Stasis dermatitis


Refers to the skin changes that occur in the leg as a result of stasis or blood pooling from insufficient venous return.

Most common cause is varicose veins.

Insufficient venous return results in increased pressure in the capillaries.

Related to venous hypertension or chronic venous insufficiency.

Most cases are caused by incompetence of the intrinsic valves in either the superficial saphenous veins or deep veins, and particularly incompetence of the communicating veins of the lower limb contacting the two venous systems.

Less commonly, venous hypertension can result from obstruction to the venous flow from thrombophlebitis, AV fistula, or failure of calf muscle pump that may occur with old age.

Can occur in the absence of varicose veins.

Affects approximately 7% of individuals over the age of 50, and 20% over the age of 70.

Has a slight female predominance.

Risk factors include: obesity, multiple pregnancies, hypertension, heart failure, renal failure, increased abdominal pressure, vein stripping, knee replacement, trauma to the leg, prolonged standing at work, and medications.

Medications associated with stasis dermatitis include: calcium channel blockers, beta blockers, minoxidil, clonidine, hydralazine, methyldopa, estrogen, nonsteroidal anti-inflammatory drugs.

Stasis dermatitis results in fluid and cells leaking out of the capillaries.

Increased venous pressure leads to permeability increases of dermal capillaries, allowing fluid and macromolecules, such as fibrinogen to leak into interstitial spaces.

Edema occurs as fluid accumulates in the interstitial spaces.

Fibrinogen polymerization to fibrin results in the formation of a fibrin cuff around dermal capillaries, serving as a barrier to oxygen diffusion, with resultant hypoxia and cell damage to the overlying skin and surrounding tissues.

The formation of fibrin cuffs and decreased fibrinolysis leads to dermal fibrosis.

Stasis dermatitis pigmentation is related to deposition of hemosiderin in the skin and melanin pigment.

Dermal hemosiderin stimulates melanogenesis.

Leaked red cells break down, with iron containing hemosiderin remaining in the skin.

The skin appears thin, brown and induated, with macules, red spots, superficial skin irritation, darkening, thickening of the skin at the ankles or legs.

It may result in weakening of the skin with the development of ulcers.

May be associated with edema of legs and ankles.

Patients may present with pruritis, edema, erythema, crusting. scaling of the lower extremities.

In the chronic stages of the disease hyperpigmentation, eczematous patches or plaques, hair loss, induration, lichenification, and thickened skin with dimpling made be seen.

Itching, pain, paresthesias may occur.

Skin barrier deterioration predisposes the entry of bacterial infection causing cellulitis infection of the leg, and stasis ulcers may form.

Usually bilateral but can be unilateral.

The medial ankle is most frequently involved, and the process can extend up the leg and down to the foot.

Upper limb involvement is unusual but may occur in patients who have AV fistula, as for hemodialysis.

Pathologic findings include hyperkeratosis, acanthosis, spongiosis in the epidermis, lobular proliferation, dilatation, capillary distention in the papillary dermis, extravasated red blood cells, hemosiderin laden macrophages, perivascular lymphocytic infiltration and dermal fibrosis.

Diagnosis is a clinical one based on the above features.

Dermoscopy can help in the diagnosis by demonstrating glomerular vessels in clusters or throughout the lesion

Ultrasound of the lower limbs should be done to demonstrate venous incompetence or DVT.

Differential diagnosis includes: atopic dermatitis, contact dermatitis, lichen simplex chronicus, lichen planus, asteatotic eczema, nummular eczema, psoriasis, tinea corporis, necrobiosis lipodica, pretibial myxedema, and cutaneous T-cell lymphoma.

Complications include ulcerations, contact sensitization, autosensitization, and superinfections along with dermatosclerosis.

Impairs quality of life and is associated with an increased risk for squamous cell carcinoma and keratocanthoma.

Prognosis depends on the underlying cause, but is usually a chronic and difficult management problem.

Treatment utilizes compression stockings or intermittent pneumatic compression pumps to decrease lower leg fluid, and topical steroid based creams.

Topical corticosteroids are the mainstay therapy.

Topical calcneurin are other options.

Patients with secondary bacterial infections should be treated with appropriate antibiotics.

Pulsed light therapy may improve pigmentation problems.

Underlying cause, if treatable, should be considered such as structural defects of veins with ligation or stripping or laser ablation, radiofrequency ablation or sclerotherapy.

Medications contributing to the process should be discontinued.

Obese patients should lose weight.

Clothing that limits circulation or movement of the lower extremities should be avoided.

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