Presenter: Dr. J. W.

Kinyanjui
Moderator: Prof. Mulimba J. A. O.
22nd July 2013
Outline
Definition
Pathophysiology
Aetiology
Presentation
Imaging
Staging
Management
Definition
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

Pathophysiology
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 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
Aetiology
Trauma
Steroids
Alcohol abuse
CT diseases eg SLE
Hematologic (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 transplantation
Radiation therapy
Gaucher disease
Malignancy (marrow infiltration,
malignant fibrous histiocytoma)
Caisson disease
Pregnancy
Bisphosphonate 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 - 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

(diagnostic)

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 formation

Histology
Definitive diagnosis
Usually retrospective/confirmatory during surgery for
treatment
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 process
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
Stage 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 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
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 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,