avascular necrosis of hip

OSTEONECROSIS OF FEMORAL HEAD

Dr.RAJESH

P.G in ORTHOPAEDICS

DEFINITION

• OSTEONECROSIS-– DEATH OF OSTEOCYTE WITH

SUBSEQUENT STRCTURAL CHANGES LEADING TO FEMORAL HEAD COLLAPSE AND SECONDARY OA OF HIP JOINT

– INCLUDES TRAUMATIC AND ATRAUMATIC

• AVASCLAR NECROSIS-– TRAUMATIC OSTEONECROSIS

DUE TO INTERRUPTION OF MAJOR NUTRIENT ARTERIES i.e, FEMORAL NECK FRACTURE AND HIP DISLOCATION

APPLIED ANATOMY• PROX END OF FEMMUR IS

SUPPLIED BY 3 GROUPS– EXTRA CAPSULAR ART RING

AT BASE FEMORAL NECK– RETINACULAR

ART/ASCENDING CERVICAL BRANCHES

– ART. OF LIGAMENTUM TERES• EXTRA CAPSULAR ART. RING

FORMED BY– POSTERIORLY-MED

CIRCUMFLEX FEM ART– ANTERIORLY-LAT

CIRCUMFLEX FEM ART– MINOR CONTRIBUTIONS

FROM INF&SUP GLUTEAL ART

ANATOMY• ASCENDING CERVICAL BRANCHES

– ARISES FROM EXTRACAPSULAR RING

– ANT PENITRATE THE CAPSULE AT IT LINE

– POST PASS BENEATH THE ORBICULAR FIBERS OF CAPSULE.

– PASS UPWARD UNDER THE SYNOVIAL REFLECTIONS TOWARDS ARTICULAR CARTILAGE.

– PROXIMITY OF THE RETINACULAR ARTERIES TO BONE PUT THEM AT RISK OF INJURY.

ANATOMY• THEY CAN BE DIVIDED INTO 4 GROUPS.

– ANTERIOR– POSTERIOR– MEDIAL AND– LATERAL

• OF THESE LATERAL GROUP PROVIDE MOST OF BLOOD SUPPLY TO FEMORAL HEAD AND NECK.

• AT THE MARIGIN OF ARTICULAR CARTILAGE THEY FORM ANOTHER RING CALLED SUBSYNOVIAL INTRA-ARTICULAR ARTERIAL RING.

• FROM THIS RING VESSELS PENETRATE HEAD-EPIPHYSEAL ARTERIES.

• THE ARTERY OF LIGAMENTUM TERES– BRANCH OF OBTURATOR ARTERY.– ALSO CALLED MEDIAL EPI-

PHYSEALART.– SUPPLIES SMALL AREA OF MEDIAL

HEAD

VARIATIONS OF VASCULAR PATTERN WITH ADVANCING GROWTH

• AT BIRTH-MAIN SUPPLY FROM – LAT EPIPHYSEAL AND – METAPHYSEAL VESSELS

• 4MONTHS TO 4YRS.– METAPHYSEAL SUPPLY DECREASES

AS OSSIFICATION CENTER BECOMES PROMINENT.

– LATERAL EPIPHYSEAL ART ASSUMES MAJOR ROLE

• 4 TO 7 YRS.– EPIPHYSEAL PLATE IS A FIRM

BARRIER BETWEEN EPIPHYSIS AND METAPHYSIS.

– ONLY SOURCE IS LATERAL VESSELS.

• 8 TO 10 YRS.– LIGAMENTUM TERES VESSELS

BECOME PROMINENT– ANASTOMOSE WITH LATERAL

EPIPHYSEAL VESSELS

VARIATIONS OF VASCULAR PATTERN WITH ADVANCING GROWTH

• ADOLESCENT PERIOD– LATERAL EPIPHYSEAL PROVIDES

MAJOR SOURCE OF BLOOD SUPPLY

• AT SKELETAL MATURITY AGAIN EPIPHYSEAL AND METAPHYSEAL VESSELS ANASTMOSES.

• IN CHILDREN UNDER 8 YRS. OF AGE INTERVAL BETWEEN THE GT AND TROCHANTERIC FOSSA IS NARROW

• CAPSULE WITH IN THIS FOSSA IS VERY THICK POSE A THREAT OF VASCULAR COMPRESSION.

