Dr. Mohammed Akbar KhanPostgraduate in OrthopaedicsAVASCULAR NECROSIS OF FEMUR HEAD

DOST- 2009 Madurai

Death of Osteocytes - Femoral head collapse & Secondary hip joint osteoarthritis

Osteonecrosis, Aseptic necrosis or Ischemic bone necrosis

Temporary or permanent loss of the blood supply - Ischemia - Death and collapse of the Bone tissue & Joint surface.

Affect several different bone.DEFINITION

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HISTORICAL REVIEW1888 - Konig - Osteochondritis dessicans of femoral head1925 - Haenish - first case - Idiopathic ischemic necrosis of femoral head in an adult1935 - Chandler - Coronary artery disease of the hip1940 - Arterial occlusion was postulated as Etiology1949 - Phemister - Femoral head drilling & Tibial bone grafting1957 - Pietrograndi - First case(AVN)-Steroid Therapy

TERMINOLOGY 1948 - Coronary artery disease of hip Aseptic necrosis Avascular necrosis or Ischemic necrosis -Osteonecrosis (Term of choice)

More neutral in its presumption of causation.

Describes main features of this condition i.e. bone death

INTRODUCTIONIschemic death of the cellular constituents - Bone & marrow 2/3 of heads removed at autopsy

Commonest site is Antero-superolateral Subchondral 50% of necrotic heads -wedge of viable area at fovea

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Foveal Live BoneDead BoneDead Bone

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Age: 3rd 5th decade

Very rare in extremes of age

Mean age of onset is 5th decade

Male : female = 4:1

Bilateral in 50 % of casesINCIDENCE

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COMMENEST SITESFemoral HeadFemoral CondylesHead of HumerusCapitulumScaphoidLunateTalus

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CLASSIFICATIONPrimary (idiopathic)Secondary to:Trauma Fracture of the femoral neckSlipped capital femoral epiphysisProximal femoral epiphysiolysisDislocation of the femoral headEpiphyseal compressionVascular traumaBurnsRadiation exposureHemoglobinopathiesSickle cell diseaseHemoglobin S or hemoglobin C Polycythemia

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Caisson disease Dysbaric osteonecrosisLocal infiltrative diseaseGaucher diseaseInfectionNeoplasmsHypercortisolismCorticosteroid medications Cushing diseaseChronic renal failureCigarette smokingCollagen vascular diseasesCongenital and developmentalCongenital dislocation of the hipEhlers-Danlos syndromeHeredity dysostosisLegg-Calv-Perthes disease

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Fabry diseaseGiant cell arteritisGout and hyperuricemiaHemodialysisHypercholesterolemiaHypercoagulable statesHyperlipidemiaHemophiliaHyperparathyroidismIntravascular coagulationOrgan transplantationAlcohol consumptionPancreatitisPregnancySystemic lupus erythematosusThrombophlebitis

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BLOOD SUPPLY OF FEMORAL HEAD

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ANATOMICAL RISK FACTORS

Subchondral part of bone - distance from the main vascular territorySubchondral trabaculae supplied by endarterioles.Vascular sinusoids of marrow No adventitial layer - compressed by marrow edema.

ETIOLOGICAL FACTORSInterruption of arterial flowIntravascular blockade of arterioles and capillariesExpansion of marrow components and capillary compressionOcclusion of venous outflow

ARTERIAL INTERRUPTIONFracture Neck of FemurDislocationSUFEInfectionsFrog leg Immmobilisation

ARTERIOLAR OCCLUSIONSickle cell diseaseVasculitis - SLECaissons diseaseHemostatic disordersGout

CAPILLARY COMPRESSION

Gauchers diseaseFatty Infiltration CorticosteroidsAlcohol abuseFamilial hyperlipidemiaRenal transplantHyperbaric conditions

MISCELLANEOUSHemarthrosisPerthes diseasePregnancyIonising radiationIatrogenic

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Sickle cell diseaseDysbaric ischemiaThrombocytopeniaFat embolismVicious cycle GauchersTuberculosisCortisoneAlchoholDysbaric ischemia

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IDIOPATHIC AVNDiagnosis of exclusionConstitutes 25% casesThrombosis of vascular supply of femoral head - unknown etiologyDiffuse osteoporosis with loss of trabeculae surrounded by sclerosis

