CLINICAL REPORT Atopic Dermatitis: Skin-Directed...

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CLINICAL REPORT Atopic Dermatitis: Skin-Directed Management abstract Atopic dermatitis is a common inammatory skin condition character- ized by relapsing eczematous lesions in a typical distribution. It can be frustrating for pediatric patients, parents, and health care providers alike. The pediatrician will treat the majority of children with atopic dermatitis as many patients will not have access to a pediatric medical subspecialist, such as a pediatric dermatologist or pediatric allergist. This report provides up-to-date information regarding the disease and its impact, pathogenesis, treatment options, and potential complica- tions. The goal of this report is to assist pediatricians with accurate and useful information that will improve the care of patients with atopic dermatitis. Pediatrics 2014;134:e1735e1744 Atopic dermatitis (AD), commonly referred to as eczema, is a chronic, relapsing, and often intensely pruritic inammatory disorder of the skin. A recent epidemiologic study using national data suggested that the pediatric prevalence is at least 10% in most of the United States. 1 AD primarily affects children, and disease onset occurs before the ages of 1 and 5 years in 65% and 85% of affected children, respectively. 1 The number of ofce visits for children with AD is increasing. 2 Up to 80% of children with AD are diagnosed and managed by primary care providers, often pediatricians. 3 Although medical subspecialists, such as pediatric dermatologists and/or pediatric allergists, may be suited to provide more advanced care for children with AD, lack of a sufcient number of such physicians, particularly pediatric dermatologists, 4 likely means the burden of AD care will continue to fall to primary care providers. Although consensus guidelines and practice parameters regarding the management of AD in children have been published, 510 considerable variability persists in clinical practice, particularly re- garding the roles that bathing, moisturizing, topical medications, and allergies play in management. Inconsistencies in opinion and treat- ment approach as well as the chronic and relapsing nature of AD can lead to frustration for the patient, family, and primary care providers when managing AD. STATEMENT OF THE PROBLEM New data support the theory that AD results from primary abnormalities of the skin barrier, 11 suggesting that skin-directed management of AD is of paramount importance. This clinical report reviews AD and provides an up-to-date approach to skin-directed management that is based on pathogenesis. Effectively using this information to create treatment plans Megha M. Tollefson, MD, Anna L. Bruckner, MD, FAAP, and SECTION ON DERMATOLOGY KEY WORDS atopic dermatitis, eczema, skin care, treatment, topical corticosteroids ABBREVIATIONS ACDallergic contact dermatitis ADatopic dermatitis IgEimmunoglobulin E MRSAmethicillin-resistant Staphylococcus aureus NIAIDNational Institute of Allergy and Infectious Diseases QoLquality of life TCItopical calcineurin inhibitor This document is copyrighted and is property of the American Academy of Pediatrics and its Board of Directors. All authors have led conict of interest statements with the American Academy of Pediatrics. Any conicts have been resolved through a process approved by the Board of Directors. The American Academy of Pediatrics has neither solicited nor accepted any commercial involvement in the development of the content of this publication. The guidance in this report does not indicate an exclusive course of treatment or serve as a standard of medical care. Variations, taking into account individual circumstances, may be appropriate. Clinical reports from the American Academy of Pediatrics benet from expertise and resources of liaisons and internal (AAP) and external reviewers. However, clinical reports from the American Academy of Pediatrics may not reect the views of the liaisons or the organizations or government agencies that they represent. doi:10.1542/peds.2014-2812 All clinical reports from the American Academy of Pediatrics automatically expire 5 years after publication unless reafrmed, revised, or retired at or before that time. PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275). Copyright © 2014 by the American Academy of Pediatrics PEDIATRICS Volume 134, Number 6, December 2014 e1735 FROM THE AMERICAN ACADEMY OF PEDIATRICS Guidance for the Clinician in Rendering Pediatric Care by guest on July 4, 2018 Downloaded from
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    Atopic Dermatitis: Skin-Directed Management