SITE PREDILICTION

– ENDARTRIOLAR SUPPLY AND LACK OF COLLATERALS

– RETROGADE BLOOD SUPPLY

– SMALL DIAMETER VESSELS AT SUB CHONDRAL REGION

– MOST OF PART IS COVERED BY ARTICULAR CARTILAGE

VASCULAR SINUSOIDS OF MARROW DON’T HAVE ANY ADVENTITIAL LAYER SO EASILY COMPRESSED BY MARROW EDEMA

PATHOGENETIC CLASSIFICATION

• TYPE 1: ARTERIAL INSUFFICIENCY– FRACTURES– DISLOCATIONS– SCFE– ART. EMBOLISM– VASCULITIS

• TYPE 2: VENOUS OCCLUSION– VENOUS THROMBOSIS– PERTHE’S DISEASE

• TYPE 3: INTRAVASCULAR CAPILLARY OCCLUSION

– SICKLE CELL DISEASE– DYSBARIC ISCHAEMIA– FAT EMBOLIS IN

HYPERCORTISONISM AND ALCOHOLIM

– SLE

• TYPE 4: INTRA MEDULLARY FACTORS

– BONE INFECTION– GAUCHER’S DISEASE– FATTY CHANGES– HYPERLIPIDAEMIA

ARTERIOLAR OCCLUSION

MARROW OEDEMA

Sinusoidal Compression

Vascular Stasis

–SICKLE CELL DISEASE–DYSBARISM –THROMBOCYTOPENIA–FAT EMBOLISM

–GAUCHER’S DISEASE–TUBERCULOSIS–CORTIO STERIODS(INCREASE FAT CELL SIZE) –DYSBARIC ISCHAEMIA–ALCOHOL

UNILATERAL VERSUS BILATERAL

• UNILATERAL – COMMON– IDIPOATHIC/SPONTANEOUS– SURGERY– TRAUMA

• UNILATERAL – UNCOMMON– GOUT– HEMOPHILIA– INFECTION

• BILATERAL-COMMON– ALCOHOLISM– CORTICOSTERIOD

THERAPY(SYSTEMIC).– SPONTANEOUS

• BILATERAL-UNCOMMON– ATHEROSCLEROSIS– CAISSON’S DISEASE– CUSHING’S DISEASE– GAUCHER’S DISEASE– HEMOGLOBINOPATHY– SLE, RA– PHEOCHROMOCYTOMA

BIOLOGICAL SEQUENCE OF REPAIR

• PHASE 1: LOSS OF CELL VIABILITY– DISINTEGRATION AND

DISAPPEARANCE OF OSTEOCYTES– VIABILITY DETERMINED WITH

FAILURE TO UP TAKE A RADIOISOTOPE 3H-CYTIDINE RIBONUCLEIC ACID WITH IN FEW HOURS

• PHASE 2: INVASION OF DEAD BONE BY PROLIFERATING CAPRILLARIES AND CELLS

• PHASE 3: INVASION OF MARROW VASCULAR SPACES OF DEAD BONE

– MICROPHAGES OBSORB NECROTIC DEBRIS

– MESENCHYMAL CELLS INVADE MARROW SPACESS BETWEEN DEAD TRABECULAE, REPLACING NECCROTIC DEBRIS

• PHASE 4: DIFFERENTIATION OF MESENCHYMAL CELLS TO OSTEOBLASTS AND FIBROBLASTS

– INCREASE IN THE MASS OF MINERALIZED BONE PER UNIT VOLUME OF TISSUE PRODUCES AN INCREASE IN RADIODENSITY

• PHASE 5: EARLY INTERNAL REMODELING OF REPAIRED CANCELLOUS BONE:

– OSTEOCLASTS PENETRATE NEW WOVEN BONE

– NEW LAMELLAR BONE FORMATION– FRACTURE OCCURS AT JUNCTION

OF REPAIRED BONE AND NECROTIC SEGMENT

– FRACTURE SITE FILLED WITH DENSE FIBROUS TISSUE ON RADIOGRAPH VISIBLE AS RADIOLUCENT LINE-CRESCENT SIGN

BIOLOGICAL SEQUENCE OF REPAIR

• PHASE 6: LATE INT. REMODELING OF CANCELLOUS BONE.

• PHASE 7: RESORPTION OF SUBCHONDRAL BONE AND ARTICULAR CARTILAGE.

– THEY ARE LOCATED FAR FROM THE REPERATIVE SITE

– AFFECTED MANY WEEKS LATER– CELLULAR EVENTS OCCURS IN

COMPACT SUBCHONDRAL BONE DEFERS FROM CANCELLOUS BONE

– RESORPTION IS GREATER THAN THE BONE FORMATION

– OVERALL RESULT IS INCREASE IN MASS OF CANCELLOUS BONE AND DECREASE IN MASS OF COMPACT SUBCHONDRAL BONE

• PHASE 8: EFFECT ON ARTICULAR CARTILAGE

– PANNUS FORMATION OVER ARTICULAR CARTILAGE

– FIBRILLATION, AND DESTRUCTION OF CARTILAGE

– OSTEOARTHRITIC CHANGES

4 ZONES IN AVN

• A-ARTICULAR CARTILAGE

• B-ZONE OF ISCHAMIA• C–REPARATIVE ZONE

• D-NORMAL BONE

AVN IN FEMURAL NECK FRACTURES

• INCIDENCE OF AVN IS EXTREMELY VARIABLE

– 10 TO 20% IN UNDISPLACED FRACTURES.

