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hand and foot fracture and management

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Orthopaedics Surgery Tutor.Com

  1. 1. Fractures<br />DefinitionsDislocation  = total loss of congruity between articular surfacesSubluxation  = partial loss of congruity between articular surfacesFracture = a break in continuity of a boneFracture healingFractures heal by restoration of bone continuityRate of healing varies with age and is quicker in childrenCancellous bone heals more quickly than cortical boneSome movement at fractures site is required for healing to occurAlso requires an uninterrupted blood supplyBone healing can arbitrarily be divided in to five stagesStage oneHaematoma formationBone ends bleedPeriosteum is stripped for variable lengthSurrounding soft tissues may be damagedStage twoAcute inflammationCell division begins within 8 hoursCell proliferation seen within periosteumStage threeCallus formationDead bone is resorbedImmature woven bone is laid downStage fourWoven bone is replaced by lamellar boneFracture becomes unitedStage fivePhase of remodellingMedullary cavity is restoredBone returns to normal shapePrinciples of fracture managementSome general principles need to be applied to fracture managementNeed to consider Reduction of the fractureImmobilisation of the fractureRehabilitationNeed for reduction varies from fracture to fractureUsually need to correct rotational or valgus or varus deformityIntra-articular fractures need anatomical reductionReduction can be performed as either an open or closed procedureImmobilisation is required until fracture unionCan be performed by external or internal methodsExternal methods include Plaster castsTractionExternal fixationInternal methods include PlatesIntramedullary nailsK-wiresIndications for internal fixationIntra-articular fractures - to stabilise anatomical reductionRepair of blood vessels and nerves - to protect vascular and nerve repairMultiple injuriesElderly patients - to allow early mobilisationLong bone fractures - tibia, femur and humerusFailure of conservative managementPathological fracturesFractures that require open reductionUnstable fracturesComplications of internal fixationInfectionNon-unionImplant failureRefractureIndications for external fixationAcute trauma - open and unstable fracturesNon union of fracturesArthrodesisCorrection of joint contractureFilling of segmental limb defects - trauma, tumour and osteomyelitisLimb lengtheningComplications of external fixationOverdistractionPin-tract infectionComplications of fracturesEarly InfectionMuscle and tendon injuriesNerve injuriesVascular injuriesVisceral injuriesLate Delayed unionNon-unionMalunionAvascular necrosisMyositis ossificansVolkmann's contractureStiffness and instabilityAlgodystrophyReflex sympathetic dystrophyCompound fracturesAll open fractures must be assumed to be contaminatedObject of treatment is to prevent them becoming infectedFirst aid treatment is the same as for a closed fracturePeripheral neurovascular status should be assessedIn addition the wound should be covered with a sterile dressingWound should be photographed so that repeated uncovering is avoided repeated exposureAntibiotic prophylaxis should be givenTetanus immunisation status should be evaluatedPicture provided by Matteo Bianchi, Trauma Centre San Paolo, Milan, ItalyManagementOpen fractures require early operationIdeally this should be performed within 6 hours of injuryAims of surgery are to: Clean the woundRemove devitalised tissueStabilise the fractureSmall clean wounds can be suturesLarge dirty wounds should be debrided and left openDebrided wounds can be closed by delayed primary suture ar 5 daysPathological fracturesGeneralised bone disease OsteoporosisMetabolic bone disease - osteomalacia, hyperparathyroidismPaget's diseaseMyelomatosisLocalised benign bone disorder Chronic infectionSolitary bone cystFibrous cortical defectChondromaPrimary malignant bone tumours OsteosarcomaChondrosarcomaEwing's tumourBibliographyForward D,  Morgan C G.  Diagnosis and immediate care of open fractures.  Hosp Med 2002;  63:  298-299.<br /> <br />Delayed and non-union<br />Union and consolidationFracture repair is a continuous processThe stages into which it is divided is an arbitrary processUnion should be regarded as incomplete repairPresent when an ensheathing callus is formedFracture site is still tenderMinimal movement at the fracture site is presentConsolidation should be regarded as complete repairRadiologically fracture line is obliteratedFracture site is non-tenderNo movement is possible at the fracture siteTime to union and consolidation depends on many factors including AgeFracture typeBlood supplyFractures heal quicker in childrenUpper limb fractures heal quicker than lower limbSpiral fractures heal quicker than transverse fracturesDelayed unionDelayed union is the prolongation of time to fracture unionNo definite timetable to define delayed union existsDelayed union is due to Inadequate blood supplyInfectionIncorrect splintageIntact fellow boneClinical featuresFracture site remains tenderBone may still move when stressedOn x-ray the fracture remains visibleMay be little callus formation or periosteal reactionManagementUsually continue previous treatment of fractureMay need to replace cast or reduce tractionFunctional bracing promotes bone unionFor tibial fracture may need to excise portion of fibulaIt union is delayed more than 6 months may need to consider Internal fixationBone graftingNon-unionNon-union has many causes including: Bone or soft tissue lossSoft tissue interpositionPoor blood supplyInfectionPathological fracturePoor splintage or fixationFracture distractionClinical featuresMovement remains present at the fracture siteMovement is often relatively painlessRadiologically the fracture is still visibleBone ends on either side of the fracture are sclerosedNon-union can be either hypertrophic or atrophicManagementNon-union is occasionally symptomlessAsymptomatic non-union may not require active treatment except splintageFor hypertrophic non-union internal or external fixation may lead to unionFor atrophic non-union bone grafting is often requiredMyositis ossificansDue to heterotopic ossification with an muscleElbow is the commonest joint involvedSeen following dislocation or muscle ruptureAlso occurs without injury in unconscious or paraplegic patientsPain is an early symptomStiffness and reduced range of movement are late featuresIn the late stage of the process a bony lump is often palpableEarly x-ray shows fluffy calcificationLate x-ray shows none formationManagementRest joint in position of functionOnce pain settles begin mobilisationAfter several months consider excision of bony massAvascular necrosisCertain bony regions are prone to bone ischaemia and necrosisThese areas include Head of femurProximal scaphoidBody of the talusInterruption of blood supply by a fracture results in avascular necrosisPain due to fracture non-union is the main symptomX-ray shows increase in bone densityManagementSurgical intervention required if there is a reduction in functionMay require arthrodesis or arthroplastyBone graftingLoss of bone can occur in several situations including TraumaTumoursMan-made prosthesesBone grafts can be used to fill the defectClassification of bone graftsAutograft = bone from the same individualAllograft = bone from another individual of the same speciesXenograft = bone from another speciesAutograftsAutogenous bone is the best graft materialMay only be available in a limited amountAlso not suitable for significant load bearingCancellous bone can be used to fill cavity defectsCortical bone can be used to provide structural supportForms scaffold into which osteoblasts and osteoclasts can growOsteoblast differentiation leads graft resorptionStimulates local bone growth by the process of osteoinductionRemodelling occurs as load is applied to the graftHarvesting of bone graftsBone can be harvested from the following sites Iliac crestProximal tibiaDistal radiusIliac crest is the most common but its use is associated with significant morbidityCortico-cancellous grafts are harvested as stripsCancellous bone can be taken from the inner or outer tableVascularised graftsSegments of bone can be transplanted as free vascularised graftsLocal rotational bone grafts may also be usedBlood supply to the graft is maintainedTechnically difficult to performResults are unpredictableAllograftsAllograft bone is more plentifulCan be harvested from living donors or cadaversDonor site morbidity is eliminatedCadaveric bone and femoral heads are stored in tissue banksBone is frozen at -20 to -86 degreesFreeze drying and storage at room temperature is occasionally usedUsed in reconstruction after: Tumour resectionRevision hip surgeryInfection is the major concern with the used of allograftsBacterial contamination may occur, especially with cadaveric graftsCan be eliminated with irradiation of the graftViral contamination with hepatitis of HIV is a concernBone should be kept in quarantine and living donors tested 90 days post surgeryAllograft bone is available as: Morsellised bone for impaction graftingStrut grafts to cover cortical boneMassive allografts to replace significant proportions of native boneBone substitutesInterest exists in artificial bone substitutesWould eliminate supply and infection problems associated with auto and allograftsPossible bone substitutes include: Calcium triphosphateHydroxyapatiteCalcium carbonateGlass-based cementsMost bone substitutes are brittleUnable to withstand significant load bearing Common and eponymous fracturesManagement of common fracturesClavicle Rest in sling or collar and cuff for two weeksActive shoulder movement started after first weekFemur - trochanteric region Fixation with dynamic hip screwEarly postoperative mobilisation is importantFemur - shaft Operative reduction usually requiredInternal fixation achieved with intramedullary nailFibula - shaft Protect limb in below knee walking cast for 3 weeksHumerus - neck In elderly disregard fracture and concentrate on shoulder movementIf fracture impacted begin mobilisation earlyHumerus - supracondylar region Reduce by manipulation under anaesthesiaPlace in full length cast with elbow at 90 degreesObserve carefully distal circulationOlecranon Undisplaced fractures need immobilisation in right angled arm plasterDisplaced and comminuted fractures require internal fixationInternal fixation can be achieved with tension band wiresPatella Undisplaced fractures should be protected in full leg cast for 3 weeksDisplaced