONE TUMOURS & CYSTS: Impt differentiating features Site of lesion Patient’s age Special x-ray features Diagnosis of Musculoskeletal Tumours 1. Imaging a. Plain X-rays i. Site of lesion ii. Solitary or multiple iii. Well-defined or ill-defined (i.e. narrow / widened zone of transition) iv. Any cortical thickening v. Any periosteal new bone formation & extension of tumour into soft tissues (malignant!) - Periosteal hypertrophy may also mean infection, stress fracture, soft tissue bruising vi. NB. stippled calcification inside a vacant area is characteristic of cartilage tumours b. CT & MRI i. Useful to assess true extent of tumour & its relationship to surrounding structures ii. Assuming that there are no metastases, the local extent of the tumour is the most important factor in deciding how much tissue has to be removed c. Radionuclide scanning with technetium i. Shows non-specific reactive changes in the bone ii. Useful to reveal site of small tumour (e.g. osteoid osteoma) or the presence of skip lesions / silent secondary deposits. 2. Biopsy --- essential for diagnosis & planning of treatment a. Open Bx more reliable b. Site is selected so that it can be included in any subsequent ablative operation
Differential diagnoses for tumours 1. Chronic osteomyelitis a. Systemic features may have been suppressed by antibiotics b. Submit tissue for histological & bacteriological examination 2. Stress fracture (young adult with localised pain near a large joint) Management Grade \ Compartment Low High
Intra-compartmental Wide excision (w/o exposing tumour)
Extra-compartmental - Radical incision - +/- bone graft OR prosthetic replacement - Radical incision and prosthetic replacement OR amputation - +/- chemo to ↓ risk of mets
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BONE TUMOUR CLASSIFICATIONS Malignant Bone tumours by frequency 1. Metastatic Common Pri site of metastatic tumours: 2. Multiple Myeloma Thyroid GI (except *Midline & paired rectum) NPC structures 3. Osteosarcoma Renal *Most are osteolytic Breasts 4. Chondrosarcoma Prostate except prostatic (blastic) Lungs 5. Ewing’s sarcoma Testes & breast (blastic & lytic)
Others
Red marrow populated areas Cartilage cap of osteochondroma OR Central medullary Pelvis
Fibrous tissue Marrow
Benign Osteoid osteoma Chondroma Osteochondroma Fibroma Eosinophilic granuloma
Children/Adolescents (<20YO)
Chondroma (arise @ puberty, presents ~30YO) Osteochondroma Osteosarcoma Osteoid osteoma (<30YO) Non-ossifying fibroma Ewing’s tumour Simple bone cyst
Young Adults (20-40YO)
Aneurysmal bone cyst Giant cell tumour Chondroma (arise @ puberty, presents ~30YO) Osteoid osteoma (<30YO)
Vascular Uncertain
Haemangioma Giant-cell tumour
Bone tumours by Site Long bones Metaphysis
Middle age / Elderly (>40YO)
Chondrosarcoma Multiple myeloma Osteosarcoma (~50YO) Metastatic tumours
Spine
Hands / feet
Malignant Osteosarcoma Chondrosarcoma
Fibrosarcoma Ewing’s sarcoma Myeloma Angiosarcoma Malignant giant-cell tumour
Osteochondroma Simple bone cyst Aneurysmal bone cyst Giant cell tumour (proximal tibia, distal radius, distal femur) Non-ossifying fibroma (cortex) Osteosarcoma (esp knee & proximal humerus) Chondrosarcoma
Diaphysis
Ewing’s tumour
Non-specific
Osteoid osteoma Chondroma Metastatic Aneurysmal bone cyst Giant cell tumours Multiple myeloma Metastatic Chondroma Giant cell tumours (calcaneum)
Metastatic
Bone tumours by Patient age
Bone tumours by cell type Cell type Bone Cartilage
Multiple myeloma Metastatic Chondrosarcoma
[MCQ] Mets to spine: disc space not eroded! [MCQ] Ewing’s and osteomyelitis can be confused by all of the following: 1. Swelling 2. Diaphyseal location 3. Periosteal bone formation 4. Exploration reveals liquefied material like pus [MCQ] child with cystic lesion at epiphysis of lnog bone, most likely diagnosis: osteoblastoma
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FEATURES OF BONE TUMOURS & CYSTS
Bone tumour
X-ray findings
Site
Age
Others
Osteoid osteoma
Small round/oval radiolucent area surrounded by dense sclerosis DDx: Brodie’s abscess May be single or multiple o Multiple exostosis has AD inheritance & low rates of malignant change 2 main types: i)conical (well defined) ii)cauliflower with partial calcification of cartilage cap Well defined rarefied area in medulla Characteristic speckles of calcification w/in area of rarefaction
Femur, tibia
<30
Aspirin (pain relief) Excision
Edge of epiphyseal plate Long bone metaphysis
Adolescence
Bony hard lump ± pain or disturbed tendon fxn Excise if symptomatic or growing (risk of malign change)
Tubular bones of hands & foot Long bones
Excise / curette & replace w bone graft Risk of malig change, esp if multiple lesions are present
Translucent areas on shaft side of growth disc Bone expansion with cortical thinning Fallen fragment sign Well defined margins around a rare area Eccentrically placed Bone expansion with cortical thinning Confined to metaphyseal side of growth plate (c.f. Giant cell tumour which extends to articular surface) Diameter of cyst usu > diameter of bone Cortex Well defined sclerosed margins
Prox ends of humerus, femur, tibia. Usually in the metaphysis Spine Metaphysis of long bones
Arises at puberty, presents ~30YO. Need to rule out chondrosarc if >30y/o Children up to puberty Young adults
Curette & filled w bone chips
Metaphysis of long bones
Child
No Rx unless #ed.