– 20 TO 40% IN DISPLACED FRACTURES

• ANTERIOR DISLOCATIONS– LESS COMMON– OCCUR IN 8% OF CASES

• ACETABULAR FRACTURES

– ASSOCIATED WITH HIGH ENERGY GROUP

– 18 TO 20% OF FRACTURES

• .

AVN IN FEMURAL NECK FRACTURES

• IN POST. DISLOCATIONS VARIES FROM 6 TO 40%

– DEPENDS ON REDUCTION TIME

– ATTEMPTS AT REDUCTION– WEIGHT BEARING AFTER

REDUCTION IS CONTROVERSIAL

– DELAYED WEIGHT BEARING HAS NO ROLE ON AVN

– IT MAY DECREASE THE SEVERITY AND DEGREE OF LATE COLLAPSE IF NECROSIS DOES DEVELOP

AVN AND STEROIDS

THE PATHOGENESIS OF AVN IN HYPERCORTISONISM IS STILL UNKNOWN

• FAT EMBOLIZATION FROM THE LIVER, FROM BONE MARROW FAT CELLS, OR FROM DESTABILIZATION AND COALESCENCE OF PLASMA LIPOPROTEINS MAY BE RESPONSIBLE.

• CORTICOSTEROIDS AND THE ASSOCIATED INSULIN RESISTANCE HYPERTENSION AND ARTERIOSCLEROSIS, MAKING AVN A SO-CALLED CORONARY DISEASE OF THE HIP

• RELATED TO PEAK DOSAG.

• ROLE OF CUMULATIVE DOSE CONTRAVERSIAL

AVN AND RENAL FAILURE

• ASSOCIATED WITH CONGENITAL ANOMALIES AND ACQUIRED RENAL DISEASE

• AVN OF THE FEMORAL NECK COULD BE A COMPLICATION OF TREATMENT WITH RECOMBINANT GROWTH HORMONE IN CHILDREN WITH RENAL DISEASE

AVN AND ALCHOHOL• RISK IN CHRONIC ALCOHOLISM DUE TO FAT EMBOLI THAT ORIGINATE

FROM AN ASSOCIATED FATTY LIVER.• PANCREATITIS, ALSO STRONGLY ASSOCIATED WITH CHRONIC

ALCOHOLISM, MAY ALSO RESULT IN AVASCULAR NECROSIS DUE TO FAT EMBOLI.

• ACCOUNTS FOR 10%-40%.• RISK INCREASES WITH CUMULATIVE DOSE.

– WEEKLY CONSUMPTIONx NUMBER OF DRINKING YEARS

AVN AND DYSBARISM

• TWO PRIMARY CAUSES– TUNNEL WORKERS-DOES NOT OCCUR BELOW 17 POUNDS OF

ATMOSPHERIC PRESSURE.– DEEP SEA DIVING-MORE THAN 30 METERS

• FORMATION OF NITROGEN BUBBLES IN BLOOD VESSELS AND PRECIPITATE ISCHAMIA

AVN AND OTHER CAUSES

• HAEMOGLOBINOPATHIES– SICKLE CELL DISEASE AND THALASAEMIAS– SLUDGING,THROMBOSIS AND INFARCTION– INCIDENSE-20-60%

• GAUCHERS DISEASE– COMPRESSION MARROW BY LIPID LADEN HISTIOCYTES

• COLLAGEN DISEASES– VASULITIS OF SMALL VESSELS– VASCULAR THROMBOSIS AND INFARCTION– CORTICOSTEROIDS

• RADIATION– OBLITERATIVE ENDARTERITIS AND CELL DEAH– THRESHOLD DOSE NEEDED 3000 RADS

CLINICAL FEATURES

• 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 CASES• ONSET – INSIDIOUS AND CHRONIC• PAIN AT GROIN RADIATING TO THIGH OR BUTTOCK• ANTALGIC GAIT

