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