fractures require internal fixation with screw or tension band wireComminuted fractures may require patellectomyPhalanges Undisplaced fractures should be strapped for 2-3 weeksDisplaced fractures may require manipulation and external fixationRadius - head If minimal displacement place in collar and cuff for 3 weeksIf severely comminuted excise radial headScaphoid Immobilise in Scaphoid cast until fracture unitedIf delayed union consider fixation with Herbert screw  Tibia - shaft Undisplaced fracture require immobilisation in full leg castDisplaced fractures may require internal fixation with intramedullary nailEponymous fracturesBennett's fracture Intra-articular fracture of the base of the first metacarpalUsually requires open reduction and internal screw fixationColle's fractures Fracture of the distal radius with dorsal and radial angulation and backward displacementClosed reduction should be followed by immobilisation in forearm cast for 6 weeksPosition should be checked by radiography one week after injuryGaleazzi fracture Fracture of the radial shaft with dislocation of the inferior radio-ulnar jointUsually requires internal fixation of the radiusMonteggia fracture Fracture of the proximal ulna with anterior dislocation of the radial headUsually requires internal fixation of the ulnaRadial head should be reduced or excisedPott's fracture A general term applied to ankle fracture'sSmith's fracture Fracture of the distal radius with anterior displacement of the distal fragmentClosed reduction may be successfulIf fails requires open reduction and fixation with a buttress plateBibliographyKrasin E,  Goldwirth M,  Gold A,  Goodwin D R.  Review of the current methods in the diagnosis and treatment of scaphoid fractures.  Postgrad Med J 2001;  77:  235-237. Hip fracturesRefers to fractures of the proximal femur60,000 hip fractures occur per year in the United KingdomMean age of patient is 80 yearsIncidence increases exponentially above the age of 65 yearsMain risk factors are female sex and osteoporosisClinical featuresUsually occurs following a fallPatient usually has other significant co-morbidityMain symptom is hip pain and inability to weight bearThe leg is shortened and externally rotatedDiagnosis confirmed by AP and lateral x-rayImpacted undisplaced fractures may present diagnostic difficultyGarden classificationStage 1 - incomplete or impacted fractureStage 2 - complete fracture with no displacementStage 3 - complete fracture with partial displacementStage 4 - complete fracture with full displacement'Practical' classificationFractures best separated into intracapsular and extracapsular fracturesIntracapsular fractures reduce the blood supply to femoral headAt high risk of delayed union, non-union or avascular necrosisIf head is to be preserved they need anatomical reductionExtracapsular fractures do not interfere with femoral head blood supplyDo not require anatomical reductionManagementAll patients require surgery if fit for an operationEarly mobilisation is associated with improved long-term prognosisIdeally surgery should be performed within 24 hoursPostoperative rehabilitation should be by a multidisciplinary teamIntracapsular fracturesThe two treatment options are: Reduction and internal fixationFemoral head replacementInternal fixation indicated in: Undisplaced fracturesDisplaced fractures in young patients (<70 years)Usually achieved with the use of three cancellous screwsComplications include non-union and avascular necrosis Femoral head replacement indicated in: Displaced fracturesPathological fracturesOptions available include: Cemented Thompson prosthesisUncemented Austin Moore prosthesisBipolar prosthesisTotal hip replacementComplications include dislocation, loosening and peri-prosthetic femoral fractureExtracapsular fracturesUsually repaired with a dynamic hip screwAllows impaction and stabilisation of fracturePrognosis related to the number of bone fragments90% of fractures proceed to uncomplicated fracture unionPrognosis40% of patients with a hip fracture die within a year50% of survivors are less independent than before the injuryMost morbidity is related to coexisting medical conditionsBibliographyLane J M,  Russell L,  Khan S N.  Osteoporosis.  Clin Orthop 2000;  372:  139-150.Parker M J,  Handoll H H.  Conservative versus operative treatment of extracapsular hip fractures.  Cochrane Database Syst Rev 2000 (2):  CD000337.Parker M.  Diagnosis and immediate care of fractured neck of femur.  Hosp Med 2002;  63:  42-43.Parker M,  Johansen A.  Hip fracture.  BMJ 2006:  333:  27-30.Schmidt A H,  Swiontkowski M F.  Femoral neck fractures.  Orthop Clin North Am 2002;  33:  97-111.  Paediatric fracturesSalter and Harris classification of epiphyseal injuriesSalter and Harris fractures occur through the growth plateTherefore they are unique to childrenClassified according to degree of involvement of physis, metaphysis and epiphysisClassification is important as it Determines treatmentDetermines prognosisType I - Epiphyseal slip - no fractureType II - Fracture through epiphyseal plate with proximal fragmentType III - Fracture through epiphysis extending into the epiphyseal plateType IV - Fracture through both epiphysis and shaft crossing the epiphyseal plateType V - Crush injury causing obliteration of the growth plateManagementIn general the following statements hold true for Slater and Harris Fractures Type I involve growth plate but growth is rarely disturbedType II fractures are the most commonType III fractures involve the joint and can result in chronic morbidityType III fractures often require surgical treatmentType IV fractures can also result in chronic morbidityType V fractures are difficult diagnose and can result in limb shorteningBibliographyPatterson J M.  Children's fractures 'not to be missed'.  Hosp Med 2002;  63:  426-428 <br /> The knee<br />AnatomyThe knee joint has two componentArticulations between the femoral and tibial condylesPatellofemoral jointIt is stabilised by the knee ligamentsAnterior cruciate ligament prevents anterior translation of the tibiaPosterior cruciate ligament prevents posterior translation if the tibiaMedial collateral ligament provides valgus stabilityLateral collateral ligament provides varus stabilityPosteromedial capsule resists external rotationPosterolateral capsule resists internal rotationThe menisci are semi-lunar shaped fibrocartilagesThey increase joint congruence and distribute load across the jointThey are avascular and heal poorly beyond the peripheriesKnee movements are complex It has dynamic stabilityThe joint is not a simple hingeClinical featuresThe history of any injury suggest which structure may be involvedDirect varus or valgus forces injure the collateral ligamentsIndirect forces injure the cruciate ligaments and menisciTwisting in flexion can damage the menisciImmediate swelling suggests a haemarthrosisAn audible 'pop' can occur with a cruciate injuryMechanical locking is characteristic of a meniscus injuryExamination should look alignment, wasting, swelling and bruisingLocalised tenderness should be elicitedThe range of passive and active movement should be assessedProvocation testsAnterior and posterior draw testLachman's testPivot shift testMcMurray's testInvestigationPlain radiographs may show avulsion fractures and exclude fractures around the kneeMRI is the most useful imaging modalityShows extent of soft tissue injuriesMeniscal injuriesMay be traumatic or degenerativeClassified by position and shapeAcute peripheral injuries can be repairedChronic central injuries often require arthroscopic partial menisectomyTotal menisectomy risk later degenerative changes and should be avoidedAnterior cruciate injuriesAcute injuries result in a haemarthrosisResults in variable amounts of pain and instabilityOften associated with medial meniscal tearTreatment options depend on expectation and life-style of patientOptions include:PhysiotherapyEarly or later cruciate ligament reconstructionThe most popular grafts are:Hamstring graftBone-patella tendon-bone graftPosterior cruciate injuriesUsually occurs following dashboard injuriesResults in knee instabilityTreatment is controversial due to less reliable surgical resultsSurgical reconstruction reserved for multiple ligament injuriesCollateral ligament injuriesMedial collateral ligament injuries are more commonClinical evaluation allows injuries to be gradedGrade 1 - Local ligament tenderness - no instabilityGrade 2 - Unstable at 20 degrees of flexion - stable in extensionGrade 3 - Unstable in flexion and extensionMRI is useful in evaluating extent of injuryGrade 1 injuries require analgesia and early mobilisationGrade 2 injuries require a hinged knee braceGrade 3 injuries require surgical repairBibliographyCook J L.  The current status of treatment for large meniscal defects.  Clin Orth Relat Res 2005:  435:  88-95Dowd G S.  Reconstruction of the posterior cruciate ligament. Indication and results.  J Bone Joint Surg Br 2004;  86:  480-491.Koon D,  Bassett F.  Anterior cruciate ligament rupture.  South Med J 2004;  97:  755-756.Smith G D,  Knutson G,  Richardson J B.  A clinical review of cartilage repair techniques.  J Bone Joint Surg Br 2005;  87:  445-449.<br />  <br />The shoulder<br />Anterior dislocationShoulder is one of the commonest joints to dislocate due to:Shallowness of glenohumeral jointRange of movementLigamentous laxity or glenoid dysplasiaVulnerability of jointDislocation usually caused by fall on handExternal rotation in abduction levers the head of the humerus out of the glenoid socketJoint capsule is often tornGlenoid labrum may be avulsed (Bankart lesion)Clinical featuresBimodal age distributionFirst peak occurs in young adult men after significant traumaSecond peak occurs in elderly women after less violencePain is often severeArm usually held in abduction and externally rotatedAll movement is restrictedLateral outline of shoulder is flattenedBulge may be felt below clavicleX-ray shows overlapping of humeral head and glenoid fossaHead of humerus seen below and medial to the jointX-ray is mandatory to exclude an humeral fractureTreatmentNumerous methods of reduction have been describedMay be reduced by simple traction / countertraction in slight abductionKocher's methodElbow flexed to 90 degreesArm slowly rotated laterally to 75 degreesElbow lifted forward and arm rotated mediallyX-ray taken to confirm reduction and exclude fractureArm rested in sling for 2-3 weeksComplicationsAxillary nerve injuryVascular injuryFracture-dislocationShoulder stiffnessUnreduced dislocationRecurrent dislocationPosterior dislocationPosterior dislocation is rareAccounts for less than 2% of shoulder dislocationsDue to indirect forces resulting in internal rotation and adductionSeen following convulsions or electric shocksInjury is easily missedAP x-ray may appear 'normal'If any doubt regarding diagnosis then CT is usefulBibliographyCicak N.  