Diagnostic Hallmarks

Distribution: ankle

History of preceding noninflammatory swelling (stasis)

Presence of varicosities

Clinical Presentation

The term "stasis" refers to the presence of chronic, noninflammatory edema of the lower leg. Stasis dermatitis occurs when the itching that often accompanies stasis leads to scratching with consequent excoriations, weeping, crusting, and int1ammation. The color of the inflammation in stasis dermatitis is violaceous rather than bright red because of pooling and deoxygenation of venous blood. In long-standing cases of stasis dermatitis, postinflammatory hyperpigmentation adds a distinctive brown hue to the underlying violaceous color. The initial changes of stasis dermatitis are almost invariably found at the ankles, but extension distally onto the foot and proximally up the lower leg is commonly seen.

Many types of eczematous disease, including atopic dermatitis and allergic contact dermatitis, occur on the ankle either as a primary disease or superimposed on stasis dermatitis. Correct identification of stasis dermatitis depends on evidence that noninflammatory edema preceded the appearance of the eruption.

Stasis ulcers frequently accompany stasis dermatitis. They appear as round to slightly irregularly shaped craters, 2 to 5 cm in diameter, with rolled violaceous borders. The center of the ulcer consists of granulation tissue that mayor may not be covered with purulent material or adherent crust. The amount of pain present is variable; often they are surprisingly asymptomatic.

Stasis ulcers begin as a result of trauma to edematous, eczematized skin. This ulcerated skin, both because of anatomically poor arterial blood supply to the lower leg and the further compromise in blood flow resulting from edema, heals very slowly. When healing finally occurs, it is accompanied by scarring. This, in turn, further compromises blood flow, allowing even minor episodes of trauma to initiate a whole new cycle. Bacterial infection in the ulcers or in the surrounding eczematized skin sometimes further complicates the process.

Course and Prognosis

Stasis dermatitis generally runs a chronic course with intermittent exacerbations and remissions. Postinflammatory hyperpigmentation remains present for months after each exacerbation.

The presence of trauma (cuts, bruises, and excoriation) to the weakened skin in stasis dermatitis sometimes leads to the development of stasis ulcers. Healing of these ulcers causes the development of tightly constricted, thickened skin around the ankle (lipodermatosclerosis). This change is sometimes mistakenly diagnosed as scleroderma. Residual edema may be found above and below the constricted area. Squamous cell carcinoma can occasionally develop in the epithelial margins of long-standing stasis ulcers.

Pathogenesis

The chronicity of stasis dermatitis depends on the continuous presence of edema. Thus, stasis dermatitis is commonly seen when the edema is due to venous valve incompetency (varicose veins) but occurs only infrequently with the intermittent edema that accompanies congestive heart failure.

Only a small proportion of patients with stasis develop stasis dermatitis. This situation is analogous to the infrequency with which dyshidrosis evolves into dyshidrotic eczema. In both diseases the eczematization occurs primarily because of the superimposition of the itch-scratch cycle, thus suggesting that atopic individuals are at particular risk.