On the Etiology of Clubbing of the Fingers

Abstract

Abstract Clubbing of the fingers and toes, and the more severe “pulmonary” osteoarthropathies and periostitides, occur when there is arterial anoxia due to congenital or acquired lesions or residence at high altitude. It occurs in many disorders in which the erythrocyte sedimentation rate is rapid, but arterial oxygen saturation normal. In all these cases the vascular bed is wide, blood flow rapid, and the tissue warmer than normal. That rapid sedimentation rates, with intravascular rouleaux formation, interfered with oxygenation of the tissues by decreasing the diffusion surface per unit of hemoglobin had long ago been suggested by Fahraeus. In this review it is suggested that with escape of rouleaux through the arteriovenous anastomoses so numerous in the fingers and toes, rapid blood flow and high levels of arterial and venous oxygen saturation may be present simultaneously with low oxygen tension in the digital tissues. Thus, rapid rates of blood flow and low tissue oxygen tension would provide the same mechanism for clubbing in chronic infections, neoplasms, or metabolic defects leading to abnormal fibrinogen and globulin levels, as in the classical cases of arterial anoxia. The most rapidly evolving and the most severe types of osteoarthropathy are seen in cases of mediastinal and lung tumors where the sedimentation rates are rapid and arterial anoxia is present. Here the two types of anoxia may coexist. In rheumatoid arthritis, in Raynaud's disease, and in Buerger's disease clubbing is rare, although tissue anoxia is severe in the latter two and rapid sedimentation rates are characteristic of the former. But in all of these, blood flow and tissue temperatures are low in the tips of the extremities. It is thereby concluded that for the development of clubbing low oxygen tensions must occur in tissues which are warm and in which the blood flow is greater than normal.