History

The chief complaint of a “red, itchy rash” is common for children with AD. The child may have a pattern of similar episodes of skin eruption in a similar distribution in the past. Certain foods, clothing, soaps, lotions, or allergenic exposures (pollen, pets) exacerbate the rash of AD. There may be a history of other atopic diseases such as food allergy, asthma, or allergic rhinitis in the child or in the immediate family.

Physical Examination

Physical examination of acute AD lesions reveals red papules and plaques that may also feature scaling, oozing, and crusting. In addition to acute lesions, children and adolescents with chronic AD may also have areas of thickened, dark skin (lichenification) at sites of prior acute lesions. The distribution of the rash is characteristic and varies by age. In infants, the cheeks, scalp, wrists, and extensor surfaces of the arms and legs are most affected (Figure 19-1). The diaper area is typically spared. The perioral and perinasal areas are rarely involved, leading to the characteristic “headlight sign” of pallor in these areas. In children and adolescents, the neck, hands, and flexor surfaces of the upper and lower extremities are more commonly affected (Figure 19-2).

Figure 19-1 Infant with atopic dermatitis.

Figure 19-2 Child with atopic dermatitis.

Complications

The defects in the epithelial barrier leave the skin susceptible to invasion by viruses and bacteria. Two common secondary infections include superinfection with Staphylococcus aureus and eczema herpeticum.

Eczema Herpeticum

Secondary infection with herpes simplex virus (HSV) is a potentially life-threatening complication that may affect children with AD of all ages. Vesicular lesions typically appear in groups superimposed on areas of skin affected by AD between 2 days and 2 weeks after exposure to HSV-1 or HSV-2. The lesions evolve to appear as “punched-out” hemorrhagic lesions with crusting (Figure 19-3). Associated symptoms may include fever, fatigue, and lymphadenopathy. Diagnosis may be made by Tzanck prep, direct fluorescent antibody, polymerase chain reaction, or viral culture from swabs of the affected area.

Figure 19-3 Eczema herpeticum.

Laboratory Testing

There are no laboratory studies essential in the diagnosis of AD. If checked for other reasons, a white blood cell count with differential may reveal an eosinophilia; a serum IgE may be elevated. In severe or refractory cases of AD, an evaluation by a pediatric allergist with skin testing (see Figure 18-3) or IgE assays for specific allergens (also known as radioallergosorbent testing [RAST]) may aid in identifying triggers that should be avoided. RAST results should be interpreted with caution because the assays often have high false-positive rates, and in the case of food allergens, subsequent elimination of foods, such as milk or eggs, poses nutritional risks.

Diagnosis

Hanifin and Rajka developed and validated a set of diagnostic criteria for AD in 1980 that remain the standard. Diagnosis is based on the presence of three major and three minor criteria (Box 19-1). The differential diagnosis of AD includes other primarily dermatologic diseases as well as systemic disease and immunodeficiency (Table 19-1).

Table 19-1 Differential Diagnosis of Atopic Dermatitis

AD, atopic dermatitis.

Approach to Therapy

The foundation of AD management includes moisturizing the skin and reducing inflammation. Moisturizing is best achieved using topical emollients with low alcohol and water content to reduce stinging when applied and drying with evaporation. Applying an effective moisturizer such as Aquaphor, Eucerin, or petroleum jelly at least twice per day helps to reduce the xerosis and heal the skin barrier. After bathing, the skin should be patted dry rather than rubbed, and moisturizer should be applied to seal in moisture. Emollients should be applied 30 minutes after any topical medications.

The first-line therapy for reducing the inflammation associated with AD is topical corticosteroids. Ointments contain less alcohol than creams and are generally preferred because of better skin penetration, although older children and adolescents may prefer creams because of their less greasy feeling. These agents are available in a wide range of potencies. Maintenance therapy is typically initiated using a low-potency corticosteroid with a low likelihood of side effects, such as hydrocortisone 1% or 2.5%. Use of medium-potency agents such as fluocinolone 0.025% or triamcinolone 0.1%, or high-potency agents such as fluocinonide 0.05% may be used for short periods of time to treat severe flares but should not be used on the face or groin. Higher-potency agents are more commonly associated with side effects, including skin atrophy, striae, telangiectasias, hypopigmentation, and hypothalamic–pituitary–adrenal axis suppression. Side effects are more likely to occur when these agents are applied to thin skin such as on the face, neck, or groin. For severe flares not controlled by topical therapy, a short course of systemic corticosteroids may be effective. Referral to an AD expert should be considered for children whose AD management is challenging (Box 19-2).

Prevention of Atopic Dermatitis in Infants

In infants, exclusive breastfeeding for the first 4 months of life has been shown to decrease the cumulative incidence of AD at 2 years of age compared with feeding with cow’s milk formula. There is no substantial evidence that supports delaying solid food introduction (including potential allergens such as cow’s milk, fish, and eggs unless the child has a suspected allergy) beyond 4 to 6 months of age as a means of preventing the development of AD.

Treatment of Complications

Treatment of S. aureus superinfection can usually be successful on an outpatient basis using oral antibiotics active against S. aureus, with consideration of antibiotics active against methicillin-resistant S. aureus (MRSA) as first-line therapy based on local resistance patterns. Small areas may respond to topical mupirocin alone. Hospitalization should be considered in young infants, those with severe disease, and children with signs of systemic illness. Ongoing therapy of the AD with moisturizers and topical steroids should be continued in children with bacterial superinfections.

Children with eczema herpeticum should be treated with acyclovir. Topical corticosteroids and TCIs should be discontinued during the acute phase of illness. Hospitalization and intravenous administration of acyclovir may be necessary in severe or disseminated cases. Ophthalmologic consultation should be considered to evaluate for herpetic keratoconjunctivitis.