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Basics

Pathogenesis

Clinical Manifestations

Diagnosis

Diagnosis-icon.jpg Differential Diagnosis

  • The diagnosis of atopic dermatitis is generally not difficult, especially in patients with an atopic history.

Contact Dermatitis (see later in this chapter)
  • Determine whether the patient was exposed to an allergen or irritant.

  • The location of the lesions is limited to the area of contact with allergen; the morphology of the lesion may suggest an external cause.

Psoriasis (see Chapter 14: Psoriasis)
  • Lesions generally appear on extensor locations—the elbows, knees, and other large joints—rather than on flexor creases.

  • Patients may have a positive family history of psoriasis.

  • Usually, psoriasis is less pruritic than eczema.

  • Psoriatic lesions tend to be clearly demarcated from normal surrounding skin, and the scale of psoriasis is adherent and silvery. However, psoriasis may at times be clinically indistinguishable from atopic dermatitis.

Scabies (see Chapter 20: Hirsutism)
  • A history of exposure is important in diagnosing scabies.

  • Symptoms are present in other household members.

  • Characteristic distribution (e.g., in the webs between the fingers and on the flexor wrists) can mimic that of eczema.

  • A positive scabies scraping is diagnostic of scabies.

Seborrheic Dermatitis
  • In infants, it may be difficult to distinguish atopic dermatitis from seborrheic dermatitis and at times both conditions overlap.

  • Seborrheic dermatitis presents earlier in infancy (1 to 3 weeks of life) and characteristically affects the skin folds, as opposed to infantile atopic dermatitis that affects the extensor surfaces.

  • The scale is greasier and has a yellow-brown color to it.

Management-icon.jpg Management

General Principles
  • Treat flares promptly with the appropriate strength topical corticosteroid until complete clearance, that is, the skin is no longer rough, red, or itchy.

  • A daily maintenance routine is required both during periods of active flares and when disease is quiescent.

  • Identification and avoidance of known and possible triggers such as extremes of temperature, outdoor and indoor allergens (i.e., dust mites, grass pollens, animal dander, molds), and irritants (i.e., sweat, harsh soaps and detergents, bubble baths, fragrances, rough synthetic fabrics, etc.).

  • Communication and education about AD is paramount. The use of a Written Action Plan (see Companion eBook) and close follow-up can help ensure adherence.

Treatment

Topical Therapy (see Chapter 13: Eczema and Related Disorders and “Introduction: Topical Therapy”)

  • Topically applied corticosteroids to areas of active dermatitis is the mainstay of AD therapy.

  • Maintenance therapy with daily gentle skin care and use of moisturizers must be a part of the treatment for all patients with AD.

Face and Body Folds
  • For the face and intertriginous regions (axillae and inguinal creases—areas that are “naturally” occluded), treatment should be initiated with a low-potency (class 6 or 7) ointment, such as hydrocortisone 2.5% ointment or desonide 0.05% ointment.

  • Protopic ointment, 0.03% or 0.1% (tacrolimus) and Elidel 1% cream (pimecrolimus) are nonsteroidal immunomodulators that have been shown to reduce the symptoms of AD and are used as an alternative to topical steroids or as part of maintenance therapy, particularly when the eruption involves the face or intertriginous areas, such as the axillae and groin, where the long-term use of high-potency steroids is limited.

  • Protopic is considered to be equivalent to a class 5 topical steroid. Protopic 0.1% is approved for the treatment of atopic dermatitis in patients >16 years and older and the 0.03% concentration is approved for patients older than 2 years.

  • Elidel 1% cream is considered to be equipotent to a class 6 topical steroid.

    For information regarding the long-term safety of these agents, see “Introduction: Topical Therapy.”

Body (Trunk, Arms, Legs, Scalp)
  • For nonintertriginous areas, treatment can be initiated with a mid-strength (class 3 or 4) cream or ointment such as mometasone 0.1% ointment (Elocon) or fluticasone 0.05% cream or 0.005% ointment (Cutivate).

  • For thicker lesions, initial therapy may be with a more potent topical steroid (class 2 or 3), such as fluocinonide 0.05% cream (Lidex) ointment.

  • Long-standing, lichenified eczematous lesions on the body or lesions on the hands and feet may require a superpotent agent such as clobetasol 0.05% ointment.

  • Topical agents should be used until the dermatitis has cleared completely, that is, the skin is no longer rough, red, or itchy. It can be helpful to find an area on the child's skin that is free of dermatitis to show the patient and parent what clear means. Skin that is clear of dermatitis can still be hypo- or hyperpigmented.

Adjunctive Therapies to Consider During AD Flares
  • Wet wraps and the “soak and smear” technique are useful adjuncts for the treatment of acute severe disease, especially when lichenified and/or localized to the upper and lower extremities.

  • Wet wrap treatment involves the application of a topical corticosteroid to the areas of active dermatitis over which a double layer, first moist then dry, of close-fitting cotton bandages are applied. Any type of close fitting cotton garment can be used (i.e., elastic tubular cotton bandage [Tubifast], old cotton bed sheets or t-shirts cut into wrappable strips). The cotton wraps can be left in place 3 to 24 hours with longer applications being more effective. Wet wrap treatment is effective when used for an average of 7 days.

  • Soak and smear involves soaking in a bath or shower for 10 to 20 minutes followed by immediate application of the topical medication while the skin is still damp. This technique allows for moisture trapping and better penetration of the medication into the skin.

  • For the child with frequent flares, especially those with a history of staphylococcal infection, “Bleach baths” with sodium hypochlorite (Clorox) (1/4 cup of household bleach in a half full bath tub or ½ cup in a full bath tub) twice weekly can be beneficial as part of the maintenance plan for atopic dermatitis.

