Stasis Dermatitis | Visual Dermatology Atlas

Illustration of the main clinical features of stasis dermatitis, showing predominant involvement of the distal lower legs in the setting of chronic venous insufficiency. The lesions appear as reddish-brown patches or plaques associated with hemosiderin-re

Clinical Images

Examples of clinical presentations.

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Stasis dermatitis : Bilateral diffuse erythema of the lower legs with marked edema, predominantly involving the distal extremities.

Source : Te Whatu Ora – Health New Zealand.

Clinical images provided for educational purposes.

General info +

AKA: Venous eczema / Venous stasis dermatitis / Gravitational eczema

• Chronic inflammatory dermatosis of the lower extremities secondary to chronic venous insufficiency and venous hypertension.
• Venous hypertension leads to extravasation of fluid, proteins, and red blood cells into the tissues, contributing to edema, inflammation, and hemosiderin deposition.
• More common in older adults, particularly those over 50 years of age.
• Frequently associated with varicose veins and chronic lower-extremity edema.
• Usually follows a chronic course with recurrent eczematous flares.
• May progress to lipodermatosclerosis and chronic venous ulceration.
• Risk factors include chronic venous insufficiency, varicose veins, previous DVT, obesity, pregnancy, prolonged immobility, and older age.

Symptoms / presentation +

• Chronic pruritus of the lower legs.
• Sensation of heavy, aching, or uncomfortable legs.
• Ankle edema, typically worse after prolonged standing and toward the end of the day.
• History of varicose veins, deep vein thrombosis, or venous ulcers may be present.
• Recurrent episodes of lower-leg eczema.
• Significant pain, warmth, rapid progression, fever, or purulent drainage should raise concern for secondary infection or another diagnosis.

Clinical exam +

• Poorly demarcated erythematous to reddish-brown patches and plaques.
• Fine scaling ± oozing and crusting during acute eczematous flares.
• Pruritus with possible excoriations.
• Pitting edema, particularly around the ankles.
• Brown hyperpigmentation caused by hemosiderin deposition.
• Varicose veins and telangiectasias may be present.
• Lipodermatosclerosis: induration and fibrosis of the lower leg; advanced disease may produce an “inverted champagne bottle” appearance.
• Atrophie blanche: small, atrophic, porcelain-white scar-like areas.
• Venous ulcers may develop in advanced disease, classically around the medial malleolus.

Distribution +

• Lower legs / “gaiter area” +++.
• Medial malleolar region +++.
• Ankles.
• May extend onto the dorsum of the foot.
• Usually bilateral, although involvement may be asymmetric.

Dermoscopy +

• Erythematous to brown background.
• Diffuse orange-brown pigmentation corresponding to hemosiderin deposition.
• Variable superficial scaling.
• Dotted, glomerular, or other nonspecific vascular structures may be present.
• Dermoscopy is mainly adjunctive and is generally not required for diagnosis.

Diagnostic +

• Primarily a clinical diagnosis based on characteristic skin findings and evidence of chronic venous disease.
• Venous duplex ultrasound if venous insufficiency has not been documented, the diagnosis is uncertain, or venous intervention is being considered.
• Ankle-brachial index (ABI) before significant compression therapy when peripheral arterial disease is suspected.
• Bacterial culture only when there are clinical signs of infection.
• Skin biopsy may be considered for atypical presentations or a chronic ulcer with suspicious features.

Differential diagnosis +

• Bacterial cellulitis.
• Allergic or irritant contact dermatitis.
• Dermatophytosis.
• Psoriasis.
• Cutaneous vasculitis.
• Lymphedema.
• Pretibial myxedema.
• Acute lipodermatosclerosis.
• Arterial or neuropathic ulcer when ulceration is present.

Treatment plan +

• Main goal: control venous hypertension and treat cutaneous inflammation.
• Graduated compression therapy = cornerstone of treatment when arterial circulation is adequate.
• Assess ABI/arterial circulation before substantial compression if peripheral arterial disease is suspected.
• Regular leg elevation to reduce edema.
• Encourage regular walking and physical activity when appropriate.
• Avoid prolonged standing or sitting without movement.
• Apply emollients daily to treat xerosis and restore the skin barrier.
• Eczematous flares: medium-potency topical corticosteroid, with a more potent agent occasionally used for a short course depending on severity and location.
• E.g., triamcinolone 0.1% once or twice daily for 1–2 weeks, followed by reassessment.
• Avoid prolonged use of potent topical corticosteroids because of the risk of skin atrophy.
• Antibiotics only for true clinical bacterial infection; colonization of a venous ulcer alone does not warrant systemic antibiotics.
• Venous ulcers: appropriate compression + wound care and dressings, with debridement when indicated.
• Chronic or complex ulcers: referral to a wound-care or vascular specialist.
• Underlying venous disease may be treated with sclerotherapy, endovenous ablation, or venous surgery depending on vascular assessment.

References +

DermNet — Venous eczema, gravitational eczema.
American Academy of Dermatology (AAD) — Stasis dermatitis.
UpToDate — Stasis dermatitis.
Bolognia JL, Schaffer JV, Cerroni L. Dermatology. Elsevier.