3 General complications ShockHypovolemic 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.
7 ShockThree types of shock may complicate fracturesHypovolemic or hemorrhagic shockThis 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 What happened? Large bulk of muscle crushed Tourniquet left for TOO longWhat happened?1st theory =Compression releasedacid myohaematin enter the circulationkidneyblocks the tubules Renal failure and death.
10 What we can see? Limb Renal Neurologically Pulseless Red Swollen Secretion diminishedLow output uraemiaAcidosisNeurologicallyDrowsynot treated DEATH
11 How to treat it? AMPUTATION 1st rule = Limb crushed severely(>6hrs) How the amputation done?Above the compression or crushed injuryBefore compression is releasedAMPUTATION
12 Venous thrombosis & Pulmonary Embolism Commonest Complications of Trauma & SurgeryMost frequentlyCalfLess frequent in proximal of thigh & pelvisPulmonary EmbolismFrom Proximal of thigh & pelvisIncidence=5% & Fatal = 0.5%
13 What cause DVT? The primary cause in surgical HYPERCOAGULABILITY of the Blooddue to activation of Factor X by Thromboplastin from damaged tissuesThrombosis occurssecondary factors areStasisPressureProlonged immobilityEndothelial damageIncrease in no & stickiness of platelet
14 What are the high risk group? Old peopleCardiovascular DiseaseBedridden patientPatients undergoing hip arthroplasty
15 What we can see in DVT? Homann’s Sign positive Pain the calf or thigh Soft tissue tendernessSudden slight increase in temperatureSudden increase in pulse rateHomann’s Sign positive
16 How to diagnose DVT? Ascending venography (bilaterally) US scanning (detecting prox DVT)Radioactive iodine labelled fibrinogen(clot)Doppler technique (measure blood flow)
17 How about pulmonary embolism? Difficult to diagnose =only minority have symptoms (chest pain, dyspnoe, heamoptysis)So high risk patients should be examine for pulmonary consolidationX-rayPulmonary angiography
18 How to prevent it? Prophylactic treatment Foot elevation Graduated compression stockingsExerciseAnticoagulant treatmentSubcut low dose heparin 5000 units preops & 3/7 postops (but CI in older patientbleeding)Change to low molecular weight heparin (less likely to cause bleeding)
19 What is the treatment? Localized DVT More extensive DVT Elastic stockingsLow dose subcut heparin (5000 unit)More extensive DVTBed restFull anticoagulationHeparin IV (10000 units 6 hourly)Continue for 5-7/7 with last 2/7 warfarin introduce
20 How to treat Pulmonary Embolism? Cardiorespiratory resuscitationOxygenLarge dose heparin ( units)Streptokinase (dissolve clot)Antibiotics (prevent lung infection)
21 TETANUS What is Tetanus? Tetanus organism live only in dead tissueexotoxin blood & lymph to CNS anterior horn cellWill developTonic clonic contractionJaw and face (trismus and risus sardonicus)Neck and trunkDiaphragm and Intercostal muscle spasmASPHYXIA
22 What is the prophylaxis? Active immunization (tetanus toxoid)Booster doses (immunized patients)Non Immunized patientsWound toilet & antibioticsIf wound contaminated antitoxin
23 Treatment for Tetanus IV antitoxin Heavy Sedation Muscle Relaxant drug Tracheal IntubationControlled respiration
24 GAS GANGRENE By clostridial infection (esp C.welchii) Anaerobic with low oxygen tensionProduce toxinsdestroy cell walltissue necrosis Spreading
25 The clinical features Within 24 hours Intense pain Swelling Brownish dischargePulse rate increasedCharasteristis smellLittle or no pyrexiaGas formation not markedToxaemiccomaDEATH
26 How to prevent it? Deep penetrating wound should be EXPLORED ALL dead tissue completely EXCISEDDoubt about tissue viabilityleft it OPENNo antitoxin
27 Treatment for gas gangrene The key = EARLY DIAGNOSISGeneral measures (fluid, IV antibiotics)Hyperbaric oxygen (limiting spread)Decompression of woundRemoval of all dead tissueAmputation (advanced case)
28 FAT EMBOLISMOnly minority patients with circulating fat globules will develop POST TRAUMATIC RESPIRATORY DYSFUNCTIONSource of fat emboli=bone marrowUsually in MULTIPLE CLOSED FRACTUREBut other condition also reported (burns, renal infarction, cardiopulmonary operation)
29 How can we detect it? Usually young adults with LL fracture Early warning signs (72 hrs. of injury)Rise in temperature and pulse rateMore pronounced caseBreathlessnessMild mental confusionPetechia (chest & conjuntival fold)Most severe caseMarked respiratory distress coma ARDS
30 How to treat it? Mild case Signs of hypoxia Monitoring of blood PO2 OxygenIf severeIntensive care with sedation and assisted ventilationSwan ganz Catheterization (monitor cardiac Fx)Fluid balanceSupportiveHeparin-thromboembolismSteroids-pulmonary oedemaAprotinin-prevent aggregation of chylomicrons
31 COMPLICATION OF FRACTURE GeneralLocalEarlyLate* Early complication : those that arise during the first few weeksfollowing injury.
