Osteonecrosis
Raymond S. Fryrear
Steven L. Moran
I. Introduction
Avascular necrosis (AVN) is defined as cellular death of bone components due to interruption of the blood supply. This results in eventual bone collapse, joint destruction, pain, and loss of joint function. AVN is associated with numerous conditions and usually involves the epiphysis of long bones, such as the femoral head, humeral head, and the femoral condyles, but the small bones of the wrist can also be affected, including the lunate, scaphoid, and capitate.
II. Etiology
AVN within the hand and wrist is often idiopathic, with no antecedent trauma or identifiable cause; however, several risk factors have been identified for the development of AVN in long bones and these include:
Corticosteroids: The most common proposed mechanism of AVN due to corticosteroid use is related to mobilized lipids from the liver that occlude end arteries in the bone. While the risks of long-term steroid use have had the most investigation, there are numerous case reports of short-term corticosteroid use resulting in AVN. The endogenous overproduction of corticosteroids, which occurs in Cushing syndrome, may also predispose to the development of osteonecrosis.
Collagen vascular disorders: Conditions such as rheumatoid arthritis, scleroderma, SLE, and dermatomyositis can produce a vasculitis, which can lead to the occlusion of arteries and arterioles resulting in the disruption of bone blood flow. Treatment of these diseases usually includes the regular use of corticosteroids placing these patients at a higher risk of AVN.
Alcoholism: Chronic alcoholism and associated fatty liver disease are thought to increase the incidence of fat emboli, which may, in turn, lead to the development of AVN. The femoral head is the most common location for this to occur.
Sickle cell disease: The sickle-shaped cells in this disease can result in small vessel thrombosis and bony infarcts. When AVN occurs in patients with sickle cell disease, it usually occurs in bones that are actively participating in hematopoiesis.
Other proposed causes of AVN may include Caisson disease, a condition where nitrogen bubbles are released out of solution from cells and result in embolism production. Gout has also been reported as a risk factor for AVN with approximately 30% of patients with gout experiencing some form of AVN.
III. Pathogenesis
The pathogenesis of osteonecrosis is commonly divided, artificially, into four different phases: the avascular phase, the revascularization phase, the repair phase, and the deformity phase. Histological and radiographic changes are associated with each of these phases.
Avascular phase: This first step in the process of osteonecrosis begins with an infarction to a section of the bone. This infarction typically takes place within fatty marrow adjacent to the subchondral cortex of the bone. The infarction at the subchondral portion of the bone leads to bone loss. As the subchondral bone becomes necrotic, the overlying cartilage hypertrophies as it attempts to convert itself to bone. The radiographic changes that correspond to this first phase are often minimal. Osteopenia or subtle soft tissue changes may be appreciated. The osteopenia is not due to the infarction itself, but hyperemia surrounding the involved area as well as synovitis and increased osteoclastic activity.
Revascularization phase: Increased osteoclastic and osteoblastic activities are seen during this stage. Radiographs may show areas of lucency and sclerosis. Increasing cell death beneath the articular surface results in fragmentation and collapse of the overlying cortex.
Repair phase: The repair phase actually begins when revascularization begins. There is a variable degree of reconstitution and healing that is dependent upon
The degree of blood loss and cell death in the initial insult
The patient’s immune system and healing response
Whether the joint is weight bearing versus nonweight bearing
Deformity phase: The deformity phase is highly variable and site specific. It is also dependent upon ongoing loading to the bone (weight-bearing areas show increase in deformities).
IV. AVN in the Hand and Wrist
AVN is most frequently found in the scaphoid, lunate, and capitate. Isolated ischemia of the other carpal bones is exceedingly rare.
AVN of the scaphoid (Preiser’s disease)
In 1910, Preiser described an osteitis of the scaphoid, which was distinct from that seen in scaphoid fractures. Preiser’s disease is defined as AVN of the scaphoid occurring in the absence of trauma and/or prior wrist procedures; where at least 80% of the scaphoid shows radiographic changes. This definition allows one to distinguish Preiser’s disease from AVN of the scaphoid, which is the direct result of fracture, most commonly proximal pole fracture. The etiology has been loosely linked to collagen vascular disease, steroid therapy, and repetitive trauma. This condition has also been reported in children.
Clinical presentation and diagnosis
Patients may present with pain within the snuff box, synovitis, or generalized wrist pain. Radiographs typically show sclerosis within the scaphoid, and there is often fragmentation of the proximal articular surfaces. MRI is valuable for identifying early cases as well as the extent of avascularity. Normal marrow elements produce high-intensity signals on T1-weighted images. Avascularity or marrow edema will lead to alterations in these signals. Preiser’s disease may be graded according to its radiographic and MRI appearance.
Stage I: Normal radiographs with a positive bone scan or avascularity on MRI
Stage II: Increased density in the proximal pole on plain radiographs with generalized osteoporosis
Stage III: Fragmentation of the proximal pole on plain radiographs, with or without pathologic fracture
Stage IV: Carpal collapse with osteoarthritis Kalainov has also described a classification system, which grades the scaphoid’s avascular status as generalized (Type I) or segmental vascular impairment (Type II). The differentiation between global ischemia and segmental ischemia is made with MRI. Those patients with Type II disease, or localized ischemia, have a more favorable clinical outcome.
Treatment
The treatment of Preiser’s disease remains controversial. Multiple treatment options have been suggested including observation, silicone replacement, arthroscopic debridement, proximal row carpectomy, and scaphoid excision with four-corner fusion. The two largest series reported on the treatment if Preiser’s disease includes the use of silicone replacement and proximal row carpectomy. Procedures that attempt to preserve the scaphoid and reverse the effects of AVN are limited to vascularized bone grafting. Salvaging the scaphoid requires that the cartilaginous shell of the bone remain intact and the radiocarpal and midcarpal joints must be free of any arthritic changes. Vascularized bone grafts from the dorsal distal radius have been reported with some success; however, equally successful results have been reported with proximal row carpectomy. Given the lack of reliable treatment options, in the absence of severe pain and disability a conservative approach may be warranted and should certainly be discussed with the patient prior to embarking on salvage surgery.
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