Atopic Dermatitis The 5 Minute Pediatric Consult


	Atopic Dermatitis

Christen Mowad

Database
Differential Diagnosis
Data Gathering
Physical Examination
Laboratory Aids
Therapy
Follow-Up
Common Questions and Answers
Bibliography

DATABASE

DEFINITION

Atopic dermatitis or eczema is a chronic, pruritic, papulosquamous eruption seen in individuals with associated personal or family history of atopy—asthma, allergies, hay fever, or rhinitis. There are often intermittent acute flares of atopic dermatitis. It most commonly begins in infancy or early childhood.

CAUSES

Etiology of atopic dermatitis is multifactorial, with genetic, environmental, physiologic, and immunologic factors.
Decreased resistance to sensitization and increased viral and dermatophyte infections seen in these patients suggest decreased cell-mediated immunity.
Patients often have elevated IgE levels and decreased chemotaxis of neutrophils.
Up to 70% of patients have a family history, but the mode of inheritance is not well defined.

PATHOLOGY

Histologic findings are dependent on the stage of atopic dermatitis—acute or chronic.
The acute form is characterized by epidermal psoriasiform hyperplasia with intercellular edema and spongiosis that can lead to vesicle formation.
Lymphocytes can be seen infiltrating the epidermis.
The chronic form shows acanthosis, hyperkeratosis, and lymphocytes in the epidermis.

GENETICS

There is a genetic trait seen in atopic dermatitis, with 30% to 70% of family members having atopy—allergies, asthma, eczema, or hay fever.
The exact mode of inheritance is not well defined and appears to be multifactorial.

EPIDEMIOLOGY

Atopic dermatitis is a common disease, occurring in up to 7% of children.
Approximately 60% of patients with atopic dermatitis will develop it in the first year of life, and 30% between the ages of 1 and 5 years.
A family history of atopy—allergies, asthma, eczema, or hay fever—is present in 30% to 70% of patients.
Atopic dermatitis is usually worse in the winter.

COMPLICATIONS

Decreased cell-mediated immunity and decreased chemotaxis can result in increased infection—viral, dermatophyte, and bacterial. Patients with atopic dermatitis have a high density of Staphylococcus aureus on their skin, and given the fissures and open excoriations, there is a risk of superinfection of these lesions.
The decreased integrity of the skin can result in widely spread cutaneous infections such as herpes simplex infection, known as Kaposi varicelliform eruption or eczema herpeticum. Similar problems can also be seen with coxsackievirus or molluscum contagiosum and used to occur with vaccinia.
Cataracts can be found in patients with atopic dermatitis, and a severe, rare complication of the disease is the development of Sézary syndrome or mycosis fungoides.

DIFFERENTIAL DIAGNOSIS

Diagnostic criteria have been established for atopic dermatitis. The differential diagnosis of atopic dermatitis includes:

Severe seborrheic dermatitis
Contact dermatitis
Allergic or irritant, psoriasis
Wiskott-Aldrich syndrome
Histiocytosis X
Acrodermatitis enteropathica
Scabies
Xerosis
Hyper-IgE syndrome
Metabolic deficiencies
- Carboxylase
- Prolidase deficiencies

DATA GATHERING

HISTORY

Age of onset
Location
Prior treatment
Bathing habits
Family history of atopy—allergies
Asthma
Eczema
Hay fever

PHYSICAL EXAMINATION

Acute flares reveal weeping and crusted erythema.
Chronic disease is characterized by hyperpigmentation or hypopigmentation, lichenification, and scaling.
The distribution of the disease is dependent on age.
- During infancy to approximately 2 years of age, the disease is widespread and includes cheeks, forehead, scalp, and extensor surfaces.
- In children from approximately 3 to 11 years, the disease involves the more characteristic flexural sites with lichenification.
- The hands and face can also be involved.
- From adolescence to adulthood, the flexures, neck, hands, and feet are frequently involved, with the face and neck flaring occasionally.
When the disease is severe, it can present as exfoliative erythroderma with diffuse scaling and erythema.
Other associated findings include geographic tongue, Dennie-Morgan folds (infraorbital folds), pityriasis alba, (dry white patches), hyperlinear palms, facial pallor, infraorbital darkening, follicular accentuation, keratosis pilaris (dry, rough hair follicles on extensor surfaces of upper arms and thighs).

