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Complications of Fractures
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COMPLICATION OF FRACTURE
General Local Early Late
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General complications
Shock Hypovolemic or hemorrhagic shock. Septic shock. Neurogenic shock. Fat embolism. Pulmonary embolism. Crush syndrome. Multiple organs failure syndrome (MOFS). Thrombo-embolism. Tetanus. Gas gangrene.
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Local complications Early
Visceral injury (the lung, the bladder, the urethra, and the rectum). Vascular injury. Nerve injury. Compartment syndrome. Haemoarthrosis. Infection. Gas gangrene. Fracture blisters. Plaster and pressure sores.
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Late Delayed union. Non-union. Malunion. Avascular necrosis. Growth disturbance. Bed sore. Myositis ossificans. Muscle contracture. Tendon lesions. Nerve compression and entrapment. Joint instability. Joint stiffness. Complex regional pain syndrome. ( algodystrophy). Osteoarthritis.
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General complications
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Shock Three types of shock may complicate fractures Hypovolemic or hemorrhagic shock This type of shock is due to blood loss due to vascular injury. The vessels may be injured by the fracture pieces or in open fractures the vessels are injured by the same cause like in missile or bullet
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injury.In hypovolemic shock there will be reduction in the circulating volume causing reduction in venous return and cardiac output. The patient usually; severely pallor, shivering, rigor, hypotensive and sometimes comatose. Treatment by 1) control of hemorrhage (may require surgery). restoration of circulating volume (fluid and blood products).
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Crush syndrome Occur in What happened? Large bulk of muscle crushed
Tourniquet left for TOO long What happened? 1st theory =Compression releasedïƒ acid myohaematin ïƒ enter the circulationïƒ kidneyïƒ blocks the tubulesïƒ Renal failure and death.
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What we can see? Limb Renal Neurologically Pulseless Red Swollen
Secretion diminished Low output uraemia Acidosis Neurologically Drowsyïƒ not treated ïƒ DEATH
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How to treat it? AMPUTATION 1st rule = Limb crushed severely(>6hrs)
How the amputation done? Above the compression or crushed injury Before compression is released AMPUTATION
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Venous thrombosis & Pulmonary Embolism
Commonest Complications of Trauma & Surgery Most frequently Calf Less frequent in proximal of thigh & pelvis Pulmonary Embolism From Proximal of thigh & pelvis Incidence=5% & Fatal = 0.5%
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What cause DVT? The primary cause in surgical
HYPERCOAGULABILITY of the Blood due to activation of Factor X by Thromboplastin from damaged tissues Thrombosis occursïƒ secondary factors are Stasis Pressure Prolonged immobility Endothelial damage Increase in no & stickiness of platelet
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What are the high risk group?
Old people Cardiovascular Disease Bedridden patient Patients undergoing hip arthroplasty
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What we can see in DVT? Homann’s Sign positive Pain the calf or thigh
Soft tissue tenderness Sudden slight increase in temperature Sudden increase in pulse rate Homann’s Sign positive
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How to diagnose DVT? Ascending venography (bilaterally)
US scanning (detecting prox DVT) Radioactive iodine labelled fibrinogen(clot) Doppler technique (measure blood flow)
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How about pulmonary embolism?
Difficult to diagnose =only minority have symptoms (chest pain, dyspnoe, heamoptysis) So high risk patients should be examine for pulmonary consolidation X-ray Pulmonary angiography
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How to prevent it? Prophylactic treatment Foot elevation
Graduated compression stockings Exercise Anticoagulant treatment Subcut low dose heparin 5000 units preops & 3/7 postops (but CI in older patientïƒ bleeding) Change to low molecular weight heparin (less likely to cause bleeding)
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What is the treatment? Localized DVT More extensive DVT
Elastic stockings Low dose subcut heparin (5000 unit) More extensive DVT Bed rest Full anticoagulation Heparin IV (10000 units 6 hourly) Continue for 5-7/7 with last 2/7 warfarin introduce
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How to treat Pulmonary Embolism?