    abstractAtopic dermatitis is a common inflammatory skin condition character-ized by relapsing eczematous lesions in a typical distribution. It can befrustrating for pediatric patients, parents, and health care providersalike. The pediatrician will treat the majority of children with atopicdermatitis as many patients will not have access to a pediatric medicalsubspecialist, such as a pediatric dermatologist or pediatric allergist.This report provides up-to-date information regarding the disease andits impact, pathogenesis, treatment options, and potential complica-tions. The goal of this report is to assist pediatricians with accurateand useful information that will improve the care of patients withatopic dermatitis. Pediatrics 2014;134:e1735e1744

    Atopic dermatitis (AD), commonly referred to as eczema, is a chronic,relapsing, and often intensely pruritic inflammatory disorder of theskin. A recent epidemiologic study using national data suggested thatthe pediatric prevalence is at least 10% in most of the United States.1

    AD primarily affects children, and disease onset occurs before the agesof 1 and 5 years in 65% and 85% of affected children, respectively.1

    The number of office visits for children with AD is increasing.2 Up to80% of children with AD are diagnosed and managed by primary careproviders, often pediatricians.3 Although medical subspecialists, suchas pediatric dermatologists and/or pediatric allergists, may be suitedto provide more advanced care for children with AD, lack of a sufficientnumber of such physicians, particularly pediatric dermatologists,4

    likely means the burden of AD care will continue to fall to primary careproviders. Although consensus guidelines and practice parametersregarding the management of AD in children have been published,510

    considerable variability persists in clinical practice, particularly re-garding the roles that bathing, moisturizing, topical medications, andallergies play in management. Inconsistencies in opinion and treat-ment approach as well as the chronic and relapsing nature of AD canlead to frustration for the patient, family, and primary care providerswhen managing AD.


    New data support the theory that AD results from primary abnormalitiesof the skin barrier,11 suggesting that skin-directed management of AD isof paramount importance. This clinical report reviews AD and providesan up-to-date approach to skin-directed management that is based onpathogenesis. Effectively using this information to create treatment plans

    Megha M. Tollefson, MD, Anna L. Bruckner, MD, FAAP, andSECTION ON DERMATOLOGY

    KEY WORDSatopic dermatitis, eczema, skin care, treatment, topicalcorticosteroids

    ABBREVIATIONSACDallergic contact dermatitisADatopic dermatitisIgEimmunoglobulin EMRSAmethicillin-resistant Staphylococcus aureusNIAIDNational Institute of Allergy and Infectious DiseasesQoLquality of lifeTCItopical calcineurin inhibitor

    This document is copyrighted and is property of the AmericanAcademy of Pediatrics and its Board of Directors. All authorshave filed conflict of interest statements with the AmericanAcademy of Pediatrics. Any conflicts have been resolved througha process approved by the Board of Directors. The AmericanAcademy of Pediatrics has neither solicited nor accepted anycommercial involvement in the development of the content ofthis publication.

    The guidance in this report does not indicate an exclusivecourse of treatment or serve as a standard of medical care.Variations, taking into account individual circumstances, may beappropriate.

    Clinical reports from the American Academy of Pediatricsbenefit from expertise and resources of liaisons and internal(AAP) and external reviewers. However, clinical reports from theAmerican Academy of Pediatrics may not reflect the views of theliaisons or the organizations or government agencies that theyrepresent.


    All clinical reports from the American Academy of Pediatricsautomatically expire 5 years after publication unless reaffirmed,revised, or retired at or before that time.

    PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).

    Copyright 2014 by the American Academy of Pediatrics

    PEDIATRICS Volume 134, Number 6, December 2014 e1735


    Guidance for the Clinician inRendering Pediatric Care

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  • and educate families should help pe-diatric primary care providers managemost children with AD, thereby im-proving patient satisfaction and clinicaloutcomes.


