Pediatric Atopic Dermatitis Treatment & Management

Updated: Feb 13, 2023
  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD  more...
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Medical Care


The most fundamental and important step in combating atopic dermatitis (AD) is rehydration of the stratum corneum. Adequate rehydration preserves the stratum corneum barrier, minimizing the direct effects of irritants and allergens on the skin and maximizing the effect of topically applied therapies, thus decreasing the need for topical steroids.

Lukewarm soaking baths lasting 10-20 minutes are ideal. [15] Extremely hot water should be avoided to prevent both vasodilation, which can trigger pruritus, and the damage to the skin barrier caused by scalding.

Small amounts of bath oils or emulsification agents may be used for added hydration benefits in older children and adolescents. Bath oils or emulsification agents result in slippery conditions; warn patients and parents of the resultant risks of trauma and drowning after a fall. Readily available over-the-counter bath agents include Aveeno Colloid Oatmeal, RoBathol, Maypo, cottonseed oil with Brij 93, or mineral oil.

Recommended soaps are mild and unscented with a neutral pH. Examples include Dove, Oil of Olay, Caress, Camay, Aveeno, and Purpose. Even these mild soaps are often too drying for atopic skin. If the children are prepubertal, bathing in water alone may be preferable. Postpubertal patients need to use soap in the axillae and groin but do not need it elsewhere.

If soaps are too irritating to the skin, hydrophobic lotions and creams, such as Cetaphil, Diprobase, and Unguentum Merck, may be used. These agents have excellent cleansing properties and low potential for irritation. They should be applied without water and rubbed gently over the skin surface until a light foaming occurs. A soft cotton cloth or tissue can then be applied to wipe away the agent, leaving behind a protective film of stearyl alcohol and propylene glycol.

Baby shampoo may be used to manage scalp dermatitis.


Baths should be followed by the immediate application of an occlusive emollient over the entire skin surface to retain moisture in the epidermis. If an emollient is not applied within 3 minutes of leaving the bath, evaporation causes excess drying of the skin. Skin should not be completely dried with a towel prior to application of the emollient; rather, lightly patting the skin with a towel to remove excess moisture is sufficient. However, preliminary evidence reported in 2020 suggests that emollients may not be beneficial for primary prevention of atopic dermatitis in infants. [27]

Frequently recommended emollients are hydrophobic and ointment-based; these include Vaseline petrolatum jelly, Crisco, vegetable oil, Aquaphor, and Elta. Occasionally, parents may find these agents too greasy for everyday use, and cream-based alternatives may be offered. Common creams include DML Forte, Moisturel, Aveeno, Curel, Purpose, Dermasil, Neutrogena, and Eucerin. This latter group of moisturizers is less effective because of the weaker occlusive effects of creams as compared to ointments; thus, they should be used only if the ointment-based emollients are not well tolerated.

The newest type of moisturizing product is a ceramide-dominant, lipid-based emollient (TriCeram) aimed at repairing the stratum corneum barrier function lost in atopic dermatitis. One study showed a significant decrease in clinical severity scores and a decrease in transepidermal water loss in children whose traditional moisturizers were replaced by TriCeram for 3 weeks. [28] Other ceramide-containing preparations are also on the market. [29]

Urea-containing products have been shown to soften and moisturize dry skin. Commonly available preparations include Aquacare cream or lotion and Ureacin Crème. Alpha-hydroxy and lactic acid preparations also are helpful as moisturizers. Name brands include Aqua Lacten Lotion, AmLactin Lotion, LactiCare Lotion, Lac-Hydrin Lotion, and Nutraderm 30. In addition, 12% ammonium lactate lotion has been shown to improve skin barrier function and even to mitigate dermal or epidermal atrophy induced by corticosteroids. [28] Because of the stinging sensation experienced by children with acute or fissured dermatoses, the 10% urea concentration is preferred over the higher concentrations, and care should also be used in the application of the alpha-hydroxy and lactic acid preparations. LactiCare-HC Lotion also contains hydrocortisone to further benefit acute flares of atopic dermatitis.

For children with repeated cutaneous infections, adding 2 teaspoons of household bleach (eg, Clorox) per gallon of bath water can help reduce the incidence of such infections. A typical bathtub holds approximately 25-40 gallons of water. During acute atopic dermatitis exacerbations, pouring 1 cup of table salt into the bath may ameliorate the stinging effect these children frequently experience while bathing.

