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The more advanced stages of venous disease, Chronic Venous Insufficiency (CVI) (C3-C6), appear to affect about 5% of the population, with the prevalence of the end stages of CVI (active and healed venous ulcers, C5+C6) estimated at 1-2% [1]. The mechanism of venous leg ulcer formation involves a sequence of pathophysiologic steps that are thought to include [1] reduction in venous outflow due to venous obstruction and/or reflux, [2] persistent venous hypertension, and subsequent increased capillary filtration and interstitial fluid load [3]. Typically, excess interstitial fluid is effectively removed by the lymphatics, but if the fluid load overwhelms the lymphatic capacity or if the lymphatics are defective, then the accumulation of interstitial fluid, macromolecules, and cytokines lead to edema (CEAP C 3 ), breakdown of subcutaneous tissue (C 4A,B ), and formation of ulcers (C 6 ) [2,3]. Thus in order to prevent development of venous leg ulcerations, treatment of the underlying venous insufficiency is imperative.

Sequential Contraction Compression Devices Reduce Leg Circumference in Patients with Chronic Venous Insufficiency