Special Questions

Excessive dryness exacerbates this disease; therefore, inquiry about bathing habits, frequency, and emollients is helpful.

LABORATORY AIDS

No tests are diagnostic of atopic dermatitis.
Biopsy can be helpful to rule out other papulosquamous disease, such as psoriasis.
IgE levels are often elevated. Cultures can help identify superinfection during acute flares and viral cultures, and Tzanck smear can identify complications of eczema herpeticum.
Patch testing can help differentiate atopic dermatitis from contact dermatitis.

THERAPY

There is no cure for atopic dermatitis.
Patients must understand that this is a chronic disease with intermittent flares and that control is the aim of treatment.
Good skin care is critical to maintenance and includes use of mild soaps, frequent use of emollients, and avoidance of excessive bathing.
Avoidance of irritants from the environment, such as wool sweaters or blankets, is recommended. Protective clothing at night to avoid scratching while sleeping is also helpful, as is trimming the nails. Antihistamines such as hydroxyzine or diphenhydramine help to decrease itching.
Topical steroids control inflammation and mid- to high-potency steroids can be used during acute flares, with tapering of steroids to milder potency when control is achieved. Once cleared, topical steroids can be held and substituted with emollients. Long-term use of steroids can lead to atrophy, telangiectasias, tachyphylaxis, and occasionally, stunting of growth. Oral antibiotics are indicated when there is superinfection of lesions.
Antivirals are needed for cases of eczema herpeticum. During acute flares with oozing and crusting and when there is superinfection with bacteria or herpes simplex virus, compresses can be helpful.
Systemic steroids are generally not used because of the chronicity of atopic dermatitis, and are reserved for when control of the eruption is very difficult, and then use should be of short duration.
Phototherapy with ultraviolet B can be used in patients with extensive disease resistant to other therapy.

FOLLOW-UP

It should be emphasized to patients that atopic dermatitis is a chronic disease and that good skin care is necessary to control disease activity. Up to 40% to 50% of children will outgrow their atopic dermatitis after the age of 5 years.

COMMON QUESTIONS AND ANSWERS

Q: Will the child outgrow this?
A: Up to 40% to 50% of children will outgrow their atopic dermatitis after the age of 5 years. In some patients, however, the disease will persist to variable extents throughout adulthood.

Q: When atopic dermatitis is controlled, is any treatment necessary?
A: Excessive dryness can exacerbate or flare disease; therefore, less use of soaps and frequent use of emollients is recommended.

Q: Do food hypersensitivities play a role in atopic dermatitis?
A: This is a debated issue. In general, the majority of patients are probably not adversely affected by foods. However, some individuals, particularly those unresponsive to routine therapy, may benefit from screening for food hypersensitivity and a trial of avoidance to any foods that test positive. The most common foods associated with exacerbation when an association can be made are eggs, milk, wheat, soy, peanuts, and fish.

ICD-9-CM 691.8

BIBLIOGRAPHY

Boguniewicz M. Advances in the understanding and treatment of atopic dermatitis. Curr Opin Pediatr 1997;9(6):577–581.

Bondi EE, Jegasothy BV, Lazarus GS. Dermatology diagnosis and therapy. Norwalk, CT: Appleton & Lange, 1991.

Burks AW, James JM, Hiegel A, Wilson G, Wheeler JG, Jones SM, Zuerlein N. Atopic dermatitis and food hypersensitivity reactions. J Pediatr 1998;132(1):132–136.

Fitzpatrick TB, Eisen AZ, Wolfe K, et al. Dermatology in general medicine, 4th ed. New York: McGraw-Hill, 1993:1543–1564.

Hill DJ, Hosking CS. Emerging disease profiles in infants and young children with food allergy. Pediatr Allergy Immunol 1997;8(10 Suppl):21–26.

Lever WF, Schaumberg_Lever G. Histopathology of the skin, 7th ed. Philadelphia: Lippincott, 1990.

Oakes RC, Cox AD, Burgdorf WH. Atopic dermatitis: a review of diagnosis, pathogenesis, and management. Clin Pediatr 1983;22(7):467–475.

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