CLINICAL FEATURES

• STAGE 1&2-ASYMPTAMATIC

• STAGE3-INTERMITTENT PAIN RADIATES TO INNER ASPET OF THIGH

• STAGE4

– SUDDEN INCREASE IN PAIN

– CLICKS-ARISING FROM CHAIR

– LIMITED HIP MOTION-ABD & INT ROTATION

• STAGE 5

– INTENSE PAIN

– CRUNCH FELT WITH EACH STEP

– CANE USED FOR SUPPORT

IMAGING

• RADIOGRAPHS• MRI• SCINTIGRAPHY• CT• LASER DOPPLER FLOWMETRY

X-RAY

• INCREASED DENSITY AFTER 2-3 MONTHS –DEPENDS ON 2 FACTORS

– RELATIVE INCREASE OF METAPHYSEAL OSTEOPOROSIS

– NEW BONE ON NECROTIC BONE• STAGE 3-IN LATERAL VIEW

– RADIO LUCENT LINE– DUE TO SUB CHONDRAL BONE

FRACT– CALLED AS-CRESCENT SIGN

• STAGE4– STEP-OF AT LATERAL MARGIN

OF INFARCT BENEATH ACTABULAR MARGIN

– WIDENING OF RADIOLUCENT LINE

CRESCENT SIGN• STAGE5-

– ASYMMETRY OF COUNTER OF FEMORAL HEAD

– PRONOUNCED FLATTENING– INCREASED DENSITY OF

DOME OF HEAD– O.A CHANGES

• STAGE6– SEVERE DEGENERATIVE

CHANGES

M R I

• VERY SENSITIVE METHOD FOR THE EARLIEST DIAGNOSIS THAN BONE SCAN

• SENSITIVITY 97% SPECIFICITY 98%

• BONE MARROW EDEMA

• COLLAPSE• INVOLVEMENT OF ACTABULUM

• STATUS OF OTHER HIP

• LOW INTENSITY SIGNAL IN T1 WEIGHTED IMAGE

• HIGH INTENSITY SIGNAL IN STIR IMAGE

MRI

• DOUBLE LINE APPEARANCE– ON T2-WEIGHTED MRI AT

THE REACTIVE INTERFACE BETWEEN ISCHEMIC (HIGH SIGNAL INTENSITY) AND NONISCHEMIC BONE (LOW SIGNAL INTENSITY).

• DETERMINATION OF EXACT STAGE & PATHOLOGICAL PROCESS

• ASSESSMENT OF THE RESPONSE OF THE OSTEONECROTIC FEMORAL HEAD TO OPERATIVE INTERVENTION

MRI T1 IMAGE signal from ischemic marrow• Single band like area of low

signal intensity.• 100% sensitivity• 98% specificity• SERPEGENOUS LINE-

– INTERFACE BETWEEN NECROTIC AND REPARATIVE ZONE

– LOCATED BETWEEN 10 O,CLOCK &2 0, CLOCK POSITION

• PITFALLS– MIMIC MULTIPLE PATHOGENIC

PROCESSES– SYNOVIAL HERNIATION PITS– FOVEA CENTRLIS– SUBCHONDRAL CYCTS– METASTASIS– INSUFFICIENCY FRACTUERS

MRI EARLY AND LATE

TRAUMATIC NECROSIS –MRI PROTOCAL

• IN FRX NOF,AND DISLOCATONS MRI ADVOCATED AFTER ONE MONTH

• WORSENING SIGNALS ON MRI AFTER 1 AND 3 MONTHS WARRANTS EARLY SURGICAL TREATMENT

CT SCAN

• ACCURATELY ASSESS THE FEMORAL HEAD COLLAPSE

• WIDH OF THE ARTICULAR CARTILAGE

• PRESENCE OF OSTEOPHYTES

• AXIAL CT SHOWING JNT SPACE NARROWING,SCLEROSIS AND OSTEOPHYTE

BONE SCAN

• EARLY DIAGNOSIS NEXT TO MRI

• USING 99MTC-SULFUR COLLOID

• HALL MARK OF VASCULARITY– PHOTOPENIC DEFECT.

• WITH REVASCULARISATION.– INCREASED UPTAKE OF

RADIONUCLIED– SUBSEQUENT INCREASED

SCINTIGRAPHIC ACTIVITY

• EARLY STAGES – COLD SPOT

• LATE STAGES - HOT SPOT

• SPECT IMPROVES DX ACCURACY

LASER DOPPLER FLOWMETRY

• MEASURES RBC INFLUX IN CAPILLARY BED

• PROBE HEAD IS APPLIED OVER TISSUE OF INTEREST

• LIGHT PENETRATES A DEPTH OF 0.5 TO 1.5 mm

• MAGNITUDE AND FREQUENCY OF DOPPLER SHIFT PROPORTIONATE TO FLOW OF BLOOD CELLS

STAGING

• FICAT• STEINBERG• ENNEKING'S • MARCUS AND ENNEKING • JAPANESE CRITERIA• SUGIOKA• ASSOCIATION RESEARCH CLASSIFICATION

OSSEOUS COMMITTEE (ARCO)-- COMBINATION

DISADVANTAGE

• DID NOT INCLUDE LESION SIZE

• NOT A SENSITIVE INDICATER OF PROGRESSION

FICAT AND ARLET CLASSIFICATION

•

stage

symptoms

X-ray findings Bone scan

Pathological finding biopsy

O PRE CLINICAL

normal uptake?

1 PRE RADIOLOGICAL

normal uptake Spontaneous repair of infarcted area

Abundant dead marrow cells,osteoblast,osteogenic cells

2A mild,PRE COLLAPSE

Sclerosis or cysts,

normal joint

lineand head contour

uptake Spontaneous repair of infarcted area

New bone deposited

2B mild Flattening

(crescent sign)

uptake Spontaneous repair of infarcted area

3 Mild

to moderate.COLLAPSE

Loss of sphericity ,collapse

uptake Subchondral #,collapse, compaction and fragmentation of necrotic segment

Dead bone trabuculae and marrow cells on both sides of fracture line

4 Moderate to severe

Joint space narrowig ,acetabular changes

uptake OA changes Degenerative changes in acetabular cartilage

STERNBERG STAGINGSTAGE CLINICAL AND LABORATORY FINDINGS

STAGE 0 . PATIENT IS ASYMPTOMATIC.

