6-09: Atopic Dermatitis

Atopic dermatitis (also known as eczema) has distinct presentations in people of different ages and races. Diagnostic criteria for atopic dermatitis must include pruritus, typical morphology and distribution (flexural lichenification, hand eczema, nipple eczema, and eyelid eczema in adults), onset in childhood, and chronicity. Also helpful are (1) a personal or family history of atopy (asthma, allergic rhinitis, atopic dermatitis), (2) xerosis-ichthyosis, (3) facial pallor with infraorbital darkening, (4) elevated serum IgE, and (5) repeated skin infections.

A. Symptoms and Signs

Itching is a key clinical feature and may be severe and prolonged. Ill-defined, scaly, red plaques (eFigure 6–9) affect the face, neck, and upper trunk. The flexural surfaces of elbows and knees are often involved. In chronic cases, the skin is dry and lichenified. In dark-skinned patients with severe disease, pigmentation may be lost in lichenified areas. During acute flares, widespread redness with weeping, either diffusely or in discrete plaques, is common. Since virtually all patients with atopic dermatitis have skin disease before age 5, a new diagnosis of atopic dermatitis in an adult over age 30 should be made only after consultation with a dermatologist.

B. Laboratory Findings

Food allergy is an uncommon cause of flares of atopic dermatitis in adults. Eosinophilia and increased serum IgE levels may be present.

Atopic dermatitis must be distinguished from seborrheic dermatitis (less pruritic, frequent scalp and central face involvement, greasy and scaly lesions, and quick response to therapy). Psoriasis is marked by sharply demarcated thickly scaled plaques on elbows, knees, scalp, and intergluteal cleft. Secondary staphylococcal or herpetic infections may exacerbate atopic dermatitis and should be considered during hyperacute, weeping flares of atopic dermatitis. An infra-auricular fissure is a cardinal sign of secondary infection.

Patient education regarding gentle skin care and exactly how to use medications is critical to successful management of atopic dermatitis.

A. General Measures

Atopic patients have hyperirritable skin. Anything that dries or irritates the skin will potentially trigger dermatitis. Atopic individuals are sensitive to low humidity and often flare in the winter. Adults with atopic disorders should not bathe more than once daily. Soap should be confined to the armpits, groin, scalp, and feet. Washcloths and brushes should not be used. After rinsing, the skin should be patted dry (not rubbed) and then immediately—within minutes—covered with a thin film of an emollient or a corticosteroid as needed. Plain petrolatum can be used if contact dermatitis resulting from additives in medication is suspected. Atopic patients may be irritated by rough fabrics, including wools and acrylics. Cottons are preferable, but synthetic blends also are tolerated. Other triggers of atopic dermatitis in some patients include sweating, ointments, and heat.

B. Local Treatment

Corticosteroids should be applied sparingly to the dermatitis once or twice daily and rubbed in well. Their potency should be appropriate to the severity of the dermatitis. In general, for treatment of lesions on the body (excluding genitalia, axillary or crural folds), one should begin with triamcinolone 0.1% or a stronger corticosteroid, then taper to hydrocortisone or another slightly stronger mild corticosteroid (alclometasone, desonide). It is vital that patients taper off corticosteroids and substitute emollients as the dermatitis clears to avoid side effects of corticosteroids. Tapering is also important to avoid rebound flares of the dermatitis that may follow their abrupt cessation. Tacrolimus ointment (Protopic 0.03% or 0.1%), pimecrolimus cream (Elidel 1%), and crisaborole (Eucrisa 2%) can be effective in managing atopic dermatitis when applied twice daily. Burning on application occurs in about 50% of patients using Protopic and in 10–25% of Elidel users, but it may resolve with continued treatment. These noncorticosteroid medications do not cause skin atrophy or striae, avoiding the complications of long-term topical corticosteroid use. They are safe for application on the face and even the eyelids but are more expensive than generic topical corticosteroids.

There is a Food and Drug Administration (FDA) black box warning for both topical tacrolimus and pimecrolimus due to concerns about the development of T-cell lymphoma. The agents should be used sparingly and only in locations where less expensive corticosteroids cannot be used. They should be avoided in patients at high risk for lymphoma (ie, those with HIV, iatrogenic immunosuppression, or prior lymphoma).