Rarefied area situated asymmetrically Extends to articular surface (MUST, otherwise excluded) Soap bubble appearance Cortex is thinned, may be ballooned / perforated
End of long bones (prox tibia, distal radius, distal femur) Vertebral body Calcaneum
20-40YO
Sunray appearance Bone areas of rarefaction in medulla Subperiosteal new bone formation Codman’s triangle = lifting of periosteum prox to tumor @ the edge of the ‘sunray’ Central medullary type: initially appears like a chondroma. Destructive medullary tumour with flecks of calcification
Metaphysis of long bones Knee & prox humerus
Bimodal distribution: 10-20YO; ~50YO (a/w Paget’s dz)
Central medullary tumour OR
>40YO
Hx of patho # High rate of recurrence if not completely excised Curette & fill with bone chips Excision & bone graft/ prosthetic replacement Metastasize readily esp to lungs ALP ↑ by 3-4X Biopsy to confirm dx ChemoRx ± RT Resection / amputation Tend to metastasize late
Osteochondroma
Chondroma (enchondroma) Simple (solitary) bone cyst Aneurysmal bone cyst
Non-ossifying fibroma (fibrous cortical defect) Giant cell tumour
Osteosarcoma
Chondrosarcoma
Intralesional steroid injection Curette & filled w bone chips
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Malig change in cartilage cap of osteochondroma type: large exostosis surrounded by flecks of calcification in the cartilage cap Bone destruction Overlying ‘onion-skin’ layers of periosteal new bone
malignant change in cartilage cap of osteochondroma Diaphysis of long bone
Multiple myeloma (single tumor = plasmacytoma)
Overall reduction in bone density Multiple punched out defects (skull XR is often shown)
Metastatic tumours
Usually osteolytic EXCEPT prostatic CA mets which are osteosclerotic Moth eaten appearance Generalised osteoporosis Look for lung metastases
Ewing’s tumour (primitive neuroectodermal tumour, PNET)
Enneking Classification Grade G0 Benign (surgical) G1 Low grade malignant G2 High grade malignant Site T0 Benign Intracapsular & intracompartmental T1 (A) Intracompartmental T2 (B) Extracompartmental Metastasis M0 No regional / distant mets M1 Regional / distant mets
10-20YO
Rare, arise from vascular endothelium Amputation, RT, adjuvant chemoRx
Areas containing red marrow. Esp skull and vertebrae
45-65YO
Areas containing red marrow Esp axial & long bones
50-70YO
Osteoporosis + high ESR Urinalysis – Bence-Jones proteins Serum/urine electrophoresis – monoclonal Ig band ChemoRx & RT, int fixation of #, brace for spinal # Other problems o Nchormic Ncytic anaemia o Hyperviscosity syndrome o Renal stones o Gout & hyperuricaemia o Abnormal globulin: albumin ratio Palliative ChemoRx & RT Int fixation of #s Sx decompression & fusion of vertebrae to prevent neuro deficit
Staging for Malignant Neoplasia IA G1 T1 M0 IB G1 T2 M0 IIA G2 T1 M0 IIB G2 T2 M0 IIIA G1 or 2 T1 M1 IIIB G1 or 2 T2 M1
Staging for Benign Neoplasia 1 Latent G0 T0 2 Active G0 T0 3 Aggressive G0 T1 or 2
M0 M0 M0 or 1 (giant cell tumour)
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Salter Harris Classification – examples
ORTHOPAEDIATRICS
FRACTURES
Prevalence in Singapore • Bimodal distribution Modal peaks: 7 and 11 years old Median age: 7.64 ± 0.05 years old • By Gender Male modal peaks: 7 yrs & 11 yrs Female modal peaks: 5 yrs & 10 yrs
Type I II III IV
Male median: 8.18 ± 0.06 yrs Female median: 6.66 ± 0.07 yrs
Basic Principles • Presence of growth plate which gets injured before ligaments ( avulsion #s) • Presence of secondary ossification centers – CRITOE • Potential for remodeling in those less than 10 years of age • Less likely for joint stiffness due to casting • Treatment is usually non surgical • Greenstick and Buckle #s • Plastic deformation • Pathological fractures • Non-accidental Injuries Growth plate
» »
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Example 11yo with ankle inversion injury Distal fibula # Distal radius # 13yo with ankle injury Tillaux # 5yo with elbow injury Lateral condylar # of humerus
Basic Mx principles of physeal #s Extra articular #s usually treated with M&R • • •
Intra articular extension Requires anatomical reduction Usually involves ORIF
All dislocation must be stably reduced ASAP. Aim for acceptable alignment based on o Age o Potential for remodeling o Plane of motion o Fractured bone o Fracture site – epiphysis, metaphysis and diaphysis o Fracture personality – spiral, oblique, transverse, ,buckle, greenstick, Bayonet and Salter Harris Reduction maintained with plaster as children are less likely to get joint stiffness
If surgery is required... » Minimal dissection to ensure no damage to growth plate » Usually smooth pins used instead of plate and screws as smooth pins produce minimal growth plate damage and periosteum » Usually combined with casting postoperative for added stability to fixation » Pins inserted percutanoeusly where possible. Remodelling - Remodelling occurs 75% at the physis, 25% at the fracture site - Physeal remodelling » Once physis is aligned, it resumes symmetrical growth - Diaphyseal remodelling » Follows Wolff’s law – ‘form follows function’. - The closer the fracture to an active physis, the greater the remodelling potential
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vi. vii.