RADIOGRAPHY FINDINGS ARE NORMAL.

HISTOLOGY FINDINGS DEMONSTRATE OSTEONECROSIS

STAGE 1 PATIENT MAY OR MAY NOT BE SYMPTOMATIC.

RADIOGRAPHY AND CT SCAN FINDINGS ARE UNREMARKABLE.

AVN IS CONSIDERED LIKELY BASED ON MRI AND BONE SCAN RESULTS (MAY BE SUBCLASSIFIED BY EXTENT OF INVOLVEMENT]).A,B AND C

HISTOLOGY FINDINGS ARE ABNORMAL

STAGE 2. PATIENT IS SYMPTOMATIC.

PLAIN RADIOGRAPHY FINDINGS ARE ABNORMAL AND INCLUDE OSTEOPENIA, OSTEOSCLEROSIS, OR CYSTS.

SUBCHONDRAL RADIOLUCENCY IS ABSENT.

MRI FINDINGS ARE DIAGNOSTIC.

STERNBERG STAGINGSTAGE 3 PATIENT IS SYMPTOMATIC.

RADIOGRAPHIC FINDINGS INCLUDE SUBCHONDRAL LUCENCY (CRESCENT SIGN) AND SUBCHONDRAL COLLAPSE.

SHAPE OF THE FEMORAL HEAD IS GENERALLY PRESERVED ON RADIOGRAPHS AND CT SCANS.

SUBCLASSIFICATION DEPENDS ON THE EXTENT OF CRESCENT, AS FOLLOWS:

STAGE IIIA: CRESCENT IS LESS THAN 15% OF THE ARTICULAR SURFACE.

STAGE IIIB: CRESCENT IS 15-30% OF THE ARTICULAR SURFACE.

STAGE IIIC: CRESCENT IS MORE THAN 30% OF THE ARTICULAR SURFA

STAGE 4 FLATTENING OR COLLAPSE OF FEMORAL HEAD IS PRESENT.

JOINT SPACE MAY BE IRREGULAR.

CT SCANNING IS MORE SENSITIVE THAN RADIOGRAPHY.

SUBCLASSIFICATION DEPENDS ON THE EXTENT OF COLLAPSED SURFACE, AS FOLLOWS:

STAGE IVA: LESS THAN 15% OF SURFACE IS COLLAPSED AND LESS THAN 2MM STEP OFF

STAGE IVB: APPROXIMATELY 15-30% OF SURFACE IS COLLAPSED AND 2-4 MM STEP OFF

STAGE IVC: MORE THAN 30% OF SURFACE IS COLLAPSED STAGE 5

. RADIOGRAPHY FINDINGS INCLUDE NARROWING OF THE JOINT SPACE, OSTEOARTHRITIS

WITH SCLEROSIS OF ACETABULUM, AND MARGINAL OSTEOPHYTES STAGE6 FINDINGS INCLUDE EXTENSIVE DESTRUCTION OF THE FEMORAL HEAD AND JOINT

SHIMUZU Classification

• BASED ON MRI IMAGES WHICH DEFINE EXTENT ,LOCATION AND INTENSITY OF ABNORMAL SEGMENT IN BONE

• FINDINGS SUGGESTED-

• EXTENT OF ISCHEMIC SEGMENT IS DETERMINED AT THE OUTSET AND NOT INCREASED WITH TIME

• 1.LESION OCCUPYING <1/4 OF HEAD AND INVOLVING M/3 OF WT BEARING AREA RARELY GO FOR COLLAPSE

• 2.LESION OCCUPYING 1/2 OF HEAD AND INVOLVING BETN 1/3 AND 2/3 OF WT BEARING AREA GO FOR COLLAPSE(30%)

• 3.LESION OCCUPYING >1/4 OF HEAD AND INVOLVING 2/3 OF WT BEARING AREA GO FOR COLLAPSE WITHIN 3 YEARS

MRI CLASSIFICATION OF TAKORI

• FEM. HEAD BUT NOT EXTEND GROUP 1 - TYPE A• FAT INTENSITY AREA CONFINED TO MED – ANTERO-SUPERIOR

ACROSS HEAD• GROUP 2- TYPE B• BEYOND THE ZENITH TO POST . PART OF HEAD• GROUP 2- TYPE C • OCCUPY THE POST. HALF • GROUP 2- TYPE D • LARGER THAN TYPE C

