Stasis dermatitis develops in patients with chronic venous insufficiency caused by valvular dysfunction, deep venous thrombosis sequelae, or muscle pump failure. Sustained venous hypertension increases capillary permeability, causing fibrinogen leakage and pericapillary fibrin cuffs, red blood cell extravasation with hemosiderin deposition, leukocyte trapping, and chronic inflammation. The lower legs, especially the medial ankle and gaiter area, are the typical sites.
Clinical findings progress from initial erythema and pruritus to scaling, weeping, crusting, hemosiderin (golden-brown) pigmentation, varicose veins, ankle pitting edema, atrophie blanche (white scarred areas), lipodermatosclerosis (fibrotic indurated subcutaneous tissue), and venous ulceration over the medial malleolus. Acute autoeczematization (id reaction) can produce widespread eczematous lesions on distant sites. Differential diagnosis includes contact dermatitis, cellulitis, asteatotic eczema, and discoid lupus.
Treatment combines compression therapy (multilayer bandaging or 30-40 mmHg compression stockings) as the cornerstone, leg elevation, emollients with ceramides, topical mid-potency corticosteroid (triamcinolone) for active dermatitis tapered to the lowest effective potency, topical calcineurin inhibitors for steroid-sparing maintenance, and antibiotics for confirmed secondary infection. Avoid topical sensitizers (neomycin, lanolin, fragrances). Definitive management of venous reflux with endovenous laser ablation, radiofrequency ablation, or sclerotherapy reduces recurrence. Pentoxifylline or aspirin may aid ulcer healing in selected cases.