Stasis dermatitis, or stasis eczema, is a common inflammatory dermatosis of the lower extremities occurring in patients with chronic venous insufficiency, often in association with varicose veins, dependent chronic edema, hyperpigmentation, lipodermatosclerosis, and ulcerations. Stasis dermatitis may rarely involve the upper limbs in patients with artificial arteriovenous (AV) fistulas for hemodialysis or congenital AV malformations .
This topic will discuss the pathogenesis, clinical presentation, complications, and treatment of stasis dermatitis. The pathophysiology, clinical and diagnostic evaluation, and treatment of lower extremity chronic venous disease are discussed separately. (See "Pathophysiology of chronic venous disease" and "Diagnostic evaluation of chronic venous insufficiency" and "Post-thrombotic (postphlebitic) syndrome" and "Medical management of lower extremity chronic venous disease".)
Skin changes related to chronic venous insufficiency, including edema, hyperpigmentation, eczema, fibrosis, atrophy, and ulceration, are reported in 1 to 20 percent of women and in 1 to 17 percent of men . In one study, stasis dermatitis was reported in 6.2 percent of patients over the age of 65 . Established risk factors for varicose veins and chronic venous insufficiency include age, family history of venous disease, female sex, standing occupation, obesity, and history of deep vein thrombosis [2,4]. Heart failure and hypertension are aggravating factors.
The epidemiology of chronic venous insufficiency is discussed separately. (See "Overview and management of lower extremity chronic venous disease", section on 'Epidemiology'.)
The final common pathway that leads to chronic venous insufficiency is the development of venous hypertension. In most cases, venous hypertension results from dysfunction of the venous valves, obstruction to the venous flow, or failure of the "venous pump" . If the valves of deep or perforator veins are incompetent, the increased pressure generated during standing or calf muscle contraction causes blood to reflux into the superficial venous system, converting it into a high pressure system. (See "Pathophysiology of chronic venous disease", section on 'Genesis and consequences of chronic venous hypertension'.)