Wet dressings are very useful for diverse types of atopic dermatitic flares and severe recalcitrant atopic dermatitis. [30] They can be used on dry lichenified lesions to improve hydration and increase the penetration of topical corticosteroids; they also work well to dry weeping or oozing lesions via evaporation. The cooling sensation on the skin that results from slow evaporation with wet dressings has an anti-inflammatory effect and suppresses itching. The mechanical barrier of the wet dressing also prevents scratching, allows more rapid healing of lesions, and offers protection from contact with allergens and bacteria. Care should be taken to use only adequately diluted corticosteroid preparations (if used) under occlusive dressings to prevent hypothalamic-pituitary-adrenal axis suppression and local adverse effects on the skin. Wet wrap implementation should be delayed at least 2-3 days after beginning antibiotic treatment for superinfected lesions to allow for observation of clinical improvement of infected sores. [3]

Burow solution 1:40 is a commonly used wet dressing because it is germicidal and directly suppresses weeping lesions by precipitation of protein. The solution is prepared easily by dissolving one Domeboro packet or effervescent tablet in a pint of tepid or lukewarm tap water. Using lukewarm water is essential because hot water induces vasodilatation with increased weeping and pruritus, whereas cold water causes vasoconstriction and secondary vasodilation. Submerge a soft cloth (eg, handkerchief, thin diaper, strips of bed sheets) into the solution until moderately wet but not dripping. Place the dressing over the affected skin site, periodically rewetting the compress. In severe cases, a topical corticosteroid may be applied after the compress for enhanced penetration and action of the medication.

Seek psychologic counseling, biofeedback, relaxation techniques, massage therapy, and behavioral modifications if emotional stressors are a contributing factor to atopic dermatitis.

Topical phosphodiesterase-4 (PDE-4) inhibitors

Crisaborole topical ointment 2% (Eucrisa) was approved by the US Food and Drug Administration (FDA) in December 2016 for mild-to-moderate atopic dermatitis in adults and children aged 2 years or older. The approval was based on two placebo-controlled trials (n=1522). Patients who received crisaborole achieved greater response with clear or almost clear skin after 28 days compared with vehicle-treated patients (P< .001). [31]

In March 2020, the FDA expanded the indication to include infants and children aged 3 months or older. Use in pediatric patients aged 3 months to less than 2 years was supported by data from a 28-day open-label, safety, and pharmacokinetics trial (n=137). [32]

Targeted biologic therapeutics in atopic dermatitis

Anti-IL-4Ra therapy (dupilumab)

Dupilumab is a monoclonal antibody that inhibits interleukin (IL)–4 and IL-13 signaling by blocking the shared IL-4Ra and originally demonstrated efficacy in phase 2 clinical trials. [33, 34] It was initially approved by the FDA for adults in 2017 who have moderate-to-severe atopic dermatitis not adequately controlled with topical prescription therapies or when those therapies are not advisable. In 2019, this indication was expanded to include adolescents aged 12 years or older, and in 2020 to include children as young as 6 years. It is a subcutaneous injection administered every 2 weeks.

Approval of dupilumab was based on clinical trials investigating dupilumab as monotherapy (SOLO 1 and SOLO 2) and in concomitant administration with topical corticosteroids (CHRONOS). Results from the SOLO 1 (n=671) and SOLO 2 (n=708) trials showed 36-38% of patients who received dupilumab had scores of 0 or 1 (clear or almost clear) on the Investigator's Global Assessment scale compared with placebo (8-10%) (P< .001). Additionally, improvement from baseline to week 16 of at least 75% on the Eczema Area and Severity Index (EASI) was reported in significantly more patients who received each regimen of dupilumab than in patients who received placebo (P< .001). [35] Approval in adolescents was based on a phase 3 trial showing statistically significant improvement of the EASI-75 in the dupilumab-treated group compared with placebo. [36]

Results from the phase 3 trial (LIBERTY AD PEDS; n = 367) in children aged 6-11 years showed 75% of those taking dupilumab plus topical corticosteroids achieved EASI-75 at 16 weeks compared with 26-28% of children using topical corticosteroids alone (P< .001). [37]