KERBOUL- MEASURING OF LESION SIZE

• MEASURING ARC OF ARTICULAR SURFACE OVER LESION IN AP & LAT VIEWS

• ADDING TWO MEASUREMENTS GIVE –COMBINED NECROTIC ANGLE

TEST FOR HEMODYNAMICFUNCTION

• USING CANNULA SALINE IS INTRODUCED INTO METAPHYSIS AND FOLLOWING ARE NOTED-

• PRESSURE BEFORE AND AFTER THE INJECTION• NORMAL-10-20MM ,RISING BY ABOUT 15MM • IN AVN-IT IS INCREASED TO 3-4 TIMES

TREATEMENT

• SURGICAL

• NONSURGICAL

NON SURGICAL

• BED REST• NSAID• BISPHOSPHONATES-HAVE A ROLE• LIMITED WEIGHT BEARING

AVN-BISPHOSPHONATES

• ALENDRONATE– WEEKLY ,7.5mg ONCE BY

MOUTH FOR 12 WEEKS– IMPROVES PAIN AND ROM– BONE CHAGES/REMODELLING

DOES’NT PROGRESS– NO NEED TO TAKE

ANALGESICS

• MOA– ANTI RESORPTIVE– CONTRACTING REMODELLING

SPACES– DELAYS BONE COLLAPSE

AVN-BISPHOSPHONATES

• IT CAN BE USED IN ANY STAGE OF THE DISEASE

• IT DELAYS THE DEFINITIVE SURGEY BY 3-4 yrs.

SURGICAL TREATMENT

• CORE DECOMPRESSION• BONE GRAFTING

– CANCELLOUS BONE GRAFTING

– OSTEO CHONDRAL GRAFT

– BUSCLE PEDICLE BG

– FREE VASCULARISED BONE GRAFT

• ELECTRICAL STIMULATION• OSTEOTOMY• ARTHROPLASTY

HEAD PRESERVATION WITHOUT COLLAPSE

• NO TX (OBSERVATION)

– DRILLING ALONE– CORE DECOMPRESSION– CD + CANCELLOUS / FREE FIBULA

GRAFT– CD + MUSCLE PEDICLE GRAFT– CD + VASCULARIZED FIBULA GRAFT

HEAD PRESERVATION WITH COLLAPSE

VALGUS OSTEOTOMY

– VARUS OSTEOTOMY– SUGIAKO ANTERIOR ROTATION

OSTEOTOMY

HEAD SACRIFICE

SURFACE REPLACEMENT (BIRMINGHAM'S)

– NON – CEMENTED THR– CEMENTED THR– CEMENTED BIPOLAR– AMP– GIRDLE STONE – EXCISION

ARTHROPLASTY

GUIDELINES FOR MANAGEMENT

• LOCATION OF LESIONTYPE A (MEDIAL) - OBSERVATION WITH PERIODIC FOLLOWUP

• TYPE B,C - CORE DECOMPRESSION

• OTHER CONSIDERATIONS: • DIAGNOSIS: SLE DO WORSE • CONTINUED STEROID: DO

WORSE • AGE AND COMPLIANCE

.

GUIDELINES FOR MANAGEMENT

– CHECK EXTENT OF LESION • LESS THAN 200 DEGREES KERBOUL COMBINED

NECROTIC ANGLES OR LESS THAN 30% HEAD INVOLVEMENT - CONSIDER OSTEOTOMY:

• • 20 DEGREES LATERALLY PRESERVED CARTILAGE-

VARUS OSTEOTOMY

• NOT ABOVE- VALGUS OSTEOTOMY

• GREATER THAN 200 DEGREES; CONSIDER BONE GRAFTING

CORE DECOMPRESSION

• STAGE 1,2A LESIONS• SMALL CENTRAL LESION IN YOUNG NONOBESE PATIENTS• THEORETICAL –IT RELIEVES INTRAOSSEOUS PRESSURE CAUSED

BY VENOUS CONGESTION THERE BY INCREASING VASCULARITY AND DECREASING THE PROGRESSION OF DISEASE

• RELIEVE PAIN IN 75%• NOT USEFUL IN POST TRAUMATIC CASES • LENNOX ET AL-100% IN STAGE I• 29%IN STAGE IIA• 0% IN STAGE IIB

PROCEDURE• HUNGERFORD METHOD : POSITION-

SUPINE• INCISION :MIDLATERAL LONGITUDINAL

INCISION CENTERED OVER SUBTROCHANTERIC REGION

• UNDER C ARM CONTROL ENTRY POINT IS PLACED OVER THE LATERAL CORTEX OF THE INFERIOR PORTION OF THE GT THEN 3.2MM THREADED GUIDE PIN IS INSERTED ,THEN OVERREAM THE GUIDE PIN WITH 8MM REAMER

• PARTIAL WT BEARING ON CRUTCHES FOR 6 WEEKS

• CAN BE PROLONGED IF DONE IN ADVANCED DISEASE.

