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AVASCULAR NECROSIS OF THE HUMERAL HEAD


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.
AVASCULAR NECROSIS OF THE HUMERAL HEAD

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.

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