Pediatric Annals

Special Issue Article 

Atopic Dermatitis: Update for Pediatricians

Katherine Grey, BA; Sheilagh Maguiness, MD


Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder present in up to 20% of children. Recent advances implicate skin barrier dysfunction as central to disease pathogenesis. Genetic defects in the filaggrin gene, the product of which is important for maintaining the epidermal barrier, are a strong predisposing factor in the development of AD. In addition to reducing identifiable triggers, treatment should focus on the four clinical characteristics of eczema: emollients for dry skin, topical anti-inflammatory agents to reduce inflammation and itch, and strategies to reduce infection/colonization, which can include diluted bleach baths. New studies demonstrate that early emollient application from birth may prevent development of AD. [Pediatr Ann. 2016;45(8):e280–e286.]


Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder present in up to 20% of children. Recent advances implicate skin barrier dysfunction as central to disease pathogenesis. Genetic defects in the filaggrin gene, the product of which is important for maintaining the epidermal barrier, are a strong predisposing factor in the development of AD. In addition to reducing identifiable triggers, treatment should focus on the four clinical characteristics of eczema: emollients for dry skin, topical anti-inflammatory agents to reduce inflammation and itch, and strategies to reduce infection/colonization, which can include diluted bleach baths. New studies demonstrate that early emollient application from birth may prevent development of AD. [Pediatr Ann. 2016;45(8):e280–e286.]

Atopic dermatitis (AD) is a chronic and relapsing inflammatory disorder of the skin. The characteristic clinical features that predominate in this disease are sensitive/dry skin, itch, inflammation, and frequently secondary infection. With a prevalence estimated between 10% and 20% of all children, AD is a disease frequently encountered by pediatricians.1 This article will equip pediatricians with an update on the pathogenesis, clinical presentation, and treatment strategies to effectively manage patients with AD.

Burden of Disease

With increasing constraints on pediatricians' time, managing AD can be frustrating and time consuming. However, studies show that AD impairs the quality of life of children more so than other chronic diseases of childhood including asthma and type 1 diabetes.2 In addition, AD is associated with psychosocial challenges in children including increased dependency, fearfulness, and sleep disturbance secondary to itch.3 Recently, associations between AD and attention-deficit/hyperactivity disorder and other behavioral disorders have been described.4 Families and caregivers of children with AD experience substantial stress due to difficult time-consuming treatment regimens, financial costs, and sleep disruption.1 However, excellent results are achievable with topical therapy for the majority of children with moderate and even severe AD (Figure 1). When clinicians partner with families through education, the burden of disease and severity of AD decreases.5,6

            Clinical photographs of atopic dermatitis (A) before and (B) after “eczema boot camp,” an intensive 2-week topical therapy outpatient regimen.

Figure 1.

Clinical photographs of atopic dermatitis (A) before and (B) after “eczema boot camp,” an intensive 2-week topical therapy outpatient regimen.


The pathogenesis of AD is complex, involving genetic, environmental, and immunologic factors. In the last 10 years, understanding of the etiology of AD has greatly evolved. Once thought of as primarily an allergic or immunologic disorder, current studies demonstrate skin barrier dysfunction as central to the disease pathogenesis. A Danish population-based twin concordance study shows the important role of genetics in development of AD, with a contribution up to 82% among identical twins.7

The epidermal barrier is made up of structural proteins, which serve to prevent transepidermal water loss (TEWL) and penetration of environmental antigens, irritants, and microbes. One of the key structural proteins in the formation of this barrier is filaggrin.8 In 2006, Palmer et al.9 demonstrated that loss of function mutations in the filaggrin gene are strong predisposing factors for AD. Further, filaggrin null mutations are associated with greater disease severity and persistence.10

