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Complications of Fractures. COMPLICATION OF FRACTURE GeneralLocal Early Late.

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Presentation on theme: "Complications of Fractures. COMPLICATION OF FRACTURE GeneralLocal Early Late."— Presentation transcript:

1 Complications of Fractures

2 COMPLICATION OF FRACTURE GeneralLocal Early Late

3 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.

4 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.

5 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.

6 General complications

7 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

8 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).

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

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

11 How to treat it? 1 st rule = Limb crushed severely(>6hrs) 1 st rule = Limb crushed severely(>6hrs) How the amputation done? How the amputation done? Above the compression or crushed injury Above the compression or crushed injury Before compression is released Before compression is released

12 Venous thrombosis & Pulmonary Embolism Commonest Complications of Trauma & Surgery Commonest Complications of Trauma & Surgery Most frequently Most frequently Calf Calf Less frequent in proximal of thigh & pelvis Less frequent in proximal of thigh & pelvis Pulmonary Embolism Pulmonary Embolism From Proximal of thigh & pelvis From Proximal of thigh & pelvis Incidence=5% & Fatal = 0.5% Incidence=5% & Fatal = 0.5%

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

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

15 What we can see in DVT? Pain the calf or thigh Pain the calf or thigh Soft tissue tenderness Soft tissue tenderness Sudden slight increase in temperature Sudden slight increase in temperature Sudden increase in pulse rate Sudden increase in pulse rate Homann’s Sign positive Homann’s Sign positive

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

17 How about pulmonary embolism? Difficult to diagnose =only minority have symptoms (chest pain, dyspnoe, heamoptysis) Difficult to diagnose =only minority have symptoms (chest pain, dyspnoe, heamoptysis) So high risk patients should be examine for pulmonary consolidation So high risk patients should be examine for pulmonary consolidation X-ray X-ray Pulmonary angiography Pulmonary angiography

18 How to prevent it? Prophylactic treatment Prophylactic treatment Foot elevation Foot elevation Graduated compression stockings Graduated compression stockings Exercise Exercise Anticoagulant treatment Anticoagulant treatment Subcut low dose heparin 5000 units preops & 3/7 postops (but CI in older patient  bleeding) 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) Change to low molecular weight heparin (less likely to cause bleeding)

19 What is the treatment? Localized DVT Localized DVT Elastic stockings Elastic stockings Low dose subcut heparin (5000 unit) Low dose subcut heparin (5000 unit) More extensive DVT More extensive DVT Bed rest Bed rest Elastic stockings Elastic stockings Full anticoagulation Full anticoagulation Heparin IV (10000 units 6 hourly) Heparin IV (10000 units 6 hourly) Continue for 5-7/7 with last 2/7 warfarin introduce Continue for 5-7/7 with last 2/7 warfarin introduce

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

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

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

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

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

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

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

27 Treatment for gas gangrene The key = EARLY DIAGNOSIS The key = EARLY DIAGNOSIS General measures (fluid, IV antibiotics) General measures (fluid, IV antibiotics) Hyperbaric oxygen (limiting spread) Hyperbaric oxygen (limiting spread) Decompression of wound Decompression of wound Removal of all dead tissue Removal of all dead tissue Amputation (advanced case) Amputation (advanced case)

28 FAT EMBOLISM Only minority patients with circulating fat globules will develop POST TRAUMATIC RESPIRATORY DYSFUNCTION Only minority patients with circulating fat globules will develop POST TRAUMATIC RESPIRATORY DYSFUNCTION Source of fat emboli=bone marrow Source of fat emboli=bone marrow Usually in MULTIPLE CLOSED FRACTURE Usually in MULTIPLE CLOSED FRACTURE But other condition also reported (burns, renal infarction, cardiopulmonary operation) But other condition also reported (burns, renal infarction, cardiopulmonary operation)

29 How can we detect it? Usually young adults with LL fracture Usually young adults with LL fracture Early warning signs (72 hrs. of injury) Early warning signs (72 hrs. of injury) Rise in temperature and pulse rate Rise in temperature and pulse rate More pronounced case More pronounced case Breathlessness Breathlessness Mild mental confusion Mild mental confusion Petechia (chest & conjuntival fold) Petechia (chest & conjuntival fold) Most severe case Most severe case Marked respiratory distress  coma  ARDS Marked respiratory distress  coma  ARDS

