Atopic dermatitis (AD) is the most common form of eczema in children and is estimated to affect 15% to 20% of children worldwide, with increasing prevalence in some countries.
Atopic dermatitis is a more precise term to describe the form of eczema that has a highly characteristic, age-specific distribution pattern and is associated with other atopic disorders such as asthma and allergic rhinitis.
Clinical hallmarks of AD include pruritus, an unpredictable course of flares and remissions, early onset, and an age-specific morphology and distribution of lesions.
Symptoms begin during infancy (usually after 2 months) in more than half of patients; and the onset is before 5 years of age in 90% of patients.
AD is typically the first manifestation of the atopic triad and precedes the development of asthma and allergic rhinoconjunctivitis. The progression from atopic dermatitis in infancy, to asthma in childhood, and allergic rhinoconjunctivitis in late childhood/early adolescence is known as the atopic march. It is estimated the 50% to 80% of children with AD will develop another atopic disease.
AD has a substantial adverse impact on the quality of life of affected children and their families and the societal economic burden is high.
AD tends to improve with age. Forty percent of children clear by 3 years of age and up to 70% clear by puberty.
Atopic dermatitis results from intrinsic defects in the epidermal barrier, alterations in cutaneous innate and adaptive immunity and environmental triggers. The complex interplay among these factors is the subject of vigorous investigation.
The traditional inside-out theory, which suggests that AD is primarily an immunologic disease, has now been complemented by the outside-in theory, which considers the barrier defect as primary.
Barrier defects in AD include mutations in filaggrin (FLG), decreased epidermal lipid content (ceramides), and increased transepidermal water loss. This barrier dysfunction explains the dry skin and vulnerability to skin infections typical of AD.
Immunologic abnormalities in AD include decreased levels of epidermal antimicrobial peptides (beta-defensins and cathelicidins), and a T-helper 2 (Th2) type response to penetrating antigens (microbial, aeroallergens, etc.), which promotes eosinophilia and IgE production. A T-helper type 1 response is noted only later, in chronic AD.
Patients invariably complain or demonstrate the presence of pruritus.
AD is a chronic condition often with an unpredictable course of flares and remissions.
The different phases of AD are not always clearly distinct and any or all manifestations (i.e., acute, subacute, or chronic; see Chapter 13: Eczema and Related Disorders) of atopic dermatitis may exist in a single patient.
Other clinical clues are often present; see Table 4.1.
Besides pruritus, other important clinical features include xerosis and other atopic stigmata (see Table 4.1); eczematous skin lesions in the typical age-specific distribution (i.e., face and extensor surfaces in infants and a flexural distribution in childhood); a chronic, unpredictable, and relapsing course; an early age at onset (usually <2 years of age); and/or a first degree relative with asthma or allergic rhinitis.
Psoriasis (see Chapter 14: Psoriasis)
Scabies (see Chapter 20: Hirsutism) Seborrheic Dermatitis
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General Principles
Treatment Topical Therapy (see Chapter 13: Eczema and Related Disorders and Introduction: Topical Therapy) Face and Body Folds
Body (Trunk, Arms, Legs, Scalp)
Adjunctive Therapies to Consider During AD Flares
Daily Maintenance Therapy Gentle Bathing Tips
Other Therapeutic Measures
SEE PATIENT HANDOUTS, Atopic Dermatitis, Written Action Plan, Soak and Smear Instruction Sheet, and Bleach Baths IN THE COMPANION eBOOK EDITION. |
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SEE PATIENT HANDOUT Atopic Dermatitis IN THE COMPANION eBOOK EDITION. |
Infantile Phase
In infancy, AD usually presents after 2 months of age with intense itching or irritability.
Skin lesions present with varying amounts of ill-defined, erythematous, edematous, papules and plaques on the cheeks, forehead, and scalp, as well as on the extensor extremities (Fig. 4.2). The eruption can also become more generalized.
The face and/or scalp is involved in almost all affected infants (Figs. 4.3 and 4.4).
There is often a history of seborrheic dermatitis or cradle cap and features of AD become prominent after the seborrheic dermatitis subsides.
Infants indicate itching by rubbing their scalp and head on crib bedding, by pinching, scratching, or tapping of affected and unaffected areas of skin.
Characteristically infantile AD spares the more moist fold areas such as the inguinal folds,
Childhood Phase
The childhood phase of AD follows the infantile phase beginning at around 2 years of age and continues through puberty.
Lesions localize to the flexural aspects of the elbows and knees (antecubital and popliteal fossae), the wrists, ankles, and posterior neck in a symmetric distribution (Figs. 4.5 and 4.6).
Facial eczema typically presents on the periorbital skin and the lips.
Lesions in childhood AD tend to be more well circumscribed, dry, and scaly.
Repeated rubbing and scratching results in lichenification (Fig. 4.7).
Pruritus may make it difficult for children to sit still in school and negatively affects attention.
In darker skin types, follicular prominence, or a goose-bump feel to the skin, especially notable on the trunk, can be a presentation of AD.
Lymphadenopathy can be severe especially in cases of long standing and untreated AD.
Adolescent Phase
Predominant areas of involvement continue to be the flexural surfaces; in addition, the dorsal aspect of the hands and feet are also commonly affected.
Lesions may also appear in other extensor locations such as the shins, ankles, feet (Fig. 4.8), and the nape of the neck. Sometimes lesions limited to the lips (atopic cheilitis; Fig. 4.9), eyelids (Fig. 4.10), vulvar or scrotal areas, or hands, which may be the only features of atopic dermatitis that persist into adolescence or adulthood.
In adolescence, the morphology of eczematous lesions may change to follicularly based papules (e.g., follicular eczema; Fig. 4.11) or deep seeded vesicles on the hands (e.g., dyshidrotic eczema; Fig. 4.12).
Nail dystrophy can occur in atopic dermatitis and represents involvement of the proximal nail fold and the underlying nail matrix (root).
Postinflammatory pigmentary changes are also more apparent during the adolescent phase.
Scratching and rubbing can result in lichenification and increase the sensation of itch resulting in the itch-scratch cycle.
Staphylococcus aureus is prevalent on AD skin and can be cultured from lesional skin in >80% of patients and clinically unaffected skin in 30% to 50% of AD patients.
Secondary skin infection is the most common complication seen in AD. S. aureus and Streptococcus pyogenes are the most frequent culprits.
The secretion of toxins (superantigens) by S. aureus may trigger flares.
Secondary infection with herpes simplex virus may result in eczema herpeticum (Kaposi varicelliform eruption) (Fig. 4.13), which more commonly occurs in childhood.
Patients with atopic dermatitis often exhibit one or more associated conditions that are listed in Table 4.2. These disorders are often found in patients with an atopic history. However, on occasion, they manifest in patients without an atopic predisposition.