Complications of Fractures

COMPLICATION OF FRACTURE General Local Early Late

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.

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.

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.

General complications

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

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).

Crush syndrome Occur in What happened? Large bulk of muscle crushed Tourniquet left for TOO long What happened? 1st theory =Compression releasedacid myohaematin enter the circulationkidneyblocks the tubules Renal failure and death.

What we can see? Limb Renal Neurologically Pulseless Red Swollen Secretion diminished Low output uraemia Acidosis Neurologically Drowsynot treated  DEATH

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

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%

What cause DVT? The primary cause in surgical HYPERCOAGULABILITY of the Blood due to activation of Factor X by Thromboplastin from damaged tissues Thrombosis occurssecondary factors are Stasis Pressure Prolonged immobility Endothelial damage Increase in no & stickiness of platelet

What are the high risk group? Old people Cardiovascular Disease Bedridden patient Patients undergoing hip arthroplasty

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

How to diagnose DVT? Ascending venography (bilaterally) US scanning (detecting prox DVT) Radioactive iodine labelled fibrinogen(clot) Doppler technique (measure blood flow)

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

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 patientbleeding) Change to low molecular weight heparin (less likely to cause bleeding)

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

How to treat Pulmonary Embolism? Cardiorespiratory resuscitation Oxygen Large dose heparin (15 000 units) Streptokinase (dissolve clot) Antibiotics (prevent lung infection)

TETANUS What is Tetanus? Tetanus organism live only in dead tissueexotoxin blood & lymph to CNS anterior horn cell Will develop Tonic clonic contraction Jaw and face (trismus and risus sardonicus) Neck and trunk Diaphragm and Intercostal muscle spasmASPHYXIA

What is the prophylaxis? Active immunization (tetanus toxoid) Booster doses (immunized patients) Non Immunized patients Wound toilet & antibiotics If wound contaminated antitoxin

Treatment for Tetanus IV antitoxin Heavy Sedation Muscle Relaxant drug Tracheal Intubation Controlled respiration

GAS GANGRENE By clostridial infection (esp C.welchii) Anaerobic with low oxygen tension Produce toxinsdestroy cell walltissue necrosis Spreading

The clinical features Within 24 hours Intense pain Swelling Brownish discharge Pulse rate increased Charasteristis smell Little or no pyrexia Gas formation not marked ToxaemiccomaDEATH

How to prevent it? Deep penetrating wound should be EXPLORED ALL dead tissue completely EXCISED Doubt about tissue viabilityleft it OPEN No antitoxin

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)

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)

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 coma ARDS

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

COMPLICATION OF FRACTURE General Local Early Late * Early complication : those that arise during the first few weeks following injury.

Early Complication Local Visceral Injury Vascular Injury Nerve Injury Compartment Syndrome Haemarthrosis Infection Gas gangrene

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

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

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).

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).

Clinical features Pt with ischemia may have 5 P’s: - paraesthesia/numbness - pain - pallor - pulselessness - paralysis Investigate if suspect vascular injury : Angiogram

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

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

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

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

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)

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:   - 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.

Injuries with a high risk of developing Compartments synd: # of the elbow # of the forearm bone # of the proximal third of the tibia

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

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  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.

- should be tested by stretching the clinically: - should be tested by stretching the muscles  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

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  debridement If muscle is healthy suture (w/o tension)/ skin grafted / simply heal by 2˚ intention. Fasciotomy :do a long incision to the fascia to release the pressure

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.

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 union will be slow and ↑ chance of refracturing. un

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

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  coma  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

swelling around the wound, brownish discharge gas formation

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

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

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

PERKINS’ TIME TABLE Upper Limb Lower Limb Callus visible 2-3 wks Union Consolidation 6-8 wks 12-16 wks

Clinical features X-Ray Fracture tenderness (Esp when subjected to stress) X-Ray Visible fracture line Very little callus formation or periosteal reaction

Severe soft tissue damage Infection Excessive traction Intact fibula

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

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

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

Hypertrophic non-union Atrophic non-union

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

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.

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

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

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

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)

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

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

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

Conditions a/w AVN Perthes’ disease Certain fractures Epiphyseal infection Sickle cell disease Caisson disease Gaucher’s disease Alcohol abuse High-dosage corticosteroid

Clinical features X-Ray Joint pain, stiffness, swelling Restricted movement X-Ray ↑ bone density Subarticular fracturing Bone deformity

Treatment Avoid weight bearing on the necrotic bone Revascularisation (using vascularised bone grafts) Excision of the avascular segment Replacement by prostheses

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

X-Ray Patchy rarefaction of the bones (patchy osteoporosis) Algodystrophy

Treatment Physiotherapy (elevation & active exercises) Drugs - Anti-inflammatory drugs - Sympathetic block or sympatholytic drugs (Guanethidine)

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

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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