A Physiological Approach to Peripheral Venous Stasis

Abstract

The therapy of such conditions as the post-phlebitic syndrome and primary varicosis has in the past often been based on certain traditional misconceptions rather than on a clear understanding of the physiopathological mechanism involved in peripheral venous stasis. Among the erroneous ideas that have long been widely accepted, two are outstanding:(1) That veins which have been the site of thrombophlebitis remain permanently obstructed.(2) That the varicose veins which often occur in the post-phlebitic state represent important collateral channels which must be preserved.The purpose of this paper is to point out the fundamental hemodynamic disturbance common both to primary varicosis and to the sequellae of deep venous thrombosis, and to outline a rational therapeutic program based on an understanding of this disturbance. _ PHYSIOLOGY _ Inasmuch as thrombosis in veins, as elsewhere, is followed by organization and canalization of the thrombus, a lumen is soon restored in veins which are the site of thrombophlebitis (8,22). However, this newly restored lumen is not only narrower than in the normal vein, but no longer contains functioning valves (5). In varicose veins, likewise, the valves are non-functional (16). Thus, when the patient assumes the upright position, the blood flows in a retrograde direction both in the deep veins in the post-phlebitic state and in the superficial veins in the presence of varicosis. It does not matter whether the varicosis is primary or secondary to an old deep thrombophlebitis. The normal direction of blood flow is maintained only in those veins of the lower extremities in which there are competent valves.When a patient with incompetent valves in the veins of the lower extremities is in an upright position, the venous pressure becomes excessively high. This increased pressure exceeds the colloid osmotic pressure of the blood, resulting in an increased quantity of lymph formation (1). If phlebitis has been the forerunner, the condition is probably aggravated by the obliteration of many of the perivenous lymphatic channels.The edema fluid of peripheral venous stasis contains a large amount of protein (18). To this high protein fluid are added cellular elements of the blood as a result of increased capillary permeability and diapedesis of the red blood cells;