30 How to treat it? Mild case Mild case Monitoring of blood PO2 Monitoring of blood PO2 Signs of hypoxia Signs of hypoxia Oxygen Oxygen If severe If severe Intensive care with sedation and assisted ventilation Intensive care with sedation and assisted ventilation Swan ganz Catheterization (monitor cardiac Fx) Swan ganz Catheterization (monitor cardiac Fx) Fluid balance Fluid balance Supportive Supportive Heparin-thromboembolism Heparin-thromboembolism Steroids-pulmonary oedema Steroids-pulmonary oedema Aprotinin-prevent aggregation of chylomicrons Aprotinin-prevent aggregation of chylomicrons

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

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

33 Local visceral Injury Fracture around the trunk are often Cx by injury to the adjacent viscera : Fracture around the trunk are often Cx by injury to the adjacent viscera : Pelvic fracture Pelvic fracture Rib fracture penetration to the lungs Rib fracture penetration to the lungs Pneumothorax Bladder and urethral rupture

34 Vascular injury Most commonly – knee, femoral shaft, elbow, and humerus. Most commonly – knee, femoral shaft, elbow, and humerus. Artery may be cut, torn, compressed or contused. Artery may be cut, torn, compressed or contused. Intima may be detached, thrombus block, artery spasm Intima may be detached, thrombus block, artery spasm Effect ?? ↓↓ bld flow coz Ischemia leads to tissue death & peripheral gangrene Effect ?? ↓↓ bld flow coz Ischemia leads to tissue death & peripheral gangrene

35 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).

36 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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38 Clinical features Pt with ischemia may have 5 P’s: Pt with ischemia may have 5 P’s: - paraesthesia/numbness - pain - pallor - pulselessness - paralysis Investigate if suspect vascular injury : Angiogram Investigate if suspect vascular injury : Angiogram

39 Treatment Emergency treatment Emergency treatment All bandages/splints removed All bandages/splints removed The fracture X-Ray again The fracture X-Ray again Circulation reassessed for next half hour Circulation reassessed for next half hour If no improvement, do vessels exploration If no improvement, do vessels exploration Suture torn vessels, vein grafting, if thrombosed do endarterectomy Suture torn vessels, vein grafting, if thrombosed do endarterectomy Aim: to restore bld flow Aim: to restore bld flow

40 Nerve Injury Variable degree of motor and sensory loss along the distribution of the nerve Variable degree of motor and sensory loss along the distribution of the nerve May be neurapraxia, axonotmesis or neurotmesis May be neurapraxia, axonotmesis or neurotmesis Radial nerve is most frequently damaged nerves. Radial nerve is most frequently damaged nerves.

41 NerveTraumaEffect 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 Foot drop

42 In closed injuries – nerve is seldom severed and spontaneous recovery should be awaited. 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. In open fractures – complete lesion(neurotmesis) : the nerve is explored during wound debridement and repaired.

43 Compartment Syndrome Definition 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. 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. A rise in pressure within these compartments may jeopardize the blood supply to the muscles & nerves within the compartment.

44 Causes: Causes: -any injury/infection leading to edema of muscle -fracture haematoma within the compartment -ischemia to the compartment leading to muscle oedema oedema -Due to tight bandages or casts Hallmark Symptoms: 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.

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

46 The vicious cycle of Volkmann’s ischaemia Arterial ischaemia blood flow Damage Direct injury oedema Compartment pressure 5P’s Pain Pallor Paraesthesia Pulseless Paralysis …………......……………. Fasciotomy

47 A vicious cycle cont. until the total vascularity of the muscles and nerves is jeopardized. 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) This result in ischaemic muscle necrosis and nerve damage. (within 12 hours) The necrotic muscle undergo healing with fibrosis, leading to Volkmann’s contracture. 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 Nerve damage may result in motor and sensory loss. In extreme case  gangrene

48 clinically: clinically: - should be tested by stretching the muscles  when the toes or fingers are muscles  when the toes or fingers are passively hyperextended there is ↑ pain passively hyperextended there is ↑ pain in the calf or forearm. in the calf or forearm. Early preventing : limb elevation Early preventing : limb elevation Dx : confirmed by direct intracompartmental pressure measuring > 40mmHg is an indication of compartment decompression and fasciotomy. Dx : confirmed by direct intracompartmental pressure measuring > 40mmHg is an indication of compartment decompression and fasciotomy.

