Primary Venous Insufficiency

The manifestations of simple primary venous insufficiency appear to be different from one another. However, reticular varicosities, telangiectasias, and major varicose veins are all elongated, dilated, and are tortuous. Investigations into valve damage and venous wall abnormalities eventually may lead to an understanding of the problem, and therefore, a solution by surgery or pharmacotherapy.1-4

Scanning electron microscopy has shown varying degrees of thinning of the varicose venous wall. These areas of thinning coincide with areas of varicose dilation and replacement of smooth muscle by collagen, which is also a characteristic of varicose veins.5,6 Our approach to this has been to assume that both the venous valve and the venous wall are affected by the elements that cause varicose veins. We and others have observed that in limbs with varicose veins, an absence of the subterminal valve at the sapheno-femoral junction is common.7 Further, perforation, splitting, and atrophy of saphenous venous valves have been seen both by angioscopy8,9 and by direct examination of surgical specimens.10

Supporting the theory of weakness of the venous wall leading to valvular insufficiency is the observation that there is an increase in the vein wall space between the valve leaf-lets.10 This is the first and most commonly observed abnormality associated with valve reflux.11 Realizing these facts, our investigations have led us to explore the possible role of leukocyte infiltration of venous valves and the venous wall as part of the cause of varicose veins. In our investigations of surgical specimens, leukocytes in great number have been observed in the venous valves, and wall and monoclonal antibody staining has revealed their precise identification as monocytes.10 Similar findings are present in the skin of patients with venous insufficiency.12

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