Chronic venous insufficiency (CVI) results from failure of return of venous blood and increased capillary pressure; the resultant changes include edema, stasis dermatitis, hyperpigmentation, fibrosis of the skin and subcutaneous tissue (lipodermatosclerosis) of the leg, and ulceration.
The valves of the deep veins of the calf are damaged and incompetent at restricting backflow of blood. The communicating veins that connect deep and superficial calf veins are damaged, which also causes CVI in that blood flows from deep veins to superficial venous plexus. Fibrin is deposited in the extravascular space and undergoes organization, resulting in sclerosis and obliteration of lymphatics and microvasculature. Perivascular fibrosis results in diminished nutrition of the epidermis, which breaks down with ulcer formation.
This cycle repeats itself: initial event - aggravation of venous stasis and varicose vein dilatation - lipodermatosclerosis - new thrombosis - stasis dermatitis - ulceration.
CVI may cause feet and calves to become swollen, often accompanied by a dull ache made worse with prolonged standing. If CVI is allowed to progress, the skin tends to darken and ulcers may occur. CVI often causes varicose veins.
Other symptoms of chronic venous insufficiency include legs that ache, feel heavy, or feel tired, especially after long periods of standing; new varicose veins; leg skin that looks and feels leathery; and flaking and itching in the affected area of the legs.
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