Journal «Angiology and Vascular Surgery» • 

2001 • VOLUME 7 • №2

LOCAL VENOUS HYPERVOLEMIA AS A CLINICAL PHYSIOPATHOLOGICAL PHENOMENON OF VARICOSE VEINS

Yu.T. Tsukanov
Postgraduate Education Department of Surgical Diseases, Omsk Medical Academy,
Omsk, Russia

Regional hypervolemia was revealed in 583 patients with varicose veins (W). Hypervolemic zones were detected in all segments of leg venous system. In 40.6±3.6% of patients daily orthostatic load caused the increase in volume of thigh and lower leg muscular parts, accompanied by feeling of heaviness in legs. Increment of lower leg circumference ranged from 1 to 3 cm (mean 1.7 cm). Mean patient height being 165-170 cm, lower leg muscular length – 16-20 cm and morning circumference – 35-40 cm, additional lower leg volume averaged 155-221 cm. Deep major venous ectasia led to 3-6-fold volume increased (p<0.05), in some cases volume increased in 10-25 times. So, fibular venous volume capacity reached 58 cm3, common femoral – 100 cm3. In 66.6±4.8% of patients diameter extension of common femoral vein during Valsalva test compared with rest breathing exceeded 0.3 cm. In some patients diameter excess reached 0.5-0.7 cm and was accompanied by 2-fold and more increase in cross sectional area. Resultant volume of deep major veins rose in 2-3 times. Intraorganic (intramuscular) and extraorganic (distension of deep and superficial outflow pathways) hypervolemias were determined, the last being divided into 2 variants: 1 variant – early stages of venous insufficiency. Deep and superficial major veins are not enlarged or functionally compromised. Intramuscular hypervolemia manifests in volume increase of lower leg muscular part. This variant takes place during capillary and inflow varices of saphenous veins and at prevariceal stage. 2 variant – late stages of venous insufficiency. Intramuscular hypervolemia is accompanied by dilatation and decompensation of major veins, separate or combined impairment of saphenous and deep veins. Mechanism of venous hypervolemia development includes what we called "pathological creep". Constant and long-term loading (daily orthostasis) causes gradual venous deformation, resulting in progressive tonus decline and enlargement of venous lumen. Ultimately pathological deposition of essential blood volume in lower extremities generates challenging mechanisms of outflow. Hypervolemia may possibly cause the development of reflux and phlebohypertension.

KEY WORDS: venous hypervolemia, lower limb varicose veins.

P. 58

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