Chronic venous insufficiency during pregnancy: causes

Risk factors for chronic venous insufficiency

Discuss a variety of risk factors for the development of chronic venous insufficiency both during pregnancy and outside it. Traditionally, they include living in industrially developed countries (due to hypodynamia), female sex, the presence of chronic venous insufficiency in relatives, constipation, obesity, repeated pregnancies.

The relative risk of developing varicose disease during pregnancy in women 30-34 years and women over 35 years is 1.6 and 4.1, respectively, compared with that of women under 29 years of age. The relative risk of chronic venous insufficiency in women who had 1 birth in the history, and women who had two births and more, is 1.2 and 3.8 compared with the risk of first-pregnancy. The presence of varicose veins in the family increases the risk of chronic venous insufficiency up to 1.6. At the same time, the relationship between chronic venous insufficiency and the body weight of the patient was not found.

Causes of chronic venous insufficiency

The main etiological factors in the development of chronic venous insufficiency outside of pregnancy include:

• weakness of the vascular wall, including connective tissue and smooth musculature;
• dysfunction and damage to the endothelium of veins;
• damage to the venous valves;
• disturbance of microcirculation.

In the presence of these factors, their aggravation occurs during pregnancy.

The compression of the inferior vena cava and iliac veins by a pregnant uterus leads to venous obstruction, an increase in venous pressure, and an increase in venous capacity accompanied by blood stasis. Venous stasis contributes to the damage of endothelial cells and makes it difficult to excrete activated clotting factors by the liver or their interaction with inhibitors (because of the low probability of their mixing among themselves). During physiological pregnancy, vessel walls usually remain intact, but the disorders listed above serve as the basis for the development of venous hypertension in both deep and surface systems. Increased pressure in the venous system leads to a disbalance between hydrostatic and colloid osmotic pressures and, as a consequence, edema. Violation of the function of capillary endothelial cells and venules [possibly due to venous stasis, activation of leukocytes, changes in the production of nitrogen monoxide (NO) during pregnancy] leads to their damage. This triggers a vicious circle of pathological changes at the microcirculatory level and leads to increased adhesion of leukocytes to the walls of the vessels, their release into the extracellular space, the deposition of fibrin in the intra- and perivascular space, the release of biologically active substances.

Adhesion of leukocytes is the main etiological factor of trophic lesions in patients with chronic venous hypertension, which is confirmed by a multitude of clinical studies in patients outside of pregnancy. However, such a mechanism can not be ruled out during pregnancy. Adhesion and migration of leukocytes cause partial obstruction of the lumen of the capillary and reduce its flow capacity. This mechanism can also contribute to the development of capillary hypoperfusion, concomitant chronic venous insufficiency. The accumulation and activation of leukocytes in the extravascular space is accompanied by the release of toxic metabolites of oxygen and proteolytic enzymes from cytoplasmic granules and can lead to chronic inflammation with the subsequent development of trophic disorders and venous thrombi.

Preservation of venous dysfunction within several weeks after birth testifies to the influence not only of venous compression of the pregnant uterus, but also of other factors. During pregnancy, the extensibility of the veins increases, and these changes persist in some patients for 1 month and even a year after childbirth. Thus, pregnancy has a negative effect on the function of the venous system.

Pregnancy and the postpartum period create prerequisites for the development of complications of chronic venous insufficiency. Thrombosis is one of the terrible complications of chronic venous insufficiency. Venous thrombi are intravascular deposits consisting mainly of fibrin and erythrocytes with a different number of platelets and leukocytes. The formation of a thrombus reflects an imbalance between thrombogenic and protective mechanisms. During pregnancy, the blood concentration of all coagulation factors increases, except for XI and XIII (their content is usually reduced). Protective mechanisms include the binding of activated clotting factors to circulating in the blood inhibitors.

Thrombinized fibrin formation increases during pregnancy and leads to hypercoagulability. During normal pregnancy, the walls of the vessels usually remain intact. However, during pregnancy and childbirth through the natural birth canal or during caesarean section, local endothelium damage of the varicose-dilated veins may occur, which will trigger the process of thrombosis. Increased aggregation of erythrocytes in chronic venous insufficiency, dysfunction of the endothelium of the affected veins and other factors make it possible to understand why chronic venous insufficiency significantly increases the risk of thrombotic complications during pregnancy.

[1], [2], [3], [4], [5], [6], [7]