Therapeutic Alternatives for Venous Ulcer

Abstract

The usual definition of venous ulcer is “an open skin lesion of the leg or foot that occurs in an area affected by venous hypertension” sic [1]. In epidemiological reports the prevalence of leg ulceration in the population C5–C6, shown by the CEAP score (Clinic estadification method for venous insufficiency, C5 Healed ulcer and C6 Open ulcer), is about 1–2%. The etiologic factors that can produce leg ulcers are diverse, but the majority of the patients have venous disease in different stages of evolution. Chronic venous insufficiency is ten times more frequent than arterial ulcers [2]. Venous ulcers affect approximately 10–35% of the total United States population, and 4% of the population who are older than 65 years show active ulcers [3]. The economic cost of this disease in the United States is one billion dollars per year. Recent epidemiological studies on chronic venous disease have been conducted in England, Sweden, and Australia; the studies included between 12,000 and 434,699 individuals. The average point prevalence for venous ulceration was 0.29%, and some interesting aspects of venous ulcer were reported: there was a strong relationship between the prevalence of arterial hypertension ulcers (63.2%) and the prevalence of venous ulcers (arterial-venous), which approached 80%. Healing was less frequent for the mixed-etiology ulcers, at 26%, than for venous ulcers alone, at 41% [4]. In regard to etiology, Koerber and Schadendorf [5]found 75.25% venous leg ulcers, 3.66% arterial leg ulcers, 14.66% ulcers of mixed origin, and 13.5% vasculitic ulcers in their study population. Diabetic leg ulcers and ulcers with an inflammatory border and skin necrosis are often associated with chronic inflammatory diseases such as ulcerous colitis or rheumatoid arthritis. Leg ulcers may also occur in patients with Klinefelter’s syndrome; in these patients with hypogonadism and testosterone deficit, slow-healing ulcers may occur with or without chronic venous disease. There is some evidence that abnormal platelet aggregability or fibrinolysis with elevated plasminogen activator inhibitor-1 activity may play an important role in ?. The most important differential diagnosis of leg ulcers is that of ulcerations caused by malignant or semi-malignant diseases, in which ulcerating tumors such as basal cell carcinoma or melanoma may mimic venous ulcerations [5]. For the correct treatment of venous ulcers we need to have the most accurate possible diagnosis, and in some cases the diagnosis is not 100% accurate. The single most helpful confirmatory test is the duplex Doppler examination; the diagnosis should not only evaluate the great saphenous vein (GSF) but all the superficial, deep, and perforating venous systems. In the Skovde study only 25% of patients with venous ulcers had detectable deep venous incompetence (DVI) [6], in contrast to the Skaraborg study, in which 60% of such patients had DVI [7]. In (a previous report about) young people with venous ulcers, 50 to 75% had only superficial and/or perforator venous incompetence (SVI/PVI) [8]. Clinical association with deep venous thrombosis occurred in 5 to 22% of the patients [9]. All these are sufficient reasons to complicate the ethiologic diagnostic in venous ulcers; in the cases where only exist venous problems, we need to locate the sources of reflux (unique o mixed). The most difficult aspect of diagnosis is that the failure of a system affects others; for example, in saphenofemoral reflux with an reentry insufficient perforating vein, can be corrected totally the perforant insufficiency by eliminating reflux in the saphenofemoral junction, while in other cases does not occur and the perforator vein remain insufficient. Similarly, in the deep venous system, there may be insufficiency in the thigh and the venous hypertension may be deflected to the superficial system in the leg or vice versa. In other cases, deep vein insufficiency of the tibialis posterior veins may be associated with post-thrombotic sequelae and perforator veins may develop a superficial circuit to compensate the changes in the venous circulation and pressure, wich them become insufficient later.