    The diagnosis of AD is primarily clinical(Table 1). Major clinical features are apruritic and relapsing eczematous der-matitis in a typical distribution thatchanges with age.9 In infancy, the cheeks,scalp, trunk, and extremities are mostcommonly affected. In early childhood,the flexural areas are characteristic,whereas in adolescents and adults,hands and feet are typically involved.Pruritus is a hallmark of AD, which isoften referred to as the itch thatrashes. Other features that supportthe diagnosis of AD include early ageof onset, personal or family historyof atopy, ichthyosis vulgaris, and/orxerosis. It is important to exclude otherinflammatory skin conditions, such ascontact dermatitis, seborrheic der-matitis, and psoriasis. Skin biopsiesand laboratory testing are usuallyunnecessary and not helpful in makingthe diagnosis of AD, although they maybe beneficial when trying to exclude

    conditions that appear similar to AD(such as those mentioned previously),particularly in patients whose symp-toms are not responding to standardskin-directed care.


    The effects of AD on the quality of life(QoL) of patients and their familiescannot be underestimated. Nearly 50%of children with AD report a severelynegative effect of the disease on QoL.12

    Factors that contribute to poor QoL inAD are fatigue and sleep deprivation(which directly correlate with itch andseverity of AD), activity restriction, anddepression. Children with severe ADalso tend to have fewer friends andparticipate in fewer group activitiesthan their peers.13 These children maybe at higher risk of depression, anxiety,and other mental health disorders.14

    AD also has a negative effect on QoL ofcaregivers and parents of affectedchildren.15 Parents of children withmoderate and severe AD spend up to3 hours per day caring for their chil-drens skin. The most commonly reportednegative effects on parents are lack ofsleep (often because of cosleeping),fatigue, absence of privacy (becauseof cosleeping, disrupted sleep of af-fected children), treatment-related fi-nancial expenditures, and feelings ofhopelessness, guilt, and depression.In fact, the depression rate in mothersof children with AD is twice as high asin mothers of children with asthma.16

    Appropriate social and community sup-port resources, such as referral to acounselor, psychologist, or patient sup-port groups, such as the NationalEczema Association (, can be helpful when QoL issuesare encountered in patients and familieswith AD.


    The pathogenesis of AD is complex andmultifactorial. Skin barrier dysfunction,

    environmental factors, genetic pre-disposition, and immune dysfunction allplay a role in its development and areclosely intertwined. In the past, em-phasis had been placed on T helper celldysregulation, production of immuno-globulin E (IgE), and mast cell hyper-activity leading to the development ofpruritus, inflammation, and the char-acteristic dermatitis.11 Recent discov-eries, however, have established thekey role of skin barrier dysfunction inthe development of AD.17

    The primary function of the skin barrieris to restrict water loss and to prevententry of irritants, allergens, and skinpathogens. The outermost layer of skin,called the stratum corneum, is criticalto the integrity of the skin barrier, withthe protein filaggrin being a key playerin stratum corneum structure andformation.18 Loss-of-function mutations(of which more than 40 have beendescribed) in FLG, which encodesfilaggrin, have been implicated in upto 50% of patients with moderate tosevere AD in some demographic pop-ulations.17,19 Mutations in FLG are as-sociated with a two- to threefoldincreased risk of having AD.20

    There are several proposed mechanismsof how filaggrin defects contribute tothe development of AD. Inadequatefilaggrin production leads to a reducedability of keratinocytes to maintain hy-dration and to restrict transepidermalwater loss, which then leads to xerosis,which in turn produces pruritus and,subsequently, AD.21 An inadequate skinbarrier might also allow for the entryof aeroallergens, leading to an in-flammatory response, causing AD.Another theory speculates that localpH may be changed with an alteredskin barrier, leading to the overgrowthof bacteria, such as Staphylococcusaureus, which then may trigger an in-nate immune response, leading tothe development of inflammatory skinlesions. Regardless of the mechanism,

    TABLE 1 Clinical Features in AD5,6,9

    Major clinical featuresItching/pruritusTypical dermatitis with a chronic or relapsing

    historyPatient or family members with atopyTypical distribution and age-specific patterns

    Minor clinical featuresEarly age of onsetDry skin/xerosisKeratosis pilarisIchthyosis vulgarisLip dermatitisHand eczemaLichenificationElevated IgE levelItching on sweatingRecurrent infectionsPityriasis albaDermatographismEye symptoms: cataracts, keratoconus,


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  • this new knowledge reinforces the pri-mary role of the skin barrier in thepathogenesis of AD and highlights theneed for skin-directed therapy to repairor enhance the function of the skinbarrier.