Cardiorespiratory resuscitation Oxygen Large dose heparin ( units) Streptokinase (dissolve clot) Antibiotics (prevent lung infection)
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TETANUS What is Tetanus?
Tetanus organism live only in dead tissueïƒ exotoxin ïƒ blood & lymph to CNS ïƒ anterior horn cell Will develop Tonic clonic contraction Jaw and face (trismus and risus sardonicus) Neck and trunk Diaphragm and Intercostal muscle ïƒ spasmïƒ ASPHYXIA
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What is the prophylaxis?
Active immunization (tetanus toxoid) Booster doses (immunized patients) Non Immunized patients Wound toilet & antibiotics If wound contaminated ïƒ antitoxin
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Treatment for Tetanus IV antitoxin Heavy Sedation Muscle Relaxant drug
Tracheal Intubation Controlled respiration
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GAS GANGRENE By clostridial infection (esp C.welchii)
Anaerobic with low oxygen tension Produce toxinsïƒ destroy cell wallïƒ tissue necrosis ïƒ Spreading
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The clinical features Within 24 hours Intense pain Swelling
Brownish discharge Pulse rate increased Charasteristis smell Little or no pyrexia Gas formation not marked Toxaemicïƒ comaïƒ DEATH
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How to prevent it? Deep penetrating wound should be EXPLORED
ALL dead tissue ïƒ completely EXCISED Doubt about tissue viabilityïƒ left it OPEN No antitoxin
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Treatment for gas gangrene
The key = EARLY DIAGNOSIS General measures (fluid, IV antibiotics) Hyperbaric oxygen (limiting spread) Decompression of wound Removal of all dead tissue Amputation (advanced case)
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FAT EMBOLISM Only minority patients with circulating fat globules will develop POST TRAUMATIC RESPIRATORY DYSFUNCTION Source of fat emboli=bone marrow Usually in MULTIPLE CLOSED FRACTURE But other condition also reported (burns, renal infarction, cardiopulmonary operation)
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How can we detect it? Usually young adults with LL fracture
Early warning signs (72 hrs. of injury) Rise in temperature and pulse rate More pronounced case Breathlessness Mild mental confusion Petechia (chest & conjuntival fold) Most severe case Marked respiratory distress ïƒ coma ïƒ ARDS
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How to treat it? Mild case Signs of hypoxia Monitoring of blood PO2
Oxygen If severe Intensive care with sedation and assisted ventilation Swan ganz Catheterization (monitor cardiac Fx) Fluid balance Supportive Heparin-thromboembolism Steroids-pulmonary oedema Aprotinin-prevent aggregation of chylomicrons
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COMPLICATION OF FRACTURE
General Local Early Late * Early complication : those that arise during the first few weeks following injury.
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Early Complication Local Visceral Injury Vascular Injury Nerve Injury
Compartment Syndrome Haemarthrosis Infection Gas gangrene
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Local visceral Injury Fracture around the trunk are often Cx by injury to the adjacent viscera : Pelvic fracture Rib fracture penetration to the lungs Bladder and urethral rupture These require Emergency Treatment…………chest tube insertion Pneumothorax
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Vascular injury Most commonly – knee, femoral shaft, elbow, and humerus. Artery may be cut, torn, compressed or contused. Intima may be detached, thrombus block, artery spasm Effect ?? ↓↓ bld flow coz Ischemia leads to tissue death & peripheral gangrene Most common artery injury is popliteal art Knee – poppliteal artery, femoral art, brachial art…….cut, torn – by initial inj or jagged by bone fragments
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Common vascular injuries may associate with the following fractures.
First rib or clavicle fracture (subclavian artery). Shoulder dislocation (Axillary artery). Humeral supracondylar fracture (brachial artery). Elbow dislocation (Brachial artery).
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5. Pelvic fracture (presacral and internal iliac).
6. Femoral supracondylar fracture (Femoral artery). 7. Knee dislocation (Popliteal artery). 8. Proximal tibia (popliteal or its branches).