Common types of #s in children 5. Clavicle #s a. Very common amongst the very young after falling off the sofa at home. b. Also as a result of birth trauma c. Almost never treated with surgery d. Arm sling will usually suffice e. ONLY # ACCEPTABLE AS NON-NAI IN THE VERY YOUNG
iii. Grade IIB (with rotation component to the #) – closed reduction & percutaneous pinning (CRPP) iv. Grade III – M & R and CRPP » Brachial artery & median nerve may kink (not rupture) » Presents as pulseless hand » Ulnar n. usually not affected (if affected, usually iatrogenic) Management – closed reduction (right) Complications i. Cubitus varus (increased extension but reduced flexion)
Axial force to correct varus alignment
6. Proximal humeral #s i. Has great potential remodeling due to the fact that the shoulder is one most mobile joint in the body. ii. Usually treated with collar and cuff OR an O slab. 7. Supracondylar #s iii. “In Singapore, the typical child who has a supracondylar fracture is a 7yo boy falling off a monkey bar with his non dominant hand” iv. Most common fracture in KKH requiring surgery v. Classification i. Grade I (posterior fat pad sign seen) – Cast Immobilisation ii. Grade IIA (Baumann angle = 75˚, anterior humeral line bisects capitulum) – M & R
Flexion to correct the extension of fragment 8. Lateral condylar #s a. Important because it’s a SH IV fracture with joint extension b. Displacements >2mm needs ORIF 125
c.
Even if undisplaced, need close surveillance to intervene if there any further displacement (by muscles) d. Can lead to non union, elbow deformity and instability if untreated 9. Radius/ulnar #s a. Unlike in adults radius/ulna can usually be treated by M&R o Immobilize with U Slab of sugar tong slab b. Surgery indicated if unable to achieve stable acceptable alignment e.g. o In older children/teenagers o Excessive rotation o Excessive angulations (>200) c. Surgery if indicated done with minimal disturbance of growth plate and periosteum d. Also think of Monteggia/Galeazzi #s e. Radial neck MUST bisect the capitulum of humerus in all views 10. Distal radius #s a. Can be different varieties b. Salter Harris II involving the distal radius epiphysis o Below elbow cast after M&R c. Distal 1/3 fracture of the radius ulna which is the most unstable. o Above elbow cast after M &R o Bayonet acceptable for those < 10 years old if delayed presentation d. Buckle fractures due to “buckling” of the periosteum o Very stable o No M&R required o May treat with Brace only 11. Femur #s a. General Concerns o Adequate pain relieve o ATLS for multiply Injured b. Be aware of possible Non Accidental Injuries NAI o In those not ambulating o Mentally retarded o Non communicative yet
c. Be aware of pathological fractures d. Treatment o Gallows traction for those less than 2 years or 20 lbs o Russell’s traction for others till next elective list o Early 1 leg hip spica. Allows for sitting. Better accepted. 12. Tibial #s a. Most common type of #s in children b. Aim is to achieve acceptable alignment o No varus or recurvatum o Angulation < 100. o No rotation c. Above knee cast backslab. d. Admit if o Concerns of Compartment syndrome Flexor hallucis longus – pain on stretching of ischaemic muscle --extend the child’s toe (small movement but great pain) o Good alignment cannot be achieved o Open fracture. Tibia is superficial therefore predisposes to osteomyelitis and nonunion (a/w poor blood supply for tibia unlike femur :. Vicious cycle) e. Beware of the Toddler’s fracture (Refuses to walk, keeps on falling) Fractures in Adolescents 5. Tibial spine #s a. In older children / adults, more likely ACL tear. b. But since ligament is stronger than bone, more likely avulsion # of tibial spine (site of attachment still has cartilaginous contact, not bone) c. Classification – Meyers & McKeever i. Type I – minimal or no displacement ii. Type II – angular elevation of anterior portion with intact posterior hinge iii. Type III - complete displacement with or without rotation
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6. Tillaux #s a. Growth plate not completely closed yet and lig > bone :. Tillaux’s fracture
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b. More growth plate = more # parts (e.g. triplane # in a 12yo girl)
Imbalance of muscle and bone growth cause tension in unfused apophysis 7. Tibial tuberosity (Osgood Schlater Disease) 8. Inferior pole of patella (Sindig Johanssen Larsen) 9. Apophysis of calcaneum (Sever’s syndrome) Tension can convert to fracture during sporting activity especially in those who are heavy for their age
• Refer early Brachial Plexus Injuries Clavicle fracture • No intervention • Reassure family • Ensure no pressure on fracture site • Exclude Brachial Plexus Injury • If the infant initially demonstrates discomfort with the fracture, the long arm sleeve of the infant's shirt can be pinned to the shirt for 7 to 10 days to provide adequate immobilization. Humerus fracture • Mechanism of injury -- -- -- -- -- -- --> Femur Fracture • Rx: pavlik harness
Specificity of Skeletal Trauma for Abuse High Specificity Moderate Specificity - Classic metaphyseal lesions - Multiple fractures, especially bilateral - Posterior rib fracture - Fractures in various stages of healing - Scapular fracture - Epiphyseal separation - Vertebral body fracture or subluxation - Spinous process fracture - Digital fracture - Sternal fracture - Complex skull fractureLow specificity - Clavicular fracture - Long-bone shaft fracture - Linear skull fracture