Janus kinase (JAK) inhibitors

Multiple proinflammatory cytokines, including type 2 cytokines, are dependent on the JAK-STAT signaling pathway to mediate their effects. [38]   Thus, in addition to cytokine receptor blockade, phase 2 clinical trials have been performed for both oral and topical JAK inhibitors and several have gain approval by the FDA for AD. In support of the direct antipruritic effect of JAK inhibitors, a 2017 study identified that neuronal JAK1 signaling critically regulates AD-associated itch in mice, independently of any effect on the immune system. [39]  Thus, these studies may explain why JAK inhibitors are demonstrating such unique anti-itch properties in clinical trials. 

Ruxolitinib topical

The first topical JAK inhibitor, ruxolitinib topical cream 1.5% (Opzelura), gained FDA approval for short-term and noncontinuous long-term treatment of mild-to-moderate atopic dermatitis in non-immunocompromised adults and adolescents whose disease is not adequately controlled with other topical prescription therapies or when those therapies are not advisable. Significantly more patients achieved success at Week 8 as measured by the Investigator's Global Assessment using ruxolitinib cream (0.75% or 1.5%) compared with vehicle cream (P < 0.0001). [40]  


The oral JAK1-selective inhibitor, upadacitinib (Rinvoq) was FDA-approved for treatment of refractory, moderate to severe AD in patients aged ≥12 years whose disease is not adequately controlled with other systemic drug products, including biologics, or who are unable to use such therapies.

Approval was based on 3 double-blind, phase 3 trials (Measure Up 1; Measure Up 2; AD Up), where 2584 patients aged ≥12 years with moderate to severe AD who were candidates for systemic therapy were randomized to receive upadacitinib 15mg and 30mg PO qDay. In Measure Up 1 and 2, upadacitinib was evaluated as monotherapy; in AD Up, upadacitinib was evaluated in combination with topical corticosteroids.

The coprimary endpoints for all the trials were the proportion of patients achieving at least a 75% improvement in the Eczema Area Severity Index (EASI 75) and a validated Investigator’s Global Assessment for Atopic Dermatitis (vIGA-AD) of clear or almost clear (0/1) at week 16. 

Results from the Measure Up 1 and Measure Up 2 trials showed a higher number of  patients treated with upadacitinib 15mg and 30mg achieved EASI 75 and vIGA-AD 0/1 at week 16 compared to placebo. Patients treated with upadacitinib met secondary endpoints including EASI 90, EASI 100, and at least a 4-point improvement in the Worst Pruritus Numerical Rating Scale (NRS) at week 16. Upadacitinib-treated group reported a reduction in itch as early as Day 2. [41]

In the AD Up trial, 65% and 77% of patients treated with upadacitinib 15mg and 30mg plus topical corticosteroids achieved EASI 75 at week 16 compared to placebo with topical corticosteroids (26%). A greater proportion of the upadacitinib/corticosteroids arm achieved vIGA-AD 0/1 at week 16 (40% and 59% [15mg and 30mg plus topical corticosteroids]) compared to 11% of patients who received placebo plus topical corticosteroids. [42]  


Another once-daily oral JAK1 inhibitor, abrocitinib (Cibinqo), is also indicated for treatment for patients aged 12 years and older with moderate to severe atopic dermatitis.  

Approval for adults was based on 5 clinical trials in a program of more than 1600 patients. The 5 clinical trials composed of 3 randomized, placebo-controlled, phase 3 trials for safety and efficacy of abrocitinib, a dose-ranging trial, and an ongoing, long-term, open-label extension trial. The FDA approved abrocitinib for adolescents in February 2023 based on clinical trials resulting in similar efficacy to that of adults.  [80, 81]  

Ultraviolet light

Ultraviolet light may benefit some patients.

Ultraviolet light in the UVB range may provide control and eliminate or markedly reduce the need for steroids. The new narrow band units are especially effective. Ultraviolet light in the UVA range has been used alone, in combination with oral psoralen administration (PUVA), or with high-dose UVA 1 (ie, 340-400 nm spectrum units).

