Discussion of the history of a subject assumes a beginning and a turning point in the course of events that separates history from present day concepts. With Kienbock's disease, the beginning is generally ascribed to the description of the disease process by the man with whose name the disease has become associated, although collapse of the lunate was originally described 70 years earlier. The turning point is more difficult to identify because presently many procedures are used for treatment of lunatomalacia. Perhaps the turning point could be defined by the recognition of the association of uInar variance in the genesis of Kienbock's disease and the potential therapeutic contribution of surgical intervention.

Anatomists, in studying cadaveric dissections, had long considered irregular or bipartite lunates to be congenital anatomic variants and classified them as lunatum partitum, bipartitum, hypolunatum. and epilunatum. 17 It was page, in 1843, who described collapse of the carpal lunate, which he believed to be secondary to fracture from trauma.' This diagnosis did not gain popularity until 1910, after the development of radiographs, when a Viennese radiologist named Robert Kienbock 7 wrote a treatise: "Concerning Traumatic Malacia of the Lunate and its Consequences: Degeneration and Compression Fractures" (translated into English in 1980 by Peltier from "Uber Traurnatische Malazie des Mondbeins und ihre Folgezustande: Entartungsformen und Kompressionsfrakturen") . Kienbock described the disease process of lunatomalacia, both the radiographic changes seen with the disease and the clinical symptomatology that accompanied it.

Radiographically, Kienbock described various changes in the lunate with the vast majority of cases beginning with disease in the proximal portion, preserving the distal portion articulating with the capitate. In some radiographs, the shape of the lunate was preserved and only the internal structure altered, with radiographs demonstrating areas of increased and decreased density. In most radiographs, however, with progression of the disease, the shape of the lunate was significantly affected, with destruction of the proximal portion and loss in height of the bone. Kienbock noted that the disease usually occurred in men in their third or fourth decade who were heavy laborers. Frequently they would have an antecedent trauma with negative radiographs and were diagnosed with a sprain. Over time, the clinical course would progress with pain, swelling, and restricted motion of the wrist. Percussion of the third metacarpal (with the hand held in a fist) produced pain in the lunate region and when comparing hands, shortening of the carpus might be evident. Radiographs demonstrated radiographic changes in the lunate and "loosening" of the radiocarpal joint, which Kienbock thought promoted mechanical damage. This loosening Probably referred to the increased radiocarpal space due -to synovitis, preceding radiocarpal arthrosis. Kienbock favored the view that the condition was due to a disturbance in the nutrition of the lunate caused by rupture of the ligaments and blood vessels from a sprain or subluxation. Leading to, rather than being a result of, compression fractures. Thus, he likened it to Preiser's disease. Kienbock believed that recovery from this disturbed nutrition only occurredin acute cases and, in late cases, could be treated only by removal of the lunate. Usually at surgery or on post mortem exammation, the lunate was found in two fragments, as previously described by anatomists, one volar and one dorsal.

It was 15 years after Kienbock's description that Goldsmith reported the first cases in the American literature and credited Speed"' with ascribing the name Kienbock's disease." He acknowledged Kienbock's theory of subluxa- tion and spontaneous reduction of the lunate causing a disruption of the dorsal ligaments and thus its nutritional supply. Goldsmith stated that because of the mildness of the symptoms and the absence of traumatic his- tory, Kienbock's disease was frequently over- looked without the use of radiographs. He described four clinical progressive stages of Kienbock's disease: joint irritation following trauma, asymptomatic stage, disease stage with severe symptoms, and stage of moderate disability. Goldsmith suggested conservative treatment in early stages, and operative extir- pation of the lunate in later stages, although the three patients in his. reported s eries re- fused operative intervention. In reviewing these three cases, all occurred in uInar-nega- tive wrists, although the association was not recognized at the time.

