Avascular necrosis Pathogenesis Clinical features

Definition: AVN or osteonecrosis is a condition where Usually by the time pt presents, lesion is often advanced
the bone has impaired blood supply or severe cell
damage which is due to traumatic and non-traumatic 1. Pain near joint a/w stiffness
conditions that will lead to ischemia n necrosis of the 2. Local tenderness
bone itself. 3. Swollen nearby joint
4. Restricted movements
Sites (most common): 5. Advanced AVN can cause bone deformity n ms
wasting
1. Femoral head 6. Neurologic deficit bcoz if the nerve affected by
2. Femoral condyles necrosis and compression of affected bones
3. Head of humerus
4. Proximal poles of scaphoid & talus Investigation

Because they lie at the outskirts of the bones main X-ray subarticular segment of increased bone density
vascular supply and are largely enclosed by articular Stage 1: Bone death w/o structural change because of reactive new bone formation in the
cartilage -> avascular structure and restrict area for surrounding living tissue which increases total mass of
entry of BV Within 48 hours after infarction there is marrow necrosis calcified bone. Usually when detected by x-ray the dz is
n cell death at advanced stage
Non-traumatic causes of osteonecrosis
Hypercortisolemia Marrow infiltration Stage 2: repair and early structure failure
Cortisol administration Gauchers Dz **
Cushings Dz Malignancy Some days/weeks after infarction, the surrounding,
Hyperlipidemia Infection living bone shows a vascular rxn: new bone is laid down
Alcohol abuse Septic arthritis upon the dead trabeculae n the increase in bone mass
Hemoglobinopathy Other shows on the x ray as exaggerated density. Despite this
Sickle-cell dz Perthes dz (children) active repair, small fractures begin to appear in the dead
Capillary occlusion SLE bone.
Dysbaric osteonecrosis Clotting disorders
Stage 3: Major structural failure MRI & CT usually show more detailed results

Pathology The necrotic portion starts to crumble and the bone

outline become distorted.
1. Severance of blood supply
2. Venous stasis and retrograde arteriolar stoppage Stage 4: Articular destruction
3. Intravascular thrombosis
4. Compression of capillaries & sinusoids by marrow Cartilage, being nourished mainly by synovial fluids, is
swelling preserved even in advanced necrosis. However, severe
distortion of the surface eventually leads to cartilage
breakdown and secondary osteoarthritis.
Radionucleotide bone scan Complication:

Better sensitivity in early stage of AVN as compared to 1. Subchondral necrosis -> subchondral fracture n
plain film better blood flow and osteoblastic activity. fracture of the bone affected
2. Deformity of the articular surface
Shows doughnut phenomenon- central area of 3. OA
decreased uptake is surrounded by an area of increased 4. In later stages, sclerosis and total destruction
uptake indicates the reactive zone surrounding the of joint can occur
necrotic area. 5. Non-union of fracture
6. secondary muscle wasting

NB **

*Gauchers Disease is a familial dz occurs predominantly

in Ashkezi Jews. Deficiency of specific enzyme cause abn
accumulation of glucocerebroside in the RE system.
Effects are seen in liver, spleen and bone marrow where
the large polyhedral Gaucher cells accumulate. Leading
to reduced circulation to affected bone and causes
osteonecrosis.
Treatment
Hip is commonly affected but lesions also appear on
1. The possible cause should be eliminated other locations.
2. Stages 1&2; bone collapse can be prevented by
combination of weight relief, splintage and https://www.gauchercare.com/en/patient/about/SignsA
surgical decompression of the bone. ndSymptoms/Adults.aspx
3. Stage 3 (bone collapse has occurred);
realignment osteotomy (transfer stress to
undamaged area) can relieve pain & prevent
further bone distortion.
4. In stage 4 tx is same as osteoarthritis (applied
only in lower limb) in upper limb, no tx
required.
5. Most ultimate tx is total hip arthroplasty.