Posterior dislocation of the shoulder.  J Bone Joint Surg Br 2004;  86:  324-332.Cutts S,  Prempeh M,  Drew S.  Anterior shoulder dislocation.  Ann R Coll Surg Engl 2009;  91:  2-7Jennings S,  Cohen B.  Common injuries of the shoulder.  Hosp Med 2002;  63:  681-683<br />  <br />Peripheral nerve injuries<br />NeuropraxiaTemporary loss of function caused by minor trauma or pressureRecovery occurs within minutesAxonotmesisLoss of function due to severe ischaemiaRecovery occurs within weeksNeurotmesisLoss of function due to division of nerveNo recovery occurs unless nerve is repairedRadial nerveOften injured in radial groove of humerusMotor paralysis results in typical 'wrist drop' due to loss of: Extension of elbow, wrist, knuckles and all joints of thumbSupinator and brachioradialisSensory loss involves dorsum of 1st, 2nd and 3rd metacarpalsMay be as small as the anatomical snuffboxPicture provided by Andrew Day, Royal Sussex County Hospital, Brighton, United KingdomMedian nerveOften injured by penetrating wounds of the forearmMotor paralysis due to loss of: The pronatorsRadial flexor of the wristFlexors of all of the proximal interphalangeal jointsFlexors of the terminal joint of the thumb, index and middle fingerAbductor and opponens pollicisSensory loss over thumb, index, middle and half of ring fingersUlnar nerveOften injured with fractures of the medial epicondyle of the elbowMotor paralysis results in 'claw hand' and hypothenar wasting due to loss of: Ulnar flexor of the wristFlexors of the terminal phalanx of the ring and little fingerMuscles of the hypothenar eminenceAdductor pollicisPalmar brevisAll the interossei and the medial two lumbricalsSensory loss over little and half of ring fingerPicture provided by Loh Yin, International Medical University, Jolam Rasah. MalaysiaPicture provided by Alan Parbhoo, Barts and Royal London Hospital, United KingdomBrachial plexus injuriesUsually occur in two situations Difficult vaginal deliveries associated with the use of forcepsTraction during a fall or road traffic accidentErb's palsyDue to damage to the upper nerve rootsUsually involves C5, C6, C7Abductors and external rotators of the shoulder are affectedLoss of finger extensionSensation is intactKlumpke's palsyDue to damage to the lower nerve rootsUsually involves C8, T1All finger muscles are paralysedLoss of sensationOften associated with unilateral Horner's syndromeBibliographyLeffert R D.  Nerve lesions about the shoulder.  Orthop Clin North Am 2000;  31:  331-345.Terzis J K,  Vekris M D,  Soucacos P N.  Brachial plexus root avulsions.  World J Surg 2001;  25:  1049-1061<br />  Upper limb disorders<br />Painful shoulderAnatomyShoulder joint is made up of a complex of five joints Sternoclavicular jointAcromioclavicular jointSubacromial spaceGlenohumeral jointScapulothoracic jointGlenohumeral joint is stabilised by a number of musclesThese include deltoid muscle and the rotator cuff musclesThe rotator cuff is made up of: SupraspinatusInfraspinatusTeres minorSubscapularisClinical featuresCauses of shoulder pain include Impingement syndromesRotator cuff tearsFrozen shoulderCalcific tendonitisRotator cuff impingementDue to abrasion of rotator cuff muscles on coracoacromial archImpingement is usually reversibleMay lead to rotator cuff tears or degenerative changes in glenohumeral jointCauses a painful arc between 60 and 120 degrees of abductionFull range of passive movement is possiblePlain radiographs may be normalTreatment includedSubacromial steroid injectionSubacromial decompressionRotator cuff tearsUsually occur in middle age and elderlyResult from either chronic impingement or acute injuryUsually present with pain and weaknessSupraspinatus and Infraspinatus are usually involvedResult in weakness if abduction and resisted external rotationUS or MRI should be obtained to:Confirm the clinical diagnosisAssess the size of the tearAssess the extent of retractionTreatment options includeConservative managementOpen or arthroscopic repairFrozen shoulderDue to chronic inflammation and fibrosis of subsynovial layerOften occurs after minor trauma or period of immobilityReduces range of active and passive movement, particularly loss of external rotationAssociated with severe painRecovery may be prolongedTreatment options includeNSAIDsPhysiotherapyManipulation under anaestheticCalcific tendonitisDue to deposition of calcium salts in supraspinatus tendonProduces severe pain over anterolateral aspect of shoulderFull range of passive movementPain is aggravated by shoulder movementCalcium deposits on x-ray are diagnosticTreatment options includeNSAIDsPhysiotherapySubacromial injectionSubacromial decompression and removal of calcium depositsLateral epicondylitisOften referred to as tennis elbowDue to inflammation at the origin of the wrist and finger extensorsIts is an enthesopathy of the lateral epicondyleClinical featuresOccurs between 30 and 50 years of ageMen and women are equally affected75% experience symptoms in their dominant armCauses pain over the lateral epicondyle radiating to the forearmTenderness is usually maximum 5 mm distal to the insertion of the tendonResisted wrist extension increases the painPlain x-ray may show calcification in the soft tissuesManagementNon surgical management involves RestNon-steroidal anti-inflammatory medicationSteroid injectionSurgical treatment if no improvement with 6 months conservative treatmentInvolves division and reattachment of the tendon85% notice a dramatic improvement in symptomsMedial epicondylitisOften referred to as golfer's elbowIt is less common than lateral epicondylitisOccurs in same age groupis is an enthesopathy of the pronator teres and flexor carpi radialis tendonCharacterised by pain over the medial aspect of the elbowPain is exacerbated by wrist flexionTenderness is distal to medial epicondyleManagement is similar to lateral epicondylitisUlnar nerve entrapment at the elbowUlnar nerve runs behind medial epicondyle at the elbowRuns in a tunnel formed by aponeurosis between tow head of flexor carpi ulnarisAponeurosis is slack in elbow extensionBecomes tight in elbow flexionDisorders of the elbow joint can result in nerve compressionSymptoms are often worse when elbow is flexedClinical featuresPain and paraesthesia in the ring and little fingerWeakness of grasp and gripLoss of manual dexterityWasting of the intrinsic muscles of the handManagementNight splints to reduce elbow flexion may improve symptomsSurgical options include Ulnar nerve decompressionMedial epicondylectomyAnterior transpositionBibliographyBuchbinder R,  Green S,  Bell S et al.  Surgery for lateral elbow pain.  Cochrane Database Syst Rev 2002;  CD003524.Green S,  Buchbinder R,  Barnsley L et al.  Non-steroidal anti-inflammatory drugs (NSAIDs) for treating lateral elbow pain in adults.  Cochrane Database Syst Rev 2002;  CD003686.Smidt N,  Assendelft W J,  van der Windt D A et al. Corticosteroids for lateral epicondylitis:  a systemic review.  Pain 2002:  96:  23-40.<br />  <br />Common disorders of the hand<br />Carpal tunnel syndromeCarpal tunnel formed by flexor retinaculum stretching across carpusForms a tight tunnel through which passes Long flexors to fingers and thumbMedian nerveSwelling within the tunnel causes nerve compression and ischaemiaCarpal tunnel syndrome affects 3% of women and 2% of men30% cases due to underlying medical conditionCausesIdiopathicHormonal - pregnancy / menopauseRheumatoid arthritisHypothyroidismDiabetesClinical featuresUsually presents in middle ageFemale : male ratio is 8:1Pain and paraesthesia in distribution of median nerveSymptoms are often worse at nightSigns are fewTapping over carpal tunnel can reproduce symptoms (Tinel's sign)Flexion of wrist for 60 seconds reproduces symptoms (Phalen's sign)Thenar wasting and loss of 2-point discrimination are late featuresDiagnosis confirmed by electomyelogramShows slowed nerve conduction across the wristManagementTreat underlying associated medical problemsNocturnal symptoms can often be controlled with night splintsSteroid injections may produce temporary symptomatic reliefTroublesome symptoms require division of flexor retinaculumMay be performed endoscopically70-90% are symptom-free following surgeryde Quervain's diseaseAlso known as stenosing tenovaginitisDue to inflammation and thickening of tendon sheaths of Extensor pollicis brevisAbductor pollicis longusOccurs where both tendons cross the distal radiusClinical featuresUsually presents in middle agePain noted over radial aspect of wristOften occurs after repetitive activityTendon sheath is thickened and tender over the radial styloidPain often worsened by abduction of thumb against resistancePassive abduction across palm often causes pain (=Finkelstein's test)ManagementSymptoms can often be improved with steroid injections into tendon sheathPersistent symptoms require surgeryTendon sheath should be split avoiding the dorsal sensory branch of radial nerveDupuytren's contractureFibroproliferative disease of the palmar fasciaFirst described in 1614Detailed anatomical study presented by Dupuytren in 1831Aetiology unclearPossibly inherited as an autosomal dominant condition with limited penetranceOccasionally associated with plantar fasciitis and Peyronie's diseaseMore common in northern EuropeMale to female ratio 4:1Affects 5% men older than 50 yearsClinical featuresThickening of palmar fascia with nodule formationFlexion contracture at MCPJ and PIPJUsually affects ring and little fingerIn late stage of the disease cords develop proximal to the nodules65% cases are bilateralRisk factorsDiabetes mellitusAlcohol excessHIV infectionEpilepsyTraumaManual labourManagementExcision or incision of the palmar fasciaOptions include fasciotomy, fasciectomy or dermofasciectomyConsider surgery if: MCP contracture is greater than 30 degreesThere is functional disabilityNeed intensive postoperative physiotherapyApproximately 20% patients develop complicationsRecurrence rate is approximately 50%GanglionsCommonest cause of swellings around the hand and wristCystic lesions arising from either the joint capsule of tendon sheathAetiology is unknownMore common in womenUsually occur between 20 and 40 yrs of age70% of ganglions occur around the wristClinical featuresMost present as smooth swellings 2-4 cm in diameterMost are painlessPain can occur due to compression of adjacent neurovascular structuresManagementIf ganglion is asymptomatic no specific treatment is requiredThe hold treatment of 'hitting with the family bible' should be condemnedAspiration can be attempted but outcome is poorExcision is the treatment of choiceLesion should be explored down to joint capsule or tendon sheathInadequate surgery results in a high recurrence rateBibliographyEngland J D.  