Lymphatic and Venous Examination of the Postphlebitic Extremity

Abstract

Ulcers of the leg secondary to vascular disease create one of the most frustrating problems in surgical practice but rarely concern the radiologist. Although numerous causes of ulceration have been described (2, 3), the most common one is “venous incompetence.” The diagnosis of this condition is generally considered simple and rarely necessitates a radiologic examination. On close scrutiny, however, the pathogenesis of these ulcers is not clear. Classically it has been taught that chronic leg ulceration is a late manifestation of the postphlebitic or post-thrombotic phenomenon, following years after the initial development of thrombophlebitis. Clinically, progressive ankle edema develops, the skin becomes bluish purple, and dermatitis and brawny induration are found. It has been thought that thrombotic occlusion of the deep veins of the leg and subsequent recanalization and destruction of the valves initiate the pathologic process. This destruction of the venous valves supposedly produces deepand communicating-vein valvular incompetence, and consequently the normal flow from the superficial to the deep system is reversed. Due to this incompetence, hypertension in the skin and in the subcutaneous veins appears and, when sufficiently high, leads to diapedesis of plasma and red blood cells. Diapedesis, in turn, causes chronic edema and deposition of hemosiderin. This concept is less than satisfactory because it does not consider a possible role for the lymphatic system. Kinmonth wondered if lymphatic damage could cause ulcers, but at that time he did not believe that the deep lymphatics were affected during the ulcerative process (6). Our study was undertaken to examine simultaneously the lymphatic and venous systems in an attempt to identify the several factors which contribute to the “post-thrombophlebitic phenomenon.” Method In this study 23 patients were selected and examined because they had or had recently had leg ulcers of the “venous stasis” variety (21 patients) or because they had had a well documented episode of recurrent, acute, lower extremity, deep thrombophlebitis with vague extremity complaints, although there had been no ulcers (2 patients). All patients were admitted to the Upstate Medical Center where, by extensive questioning, we attempted to establish whether or not they had had a previous episode of lower extremity, deep thrombophlebitis, the so-called “milk-leg.” Each patient was then examined by photography, peripheral venography, and lymphangiography. Venography always preceded lymphangiography, although on occasion the patent blue was injected prior to venography. Scalp vein needles were introduced into an adequate vein in the dorsum of each foot and connected to an infusion apparatus containing isotonic saline. The patient was placed in the semierect position, and tourniquets were applied above the malleoli.