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In Kienböck disease, also known as lunatomalacia, the collapse of the carpal lunate occurs because of avascular necrosis. The disease occurs most often in young adults between 15 and 40 years of age and is usually unilateral. The actual cause of the vascular impairment has not been determined, although several etiologic factors have been proposed: (1) single or repetitive microfractures that result in vascular embarrassment; (2) traumatic disruption of circulation or ligamentous injury with subsequent degeneration; (3) primary circulatory disease; and (4) shortening of the ulna relative to the radius, which decreases the support for the lunate. The current theory is that the disease occurs in persons with a mechanical and/or vascular predisposition, when repetitive compression of the lunate between the capitate and distal radius disrupts the intraosseous structures. Chronic compression of the lunate (which is unavoidable in normal wrist function), effusion, and synovitis may interfere with healing and provide a mechanism for progressive collapse of the bone.


The primary signs and symptoms of Kienböck disease are wrist pain that radiates up the forearm and stiffness, tenderness, and swelling over the lunate. Passive dorsiflexion of the middle finger produces the characteristic pain. Physical examination reveals limitation of wrist motion, usually dorsiflexion, and a striking weakness of grip. The pain and weakness increase as the lunate collapses and degenerative changes develop, making the disability both severe and chronic.

The avascular necrosis of the lunate may vary in degree but produces consistent and typical radiographic changes. Initial radiographic findings may be normal except for a short ulna, but sclerosis of the lunate the radiographic hallmark of the disease develops with time. The lunate progressively loses height and eventually fragments. Further lunate collapse leads to carpal instability and resultant degenerative joint changes, including the formation of cysts within the lunate. The degenerative changes may ultimately involve the entire wrist. The Lichtman classification utilizes radiographic findings to stage disease severity (see table on Plate 3-37). This classification helps guide treatment and allows the evaluation of disease progression with time.

Because the specific etiology of Kienböck disease is not fully understood, no reliable treatment has been established, although many have been proposed. Prolonged immobilization relieves symptoms, but the revascularization of the lunate does not occur readily in adults, and a decrease in range of motion in the wrist and grip strength gradually occurs. A simple excision of the lunate produces good results initially, but, ultimately, the remaining carpal bones migrate, leading to joint incongruity, limited wrist motion and grip strength, and degenerative osteoarthritis.
Current surgical options aim to either unload the lunate, revascularize the lunate, or perform limited or complete wrist fusions to halt disease progress and diminish symptoms. Joint-leveling procedures (shortening the radius) have produced excellent long-term results, particularly if performed early in the disease process. Wrists that have either neutral or positive ulnar variance cannot reliably be treated with shortening of the radius. Capitate shortening has been utilized to unload the lunate in these situations. Vascularized bone grafting, most frequently from the dorsal radius, is often combined with these unloading procedures with the aim of improving the likelihood for lunate revascularization. Recently, there have been reports of decompressing the distal radial metaphysis via a limited radial incision; this simple procedure has shown promise in earlier stages of Kienböck disease. With advancing stages of collapse and/or degenerative changes, surgical options are limited to partial versus complete wrist fusion.