Avascular Necrosis

Presenter: Dr. J. W. Kinyanjui
Moderator: Prof. Mulimba J. A. O.
22nd July 2013
 Definition
 Pathophysiology
 Aetiology
 Presentation
 Imaging
 Staging
 Management
 Cellular 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
 Interruption of blood flow to bone
 Affect bones with single terminal blood supply:
 Talus
 Carpals, tarsals
 Proximal humerus
 Proximal femur
 Femoral 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
 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
Alcohol abuse
CT diseases eg SLE
Hematologic (sickle cell disease,
 Metabolic
(hyperlipidemia, gout, renal
 Orthopedic disorders (slipped
capital femoral epiphysis,
developmental dysplasia of the
hip, Legg-Calve-Perthes disease)
Infection (osteomyelitis, HIV])
Renal transplantation
Radiation therapy
Gaucher disease
Malignancy (marrow
infiltration, malignant fibrous
 Caisson disease
 Pregnancy
 Bisphosphonate use
 Severance of blood supply – displaced femoral neck
 Scaphoid and talus – proximal osteonecrosis due to
distal origin of vessels
 Osteoarticular impact – localised osteonecrosis in
convex surfaces (osteochondroses)
Non traumatic osteonecrosis
Presentation - History
 Trauma
 Corticosteroid use
 Alcohol intake
 Medical conditions – malignancy, thrombophilia, SLE, SCD
 Pain – progressive, severity correlates with size of infarct
 Deformity and stiffness – later stages
Presentation - examination
 Limp
 Antalgic gait
 Restricted ROM
 Tenderness around bone
 Joint deformity
 Muscle wasting
Imaging: X ray
 Initially 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: MRI
 90% sensitive
 Reduced subchondral intensity on T1 representing
boundary between necrotic and reactive bone
 Low signal on T1 and high signal on T2 – reactive zone
 Changes detected early
Radionuclide scan
 Donut 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
 Definitive diagnosis
 Usually retrospective/confirmatory during surgery for
 Occasionally biopsy of sclerotic lesion
 Necrosis 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
Intramedullary pressures
 Cannula 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 Staging
Clinical and radiological findings
Asymptomatic, radiology normal, histological diagnosis
+-symptoms, normal CT and X ray, early changes on MRI
Symptomatic, bone density changes on X ray, diagnostic MRI findings
Cresent sign. IIIa - <15% articular surface, IIIb 15 – 30%, IIIc >30%
Collapse of head IVa - <15% surface collapsed, IVb 15 – 30%. IVc >30%
OA – narrowed joint space, acetabular sclerosis, marginal osteophytes
Extensive destruction of joint and involved bone
Management principles
 Early stages (I & II):
 Bisphosphonates prevent collapse
 Unloading osteotomies
 Medullary decompression + bone grafting
 Intermediate stage (III & IV):
 Realignment osteototmies, decompression
 Arthrodesis
 Late stage (V & VI):
 Analgesia, activity modification
 Arthrodesis
 Arthroplasties
Management - conservative
 Offloading affected joints with use of crutches
 Immobilisation
 Analgesia
 Bisphosphonates to delay femoral head collapse
 Statins in patients on high dose corticosteroids –
reduced lipid deposition
Core decompression
 Indicated 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 osteotomy
 Indicated 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
 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 syndromes
 Kienbock’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,
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