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FEMORAL HEAD DISLOCATIONInjury to the ligementum Teres Disrupts the blood supplySuperior retinacular arteries may be injuredReduction returns the bone to its normal stress - bearing state

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FEMORAL NECK FRACTUREExtensive interruption of blood flowSinusoidal vascular bed interrupted Subsynovial retinacular vessels disruptedOnly supply from Ligamentum teresValgus reduction helps in union but blood supply

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STEROIDSPathogenesis of AVN in hypercortisolism is unknown. 1. Fat embolization from the liver, Bone marrow fat cells, or destabilization and coalescence of plasma lipoproteins. 2. Corticosteroids along insulin resistance hypertension & arteriosclerosis - Coronary disease of the hip 3. Corticosteroid Osteoporosis Microfractures AVN4. Peak doses of steroid are significant than duration of treatment

RENAL FAILURE Congenital anomalies and Acquired renal disease Complication of treatment with recombinant growth hormone in children with Renal disease.

COLLAGEN VASCULAR DISEASEThickening & Necrosis of vessel basement membrane - occlusion of vessels.Rheumatoid arthritis Scleroderma SLEDermatomyositis Corticosteroids used for treatment.

ALCHOHOLFatty Liver - Fat embolism.Ac. or Ch. Pancreatitis - Circulating lipases - Fat necrosis in bone

SICKLE CELL DISEASESluggish blood flow - sickle shaped cells - diminished blood supply - infarction of epiphyseal & metadiaphyseal bone -AVNBone within bone appearance in x-ray - Infarction of inner 1/3 of cortex

ENDOSTEAL SCLEROSISBONE WITHIN BONE APPEARANCE

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AREAS OF MOTTLING AND SCLEROSIS SEQUESTRUM FORMATION (BONE WITHIN A BONE)

LIGHT NECROTIC AREAS DEMARCATED FROM VIABLE BONE

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IRRADIATIONDirect cell damage Damage to cells in the walls of blood vessels with obliteration of vesselsHighest risk seen in patients with Hodgkin's and NHL receiving RT,CT and Steroids

DYSBARIC DISORDERSDirectly related toDepth of dive Number of divesUncontrolled decompressionLow oxygen saturationAccumulation of undissolved nitrogen bubbles in vascular & interstitial spaces

DYSBARIC OSTEONECROSIS

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GAUCHERS DISEASEMarrow sinusoids packed with glucocerebrocide filled histiocytes (gaucher cells) - Increased pressureDirect affection of femoral head Liver disease

Fat embolism

AVN

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PREGNANCYLast trimester Venous stasis with increased marrow pressure

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PATHOGENESISFour phases 1) Avascular phase, 2) Revascularization phase, 3) Repair phase, 4) Deformity phase.

AVASCULAR PHASEInfarction within fatty marrow adjacent to subchondral cortex of the bone necrotic - overlying cartilage hypertrophies (attempt to convert itself to bone).Radiographic appearance - Minimal osteopenia or subtle soft tissue changes.Increase in the medial joint space between Kohler's tear drop and the femoral head - 2 mm difference - (Waldenstrom's sign)

Kohlers tear drop Increase Medial Joint Space WALDENSTORMS SIGNFemoral Head

REVASULARIZATION PHASEOsteoclastic & osteoblastic activity. Mixed areas of luceny & sclerosis.Cell death - beneath articular surface bone - fragmentation and collapse of the overlying cortex indication of collapse - Crescent sign.Further collapse - Step signSnow Cap Sign - Diffuse sclerosis - Repair is sufficient in revascularization phase.

Thin curvilinear lucency in immediate subchondral bone & located on the weight bearing portion. Further collapse may result in a "step sign" in which cortical offset is actually noted on the film CRESCENT SIGN & STEP SIGN

Diffuse sclerosis of femoral head SNOW CAP SIGN

CRESCENT SIGNSNOW CAP SIGN

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REPAIR PHASEBegins with revascularization. Variable degree of reconstitution and healing -Degree of blood loss and cell death - initial insult-Patient's immune system and healing response -Joint is weight-bearing vs. non-weight bearing

DEFORMITY PHASEHighly variable - severity of other phases - site specific & stresses in the area (weight-bearing areas - increase in deformities)Early and severe degenerative joint disease - incongruent joint surfaces early hip replacement Cell death - process will cascade - severe & debilitating degenerative joint disease.Fortunate aspect - Treatable if discovered early.