The treatment of atopic dermatitis is dictated by the pattern and stage of the dermatitis—acute/weepy, subacute/scaly, or chronic/lichenified.

1. Acute weeping lesions

Staphylococcal or herpetic superinfection should be formally excluded. Use water or aluminum subacetate solution (Domeboro or burow solution), or colloidal oatmeal as a bath or as wet dressings for 10–30 minutes two to four times daily. Lesions on extremities may be bandaged for protection at night. Use high-potency corticosteroids after soaking, but spare the face and body folds. Tacrolimus is usually not tolerated at this stage. Systemic corticosteroids may be required. An allergic or irritating contactant should also be considered when acute weeping lesions are present, since contact dermatitis is more likely to develop in atopic patients.

2. Subacute or scaly lesions

At this stage, the lesions are dry but still red and pruritic. Mid- to high-potency corticosteroids in ointment form should be continued until skin lesions are cleared and itching is decreased substantially. At that point, patients should begin a 2- to 4-week taper from twice-daily to daily dosing with topical corticosteroids to reliance on emollients, with occasional use of corticosteroids only to inflamed areas. It is preferable to switch to daily use of a low-potency corticosteroid instead of further tapering the frequency of usage of a more potent corticosteroid. Tacrolimus and pimecrolimus may be substituted if corticosteroids cannot be stopped completely.

3. Chronic, dry, lichenified lesions

Thickened and usually well demarcated, they are best treated with high-potency to ultra–high-potency corticosteroid ointments. Nightly occlusion for 2–6 weeks may enhance the initial response. Adding tar preparations, such as liquor carbonis detergens (LCD) 10% in Aquaphor or 2% crude coal tar may be beneficial.

4. Maintenance treatment

Once symptoms have improved, constant application of effective moisturizers is recommended to prevent flares. In patients with moderate disease, use of topical anti-inflammatories only on weekends or three times weekly can prevent flares.

C. Systemic and Adjuvant Therapy

Systemic corticosteroids are indicated only for severe acute exacerbations. Oral prednisone dosages should be high enough to suppress the dermatitis quickly, usually starting with 1 mg/kg daily. The dosage is then tapered off over a period of 2–4 weeks. Owing to the chronic nature of atopic dermatitis and the side effects of long-term systemic corticosteroids, ongoing use of these agents is not recommended for maintenance therapy. Bedtime doses of hydroxyzine, diphenhydramine, or doxepin may be helpful via their sedative properties to mitigate perceived pruritus. Phototherapy can be an important adjunct for severely affected patients. Properly selected patients with recalcitrant disease may benefit greatly from therapy with UVB with or without coal tar or (psoralen plus ultraviolet A [PUVA]). Dupilumab is a targeted immunomodulator with minimal systemic adverse effects and requires minimal laboratory monitoring. Oral cyclosporine, mycophenolate mofetil, methotrexate, tofacitinib, or azathioprine may also be used for the most severe and recalcitrant cases.

The clinician should monitor for skin atrophy. Eczema herpeticum, a generalized herpes simplex infection manifested by monomorphic vesicles, crusts, or scalloped erosions superimposed on atopic dermatitis or other extensive eczematous processes, is treated successfully with oral or intravenous acyclovir (eFigure 6–10). Smallpox vaccination is absolutely contraindicated in patients with atopic dermatitis or a history thereof because of the risk of eczema vaccinatum (widespread vaccinia infection, preferentially in areas of dermatitis). Fissures, crusts, erosions, or pustules indicate staphylococcal or herpetic infection clinically. Systemic antistaphylococcal antibiotics—such as a first-generation cephalosporin or doxycycline if methicillin-resistant Staphylococcus aureus is suspected—should be given only if indicated and guided by bacterial culture. Cultures to exclude methicillin-resistant S aureus are recommended. In this setting, continuing and augmenting the topical anti-inflammatory treatment often improves the dermatitis despite the presence of infection.

Atopic dermatitis runs a chronic or intermittent course. Affected adults may have only hand dermatitis. Poor prognostic factors for persistence into adulthood in atopic dermatitis include generalized disease or onset early in childhood and asthma. Only 40–60% of these patients have lasting remissions.