Atopic Dermatitis

Key Points

  • Atopic dermatitis is an often chronic, intermittent disease.
  • It is commonly found in association with allergic rhinitis, asthma, or other manifestations of atopy.
  • There are two likely-related pathophysiologic mechanisms underlying the disease: skin inflammation and impaired skin barrier. Both must be targeted by effective therapy.
  • Treatment involves an initial therapy to reduce inflammation as well as a long-term maintenance regimen. Dry skin care is critical to the initial treatment and to this maintenance plan.


The prevalence of atopic dermatitis in developed countries is estimated 15-20% for children and 2-10% for adults.

Clinical overview

In newborns or infants, the first eczematous lesions usually present on the cheeks and scalp and on the extensor surface of the knees and elbows. Scratching, which frequently starts a few weeks later, causes crusted erosions. During childhood, lesions involve flexures (knee and elbow), the nape, and the dorsal aspect of the limbs. In adolescence and adulthood, lichenified plaques affect the flexures, head, neck and hands.

Initial Evaluation

Erythematous, scaly, excoriated symmetric plaques on the face, with sparing of the nasal tip. Face and neck involvement is common.

Other body areas can be affected with more erythema or more dull, less erythematous eczematous plaques.

Excoriated, fissured, lichenified erythematous plaques of atopic dermatitis in a bilateral, symmetric distribution affecting the popliteal fossa, a commonly-affected site.

Lichenification resulting in loss of the lateral aspect of the eyebrows, also known as Hertoghe’s sign.

Hypopigmented patches with subtle scale in atopic dermatitis, also known as pityriasis alba.

Fissuring is common in the retroauricular fold.

Bacterial superinfection (seen as crusting) within fissures is a common complication.

Keratosis pilaris or follicular hyperkeratosis in atopic dermatitis.

Hyperlinearity of the palms.

Principles of Management of Atopic Dermatitis

Effective management must address 4 major issues:

  1. Skin barrier: Repairing the barrier through hydration and emollients
  2. Inflammation:
    • Use of an anti-inflammatory agent, either topical or systemic
    • In most cases, this is usually a topical corticosteroid
  3. Address secondary infection, commonly by Staphylococcus aureus (impetiginization) and sometimes by herpes simplex virus (eczema herpeticum)
  4. Pruritus:
    • can exacerbate atopic dermatitis
    • carries significant morbidity (i.e., lack of sleep, excoriations that further impair the skin barrier and predispose to secondary infection)

Therapy should be based on the extent (severity) of skin involvement (i.e., generalized vs. localized disease).

  • Localized disease: usually managed by topical corticosteroids and liberal use of emollients, reduction of bacterial colonization, and reduction of pruritus.
  • Generalized disease: may require use of topical corticosteroids and emollients, or alternatively systemic immunosuppression; reduction of bacterial colonization and pruritus management are essential.


Initial therapy

  1. Hydration:
  2. Suppression of inflammation:
    • A topical corticosteroid should be applied to the rash b.i.d. The formulation (ointment, cream, lotion) should offer the most emollient. The potency of the corticosteroid should be matched to the severity of disease and to the site:

Low potency steroids: Hydrocortisone 1% or 2.5% lotion, cream, ointment.

Low-medium potency steroid: 

  • Hydrocortisone butyrate 0.1% (such as Locoid) ointment, cream, crelo
  • Desonide 0.05% (such as Desonate, Desowen, LoKara, Verdeso) lotion, cream, ointment, or foam
  • Mometasone furoate 0.1% (such as Elocon) lotion, cream, ointment

Medium potency steroid: Triamcinolone acetonide 0.1% lotion, cream, ointment.

Potent steroid: Fluocinonide 0.05% or 0.1% (such as Lidex or Vanos) lotion, cream, ointment.

Superpotent steroid: Clobetasol propionate 0.05% (such as Clobex, Embeline, Olux, Temovate) foam, gel, lotion, cream, ointment.

Site Best vehicle Mild disease Moderate severity Severe disease Frequency
Face, axillae, groin cream Hydrocortisone 1% or 2.5% Desonide 0.05% Mometasone 0.1% (ointment used q. day up to 5-7 days) Daily to b.i.d.
Scalp lotion or foam Desonide 0.05% or Triamcinolone 0.1% Fluocinonide 0.05% Clobetasol 0.05% Daily to b.i.d.
Trunk, extremities cream or ointment Desonide 0.05% or Triamcinolone 0.1% Triamcinolone 0.1% Mometasone 0.1% Fluocinonide 0.05% Mometasone 0.1% Fluocinonide 0.05% Clobetasol 0.05% b.i.d.
Palms, soles ointment Desonide 0.05% or Triamcinolone 0.1% Triamcinolone 0.1% Mometasone 0.1% Fluocinonide 0.05% Mometasone 0.1% Fluocinonide 0.05% Clobetasol 0.05% b.i.d.