SEQUENCE OF REPAIR8 PHASESPhase 1< 24 hours loss of cell viability2-4 days Pyknosis and karyolysisPhase 2Invasion of marrow vascular spaces by capillaries, primitive mesenchymal cells and inflammatory cellsOccurs in adjacent live bone

SEQUENCE OF REPAIRPhase 3Invasion of capillaries and cells in dead bonePhase 4Synthesis of new boneMesenchymal cells differentiate into osteoblastsPhase 5 Early internal remodellingPhase 6Late internal remodelling

SEQUENCE OF REPAIRPhase 7Resorption of subchondral boneBone resorption > bone formationPhase 8Pannus formation over articular cartilage

Fibrillation and destruction of cartilage

Osteoarthritic changes

ZONES IN AVNFour zonesA - Central zone of cell deathB - Zone of ischemic injuryC - Active hyperemiaD - Normal tissue

AVN- 4 zones

ABBCD

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FISSURING

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BREAKING UP

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DESTROYED JOINT SURFACE

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HISTOPATHOLOGY Wedge shaped area of necrosis - subchondral portion of the head of femur at anterosuperolateral part - weight bearing portion of the femoral head

Invasion of the vascularised cellular tissue from surrounding living marrow into the necrotic segment

Necrotic trabeculae are ensheathed by the newly deposited bone through reparative process Increased radiological density

STAGINGFICAT & ARLETSHIMIZU et alRATLIFFEMARCUS et alHUNGERFORD & ZIZICAAOSSTEINBERG et alARCO

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FICAT AND ARLET CLASSIFICATION

StasympX-rayB-scanpathoBiopsy 0NoneNormal?Uptake 1None/ mildNormalCold spotInfarctionDead marrow2-A2-BmildSclerosis flatteningUptakeRepairNew bone 3modCollapseUptake Subcho#Dead bone 4severeJoint space Uptake OA changesDeg. change

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FICAT AND ARLET CLASSIFICATIONSTAGE IISTAGE III STAGE IV

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SHIMIZU et alGrade 1 Restricted to medial part Grade 2 Occupy upto of head & bet. 1/3 to 2/3 of wt. bearing surfaceGrade 3 Occupy large part of head & more than 2/3 of wt. bearing surface

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RATLIFFE CLASSIFICATION# NOF IN CHILDREN

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MARCUS et al (1973)STAGECLINICAL RADIOGRAPHIAsymptomatic Mottled densitiesIIAsymptomatic Infarcted demarcated by densityIII Pain-mild & intermittentCrescent signIVPain with activity Depression of infarctVPain with activityFlattening & compressionVI Pain at rest Degenerative arthritis

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HUNGERFORD & ZIZIC (1978)1. Normal x-ray May / may not be painful2. X-ray show dense line but intact femoral head3. Subchondral fracture sequestration of cartilage4. OA with joint Space narrowing

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AAOS

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STEINBERG et alStage Criteria0 Normal or nondiagnostic x rays, bone scan & MRII Normal x rays, abnormal bone scan, and/or MRIII Abnormal x rays (cystic, sclerotic without collapse)III Subchondral collapseIV Flattening of the femoral head without joint spacenarrowing or acetabular involvement.VJoint narrowing and/or acetabular involvementVI Advanced degenerative changes

Staging - extent of lesion (A, B & C) - size by MRI /x-ray.

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STEINBERG

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MRI CLASSIFICATIONTAKORIGroup 1 - Type AFat intensity area confined to med antero-superior fem. Head but not extend across headGroup 2 - Type BBeyond the zenith to posterior part of headGroup 2 - Type C occupy the posterior Half Group 2 - Type D Larger than Type CUseful in pts at risk of AVN

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OHZONO PROGNOSTIC

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Sakamoto et al - extent of lesion on MRI

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ARCOFicat Arlet staging system Hungerford-Lennox modification (Steinberg) concept of prognosis based on location (Ohzono)

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ARCO ARCO

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CLINICAL FEATURESAsymptomatic - Discovered on radiographyOnset insidious and chronicPain is throbbing, deep & intermittent at groin radiating to thigh or buttock exacerbated by weight bearing and coughingInitially mild but progressively worsens over time and with use - present at rest and may present or worsen at nightAntalgic gait

SIGNSInitial findings are unrevealing.Latter stages - Joint function deterioratesLimp Loss of range of motion( active and passive) - Flexion, abduction, & internal rotation, - Femoral head collapseTenderness around the affected area.Neurological deficit.