Traumatic Birth Injuries - Osteogenesis imperfecta • Life-threatening condition 127
Able to hyperextend the elbow (beyond 10 degrees) Left Right Able to put hands flat on the floor with knees straight Able to hyperextend knees (beyond 10 degrees) Left Right
1 1 1 1 1
CONGENITAL, DEVELOPMENTAL AND PHYSIOLOGICAL CONDITIONS TORTICOLLIS (AKA WRY NECK) Classification • Primary/Muscular/idiopathic – tight SCM • Secondary – always exclude & treat this first since this is the underlying cause – Squint – Hearing problems – Flat head (plagiocephaly) – Bony fusion of cervical spine (Klippel Feil) – Tumours and infections in the neck – Trauma OSSIFICATION CENTRES
Clinical Features • Childs tilts or looks to the sides opposite to the tight SCM • Facial asymmetry on the side of the torticollis • Limited lateral rotation on the same side of torticollis • Limited lateral flexion on the opp side of torticollis
CRITOE – ossification starts at 1. capitalium (1yo), 2. internal/medial epicondyle (3yo), 3. trochlea (5yo), 4. olecranon (7yo), 5. external/lateral epicondyle (9yo) LIGAMENTOUS LAXITIES Assessed using Beighton scoring (out of 9) Test
Able to bend thumb backwards to touch volar forearm Left Right Able to bend little finger back (beyond 90 degrees) Left Right
Points 1 1
Management • Exclude secondary causes • If under 1 year can be treated effectively with stretching (physio) • Surgery usually needed for those above 1 year old. • Release of the SCM is done with or without a reconstruction of the sternal head • Post op aggressive physiotherapy with use of custom made cervical collar for immediate post op period.
1 1 128
APPROACH TO LIMPING CHILD Presentation: limping child / delayed walking / abnormal gait Things to consider 1) Site/location 2) Painful versus painless 3) Age (NB. regardless of age, must always include trauma & infection [septic arthritis, OM, synovitis] under painful causes) <3yo
3yo to schoolgoing
Painful Most commonly due to infection Trauma (exclude NAI) Toddler’s # (1-4yo): distal tibial # Transient synovitis DX OF EXCLUSION Inability to bear weight a/w excessive running May be related to upper respiratory infection Gets better with rest Growing pain Diagnosis of exclusion Usually between 4-5yo and during puberty Bone growth rate faster than rate of increase in length of muscle & tendon Pain occurs usually at the end of the day, often relieved with massage / after a good night’s rest Leukaemia (4-10yo)
Schoolgoing through adolescence
Perthe’s disease (4-8yo) Loss of blood supply to the hip Unknown cause Can cause early degenerative disease
Painless Limb length discrepancies Bone: femur versus tibia shortening Joint: commonly DDH Generalised o Muscle hypertrophy on one side; causes: nerves (NF), vessels (haemangiomas) o Polio infection Physiological o Metatarsal adductors o Tibial torsion o Femoral anteversion o Flat foot Biggest concern: undiagnosed dislocated hip ( DDH) Significant limb length discrepancy Asymmetrical thigh crease Hip clicks Limited/asymmetrical abduction
Adolescents
Transient synovitis Commonest cause of irritable hip Epidemiology: boys 2x more than girls, 3-10yo History o Unilateral groin/hip pain o Antalgic limp o Very young children: no other symptoms except crying at night o Recent Hx of URTI, pharyngitis, bronchitis or otitis media (in >50% of cases) o No definitive cause known Slipped Upper Femoral Epiphysis (~15yo) – Thought to be due to excessive weight on a predisposed hip – Maybe due to an endocrine abnormalities (Pituitary, growth, thyroid and parathyroids, gonadal hormones) – Diagnosis delayed because they can present with knee pain – Always need surgery to stop progression Growing pain (see above)
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DDH •
•
•
Incidence – 1:1000 live births – Common enough for the condition to be screened by the neonatologists Risk factors – 1st female child – Family history – Breech – Condition predisposing to crowding of uterus (multiple pregnancies, oligohydramnios, fibroids, baby too big, mother too small) Diagnosis: – Diagnosis is CLINICAL • Barlow maneuver – test of “dislocatability” • see if hip can come out or not, test positive when it goes back in on the way • Ortolani maneuver – test of “reducibility” • pushing a hip that is already out; clunk only when it moves over labrum – U/S or X-rays can be used but not to diagnose at birth • X-ray: radiation PLUS hip is not ossified • U/S not done at birth because laxity of hip joint, may get spurious reading at birth (in order for baby to come out of birth canal) – hence earliest U/S is at 6 weeks – When to do U/S • For high-risk cases (e.g. breech) / hip laxity / hip clicks • To ensure concentric stable reduction after treatment • Weekly after with splint to ensure reduction and correct application of splints • Every 6 weeks after once hip reduced • Most effect <3 months old (3 months onwards :X-rays; must ensure concentric reduction with good acetabular cover, if not mechanical forces of hip not evenly distributed may get OA) – When to do X-rays • 3 months onwards
•
Each Xray must show concentric reduction with good acetabular cover
Management – Goals •
–