Daily “soak & smear” bathing: Instruct the patient to soak for 20 minutes daily in tepid to lukewarm water. Three minutes after the bath with or without drying the skin with a soft towel, apply steroid ointment to the affected areas with occlusion under plastic kitchen wrap (for localized areas).

Other alternatives to occlusion in generalized disease are: Sauna suit or wet wraps (2 layers of pajamas: the inner layer is moistened with water, and the outer layer is dry).

Other considerations: The simplest treatment regimen is highly recommended, as the prescription of multiple medications can result in confusion about the strength, frequency, or site of application. Explicit instructions on the prescription label itself (including site of application) or use of a treatment plan handout may be helpful to avoid under- or over-treatment of skin disease. See patient handout  Treatment Plan for Atopic Dermatitis.

  1. Suppression of pruritus:
    • All effective anti-pruritic agents can result in drowsiness as a side effect.
    • Start by prescribing an evening dose, taken approximately 1 hour prior to bedtime. Give oral antihistamines (hydroxyzine, such as Atarax or Vistaril, initially 10 mg at bedtime to four times daily, increasing to 50 mg up to four times daily until pruritus is suppressed, or until specific side effects limit dosage).
    • Diphenhydramine (such as Benadryl) 50-100 mg may be substituted for hydroxyzine as it has less of a sedating effect.
    • Less sedating antihistamines like loratadine (such as Claritin) and cetirizine hydrochloride (such as Zyrtec) suspension can be also used.
    • In December 2016, the US FDA approved crisaborole 2% ointment, the first of a new class of topical phosphodiesterase 4 (PDE4) inhibitors.

Ancillary therapy

  1. Treatment of secondary infection: Superinfection with S. aureus is common.
    • Symptoms of bacterial superinfection are:
      • increased erythema
      • honey-crusting
      • serous weeping
    • It is imperative to perform bacterial swab cultures to determine the causative agent and to determine its antibiotic sensitivities.
    • Patients with obvious bacterial superinfection can be treated empirically with erythromycin (such as Erythrocin), cephalexin (such as Keflex) 500-750 mg t.i.d. to 4 times daily, or a semisynthetic penicillin (e.g., dicloxacillin 1 g/day for 7-10 days).
    • Periodic bleach baths (prepared with 1/4 cup of household bleach in a full bathtub of lukewarm water) several times a week (soaking 20 minutes each) may also be an important step towards reducing/preventing bacterial colonization (See patient handout Skin Care in Atopic Dermatitis).
    • Secondary infection with herpes simplex virus is also possible, and appropriate viral cultures and/or empiric treatment with anti-viral therapy should be initiated if this is suspected.

Erythematous scaly, excoriated plaques with fissures and honey-colored crusting, especially evident on the glabella, on the upper cutaneous lip, chin, and in the peri-ocular area. This is highly suggestive of impetiginized (superinfected) facial eczema.

  1. Gentle skin care is paramount (see patient handout Skin Care in Atopic Dermatitis).

Subsequent therapy (after rash abates, usually in 7-10 days)

  1. Continue dry skin care: Use emollients daily between flares.
  2. Suppression of inflammation:
    • Screen frequently for potential adverse effects of long-term topical corticosteroid use (skin atrophy, erythema, striae, or telangiectasias).
    • Adjust the treatment regimen or patient education on the potencies of their prescribed medications and how to increase or reduce the potency based on the skin inflammation they are observing.
  3. Suppression of pruritus:
    • Continue antihistamines as needed.

Alternative treatment

Treatment in moderate-to-severe cases: Refer to dermatologist to introduce phototherapy (narrowband-UVB, UVA, PUVA) or systemic immunosuppression (prednisone, cyclosporine, mycophenolate mofetil, azathioprine, or interferon-gamma).

Adjunctive care

  • Education programs for the parental management of atopic dermatitis in children, and self-management in adolescents, improve disease control and should be integrated into daily routine.
  • Patient education on the role of skin care should be provided using the simplest explanations possible. This will allow integration of proper skin care practices into daily routine.
  • Identification and avoidance of trigger factors is part of the education to prevent flares from occurring.
  • It is widely accepted that stress can induce and exacerbate atopic dermatitis. Stress-reduction is a possible adjunctive treatment for patients.