  • Oral first generation H1 antihistamines such as diphenhydramine (Benadryl) and hydroxyzine (Atarax) probably do not reduce itching, but they are sometimes useful as inducers of sleep, a positive side effect for many patients.

  • If outdoor or indoor allergens are identified as a potential exacerbating factor, daily nonsedating antihistamines such as loratidine (Claritin) or cetirizine (Zyrtec) can be beneficial.

Daily Maintenance Therapy
Gentle Bathing Tips
  • Despite popular belief, patients with AD, especially children, should bathe daily.

  • The benefits include removal of excess dirt, potential irritants and allergens and surface microbes; hydrating the skin and allowing for better delivery of corticosteroids and moisturizers.

  • Baths should be short (no longer than 10 minutes) and with tepid water.

  • Use mild, moisturizing soaps such as Dove (sensitive skin beauty bar) or nonsoap cleansers such as Cetaphil Gentle cleanser.

  • After bathing, pat (do not rub) the skin dry; and then immediately (within 3 minutes) apply topical corticosteroid to areas of active dermatitis first, then apply moisturizer to all skin including over topical steroid.

  • Moisturizers should be fragrance-free creams or ointments and contain ceramides.

  • Suggested ointments: Vaseline Petroleum Jelly, Aquaphor

  • Suggested creams: CeraVe cream, Eucerin Daily Repair Creme, Cetaphil Cream

  • Atopiclair, MimyX, and Epiceram and Eletone are newer, multiple-ingredient nonsteroidal barrier repair creams that are available via prescription.

Other Therapeutic Measures
  • For patients with secondary staphylococcal infection, oral antistaphylococcal therapy with cephalexin (or other agent) is required. Bacterial cultures should always be performed before starting an oral antibiotic.

  • If infection with methicillin-resistant S. aureus (MRSA) is detected or suspected, therapy with clindamycin, doxycycline (if patient is older than 8 years), or trimethoprim-sulfamethoxazole is required.

  • For patients with secondary herpes simplex infection (Kaposi varicelliform eruption), oral antiviral therapy and, possibly, hospitalization may be required. A viral culture taken from the base of a fresh vesicle should be sent before initiating antiviral therapy.

  • When the child continues to have severe disease such that the condition is causing significant disruption in the child's and/or family's life, more aggressive systemic therapy is warranted.

  • Before resorting to systemic therapy, “soak and smear” and/or wet wraps with potent topical corticosteroids should be attempted. (See above and “Introduction: Topical Therapy.”)

  • Systemic steroids should not be used for the treatment of flares of AD because of the unfavorable risk to benefit profile and the severe rebound flares of disease that often occurs upon tapering.

  • Phototherapy with narrowband ultraviolet B rays and, less commonly, ultraviolet A rays, is often very effective for widespread skin involvement.

  • Systemic immunosuppressive agents such as cyclosporine, mycophenolate mofetil, or azathioprine is sometimes necessary in patients with severe generalized atopic dermatitis that is refractory to topical and adjunctive therapies.

SEE PATIENT HANDOUTS, “Atopic Dermatitis,” “Written Action Plan,” “Soak and Smear Instruction Sheet,” and “Bleach Baths” IN THE COMPANION eBOOK EDITION.

Helpful-Hint-icon.jpg Helpful Hints

  • Patients and their parents, caregivers, and teachers should be educated about the manifestations and management of atopic dermatitis at each visit.

  • When topical steroids are applied immediately after bathing, their penetration and potency are increased.

  • The “gooiest” and cheapest moisturizer is petrolatum.

  • The National Eczema Association can be contacted at:

Point-Remember-icon.jpg Points to Remember

  • Topical steroids should be applied only to areas of active disease (inflamed, rough, red skin) and not for postinflammatory hyper- or hypopigmentation.

  • The application of an appropriately chosen topical steroid (more potent for thicker lesions and less potent for thinner lesions) can clear even the most severe dermatitis.

  • “Stronger” is often preferable to “longer” in the use of topical steroids, because long-term application is more often associated with cutaneous side effects (i.e., striae, telangiectasias, atrophy, acne).

  • Low-potency topical steroids or topical calcineurin inhibitors are recommended for use on the face and in skin folds, such as the perineal area and underarms.

SEE PATIENT HANDOUT “Atopic Dermatitis” IN THE COMPANION eBOOK EDITION.

Common Myths About Atopic Dermatitis

Myth: Soy formulas improve eczema in infants.

Fact: Food allergies contribute to flares of atopic dermatitis in less than 10% of patients. Thus, changing a formula from cow's milk protein to soy protein usually does not affect eczema. Urticaria (hives) is the usual skin manifestation of a food allergy.

Myth: Infants and children who have atopic dermatitis should be bathed infrequently.

Fact: The advantages of bathing (removal of scale, surface bacteria, etc.) far outweigh its disadvantages (see following) and potential drying effect of water on the skin.

Myth: Laundry detergents are a common cause of eczema.

Fact: This is very rarely the case. Most detergents are rinsed out, with very little soap remaining to trigger a flare of atopic dermatitis.

Myth: Potent topical steroids should not be used on infants or young children.

Fact: Topical steroids, when used properly, are quite safe. Choosing a topical steroid of adequate potency (even if potent or superpotent) to clear eczema completely will result in less overall use than the use of a mild topical steroid for a longer period of time. Not using topical steroids of adequate potency can lead to undertreatment, which can interfere with the child's and family's daily activities.

Other Information

Description of Lesions !!navigator!!

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,

  • diaper area, nasolabial folds, and axillae.

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.

  • Lichenification is often seen.

  • 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.

Clinical Sequelae and Possible Complications !!navigator!!

Associated Conditions !!navigator!!

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.


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