Entrapment neuropathies.  Cur Opin Neurol 1999;  12:  597-602.Frank P L.  An update on Dupuytren's contracture.  Hosp Med 2001;  62:  6780681.Gerritsen A A M,  Uitehaag B M J,  van Geldere D,  Scholten R J P M,  de Vet H C W,  Bouter L M.  Systematic review of randomised clinical trials of surgical treatment for carpal tunnel syndrome.  Br J Surg 2001;  88:  1285-1295.Gudmundsson K G,  Jonsson T,  Amgrimsson R.  Guillamme Dupuytren and finger contractures.  Lancet 2003;  362:  165-168.Hart M G,  Hooper G.  Clinical association of Dupuytren's disease.  Postgrad Med J 2005;  81:  425-428.Katz J N,  Simmons B P.  Carpel tunnel syndrome.  New Eng J Med 2002;  346:  1807-1812.Kloen P.  New insights in the development of Dupuytren's contracture:  a review.  Br J Plast Surg 1999;  52:  629-635.Marshall S,  Tardif G,  Ashworth N.  Local corticosteroid injection for carpal tunnel syndrome.  Cochrane Database Syst Rev 2000:  4:  CD001554.Preston D C.  Distal median neuropathies.  Neurol Clin 1999;  17:  407-424.Saar J D,  Grothaus P C.  Dupuytren's disease:  an overview.  Plast Reconstr Surg 2000;  106:  125-134Sen D,  Chhaya S,  Morris V H.  Carpel tunnel syndrome.  Hosp Med 2002;  63:  392-395.Stenback G.  The carpal tunnel syndrome.  J Emerg Med 1999;  17:  519-253.Tennent T D,  Goddard N J.  Carpal tunnel decompression: open vs. endoscopic.  Br J Hosp Med 1997;  58:  551-554.Thornburg L E.  Ganglions of the hand and wrist. J Am Acad Orthop Surg 1999;  7:  231-238.Thurston A J.  Dupuytren's disease.  J Bone Joint Surg [Br] 2003;  85:  496-505.<br />  <br />Lower limb disorders<br />Achilles tendon ruptureAnatomyAchilles tendon formed from combined tendons of soleus and gastrocnemiusApproximately 15 cm in lengthOften transmits forces ten time body weightTendon is enclosed with a paratenon rather than synovial sheathBlood supply is tenuous 3-6 cm proximal to calcaneal insertionPathologyRupture usually occurs in fit, active menCommonest age is 20 to 40 yearsRupture occurs within tendonUsually occurs 3-4 cm proximal to insertionRupture is usually caused by sudden force to dorsiflexed footPicture provided by J M Gauer, Kantonsspital Schaffhausen, SwitzerlandClinical featuresUsually no preceding pain or history of traumaPresents with snapping sensationFollowed by acute pain over the tendonPlantar flexion of the foot is reducedOften a gap is palpable at the site of the ruptureWith the patient prone, plantar flexion on calf compression is abolished (Thompson's test)ManagementAim is to restore continuity of the tendonCan be achieved with surgical or non-operative approachesSurgery is probably more appropriate in fit, active individualsNon-operative management is probably more appropriate in elderly or unfitSurgeryCan be performed by either an open or percutaneous techniqueDuring open surgery Incision is made over the tendonParatenon is openedEnds of tendon are apposed using a non-absorbable sutureRepair performed using either a Kessler or Bunnell TechniqueParatenon is closed over repairSame can be achieved using a percutaneous techniquePatient requires an equinus splint for 2 weeksThe ankle is then gradually dorsiflexedRe-rupture rate is less than 5%Picture provided by J M Gauer, Kantonsspital Schaffhausen, SwitzerlandNon-operative approachPatient is maintained in short-leg equinus cast for at least 6 weeksRe-rupture rate as high as 40% have been recordedBibliographyCoull R,  Williams R L.  Common injuries of the foot and ankle.  Hosp Med 2002;  63:  624-625.McClelland D,  Maffulli N.  Percutaneous repair of ruptured Achilles tendon.  J R Coll Surg Ed 2002;  47: 613-618.Maffulli N.  Rupture of the Achilles tendon. J Bone Joint Surg Am 1999;  81:  1019-1036.<br /> Common problems of the foot<br />Hallux valgusCommonest deformity of the footResults in excessive valgus angulation of the big toeOnly seen in populations that wear shoesSplaying of the forefoot with varus angulation of the first metatarsal predisposesThe anatomical deformity consists of: Increased forefoot widthLateral deviation of the halluxProminence of the first metatarsal headAs deformity increases long tendons of the hallux are shifted laterallyClinical featuresMore common in womenOften bilateralSymptoms result from A bursa over metatarsal head = bunionHammer toesMetatarsalgiaOsteoarthritis of the first MTPJDiagnosis can be confirmed on x-rayIntermetatarsal angle should be less than 20 degreesHallux angle should be less than 15 degreesPicture provided by Ronan Caspi, Tel Aviv, IsraelManagementSurgical management should be considered if patient is symptomaticOptions include: First metatarsal osteotomyExostectomy and capsulorraphyExcision of proximal one-third of proximal phalanx (Keller operation)ArthrodesisHallux rigidusDue to osteoarthritis of first MTPJAffects men more often than womenResults in pain on walking, especially on rough groundThere is no valgus deviation of the halluxMTPJ is swollen and enlargedDorsiflexion of the MTPJ is reducedA rocker-soled shoe may improve symptomsIf significant symptoms occur then surgery may be requiredOptions include: Extension osteotomyCheilectomyArthroplastyArthrodesisClaw toesResults from: Flexion of the interphalangeal jointsHyperextension of the metatarsophalangeal jointsOften idiopathicCan be associated with: Rheumatoid arthritisPoliomyelitisPeroneal muscular atrophyClinical featuresPain in the forefoot = metatarsalgiaSymptoms are usually bilateralWalking may be restrictedPainful callosities on the dorsum of the toes or under the metatarsal headsPicture provided by Ronan Caspi, Tel Aviv, IsraelManagementIf the toes can be passively straightened than a 'metatarsal bar' may helpSpecial footwear may reduce symptomsIf non-operative management fails then surgical options include Interphalangeal arthrodesisJoint excisionMetatarsal osteotomyDigital amputationPlantar fasciitisSelf-limiting condition that occurs in middle agePresents with intermittent inferior heal painUsually unilateral but 15% cases are bilateralPain often worse early in the morningExamination show tenderness over the medial plantar aspect of the calcaneal tuberosity50% have heel spur on plain x-rayDifferential diagnosis includes: Reiter's syndromeEntrapment neuropathyCalcaneal stress fractureManagement should involve the use of Supportive heel pads and other orthotic devicesNon-steroidal anti-inflammatory drugsSurgery is rarely indicatedMorton's neuromaPainful forefoot disorderCaused by thickening and fibrosis of interdigital nervesAetiology is unknownUsually affects second or third web spaceCauses plantar pain at level of metatarsal headsMay be associated with distal sensory lossDifferential diagnosis includesMetatarsalgiaMetatarsophalangeal synovitisStress fractureFrieberg's infarctionInitial management is non-operativeSurgical excision of the neuroma should be considered if symptoms fail to settleBibliographyCoughlin M J.  Hallux valgus.  J Bone Joint Surg Am 1996;  78; 932-936Ferrari J,  Higgins J P,  Williams R L.  Interventions for treating hallux valgus (abductovalgus) and bunions.  Cochrane Database Syst Rev 2000;  CD000964.Singh S K,  Loli J P,  Chiodo C P.  The surgical treatment of Morton's neuroma.  Current Orthopaedics 2005:  19:  379-384<br />  <br />Degenerative and rheumatoid arthritis <br />OsteoarthritisOsteoarthritis is the commonest condition affecting synovial jointsNo longer considered simple joint 'wear and tear'Change in cartilaginous matrix is probably importantPrimary OA is of unknown aetiologySecondary OA is the result of congenital, infective joint disorders or traumaPathology characterised by: Loss of hyaline cartilageSubchondral bone sclerosisSubchondral cyst formationOsteophyte formationSeveral patterns of joint involvement recognised including: Generalised nodular OALarge joint osteoarthritisClinical featuresJoint pain - worse after exercise or at end of dayPain relieved by restLimited early morning stiffnessLimited stiffness after restBony joint swellingFew systemic featuresManagementAims of treatment are to: Reduce joint painImprove joint functionIn early stages pain can often be improved with simple analgesiaLife style modification is also importantNSAIDs can often helpIntra-articular steroids can reduce symptomsIf fails to improve with conservative measures surgery may be requiredSurgical options for degenerative joints are Arthroscopic lavage and debridementOsteotomy - alteration of joint alignmentArthroplasty - replacement of diseased jointArthrodesis - fusion of disease jointRheumatoid arthritisRheumatoid arthritis is an autoimmune inflammatory synovial diseaseAetiology if unknownWorldwide prevalence is approximately 1%Female : male ratio is 3:1Onset most often seen between 20 and 40 yearsUsually symmetrically affects multiple jointsCommonest joints affected are hand, elbow, knee and cervical spineAlso affects synovium of tendon sheathsOften part of a systemic inflammatory processMore common in those with HLA DR4 and DW4Pathologically characterised by: An inflammatory process within the synoviumJoint destruction and pannus formationPeriarticular erosionsClinical featuresJoint pain - worse during exercisePain relieved by movementProlonged early morning stiffnessProlonged stiffness after restMarked soft tissue swelling and erythemaSystemic features often presentExtra-articular manifestationsOccur in approximately 20% of patientsOcular Keratoconjunctivitis siccaEpiscleritisScleritisPulmonary Pulmonary nodulesPleural effusionFibrosing alveolitisCardiac Pericarditis / pericardial effusionValvular heart diseaseConduction defectsCutaneous Palmar erythemaRheumatoid nodulesPyoderma gangrenosumVasculitic rashes and leg ulcerationNeurological Nerve entrapmentCervical myelopathyPeripheral neuropathyMononeuritis multiplexManagementRequires a multidisciplinary approachDisease modifying drugs include: NSAIDsMethotrexate, sulphasalazine, penicillamine, goldCorticosteroidsCytotoxic drugsSpecific syndromesSeveral syndromes have been described associated with rheumatoid arthritisFelty's syndrome Rheumatoid arthritisNeutropeniaLymphadenopathySplenomegalyStill's disease Rheumatoid arthritis in childhoodRashFeverSplenomegalySjogren's syndrome Rheumatoid arthritisReduced lacrimal and salivary secretionBibliographyGrainger R,  Cicuttini F M.  