The following year, Henderson reported on two cases of Kienbock's disease and stated that according to Muller, three types of lesions were identified: traumatic, occupational (repeated minor injuries), and anatomic (pressure from associated anomalies). He also 'found an asymptormatic interval between the inciting event and the development of lunate disease. He advised splinting as treatment, even of advanced cases. That same year, Webb" reported on one patient with Kienbock's disease who had a lunate excision with relief of pain; however, range of motion of the wrist remained limited to 27' of flexion in this patient. These reports of Kienbock's disease were the first to recognize a potentially causative event in the development of lunatomalacia and thus link the disability with a previous trauma. The import of this finding on the settlement of insurance claims was addressed in many of these articles.

It was 2 years later, in 1928, 18 years after the description of Kienbock's disease, that Hulten made the association between uInar variance and lunatomalacia. He evaluated 400 normal wrists radiographically and found that uInar variance fell in a bell-shaped curve, with 61% being uInar neutral. Twenty-three percent of ulnas were shorter than the radius (uInar negative), and sixteen percent were longer than the radius (uInar positive). He then examined 23 cases of Kienbock's disease and found that in 17 (74%), the ulna was shorter than the radius (uInar negative), and in 6 patients (26%), the ulna was equal in length to the radius. He noted that no wrist in which the ulna was longer than the radius developed Kienbock's disease. The ulnar-positive wrists did develop a cyst-like rarefaction in the uInar aspect of the lunate, similar to what we now call uInar impaction syndrome.

Hulten believed that the cause of Kienbock's disease was a primary fracture and not a soft-tissue disruption causing avascularity as Kienbock had originally described. He thought that the anatomic considerations of the lunate contributed to the production of the fracture and its unusual course. Because the lunate was mostly articular, with only a small portion covered by periosteum and responsible for pain sensation, Hulten asserted that painful sensations from this bone were slight. This lack of periosteum was especially true of the proximal pole in which most of the changes were found. Therefore, a compression fracture could occur without causing severe enough pain for the patient to remember. It was generally accepted that the lines of force emanating from the hand converged to meet on the lunate, and thus the lunate was subjected to a greater pressure than any of the other wrist bones. Additionally, histologically examined lunates with malacia demonstrated no evidence of ligamentous disruption. The continuous stress on the lunate and its poor osteogenic potential led to its further collapse, and the production of a painful stiff wrist of which the patient gradually became aware.

Molten, having noted the association of Kienbock's disease and uInar variance, implicated the ulnar-negative wrist as a cause in fractures of the lunate and published a report of one case using radial shortening to treat lunatomalacia. He still advocated conservative treatment-for early disease with immobilization for as long as 4 months and extirpation of the lunate for late disease. Hulten's work contributed not only to understanding of the cause of lunatomalacia but also created a foothold for the development of surgical treatment to halt progression of disease and was a turning point in the history of Kienbock's disease. By the mid 1940s, there was consensus in the literature that lunatomalacia was caused by a primary fracture of the lunate due to its anatomic vulnerability, perhaps interrupting the vascular supply to the remaining lunate, and Kienbock's theory of ligamentous disruption was losing favor. Arguments still existed that the primary trauma was not great enough to produce fracture and that the interval from trauma to disease was too great. Hulten argued against an initial fracture being visible on a radiograph because the lunate was mostly cartilage and spongy bone and thus elastic and able to resume its normal appearance after compression. Only later did radiographic changes set in secondary to avascularity. Hollers theory of "occupational" lunatomalacia or chronic traumatization either causing microfracture or endarteritis also gained popularity. In those patients that did not have "occupational" lunatomalacia an ulnar-negative variance of the wrist was found.

Most practitioners still advocated conservative treatment, although the results were universally poor. Operative extirpation of the lunate was reserved for advanced cases with pronounced arthrosis but was noted to give poor late results because of rearrangement of the remaining carpal bones and subsequent arthrosis. Hulten's work had created a precedent for operative intervention to halt the progression of Kienbock's disease.