The exact mechanism for disease conferred from filaggrin deficiency is unknown. Irvine et al.11 proposed several biophysical and structural consequences of filaggrin deficiency that help explain its role in AD pathogenesis. These include increased pH of the skin and subsequent Staphylococcus aureus colonization, enhanced protease activity leading to inflammation, and impaired filament aggregation with subsequent barrier dysfunction. Beyond AD, filaggrin mutation carriers demonstrate an increased risk for asthma, hay fever, contact allergy, and peanut allergy.11

Filaggrin mutations do not account for all cases of AD, with an overall odds ratio of 3.12 to 4.78.11 Kelleher et al.12 demonstrated that increased TEWL, a marker for epidermal barrier dysfunction, at age 2 days and age 2 months is antecedent and predicative of AD development, independent of filaggrin mutation.12 Other genetic defects in epidermal proteins may account for some cases of AD. For example, mutations in desmosome proteins DSG1 and CDSN underlie some cases of severe AD.13 Further, environmental triggers and immune dysregulation seem to incite AD in genetically susceptible people. As antigens cross the impaired epidermal barrier, they prime a predominately Th2 response. Although many possible mechanisms may be at play, understanding the role of skin barrier dysfunction in the development of AD is crucial for successful topical management and perhaps even the prevention of this chronic skin disease.

Role of Bacterial Colonization and Infection

The role of microbial colonization in patients with AD cannot be overemphasized. Infection and colonization, in particular with S. aureus, is an important comorbidity in AD and leads to increased severity and prolonged duration of disease. The impaired barrier structure of the skin in AD facilitates colonization of numerous bacterial, fungal, and viral pathogens including S. aureus, Streptococcus pyogenes, herpes simplex virus, molluscum contagiosum, and Malazessia species. S. aureus is the predominant pathogen among patients with AD, colonizing up to 90% of AD patients compared to 5% of healthy people.14 Of note, S. aureus counts correlate with disease severity.15

S. aureus leads to worsening of AD severity through production of superantigens including staphylococcal enterotoxins A and B and toxic shock syndrome toxin-1. Superantigens have many deleterious effects in AD, primarily through modulation of the immune system. They cause proliferation of T cells with a dominant Th2 response. Further, superantigens induce corticosteroid insensitivity, hindering treatment.14

Clinical Characteristics

AD is a clinical diagnosis made largely by clues of lesion morphology, location, and associated symptoms. Numerous working groups have established criteria for diagnosis.16,17 Two criteria considered essential to a diagnosis of AD include pruritus and eczematous patches in an age-specific distribution. Xerosis, personal and/or family history of atopy, and early onset of disease (typically between ages 3 and 6 months) are supportive of an AD diagnosis.

The distribution of lesions often follows a pattern based on age. Infants tend to have involvement of the face, scalp, neck, and extensors. Childhood and adult lesions more commonly localize to flexures. It is not typical for lesions to appear in the groin or axillae at any age.

The morphology of eczematous lesions differs according to stage. New lesions tend to be erythematous, pruritic papules with overlying excoriations and/or exudates. Lesions typically progress to lichenified plaques secondary to excoriation. Clinical signs of infection include formation of pustules, crusting, or weeping18 but also may manifest by dermatitis unresponsive to previously adequate treatments.

Red Flags: What Not to Miss?

Atypical or Early Atopic Dermatitis and Eczema Herpeticum

Although AD typically follows the aforementioned patterns, there are atypical presentations that pediatricians should note that warrant further evaluation and unique treatment plans. If eczematous lesions appear prior to age 2 months, immunodeficiency should be considered. Several immunodeficiency disorders including hyper-IgE syndrome, Wiskott-Aldrich syndrome, severe-combined immunodeficiency syndrome, IPEX syndrome, and others may present with an eczematous rash in the first weeks after birth.13 Early, severe, and extensive dermatitis accompanied by severe or recurrent infections may indicate an underlying genetic cause for disease.