32 Early Complication Local Visceral Injury Vascular Injury Nerve Injury Compartment SyndromeHaemarthrosisInfectionGas gangrene
33 Local visceral InjuryFracture around the trunk are often Cx by injury to the adjacent viscera :Pelvic fractureRib fracture penetration to the lungsBladder and urethralruptureThese require Emergency Treatment…………chest tube insertionPneumothorax
34 Vascular injuryMost commonly – knee, femoral shaft, elbow, and humerus.Artery may be cut, torn, compressed or contused.Intima may be detached, thrombus block, artery spasmEffect ?? ↓↓ bld flow coz Ischemia leads to tissue death & peripheral gangreneMost common artery injury is popliteal artKnee – poppliteal artery, femoral art, brachial art…….cut, torn – by initial inj or jagged by bone fragments
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).
38 Clinical features Pt with ischemia may have 5 P’s: - paraesthesia/numbness- pain- pallor- pulselessness- paralysisInvestigate if suspect vascular injury : Angiogram
39 Treatment Emergency treatment All bandages/splints removed The fracture X-Ray againCirculation reassessed for next half hourIf no improvement, do vessels explorationSuture torn vessels, vein grafting, if thrombosed do endarterectomyAim: to restore bld flowIn this operation, the fracture can be fixed internally at the same time
40 Nerve InjuryVariable degree of motor and sensory loss along the distribution of the nerveMay be neurapraxia, axonotmesis or neurotmesisRadial nerve is most frequently damaged nerves.Radial N – Humerus fractureNeurapraxia-minimal damage, axonotmesis- axon damage but sheath intact, neurotmesis- complete damage
41 Dislocation of shoulder Deltoid paralysis Radial # of humerus NerveTraumaEffectAxillaryDislocation of shoulderDeltoid paralysisRadial# of humerusWrist dropMedianSupracondylar # of humerusPointing indexUlnar# medial epicondyl humerusClaw handSciaticPost dislocation of hipFoot dropCommon peronealKnee dislocation # neck of fibula
42 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
43 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)
44 Causes:-any injury/infection leading to edema of muscle-fracture haematoma within the compartment-ischemia to the compartment leading to muscleoedema-Due to tight bandages or castsHallmark 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: # of the elbow# of the forearm bone# of the proximal third of the tibia
46 The vicious cycle of Volkmann’s ischaemia 5P’sPainPallorParaesthesiaPulselessParalysisArterial ischaemia blood flowDamageDirectinjury…………......…………….oedemaFasciotomyCompartmentpressure
47 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 gangreneThis 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.
48 - should be tested by stretching the clinically:- should be tested by stretching themuscles when the toes or fingers arepassively hyperextended there is ↑ painin the calf or forearm.Early preventing : limb elevationDx : 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 pressureWithin 6 hour in total ischema…muscles necrosis
50 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 debridementIf 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
53 HaemarthrosisFractures 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.
54 InfectionCauses: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
55 Excising all devitalised tissue Treatment:AntibioticExcising all devitalised tissueIf Sx of acute infx and pus formation : tissue around the fracture should be opened & drainedAll open fracture shud be regarded as potentially infecte
56 Gas gangrene Produced by anaerobic orgs : Clostridium sp infections. These orgs can survive in ↓ O2 tensionToxins produced will destroy the cell wall and leads to tissue necrosisC/feature: within 24hr. Pt complains:- intense pain- swelling around the wound- brownish discharge- gas formation- pyrexia- characteristic smelling- PR ↑- toxaemic coma deathInability to recognize may lead to unnecessary amputation for the non-lethal cellulitis.C.perfringens, welchiiCth dead muscle, dirty wound, inadequate debridementOnce experienced this will never be forgotten
57 swelling around the wound, brownish dischargegas formation
58 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 woundTreatment:Early Dx is life savingGeneral measures:Fluid replacement & IV Antibiotic (immediate)Hyperbaric O2 (limiting the spread of gangrene)Mainstay : prompt decompression & remove dead tissue
59 LATE COMPLICATIONS Joint instability Muscle contracture Delayed union (Volkmann’s contracture)Tendon lesionsNerve compressionGrowth disturbanceBed soresDelayed unionNon-unionMalunionJoint stiffnessMyoisitis ossificansAvascular necrosisAlgodystrophyOsteoarthritis