Medical management of osteoarthritis of the knee and hip.  Med J Aust 2004;  180:  232-236.Gupta K B,  Duryea J,  Weissmann B N.  Radiographic evaluation of osteoarthritis.  Radiol Clin North Am 2004;  42:  1-9. Haq I,  Murphy E,  Dacre G.  Osteoarthritis.  Postgrad Med J 2003;  79:  377-383.Hunter D J,  Felson D T.  Osteoarthritis.  BMJ 2006;  332:  639-342Scott D L.  Advances in the medical management of rheumatoid arthritis.  Hosp Med 2002:  63:  294-297.Walker-Bone K,  Javaid K,  Arden N,  Cooper C.  Medical management of osteoarthritis.  Br Med J 2000;  321:  936-940.<br />  Osteoporosis<br />Osteoporosis is a systemic skeletal disease characterised by: Low bone massMicro-architectural deteriorationIt is associated with increased bone fragility and susceptibility to fracturesIt is defined as a bone mineral density less than 2.5 standard deviations below the meanEstablished osteoporosis is a low bone mineral density associated with an osteoporosis-related fracturePathophysiologyBone undergoes continuous resorption and formation10% of adult skeleton is remodelled each yearBone loss results from an imbalance between resorption and formationHuman skeleton comprises approximately 80% cortical bone20% trabecular boneOsteoporotic fractures occur at sites with more than 50% trabecular bone Vertebral bodyProximal femurDistal forearmBone loss leads to thinning of the trabecular platesThis causes a disproportionate loss of bone strengthPeak bone mass is achieved by the age of 30 yearsAfter skeletal maturity bone is lost at about 1% per yearWomen experience accelerated bone loss after the menopauseFactors associated with increased bone loss include: InactivityCigarette smokingPoor dietFamily historyEarly menopauseEndocrine disease - Cushing's syndrome, diabetes, hyperthyroidismDrugs - Steroids, thyroxine, diureticsClinical featuresOsteoporosis-related fracturesIncreased mortalityPainDeformityLoss of independenceInvestigationRadiologyDual-energy x-ray absorptionometryQuantitative CT scanningQuantitative ultrasoundBone biopsyBiochemical markers of bone turnoverPreventionOptimisation of peak bone mass ExerciseDietary calciumReduce rate of bone loss Hormonal replacement therapyModerate alcohol intakeStop smokingBibliographyChristodoulou C.  Cooper C.  What is osteoporosis?  Postgrad Med J 2003;  79:  133-138.Compston J.  Prevention and treatment of osteoporosis.  Clinical guideline and new evidence.  J R Coll Physicians Lond 2000;  34:  518-521.Eastell R.  Treatment of postmenopausal osteoporosis.  N Engl J Med 1998;  338:  736-746. Kanis J A.  Diagnosis of osteoporosis and assessment of fracture risk.  Lancet 2002;  359:  1929-1936.Theodorou S J,  Theodorou D J,  Sartoris D J.  Osteoporosis and fractures;  the size of the problem. Hosp Med 2003;  64:  87-9.<br /> Metabolic bone disease<br />Bone is composed of both cells and matrixAlso contains blood vessels, nerves and haemopoeitic systemBones cells Osteoblasts are responsible for bone formationOsteoclasts are responsible for bone resorptionSerum alkaline phosphatase reflects osteoblastic activityMatrix Has both mineralised and unmineralised componentsMineralised component is made up of hydroxyapatiteOsteoid is the unmineralised componentMade up of 90% collagen and 10% non-collagenous proteinsNon-collagenous proteins include proteoglycans and glycoproteinsCalcium homeostasis98% of bodies calcium is stored within the skeletonAt homeostasis turnover results in equal flux in and out of skeletonCalcium homeostasis is maintained by parathyroid hormone, Vitamin D3 and calcitoninParathyroid hormone84 amino acid protein produced by parathyroid glandsIncreases serum calciumIncreases renal calcium reabsorptionIncreases skeletal turnoverIncreases renal production of dihydroxy-vitamin D3CholecalciferolIs vitamin D3Under normal circumstances is produced in the skin by action of sunlight on precursorsHydroxylated in the liver to 25-hydroxy-vitamin D3Hydroxylated in kidney to 1,25 dihydroxy-vitamin D3Increases renal reabsorption of calciumIncreases gastrointestinal absorption of calciumIncreases skeletal calcium resorptionCalcitoninProduced by thyroid parafollicular C cellsReduces serum calciumInhibits bone calcium resorptionOsteomalacia and ricketsVitamin D deficiency results in incomplete osteoid mineralisationIn childhood, prior to epiphyseal closure, causes ricketsIn adults causes osteomalaciaCausesVitamin D deficiency MalabsorptionPost-gastrectomy or bowel resectionCoeliac diseaseCirrhosisRenal disease Renal tubular disorder (e.g. familial hypophosphataemic rickets)Chronic renal failureAnticonvulsant therapyTumoursClinical featuresOsteomalacia usually due to dietary deficiency in the elderly or Asian populationRickets usually due to familial hypophosphataemic ricketsRickets usually presents in early childhood with Failure to thriveValgus or varus long bone deformitiesSkull deformities = craniotabesEnlarged costochondral junctions = Rickety rosaryLateral indentation of the chest wall = Harrison's sulcusX-ray shows widened epiphyses and cupped distal metaphysisOsteomalacia presents with Bone pain and tendernessProximal myopathyTrue pathological or pseudo-fracturesX-ray shows translucent bands in medical femoral cortex, pubic ramus or scapula= Looser's zones   In osteomalacia Serum calcium and phosphate are lowAlkaline phosphatase is increasedIn familial hypophosphataemic rickets Serum calcium is normal and phosphate is lowBone biopsy would show increased unmineralised osteoidTreatmentVitamin D replacement therapyPhosphate supplements in familial hypophosphataemic ricketsBibliographyRenton P.  Radiology of rickets, osteomalacia and hyperparathyroidism.  Hosp Med 1998;  59:  399-403.<br /> Paget's disease of bone<br />Named after Sir James Paget (1814-1899)First described osteitis deformans in 1877Aetiology is unknown - possibly due to a viral infectionOften an incidental finding on x-ray in an asymptomatic patientIf symptomatic usually causes bone painClinical signs include characteristic skull and long bone deformitiesComplicationsPathological fractures - complete or incompleteNeurological effects Cranial nerve lesionsSpinal cord lesionsOsteoarthritisSarcomasCardiac failureHistological featuresOsteoclasts are enlargedIncreased bone turnover produces a mosaic pattern of lamellar boneThree phases recognised - osteolytic, mixed and scleroticRadiological featuresOsteolytic phase can produce osteoporosis circumscriptaBone softening can produce bowing, platybasia, protrusion acetabuli or greenstick fracturesMixed phase shows generalised bone enlargementSclerotic phase shows increased density, trabeculae and cortical thickeningBiochemistrySerum calcium and phosphate are usually normalSerum alkaline phosphatase is increasedUric acid increased in about 30% of patientsTreatmentNon-steroidal anti-inflammatory agents will control bone painBiphosphonates will reduced bone turnoverNeurological complications and fractures may require surgical interventionPaget's sarcomasMost osteosarcomas that develop lat in life are associated with Paget's diseaseMalignant change occurs in less than 1% patients with Paget's disease50% are osteosarcomas25% are fibrosarcomas25% are giant-cell sarcomasThe commonest site is the femurPrognosis of Paget's sarcomas is poorMedian survival is one yearOnly 5% alive at five yearsBibliographyKeen R W.  The current status of Paget's disease of bone.  Hosp Med 2003;  64:  230-232.Ooi C G,  Fraser W D.  Paget's disease of bone.  Postgrad Med J 1997;  73:  69-74.<br /> Hip replacement surgery <br />Operation developed by Sir John Charnley in 1960sMore than 50,000 hip replacements are performed each year in United KingdomOver one million hips have been replaced worldwideOver 100 different types of prosthesis have been usedThe 'gold standard' is the Charnley cemented prosthesisPrinciple componentsAcetabular componentUsually made of high density polyethyleneBiocompatible, low coefficient of friction, low rate of wearCeramic acetabular component have improved surface propertiesAre expensive and have tendency to brittle failureMetal cups are obsolete due to high friction, loosening and wearFemoral componentUsually made of stainless steel, titanium or cobalt chrome alloyResistant to corrosion with high enduranceImproved longevity seen with small femoral headPolymethylmethacrylate cementActs as a filling agent without adhesive propertiesMacrolocking occurs with cement in drilled holesMicrolocking occurs with cement in interstices of cancellous boneProduces an exothermic reaction during preparationAddition of barium weakens the cementAntibiotic impregnation may increase resistance to infectionRecently uncemented prostheses have been developedRequire more exacting insertion techniqueAnchored by interference fit achieved by porous surface or hydroxyapatite coatingUncemented prostheses have a tendency early failureIndicationsOsteoarthritisRheumatoid arthritisStill's diseaseAnkylosing spondylitisCongenital dysplastic or dislocated hipsPaget's diseaseTrauma or avascular necrosisSeptic arthritisContraindicationsUncontrolled medical problemsSkeletal immaturityActive infectionNeuropathic jointProgressive neurological diseaseMuscle weaknessAims of surgeryPatients should have significant pain, functional disturbance and failed conservative therapyThe principle aims of surgery are: To reduce joint painImprove joint functionOperative techniqueAvoid operation in patients with a septic focusThorough skin preparation with sterile adhesive plastic drapesOperating team should wear two pairs of glovesBody exhaust suites may be wornLaminar air flow should be provided in operative fieldAntibiotic prophylaxis should be givenSpecific complicationsNeurovascular injuriesLeg length discrepancyDislocationInfectionAseptic looseningImplant wear and failureHeterotopic ossificationFemoral fracturesTrochanteric non-unionAbductor mechanism weaknessOutcomeOutcome is affected by many factors including Type of implant usedUnderlying diagnosisSex of patientCement typeCementing techniqueSurgical approachJoint resurfacingOutcome of joint replacement surgery in less predictable in Younger patientsThose with active life styleMetal on metal hip resurfacing developed for use in younger patientsHead of femur preserved which is developed into chamfered cylinderMetal head is cemented in placeMetal cup is placed in acetabulumCompared to THR, has lower risk of complicationsLower risk of dislocationLess bone lossLower risk of component loosingShort-term results are very encouragingLong-term outcome unclearBibliographyClarke I C,  Donaldson T,  Bowsher J G et al.  