The current status of the etiopathogenesis of chronic venous insufficiency and the formation of trophic ulcer
DOI:
https://doi.org/10.32782/2415-8127.2022.66.5Keywords:
chronic venous insufficiency, microcirculation, trophic venous ulcers, deep vein thrombosis, valvular insufficiency.Abstract
Introduction. In the review of literature based on clinical and experimental researches of various authors, a modern view on etiopathogenesis of chronic venous insufficiency and the principles of formation of trophic ulcers is highlighted. Aim. In order to improve the results of treatment of patients with chronic venous insufficiency in the stage of decompensation, evaluate the current state of the etiopathogenesis of the formation of chronic venous insufficiency and trophic ulcers. Results. The main causes of the occurrence of trophic ulcers are the violation of venous blood circulation, which occurs in varicose veins and post-thrombophlebitic syndrome. As a result of valvular insufficiency of subcutaneous, penetrating and deep veins, blood outflow from the extremities is disturbed, chronic venous hypertension is formed, which initiates the next chain of pathological reactions, leading to trophic changes and ulcers. One of the most frequent causes of the development of valvular insufficiency of the veins of the lower extremities is post-thrombophlebitic syndrome. On the basis of morphological studies, it was established that under the influence of venous hypertension, the architecture of the capillary network undergoes significant changes. The number of capillaries increases, the capillaries become tortuous, resembling kidney glomeruli. These changes, as a rule, are most pronounced in the area of the ankle-foot joint. Under the influence of venous hypertension, the venous bed is overloaded, the venules gradually lengthen, which leads to the appearance of telangiectasias. The role of ischemia is confirmed by a significant decrease in the partial pressure of oxygen in the area of venous ulcers and in the tissues adjacent to them. In addition, the absorption of oxygen from the blood is reduced in the area of venous ulcers. Conclusions. The development of CVI follows the following simplified scheme: the development and progression of venous hypertension with subsequent imbalance of the microcirculatory signaling pathway (MFRS and MDS systems), activation of macrophages and endothelial cells, imbalance between MMP/TIMMP, which leads to pathological remodeling of the vein wall and surrounding tissues with the formation venous ulcers.
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