Stasis Dermatitis

Stasis dermatitis (also called gravitational dermatitis) is an eczematous eruption that is most commonly located on the lower legs. It often appears on the medial ankles of middle-aged and elderly patients and rarely occurs before the fifth decade of life.
The dermatitis is a consequence of chronic venous insufficiency (“leaky valves”) and is seen more often in women, particularly those with a genetic predisposition to develop varicosities. It may also occur in patients with acquired venous insufficiency resulting from surgery (e.g., vein stripping or harvesting of saphenous veins for coronary bypass), deep venous thrombosis, or other types of traumatic injury to the lower venous system.
Contributing factors include: congestive heart failure (CHF), dependent leg edema, long-standing hypertension.

Traditionally, the following sequence of events has been proposed to explain the pathogenesis of stasis dermatitis:
Varicose veins Reversed flow through incompetent valves Diminished venous return Increased hydrostatic capillary pressure Pooling of blood Peripheral edema and relative tissue hypoxia
Fibrin Cuff Theory: The preceding schema may account for the pruritic, eczematous eruption seen in the early stages of stasis dermatitis; however, the fibrin cuff theory offers an explanation at the tissue level.
- Instead of pooled, stagnant blood with low oxygen tension, leg veins in patients with venous insufficiency have increased flow rates and high oxygen tension.
- An increase in permeability of dermal capillaries enables macromolecules, such as fibrinogen, to leak out into the pericapillary tissue, polymerization of fibrinogen to fibrin results in the formation of a fibrin cuff around the capillaries serving as a barrier to oxygen diffusion, with resulting tissue hypoxia and cell damage.

Lesions begin with erythema and scale (eczematous dermatitis) (Fig. 13.44). Later, the rash may become subacute, with more intense erythema, edema, erosions, crusts, and secondary bacterial infection (Fig. 13.45). The eruption may progressively lead to the chronic stages of stasis dermatitis, in which pigmentary changes occur. After an initial redness (from extravasated red blood cells), affected areas turn reddish brown (from iron that is left from the breakdown of red blood cells).
Postinflammatory hyperpigmentation (from melanin) also occurs. These colors may overlie a cyanotic background.
Ultimately, the skin may thicken and become less supple and nonpitting, and feel permanently bound down and fibrotic (“woody”) on palpation.
Most cases of stasis dermatitis and associated ulcers are located on the medial malleolus. When symptoms progress, lesions may spread to the foot or calf.
Large venous varicosities may be evident proximal to the eruption, and superficial varicosities may surround the affected area (Fig. 13.46).
Pruritus may occur.
Ankle edema that is initially pitting later may become fibrotic and nonpitting.

The diagnosis is made clinically. Skin biopsy of stasis dermatitis is rarely indicated.
Blood tests may be helpful only rule out underlying hypercoagulable states.
Radiologic/Doppler studies can rule out deep venous thrombosis or severe valve damage due to past thrombosis.

Differential Diagnosis

Cellulitis

Stasis dermatitis is often confused with cellulitis (Fig. 13.50), an acute infection of skin and soft tissues characterized by localized pain, swelling, tenderness, erythema, and warmth. It is usually caused by gram-positive aerobic cocci (e.g., S. aureus, S. pyogenes).

Other Diagnoses

When ulcerations are present, the differential diagnosis includes vasculitis, arterial disease, cryoglobulinemia, the antiphospholipid syndrome, protein C deficiency, skin cancer, or pyoderma gangrenosum.

Management

Stasis Dermatitis (Eczematous Eruption): Topical Therapy

Weeping, oozing, or infected areas may be soaked with Burow Solution followed by a midpotency topical corticosteroid such as triamcinolone 0.1% ointment for reducing inflammation and itching during acute flares.
Higher-potency topical corticosteroids should be avoided.
Patients should be advised not to apply topical corticosteroid preparations directly to stasis ulcers because the preparations may interfere with healing.
Plain white petrolatum (Vaseline Petroleum Jelly) is a cheap occlusive moisturizer/dressing with no potential to develop ACD.
Possible OTC sensitizers such as lanolin, neomycin, and bacitracin should be avoided since patients with stasis dermatitis tend to develop ACD quite readily.

Edema

Significant edema may be managed with compressive therapy, the mainstay of therapy for venous insufficiency.
Support hose, elastic bandages, and specialized compression stockings (Jobst, Sigvaris) that deliver a controlled gradient of pressure should be strongly recommended.
The patient's peripheral arterial circulation should be assessed clinically or with a Doppler or Duplex study before compression is recommended. Adding compression to a leg with compromised arterial circulation could increase claudication and put the patient at risk for ischemic damage.

Infection

Obvious superficial infections (impetiginization) should be treated with systemic antibiotics that have activity against S. aureus and Streptococcus species (e.g., dicloxacillin, cephalexin, or a fluoroquinolone).
A widespread autoeczematized eruption may require treatment with both systemic corticosteroids and oral antibiotics.

Stasis Ulcers

Stasis ulcers are managed by treating the underlying eczematous dermatitis, controlling weight, preventing infection, and using compression. Venous ulcers at times produce a dull pain that is relieved by elevation.
An Unna boot is best applied in the morning, before edema progresses. After application, the bandage hardens into a cast. The boot decreases edema, promotes healing, and serves as a barrier from trauma (e.g., scratching). It should be changed weekly until the ulcer heals.
If feasible, corrective surgery, such as skin grafts or vascular procedures, may be another option.

Prevention of Diminished Venous Return

Venous return can be increased by engaging in regular exercise, such as brisk walking and bicycling. Such activities augment the “calf pump.”
Furthermore, the affected leg(s) should be elevated above the level of the heart or at least to hip level if the patient has congestive heart failure (sitting with the leg elevated by a stool is inadequate).
At night, leg elevation can be accomplished by propping up the foot end of the bed with 2 to 3 in of plywood or a bedding fabric such as sheets (Fig. 13.51).
Compression of lower extremities with support hose or elastic bandages can help venous return and should be strongly encouraged as an essential component of prevention.

SEE PATIENT HANDOUT “Burow Solution” IN THE COMPANION eBOOK EDITION.

Helpful Hints

Stasis dermatitis is often misdiagnosed as cellulitis.
Infected stasis dermatitis should be considered in patients who develop a sudden onset of extensive generalized eczematous dermatitis (autoeczematization).
Compression is the mainstay of therapy for venous insufficiency and venous leg ulceration.

Helpful Hints

Sitting in a reclining chair while reading or watching television can help promote venous return.
Compression stockings should be applied early in the morning, before the patient rises from bed, to facilitate application when leg edema is at its lowest point.
Walking regularly at a brisk pace should be encouraged.
Physical therapy should be considered.
Smoking and long periods of standing or sitting should be discouraged.

Clinical Sequelae and Possible Complications

Venous stasis ulcers may develop and be exacerbated by trauma (e.g., scratching), bacterial infection, or improper care of the eczematous rash (Fig.13.47). Ulcers are often asymptomatic but can sometimes produce a dull pain.
Induration may progress to lipodermatosclerosis, which has a classic “inverted water bottle” appearance (Fig. 13.48).
Autoeczematization is a widespread, often explosive, acute eczematous eruption that is presumably triggered by secondary bacterial infection (impetiginization) of eczema, with resultant circulating immune complexes released from the site of the stasis dermatitis lesions (Figs. 13.49A,B). It is hypothesized that patients become sensitized to their own tissue breakdown products.

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Basics ⬇

Pathogenesis ⬆ ⬇

Clinical Manifestations ⬆ ⬇

Diagnosis ⬆ ⬇

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