Current concepts of metal-on-metal hip resurfacing.  Orth Clin North Am 2005;  36:  143-162.Grigoris P,  Roberts P,  Pabousis K et al.  The evolution of hip resurfacing arthroplasty.  Orth Clin North Am 2005;  36:  125-134. Latham J,   Treacy R B C,  Shetty V D,  Villar R N.  To resurface or replace the hip in the under 65-year old.  Ann R Coll Surg Engl 2006;  88:  349-353Salah K J,  Kassim R,  Yoon P,  Vorlicky L N.  Complications of total hip arthroplasty.  Am J Orthop 2002;  31:  485-488. <br />  Infected joint replacement<br />Over 100,000 knee and hip replacements are performed in the UK each yearMost are carried out with few complicationsInfections is an uncommon but devastating complicationOccurs in approximately 1% casesResults in major morbidity and considerable costRisk can be reduced by: Excluding patients who have active infectionAntibiotic prophylaxisCareful theatre techniqueMicrobiologyCommonest organisms identified are: Coagulase-negative staphylococcus (45%)Staph. aureus (35%)Streptococci (10%)Gram-negative bacteria (<5%)Early infection results form intraoperative contaminationLate infection usually results from haematogenous spreadBacteria adhere to prosthetic material and produce a biofilmBiofilm isolates the bacteria from host defences and antibioticsSignificant infection can result from small bacterial inoculumA low-grade inflammatory process then occursThis leads to bone erosion and loss of bone stockClinical featuresAcute infection presents with sign of a wound infectionA purulent discharge from the wound is often presentChronic infection presents more insidiouslyPain is often the prominent symptomThe diagnosis of chronic infection can be difficultInvestigationThe following investigations should be considered Microbial cultureInflammatory markersPlain radiographyBone scanHistologyMolecular methodsDiagnosis depend on identification of bacteria from fluid around jointManagementAntibiotics should be started once diagnosis is consideredRarely eradicate establish infectionAntibiotic choice should be based on culture resultsIf cultures are negative or unavailable then vancomycin is the organism of choiceSurgeryIn acute infection joint debridement and washout may be appropriateIn chronic infection with a loose joint, implant should be removedRevision surgery can be performed as a one-stage or two-stage procedureIf insertion of new prosthesis is impossible consider: Excision arthroplastyJoint fusionComplications following revision joint surgery include: Massive bone lossPeriprosthetic fractureRecurrence of infectionBibliographyGillespie W J.  prevention and management of infection after total joint replacement.  Clin Infect Dis 1997;  25:  1310-1317.Nelson C L.  Primary and delayed exchange for infected total knee arthroplasty.  Am J Knee Surg 2001:  14;  60-64.Kaltas D S.  Infection after total hips arthroplasty.  Ann R Coll Surg Engl 2004;  86:  267-271.<br /> Acute osteomyelitis<br />Acute osteomyelitis usually occurs in childrenUsually a haematogenous infection from distant focusOrganisms responsible include: Staph. aureusStrep. pyogenesH. influenzaeGram-negative organismsSalmonella infections are often seen in those with sickle-cell anaemiaInfection usually occurs in metaphysis of long bonesPathologyAcute inflammation results in raised intraosseous pressure and intravascular thrombosisSuppuration produces a subperiosteal abscess that may discharge into soft tissuesSpread of infection into epiphysis can result in joint infectionWithin days bone death can occurFragments of dead bone become separated in medullary canal (sequestrum)New bone forms below stripped periosteum (involucrum)If infection rapidly controlled resolution can occurIf infection poorly controlled chronic osteomyelitis can developClinical featuresChild usually presents with pain, malaise and feverOften unable to weight bearEarly signs of inflammation are often fewBone is often exquisitely tender with reduced joint movementLate infection presents with soft-tissue swellings or discharging sinusDiagnosis can be confirmed by aspiration of pus from abscess or metaphysis50% of patients have positive blood culturesRadiologyX-rays can be normal during first 3 to 5 daysIn the second week radiological signs include: Periosteal new bone formationPatchy rarefaction of metaphysisMetaphyseal bone destructionIn cases of diagnostic doubt bone scanning can be helpfulDifferential diagnosisCellulitisAcute suppurative arthritisRheumatic feverSickle-cell crisisManagementGeneral supportive measures should include intravenous fluids and analgesiaPainful limb often requires a splint of skin traction to relieve symptomsAggressive antibiotic therapy should be institutedFlucloxacillin is often the antibiotic of choiceIf fails to respond to conservative treatment surgery may be requiredA subperiosteal abscess should be drainedDrilling of metaphysis is occasionally requiredOverall, about 50% of children require surgeryComplicationsMetastatic infection can occurs at distant sites (e.g. brain, lung)Spread into joint can result in a septic arthritisThis complication occurs in: Young children in whom the growth plate is permeableBones in which the metaphysis is intracapsularEpiphysis of bones involved in metastatic infectionInvolvement of physis can result in altered bone growthFailure to eradicate infection can result in chronic osteomyelitisBibliographyBerendt T,  Byren I.  Bone and joint infection.  Clin Med 2004;  4:  510-518Frank G,  Mahoney H M,  Eppes S C.  Musculoskeletal infections in children.  Pediatr Clin North Am 2005;  52:  1083-1106.Lazzarini L,  Mader J T,  Calhoun J H.  Osteomyelitis in long bones.  J Bone Joint Surg Am 2004;  38:  1855-1859.Lew D P,  Waldvogel F A.  Osteomyelitis.  Lancet 2004;  364:  369-379.Ray P S,  Simonis R B.  Management of acute and chronic osteomyelitis.  Hosp Med 2002;  63:  401-407.Parsons B,  Strauss E.  Surgical management of chronic osteomyelitis.  Am J Surg 2004;  188 (Suppl 1):  57-66<br />  Septic arthritis<br />Acute inflammatory condition of a jointUsually results from bacterial infectionUntreated it will lead to destruction of the articular cartilage50% cases occur in children less than 3 years of ageIn infants less than one year old the hip is the commonest joint involvedIn older children the knee is the commonest joint affected10% of patients have multiple joints involvedMicrobiologyInfecting organism depends on ageChildrenAdults<  3 years old> 3 years old< 50 years old> 50 years oldH. influenzaeStaph aureusStaph aureusStaph aureusStaph aureusH. influenzaeNeisseria gonorrhoeaGram-negativeColiformsStreptococci Organism can enter joint via a number of routes Penetrating woundFrom epiphysis or metaphysisHaematogenous spreadProvoke an acute inflammatory responseLarge number of neutrophils accumulate in jointRelease proteolytic enzymes that break down the articular cartilageResults in joint effusion and reduced synovial blood supplyComplications of septic arthritis include Avascular necrosis of epiphysisJoint subluxation / dislocationGrowth disturbanceSecondary osteoarthritisPersistent or recurrent infectionClinical featuresExact presentation depends on ageChildren are usually systemically unwellPresent with pain in the affected jointAll movements of the joint are painfulReluctant to stand on weight-bearing jointsAffected joint is usually swollen, red and warmHip involvement results in flexion and external rotationIn adults septic arthritis is usually associated with immunosuppressionPicture provided by Mohamed Atanis,  El Wafa Clinic, Al Marj, LibyaInvestigationsKey investigation is culture of a joint aspirateShould be performed prior to the administration of antibioticsOther appropriate investigations should include Inflammatory markersPlain x-raysBone scanDifferential diagnosisIrritable hipPerthe's diseaseOsteomyelitisGoutPseudogoutManagementAntibiotics should be started after joint aspirationEmpirical therapy should be commenced based on likely organismsAdjusted depending antibiotic sensitivityAntibiotics should be continued for 6 weeksSurgeryInvolves joint drainage and lavageMay be performed arthroscopicallyEarly joint mobilisation should be encouragedBibliographyGarcia De la Torre I.  Advances in the management of septic arthritis.  Rheum Dis Clin North Am 2003;  29:  61-75.Shirtliff M E,  Mader J T.  Acute septic arthritis.  Clin Microbiol Rev 2002;  15:  527-544.<br /> Other bone infections<br />Pott's diseasePott's disease is tuberculous spondylitisWell recognised in Egyptian mummiesDescribed by Percival Pott in 1779Now rare in western countriesStill prevalent in the developing worldPathologyUsually occurs secondary to infection elsewhereDue to a combination of osteomyelitis and arthritisOften occurs at more than one vertebral levelUsually affects anterior part of vertebral bodyMore common in thoracic spineBone destruction lead to vertebral collapse and kyphosisSpinal cord can be narrowed resulting in cord compression and neurological deficitClinical presentationBack pain is the commonest symptomPain may be present for several monthsPain can be both spinal and radicular50% patients have neurological signs at presentationMost patients have some degree of kyphosisCold abscess may point in the groinInvestigationsSerum ESR is usually massively raisedTuberculin skin test is usually positivePlain x-rays may showLytic destruction of anterior vertebral bodyAnterior vertebral collapseReactive sclerosisEnlarged psoas shadowCT or MRI provides information on disc space and neurological involvementAs allows CT guided biopsy to obtain microbiological and pathological specimensPicture provided by Christine Breynoert, Hospital Saint-Elizabeth, Zottegen, BelgiumTreatmentTreatment involves both tuberculous chemotherapy and possible surgeryNine months of combination chemotherapy should be usedThis involves 3 or 4 drugsIsoniazid and rifampicin should be given for full nine monthsPyrazinamide, ethambutol or streptomycin should be give for first 2 monthsSurgery is indicated if:Neurological deficitSpinal deformity with instabilityNo response to medical treatmentNon-diagnostic percutaneous biopsySurgical approach depends on extent of disease and level of spinal involvementUsually involves radical debridement and posterior stabilisationBibliographyAlmeida A.  Tuberculosis of the spine and spinal cord.  Eur J Radiol 2005;  55:  193-201.Busteed S,  Beeching N J,  Nye F J et al.  Tuberculous osteomyelitis:  chasing the elusive tubercle.  