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Clinical features Pt with ischemia may have 5 P’s:
- paraesthesia/numbness - pain - pallor - pulselessness - paralysis Investigate if suspect vascular injury : Angiogram
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Treatment Emergency treatment All bandages/splints removed
The fracture X-Ray again Circulation reassessed for next half hour If no improvement, do vessels exploration Suture torn vessels, vein grafting, if thrombosed do endarterectomy Aim: to restore bld flow In this operation, the fracture can be fixed internally at the same time
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Nerve Injury Variable degree of motor and sensory loss along the distribution of the nerve May be neurapraxia, axonotmesis or neurotmesis Radial nerve is most frequently damaged nerves. Radial N – Humerus fracture Neurapraxia-minimal damage, axonotmesis- axon damage but sheath intact, neurotmesis- complete damage
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Dislocation of shoulder Deltoid paralysis Radial # of humerus
Nerve Trauma Effect Axillary Dislocation of shoulder Deltoid paralysis Radial # of humerus Wrist drop Median Supracondylar # of humerus Pointing index Ulnar # medial epicondyl humerus Claw hand Sciatic Post dislocation of hip Foot drop Common peroneal Knee dislocation # neck of fibula
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In closed injuries – nerve is seldom severed and spontaneous recovery should be awaited.
In open fractures – complete lesion(neurotmesis) : the nerve is explored during wound debridement and repaired. About 90% cases recover within 4 months
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Compartment Syndrome Definition
Compartment syndrome involves the compression of nerves and blood vessels within an enclosed space, leading to impaired blood flow and nerve damage. Fascia separate groups of muscles in the arms and legs from each other. Inside each layer of fascia is a confined space, called a compartment, that includes the muscle tissue, nerves, bones and blood vessels. A rise in pressure within these compartments may jeopardize the blood supply to the muscles & nerves within the compartment. If blood supply is impaired more than 12 hours, coz necrosis of the muscles and nerves within the compartments. Nerve is still capable of regeneration but muscles once infarcted, can never recover n will be replaced by inelastic fibrous tissue.(volkmann’s contracture)
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Causes: -any injury/infection leading to edema of muscle -fracture haematoma within the compartment -ischemia to the compartment leading to muscle oedema -Due to tight bandages or casts Hallmark Symptoms:Â Â - severe pain that does not respond to elevation or pain medication. - In more advanced cases, there may be decreased sensation, weakness, and paleness of the skin.
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Injuries with a high risk of developing Compartments synd:
# of the elbow # of the forearm bone # of the proximal third of the tibia
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The vicious cycle of Volkmann’s ischaemia
5P’s Pain Pallor Paraesthesia Pulseless Paralysis Arterial ischaemia blood flow Damage Direct injury …………..... .……………. oedema Fasciotomy Compartment pressure
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A vicious cycle cont. until the total vascularity of the muscles and nerves is jeopardized.
This result in ischaemic muscle necrosis and nerve damage. (within 12 hours) The necrotic muscle undergo healing with fibrosis, leading to Volkmann’s contracture. Nerve damage may result in motor and sensory loss. In extreme case ïƒ gangrene This results in further swelling, a further increase in pressure, and a further reduction in capillary blood flow. Necrosis develops within about 12 hours - nerve function may be recoverable in time but infarcted muscle is damaged permanently. Eventually, the dead muscle fibroses and shortens, and an ischaemic contracture results.
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- should be tested by stretching the
clinically: - should be tested by stretching the muscles ïƒ when the toes or fingers are passively hyperextended there is ↑ pain in the calf or forearm. Early preventing : limb elevation Dx : confirmed by direct intracompartmental pressure measuring > 40mmHg is an indication of compartment decompression and fasciotomy. As ischemic muscles is sensitive to stretch, Different pressure btwn diastolic pressure and compartment pressure Within 6 hour in total ischema…muscles necrosis
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Treatment First removed all the bandages & dressing.