60 DELAYED UNION Fracture takes more than the usual time to unite. Causes Inadequate blood supplySevere soft tissue damagePeriosteal strippingExcessive tractionInsufficient splintageInfection
61 PERKINS’ TIME TABLE Upper Limb Lower Limb Callus visible 2-3 wks Union Consolidation6-8 wks12-16 wks
62 Clinical features X-Ray Fracture tenderness (Esp when subjected to stress)X-RayVisible fracture lineVery little callus formation orperiosteal reaction
63 Severe soft tissue damage InfectionExcessive tractionIntact fibula
64 Treatment Conservative - To eliminate any possible cause - Immobilization- ExerciseOperative- Indication :Union is delayed > 6 mthsNo signs of callus formation- Internal fixation & bone grafting
65 NON-UNIONCondition when the fracture will never unite w/o interventionHealing has stopped.Fracture gap is filled by fibrous tissue (pseudoarthrosis)CausesImproper Tx of delayed unionToo large a gapInterposition of periosteum, muscle or cartilage between the fragments
66 Clinical features X-Ray Painless movement at the fracture site Fracture is clearly visibleFracture ends are rounded, smooth and scleroticAtrophic non-union : - Bone looks inactive(Bone ends are often tapered / rounded)- Relatively avascularHypertrophic non-union : - Excessive bone formation` - on the side of the gap- Unable to bridge the gap
68 Treatment Ununited scaphoid fracture → asymptomatic Hypertrophic non-union (Esp long bone)→ Rigid fixation (internal / external)sometimes need bone graftingAtrophic non-union→ Fixation & bone grafting
69 MALUNIONCondition when the fragments join in an unsatisfactory position (unaccepted angulation, rotation or shortening)CausesFailure to reduce a fracture adequatelyFailure to hold reduction while healing proceedsGradual collapse of comminuted or osteoporotic bone.
70 Clinical features Treatment Deformity & shortening of the limb Limitation of movementsTreatmentAngulation in a long bone (> 15 degrees)→ Osteotomy & internal fixationMarked rotational deformityShortening (> 3cm) in 1 of the lower limbs→ A raised boot ORBone operation
72 JOINT STIFFNESSCommon complication of fracture Tx following immobilizationCommon site : knee, elbow, shoulder,small joints of the handCausesOedema & fibrosis of the capsule, ligaments, muscle around the jointAdhesion of the soft tissue to each other or to the underlying bone (intra & peri-articular adhesions)Synovial adhesions d/t haemarthrosis
73 Treatment Prevention : Joint stiffness has occurred: - Exercise - If joint has to be splinted → Make sure in correct positionJoint stiffness has occurred:- Prolonged physiotherapy- Intra-articular adhesions→ Gentle manipulation under anaesthesiafollowed by continuous passive motion- Adherent or contracted tissues→ Released by operation
74 MYOSITIS OSSIFICANSHeterotopic ossification in the muscles after an injuryUsually occurs inDislocation of the elbowA blow to the brachialis / deltoid / quadricepsCauses(thought to be due to) muscle damagew/o a local injury (unconscious / paraplegic patient)
75 Clinical features X-Ray Pain, soft tissue tenderness Local swelling Joint stiffnessLimitation of movementsExtreme cases: - Bone bridges the joint- Complete loss of movement(extra-articular ankylosis)X-RayNormalFluffy calcification in the soft tissue
76 Treatment Early stage : Joint should be rested Then : Gentle active movementsWhen the condition has stabilized :Excision of the bony massAnti-inflammatory drugs may ↓ joint stiffness
77 AVASCULAR NECROSIS Circumscribed bone necrosis Common site : Causes Interruption of the arterial blood flowSlowing of the venous outflow leading to inadequate perfusionCommon site :Femoral headFemoral condylsHumeral headCapitulum of humerusScaphoid (proximal part)Talus (body)Lunate
81 Treatment Avoid weight bearing on the necrotic bone Revascularisation (using vascularised bone grafts)Excision of the avascular segmentReplacement by prostheses
82 ALGODYSTROPHY (COMPLEX REGIONAL PAIN SYNDROME) Previosly known as Sudeck’s atrophyPost-traumatic reflex sympathetic dystrophyUsually seen in the foot / hand(after relatively trivial injury)Clinical featuresContinuous, burning painEarly stage : Local swelling, redness, warmthLater : Atrophy of the skin, musclesMovement are grossly restricted
83 X-Ray Patchy rarefaction of the bones (patchy osteoporosis) Algodystrophy
84 Treatment Physiotherapy (elevation & active exercises) Drugs - Anti-inflammatory drugs- Sympathetic block or sympatholytic drugs(Guanethidine)
85 OSTEOARTHRITIS Post-traumatic OA 2O OA Joint fracture wt severely damaged articular cartilageWithin period of months2O OACartilage healsIrregular joint surface may caused localized stress → 2O OAYears after joint injury