The Venous Valvular System

The number of venous valves of the leg veins has been found to be decreased in patients with varicose veins when compared with patients without varicose veins [2]. Age or gender does not correlate with a decrease in valvular number. Therefore, other factors must contribute to the decrease in the number of venous valves. Additional potential mechanisms of valvular dysfunction contributing to varicose veins include fibrosis of these valves caused by turbulent high-pressure blood flow, a hereditary defect in either vein wall and/or valvular structure, and an increase in deep venous pressure (Table 8.1). Since competent venous valves are able to withstand pressures of up to 3 atmospheres, the normal vein diameter must first dilate in order to cause valvular incompetency [2]. Chronic venous dilation from chronic venous hypertension may likely produce stress on the valvular system, leading to dysfunctional fibrosis of the valves(s) These dysfunctional valves lead to the development of valvular insufficiency, which in turn causes a reversal of blood flow from the deep venous system to the superficial veins through incompetent perforating/ communicating veins. This reversal of flow by incompetent valves of perforating veins may be beneficial, however, during sclerotherapy. When a superficial varicosity is injected, the reversal of blood flow forces the direction of the sclerosant to flow distally to the smaller branching veins away from the deep veins thereby preventing thromboembolic disease of the deep venous system. In summary, pathologic development of incompetent valves and varicose veins can be divided into the following four categories: increased deep venous pressure, primary valvular incompetence, secondary valvular incompetence, and heredity factors.

Table 8.1. Factors involved in the development of varicose veins Increased deep venous pressure    Proximal causes Pelvic obstruction (indirect venous obstruction) Increased intraabdominal pressure (straining at defecation or micturition, wearing constrictive clothing, prolonged standing, chair sitting, leg crossing, squatting, obesity, or running) Saphenofemoral incompetence Venous obstruction    Distal causes Communicating or perforating vein valvular incompetence Venous obstruction Arteriovenous anastomoses Primary valvular incompetence Venous obstruction (thrombosis) Thrombophlebitis with destruction of venous valves Congenital absence of the venous valves (agenesis) Decreased number of venous valves Secondary valvular incompetence Deep venous obstruction Increased venous distensibility Hormonal (pregnancy; estrogens, progesterone, and their relative concentrations) Heredity Vein wall weakness Inherited deficiency of vein wall collagen Primary valvular dysfunction / agenesis ABO blood group     Source: This has been modified from Goldman MP (1991) Sclerotherapy: Treatment of varicose and telangiectatic leg veins. Mosby, St. Louis, p 56,with permission from the author