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50 Treatment First removed all the bandages & dressing. First removed all the bandages & dressing. Fasciotomy is performed. Fasciotomy is performed. The wound should be left open and inspected 2 days later. The wound should be left open and inspected 2 days later. If there is muscle necrosis  debridement If there is muscle necrosis  debridement If muscle is healthy  suture (w/o tension)/ skin grafted / simply heal by 2˚ intention. If muscle is healthy  suture (w/o tension)/ skin grafted / simply heal by 2˚ intention.

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53 Haemarthrosis Fractures involve joints, leads to acc. of blood within the joints. 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. 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. Tx : the blood should be aspirated before dealing with the fracture.

54 Infection Causes: Causes: Open fracture (common) Open fracture (common) Use of operative method in the Tx of # Use of operative method in the Tx of # Wound becomes inflamed and starts draining seropurulent fluid. Wound becomes inflamed and starts draining seropurulent fluid. Infection may be superficial, moderate (osteomyelitis), severe (gas gangrene). 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. Post-traumatic wound infx is most common cause of chronic osteomyelitis  union will be slow and ↑ chance of refracturing.

55 Treatment: Antibiotic Antibiotic Excising all devitalised tissue Excising all devitalised tissue If Sx of acute infx and pus formation : tissue around the fracture should be opened & drained If Sx of acute infx and pus formation : tissue around the fracture should be opened & drained

56 Gas gangrene Produced by anaerobic orgs : Clostridium sp infections. Produced by anaerobic orgs : Clostridium sp infections. These orgs can survive in ↓ O 2 tension These orgs can survive in ↓ O 2 tension Toxins produced will destroy the cell wall and leads to tissue necrosis Toxins produced will destroy the cell wall and leads to tissue necrosis C/feature: within 24hr. Pt complains: 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. Inability to recognize may lead to unnecessary amputation for the non-lethal cellulitis.

57 swelling around the wound, brownish discharge gas formation

58 Prevention: 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 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 woundTreatment: Early Dx is life saving Early Dx is life saving General measures: General measures: Fluid replacement & IV Antibiotic (immediate) Fluid replacement & IV Antibiotic (immediate) Hyperbaric O 2 (limiting the spread of gangrene) Hyperbaric O 2 (limiting the spread of gangrene) Mainstay : prompt decompression & remove dead tissue Mainstay : prompt decompression & remove dead tissue

59 LATE COMPLICATIONS Delayed union Delayed union Non-union Non-union Malunion Malunion Joint stiffness Joint stiffness Myoisitis ossificans Myoisitis ossificans Avascular necrosis Avascular necrosis Algodystrophy Algodystrophy Osteoarthritis Osteoarthritis Joint instability Joint instability Muscle contracture Muscle contracture (Volkmann’s contracture) Tendon lesions Tendon lesions Nerve compression Nerve compression Growth disturbance Growth disturbance Bed sores Bed sores

60 DELAYED UNION Fracture takes more than the usual time to unite. Fracture takes more than the usual time to unite. Causes Causes  Inadequate blood supply  Severe soft tissue damage  Periosteal stripping  Excessive traction  Insufficient splintage  Infection

61 PERKINS’ TIME TABLE Upper Limb Lower Limb Callus visible 2-3 wks Union 4-6 wks 8-12 wks Consolidation 6-8 wks wks

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

63 Severe soft tissue damage Infection Excessive traction Intact fibula

64 Treatment Treatment  Conservative - To eliminate any possible cause - To eliminate any possible cause - Immobilization - Immobilization - Exercise - Exercise  Operative - Indication : - Indication : Union is delayed > 6 mths Union is delayed > 6 mths No signs of callus formation No signs of callus formation - Internal fixation & bone grafting - Internal fixation & bone grafting

65 NON-UNION Condition when the fracture will never unite w/o intervention Condition when the fracture will never unite w/o intervention Healing has stopped. Healing has stopped. Fracture gap is filled by fibrous tissue (pseudoarthrosis) Causes Causes  Improper Tx of delayed union  Too large a gap  Interposition of periosteum, muscle or cartilage between the fragments

