AVASCULAR NECROSIS

Aldwin Ardwiyardi
Helena A. K. Cantika P.
Gaza Muhammad Anjartama
Avascular Necrosis
• Avascular Necrosis or
osteonecrosis is the death of
bone tissue due to lack of
blood supply
• Affected bone cells die, and
the dead bone weakens and
may begin to fracture and
collapse
• It most commonly affects the
head of femur, but can also
affect other bones
Symptoms
• Avascular necrosis can cause pain and loss of mobility
• Pain may be most noticeable during physical activity
• But eventually may hurt even when at rest
Risk factor
• Trauma (injury)
• Steroid use (high dose)
• Excesive alcohol use
• Clotting disorder
• Disease (SLE, HIV, Cancer)
Treatment
• Avascular necrosis of the hip will tipically treated with surgery
• Surgical options may include core decompression, bone reshaping,
osteotomy, bone grafting, or joint replacement
Alcohol and AVN
• Very common risk factor is excessive use of alcohol
• The greater the consumption of alcohol, the higher the risk of
developing AVN
• The exact mechanism of how alcohol, causes AVN is not absolutely
understood, but it is believed that excessive fatty substances are
produced and build up in the very small blood vessels of the bone.
Blockage then occurs which decreases blood flow to the femoral head
causing bone death.
pathogenesis of osteonecrosis in relation to
alcohol use
• The pathogenesis of osteonecrosis in relation to alcohol use, with fat
emboli produced by the liver occluding vessels in the subchondral
bone
• It was previously assumed that osteonecrosis was caused by the
active metabolites of ethanol
• The direct cytotoxicity of lipid peroxidation, caused by alcohol and its
metabolites, might further insult ischemic osteocytes, resulting in an
irreversible state of the injury, leading to cell death, and finally
osteonecrosis
• Changes in the bone marrow after alcohol abuse can also lead to
venous stasis, increased intraosseous pressure, decreased perfusion
and bone death
• There is still controversy regarding length and quantity of alcohol
abuse that results in osteonecrosis, with Jones5stating that the
alcohol threshold for alcohol-associated osteonecrosis being a
consumption of 150 litres of 100% ethanol at 400ml or more of
absolute ethanol a week
Fat emboli
• Alterations in lipid metabolism cause hyperlipidemia with fat
mobilization and embolisation to the subchondral arterioles.
Overload of subchondral fat results in vascular stasis, local
hypercoagulability, endothelial damage, and subsequent intravascular
coagulation. The use of lipid lowering agents has been consistently
shown to improve this alteration in blood flow.
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