A significant decline in the usage of UVA light therapy and psoralen has been observed because this regimen clearly accelerates photoaging and increases the risk of skin cancer. UVA 1 spectrum light works by reducing cellular immunoglobulin E (IgE) binding sites and inducing apoptosis in inflammatory cells and has demonstrated significant efficacy in treating atopic dermatitis. A small number of patients develop erythema or disease flares with light treatment.

Allergen immunotherapy

Allergen immunotherapy is currently indicated only for patients with allergic rhinitis or allergic asthma. However, several small randomized controlled trials have shown a significant clinical benefit of subcutaneous immunotherapy or sublingual immunotherapy with house dust mite extract in patients sensitized to the house dust mite. Larger randomized, double-blind, placebo-controlled trials are needed to confirm these findings. [43]

Sublingual immunotherapy with drops of the house dust mite species, Dermatophagoides farinae, for pediatric atopic dermatitis has been evaluated as safe and effective. [44]



Consider consultation with an allergist/immunologist or dermatologist for the following conditions:

  • Atopic dermatitis that is severe (eg, 20% skin involvement, 10% skin involvement with eyelids/hands/intertriginous areas affected) or is refractory to first-line treatments

  • Erythroderma or extensive exfoliation

  • Infectious complications

  • Ocular complications

  • Psychosocial complications

  • Coexisting asthma or allergic rhinitis

  • Impaired quality of life

  • Identification of triggers and allergens

  • Atopic dermatitis requiring hospitalization or more than one course of systemic steroids

  • Uncertain diagnosis



Whether breastfeeding can help prevent development of atopic dermatitis in children remains unclear. A clinical report from the American Academy of Pediatrics recommended exclusive breastfeeding as opposed to cow's milk formula feeding over the first 4 months of life to prevent development of atopic dermatitis in infants at high risk of developing atopy. [45] However, several studies have found no protective benefit of exclusive breastfeeding in the first 3-6 months of life. [46, 47]

Supplementation with extensively hydrolyzed formulas in infants at high risk of developing atopic dermatitis appeared to be more effective at preventing atopic dermatitis than supplementation with partially hydrolyzed formulas or cow's milk formulas. [45] However, partially hydrolyzed cow's milk formula may be beneficial in treating infants with mild-to-moderate atopic dermatitis during the first 6 months of their life without affecting their nutritional status. [48]

For children older than 5 years, nutritionally adequate elimination diets are the goal if double-blind placebo-controlled trials indicate a clinically significant food allergy. However, most skin tests, radioallergosorbent tests (RASTs), and enzyme-linked immunosorbent assays (ELISA) that reveal positive results against food allergens are not borne out to cause disease flares in clinical trials; thus, elimination diets are only rarely indicated.



Prohibit smoking in the home and in other areas that are frequented by children with allergies.

Implement dust mite control measures for children with documented sensitivity to dust mites. Counsel parents to use dust mite–proof plastic cases around pillows, mattresses, and box springs. Wash bedding in hot water weekly to remove dust mites. Remove carpets and drapes from the bedroom or vacuum carpets and drapes weekly to remove dust mites.

In the subgroup of children with atopic dermatitis who also experience respiratory allergies to animal allergens, parents should consider removing animals from the home or confining them to areas of the house where susceptible children do not come into contact with their dander or saliva.

Avoid irritants that trigger the itch-scratch-itch cycle (eg, soaps, detergents, chemicals, abrasive clothing, extremes of temperature and humidity).

Use pH-neutral minimally defatting soaps (eg, Dove). Avoid excessive drying of the skin with alcohol-containing astringents. Launder new clothes before wearing to remove manufacturing chemicals. Use liquid detergent rather than powder detergent and add a second rinse cycle to remove all residual detergent.

Wear loose fitting open-weave cotton or cotton-blend clothing; avoid wool.

Use a humidifier in the winter to prevent excessive skin dryness and an air conditioner in the summer to prevent sweating and associated macerative effects on the skin. Decreased humidity indoors helps prevent the growth of mold.



The most common complication of atopic dermatitis is secondary infection.

Staphylococcus species and group A beta-hemolytic streptococci are the most frequent organisms cultured from skin lesions. Superinfected eczematoid lesions appear as erythema associated with serous or purulent exudates and crusting. Greasy moist scales on the surface of the lesions and small pustules at the advancing edges may be present. Always consider infection in acute flares of chronic atopic dermatitis or in cases that are unresponsive to appropriate therapy.