In 1945, Persson" published his series of 19 cases of Kienbock's disease treated with corrective osteotomy, 3 with radial shortenings, and 16 with uInar lengthenings. The structure of the lunate improving in 50% of the cases. The ulna was lengthened through an oblique osteotomy, and the distal fragment drawn distally 3 or 4 mm. The osteotomy was then fixed with two cerclage wires. Because of poor fixation, two of the radial shortenings healed with angular displacement, and the third developed a pseudarthrosis. Only two failures of ulnar lengthening occurred secondary to inadequate tightening of the cerclage wires, with shortening of the ulna and progression of the lunatomalacia. Because of the difficulty with fixation and healing of the radial osteotomy, Persson abandoned radial shortening and advocated ulnar lengthening in the treatment of Kienbock's disease.

Two years later, in 1947, RAU' through the use of arteriograms demonstrated that the volar circulation (not the dorsal as Kienbock had suggested) was the important Vascular supply to the lunate. The vessels were smaller in caliber than those to the scaphoid and, he postulated, potentially more sensitive to trauma. He disagreed with Persson and thought that the good results-that Persson achieved were secondary -to the prolonged period of immobilization required for the osteotomy to heal. Stahl published the results of his using immobilization for more than 2 months and found that nearly two thirds of patients under 25 years old had reconstitution of the lunate. Most of his patients were men in their thirdor fourth decade, engaged in heavy labor. The earlier the treatment was begun, the better the late results. In wrists immobilized for more than 2 months, only one in six had a "bad" result, with 50% demonstrating reconstitution of the lunate. In those patients with immobilization of longer than 2 months, strength was 82% of the uninjured side, compared with strength of 69% of the unuinjured side in those with less than 2 months immobilization. Stahl condemned extirpation of the lunate as not being possible in its entirety and yielding poor late results. He defined five stages of lunate osteomalacia: stage 1, radiographs demonstrated a radiodense fracture; stage 2, secondary resorption with development of a rarefaction line; stage 3, sclerosis; -stage 4, secondary fractures with fragmentation; and stage 5, arthrosis. Most patients presented with stage 3 or 4 disease, with ulnar-negative variance predominating.

Excision of the lunate continued to have proponents. Doman,' in 1949, reported on 16 patients treated with excision of the lunate bone. Follow-up averaged 3 years, and 44% of patients had excellent results with complete return to work, with another 25% only having symptoms after heavy work. He ad vised excision Of the lunate in those patients that continued to have pain after a satisfactory trial of immobilization; however, longterm results from this study were lacking.

In 1950, Persson reported a further series of 14 patients all treated with ulnar lengthen- ing osteotomies with excellent results. Only one patient was required to change occupa tion because of pain. Strength was 90% that Of the normal hand (compared with Stahl's - 82% for long immobilization and 69% for short), and range of motion of the wrist was greater than that achieved with immobiliza- tion (84% versus Stahl's 69% and 61%). Pers- son postulated that after a surgical uInar lengthening, the pressure on the Iunate bone decreased. Even if the lunate did not radio-- graphically reconstitute, the "pseudarthrosis" could be clinically "healed" because the de creased load across the lunate rendered it asympto matic Like stahl, he found that the older the patient, the less tendency toward radiographic healing of the lunate and the greater tendency toward arthritis. Still, ulnar lengthening offered clinically and radio graphically superior results to prolonged im-- mobilization 'and supported the fracture the- ory of Kienbock's disease.

Thus by the 1970s, methods of treating pa tients with Kienbock's disease were still de- veloping, nearly 60 years after its description. Immobilization was used for mild cases with no radiographic changes and joint leveling procedures for radiographically evident dis- ease to prevent progression. The advent of successful methods of internal fixation would make the latter choice more popular. For late disease, lunate excision was an option, al- though late results of lunate excision were worsened by the carpal shift that occurred to fill the lunate void. If the space created from excision of the lunate was filled, then perhaps the late collapse could be prevented. Swan- son," in 1970, advocated silicone replacement arthroplasty of the lunate and Nahigian et al reported on a modification of lunate excision with a dorsal flap arthroplasty similar to that done for trapezial excision. The latter series was small (four patients) and the follow-up short (average 2.4 years), but all patients had relief of pain with return of grip to normal. In the two cases presented, radiographs showed no carpal shift.

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