AVASCULAR NECROSIS OF
THE HUMERAL HEAD
Avascular necrosis (AVN) of the humeral head is
caused by loss of blood flow to a portion of the humeral head. This can be
associated with trauma, as seen in multiplepart fracture-dislocations. AVN can
also be seen in a wide variety of systemic diseases associated with sickle cell
anemia, caisson disease (deep sea diver decompression sickness),
mucopolysaccharidoses, or the use of systematically administered corticosteroids,
particularly when used at high dosage.
Early AVN has almost no symptoms of
pain, weakness, or stiffness. In most cases it is due to a single insult to the
bone, although in some patients with systemic disease the vascular loss may
result in multiple infarcts to the bone and, as such, the areas of AVN can
become larger over time. In all of these cases the symptoms occur secondary to
humeral head deformity associated with humeral head collapse, subchondral
fracture, or secondary damage to the cartilage surface due to joint
incongruity. When a late pathologic process and symp- toms occur, joint
replacement is often needed. In many of these cases the patients are young and
active and long-term survivorship of the prosthetic components is shorter than
in patients who are older and less active. For these reasons, early screening
of the joints at risk is recommended in patients with known risk factors and
when one joint is diagnosed with AVN. Multiple joint involvement is common in
patients with systemic causes for AVN. In most cases, the weight-bearing joints
will become symptomatic first, followed by the non weight-bearing joints. A
skeletal survey or a bone scintiscan to screen for AVN in other asymptomatic
joints is the most cost-effective means for detecting early AVN. MRI is the
most sensitive test for AVN but may be less practical for screening owing to
cost and time needed for each scan.
AVN in the humeral head is
characterized by a segmental loss of blood supply and is seen on radiography
and MRI as an area of sclerosis with well-demarcated margins. In more advanced
stages, the humeral segment involved undergoes collapse, initially seen as a
crescent sign below the subchondral surface. A crescent sign represents a sheer
fracture between the subchondral bone and the avascular segment of cancellous
bone below the articular surface. Later collapse of the humeral head will
result in nonspherical head and, later, arthritic changes, which are most
severe on the humeral side.
In later stages of the disease, secondary
damage occurs to the glenoid surface when articulated with a deformed humeral
head over a long period of time. In patients with significant articular
deformity and chronic and refractory pain, joint replacement either as
hemiarthroplasty or total shoulder arthroplasty is performed.
When both sides of the joint are
significantly involved, total shoulder arthroplasty is preferred to treat both
sides of the joint.
In early stages of AVN, surgeons some
have advo- cated surgical decompression of the avascular segment by drilling of
small holes into the bone from the distal aspect of the bone proximally into
the lesion. This is generally done by per utaneous methods using fluoroscopic
image control.
