Abstract

Clinical and phlebographic evidence exists that correlates the presence of varices of the vulva, posterior thigh, and the pelvic congestion syndrome with insufficiency of the internal iliac venous system (pelvic dumping syndrome). Information in the modern medical literature regarding the valvular anatomy of the internal iliac veins and its tributaries is limited. We dissected 82 iliac venous system specimens in 42 human cadavers (29 men, 13 women) to gain information on the relationship between the disease described and the anatomy of the region. Each specimen contained common, external, and internal iliac veins, including the tributaries of the latter. We recorded the anatomic variations of the internal iliac vein trunk and the location of valves in the complete iliac venous system, including 485 tributaries of the internal iliac veins. Five specimens of internal iliac vein had calcified thrombosis or were extensively involved with pelvic carcinoma and were not suitable for valve study, which left 79 specimens for analysis. The internal iliac vein drained into the external iliac venous system by means of a single trunk in 73% of the specimens and by two well-formed and separated trunks in 27% of the specimens. In one specimen (1.2%) the internal iliac vein drained directly into the inferior vena cava (parallel internal and external iliac veins). One specimen had a well-developed valve in the common iliac vein (1.2%). The external iliac vein had one valve in 26.2% of the specimens. This vein had three times as many valves on the right side as in the left (39.6% vs 14.6%: p = 0.0106). The internal iliac vein had valves present in 10.1% of its main trunks and in 9.1% of the 485 tributaries dissected. This is the first time that well-developed valves have been demonstrated in the internal iliac vein and their location described in a series of human cadaver dissections. The scarcity of valves in the pelvic veins, however, led us to consider that varicose veins in the vulva or elsewhere develop not only because of valvular insufficiency but also because of genetic structural venous wall anomalies as well as hormonal and hemodynamic factors present during pregnancy.

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