THE CAUSE OF CHRONIC VENOUS ULCERS
Elevated venous pressure is the underlying cause of the skin and tissue changes that lead to chronic ulceration (Figure (Figure11). This elevated venous pressure is the result of failure of the venous valves in the deep or superficial veins or both. Two forces are at work in this venous hypertension: 1) the weight of the column of blood from the right atrium to the valveless inferior vena cava and from the iliac veins to the femoral vein and 2) the relatively high pressure generated by the contracting leg muscles that is transmitted through incompetent perforator veins of the leg. The elevated venous pressure, which is transmitted to the venules and capillaries of the skin and subcutaneous tissues, causes a series of clinical changes, including edema, lipodermatosclerosis or stasis dermatitis, and development of hyperpigmentation, hyperkeratosis, and atrophie blanche and ultimately a chronic nonhealing ulcer (9).
On a microscopic level, lymphatic vessels are enlarged (10) and capillaries are elongated and dilated (11), with the functional number of capillaries being reduced (10, 11). Capillaries often show occlusive microthrombi (12) and sludging of white blood cells (13). Plasma proteins and red blood cells leak into the interstitium, where hemosiderin and fibrin deposition occurs as well as fibrinoblastic activity (12). These microscopic changes result in the reduction and stagnation of blood flow and decreased oxygen levels at the capillary level in the preulcer skin, and increased flow and arteriovenous shunting in nearby tissues (11, 14). The protein-rich edema, acting as a diffusion barrier to oxygen transport, probably plays a major role in tissue hypoxia (14).
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Some investigators have advanced the “cutaneous leukocyte trapping hypothesis” (15), which invokes white cell activation resulting in tissue damage from release of proteolytic enzymes and free radicals (16, 17). Others doubt the causative nature of these inflammatory responses and believe that the hemodynamic changes at the microvascular level are sufficient to explain the development of venous ulcerations (18). The end result is an area of skin in which capillaries are either missing or severely damaged and altered. In this setting, slight trauma or infection can lead to a nonhealing ulcer.
It is important to stress that other causes of leg ulceration must be considered before treatment is initiated. Arterial insufficiency must be ruled out before treatment, as compression bandaging is contraindicated in such cases. Diabetic foot ulcers, which are usually the result of neuropathy, may be combined with arterial insufficiency from distal small vessel arteriosclerotic occlusions. Decubitus ulcerations, infectious causes, and vasculitis should also be considered. Rare causes of leg ulcerations include pyoderma gangrenosum and primary and metastatic malignancies.
Venous ulcers are found in patients with superficial, deep, or perforator incompetence or a combination of two or all three. Duplex scanning has documented the importance of superficial venous reflux and the relatively infrequent finding of deep reflux in patients with venous ulcers (19–21). Labropoulos et al (22) studied 112 limbs with ulcers and distributed venous incompetence in superficial, deep, and perforator systems using color duplex imaging. They found that 64% of limbs had more than one system involved, 32% had only one system showing reflux, 6% had isolated deep system reflux, and 23% had isolated superficial vein incompetence. Deep system reflux was noted in 50% of patients with ulcers. Others have found superficial TenBrook et al venous reflux in 17% to 53% of patients with leg ulcers (19–21, 23, 24). Most deep venous reflux in limbs disappears when the superficial reflux is eliminated (25).
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The importance of incompetent perforators has been em by several investigators including Labropoulos (26), who found them present in 48.8% of patients with skin changes and in 60.8% of patients with ulceration. Others (27, 28) have documented a similar distribution. The presence of incompetent calf perforators occurring with either superficial or deep system reflux has been reported in 73% of limbs with venous ulceration (29). The perforating veins are usually located near the ulcerations and transmit elevated venous pressure directly to the small vessels of the skin and subcutaneous tissues (11, 18).