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SIGNSTrendelenburg sign - Positive.Click - patient rises from a chair or after external rotation of the abducted hip. Advanced disease - Joint deformity & muscle wasting

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X-RAYEvident only after 2-3 monthsSclerosis & cystSubchondral FracturesCrescent signCollapseJoint space narrowing & osteophytesAcetabular changes

SCLEROSIS

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CRESCENT SIGN

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CRESCENT SIGN

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SUBCONDRAL SCLEROSISSNOW CAP LESION

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CT SCANExtent of involvement, - Subchondral lucency & sclerosis Reparative stage (before the collapse of the femoral head) Detecting femoral head collapse Early degenerative joint disease Presence of loose bodies -Multiplanar reconstruction

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M R ISensitive method for earliest diagnosis Sensitivity 97% specificity 98%Low intensity signal in T1 weighted imageHigh intensity signal in STIR imageDouble line appearance on T2 weighted - Reactive interface between ischemic & non-ischemic bone. Accurate staging - clearly depicting the size of the lesion- multiplanar imaging- excellent soft tissue resolutionPrognosis - Osteonecrotic femoral head - Operative

DOUBLE LINE SIGN

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DOUBLE LINE SIGN

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INCREASED SIGNAL INTENSITY

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SPECTAlternative - MRI cannot be performed - MRI results are indeterminate.Difficult to use - Requires remaining still for long periods of time. Bladder artifacts - Frequent problem

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BONE SCANEarly diagnosis next to MRI99mTc-sulfur colloidEarly stages - Cold spotLate stages - Hot spotScintigraphic imagingCentral area of decreased uptake, surrounded by area of increased uptake -Doughnut sign or cold in hot sign

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OTHER IMAGING STUDIESRadionuclide scintigraphy Sr 87m and Tc 99m MDP scanTc isotope pickupRadioisotope clearance of Na 24Radio phosphorous pickupArteriography

BIOPSYUsually done with core decompressionEmpty lacunae in trabecular bone Common finding is old & new hemorrhage in bone marrow

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FUNCTIONAL INVESTIGATION (intra osseous pressure measurement)Normal baseline IO pressure 10 - 20 mm Hg Stress test - transient mild Pressure elevation io venogram - Contrast cleared within 5 Mts AVNFH > 30 mm Hg

> 10mm Hg for > 5mts

venous stasis

TREATEMENTGoal keep joints from breaking down - severe pain and limitation in movement.Arrest progression & prevent late collapse & AVN Before collapse no treatment - Arresting progressionAge of the patient, stage of the disease, location & amount of bone affected and underlying cause SURGICALNONSURGICAL

NON SURGICALBed restStatin therapy, Bisphosphonates or NSAIDSContinuous tractionNon weight bearing - No effect on final outcome

OPERATIVESALVAGE PROCEDURECore decompressionCore decompression & Bone graftingTranstrochanteric rotational OsteotomyIntertrochanteric osteotomyHip arthrodesisTrap door procedureResurfacing arthroplastyRECONSTRUCTIONTotal hip replacement

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BONE GRAFTINGTYPESCancellous iliac graftPhemister Free fibular graftMuscle pedicle graft - Tensor fascia lata - Quadratus femoris graft(meyers) - SartoriusVascular pedicle graft Iliac crest

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OSTEOTOMYFlexionVarusSugiokas ventral rotation

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CORE DECOMPRESSIONStage 1, 2A lesionsSmall central lesion in young non-obeseRelieve pain in 75%Not useful Post-traumatic cases Decompression of rigid interosseous chamber Improvement of vascularityPrevention of additional ischemic episode

HungerfordSupine - Fracture table or lateral decubitus2 3 cm longitudinal incision centered over subtrochanteric region.3.2mm threaded guide pin - lateral cortex of inferior portion of greater trochanter & distal portion of lesser trochanter. Direct tip of guide pin - Center of diseased bone Overream the guide pin 8 mm reamer. Histology - Core reamerCORE DECOMPRESSION

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AFTER TREATMENTPartial weight bearing (50%) on crutches is continued for at least 6 weeks Patients with advanced disease, protected weight bearing is prolonged

