Hemodynamics and Mechanism of the Venous Ulcer

Joh, Jin Hyun

Abstract

Venous ulcer is a severe clinical manifestation of chronic venous insufficiency (CVI). Open venous ulcers occur in about 0.3% of the adult population and a history of open or healed ulceration occurs in about 1%. The prevalence of the venous ulcer increases with age. It is responsible for about 70% of chronic ulcers of the lower limbs. The high prevalence of venous ulcer has a significant socioeconomic impact in terms of medical care, daily work and reduced quality of life. The pathophysiology of venous ulcer and CVI are directly related. CVI is caused by a dysfunction in the muscular pump of the calf which is the primary mechanism to return blood from the lower limbs to the heart. This dysfunction leads to the ambulatory venous hypertension (AVH). AVH is the primary event result in the venous ulcer. There are many theories regarding the pathogenesis of venous ulcer. The oldest theories are venous stasis and arteriovenous shunts. The more recent theories have associated CVI with microcirculatory abnormalities, with the generation of an inflammatory response: pericapillary fibrin cuff formation; leukocyte adhesion and activation; tumor necrosis factor alpha (TNF-alpha); macromolecules, extravasation and fibrinolysis abnormalities; aggregate monocyte-platelet formation. Despite the many studies, the real mechanism of venous ulcer is still unknown. It is possible that each mechanism is important in some cases. Therefore, the pathophysiology of venous ulcer is still the subject of many current studies.