Primary incompetent veins and valves may occur in segmental or axial distribution. Axial reflux occurs most frequently in the saphenous veins, and often is limited to the saphenous veins in primary disease. The presence of axial reflux in the deep veins is significant in the more serious cases of primary reflux, which present with extensive aching, swelling, and disability.
This distribution of reflux is different than that of post-thrombotic disease where isolated reflux is often found in the deep veins but rarely in the saphenous veins. It is common to find the saphenous vein enlarged and still competent in late post-thrombotic disease, but this would be extremely rare in primary disease. Volume flow studies often indicate the competent great saphenous vein is the major outflow tract in the post-thrombotic extremity when the femoral and profunda veins have prominent elements of obstruction.
In a series of 98 cases of venous ulcers20 in which the distribution of reflux was studied, the deep veins showed reflux in 73% of cases, perforators in 80%, and saphenous in 86%. The etiologies in these cases were 67% primary and 33% post-thrombotic disease. It is cogent that the deep veins demonstrated axial incompetence in one-third of primary cases and in two-thirds of secondary cases, and the great saphenous veins demonstrated axial incompetence in two-thirds of primary and one-third of post-thrombotic cases. Even in these far-advanced cases of CVD the preponderance of deep vein reflux in post-thrombotic disease contrasts with the preponderance of superficial reflux in the primary cases.
The source of the reflux and wall dilation in primary disease remains controversial between the top-down valvular theory and the contrasting theory that the basic problem begins with degeneration of the vein wall and involves the valves secondarily. Clinical evidence that the initial weakness occurs in the vein wall in primary disease has been presented,21 and theoretical support for the primacy of wall changes can be deduced from the histologic changes in the vein wall described in the earlier section that described the pathologic changes of femoral-popliteal valves. It is entirely possible that the wall changes result in dysfunction of the valve. Regardless of the initial event, elements of both wall weakness and valvular reflux clearly coexist as the degenerative process of primary disease matures.
The development of primary disease as a progressive phenomenon is well supported by the Bochum investiga-tions,22 in which young students were followed serially in four-year increments during primary and secondary school and demonstrated progressive reflux in the saphenous and perforator veins, with minimal involvement of the deep veins. This is consistent with the observation that large numbers of early primary cases with varicose veins have no reflux in the deep veins, but progressive involvement beyond the saphenous and into the perforator veins and later into the deep veins is found in patients with more severe degrees of clinical disease as skin changes and ulceration becomes manifest. This contrasts sharply with the natural history of post-thrombotic disease, which nearly always begins in the deep veins and spares the superficial veins.
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