ADVANTAGES

• DECOMPRESSION OF RIGID INTEROSSEOUS CHAMBER• IMPROVEMENT OF VASCULARITY• PREVENTION OF ADDITIONAL ISHEMIC EPISODE • RELIEVES PAIN

BONE GRAFTING - TYPES

• CORE DECOMPRESSION + BG + ELECTRICAL STIMULATION- LESS BENEFICIAL

• CORE DECOMPRESSION+ NONVASCULARISED FIBULAR GRAFT – FOR STAGE 1 & 2

• MUSCLE PEDICLE GRAFT• VASCULARISED FIBULAR GRAFT

OTHER GRAFTING METHODS

• GANGJI- INJECTION OF AUTOLOGOUS BONE MARROW ASPIRATE AT CORED FEMORAL HEAD

• LIEBERMAN & URIST – HUMAN BMP– USEFUL IN 2A STAGE– 93% SUCCESS

NON VASCULARISED GRAFT

• PHEMISTER

• FOR STAGES 1 & 2

• NOT PROVED OF MUCH VALUE

• COMBINED WITH CORE DECOMPRESSION

VASCULARISED BONE GRAFT

• USING CORTICAL ,CANCELLOUS, VASCULARISED BONE GRAFT AND

• ACCURATE PLACEMENT WITHIN THE LESION AND UNDER SUBCHONDRAL BONE.

• ACCORDING TO URBANIAK ET AL –• 1.DECOMPRESSION OF THE HEAD MAY

INTERRUPT THE ISCHEMIA AND INTRAOSSEOUS HYPERTENSION

• 2.EXICISION OF THE SEQUESTRUM WHICH MIGHT INHIBIT REVASCULARIZATION.

• 3.FILLING THE DEFECT WITH OSTEOINDUCTIVE BONE GRAFT AND A VIABLE CORTICAL STRUT TO SUPPORT THE SUBCHONDRAL SURFACE AND TO ENHANCE REVASCULARIZATION.

• 4.PROTECT OF HEALING CONSTRUCT BY PERIOD OF LIMITED WT BEARING.

• TWO TEAMS NEEDED• POSITION –LATERAL • APPROACH-ANTEROLATERAL EXPOSE THE PROXIMAL

FEMUR• UNDER CARM CONTROL INSERT GUIDE PIN (AVOID

PENETRATION INTO ARTICULAR SURFACE) AND BY USING SEQUENTIAL REAMING CREATE CORE DIAMETER OF 16 -21MM BEGINNING FROM THE LATERAL CORTEX JUST DISTAL TO VASTUS RIDGE AND CORE EXTENDS WITHIN 3-5MM OF THE ARTICULAR SURFACE.

• HARVEST CANCELLOUS GRAFT FROM GT AND PACK IT INTO THE CAVITY USING IMPACTOR AND PLACEMENT CONFIRM WITH C-ARM AND CONTRAST MEDIUM

• 13CM LONG FIBULA WITH AS LONG A PEDICLE OF • PERONEAL ARTERY AND VEIN CAN BE

OBTAINED.• LEAVE AT LEAST 10CM OF FIBULA PROXIMAL TO

ANKLE MORTISE.• PEEL 3-4MM OF PERIOSTEUM FROM DISTAL END

OF GRAFT AND ROLL IT OVER THE BONE AND PLACE 3-0 ABSORBALE SUTURE CIRCUMFERENTIALLY TO SECURE THE PERIOSTEUM AND VASCULAR PEDICLE SO THAT IT IS NOT STRIPPED WHEN GRAFT IS INSERTED

• DIAMETER OF CORE IS 1-2MM LARGER THEN FIBULA DIAMETER

• ORIGINS OF VASTUS INTERMEDIUS AND LATERALIS IS RELEASED SO THAT PERONEAL AND LATERAL FEMORAL CIRCUMFLEX VESSELS CAN ANASTOMOSED WITHOUT TENSION.

• BLEEDING FROM THE CORTICAL BONE AT THE BASE OF GRAFT CONFIRMS THE VASCULARITY

• STABILSE THE GRAFT WITH .62MM K-WIRE

• DON’T REATTACH THE ORIGIN OF VASTUS MUSCLES

VASCULARISED BONE GRAFT

POST OP PERIOD.• BK SLAB• ON 3 RD DAY SLAB REMOVED• PROPHYLACTIC ANTICOAGULANT USING 500ML

LMW DEXTRAN - 5 DAYS,300MG ASPIRIN BDX6 WEEKS.

• DIGITAL SUBSTRACTION ANGIOGRAM TAKEN ON5TH DAY TO EVALUATE THE FUNCTION OF ANASTOMOSIS

• NO WT BEARING TILL 6 WEEKS• GRADUAL WT BEARING IN NEXT 3 MONTHS AND

FULL UNASSISTED AT 6 MONTHS

MUSCLE PEDICLE BONE GRAFT

• MEYER’S

• USES QUADRATUS FEMORIS

• POSTERIOR APPROACH-MOORE’S

• FOR STAGES 1 &2

IN B/L CASES

• SECOND GRAFT CAN BE DONE AFTER 3 MONTHS AFTER FIRST PROCEDURE

• 6 WEEKS BEFORE THE OPERATION ON THE SECOND HIP WT BEARING ON THE SIDE OF THE FIRST OPERATION IS

INCREASED TO 50%.

