AVASCULAR NECROSIS (AVN)

Osteonecrosis
Arif@Khin Maung Ohn
 Avascular necrosis

After the completion of this lecture, the students should be able to:

Define osteonecrosis.

Describe the various site of avascular necrosis

Discuss the incidence of osteonecrosis and identify the four most common causes

Describe the pathophysiology of avascular necrosis.

Describe the methods used in the diagnosis and treatment of osteonecrosis of

femoral head.
 Definition
Cellular death of bone components secondary
to interruption of blood supply

Consequent collapse of bone components

Proximal epiphysis of femur most commonly

affected
 various site of avascular necrosis
Interruption of blood flow to bone
Affect bones with single terminal blood supply:
Talus
Scaphoid
Carpals, tarsals
Proximal humerus
Proximal femur
Femoral condyles
Bone marrow, medullary bone and cortical bone
necrosis results
AVN Talus
AVN Humeral Head
AVN Scaphoid
 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 Infection (osteomyelitis, HIV])
Alcohol abuse Renal transplantation
CT diseases eg SLE Radiation therapy
Hematologic (sickle cell disease, Gaucher disease
hemoglobinopathies, Malignancy (marrow infiltration,
thrombophilia) malignant fibrous histiocytoma)
Metabolic (hyperlipidemia, gout, Caisson disease
renal failure) Pregnancy
Orthopedic disorders (slipped
Bisphosphonate use
capital femoral epiphysis,
developmental dysplasia of the
hip, Legg-Calve-Perthes disease)
 Trauma

Severance of blood supply displaced femoral

neck fractures
Scaphoid and talus proximal osteonecrosis
due to distal origin of vessels
Non traumatic osteonecrosis
 Presentation - History
Trauma

Corticosteroid use

Alcohol intake

Medical conditions malignancy, thrombophilia, SLE

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 up to 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
Kienbocks disease idiopathic avascular necrosis of
the lunate bone that leads to collapse and
progressive carpal arthritis.
 Legg-Calve-Perthess idiopathic
osteonecrosis of femoral capital epiphysis in
children. Treated with orthotics, traction,
surgery to rotate the femoral head
 Caterall head-at-risk signs
Associated with poor results

lateral subluxation (most important)

calcification lateral to the epiphysis

Gage's sign: V shaped defect laterally

metaphyseal cysts

horizontal growth plate

terall head-at-risk sig

metaphyseal cysts