Topical antibiotic therapy is useful for localized infections; however, systemic treatment is preferred for recurrent or widespread infections. The agent of choice is penicillin G if group A streptococci is the known infectious organism. Use erythromycin or a semisynthetic penicillin (eg, nafcillin, oxacillin, dicloxacillin) if S aureus is a possible cause. Hospitalization and use of intravenous antibiotics are indicated in cases of invasive infection (eg, osteomyelitis). Perform urinalysis and closely observe patients for symptoms for at least 7 weeks after treatment in endemic areas because systemic antibiotic treatment does not prevent postinfectious glomerulonephritis after a cutaneous infection with nephritogenic M strains of streptococci.

Less commonly, patients with atopic dermatitis may develop an explosive vesicular eruption known as Kaposi varicelliform eruption or eczema herpeticum. Vesicles and pustules are typically umbilicated and are initially confined to eczematous skin but may later spread to normal skin. Later in the course of the disease, erosions may be commonplace and confluent, resulting in denuded areas. Tzanck smear of vesicles or a viral culture confirms the diagnosis. Treatment is with acyclovir (if mild, administer 25-30 mg/kg/d, up to 200 mg 5 times per day orally; if severe, administer 5 mg/kg/dose every 8 h or 1.5 g/m2/d intravenously).

Atopic dermatitis nearly doubles an individual's risk of developing lymphoma. This risk increases with usage of potent topical steroids, especially for prolonged time periods. [49]

Sleep disturbances are common in those with atopic dermatitis. [50, 51] They have reduced sleep efficiency, longer sleep onset latency, more sleep fragmentation, and less nonrapid eye movement sleep. Reduced nocturnal melatonin secretion may be linked. Mothers may also experience sleep disturbance and exhaustion as a result of their child’s atopic dermatitis. [52]



Prevention of acute flares and the subsequent development of chronic lesions of atopic dermatitis are indicators of successful treatment for this disease. Maintenance of adequate hydration of the stratum corneum, avoidance of known or probable allergens and irritants, rapid self-treatment with the proper class of topical steroids, and judicious use of complementary therapies (eg, antipruritics, stress relievers, antibiotics) are the cornerstones of ensuring a high quality of life unimpeded by the more severe aspects of this disease.

Nonspecific triggers of inflammation in patients with atopic dermatitis may include physical or chemical irritants. The following simple measures should be followed in daily life to reduce the frequency and severity of irritant-induced atopic dermatitis flares [53] :

  • Skin care products that contain alcohol and astringents should be avoided.

  • New clothes should be laundered before use to remove formaldehyde and other chemicals.

  • Liquid detergents are preferred over powder detergents for laundering clothes, as liquids are easier to rinse out. A second rinse cycle may also improve removal of residual detergent.

  • Patients should shower immediately after swimming in chlorinated pools and should subsequently apply moisturizer.

  • Fragrance-free skin products that are hypoallergenic or made for "sensitive skin" may be less irritating than other kinds of skin products.

Prenatal and postnatal probiotic supplementation may be helpful in preventing the development of atopic dermatitis in young children. In a 2008 meta-analysis, the most commonly studied probiotic was Lactobacillus rhamnosus GG. [54] Larger, randomized controlled studies are needed to confirm these initial findings.

A dog living in the home at the time of birth has been associated with a 50% decrease in the incidence of atopic dermatitis at age 3 years. [6] One study found that, at age 4 years, dog-sensitized children experienced less risk for eczema, whereas cat sensitization significantly increased the risk. [55]

Children with ichthyosis vulgaris should avoid neonatal cat exposure to prevent atopic dermatitis. [56]

Breastfeeding during the first 4 months of life may reduce in incidence and severity of childhood atopic disease but only modestly and only in those at high risk. [57]


Long-Term Monitoring

Frequent follow-up is needed early in the course of atopic dermatitis (AD) to ensure compliance and assess patient responsiveness to therapy. Analyze treatment failures for the presence of resistant organisms, contact dermatitis to a medication (eg, preservatives in steroid preparations, bacitracin), or parental noncompliance.

There is no evidence to date that AD is an independent risk factor for acquiring coronavirus disease 2019 (COVID-19) or having it with enhanced severity, at least in adults. [58]