eMedicine Specialties > Orthopedic Surgery > Hand & Upper Extremity
Kienböck Disease
Updated: Jul 11, 2007
Introduction
Kienböck disease is a condition of uncertain etiology that results in osteonecrosis of the carpal lunate.
History of the Procedure
In 1843, Peste presented the initial description of lunate collapse in the French literature. Nearly 70 years later, a Viennese radiologist named Robert Kienböck introduced the term "lunatomalacia" to describe the condition that bears his name. Kienböck believed that traumatic rupture of the ligaments and vessels around the lunate produced lunate fracture with subsequent collapse.
In 1928, Hulten noted an association between Kienböck disease and the presence of negative ulnar variance. He advanced the progress of treatment by advocating shortening of the radius. Shortly thereafter, Persson presented the option of lengthening the ulna to restore normal ulnar variance.
Problem
The true natural history of this condition is not well understood, and this has hampered the determination of the ideal treatment. As with many conditions that affect the wrist, the clinical condition of the patient does not necessarily correlate well with the radiographic appearance.
Frequency
Kienböck disease usually affects the dominant wrist of men aged 20-40 years.
Etiology
Although the underlying etiology is not known, the final results of fragmentation and collapse are secondary to osteonecrosis. Intrinsic and extrinsic factors have been implicated.
Intrinsic factors
Vascular supply
The vascular supply of the lunate has been well studied by Gelberman.1,2 It consists of both extraosseous and intraosseous vessels running in the dorsal and volar radiocarpal ligaments. Three vessel patterns of intraosseous supply have been noted. In 70% of lunates, multiple vessels enter either volarly or dorsally (X or Y pattern). In the remaining 30% (I pattern), only a single vessel is present palmarly and dorsally, which theoretically places these lunates at increased risk of losing vascular supply. Kienböck disease has not been reported following perilunate dislocations where the vascular supply has been damaged completely. Early signs of osteonecrosis (eg, increased radiodensity on plain radiographs) may be seen but have not been followed by progression to collapse. Increased intraosseous pressure has been shown to occur in lunates with Kienböck disease, but it is unclear whether this is a primary or secondary finding.
Lunate and distal radius geometry
Zapico has classified lunate geometry into 3 types: Type I lunates occur in ulnar-negative wrists, while type II and III lunates are seen in ulnar-neutral or ulnar-positive wrists. His thesis was that the weakest trabecular pattern was seen in the type I lunate, thereby helping to explain the relationship between the ulnar-minus variant and the disease. Later work by Tsuge, however, failed to show an association between lunate geometry and Kienböck disease. Mirabello demonstrated that patients with Kienböck disease with decreased radial inclination developed the disease at an earlier age. The exact biomechanical effect of de novo decreased radial inclination has not been determined.
Extrinsic factors
Relationship between the radii of curvature of the lunate and capitate
Compressive axial forces are concentrated on the distal articular surface of the lunate because the radius of curvature of the capitate is less than that of its articulating surface on the lunate. As the capitate settles proximally later in the disease process, it can act as a wedge to split the lunate into dorsal and volar halves.
Repetitive trauma
While no specific data support a causal relationship, a history of repetitive microtrauma is often noted in patients with Kienböck disease.
Ulnar variance
While not thought to be causal, a statistical relationship between negative ulnar variance and Kienböck disease appears evident. In Hulten's original work, he noted that 23% of the general population has negative ulnar variance, while 74% of his patients with the disorder were ulnar minus. The ulnar-minus variant has been shown experimentally to cause an abnormal increase in the force transmitted across the lunate. In addition, the triangular fibrocartilage complex (TFCC) is thicker in these patients, and the differential loading between it and the ulnar edge of the radius is increased. De Smet, however, counters that true correlation between the ulnar-minus variant and Kienböck disease has not been proven when appropriate sex- and age-matched controls and radiographs have been used.3
The etiology of Kienböck disease has not been clearly determined. Most likely, it occurs as a result of repeated loads to a "lunate at risk" by virtue of its unique vascular or mechanical environment.
Pathophysiology
Force transmission studies have formed an important part of the understanding of the pathophysiology of Kienböck disease. In the normal wrist in neutral alignment, 80% of the axial load through the wrist is transmitted through the radiocarpal joint, while the remaining 20% goes through the ulnocarpal joint. Two-dimensional theoretical models of force transmission in patients with Kienböck disease have demonstrated that in the early stages of the disease (II and IIIa), the normally positioned scaphoid prevents excessive forces on the lunate. However, as the scaphoid assumes its flexed position in stage IIIB, loads across the lunate are increased. These excessive loads may further accelerate the process of fracture and fragmentation leading to collapse.
Presentation
The most common patient with Kienböck disease is a man aged 20-40 years who is either a manual laborer or one who participates in recreational activities that repetitively load the wrist. Patients present with reports of activity-related dorsal wrist pain, decreased wrist motion in the flexion-extension arc, and poor grip strength. The symptoms tend to occur more often in the dominant hand. Dorsal wrist swelling and tenderness are frequently present over the radiocarpal joint. A history of trauma is variable and may be in the distant past. A recent review that focused on Kienböck disease in women revealed that men and women have different presentations of Kienböck disease. Women had roughly equivalent involvement of the dominant and nondominant sides, and they tended to present at a much older age (46 years versus 31 years for men).
Indications
The primary indication for operative treatment in Kienböck disease is persistent pain not responsive to conservative treatment such as nonsteroidal anti-inflammatory drugs (NSAIDs) and immobilization. Most patients with Kienböck disease who have moderate-to-severe symptoms are candidates for operative intervention. The choice of operative technique is based on patient age, stage of disease, and the presence or absence of ulnar variance.
Relevant Anatomy
See Surgical therapy.
Contraindications
The primary contraindication to consider in the operative treatment of Kienböck disease is ulnar-positive or ulnar-neutral variance because in patients with such variance, joint-leveling procedures (radial shortening and ulnar lengthening) cannot be performed.
More on Kienböck Disease |
 Overview: Kienböck Disease |
| Workup: Kienböck Disease |
| Treatment: Kienböck Disease |
| Follow-up: Kienböck Disease |
| References |
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References
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Further Reading
Keywords
avascular necrosis of the lunate, osteonecrosis of the carpal lunate, wrist injury, wrist pain, lunatomalacia, Kienbock disease, triangular fibrocartilage complex, TFCC, ulnar, ulnar variance, negative ulnar variance, positive ulnar variance, radial shortening, ulnar lengthening, lunate collapse, scaphoid rotation, lunate excision, scaphotrapeziotrapezoid, triscaphe, STT, STT fusion, STT arthrodesis, scaphocapitate, capitohamate, carpectomy, proximal row carpectomy, PRC, ulnar-negative variance, ulnar-positive variance