Situations requiring dermatologic consultation

The following clinical signs should prompt dermatologic consultation:

  • Frequent or uncontrolled flares.
  • For management of systemic immunosuppression or phototherapy.
  • Suspicion of an immunodeficiency syndrome or metabolic disease
  • frequent superinfection.
  • In children, if there is a parental concern regarding food allergy, and significant food restrictions have been implemented, consultation with a dermatologist and/or allergist should be obtained.

Clinical Cases

Case 1

Mild disease

  • 9-year-old girl with chronic dry skin, who developed hypopigmented, fine scaling patches on the face and trunk
  • She reports new pruritus of the skin
  • No prior treatment


  • Counseling on daily skin care (cleansing: soap-free cleanser over the body, mild soap only in the axilla, groin, hands, feet; moisturizing: emollients used immediately after bathing)
  • Face: hydrocortisone 2.5% ointment b.i.d.
  • Body: desonide 0.05% ointment b.i.d.
  • hydroxyzine at bedtime, as needed for pruritus (max. 100 mg/day)
  • follow-up in 4 weeks

Follow-up evaluation

  • She returns to the clinic with much improved comfort of the skin. There is less scale and her skin appears well-moisturized but the hypopigmentation persists.
  • Recommend hydrocortisone 1% ointment b.i.d. (face) and hydrocortisone 2.5% ointment b.i.d. (body)
  • Continue dry skin care, emphasizing that a maintenance regimen is critical to prevent future flares
  • Reassurance that the skin pigmentation will be restored with time and ongoing maintenance therapy

Case 2

Moderate disease

  • 42-year-old man with eczema since childhood, now generalized despite topical corticosteroid use
  • He presents with extensive skin disease, much of which is lichenified plaques with thick scale
  • He reports severe pruritus and difficulty sleeping
  • A bacterial culture sent several weeks ago did not reveal bacterial superinfection


  • Continue topical corticosteroid use now with escalated potency of his medications:
    • Face: mometasone ointment q. day
    • Body: clobetasol ointment b.i.d.
    • Soak & smear with plastic wrap or sauna suit occlusion at night
    • hydroxyzine at bedtime
  • Follow-up in 2 weeks

Follow-up evaluation

  • The patient is improved, now less erythematous but still with lichenified pruritic plaques
  • Recommend continuing topical regimen with addition of NB-UVB three times a week
  • Follow-up in 1 month to determine whether phototherapy must be continued and to decide about systemic immunosuppression (such as prednisone or cyclosporine) if the disease is worsening

Case 3

Severe disease with superinfection

  • 4-year-old child with long standing atopic dermatitis of the face, trunk, arms, and legs, now presenting with acute onset of increased erythema, honey-colored crusting of eczematous plaques, and excoriations of his skin
  • He was previously well managed with hydrocortisone 1% cream and emollient, used once daily
  • One day of low-grade fevers, and he is not sleeping well due to severe pruritus and itching


  • Bacterial culture sent to microbiology lab
  • Empiric treatment:
    • Face: desonide ointment 0.05% b.i.d.
    • Body: triamcinolone ointment 0.1% b.i.d. with wet-wrap occlusion
    • bleach baths (1/4 cup bleach in full bathtub of water, with rinsing afterwards), nightly
    • cephalexin t.i.d. for 2 weeks
    • hydroxyzine at bedtime (max. 50 mg/day) or cetirizine hydrochloride syrup (max. 5 mg/day)
  • Follow up in 2 weeks

Follow-up evaluation

  • The bacterial culture reveals methicillin-sensitive Staphylococcus aureus
  • The patient’’s skin is much improved
  • Recommendations:
    • Face: hydrocortisone 1% ointment b.i.d.
    • Body: hydrocortisone 2.5% ointment b.i.d.
    • bleach baths three times a week
    • hydroxyzine at bedtime, as needed


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Bieber T. (2008). Atopic dermatitis. N Engl J Med, 3;358(14):1483-94.

Darsow U, Wollenberg A, Simon D, et al. (2009) ETFAD/EADV eczema task force 2009 position paper on diagnosis and treatment of atopic dermatitis. J Eur Acad Dermatol Venereol, Epub ahead of print.

Paller AS, Tom WL, Lebwohl MG, et al. (2016). Efficacy and safety of crisaborole ointment, a novel, nonsteroidal phosphodiesterase 4 (PDE4) inhibitor for the topical treatment of atopic dermatitis (AD) in children and adults. J Am Acad Dermatol, 75(3):494-503.e4.

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