avascular necrosis

Presenter: Dr. J. W. KinyanjuiModerator: Prof. Mulimba J. A. O.

22nd July 2013

OutlineDefinitionPathophysiologyAetiologyPresentationImagingStagingManagement

DefinitionCellular death of bone components secondary

to interruption of blood supply

Consequent collapse of bone components

Pain, loss of function of joints

Proximal epiphysis of femur most commonly affected

PathophysiologyInterruption of blood flow to boneAffect bones with single terminal blood

supply:TalusCarpals, tarsalsProximal humerusProximal femurFemoral condyles

Bone marrow, medullary bone and cortical bone necrosis results

Final pathway from multiple causes

Predisposing factors

Distance from vascular territory of bone

Enclosed by cartilage limiting vascularity

Endarterioles supply trabelcular bones

Pathways to necrosis

Vascular occlusion – direct trauma, stress fracture, SCD, venous stasis

Intravascular coagulation – hypercoaguable states

Primary cell death – alcohol, steroids, transplant patients

Bone necrosis after 12 – 48 hrs of anoxia

Reactive new bone formation around necrotic bone

Granulation tissue over necrosed bone – sclerosis

Structural failure – subchondral fracture 1st

Segmental collapse dependant on stress and area of necrosis

AetiologyTraumaSteroidsAlcohol abuseCT diseases eg SLEHematologic (sickle cell

disease, hemoglobinopathies, thrombophilia)

Metabolic (hyperlipidemia, gout, renal failure)

Orthopedic disorders (slipped capital femoral epiphysis, developmental dysplasia of the hip, Legg-Calve-Perthes disease)

Infection (osteomyelitis, HIV])

Renal transplantationRadiation therapyGaucher diseaseMalignancy (marrow

infiltration, malignant fibrous histiocytoma)

Caisson diseasePregnancyBisphosphonate use

Trauma

Severance of blood supply – displaced femoral neck fractures

Scaphoid and talus – proximal osteonecrosis due to distal origin of vessels

Osteoarticular impact – localised osteonecrosis in convex surfaces (osteochondroses)

Non traumatic osteonecrosis

Presentation - HistoryTrauma

Corticosteroid use

Alcohol intake

Medical conditions – malignancy, thrombophilia, SLE, SCD

Pain – progressive, severity correlates with size of infarct

Deformity and stiffness – later stages

Presentation - examinationLimp

Antalgic gait

Restricted ROM

Tenderness around bone

Joint deformity

Muscle wasting

Imaging: X rayInitially normal upto 3 months

Sclerosis

Flattening

Subchondral radiolucent lines (cresent sign)

Collapse of cortex

OA

Imaging: CT scan

Used to assess extent of disease and calcification

Clearly shows articular deformity

Calcification and bone collapse

Central sclerosis in femoral head produces asterix sign

Imaging: MRI90% sensitive

Reduced subchondral intensity on T1 representing boundary between necrotic and reactive bone

Low signal on T1 and high signal on T2 – reactive zone (diagnostic)

Changes detected early

Radionuclide scanDonut sign – central reduced uptake with

surrounding rim of increased uptake

More sensitive than plain films in early AVN

Less sensitive than MRI

Necrotic zone surrounded by reactive new bone formation

HistologyDefinitive diagnosisUsually retrospective/confirmatory during

surgery for treatmentOccasionally biopsy of sclerotic lesionNecrosis of cortical bone is followed by a

regenerative process in surrounding tissues. Increased osteoclastic activity to remove

necrotic bone and increased osteoblastic activity as a reparative process

Intramedullary pressuresCannula into metaphysis

Measure at rest and after saline injection

Femoral head:10 – 20 mmHg, increasing by 15 mmHg after

saline

Markedly increased values in AVN (3 to 4 fold)

Less marked increase in OA

ARCO StagingStage Clinical and radiological findings

0 Asymptomatic, radiology normal, histological diagnosis

I +-symptoms, normal CT and X ray, early changes on MRI

II Symptomatic, bone density changes on X ray, diagnostic MRI findings

III Cresent sign. IIIa - <15% articular surface, IIIb 15 – 30%, IIIc >30%

IV Collapse of head IVa - <15% surface collapsed, IVb 15 – 30%. IVc >30%

V OA – narrowed joint space, acetabular sclerosis, marginal osteophytes

VI Extensive destruction of joint and involved bone

Management principlesEarly stages (I & II):

Bisphosphonates prevent collapseUnloading osteotomiesMedullary decompression + bone grafting

Intermediate stage (III & IV):Realignment osteototmies, decompressionArthrodesis

Late stage (V & VI):Analgesia, activity modificationArthrodesisArthroplasties

Management - conservativeOffloading affected joints with use of

crutchesImmobilisationAnalgesiaBisphosphonates to delay femoral head

collapseStatins in patients on high dose

corticosteroids – reduced lipid deposition

Core decompressionIndicated in ARCO I and II

8 – 10 mm anterolateral core of bone

Filled with bone graft (vascularised/non vascularised)

Decompresses medullary cavity, reduces pain

Cortical (osteoconductive) or cancellous(osteoinductive) bone graft

Vascularised graft may reverse necrosis

Realignment osteotomyIndicated in ARCO III & IV

Used to relocate necrotic area from weight bearing portion of femoral head

Angular osteotomies more common

Multiple techniques for holding the fixation

Sugano intertrochanteric rotational osteotomy technically demanding but higher success rate

Arthroplasty

Indicated in ARCO IV onwards

Main aim is pain reduction

Young patients will need revision

Higher failure rates than in OA

Hemi arthroplasty an option

Eponymous syndromesKienbock’s disease – idiopathic avascular

necrosis of the lunate bone that leads to collapse and progressive carpal arthritis. PRC as treatment

Legg-Calve-Perthes’s – idiopathic osteonecrosis of femoral capital epiphysis in children. Treated with orthotics, traction, surgery to rotate the femoral head

Preiser's disease – idiopathic osteonecrosis of scaphoid. Collapse with progressive arthritis. PRC, Excision and fusion,