Fasciotomy is performed. The wound should be left open and inspected 2 days later. If there is muscle necrosis ïƒ debridement If muscle is healthyïƒ suture (w/o tension)/ skin grafted / simply heal by 2Ëš intention. Fasciotomy :do a long incision to the fascia to release the pressure
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Haemarthrosis Fractures involve joints, leads to acc. of blood within the joints. C/Feature :The joint is swollen and tense and patient will resists any movement. Tx : the blood should be aspirated before dealing with the fracture.
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Infection Causes: Open fracture (common) Use of operative method in the Tx of # Wound becomes inflamed and starts draining seropurulent fluid. Infection may be superficial, moderate (osteomyelitis), severe (gas gangrene). Post-traumatic wound infx is most common cause of chronic osteomyelitis ïƒ union will be slow and ↑ chance of refracturing. un
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Excising all devitalised tissue
Treatment: Antibiotic Excising all devitalised tissue If Sx of acute infx and pus formation : tissue around the fracture should be opened & drained All open fracture shud be regarded as potentially infecte
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Gas gangrene Produced by anaerobic orgs : Clostridium sp infections.
These orgs can survive in ↓ O2 tension Toxins produced will destroy the cell wall and leads to tissue necrosis C/feature: within 24hr. Pt complains: - intense pain - swelling around the wound - brownish discharge - gas formation - pyrexia - characteristic smelling - PR ↑ - toxaemic ïƒ coma ïƒ death Inability to recognize may lead to unnecessary amputation for the non-lethal cellulitis. C.perfringens, welchii Cth dead muscle, dirty wound, inadequate debridement Once experienced this will never be forgotten
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swelling around the wound,
brownish discharge gas formation
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Prevention: Treatment:
deep penetrating wound in muscular tissue are dangerous;should be explored, all dead tissue should be completely excised, and if there doubt about the tissue viability should left open the wound Treatment: Early Dx is life saving General measures: Fluid replacement & IV Antibiotic (immediate) Hyperbaric O2 (limiting the spread of gangrene) Mainstay : prompt decompression & remove dead tissue
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LATE COMPLICATIONS Joint instability Muscle contracture Delayed union
(Volkmann’s contracture) Tendon lesions Nerve compression Growth disturbance Bed sores Delayed union Non-union Malunion Joint stiffness Myoisitis ossificans Avascular necrosis Algodystrophy Osteoarthritis
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DELAYED UNION Fracture takes more than the usual time to unite. Causes
Inadequate blood supply Severe soft tissue damage Periosteal stripping Excessive traction Insufficient splintage Infection
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PERKINS’ TIME TABLE Upper Limb Lower Limb Callus visible 2-3 wks Union
Consolidation 6-8 wks 12-16 wks
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Clinical features X-Ray Fracture tenderness
(Esp when subjected to stress) X-Ray Visible fracture line Very little callus formation or periosteal reaction
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Severe soft tissue damage
Infection Excessive traction Intact fibula
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Treatment Conservative - To eliminate any possible cause
- Immobilization - Exercise Operative - Indication : Union is delayed > 6 mths No signs of callus formation - Internal fixation & bone grafting
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NON-UNION Condition when the fracture will never unite w/o intervention Healing has stopped. Fracture gap is filled by fibrous tissue (pseudoarthrosis) Causes Improper Tx of delayed union Too large a gap Interposition of periosteum, muscle or cartilage between the fragments
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Clinical features X-Ray Painless movement at the fracture site
Fracture is clearly visible Fracture ends are rounded, smooth and sclerotic Atrophic non-union : - Bone looks inactive (Bone ends are often tapered / rounded) - Relatively avascular Hypertrophic non-union : - Excessive bone formation ` - on the side of the gap - Unable to bridge the gap
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Hypertrophic non-union
Atrophic non-union
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Treatment Ununited scaphoid fracture → asymptomatic
Hypertrophic non-union (Esp long bone) → Rigid fixation (internal / external) sometimes need bone grafting Atrophic non-union → Fixation & bone grafting
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MALUNION Condition when the fragments join in an unsatisfactory position (unaccepted angulation, rotation or shortening) Causes Failure to reduce a fracture adequately Failure to hold reduction while healing proceeds Gradual collapse of comminuted or osteoporotic bone.