66 Clinical features Clinical features  Painless movement at the fracture site  X-Ray  Fracture is clearly visible  Fracture ends are rounded, smooth and sclerotic  Atrophic non-union : - Bone looks inactive (Bone ends are often tapered / rounded) (Bone ends are often tapered / rounded) - Relatively avascular - Relatively avascular Hypertrophic non-union : - Excessive bone formation Hypertrophic non-union : - Excessive bone formation ` - on the side of the gap - Unable to bridge the gap - Unable to bridge the gap

67 Hypertrophic non-union Atrophic non-union

68 Treatment Treatment  Ununited scaphoid fracture → asymptomatic  Hypertrophic non-union (Esp long bone) → Rigid fixation (internal / external) → Rigid fixation (internal / external) sometimes need bone grafting sometimes need bone grafting  Atrophic non-union → Fixation & bone grafting → Fixation & bone grafting

69 MALUNION Condition when the fragments join in an unsatisfactory position (unaccepted angulation, rotation or shortening) Condition when the fragments join in an unsatisfactory position (unaccepted angulation, rotation or shortening) Causes Causes  Failure to reduce a fracture adequately  Failure to hold reduction while healing proceeds  Gradual collapse of comminuted or osteoporotic bone.

70 Clinical features Clinical features  Deformity & shortening of the limb  Limitation of movements  Treatment  Angulation in a long bone (> 15 degrees) → Osteotomy & internal fixation → Osteotomy & internal fixation  Marked rotational deformity → Osteotomy & internal fixation → Osteotomy & internal fixation  Shortening (> 3cm) in 1 of the lower limbs → A raised boot OR → A raised boot OR Bone operation Bone operation

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72 JOINT STIFFNESS Common complication of fracture Tx following immobilization Common complication of fracture Tx following immobilization Common site : knee, elbow, shoulder, Common site : knee, elbow, shoulder, small joints of the hand small joints of the hand Causes 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

73 Treatment Treatment  Prevention : - 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 → Gentle manipulation under anaesthesia followed by continuous passive motion followed by continuous passive motion - Adherent or contracted tissues → Released by operation → Released by operation

74 MYOSITIS OSSIFICANS Heterotopic ossification in the muscles after an injury Heterotopic ossification in the muscles after an injury Usually occurs in 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)

75 Clinical features Clinical features  Pain, soft tissue tenderness  Local swelling  Joint stiffness  Limitation of movements  Extreme cases: - Bone bridges the joint - Complete loss of movement - Complete loss of movement (extra-articular ankylosis) (extra-articular ankylosis)  X-Ray  Normal  Fluffy calcification in the soft tissue

76 Treatment Treatment  Early stage : Joint should be rested  Then : Gentle active movements  When the condition has stabilized : Excision of the bony mass Excision of the bony mass  Anti-inflammatory drugs may ↓ joint stiffness

77 AVASCULAR NECROSIS Circumscribed bone necrosis Circumscribed bone necrosis Causes Causes  Interruption of the arterial blood flow  Slowing of the venous outflow leading to inadequate perfusion Common site : Common site :  Femoral head  Femoral condyls  Humeral head  Capitulum of humerus  Scaphoid  Scaphoid (proximal part)  Talus  Talus (body)  Lunate

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

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

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

82 ALGODYSTROPHY ( COMPLEX REGIONAL PAIN SYNDROME ) Previosly known as Sudeck’s atrophy Previosly known as Sudeck’s atrophy Post-traumatic reflex sympathetic dystrophy Post-traumatic reflex sympathetic dystrophy Usually seen in the foot / hand Usually seen in the foot / hand (after relatively trivial injury) Clinical features Clinical features  Continuous, burning pain  Early stage : Local swelling, redness, warmth  Later : Atrophy of the skin, muscles  Movement are grossly restricted

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

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

85 OSTEOARTHRITIS Post-traumatic OA Post-traumatic OA  Joint fracture wt severely damaged articular cartilage  Within period of months  2 O OA  Cartilage heals  Irregular joint surface may caused localized stress → 2 O OA  Years after joint injury

86 Clinical features Clinical features  Pain  Stiffness  Swelling  Deformity  Restricted movement Treatment Treatment  Pain relief : Analgesics Anti-inflam agent  Joint mobility : Physiotherapy  Load reduction : wt reduction  Realignment osteotomy (young pt)  Arthroplasty (pt > 60yr)

87 Thank You


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