CONCENTRICALLY REDUCED AND STABLE HIPS WITH GOOD ACETABULAR COVER • To Avoid Early Degenerative Disease of the Hips Treatment • WATCH – observe if • Hip laxity only • Hip clicks • Repeat U/S at 4-6 weeks • If hips reduced and stable, no further tx • Otherwise treat as DDH • ABDUCTION SPLINT 0 to 6 months • Abduction splint (old mtd) or Pavlik Harness • Repeat U/S in harness after 1 week and out of harness at 6 weeks • Worn for at least 3 months until 1st Xrays • If Xrays show concentric hips with good acetabular cover, then wean off splints In Human position: 50deg of abduction of each side and 100deg of flexion
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•
•
CLOSED REDUCTION & HIP SPICA 0 to 6 months • If unable to achieve stable reduction with splints then closed reduction and hip spica attempted OPEN REDUCTION & HIP SPICA 6 to 12 months • Closed reduction can still be attempted but more difficult to achieve stability • Open reduction then done 12 to 18 months • Child is already weight bearing • Open reduction usually involves femoral derotation and shortening • Acceptable is thought to remodel accordingly Above 18 months • Potential for acetabular remodeling is less • Both acetabular and proximal femoral surgery will be required. • Acetabular surgery (Salter osteotomy) FOR CHRONICALLY NEGLECTED CONDITIONS (RARE) Reductions not usually attempted if • > 8 years for unilateral (no more remodelling past 8yo, so reduction would cause OA) • > 5 years for bilateral Consequences of not reducing • Partially dislocated (formation of false joint) – • Completely dislocated – will have Trendelenburg gait, cost of energy to walk will be high hence not ideal (have to sit on side back pain, will get scoliosis • Bilateral: waddling gait, hips dislocated behind so nothing to hold pelvis in between, would get lordosis • Will ALL will walk assuming muscles and nerves are functional
CLUBFOOT (CONGENITAL TALIPES EQUINOVARUS) Incidence • 1:1000 • 2x more common in males, bilateral in 1/3 of patients • a/w spina bifida & arthrogryposis (non-progressive condition characterized by multiple joint contractures found throughout the body at birth) • Also screened at birth by neonatologist Types - Structural o Something wrong with the structure, intervention required o Mainly Idiopathic o Neuromuscular [muscle imbalance – peroneals not working (S1)] o Syndromic – e.g. - Positional (if able to dorsiflex foot then positional) o When you examine the feet flexible, due to position in the womb Clinical Features
Hindfoot equinovarus
Forefoot supination
Forefoot adduction
Cavus 131
Management I) Ponseti casting - Serial casting and manipulations soon after birth. - Foot corrected distal to proximal o Weekly for 4 weeks o Fortnightly for 4 weeks until external rotation of 60° achieved o Then assess need for TA tenotomy if hindfoot still uncorrected. #1 #2
#5
SUMMARY: • External rotation: tilt toe and turn out 60deg in relation to the knee • Principle: serial casting & manipulation • FOREFOOT: casting (forefoot corrected first then hindfoot!) • HINDFOOT: cut the tendon (if force into casting, will cause vertical talus) • Then BOOTS & BARS
II) Boots & Bars - 23hrs/ day for 3 months - Then wean till child being to cruise - Then night and nap till 4 years old. #3 FLATFEET (PES CAVUS)
#4
Classification Two diagnostic groups • Dynamic – Due to generalised ligamentous laxity • All children have this till about 7yo • Ask patient to tip toe – tightening of plantar fascia arches indicative of ligamental problems • Jack’s Test (reverse of tip-toe; pull toe up arch appears) – Due to tight TA • Growth spurts creates muscle tightness esp TA due to imbalance of muscle and bone growth – Due to collagen tissue disorders, e.g. Marfan’s • Fixed Flatfeet – Neuromuscular e.g. CP – Idiopathic – Tarsal coalition with/without peroneal spasm 132
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Calcaneo Navicular • 9 to 12 years • Do an oblique x-ray Talo - calcaneum • 12 to 15 years; 50% bilateral • Do a CT
Management Dynamic with no tight TA Dynamic with tight TA Fixed - Tarsal coalition
Watch and Masterly Inactivity Stretching, Good Shoeing and Medial Arch Support Treat underlying problem - usually needs surgery - Treat if < 30% involved, with soft tissue interposition (fat & extensor digitorum brevis)
LOWER LIMB MALALIGNMENT
• • • •
At birth: all children will have varus up to 2yo 4yo: maximal valgus occurs (reassure parents & monitor child’s inter-malleolar distance every 6 months to record progress) 7yo: resolves spontaneously; should a marked deformity persist past 10yo, operative correction should be advised Normal adults/teens: Slight valgus, about 6deg or so
Importance of aligning early: • Accept valgus till about 5-7yo • If valgus <7yo, mechanical axis will be lateral (i.e. pressure at lateral portion of growth plate) inhibition of lateral growth plate compared to medial • OA of lateral compartment (about 30-40yo) Causes Child Toddler Infant
HIP: Medial femoral torsion (femoral anteversion) - Usually bilateral LEG: Medial tibial torsion (commonest cause of bow-leggedness in 1yo’s) FOOT: Metatarsus adductus 1. Metatarsus deviate medially 2. Kidney-shaped sole 3. Splaying of first webbed space 4. Inverted sole
SCOLIOSIS Classification - Idiopathic - Neuromuscular » CP » SMA » Myelomeningocoele » Muscular dystrophies - Congenital » Hemivertebrae » Block vertebrae - Syndromic » Ehler-Danlos » Marfan’s » Neurofibromatosis » VACTERL
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Clinical Assessment - General assessment + height - Back examination » Scoliometer (in clinic) » Spinal balance: plumbline » Screening test: Adam’s Forward Bending Test
Why positive?