Hosp Med 2004;  65:  438-439.Moore S L,  Rafii M.  Imaging of musculoskeletal and spinal tuberculosis.  Radiol Clin North Am 2001;  39:  329-342.<br />  <br />Low back pain and sciatica<br />Lumbar back pain is one of the commonest causes of chronic disabilityUsually due to abnormality of intervertebral discs at L4/5 or L5/S1 levelPathologyWith age nucleus pulposus of disc dries outAnnulus fibrosis also develops fissuresNuclear material may herniate through annulusMay perforate vertebral end-plate to produce a Schmorl nodeFlattening of the disc with marginal osteophyte formation is known as spondylosisOsteoarthritis may develop in the facet jointsOsteophyte formation may narrow lateral recesses of spinal canalThese can encroach on spinal canal and result in spinal stenosisAcute herniation of disc contents can occurUsually occurs to one side of the posterior longitudinal ligamentPosterolateral rupture can compress nerve rootsCentral posterior rupture can compress the cauda equinaAcute disc ruptureCan occur at any ageUsually occurs in fit adults between 20-45 yearsClinical featuresPresents with acute low back pain on stooping or liftingPain often radiates to buttock or legMay be associated with paraesthesia or numbness in the legCauda equina compression can cause urinary retentionExamination may show a 'sciatic' scoliosisAll back movement is restrictedMay be lumbar tenderness and paravertebral spasmStraight leg raising is often restrictedNeurological examination is essentialL5 root signs include: Weakness of hallux extensionLoss of knee reflexSensory loss over the lateral aspect of the leg and dorsum of the footS1 root signs include: Weakness of foot plantar flexionLoss of ankle reflexSensory loss over the lateral aspect of the footCauda equina compression causes Urinary retentionLoss or perianal sensationImagingLumbar spine x-ray will exclude other bone lesionsMyelography is a historical investigationMRI is now the investigation of choiceManagementBed rest is of unproven benefitRecovery is not hasten by tractionNSAID provide symptomatic reliefThe role of epidural steroid injection is unclearChemonucleolysis is less effective than surgical discectomySurgery is required if: Cauda equina compression - neurosurgical emergencyNeurological deterioration with conservative managementPersistent symptoms and neurological signsSurgical options are: Partial laminectomyMicrodiscectomyPostoperative rehabilitation and physiotherapy are essentialFacet joint dysfunctionUsually present with recurrent low back painPain often related to physical activityMay be referred to the buttockOften relieved by lying downLumbar spine movement is often goodNeurological signs may be fewLumbar spine x-rays show narrowing of the disc spaceOblique views may show facet joint malalignmentTreatment includes: PhysiotherapyAnalgesiaFacet joint injectionsSpinal fusionSpinal stenosisNarrowing of the spinal canal due to hypertrophy of the posterior disc marginMay be compounded by facet joint osteophyte formationSpinal stenosis may also be associated with: AchondroplasiaSpondylolisthesisPaget's diseaseUsually presents with either unilateral or bilateral leg painInitiated by standing or walkingRelieved by sitting or leaning forward - 'spinal claudication'Patient prefers to walk uphill rather than downhillX-rays often show degenerative spondylolisthesisDiagnosis can be confirmed by MRIOften treated conservativelySurgery involves wide laminectomy and decompressionSpondylolisthesisSpondylolisthesis means forward shift of the spineOccurs at L4/L5 or L5/S1 levelCan only occur if facet joint locking mechanism has failedClassified as: Dysplastic - 20%Lytic - 50%Degenerative - 25%Post-traumaticPathologicalPostoperativeIn lytic spondylolisthesis the pars interarticularis is in two pieces (spondylolysis)Vertebral body and superior facet joints subluxate and dislocate forwardDegree of overlap is usually expressed as percentageCauda equina or nerve roots may be compressedPresents with back pain and neurological symptomsPatients have a characteristic stanceA 'step' in the lumbar spine may be palpableDiagnosis can be confirmed on a plain x-rayMost patients improve with conservative managementSurgery may be required if: Disabling symptomsProgressive displacement more than 50%Significant neurological compromiseAnterior or posterior fusion may be requiredBibliographyDeyo R A,  Weinstein J N.  Low Back Pain. N Engl J Med 2001;  344:  363-370.Hagen H D,  Hilde G,  Jamtvedt G,  Winnem M.  Bed rest for acute low back pain.  Cochrane Database Syst Rev 2000;  2: CD001254.Koes B W,  van Tulder M W,  Thomas S.  Diagnosis and treatment of low back pain.  BMJ 2006; 332:  1430-1434.Nelemas P J,  de Bie R A,  de Vet H C,  Sturmans F.  Injection therapy for subacute and chronic low back pain.  Cochrane Database Syst Rev 2000;  2: CD001824.van Tulder M W,  Scholten R J,  Koes D C V,  Deyo R A.  Non-steroidal anti-inflammatory drugs for low back pain.  Cochrane Database Syst Rev 2000;  2: CD000396.<br />  Spinal cord compression<br />The clinical features of a spinal cord lesion depend on its rate of developmentTrauma produces acute compression with rapidly developing effectsBenign neoplasms can cause substantial compression with little neurological deficitAnatomyThe spinal cord is shorter than spinal canalThe cord ends at the interspace between the L1 and L2 vertebraeBelow the termination of the cord the nerve roots form the cauda equinaWithin cervical spine segmental levels of cord correspond to bony landmarksBelow this level there is increasing disparity between levelsSpinal pathology below L1 presents with only root signsAetiologyTrauma - vertebral body fracture or facet joint dislocationNeoplasia - benign or malignantDegenerative - prolapsed intervertebral disc, osteophyte formationVascular - epidural or subdural haematomaInflammatory - rheumatoid arthritisInfection - tuberculosis  or pyogenic infectionsClinical presentationClinical features depend on extent and rate of development of cord compressionMotor symptoms include easy fatigue and gait disturbanceCervical spine disease produces quadriplegiaThoracic spine disease produces paraplegiaLumbar spine disease affects L4, L5 and sacral nerve rootsSensory symptoms include sensory loss and paraesthesiaLight touch, proprioception and joint position sense are reducedTendon reflexes are often: Increased below level of compressionAbsent at level of compressionNormal above level of compressionReflex changes may not coincide with sensory levelSphincter disturbances are late features of cervical and thoracic cord compressionCauda equina compression due to central disc prolapse produces: Loss of perianal sensation'Root pain' in both legsPainless urinary retentionMost patients with surgical treatable causes of spinal compression have spinal painMovement induce pain suggests vertebral fracture or collapseExquisite tenderness suggests an epidural abscessLow-grade background pain suggests tumour infiltration or osteomyelitisInvestigationPlain x-rays may show bone or paravertebral soft tissue diseaseFeatures include vertebral collapse, lytic lesions, loss of pedicleIntegrity of disc may indicate diagnosis'Good disc = bad news' often indicates malignancy'Bad disc = good news' may indicate infectionMRI is investigation of choice to define extent of soft tissue diseaseBone scan may indicate pattern and extent of bone pathologyManagementAcute cord compression is a 'surgical' emergencyIn those with malignant disease radiotherapy may be treatment of choiceIn general, tumour, infection and disc disease produces anterior compressionSurgical decompression should be achieved through an anterior approachCervical spine can be approached between larynx medially and carotid sheath laterallyThoracic spine can be approached through chest by a posterior thoracotomy or costotransversectomyBibliographyAbraham J.  Management of pain and spinal cord compression in patients with advanced cancer.  Ann Intern Med 1999;  131:  37-46.Gleave J R W,  MacFarlane R.  Cauda equina syndrome:  what is the relationship between timing of surgery and outcome?  Br J Neurosurg 2002;  16:  325-328.Healey J H,  Brown H K.  Complications of bone metastases.  Cancer 2000;  88 (Suppl 1): 2940-2951.Markman N.  Early recognition of spinal cord compression in cancer patients.  Cleve Clin Med J 1999;  66:  629-631.<br /> Scoliosis<br />A scoliosis is an apparent lateral curvature of the spineIt is a triplanar deformity with lateral, anteroposterior and rotational componentsPostural scoliosis is secondary to pathology away from the spine (e.g. short leg or pelvic tilt)Curvature disappears when patient sits downStructural scoliosis is a non-correctable deformityVertebral rotation results in spinal processes swinging to concavity of curveSecondary changes occur to counterbalance primary deformityMost cases of structural scoliosis are idiopathicCan also result from bone, neurological or muscular diseaseClinical featuresA scoliosis shows a typical deformity with a skew back and rib humpThe hip normally protrudes on the concave sideThe scapula normally protrudes on the convex sideThe level and direction of the major curve convexity should be notedConvexity of curvatures determines the nomenclature of the lesione.g.  A right thoracic scoliosis has the thoracic spine convex to the rightA balanced deformity keeps occiput in midlineA fixed scoliosis become more obvious on flexionThe younger the child and greater the curvature the worse the prognosisRadiologyFull length PA and lateral films of the spine are requiredUpper and lower ends of spinal curve can be identifiedAngle of curvature (Cobb's angle) can be measuredLateral bending view can assess degree of correctabilitySkeletal maturity important as scoliosis can progress during skeletal growthIdiopathic scoliosis80% of scoliosies are idiopathicPatients often have a family historyMany patients have a trivial curvatureAbout 0.2% of population have greater than 30° of curvatureAge of onset defines three groups as adolescent, juvenile and infantileAdolescent idiopathic scoliosisOccurs with an onset older than 10 years90% patients are femaleProgression is not inevitableWith curvature of less than 20° spontaneous resolution can occurPredictors of progression include young age, marked curvature and skeletal immaturityMain aim of treatment is to prevent mild deformity becoming severeIf mild scoliosis with progression consider braceIf greater than 30° and progressing operative intervention may be requiredHarrington rods used to reduce rotational deformity and lateral curvatureJuvenile idiopathic scoliosisOccurs with an onset between 4 and 9 yearsRelatively uncommon conditionPrognosis is worse than adolescent groupSpinal fusion may be necessary before pubertyInfantile idiopathic scoliosisOccurs with an onset less than 3 yearsIs a rare condition60% patients are boysIn 90% the deformity resolves spontaneouslyIn those in whom progression occurs the curvature can be severeAssociated with a high incidence of cardiopulmonary dysfunctionOsteopathic scoliosisAssociated with hemivertebrae, wedged vertebrae and fused vertebraeOverlying tissue often shows angiomas, naevi  and skin dimplesScoliosis usually mildBefore considering surgery need to exclude and meningomyeloceleNeuropathic / myopathic scoliosisAssociated with polio, cerebral palsy and muscular dystrophyScoliosis is typically long and convex towards side of muscle weaknessX-rays with traction with assess the degree of correctabilityBibliographyBridewell K H.  