Eczema herpeticum is a complication arising in the setting of preexisting AD that is caused by disseminated herpes simplex viral infection and requires emergent intervention. Characteristic lesions include “punched out” erosions and vesicles. Patients often have fever, malaise, and/or lymphadenopathy accompanying skin lesions. Emergent antiviral treatment is necessary and in the case of widespread or facial involvement, admission to a hospital for intravenous administration of antivirals may be warranted to prevent keratoconjunctivitis or multiorgan involvement.13


Treatment strategies in AD should focus on improving the skin barrier dysfunction by addressing the clinical characteristics of eczema: dry skin, itch, inflammation, and infection. All four clinical features need to be addressed simultaneously for optimal response (Figure 2).

            A diagram of the basic treatment strategies for atopic dermatitis.

Figure 2.

A diagram of the basic treatment strategies for atopic dermatitis.

Optimizing the Skin Barrier

Restoring moisture that is lost secondary to TEWL from the impaired epidermal barrier is essential. Regular application of a thick emollient should be included in the treatment regimen of all cases of AD as well as maintenance regimens for inactive AD. Emollients (moisturizers) can reduce both disease severity and the need for topical steroids.19 Although there are numerous options for moisturizers, ointments and creams are preferred. White petrolatum is an inexpensive occlusive agent, highly effective in forming a barrier that prevents TEWL. Lotions should be avoided as they can have high water and alcohol content, which may lead to worsening of TEWL and stinging or burning on application. Emollients should be reapplied often; encourage at least twice daily moisturizing.

There is insufficient evidence for recommended frequency or duration of bathing among children with AD.19 However, many pediatric dermatologists favor daily bathing in a tub over showering. Bathing restores moisture to the skin and is effective in removing debris and allergens. Patients with AD can soak daily for 10 minutes in a lukewarm bath, followed by “patting” the skin dry. To prevent further evaporation of water from the skin, recommend immediate application of an emollient after bathing. Cleansers are not necessary but nonsoap, fragrance-free cleansers can be used to clean the groin, axillae, hands, and feet if desired.


Topical corticosteroids (TCS) are most effective in treating active inflammation and are typically introduced after failure to respond to regular moisturizing alone as outlined above. TCS act on immune cells, interfering with antigen processing and the release of inflammatory mediators. Beyond anti-inflammatory effects, TCS can help reduce itch associated with AD. TCS are classified by strength from I (very high potency) to VII (lowest potency). Choice of corticosteroids depends primarily on lesion location and patient age. In acute flares, use medium-potency TCS (ie, triamcinolone 0.1% ointment) twice daily on body lesions for 2 weeks or until lesions significantly improve and then taper. For facial lesions, use a lower potency TCS (ie, hydrocortisone 2.5% ointment).

Children have a greater body surface area to weight ratio, and therefore experience greater absorption of TCS. It is necessary to monitor for cutaneous side effects of TCS including striae, telangiectasias, and atrophy, although they are rare. TCS should be discontinued in the setting of any of the aforementioned signs on examination. Systemic side effects, including hypothalamic-pituitary-adrenal axis suppression, are rare and no specific monitoring is recommended for pediatric patients.19 It is important to discuss strength of steroids and their appropriate treatment locations with caregivers. When used appropriately, topical steroids are extremely safe and effective in the management of AD in all age groups.20

Topical calcineurin inhibitors (TCI) are another option for treatment of AD lesions. By selectively blocking proinflammatory cytokine transcription in activated T cells, TCI can be used as steroid-sparing agents for patients requiring long-term anti-inflammatory treatment. Additionally, TCI do not cause skin atrophy, making them safe for use on facial lesions and for longer durations. Currently, pimecrolimus and tacrolimus are approved for children age 2 years and older13 as a second-line treatment for failure or intolerance to corticosteroids. The main side effect of TCI is transient burning with application that should subside after a few applications. Initially, concerns over long-term safety were raised with TCIs but studies over the last decade have not substantiated this concern in the mid-term.21

Reducing Pruritus

The most effective way to manage itch associated with AD is through emollient skin barrier repair and anti-inflammatory topical medications. Oral antihistamines (H1 antagonists) may be incorporated as add-on therapy. A 2014 Cochrane review found no high-level evidence to support oral antihistamine use in AD, as there have been no randomized controlled trials comparing oral H1 antihistamines with placebo.22 The main benefit of oral antihistamines may be due to their sedating effects, helping patients sleep and decreasing scratching during the night.