Idiopathic scoliosis: important points in history-taking - Chronological age - Menarche - Family history -
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Neurological examination Cobb’s angle (X-ray)
Time of diagnosis Severity of first X-ray Any previous treatment Associated symptoms » Back Pain » Neurological: clumsiness/weakness, bowel/bladder function
Red flags that scoliosis may NOT be idiopathic History - Back pain that is well-localised and constant - Pain that is becoming progressively worse over time - Feelings of weakness or clumsiness - Episodes of bowel or bladder incontinence - Ejaculation problems 134
Physical Examination - Foot deformity, particularly unilateral - A lack of rotational deformity on Adam’s forward bending test - Hyperkyphosis - Tight hamstrings (popliteal angle > 50‐60 deg) - Abnormal curve pattern : Not R thoracic and/or L lumbar - Unequal or abnormal reflexes X-rays - Widened pedicles - Kyphosis - Atypical curve pattern - Lack of vertebral rotation - Rapid curve progression (>1 degree / month) - Absent pedicles (`winking owl’) - Limb length discrepancy MRI When to order o Neurologic abnormalities on physical exam (don’t forget the feet) o Structural (congential) abnormalities on plain film o Excessive kyphosis o Apex left thoracic or thoracolumbar curves o Early onset scoliosis o Syndromic features present What to look for Syringomyelia Chiari malformations Tethered cord Diastematomyelia Treatment
CEREBRAL PALSY Definition Non progressive insult on a developing brain • The brain lesion is permanent and non progressive, but the natural history of cerebral palsy is not static. • If non-progressive insult on a developed brain = stroke Aetiology • About 10 to 15% of patients documented perinatal hypoxia. • Cerebral palsy is not solely the result of prematurity because 60 to 65% of afflicted children were born at full term • Although only approximately 10% of cerebral palsy patients weigh less than 1,500 grams at birth, in this low birth weight group the risk of having cerebral palsy is 90 per 1,000, compared with 3 per 1,000 if weighing more than 2,500 grams and appropriate for gestational age • Low birth weight for gestational age & prematurity are commonly associated with the development of spastic diplegia Types Neuropathic Types*** • Spastic – Overactive Golgi apparatus – The only one in which Ortho team can intervene • Ataxic • Athetoid • Hypotonic • Mixed
Anatomic Patterns*** • Hemiplegic • Diplegic • Quadriplegic • Total body Others • Triplegic • Monoplegic
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Management is dependent on functional assessment of the child! (See right) Type Functional Aim Hemiplegic
Diplegic
Quadriplegic
•
• Walker •
Efficient Walking – Supple Hamstrings – Supple TA Upper Limb is the best position for function
Efficient walking – No crouch/jump gait – No tiptoeing – Feet in neutral position – No scissoring • Consider need for assistance if power and control poor • Dietary control (optimal BMI; too heavy, patient cannot bear weight) • All should walk !! (if not, could be due to poor parental support, laziness [rehab into society would be even more difficult]) Non Walker • Investigate reason • If reason for inability to walk is neurological then aims same as quadriplegic sitter • Painless seating – Seating Clinic • Spine fairly straight and stable • Hips painless and reduced • No pelvic tilt • Adequate abduction for hygiene care • Adequate knee flexion
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Botulinum A Toxin • intramuscular injection of a neurotoxin produced by Clostridia bacteria. • It is delivered into or near sites of nerve arborization, and blocks the release of acetylcholine from presynaptic vesicles at the myoneural junction. • Recovery of tone results from the sprouting of new nerve terminals, which peaks at about 60 days • The agent is injected using a 23- or 25-gauge needle, usually without local or general anesthesia • The muscles are located by palpation. • To reach muscles that are deep or difficult to localize, electromyographic guidance and electrical stimulation have been used • BTX diffuses readily, so the injection should be placed in the muscle belly
Done percutaneously in very young
•
Hamstring release • In those with very severe crouch gait and popliteal angles usually exceeding 45o • Release of semitendinosus • Fractional lengthening of semimembranosus and biceps femoris
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Adductor release • Done for significant scissoring in walker • Uncorrectable tight adductor in non- walker such that perineal hygiene is compromised • Painful subluxed hips
Soft tissue surgery: basic principles • Surgery only done when deformity progresses to contracture and is not dynamic anymore (not dynamic = passive ROM still possible) • Surgery is CONTRAINDICATED in joints with correctible deformity • Surgery done with functional aim in view • Cosmesis only a consideration in Upper Limb • Tendo-Achilles Lengthening • Indicated when ankle cannot be dorsiflexed to neutral in walker 137