Surgical treatment of idiopathic adolescent scoliosis.  Spine 1999;  24:  2607-2616.Dobbs M B,  Weinstein S L.  Infantile and juvenile scoliosis.  Orthop Clin North Am 1999;  30:  331-341.Sarwark J F,  Kramer A.  Pediatric spinal deformity.  Curr Opin Pediatr 1998;  10:  82-86.Weinstein S L,  Dolan L A,  Cheng J C et al.  Adolescent idiopathic scoliosis.  Lancet 2008;  371:  1727-1537.<br /> Thoracic outlet compression syndrome<br />Describes a collection of upper limb neurological and vascular symptomsArise from proximal compression of neurovascular structuresUsually affects middle aged womenMale : female ratio is  1:310% have bilateral symptomsPathophysiologyCompression can result from a bone, muscle or fibromuscular bandCompressing lesion is usually congenital30% of cases follow trauma (e.g. whiplash injury)Clinical featuresNeurological features are more common than vascularSubclavian artery aneurysm and axillary vein thrombosis are uncommonSymptoms often worsened by carrying weights or lifting arms above headDifferential diagnosis includes: Cervical spondylosisDistal nerve compressionPancoast's tumourConnective tissue disordersVascular and venous embolic diseaseDiagnosis depends mainly on the historySigns are few but diagnosis may be confirmed with the Roos test - Reproduction of symptoms with arms flexed and abductedSubclavian compression tests (e.g. Adson's manoeuvre)Loss of radial pulse with head turned to opposite side and neck extendedInvestigationsThe results of investigations are often normalA CXR may show a cervical ribNerve conduction studies may be needed to exclude a distal nerve compressionArch aortogram may show a subclavian artery aneurysmDuplex scanning may show arterial or venous compression and the effect of positionPicture provided by Andrew McIrvine, Darent Valley Hospital, Dartford, United KingdomTreatmentSymptoms may improve with physiotherapyIf disabling symptoms need to consider surgical decompressionInvolves resection of most of first ribCan be achieved through either a supraclavicular or transaxillary approach10% will develop a pneumothoraxPrognosis80% report a symptomatic improvementMore than 50% of patients are usually symptom freeFailure to improve is often due to: A double crush compression syndromeIncomplete division of compressing structureBibliographyEdwards D P,  Mulkern E,  Raja A N,  Barker P.  Trans-axillary first rib excision for thoracic outlet syndrome.  J R Coll Surg Ed 1999;  44:  362-365.Thompson R W,  Petrinec D.  Surgical treatment of thoracic outlet compression syndromes:  diagnostic considerations and transaxillary first rib resection.  Ann Vasc Surg 1997;  11:  315-323. Urschel H C,  Razzuk M A.  Neurovascular compression in the thoracic outlet:  changing management over 50 years.  Ann Surg 1998;  228:  609-617.<br /> Primary bone tumours<br />Primary bone tumours are rareSecondaries tumours are more common especially in the elderlyClassificationCell typeBenignMalignantBoneOsteoid osteomaOsteosarcomaCartilageChondromaChondrosarcomaOsteochondromaFibrous tissueFibromaFibrosarcomaBone marrowEosinophilic granulomaEwing's sarcomaMyelomaVascularHaemangiomaAngiosarcomaUncertainGiant-cell tumourMalignant giant cell tumourClinical featuresMost present with pain, swelling and localised tendernessRapid growth and erythema are suggestive of malignancyMay cause pathological fracturesDiagnosis confirmed by: Plain x-rayCT scanBone scanCarefully planned biopsyOsteoid osteomaBenign bone tumourUsually less than 1 cm in diameter and surround by dense osteoidOccurs in young adultsTibia and femur are the commonest sitePain (relieved by aspirin) is presenting complaintXray has characteristic appearance of a radiolucency surrounded by dense boneLocal excision is curativeOsteochondromaCommonest bone tumourLesions can be single or multipleAppears in adolescence as cartilaginous overgrowth at epiphyseal plateGrows with underlying boneMetaphyses of long bones are the commonest sitesPresents as painless lump or occasionally joint painExcision should be considered if causing significant symptomsChondromaBenign tumour of cartilageLesions may be single or multiple (Ollier's disease)Appears in tubular bones of hands and feetXray shows well defined osteopenic area in the medullaLesion should excised and bone graftedGiant-cell tumour (Osteoclastoma)Equal proportions are benign, locally invasive and metastaticFound in sub-articular cancellous region of long bonesOnly occurs after closure of epiphysesPatients are usually between 20 and 40 yearsXray shows an asymmetric rarefied area at the end of a long boneCortex is thinned or even perforatedTreatment by local excision and grafting often leads to recurrenceWide excision and joint replacement is the treatment of choiceAmputation if malignant or recurrent tumourOsteosarcomaOccurs in the metaphyses of long bonesCommonest sites are around the knee or proximal humerusDestroys bone and spreads into the surrounding tissueRapidly metastasizes to the lungUsually occurs between 10 and 20 yearsIn later life is seen associated with Paget's diseaseX-ray shows combination of bone destruction and formationPeriosteum may be lifted (Codman's triangle)Soft tissue calcification produces a 'sunburst' appearanceTreatment involves amputation and chemotherapyAmputations are often limited with prosthetic replacement50% five years survivalWorst prognosis seen with proximal and axial skeletal lesionsPicture provided by Sathar Thajam, Monkland's Hospital, Airdrie, ScotlandChondrosarcomaOccurs in two forms'Central' tumour in pelvis or proximal long bones'Peripheral' tumour in the cartilaginous cap of an osteochondromaTend to metastasise lateWide local excision is often possibleBibliographyHam S J,  Schraffordt-Koops H,  van der Graaf W T,  van Horn J R,  Postma L, Hoekstra H J.  Historical, current and future aspects of osteosarcoma treatment.  Eur J Surg Oncol  1998; 24: 584-600.Witt J.  Management of osteoid osteoma.  Hosp Med 2002;  63:  207-209.<br /> Bone metastases<br />30% of patients with malignant disease will develop bone metastases10% of these patients will develop a pathological fractureTumours spread to bone by: Direct invasionHaematogenous spreadLymphatic spreadSpread via paravertebral venous plexusCommonest sites lumbar vertebrae, pelvis and ribsPrimary tumours which spread to boneBreast  (35%)Prostate  (30%)Bronchus (10%)Kidney  (5%)Thyroid  (2%)Others (18%)Clinical featuresPain or localised bone lumpPathological fractureHypercalcaemiaCord compressionRadiologyPlain x-rays can be normalIf abnormal will show either an osteolytic or sclerotic lesionBone scan has higher sensitivity than x-raysMay identify other asymptomatic lesionsDifferential diagnosisCalcified enchondromaHyperparathyroidismChronic sclerosing osteomyelitisBone infarctMyeloma depositTreatmentThe aims of treatment are to relieve pain and preserve mobilityIf pathological fracture consider internal fixation for early mobilisation and pain reliefConsider radiotherapy for back painSpinal decompression may be needed for cord compressionProphylactic internal fixation may be required if: Greater than 50% erosion of a long bone cortexA metastasis of more than 2.5 cm in diameterMetastasis in high risk area (e.g. subtrochanteric femur)Metastasis with persistent painBibliographyBritish Association of Surgical Oncology Guideline.  The management of metastatic bone disease in the United Kingdom.  The Breast Speciality Group of the British Association of Surgical Oncology.  Eur J Surg Oncol 1999;  25:  3-23.Downey S E,  Bundred N J.  Bone metastases.  In:  Johnson C D,  Taylor I eds.  Recent advances in surgery 19.  Churchill Livingstone, Edinburgh 1996;  109-128.Major P P,  Cook R.  Efficacy of bisphosphonates in the management of skeletal complications of bone metastases and selection of clinical end-points.  Am J Clin Oncol 2002;  25 (Suppl1);  S10-S18.Radford M,  Gibbons C L.  Management of skeletal metastases.  Hosp Med 2002;  63:  722-725Rosenthal D I.  Radiologic diagnosis of bone metastases.  Cancer 1997;  80 (Suppl 8):  1595-1607.Ryan P J.  Fogelman I.  The bone scan:  where are we now?  Semin Nucl Med 1995;  25:  76-91.<br /> Multiple myeloma<br />Multiple myeloma is a malignant disease of plasma cells in bone marrowAccounts for 1% of all cancers2,500 new cases each year in United KingdomMost patients are over 60 years of ageCharacterised by production of monoclonal immunoglobulinsThese can be detected in serum, urine or bothPathogenesisMonoclonal overgrowth of one clone of plasma cells occursProduces monoclonal immunoglobulin or paraproteinIn 80% patients an IgG or IgA is detectable in serumIn 20% no paraprotein is detectable in the serumFree light chains may cross glomerulus and appear in urineThese are known as Bence-Jones proteinsClinical featuresBone pain - especially back painPathological fractureCord compression may occurHypercalcaemiaRenal failureAnaemiaImmunosuppressionAmyloidosisInvestigationsDiagnosis confirmed by: Paraprotein in serum or urine on electrophoresisLytic lesions on radiographyBone marrow aspirate with more than 10% plasma cellsManagement70% patients respond to therapyComplete remission is rareMedian survival is 3 yearsTreatment options Melphalan chemotherapyInterferon-alphaBone marrow transplantationTreatment of complications Dialysis for renal failureBisphosphonates for hypercalcaemiaRadiotherapy for localised bone painBibliographyBataille R,  Harousseau J L.  Multiple myeloma.  N Engl J Med 1997;  336:  1657-1663.Berenson J, Lichtenstein A,  Porter L et al.  Efficacy of pamidronate in reducing skeletal events in patients with advanced multiple myeloma.  N Engl J Med 1996;  334:  488-493.<br /> <br />