OR WAIT 15 SECS
Venous reflux from pelvic sources is often overlooked when evaluating gynecologic patients, argues an advocate of the newer discipline of phlebology. Pay special attention, he urges to those patients having pelvic pain and chronic venous insufficiency in their legs.
Phlebology, the medical discipline devoted to venous disease, is recognized by the AMA as a self-designated practice specialty. Chronic venous insufficiency (CVI) a frequently overlooked medical disorder, affects at least 25% of women and 15% of men.1,2 Left untreated, CVI can cause leg pain, swelling, thromboses, and varicose veins. In addition, patients may develop dermatologic skin changes of hyperpigmentation, lipodermatosclerosis, and venous stasis ulcers.3
Pelvic venous anatomy 101
As the CFV continues cephalad, it crosses below the inguinal ligament to become the external iliac vein. This vessel merges with the internal iliac (hypogastric) vein to form the common iliac vein. On the right side, this vein lies posterior and then medial to the iliac artery. On the left side, it courses entirely along the medial aspect of the iliac artery. At the level of the fifth lumbar vertebra, the right and left common iliac veins unite to give rise to the inferior vena cava (Figure 1). Here, the left common iliac vein courses behind the right common iliac artery.
The internal iliac (hypogastric) vein drains the pelvic viscera. Venous branches include the gluteal, internal pudendal, and obturator veins. The latter two provide venous drainage for the vulva.
The right ovarian vein drains directly into the inferior vena cava while the left ovarian vein drains into the left renal vein (Figure 1). The left renal vein often lies between the superior mesenteric artery and the abdominal aorta.
Pathophysiology of pelvic venous insufficiency and thrombosis
Venous insufficiency develops when a component of the venous system fails. Reflux and obstruction are contributing factors. Reflux develops as vein valves weaken, with veins subsequently dilating and elongating. Genetic predisposition, along with anatomical variants in venous anatomy, can lead to an obstruction in venous drainage, which gives rise to venous insufficiency.
In women, this can be due to pelvic masses such as myomas and ovarian cysts. In pregnancy, the gravid uterus can contribute to this phenomenon. In addition, the increased progesterone levels typical of pregnancy and the luteal phase of the menstrual cycle relax the smooth muscles. This further weakens vein walls and contributes to venous stasis.7 Thrombosis may subsequently develop.
In some patients, a tendency towards thrombosis is due to an underlying thrombophilia. These hypercoagulable conditions can be classified as either primary (inherited) or secondary (acquired).8,9 The common primary conditions are antithrombin III, protein C, and protein S deficiencies, along with activated protein C resistance (factor V Leiden mutation). Secondary hypercoagulable conditions consist of disorders ranging from well-known ones that predispose to thrombosis (pregnancy, malignancy, trauma, and postoperative immobility) to medical conditions (antiphospholipid syndrome and hyperhomocystinemia). In addition, oral contraceptives, estrogen, and tamoxifen are known to result in hypercoagulability.10