Bony surgery: basic principles • Usually in older children • When soft tissue surgery had failed with recurrence of deformity [aka once joints are stuck/immobile] • In areas where soft tissue surgery alone inadequate – Spine – Unstable hips – Severely deformed feet due to uncorrected muscle imbalance. • Spine – Paralytic scoliosis due to muscle imbalance – Not treatable with bracing – Seating is difficult for Quadriplegics if uncorrected • Unstable hips – Hips need to be reduced because • Pain • Severe pelvic tilt causing 2o scoliosis • Pressure sores due to unequal pressure when sitting – Not the same as DDH – Usually needs Open Reduction – With or without femoral and/or acetabular osteotomy • Feet – Usually done in older age group – Many methods described – Principle is to correct the foot alignment – Indicated in walkers with passively uncorrectable deformities – Valgus feet • Calcaneal Shift, Grice Extra-articular Fusion
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Tendon Transfers • Split Posterior Tibialis Tendon Transfer
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Triple Arthrodesis • Salvage procedure
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IMPORTANT CLASSIFICATIONS FOR ORTHOPAEDICS FRACTURE TYPES Simple Comminuted
Hairline Greenstick
Compression Avulsion
Impacted
Transverse (<30o) Oblique (>30o) Spiral Spiral wedge – torsional forces Bending wedge – characteristic butterfly fragment Comminuted wedge – bending wedge # with fragmented butterfly fragment Complex spiral – >1 spiral fragments Complex segmental – double # Complex irregular – bone lying btw main elements is fragmented If not detected on XR initially: Do oblique XR Repeat film after 7-10 days Children Elastic spring of periosteum may cause recurrence of angulation, hence plaster fixation must be well done. Rapid healing Common sites Vertebral bodies Heels Common sites Base of 5th metatarsal (peroneus brevis) Tibial tuberosity (quadriceps) (Osgood-Schlatter’s disease) Lower pole of patella (Johansson-Larsen’s disease) Upper pole of patella (quadriceps) Lesser trochanters (iliopsoas) One fragment driven into another
DESCRIBING FRACTURES 1. Level Anatomical – epiphysis, epiphyseal plate, metaphysic, diaphysis OR Thirds – proximal, middle, distal 2. Displacement Direction of displacement in terms of movt of distal fragment Degree of displacement in % of # surfaces in contact 3. Angulation Described in terms of the direction the point of # angulation is pointing towards (eg anterior angulation in Colles’ #) 4. Axial rotation Easily missed, examine the joints above & below the # 5. Open / Close Open
Gustilo Classification Open from within or without – latter has ↑ risk of infxn, hemorrhage & injury to muscles, nerves or bld vessles. Also usually comminuted & more difficult to manage.
OPEN FRACTURES: Gustilo Classification Type I <1cm AND clean Type II >1cm AND no extensive soft tissue damage, avulsions or flaps Type IIIA Extensive soft tissue damage, avulsions or flaps but adequate soft tissue coverage of bone OR High-energy trauma cause irregardless of size of wound Type IIIB Extensive soft tissue loss + periosteal stripping + bone exposure Massive contamination common Type IIIC Arterial injury requiring repair HAEMORRHAGE IN FRACTURES Close # of femoral shaft Haemothorax Pelvic #
2-3L 3-5L 3-5L
EPIPHYSEAL PLATE INJURIES: Salter-Harris Classification Type 1 Whole epiphysis separated from shaft Type 2 Epiphysis is displaced together with a metaphyseal fragment Type 3 Separation of part of the epiphysis Type 4 Separation of part of the epiphysis with a metaphyseal fragment Type 5 Crushing of part or all of the epiphysis *Cxs: avascular necrosis, growth arrest UPPER LIMB Colles’ #
Smith’s # Galeazzi #dislocation Monteggia #dislocation
# distal radius w/in 2.5 cm of wrist (aka dinner-fork #) Anterior & ulnar angulation Dorsal & radial displacement of distal fragment Impaction of fragments. # distal radius w posterior angulation ± anterior displacement (aka reversed Colles’ #) # of radius, inferior radioulnar joint dislocation (GUD) Ulna fracture + anterior dislocation of head of radius (MUF) 139
Features Pain, no trigger Correctable by active extension Correctable by passive extension Fixed flexion deformity
Mx NSAIDs H&L H&L, Sx sheath incision Sx release
PELVIC FRACTURES: Tile classification Type Stable #s A No involvement of pelvic ring A 1 A Stable, minimally displaced # of pelvic ring 2 Type B Rotationally B1 AP compression # (“open book” #) unstable, B2 Lateral compression #, ipsilateral vertically stable B3 Lateral compression #, contralateral Type C Rotationally & C1 Unilateral vertically C2 Bilateral unstable C3 Associated acetabular # PERTHES’ DISEASE Catterall grading– according to degree of femoral head involvement Grade Severity Px 1 involve anterior portion of epiphysis Revascularisation may be only. No collapse or sequestrum complete w/o bone collapse 2 ≤ 50 % involvement with a sequestrum Bony collapse inevitable 3 ~75% involved, with collapse & Bony collapse inevitable. Poor sequestrum Px 4 whole epiphysis involved INTERTROCHANTERIC FRACTURE OF THE FEMUR Evans’ Classification I 2 fragments, undisplaced II 2 fragments, displaced III 3 fragments w/o posterolateral support (ie # of the greater trochanters) IV 3 fragments w/o medial support (ie # of the lesser trochanter) V 4 fragments R Reversed oblique # - prone to displacement *Alternative classification: according to number of fragments + reversed oblique #