BAKSI

• USES TENSOR FASCIA LATA• USUALLY ANTERIOR APPROACH• FOR STAGES 1 & 2

OSTEOTOMIES

• TRANSTROCHANTERIC ROTATIONAL OSTEOTOMY• SUGIOKA – 1978• AGE <55 YRS• <30% HEAD INVOLVEMENT• IN IDIOPATHIC AND POST TRAUMATIC• FOR STAGE 1 & 2• REPOSITION OF NECROTIC ANTEROSUPERIOR PART TO NON

WT. BEARING LOCALE• PREVENTS PROGRESSIVE COLLAPSE• IMPROVE THE CONGRUITY

SUGIOKA ANT ROTATIONAL OSTEOTOMY

• PREVENTS PROGRESSIVE COLLAPSE OF ART SURFACE

• TO IMPROVE CONGRUITY OF JOINT

• REPOSITION THE NECROTIC ANT,SUP PART OF HEAD TO ANON WT BEARING AREA

• HEAD AND NECK SEGMENT ROTATED ANT.LY AROUND ITS LONG AXIS

• WT BEARING IS TRANSMITTED TO THE POST ARTICULAR SURFACE.

SUGIOKA ANT ROTATIONAL OSTEOTOMY-TECH

• LATERAL APPROACH– EXPOSE CAPSULE

– OSTEOTOMISE GT,REFLECT PROXIMALLY WITH TENDONS OF GLU MED,MIN ANDPIROFORMIS

– TRANSECT SHORT EXT ROTATORS

– INCISE CAPSULE CIRCUMFERENTIALLY

– PROTECT POST BRANCH OF MED CIR FEMORAL ART

– PLACE TWO PINS IN GT, LAT TO MED

– TROCHANTERIC OSTEOTOMY 10MM DISTAL TO IT LINE ,PERPENDICULAR TO LONG AXIS OF NECK

• SECOND OSTEOTOMY PERPENDICULAR TO FIRST OVER SUP MED ASPECT OF LT

• USE PROX PIN TO ROTATE PROXIMAL FRAGMENT 45 TO 90 degrees

• FIX THE OSTEOTOMY WITH 3 CC SCREWS OR NAIL AND PLATE

POST OP PERIOD

• CONTINUOUS SKIN TRACTION FOR 1ST WEEK(2 KG)• ONLY IN NIGHT FOR ANOTHER 2 WEEKS• ACTIVE MOVEMENTS ON 10 TO 14 DAY• PARTIAL WT BEARING AT 8 WEEKS• USE CRUTCHES UPTO 6 MONTHS

ROTATIONAL OSTEOTOMY

• GRADE

1

2

3

4

• SUCCES RATE

88%

83%

74%

70%

OTHER OSTEOTOMIES

• INTERTROCHANTERIC• FLEXION• EXTENSION• VARUS OR• VALGUS• FOR STAGE 2 AND 3 AVN WITH <30% HEAD INVOLVEMENT• SCHER AND JAKIM- VALGUS EXTENSION IT OSTEOTOMY

WITH CURETTAGE AND BG

ARTHROPLASTY - TYPES

• RESURFACING ARTHROPLASTY(BIRMINGHAM)• UNIPOLAR AND BIPOLAR HEMIARTHROPLASTY• THR

RESURFACING HEMIARTHROPLASTY

• WHEN AVN INVOLVES MORE THAN 30% HEAD

• INTRA OP ASSESSMENT OF THE ACETABULAR CARTILAGE TO BE DONE IF ANY DOUBT THEN THR SHOULD BE PERFORMED.

• GOOD ALTERNATIVE FOR YOUNG PATIENTS WITH ADVANCED AVN AS LITTLE BONE IS SACRIFICED

STAGE 3 & 4 CASES

• TOTAL HIP REPLACEMENT ARTHROPLASTY• PATIENT AGED 50 & MORE • ADVANCE OSTEOARTHRITIS AND REDUCTION OF JOINT

SPACE.• RADIATION NECROSIS • RESULT LESS THAN IDEAL. – NECROTIC BONE• POOR IN SICKLE CELL DISEASE.• CEMENTLESS ARE SUPERIOR OVER CEMENTED THR

Why separate treatment?

CARRY HOME MESSAGE

• MC CAUSE- IDIOPATHIC • STEROIDS – PEAK DOSES MORE SIGNIFICANT• # NOF- DISPLACED # AND MALREDUCED #• ONCE NECROSIS OCCURS CHANGES IRREVERSIBLE• MRI- EARLIEST TO DIAGNOSE• NO ROLE OF CONSERVATIVE TREATMENT TO PRESERVE

HEAD• EARLY DIAGNOSIS & JOINT PRESERVING MEASURES

RESULT IN BETTER PROGNOSIS• RESULTS OF REPLACEMENT ARE POOR IN YOUNGER THAN

OLDER AGE

THANK YOU

FOR PATIENT LISTENING