Atrophy of Terminal Phalanges in Clubbing and Hypertrophic Osteoarthropathy

Abstract

The pathogenesis of clubbing of the fingers and toes has remained obscure in spite of numerous investigations. Since Hippocrates' original description of this phenomenon in a patient with empyema it has been found associated with various conditions such as cardiac, pulmonary, and gastro-intestinal disease. Clubbing has been recognized as both acquired and hereditary in type and has been classified as idiopathic in cases in which an etiologic factor has not been established. Hypertrophic osteoarthropathy is now generally believed to be a more pronounced and advanced stage of the same process (1). The bone changes occurring in hypertrophic osteoarthropathy have attracted considerable attention since the original investigations of Bamberger (2) and Pierre Marie (3). The condition is characterized by an irregular periosteal thickening of the shafts of the involved bones. In advanced stages subperiosteal new bone formation may be so pronounced as to result in marked thickening of the bone shafts and in conspicuous swelling of the involved parts. The bones most frequently affected are the long bones of the extremities, the metacarpal and the metatarsal bones, the proximal phalanges, and clavicles. The vertebrae and ribs are rarely involved. The bone changes taking place in the terminal phalanges in simple clubbing and hypertrophic osteoarthropathy deserve special consideration. Earlier observers believed the enlargement of the distal portions of the fingers and toes to be the result of bony overgrowth (2). This conception was revised after roentgenologic studies showed the clubbing to be attributable chiefly to enlargement of the soft tissues. In most instances no changes whatsoever were observed in the terminal phalanges. Thus, Hodges, Phemister, and Brunschwig (4) claim that “almost invariably there are no bone changes of the terminal phalanges at the site of clubbing.” In some cases, however, a characteristic burr-like overgrowth of the unguinal process of the phalanx was observed. Locke (1), who examined a large series of patients, noted hypertrophic changes of the terminal phalanges in 28 per cent of those with simple clubbing. Of 5 patients with advanced hypertrophic osteoarthropathy observed by this investigator, all showed hypertrophic changes of the terminal phalanges. Mendlowitz (5), in his review of clubbing and hypertrophic osteoarthropathy, refers to a small number of cases which showed characteristic atrophic changes of the terminal phalanges. These cases are reported in the foreign literature. To our knowledge, no similar reports have appeared in the American and English literature.2 The recognition of these atrophic changes in clubbing and hypertrophic osteoarthropathy would seem to be of importance to the roentgenologist, in the differential diagnosis of conditions characterized by destructive changes in the terminal phalanges.