Reducing Infection and Colonization

Finally, bacterial colonization should be considered in all patients with AD, and addressing this should be included in the treatment regimens of patients unable to easily clear flares and reduce their recurrence. In cases of overtly infected lesions (overlying honey-colored crusting or pustules), obtain a culture and prescribe oral antibiotics based on susceptibilities. For long-term suppression of bacterial colonization, consider recommending diluted sodium hypochlorite (bleach) baths for patients with AD (Table 1).

            Bleach Bath Directions

Table 1:

Bleach Bath Directions

Huang et al.23 demonstrated significantly reduced disease involvement and severity among AD patients treated twice weekly with diluted bleach baths and intranasal mupirocin compared to placebo (plain water baths) and intranasal mupirocin.23 The efficacy of diluted bleach baths may go beyond antimicrobial effects. Leung et al.24 reported reduction in nuclear factor-kappa B–mediated epidermal pathology, an important signaling protein in the proinflammatory pathway, with topical diluted bleach.24 Caregivers may express reservations regarding the addition of bleach to their child's bath. A diluted bleach bath is akin to chlorinated swimming pool water. Further, patients using bleach baths do not show increased susceptibility to resistant strains of S. aureus.23 Finally, a 5-day course of intranasal mupirocin can be used to treat S. aureus carriage among patients with AD and their household members although re-colonization is common.

Intensive Topical Therapy: Eczema Boot Camp

Severe or refractory cases of AD require intensive topical therapy regimens that can lead to significant improvement. Wet wrap therapy (WWT) is a safe and effective adjunctive modality useful in the setting of flares to quickly calm disease severity. WWT prevents TEWL and provides occlusion of topical steroids and emollients for maximum benefit. WWT can be performed at home by dressing the patient in moist pajamas (dampened by warm water) covered by a pair of dry pajamas overnight. This should follow application of topical steroids and/or emollient therapy. The temperature in the child's room should be warm to prevent chilling. Occlusive dressings will increase the absorption of TCS; therefore, taper WWT once the flare is controlled. Dabade et al.25 reported that 83% of patients treated at the Mayo Clinic with an intensive regimen of topical steroids and wet dressings showed >50% improvement of AD disease severity in a short time period (mean 3.6 days).25 WWT is generally safe and well tolerated. Side effects are few, but can include folliculitis, decreased body temperature in small infants, and possible systemic absorption of topical steroid.

A 2-week intensive skin care regimen, including daily diluted bleach baths, appropriate strength topical steroids, emollients, and wet wraps, is an effective modality that results in rapid clearance of AD even in the most severe cases. In our practice, we refer to this intensive topical regimen as “eczema boot camp” and in most cases patients respond extremely well (Figure 1). Treatments should be tapered after 2 weeks and topical steroids reduced or discontinued followed by a maintenance gentle skin care plan.

Prevention of Atopic Dermatitis

Currently, there is no cure for AD. However, a growing body of literature supports early repair of the skin barrier and oral introduction of allergens in prevention of allergy. Two randomized controlled studies show that early emollient application from birth may prevent AD in genetically susceptible people. Simpson et al.26 showed a relative risk reduction of 50% for development of AD at 6 months among infants treated with full body emollient therapy at least once daily compared to infants treated with no emollients. Similarly, Horimukai et al.27 demonstrated a 32% risk reduction in AD among infants treated with a daily emollient. Importantly, there were no adverse events related to emollient use. Early emollient use likely repairs the skin barrier function of the epidermis, preventing penetration of antigens and TEWL. These studies offer a safe, inexpensive, practical intervention for primary prevention of AD (Table 2).