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Clinical features Treatment Deformity & shortening of the limb
Limitation of movements Treatment Angulation in a long bone (> 15 degrees) → Osteotomy & internal fixation Marked rotational deformity Shortening (> 3cm) in 1 of the lower limbs → A raised boot OR Bone operation
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JOINT STIFFNESS Common complication of fracture Tx following immobilization Common site : knee, elbow, shoulder, small joints of the hand Causes Oedema & fibrosis of the capsule, ligaments, muscle around the joint Adhesion of the soft tissue to each other or to the underlying bone (intra & peri-articular adhesions) Synovial adhesions d/t haemarthrosis
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Treatment Prevention : Joint stiffness has occurred: - Exercise
- If joint has to be splinted → Make sure in correct position Joint stiffness has occurred: - Prolonged physiotherapy - Intra-articular adhesions → Gentle manipulation under anaesthesia followed by continuous passive motion - Adherent or contracted tissues → Released by operation
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MYOSITIS OSSIFICANS Heterotopic ossification in the muscles after an injury Usually occurs in Dislocation of the elbow A blow to the brachialis / deltoid / quadriceps Causes (thought to be due to) muscle damage w/o a local injury (unconscious / paraplegic patient)
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Clinical features X-Ray Pain, soft tissue tenderness Local swelling
Joint stiffness Limitation of movements Extreme cases: - Bone bridges the joint - Complete loss of movement (extra-articular ankylosis) X-Ray Normal Fluffy calcification in the soft tissue
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Treatment Early stage : Joint should be rested
Then : Gentle active movements When the condition has stabilized : Excision of the bony mass Anti-inflammatory drugs may ↓ joint stiffness
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AVASCULAR NECROSIS Circumscribed bone necrosis Common site : Causes
Interruption of the arterial blood flow Slowing of the venous outflow leading to inadequate perfusion Common site : Femoral head Femoral condyls Humeral head Capitulum of humerus Scaphoid (proximal part) Talus (body) Lunate
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Conditions a/w AVN Perthes’ disease Certain fractures
Epiphyseal infection Sickle cell disease Caisson disease Gaucher’s disease Alcohol abuse High-dosage corticosteroid
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Clinical features X-Ray Joint pain, stiffness, swelling
Restricted movement X-Ray ↑ bone density Subarticular fracturing Bone deformity
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Treatment Avoid weight bearing on the necrotic bone
Revascularisation (using vascularised bone grafts) Excision of the avascular segment Replacement by prostheses
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ALGODYSTROPHY (COMPLEX REGIONAL PAIN SYNDROME)
Previosly known as Sudeck’s atrophy Post-traumatic reflex sympathetic dystrophy Usually seen in the foot / hand (after relatively trivial injury) Clinical features Continuous, burning pain Early stage : Local swelling, redness, warmth Later : Atrophy of the skin, muscles Movement are grossly restricted
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X-Ray Patchy rarefaction of the bones (patchy osteoporosis)
Algodystrophy
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Treatment Physiotherapy (elevation & active exercises) Drugs
- Anti-inflammatory drugs - Sympathetic block or sympatholytic drugs (Guanethidine)
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OSTEOARTHRITIS Post-traumatic OA 2O OA
Joint fracture wt severely damaged articular cartilage Within period of months 2O OA Cartilage heals Irregular joint surface may caused localized stress → 2O OA Years after joint injury
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Clinical features Treatment Pain Stiffness Swelling Deformity
Restricted movement Treatment Pain relief : Analgesics Anti-inflam agent Joint mobility : Physiotherapy Load reduction : wt reduction Realignment osteotomy (young pt) Arthroplasty (pt > 60yr)
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Thank You
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