The document discusses fractures, including their definition, causes, types, healing processes, and complications. It provides details on the principle management of fractures, including reduction, immobilization, and internal or external fixation. Key complications discussed are shock, diffuse coagulopathy, respiratory dysfunction, crush syndrome, deep vein thrombosis, fat embolism, gas gangrene, and tetanus.
CAUSESSudden traumadirect(fracture ofthe ulna caused by blow on the arm)indirect(spiral fractures of the tibia and fibula due to torsion of the leg, vertebral compression fractures, avulsion fractures)Stress or fatigue-repetitive stress(athletes, dancers, army recruits)Pathological(osteoporosis, Paget’s disease, bone tumour)
FRACTURES DISPLACEMENTAfter acomplete fracture the fragments usually displaced:partly by the force of injurypartly by gravitypartly by the pull of muscles attached to them.4 types: Translation/ShiftAlignment/AngulationRotation/TwistAltered length
Healing by callusCallusis the response to movement at the fracture site to stabilize the fragments as rapidly as possible.Steps:
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Healing without callusForfracture that is absolutely immobile:impacted fracture in cancellous bone.fracture rigidly immobilized by internal fixationNew bone formation occurs directly between fragments.Gaps between the fracture surfaces are invaded by new capillaries & bone forming cells growing in from edges.For very narrow crevices(<200um), osteogenesis produces lamellar bone(mature).For wider gaps, osteogenesis begins with woven bone (immature) first which is then remodelled to lamellar bone (mature bone).
First aid managementAirway, Breathing and CirculationSplint the fracture Look for other associated injuriesCheck distal circulation – is distal circulation satisfactory? Check neurology – are the nerve intact?AMPLE history- Allergies, Medications, Past medical history, Last meal, Events Radiographs – 2 views, 2sides, 2 joints, 2 times.
ReduceAim for adequateapposition and normal alignment of the bone fragmentsThe greater contact surface area between fragments, the more likely is healing to occur
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However, there aresome situations in which reduction is unnecessary:When there is little or no displacementWhen displacement does not matter (e.g. in some fractures of the clavicle)When reduction is unlikely to succeed (e.g. with compression fracture of the vertebrae)
Most effective whenthe periosteum and muscles on one side of fracture remain intactUnder anaesthesia and muscle relaxation, a threefold manoeuvre applied:Distal part of the limb is pulled in line of the boneDisengaged, repositionedAlignment is adjusted
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Mechanical TractionSome fractures (example fracture of femoral shaft) are difficult to reduce by manipulation because of powerful muscle pullHowever, they can be reduced by sustained muscle mechanical traction; also serves to hold the fracture until it starts to unite
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Open ReductionOperative reductionunder direct visionIndications:When closed reduction failsWhen there is a large articular fragment that needs accurate positioningFor avulsion fractures in which the fragments are held apart by muscle pullWhen an operation is needed for associated injuriesWhen a fracture needs an internal fixation
Disadvantage and complicationsPatientkept on bed for long timePressure ulcerGeneral weaknessPulmonary infectionContracturePin tract infectionThromboembolic eventMethodsTraction by gravityBalanced tractionFixed traction
Fixed TractionPrinciple =balanced tractionUseful for when patient has to be transportedThomas’s splint
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Cast SplintageMethods:Plaster ofParis FibreglassEspecially for distal limb # and for most children #Disadvantage: joint encased in plaster cannot move and liable to stiffenCan be minimized:Delayed splintage (traction initially)Replace cast by functional brace after few weeks
ExercisePrevention of edemaactiveexercise and elevationActive exercise also stimulates the circulation. Prevents soft-tissue adhesion and promotes fracture healing.Preserve the joint movementRestore muscle powerFunctional activity
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Management of OpenFracturesAbreakin skin and underlying soft tissues leading directly to communicating with the fracture
