TO THE EDITOR:
The etiology of Kienböck disease has been a matter of debate for many years. Bonzar et al., in "Kienböck Disease and Negative Ulnar Variance" (80-A: 1154—1157, Aug. 1998), confirmed an association between negative ulnar variance (shortness of the ulna relative to the radius) and Kienböck disease, and they concluded that their findings support the hypothesis proposed by Hultén2 that relative shortness of the ulna may predispose to Kienböck disease. However, because relative shortness of the ulna seemed to be a predisposing rather than a causative factor, they suggested that unknown factors may influence the development and expression of Kienböck disease. Thus, it seems justified to call attention to a theory on the etiology of Kienböck disease4,5, which postulates that relative shortness of the ulna has a secondary influence on a primary necrotic lunate.
Hemarthrosis in the hip joint may cause avascular necrosis of the femoral head because of increased intra-articular pressure (joint tamponade) after an undisplaced intra-articular fracture1,8,9. In contrast, when the joint capsule is ruptured during a displaced fracture, no joint tamponade occurs because the intra-articular bleeding is drained8,9.
Analogously, the fact that Kienböck disease is often preceded by minor trauma10 but is rare after dislocation of the lunate7 indicates that it might be the result of tamponade of the wrist joint. An intra-articular pressure of ten kilopascals due to hemarthrosis has been recorded after an undisplaced fracture of the scaphoid4. As is the case when there is tamponade of the hip joint in association with an undisplaced fracture8,9, aspiration of the intra-articular hematoma may prevent the development of osteonecrosis.
According to this theory, the association between shortness of the ulna and Kienböck disease may be related to deformation of the necrotic lunate by the relatively elongated radius. The success of operative ulnar lengthening (or radial shortening), when performed before advanced fragmentation and collapse has occurred, can be explained by the role of the triangular fibrocartilage complex, which reduces the stress from the corner of the radius on the lunate6 during the healing period.
Interestingly, Kienböck3 asserted as early as 1910 that there was primarily a nutritional disturbance of the lunate (which he thought was due to a rupture of the ligaments) and secondarily a fracture of the weakened bone.
Bengt Mjöberg, M.D., Ph.D.: Department of Orthopedics, Uppsala University Hospital, SE-751 85 Uppsala, Sweden
Dr. McCabe replies:
Dr. Mjöberg's insightful letter suggests that negative ulnar variance may be important as a factor in collapse, but not necrosis, of the lunate. This is an interesting perspective that requires additional observation and study. Dr. Mjöberg also makes a great educational point about the important distinction between association and causation. As he points out, our article supports the association between ulnar variance and Kienböck disease but does not prove causation. His suggestion that increased pressure in the wrist can cause necrosis and subsequent collapse of the bone in susceptible individuals clearly demonstrates how this can occur. We thank him for his comments.
Steven J. McCabe, M.D., F.R.C.S.: Christine M. Kleinert Institute for Hand and Micro Surgery, 225 Abraham Flexner Way, Louisville, Kentucky 40204-3840