            Gentle Skin Care Practices for Newborns and Infants That May Reduce Clinical Manifestations of Atopic Dermatitis

Table 2:

Gentle Skin Care Practices for Newborns and Infants That May Reduce Clinical Manifestations of Atopic Dermatitis

A strategy for prevention of allergy is early oral introduction of foods. Strid et al.28 showed that early environmental exposure of allergens (through barrier-disrupted skin) may account for sensitization. Conversely, oral introduction of allergens produces a tolerance through immune unresponsiveness in animal models.29 Du Toit et al.30 recently reported a 70% to 86% relative risk reduction in prevalence of peanut allergy among infants with either severe AD or egg allergy who were introduced early (before age 11 months) to peanuts through the gut versus those who avoided peanuts until age 60 months.30 Further, infants who were introduced early to peanuts showed significantly greater peanut-specific immunoglobulin G by age 60 months, a sign of successful immune modulation. There were no differences in adverse events between the two groups. These findings may refute overused elimination diets among children with AD and instead support early and sustained introduction of allergens in the diet. Finally, skin testing and serum assays for food allergies in children should be limited due to their low positive-predictive value.31


AD is common and can be challenging to treat. Most patients can be successfully managed with topical therapies and gentle skin care. However, time and education are needed among pediatricians and primary care providers to help patients and families understand and optimize their treatments. Addressing the role of infection and colonization in AD is important, and considering diluted bleach baths as an adjunctive therapy to a successful topical regimen may be beneficial. The role of skin barrier dysfunction has transformed our understanding of this complex disease and paved the way for possible preventive measures such as identifying infants at risk for AD development and recommending early emollient therapy.