Surgical DebridementType IIand type III require surgical debridement. Important aspect of wound management.Reduce bacteria, remove foreign bodies, remove devitalized tissue. Removal of dead tissue reduces bacterial burden and accelerate healing. 89
Wound ClosureUncontaminated I& II can be sutured – provided without tensionAll other wounds left open, packed with moist sterile gauze, to be inspected 24-48 hours – primary delayed closureIf wound cannot be closed without tension – skin grafting
Stabilization of thefractureTo reduce infection and assist recovery of soft tissueDepends on:degree of contaminationlength of time from injury to operationamount of soft tissue damageIf <8 hours: up to IIIA treated as closed fractures:SplintageIntramedullary nailingPlating External fixationOthers: External fixation
General 1: ShockAlteredphysiologic status with generalized inadequate tissue perfusion relative to metabolic requirements. irreversible damage to vital organs
General 4: CrushSyndrome[traumatic rhabdomyolitis]Serious medical condition characterized by major shock & renal failure following a crushing injury to skeletal muscles or tourniquet left too longBywaters’ Syndrome
General 5: Deepvein thrombosis and pulmonary embolism.Virchow’s triad factor Clot formation in large vein thrombus breaks off EmboliSite: leg, thigh and pelvic vein.Risk factors:
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General 5: ManagementDeep vein thrombosis and pulmonary embolism.AnticoagulationAmbulate patientEstablished thrombosis/embolismLimb elevationHeparinizationThrombolysisOxygenation or ventilationPREVENTIONCorrect hypovolemiaCalf muscle exerciseProper positioningWell fitting bandages & castLimb elevationGraduated compression stockingsCalf muscle stimulation
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General 6: FatEmbolismFat globules from marrow pushed into circulation by the force of trauma that causing embolic phenomena
General 7: GasGangreneRapid and extensive necrosis of the muscle accompanied by gas formation and systemic toxicity due to clostridium perfringens infection
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General 7: GasGangrenePrevention: ALL DEAD TISSUE [4C] SHOULD BE COMPLETELY EXCISED,
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General 8: TetanusAcondition after clostridium tetani infection that passes to anterior horn cells where it fixed and cant be neutralized later produces hyper-excitability and reflex muscle spasm
Early 1: VisceralinjuryFractures around the trunk are often complicated by visceral injury.E.g. Rib fractures pneumothorax / spleen trauma / liver injuries.E.g. Pelvic injuries bladder or urethral rupture / severe hematoma in the retro-peritoneum .Rx: Surgery of visceral injuries
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Early 2: VascularinjuryCommonly associated with high-energy open fractures. They are rare but well-recognized.Mechanism of injuries:The artery may be cut or torn. Compressed by the fragment of bone. normal appearance, with intimal detachment that lead to thrombus formation.segment of artery may be in spasm.It may causeTransient diminution of blood flowProfound ischaemiaTissue death and gangrene
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Early 2: VascularinjuryX-ray: suggest high-risk fracture.Angiogram should be performed to confirm diagnosis.
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Early 2: Vascularinjurymuscle ischaemic is irrevesible after 6 hours.Remove all bandages and splint & assess circulationSkeletal stabilization – temporary external fixation.Definitive vascular repair.Vessel suturedendarterectomy
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Early 3: CompartmentSyndromeA condition in which increase in pressure within a closed fascial compartment leads to decreased tissue perfusion. Untreated, progresses to tissue ischaemia and eventual necrosis
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Early 3: CompartmentSyndromeMost common sites (in ↓ freq): leg (after tibial fracture) -> forearm -> thigh -> upper arm. Other sites: hand, foot, abdomen, gluteal and cervical regions.High risk injuries:# of elbow, forearm bones, and proximal 3rd of tibia (30-70% after tibial #)multiple fracture of the foot or handcrush injuriescircumferential burns
Early 3: CompartmentSyndrome Vicious cycle↑ fluid contentConstriction of compartment↑ INTRACOMPARTMENTAL PRESSURECapillary basement membranes become leaky -> oedemaObstruct venous returnVascular congestionMuscle and nerve ischaemiaFurther ↑ intracompartmental pressure↓ capillary perfusionCompromise arterial circulation-> PROGRESSIVE NECROSIS OF MUSCLES AND NERVES !!
