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Dry eczema
Last reviewed: 04.07.2025

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Epidemiology
The disease is more common among patients with atopic diathesis, especially in later years of life. Most patients have a history of similar outbreaks of the disease. The incidence peaks at the end of winter and decreases in summer, especially in countries with dry, cold climates.
Causes dry eczema
Dry (asteatotic) eczema is a form of subacute eczematous dermatitis that tends to be slowly chronic with seasonal flare-ups in winter due to low humidity. Men and women are affected equally. Any area of the skin may be affected, although the lower extremities are most commonly affected. At the onset of the disease, patients often notice that their skin looks and feels dry. As the disease progresses, itching and increasing inflammation become the most prominent symptoms. Patients may feel a burning sensation, and in severe cases, cracks and crusts may form.
Symptoms dry eczema
The symptoms of dry eczema are typical of subacute eczematous dermatitis. Xerosis with an accentuated skin pattern is characteristic from the onset of the disease. Inflammation is initially mild but becomes more pronounced with time. Mild, ill-defined erythema progresses to bright red, acutely eczematous papules that coalesce into broad plaques. Vesicles are usually not formed, and excoriations are almost always present. Dry, thin desquamation progresses to the formation of fine superficial fissures to a picture known as "eczema craquele", when the skin resembles cracked porcelain or a dry river bed. The skin is very dry with fine and deep fissures. It can be painful. As it progresses, dry eczema becomes acute, with weeping, crusting, and intense erythema.
Seasonal relapses during the winter months are to be expected. Mild seasonal outbreaks with pruritus and xerosis improve with warm weather and with continued use of emollients. Active subacute inflammation usually responds to moderate-strength corticosteroid ointments and also improves with the onset of warm weather. Severe localized outbreaks with acute features such as oozing and crusting also respond to individualized topical therapy, which is discussed later. Severe outbreaks should be treated aggressively because they may become generalized.
Diagnostics dry eczema
The symptoms of dry eczema are so eloquent that a skin biopsy is rarely needed to make a diagnosis. Skin biopsy confirms the presence of epidermal spongiosis with inflammation of the dermis and often secondary impetiginization.
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Differential diagnosis
The differential diagnosis includes other subacute eczematous dermatoses such as stasis dermatitis, irritant contact dermatitis, atopic dermatitis, allergic contact dermatitis, and cellulitis. Features of several dermatoses may be present simultaneously. A second dermatosis may mask or worsen the primary eczematous process. Irritant and allergic contact dermatitis may develop as a result of the patient's own efforts to self-medicate. The patient should be asked about what he or she applies to the affected areas. Stasis dermatitis usually affects the shins in elderly patients. The anamnesis records venous insufficiency and swelling of the legs, as well as the presence of brown pigmentation (hemosiderosis) of the skin.
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Treatment dry eczema
Treatment of dry eczema depends on the stage of dry eczema (acute, subacute, or chronic) and the degree of inflammation. Treatment of xerosis involves measures for sensitive skin, namely, limited use of mild soaps only and generous use of emollients. Vaseline may be recommended as a preservative-free emollient, although patients do not always agree to use it. Moisturizers containing lactic acid, urea, or glycolic acid may also be useful. Early inflammation is best treated with medium-strength topical corticosteroids, preferably in an ointment base.
Treatment of dry eczema should be continued until erythema and scaling resolve. Liberal application of emollients should be continued as a prophylaxis against relapse. Unscented, soothing emollients are best. Localized flares with signs of acute eczematous process such as oozing and crusting should be treated initially as acute eczema. Patients require close monitoring during this stage as localized flares may become generalized. Recurrent acute flares should be evaluated by a dermatologist for allergic contact dermatitis. Wet compresses with Burow's solution and a medium-strength topical corticosteroid cream are effective in wound debridement and inflammation reduction. Systemic antibiotics may be indicated for secondary impetiginization, indicated by sticky, honey-colored crusts. Once the oozing, inflammation, and crusting have resolved, wet compresses should be discontinued to avoid excessive drying of the lesions. Medium-strength corticosteroid ointments (Group II or IV) should be continued until the redness and scaling have resolved, approximately 2 to 3 weeks. Sensitive skin care measures, including emollients, are then used to reduce recurrence. Systemic corticosteroids are rarely used to treat dry eczema.