  1. Carroll CL, Balkrishnan R, Feldman SR, Fleischer AB Jr, Manuel JC. The burden of atopic dermatitis: impact on the patient, family, and society. Pediatr Dermatol. 2005;22(3):192–199. doi:10.1111/j.1525-1470.2005.22303.x [CrossRef]
  2. Beattie PE, Lewis-Jones MS. A comparative study of impairment of quality of life in children with skin disease and children with other chronic childhood diseases. Br J Dermatol. 2006;155(1):145–151. doi:10.1111/j.1365-2133.2006.07185.x [CrossRef]
  3. Solomon CR, Gagnon C. Mother and child characteristics and involvement in dyads in which very young children have eczema. J Dev Behav Pediatr. 1987;8:213–220. doi:10.1097/00004703-198708000-00005 [CrossRef]
  4. Chen MH, Su TP, Chen YS, et al. Is atopy in early childhood a risk factor for ADHD and ASD? A longitudinal study. J Psychosom Res. 2014;77(4):316–321. doi:10.1016/j.jpsychores.2014.06.006 [CrossRef]
  5. Broberg A, Kalimo K, Lindblad B, Swanbeck G. Parental education in the treatment of childhood atopic eczema. Acta Derm Venereol. 1990;70:495–499.
  6. Staab D, Von Rueden U, Kehrt R, et al. Evaluation of a parental training program for the management of childhood atopic dermatitis. Pediatr Allergy Immunol. 2002;13:84–90. doi:10.1034/j.1399-3038.2002.01005.x [CrossRef]
  7. Thomsen SF, Ulrik CS, Kyvik KO, et al. Importance of genetic factors in the etiology of atopic dermatitis: a twin study. Allergy Asthma Proc. 2007;28(5):535–539. doi:10.2500/aap2007.28.3041 [CrossRef]
  8. O'Regan GM, Sandilands A, McLean WH, Irvine AD. Filaggrin in atopic dermatitis. J Allergy Clin Immunol. 2009;124(3):R2–R6. doi:10.1016/j.jaci.2009.07.013 [CrossRef]
  9. Palmer C, Irvine AD, Terron-Kwiatkowski A, et al. Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nat Genet. 2006;38(4):441–446. doi:10.1038/ng1767 [CrossRef]
  10. Henderson J, Northstone K, Lee SP, et al. The burden of disease associated with filaggrin mutations: a population-based, longitudinal birth cohort study. J Allergy Clin Immunol. 2008;121(4):872–877.e9. doi:10.1016/j.jaci.2008.01.026 [CrossRef]
  11. Irvine AD, McLean WH, Leung D. Filaggrin mutations associated with skin and allergic diseases. N Engl J Med. 2011;365(14):1315–1327. doi:10.1056/NEJMra1011040 [CrossRef]
  12. Kelleher M, Dunn-Galvin A, Hourihane J, et al. Skin barrier dysfunction measured by transepidermal water loss at 2 days and 2 months predates and predicts atopic dermatitis at 1 year. J Allergy Clin Immunol. 2015;135(4):930–935.e1. doi:10.1016/j.jaci.2014.12.013 [CrossRef]
  13. Lyons JJ, Milner JD, Stone KD. Atopic dermatitis in children: clinical features, pathophysiology, and treatment: clinical features, pathophysiology, and treatment. Immunol Allergy Clin N Am. 2015;35(1):161–183. doi:10.1016/j.iac.2014.09.008 [CrossRef]
  14. Roll A, Cozzio A, Fischer B, Schmid-Grendelmeier P. Microbial colonization and atopic dermatitis. Curr Opin Allergy Clin Immunol. 2004;4(5):373–378. doi:10.1097/00130832-200410000-00008 [CrossRef]
  15. Brussow H. Turning the inside out: the microbiology of atopic dermatitis. Environ Microbiol. 2015; doi:10.1111/1462-2920.13050 [CrossRef]. [Epub ahead of print].
  16. Hanifin JM, Rajka G. Diagnostic features of atopic dermatitis. Acta DermVenereol Suppl. 1980;92:44–47.
  17. Eichenfield LF, Tom WL, Chamlin SL, et al. Guidelines of care for the management of atopic dermatitis. Section 1. Diagnosis and assessment of atopic dermatitis. J Am Acad Dermatol. 2014;70(2):338–351. doi:10.1016/j.jaad.2013.10.010 [CrossRef]
  18. Raimer SS. Managing pediatric atopic dermatitis. Clin Pediatr. 2000;39(1):1–14. doi:10.1177/000992280003900101 [CrossRef]
  19. Eichenfield L, Tom WL, Berger TG, et al. Guidelines of care for the management of atopic dermatitis Section 2. Management and treatment of atopic dermatitis with topical therapies. J Am Acad Dermatol. 2014;71:116–132. doi:10.1016/j.jaad.2014.03.023 [CrossRef]
  20. Hong E, Smith S, Fischer G. Evaluation of the atrophogenic potential of topical corticosteroids in pediatric dermatology patients. Pediatr Dermatol. 2011;28(4):393–396. doi:10.1111/j.1525-1470.2011.01445.x [CrossRef]
  21. Siegfried EC, Jaworski JC, Hebert AA. Topical calcineurin inhibitors and lymphoma risk: evidence update with implications for daily practice. Am J Clin Dermatol. 2013;14(3):163–178. doi:10.1007/s40257-013-0020-1 [CrossRef]
  22. van Zuuren EJ, Apfelbacher CJ, Fedorowicz Z, Jupiter A, Matterne U, Weisshaar E. No high level evidence to support the use of oral H1 antihistamines as monotherapy for eczema: a summary of a Cochrane systematic review. Syst Rev. 2014;3:25. doi:10.1186/2046-4053-3-25 [CrossRef]
  23. Huang JT, Abrams M, Tlougan B, Rademaker A, Paller AS. Treatment of Staphylococcus aureus colonization in atopic dermatitis decreases disease severity. Pediatrics. 2009;123(5):e808–814. doi:10.1542/peds.2008-2217 [CrossRef]
  24. Leung TH, Zhang LF, Wang J, Ning S, Knox SJ, Kim SK. Topical hypochlorite ameliorates NFKB-mediated skin diseases in mice. J Clin Invest. 2013;123(12):5361–5370. doi:10.1172/JCI70895 [CrossRef]
  25. Dabade TS, Davis DM, Wetter DA, et al. Wet dressing therapy in conjunction with topical corticosteroids is effective for rapid control of severe pediatric atopic dermatitis: experience with 218 patients over 30 years at Mayo Clinic. J Am Acad Dermatol. 2012;67(1):100–106. doi:10.1016/j.jaad.2011.06.025 [CrossRef]
  26. Simpson EL, Chalmers JR, Hanifin JM, et al. Emollient enhancement of the skin barrier from birth offers effective atopic dermatitis prevention. J Allergy Clin Immunol. 2014;134(4):818–823. doi:10.1016/j.jaci.2014.08.005 [CrossRef]
  27. Horimukai K, Morita K, Narita M, et al. Application of moisturizer to neonates prevents development of atopic dermatitis. J Allergy Clin Immunol. 2014;134(4):824–830.e6. doi:10.1016/j.jaci.2014.07.060 [CrossRef]
  28. Strid J, Hourihane J, Kimber I, Callard R, Strobel S. Epicutaneous exposure to peanut protein prevents oral tolerance and enhances allergic sensitization. Clin Exp Allergy. 2005;35(6):757–766. doi:10.1111/j.1365-2222.2005.02260.x [CrossRef]
  29. Strid J, Thomson M, Hourihane J, Kimber I, Strobel S. A novel model of sensitization and oral tolerance to peanut protein. Immunology. 2004;113(3):293–303. doi:10.1111/j.1365-2567.2004.01989.x [CrossRef]
  30. Du Toit G, Roberts G, Sayre PH, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med. 2015;372(9):803–813. doi:10.1056/NEJMoa1414850 [CrossRef]
  31. Boyce JA, Assa'ad A, Burks AW, et al. Guidelines for the diagnosis and management of food allergy in the United States: summary of the NIAID-sponsored expert panel report. J Allergy Clin Immunol. 2010;126(6):1105–1118. doi:10.1016/j.jaci.2010.10.008 [CrossRef]

