THE CONTRIBUTION OF VENOUS HYPERTENSION TO THE DEVELOPMENT OF CHRONIC VENOUS INSUFFICIENCY IN PATIENTS WITH LOWER LIMB VARICES

B.S. Sukovatykh, P.M. Nazarenko, L.N. Belikov, O.A. Rodionov, S.A. Abramova, A.N. Scherbakov

Mechanisms of the development and the course of venous hypertension, as well as its impact on the arterial flow and microcirculation of lower limb were studied in 539 variceal patients by means of Doppler ultrasound, retrograde phlebography, phlebometry, rheovasography and photoplethysmography. Ultrasonography and radiological examinations revealed 2 mechanisms of venous hypertension genesis: superficial and deep. The first one (84.4%) was characterized by isolated emergence of retrograde flow in some segments of venous system caused by primary impairment of valve leaves at different levels of lower limbs. Venous hypertension development in this group was determined by deleterious effect of superficial and perforant venous refluxes. Deep reflux had no essential hemodynamic influence. According to the second mechanism (15.2%) reflux formation was preceded by descendant ectasia of deep veins followed by valve insufficiency. In the second group the primary and determining factor of the venous hypertension development was deep blood reflux that elicited secondary refluxes in superficial and communicating veins. Phlebometry revealed 3 forms of venous hypertension: subankle, superankle and mixed. Superankle form (73.1%) was determined by dysfunction of femoral and calf muscle-venous pumps, subankle (10.2%) – of calf and foot pumps, mixed (16.7%) – of all three pumps. Isolated supra- and sunankle venous hypertension was clinically favorable for a long time, mixed form rapidly elicited outflow decompensation. Rheovasographic and photopletysmographic studies demonstrated that the decrease of arterial blood filling in crus and foot was an adaptive reaction to venous hypertension. Critical levels of venous hemodynamic and microcirculatory deviations after functional loading of muscle pumps were determined, leading to the development of trophic disturbances: decrease of venous pressure on <12% from the basal level, capillary gradient <25%, increase of venous outflow deficit >20%.

KEY WORDS: venous hypertension, chronic venous insufficiency.

P. 63

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