Pruritus is the sine qua non of AD, which is often referred to as “the rash that itches.”3 Acute skin lesions present as ill-defined erythematous patches, papules, and plaques absent of scaling. Skin may appear edematous with widespread involvement. Moist and cracked erosions are often present with linear or punctate lesions from scratching. If secondary infections are present, erosions may have oozing, pustules, crusting, increased warmth to touch, and surrounding erythema. Other symptoms of atopy such as conjunctival and pharyngeal itching, lacrimation, allergic rhinitis, and obstruction of nasal passages may be noted.5
In chronic AD, skin thickening (lichenification) with accentuation of natural skin markings is present. Periorbital pigmentation, infraorbital folds below the eyelids (known as the Dennie-Morgan sign), and alopecia of the lateral one-third of the eyebrow from chronic rubbing may be present. Clinical manifestations of AD vary based on age and the individual patient. The scalp, face, neck, trunk, and extensor surfaces of the extremities are typical affected areas in infants, usually sparing the diaper area. Infantile AD may present with erythema and tiny vesicles. Childhood-type AD presents on the neck, face, and antecubital and popliteal fossae as lichenified plaques, erosions, crusts, and papular lesions. In adolescent and adult-type AD, the hands, feet, and flexural surfaces of the extremities are usually affected, with the condition manifesting as excoriated and lichenified skin often with painful fissures. In severe cases, disease may be generalized. Forms of AD include hand dermatitis, nummular eczema, and exfoliative dermatitis.
Ethnicity may affect the appearance of AD. In patients with dark brown and black skin, lesions may present with discrete follicular papules involving hair follicles. White dermatographism, the blanching of skin evoked by stroking, may be an associated finding.
The differential diagnosis includes seborrheic dermatitis, irritant dermatitis, allergic contact dermatitis, lichen simplex chronicus, psoriasis, ichthyosis, cutaneous T-cell lymphoma, and infectious skin diseases such as dermatophytosis, impetigo, and scabies. Congenital immunodeficiencies such as hyper-IgE syndrome, Wiskott-Aldrich syndrome, and Omenn syndrome may have an eczematoid component. In patients presenting with AD later in life with resistance to therapy, mycosis fungoides must be considered.
Diagnosis is usually based on history and clinical appearance. Although various criteria have been suggested for the diagnosis of AD, there is no gold standard. Williams et al provides a simplified criterion with high sensitivity and specificity.10 The presence of itchy skin plus 3 or more minor criteria depending on the patient’s age are required for the diagnosis of AD. Minor criteria in older children and adults include history of itchiness in skin creases, personal history of asthma or allergic rhinitis, personal history of general dry skin in the last year, visible flexural dermatitis, and onset before the age of 2 years.10
In cases with atypical presentation or if history and physical examination are not diagnostic, punch biopsy may be necessary with evaluation by a dermatopathologist. Spongiosis, a manifestation of intercellular edema, is a characteristic finding. Impetiginized or vesiculated areas may warrant bacterial or viral cultures.
Course and Prognosis
When arising in childhood, approximately 70% of individuals will experience remission by adolescence.5,6 Adult-onset AD is often severe and may persist for decades. Patients with widespread disease and those with concomitant atopic conditions such as allergic rhinitis and asthma have a less sanguine prognosis.