Bleach Bath Directions


Bleach baths should be prepared by an adult and fully mixed prior to the patient entering the tub


Both the caregiver and patient should avoid direct contact with undiluted bleach


For a full bathtub: use one-half cup of plain bleach (∼6% sodium hypochlorite) or one-fourth cup of concentrated bleach (∼8% sodium hypochlorite)


For an infant tub: 1–2 tablespoons of plain bleach


Gentle Skin Care Practices for Newborns and Infants That May Reduce Clinical Manifestations of Atopic Dermatitis


Bathing: A daily tub (soaking) bath for about 10 minutes. This must be followed by immediate application of a bland emollient


Cleansers: Synthetic detergents (nonsoap cleansers) are preferred. Limit use to 2–3 times weekly if possible


Emollient: 1–2 times daily application of a bland emollient. Ointment/occlusive agent is recommended and may prevent the development of atopic dermatitis. Cream is another option. Lotions may not be as well tolerated


Katherine Grey, BA, is a fourth-year Medical Student, University of Minnesota Medical School. Sheilagh Maguiness, MD, is an Assistant Professor, Department of Dermatology, University of Minnesota.

Address correspondence to Sheilagh Maguiness, MD, Department of Dermatology, University of Minnesota, 420 Delaware Street SE, MMC 98, Minneapolis, MN 55455; email:

Disclosure: The authors have no relevant financial relationships to disclose.


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