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ELECTRICAL STIMULATIONCore decompression + CBG + Electrical stimulation- More beneficialCore decompression + non-vascularised fibular graft for stage 1 & 2

OTHER GRAFTING METHODSGangji - Injection of autologous bone marrow aspirate at cored femoral headLieberman & Urist Human BMPUseful in 2A stage93% success

NON VASCULARISED GRAFTPHEMISTERFor stages 1 & 2Not proved of much valueCombined with core decompression

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VASCULARISED FIBULAR GRAFTDecompression of femoral headExcision of sequestrumFilling of defect with osteoinductive graftProtection of graft by a period of limited weight bearing

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MUSCLE PEDICLE BONE GRAFTMEYERSUses quadratus femorisPosterior approachFor stages 1 & 2

BAKSIUses Tensor fascia lataUsually anterior approachFor stages 1 & 2

OSTEOTOMIESTranstrochanteric Rotational OsteotomySUGIOKA 1978Age < 55 yrs< 30% head involvementIn idiopathic and post traumaticFor stage 1 & 2Reposition of necrotic anterosuperior part to non wt. bearing localePrevents progressive collapseImprove the congruity

ROTATIONAL OSTEOTOMYDeveloped by sugiokaAllows greater movement of diseased portion of femoral headCapsule is incised circumferentially to allow adequate rotationSupplemented by mild varus with Retroversion of neck

ROTATIONAL OSTEOTOMYCapsule incised circumferentiallyNear the acetabular rimTrans trochanteric osteotomy-10mm distal to inter trochanteric crest at 90* to the long axis of neckNear the base of inter trochanteric osteotomy line be 90* cephalad

ROTATIONAL OSTEOTOMY

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ROTATIONAL OSTEOTOMY GRADE 1 2 3 4SUCCES RATE 88% 83% 74% 70%

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OTHER OSTEOTOMIESIntertrochanteric Flexion Extension Varus or ValgusStage 2 and 3 AVN with < 30% head involvementScher and jakim - valgus extension IT osteotomy with curettage and Bone Grafting

TRAP DOOR PROCEDUREIntroduced in 1998Necrotic area is exactly locatedCartilage overlying is opened like a doorNecrotic bone curetted out and filled with cancellous bone, door is closed.Good results in stage 3

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STAGE 3 & 4 CASESTOTAL HIP REPLACEMENT ARTHROPLASTY

ARTHROPLASTY - TYPESResurfacing hemiarthroplastyTotal resurfacing arthroplasty (Birmingham)Unipolar and bipolar hemiarthroplastyTHR

RESURFACING ARTHROPLASTYExcellent interim procedure that allows revision to THR in young patients.High failure rateTotal articular resurfacing arthroplasty [TARA]Part of AVN head is removed, metal component is attached through neck and trochanter and is uncementedAcetebular component is poly ethylene & fixed with cement

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RESURFACING ARTHROPLASTYAdvantage: Preservation of normal anatomy for later THR with little FB implantedDisadvantage: Acetabular bone stock compromised by osteolysisNot useful in B/L AVN

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THRUsually done more than 50 yrsMany AVN are in 25-45 yrsUncemented THR in these group is not satisfactoryRecurrent dislocation , infection and osteolysis are common complications.Use of cementless THR under evaluation.

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Why separate treatment?

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,

THE JOURNAL OF BONE AND JOINT SURGERY

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OSTEONECROSIS OF THE FEMORAL HEAD: CURRENT CONCEPTS AND CONTROVERSIES - Brian D. Mulliken, M.D.

Further research is needed to assess the natural history of early AVN and evaluate the role of surgery in preventing progression

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Osteonecrosis of the Femoral Head Carlos J. Lavernia, Rafael J. Sierra, , and Francisco R. Grieco, J Am Acad Orthop Surg 1999;7:250-261

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Carry home messageMC Cause - Idiopathic Steroids - peak doses more significant# NOF - displaced # and malreduced #Once necrosis - IrreversibleMRI - Earliest to diagnoseNo role of conservative treatment to preserve headEarly diagnosis & joint preserving measures -Better prognosisResults of replacement are poor in younger than older age

BIBILOGRAPHYCampbell operative OrthopaedicsTurek OrthopaedicsApleys Orthopaedics

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THANK YOU

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