FRACTURE OF NECK OF FEMUR: (A) Gardens Classification Type Incomplete fracture (Inferior cortex 1 not broken) No displacement Abduction # Trabeculae are angulated Type Complete fracture line (inf. cortex 2 broken) No displacement Trabecular lines interrupted but not angulated Type Complete fracture line 3 Slight-moderate displacement Rotation of femoral head – prox frag abducted & int. rotated Type Severe displacement 4
(B) Anatomical Classification A Subcapitate B Transcervical C Basilar
10 Fixation by: Cannulated screws / pins DHS
>65YO – hemiarthroplasty. o Unipolar (Moore’s or Thompson’s) o Bipolar – for younger PTs <65YO – attempt joint salvage
20 Risk of AVN (%)
TRIGGER FINGER Stage Pre-triggering Triggering Triggering & Lock Contracture
30
40
Intracapsular – risk of severing retinacular vessels resulting in AVN (12-33% of all #NOF Extracapsular
(C) Phases of AVN I Only head involvement II Progress to secondary OA & acetabulum is affected as well ANKLE FRACTURES Weber’s classification Type Level of fibular # A Distal to syndesmosis B Involve the syndesmosis C Proximal to syndesmosis
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Pott’s Classification First degree # of a single malleolus (medial or lateral) Second degree # of both medial & lateral malleoli Third degree # of medial, lateral & posterior malleoli SCOLIOSIS List of Causes Non structural Structural
Limb length discrepancy (apparent or true shortening of one leg) Hip contracture Muscle spasm – eg 2o to PID Adolescent idiopathic (commonest, 80%) Infantile idiopathic – may resolve or progress Osteopathic – due to congenital vertebral anomalies Neuropathic – eg 2o to polio or CP. Due to asymmetrical muscle weakness Myopathic – due to muscular dystrophies Neurofibromatosis
SPONDYLOLISTHESIS Causes 1. Dysplasia – congenital lumbosacral facet jt dysplasia 2. Isthmic (spondylolytic) – break in the pars interarticularis 3. Elderly (degenerative) – OA degeneration of facet joints 4. Trauma 5. Suspicious (pathological) – neoplasm 6. Post-op – due to laminectomy for decompression
Meyerding classification Grade % translation of VB I 0-25 II 25-50 III 50-75 IV 75-100
BONE TUMOURS Enneking’s Classification Grade G0 Benign (surgical) G1 Low grade malignant G2 High grade malignant Site T0 Benign Intracapsular & intracompartmental T1 (A) Intracompartmental T2 (B) Extracompartmental Metastasis M0 No regional / distant mets M1 Regional / distant mets Staging for Malignant Neoplasia IA G1 T1 M0 IB G1 T2 M0 IIA G2 T1 M0 IIB G2 T2 M0 IIIA G1 or 2 T1 M1 IIIB G1 or 2 T2 M1 Staging for Benign Neoplasia 1 Latent G0 T0 2 Active G0 T0 3 Aggressi G0 T1 or 2 ve OSTEOPOROSIS BMD T-score >-1 -1 to -2.5 <-2.5 <-2.5 + fragility fracture
M0 M0 M0 or 1 (giant cell tumour)
Definition Normal Oteopenia Osteoporosis Severe osteoporosis
RHEUMATOID ARTHRITIS Stage 1 (synovitis) – pain, chronic swelling, large effusion, thickened synovium Stage 2 (articular erosion) – joint instability, ↓ROM. X-ray: loss of jt space & marginal erosion, but lack of osteophytes c.f. OA Stage 3 (deformity) – pain, deformity, instability & disability. X-ray: bone destruction 141
DISEASES MNEOMONICS
1. Osteosarcoma: risk factors PRIMARY: Paget's, Radiation, Infaction of bone, Male, Alcohol, poor diet, sedentary lifestyle [adults only] Retinoblastoma, Li-Fraumeni syndrome, Young [10-20 yrs]. Osteosarcoma is the most common primary malignant tumor of bone. 2. Osteosarcoma: features PEARL HARBOR: Paget's disease (10-20%)*, Early age (10-20 yrs), Around knee, Raised periosteum by expanding tumor: "sunburst pattern", Lace-like architecture, Hyaline arteoriosclerosis, Alkaline phosphatase increased, Retinoblastoma*, Boys, predominantly, Osteomyelitis DDx, Radiation* · Sunburst pattern was Japanese Navy emblem during WWII. *: Predisposing factors.
8. Deep tendon reflexes: root supply "1,2,3,4,5,6,7,8": S1-2: ankle, L3-4: knee, C5-6: biceps, supinator, C7-8: triceps 9.
Monoarthritis differential GHOST: Gout, Haemarthrosis, Osteoarthritis, Sepsis, Trauma
10. Can H&L (hydrocortisone and lignocaine) everything except plantar fascitis and archilles tendonitis
3. Sacroiliitis: causes PUB CAR: seronegative arthropathies + Bechet’s Psoriasis, Ulcerative colitis, Behcet's disease, Crohn's disease, Ankylosing spondylitis, Reiter's disease 4. Rheumatoid arthritis: features RHEUMATOID: Ragocytes/ Rheumatoid factor (anti-IgG), HLA-DR4/ HLA-Dw4, ESR increase/ Extra-articular features (restrictive lung disease, subcutaneous nodules), Ulnar deviation, Morning stiffness/ MCP joint, Ankylosis/ Atlantoaxial joint subluxation/ Autoimmune/ ANA, T-cells (CD4)/ TNF, Osteopenia Inflammatory synovial tissue/ Idiopathic/ IL-1, Deformities (swan-neck, boutonniere) 5. Seronegative spondyloarthopathy: diseases PAIR: Psoriatic arthitis, Ankylosing spondylitis, IBD, Reiter's syndrome 6. Osteomalacia: features "Vit-D deficiency in ADULT": Acetabuli protrusio, Decresed bone density, Under mineralization of osteoid, Looser's zone (pseudofracture), Triradiate pelvis (females) 7. Osteomyelitis: complications FIBRES: Fractures, Intraosseous (broidie) abscesses, Bacteremi/ Brodie abscess, Reactive amyloidosis, Endocarditis, Sinus tracts/ Squamous cell CA
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