Stasis dermatitis is inflammation of the skin of the lower legs caused by chronic venous insufficiency. Symptoms are itching, scaling, hyperpigmentation, and sometimes ulceration. Diagnosis is clinical. Treatment is directed at the chronic venous insufficiency and preventing occurrence or progression of associated ulcers.
Stasis dermatitis occurs in patients with chronic venous insufficiency (see Chronic Venous Insufficiency and Postphlebitic Syndrome) because pooled venous blood in the legs compromises the endothelial integrity in the microvasculature, resulting in fibrin leakage, local inflammation, and local cell necrosis.
Symptoms and Signs
In the early stage, eczematous changes develop and manifest as erythema, scaling, weeping, and crusting, all of which can be made worse by bacterial superinfection or by contact dermatitis caused by the many topical treatments often applied. Hyperpigmentation and red-brown discoloration can occur secondary to venous stasis and be present before stasis dermatitis develops. Hyperpigmentation can also appear after stasis dermatitis develops, as a secondary change. When chronic venous insufficiency and stasis dermatitis are both inadequately treated, stasis dermatitis progresses to frank skin ulceration, chronic edema, thickened fibrotic skin, or lipodermatosclerosis (a painful induration resulting from panniculitis, which, if severe, gives the lower leg an inverted bowling pin shape with enlargement of the calf and narrowing at the ankle).
Diagnosis is clinical based on the characteristic appearance of the skin lesions and other signs of chronic venous insufficiency. Consultation with a vascular specialist and testing (such as ultrasonography) may be needed.
Chronic venous insufficiency must be adequately treated with leg elevation and compression stockings (see Treatment). For acute stasis dermatitis (characterized by crusts, exudation, and superficial ulceration), continuous and then intermittent tap water compresses should be applied. For a weeping lesion, a hydrocolloid dressing may be best. For less acute dermatitis, a corticosteroid cream or ointment should be applied 3 times/day or incorporated into zinc oxide paste.
Ulcers are best treated with compresses and bland dressings (eg, zinc oxide paste); other dressings (eg, hydrocolloids) are also effective (see also Direct ulcer care). Ulcers in ambulatory patients may be healed with an Unna paste boot (zinc gelatin), the less messy zinc gelatin bandage, or a colloid dressing (all are available commercially). Colloid-type dressings used under elastic support are more effective than an Unna paste boot. It may be necessary to change the dressing every 2 or 3 days, but as edema recedes and the ulcer heals, once or twice/wk is sufficient. After the ulcer heals, an elastic support should be applied before the patient rises in the morning. Regardless of the dressing used, reduction of edema (usually with compression) is paramount for healing.
Oral antibiotics (eg, cephalosporins, dicloxacillin) are used to treat superimposed cellulitis. Topical antibiotics (eg, mupirocin, silver sulfadiazine) are useful for treating erosions and ulcers. When edema and inflammation subside, split-thickness skin grafts may be needed for large ulcers.
Complex or multiple topical drugs or OTC remedies should not be used. The skin in stasis dermatitis is more vulnerable to direct irritants and to potentially sensitizing topical agents (eg, antibiotics; anesthetics; vehicles of topical drugs, especially lanolin or wool alcohols).
Last full review/revision October 2014 by Karen McKoy, MD, MPH
Content last modified October 2014