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A vicious circlethat ends after 12 hours or lessNecrosis of the nerve and muscle within the compartmentNerve-capable to regenerateMuscle-infarctedNever recoverReplaced by inelastic fibrous tissue( Volkmann’s ischaemic contracture)
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Investigations of compartmentsydromesIntra-compartment Pressure Measurement (ICP)Use of slit catheter; quick and easyIndications:Unconscious patientThose who are difficult to assessConcomitant neurovascular injuryEquivocal symptomsEspecially long bone # in lower limbPerform as soon as dx considered> 40mmHg – urgent Rx! (normal 0 – 10 mmHg)
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Investigations of compartmentsyndromesOther Ix – limited value; +ve only when CS is advancedPlasma creatinine and CPKUrinanalysis – myoglobinuriaNerve conduction studies Ix to establish underlying cause or exclude differentialsX-ray of affected extremity Doppler US/arteriograms – determine presence of pulses; exclude vascular injuries and DVTPT/APTT – exclude bleeding disorder
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ManagementPrompt DECOMPRESSION ofaffected compartmentRemove all bandages, casts and dressingsExamination of whole limbLimb should be maintained at heart levelElevation may ↓ arterio-venous pressure gradient on which perfusion dependsEnsure patient is normotensive. Hypotension ↓ tissue perfusion, aggravate the tissue injury.
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ManagementMeasure intra-compartment pressureIf> 40mmHgImmediate open fasciotomyIf < 40mmHgClose observation and re-examine over next hourIf condition improve, repeated clinical evaluation until danger has passedDon’t wait for the obvious sings of ischemia to appear. If you suspect An impending compartment syndrome, start treatment straightaway
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FasciotomyOpening all 4compartmentsDivide skin and deep fascia for the whole length of compartmentWound left openInspect 5 days laterIf muscle necrosis, do debridementIf healthy tissue, for delayed closure or skin grafting
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ComplicationsVolkmann’s ischaemiccontracture Motor/sensorydeficitsKidney failure from rhabdomyolysis (if very severe)Infection – fasciotomy converts closed # to open #Loss of limbDelay in bone unionPrognosisexcellent to poor, depending on how quickly CS is treated and whether complications develop
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Early 4: NerveInjuryIt’s more common than arterial injuries.The most commonly injured nerve is the radial nerve [in its groove or in the lower third of the upper arm especially in oblique fracture of the humerus]Common with humerus, elbow and knee fracturesMost nerve injuries are due to tension neuropraxia.
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Early 4: NerveInjuryDamaged by laceration, traction, pressure or prolonged ischaemia
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Early 4: NerveInjuryInvestigationsElectromyographyNerve conduction studyMay help to establish level and severity of lesionClinical featuresNumbness and weaknessSkin smooth and shiny but feels dryMuscle wasting and weaknessSensation bluntedTinel’s sign +ve
Early 5: HaemarthrosisBleedinginto a joint spaces.Occurs if a joint is involved in the fracture.Presentation:swollen tense joint; the patient resists any attempt to moving ittreatment:blood aspiration before dealing with the fracture; to prevent the development of synovial adhesions.
