Atopic Dermatitis (Eczema)

Atopic dermatitis is a chronic relapsing and remitting inflammatory skin disease characterized by dermatitis with typical morphology and distribution.

Eczema is a generic term for a constellation of clinical signs, whereas atopic dermatitis is a term that specifically connotes an allergic contribution to the etiology of the eczema.

The overall prevalence of atopic dermatitis in the United States is 17% among school-aged children, leading to considerable disease-related morbidity, including irritability, secondary skin infections, sleep disturbance, school absenteeism, and poor self-image.

History

• Age of onset is a consideration, with 45% of affected individuals manifesting atopic dermatitis in the first 6 months of life, 60% by the first year, and 85% by school age.
• Pruritus is a cardinal feature of eczema, often described as the “itch that rashes.” Scratching leads to further compromise in the skin barrier and augments inflammation.
• Xerosis (dry skin) also involves nonlesional skin. (In other conditions, commonly mistaken for atopic dermatitis (seborrheic dermatitis, nummular eczema, and psoriasis), the uninvolved skin is generally healthy.)
• Patients may have a personal and family history of atopy (asthma, hay fever, food allergy).
• Exacerbating factors include food allergens (most frequently egg, milk, wheat, soy, peanut, tree nuts, shellfish) and inhalant allergens (e.g., pet dander, house dust mite).
• Systemic involvement, with failure to thrive, chronic diarrhea, and/or recurrent infections should prompt consideration of underlying systemic disease, such as immunodeficiency (e.g., Wiskott-Aldrich syndrome, Netherton syndrome, immune dysregulation polyendocrinopathy enteropathy X-linked (IPEX) syndrome, and hyper-IgE syndrome), or malabsorption (e.g., zinc deficiency or cystic fibrosis).

Physical Examination

• Xerosis (dry skin)
• Morphology of lesions
• Acute lesions: pruritic papules with excoriation and serous exudation
• Chronic lesions: lichenified papules and plaques
• Superficial linear abrasions from scratching
• Indistinct lesional borders, unlike that of psoriasis

Areas of involvement. Although atopic dermatitis may appear anywhere on the body, characteristic patterns include:

• Infants: cheeks, forehead, and extensor surface of extremities
• Children/adolescents: flexor surface of extremities popliteal and antecubital fossae, and ventral surface of wrists and ankles
• Atypical areas: diaper region (as a result of a lack of access to scratch the area) and nasolabial folds (commonly involved in seborrheic dermatitis)

Evaluation
Diagnosis is based on clinical features. Skin biopsy is not essential for diagnosis. Identify factors that exacerbate atopic dermatitis.

Food allergy
One third of children with moderate to severe atopic dermatitis experience worsening of eczema when exposed to food allergens.
Percutaneous skin tests, food-specific serum IgE, and oral food challenges may help identify specific foods.

Aeroallergen sensitivity

Infections

• Bacteria. Staphylococcus aureus colonizes (cutaneous, nasal, or both) 80%–90% of individuals with atopic dermatitis, potentially leading to superinfection and/or production of superantigens and augmenting cutaneous inflammation.
• Cutaneous viruses
• Herpes simplex virus (eczema herpeticum). These vesicles and/or individual “punched out” lesions have an erythematous base. Confirm by herpes simplex virus polymerase chain reaction test or Tzanck smear from a newly unroofed vesicle.
• Molluscum contagiosum
• Malassezia sympodialis (formerly Pityrosporum ovale): Consider in individuals with recalcitrant eczema, especially with lesions concentrated on the head, neck, and upper torso. Sensitivity to M. sympodialis (by skin prick test or specific IgE determination) is diagnostic. Treatment is oral antifungal therapy (itraconazole).

Differential diagnosis

• Dermatologic disease: seborrheic dermatitis, psoriasis, nummular eczema, irritant or allergic contact dermatitis, keratosis pilaris, ichthyosis, lichen simplex chronicus, and Netherton syndrome
• Infections: scabies, tinea corporis, tinea versicolor, and HIV-associated eczema
• Metabolic disease: zinc or biotin deficiency and phenylketonuria
• Immunodeficiency: see earlier discussion
• Neoplastic disease: mycosis fungoides (cutaneous T-cell lymphoma) and Langerhans histocytosis

Treatment
1, Limiting exposure to triggers
2, Nonspecific irritants. Wear nonocclusive clothing, and avoid wool or synthetic material.
3, Allergens. Eliminate contact with established allergic triggers (food or aeroallergen) if identified.
4. Topical therapy

• Emollients. Rehydration of the skin is key to stopping the “itch-scratch” cycle by the “soak and seal” method. Daily baths with lukewarm water for 10–20 minutes followed by application of a thick emollient cream are necessary.
• Topical steroids, which are the gold standard of therapy for treatment of acutely inflamed areas
• Use mild to moderate potency steroids in children (e.g., hydrocortisone 1% ointment and triamcinolone 0.1% ointment, respectively).
• Use only mild potency steroid on face, genital, and intertriginous areas.
• Topical calcineurin inhibitors, such as pimecrolimus and tacrolimus
• Nonsteroidal topical agents are effective in treating atopic dermatitis and are approved for children 2 years of age and older.

A U.S. Food and Drug Administration “black box” warning exists for topical calcineurin inhibitors, recommending these drugs as second-line treatment options.

5. Wet-wrap therapy. This involves applying a damp wet layer of cotton dressing (or cotton pajamas) over the topical emollients and then placing a layer of dry clothing above.

6. Antimicrobial therapy

• Topical antiseptics (mupirocin, triclosan, or chlorhexidine) may be applied to open excoriated areas. Intranasal mupirocin may be used to eradicate nasal carriage of S. aureus if detected. Neomycin should be avoided because it can cause contact dermatitis.
• Bleach baths, which may decrease colonization. Add 1–2 cups of household bleach per bathtub (adding a cup of table salt may diminish the stinging sensation).
• Systemic antibiotics: If there is evidence of bacterial superinfection (e.g., honey-crusted lesions), systemic antistaphylococcal antibiotics are indicated; a 5- to 10-day course is usually sufficient.

7. Prophylactic therapy is not advised because of the emergence of bacterial resistance.

8. Systemic corticosteroids. These agents are effective in short courses, but the systemic side-effect profile limits long-term applicability.

9. Systemic antihistamines
The major therapeutic value of systemic antihistamines resides in the sedative effect of first-generation histamine blockers, which helps minimize scratching and discomfort at night. Nonsedating antihistamines provide a modest reduction in pruritus.
Topical antihistamines should be avoided because they may cause sensitization and worsen disease.
Other therapies: ultraviolet light (PUVA), systemic cyclosporine, azathioprine, and immunotherapy

Special Considerations

• Associated atopic disorders. Atopic dermatitis in early childhood may herald progression toward other allergic conditions. This is known as the atopic march (allergic rhinitis and asthma).

Prevention

• Exclusive breastfeeding for at least 4 months reduces the risk of atopic dermatitis, although the protective effect wanes by 3 years of age.
• In infants with atopic dermatitis, consider delaying introduction of commonly allergenic food: cow’s milk until 12 months; eggs until 24 months; and peanuts, tree nuts, and seafood until 36 months.

Natural history. Among children with onset of atopic dermatitis before 2 years of age, 60% experience complete remission, 20% have intermittent symptoms, and 20% have persistent disease by 7 years of age.