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Avascular Necrosis and Related Disorders


The different causes of true osteonecrosis are numerous with differing ways that the blood supply becomes obliterated. This section will only deal with the causes while the following section will discuss the pathogenesis of true osteonecrosis.


Avascular necrosis due to no apparent reason is the most common presentation. This classically involves the hip of a child, 4-8 years old, that presents to the clinician with a painful limp. This scenario is termed Legg Calve Perthes disease and will be discussed later.


Probably the most common known cause for osteonecrosis is long term systemic corticosteroid use. Because the goal of corticosteroids is to reduce inflammation, it is important to ask those patients with inflammatory diseases, e.g., rheumatoid arthritis, seronegative spondyloarthropathies, scleroderma, and systemic lupus erythematosus (SLE), if they are taking corticosteriods. The most common proposed mechanism of infarction due to corticosteroid use is related to mobilized lipids from the liver that occlude end arteries in the bone. While long term use is the most investigated, there are numerous reports of short term corticosteroid use resulting in avascular necrosis. Not only exogenous (therapeutic) corticosteroids give rise to osteonecrosis. Excess endogenous corticosteriods, Cushing syndrome, may as well. The proposed mechanism of infarction for endogenous is exactly the same as exogenous corticosteroid use.


Trauma is also a common cause of osteonecrosis. Both dislocation and fracture may result in a deficient blood supply. Dislocation and fracture of the proximal femur and fracture of the scaphoid are probably the most popular. Dislocation of the proximal femur will rupture the ligamentum teres and circumflex arteries that supply blood to the femoral head. Regarding two types of proximal femur fractures, extracapsular and intracapsular, it is the intracapsular fracture that is most associated with osteonecrosis. Management of these fractures is key to restoring the possible disruption of arterial supply. Close approximation and stability at the fracture site to avoid nonunion seems to be especially important. This concept holds true for all fractures, but emphasis has historically been put on the proximal femur and scaphoid fractures.


Conditions such as rheumatoid arthritis, scleroderma, SLE, and dermatomyositis result
in thickening and necrosis of vessel basement membrane which can lead to occlusion of vessels. Because these are inflammatory diseases, treatment usually includes corticosteroids which, as discussed above, will at least contribute to the possibility of getting avascular necrosis.


Osteonecrosis is a definite risk in chronic alcoholism due to fat emboli that originate from an associated fatty liver. The femoral head is the most common location for this to occur. Pancreatitis, also strongly associated with chronic alcoholism, may also result in avascular necrosis due to fat embolism.


The sluggish blood flow of the sickle-shaped cells in this disease results in a diminished blood supply leading to avascular necrosis. Unlike other causes of avascular necrosis, the location in the skeleton due to sickle cell disease takes place in areas of active hematopoiesis.

There are many other causes of avascular necrosis including Caisson's disease (Nitrogen bubbles released out of solution from cells and causing embolism - "The Bends"). Gout - it is reported that approximately 30% of patients with gout experience avascular necrosis. Pregnancy is also a known risk factor.

So...how can we remember such a long list of causes for avascular necrosis? MEMORIZE THEM...or remember "ASEPTIC"

A - Alcoholism

S - Sickle cell disease

E - Exogenous and Endogenous steroids

P - Pancreatitis and Pregnancy

T - Trauma

I - Idiopathic

C - Collagen vascular disease or Caisson's disease

How do you remember that gout is a risk factor? MEMORIZE IT (I don't have any other hints.)


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