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Early 6: INFECTIONClosedfractures – hardly everOpen fractures – may become infectedPost traumatic wound – may lead to chronic osteomyelitis
Late 1: DELAYEDUNION Union of the upper limbs - 4-6 weeksUnion of the lower limbs - 8-12 weeks(rough guide)Any prolong time taken is considered delayed
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Late 1: DELAYEDUNIONFactors are either biological or biomechanicalBiological :Poor blood supplyTear of periosteum, interruption of intramedullary circulationNecrosis of surface# and healing process will take longerSevere soft tissue damageMost important factorLonger time for bone healing due less inflammatory cell supplyInfection: bone lysis, tissue necrosis and pus Periosteal strippingLess blood circulation to bone
Clinical features:Tenderness persistAcutepain if bone is subjected to stress*( * ask pt to walk, move affected limb)X RAYS -visible line# and very little callus formation/periosteal reaction - bone ends are not sclerosed/ atrophic (it will eventually unite)Late1: DELAYED UNION
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Tx: conservative andoperativeEliminate possible causes of delayPromote healingImmobilization should be sufficient to prevent movement at # site(cast / internal fixation)Not to neglect # loading so, encourage muscle exercise and weight bearing in the cast/braceOperation> 6 mths & no signs of callus formationInternal fixation and bone graffting(operation-least possible damage to the soft tissue)Late 1: DELAYED UNION
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Late 2: NON-UNIONIn a minority of cases, delayed union--non-unionFactors contributing to non-union:-inadequate treatment of delayed union too large gapinterposition of soft tissues between the fragmentsThe growth has stopped and pain diminished- replaced by fibrous tissue - pseudoarthrosisTreatment :-conservative / operativeatrophic non-union – fixation and grafting hypertrophic non-union – rigid fixation
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Late 2: NONUNIONbone ends are rounded off or exuberantHypertrophic non unionBone ends are enlarged, osteogenesis is still active but not capable of bridging the gap‘elephant feet’ on X rayAtrophic non unionCessation of osteogenesisNo suggestion of new bone formation
Late 2: NonunionTx:Mostly symptomlessConservativeRemovable splintFor hypertrophic non-union, functional bracing-induce unionPulsed electromagnetic fields and low frequency pulsed u/s can also be used to stimulate union.OperativeHypertrophic--Rigid fixation (internal or external)Atrophic--Excision of fibrous tissue ,sclerotic tissue at bone end, bone grafts packed around the fracture
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Late 3: MALUNIONFactors:-failure to reduce the fracturefailure to hold the reduction while healing proceedgradual collapse of comminuted / osteoporotic bone
Late 3: Mal-unionX-ray are essential to check the position of the fracture while uniting. important- the first 3 weeks so it can be easily corrected Clinical features:Deformity usually obvious , but sometimes the true extent of malunion is apparent only on x-rayRotational deformity can be missed in the femur, tibia, humerus or forearm unless is compared with it’s opposite fellow
Late 4: AVASCULARNECROSISCertain region-known for their propensity to develop ischaemia and bone necrosisHead of femur Proximal part of scaphoidLunateBody of talus(Actually this is an early complication however the clinical and radiological effects are not seen until weeks or even months)No clinical feature of avascular necrosis but if there is a failure to unite or bone collapse-pain
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ABThe cardinal X-rayfeature – increased bone density in the weight-bearing part of the joint(new bone ingrowth in necrotic segment)
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Treatment:- Avascular necrosiscan be prevented by early reduction of susceptible fractures and dislocations. Arthroplasty - Old people with necrosis of the femoral head.Realignment osteotomy or arthrodesis - for younger people with necrosis of the femoral head Symptomatic treatment for scaphoid or talus
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Late 5: OSTEOARTHRITISAfracture-joint may damage the articular cartilage and give rise to post traumatic osteoarthritis within a period of months.Even if the cartilage heals, irregularity of the joint surface may cause localized stress and so predispose to secondary osteoarthritis years later
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Late 6: JOINTSTIFFNESSCommonly occur at the joints close to malunion or bone loss eg: knee, elbow, shoulder Causes of joint stiffnesshaemarthrosis -> lead to synovial adhesionoedema and fibrosis adhesion of the soft tissuesWorsen by prolong immobilizationTreatment prevented with exercisephysiotherapy
#90 Type I open fracture can be managed with non-operative approach and closed reduction.
#99 may lead to irreversible damage of the life supporting organs.Thirst, rapid shallow breathing, the lips and skin are pale and the extremities feel cold,if the compansation fails….. impaired renal function test and decreased urinary output.
#104 It’s a re-perfusion injury seen after the release of crushing pressure, there will be release of muscular breakdown products(myoglobin,k+,p) which have nephrotoxic effect on the kidneyFirst describe by Eric Bywaters
#105 It’s a re-perfusion injury seen after the release of crushing pressure, there will be release of muscular breakdown products(myoglobin,k+,p) which have nephrotoxic effect on the kidneyFirst describe by Eric Bywaters
#112 4C – Colour – blue-black purpleConsistency – MushyContractibility – unableCut – not capable to bleedDeep, penetrating wound in muscular tissue should be explored, ALL DEAD TISSUE SHOULD BE COMPLETELY EXCISED, if there is doubt about tissue viability, the wound should be left opened