    The relationship between AD and foodallergy is complex but likely over-emphasized. More than 90% of parentsincorrectly believe that food allergy isthe sole or main cause of their childsskin disease.22 The resulting focus onfood allergy can result in eliminationdiets; potential nutritional concerns,such as protein or micronutrient mal-nutrition or deficiencies; and mis-direction of treatment away from theskin, thereby leading to undertreat-ment. Effective treatment of the skintends to allay parental concern re-garding food allergy.23

    True food-induced AD is rare. The mostcommon cutaneous manifestations offood allergy are often IgE-mediated andconsist of acute urticaria, angioedema,contact reactions, or in some cases, anincrease in AD symptoms.24,25 In thecase that AD is worsened by exposureto a food allergen, these reactions arenot IgE-mediated but rather delayed-type hypersensitivity reactions andusually develop 2 to 6 hours after theexposure to the food.26

    The accentuated role of food allergiesin AD may stem from the observationthat food allergies are prevalent inpatients with AD. The prevalence offood allergy in all children in the first 5years of life is approximately 5%.24 Inchildren with AD, however, the preva-lence of food allergy is approximately30% to 40%,25 and up to 80% will havehigh food-specific IgE concentrations,even in the absence of a true foodallergy.27 In addition, patients whohave food allergy often have earlier-onset and more severe AD, and pa-tients with early-onset AD have a higher

    risk of developing food allergies thanthose with later-onset AD.28 However, it isimportant to stress that this relationshipis not causative. Rather, the presence offood allergy predicts a poor prognosis ofsevere and persistent AD, but food al-lergy does not necessarily cause AD.

    Recent guidelines set forth by the Na-tional Institute of Allergy and InfectiousDiseases (NIAID) support this position.In these guidelines, the NIAID states: Insome sensitized patientsfood aller-gens can induce urticarial lesions,itching and eczematous flares, all ofwhich may aggravate AD but do notcause AD. They also state that, in theabsence of documented IgE- or non-IgEmediated food allergy, there islittle evidence to support the rolefor food avoidance in the treatment ofAD.25 Egg allergy may be one excep-tion, as up to half of infants with egg-specific IgE may have improvement intheir AD when following an egg-freediet.29 The NIAID guidelines state thatallergy evaluation (specifically to milk,egg, peanut, wheat, and soy) should beconsidered in children younger than 5years with severe AD if the child haspersistent AD despite optimal man-agement and topical therapy or if thechild has a reliable history of an im-mediate cutaneous reaction after in-gestion of a specific food.

    The atopic march is the concept thatAD is the first stop in the progressionto other allergic disorders, such asasthma and allergic rhinitis.30 It hasbeen suggested that early optimal andsuccessful treatment of AD may preventor attenuate the development of otheratopic conditions.31 The recent findingsof the role FLGmutations play in causingepidermal barrier defects, thus allowingfor the entry of aeroallergens and otherallergens into the skin and subsequentepicutaneous sensitization, lends strongsupport to this possibility and highlightsthe importance of effective skin-directedtreatment of AD.

    Allergic contact dermatitis (ACD) is adelayed hypersensitivity reaction tocutaneous allergens that is under-estimated in the pediatric populationand likely plays a greater role inperpetuating AD than was previouslybelieved. Up to 50% of children withdifficult-to-control AD have at least 1 pos-itive patch test reaction to a cutaneousallergen.32 Not all positive reactionsmay be relevant, however. Most studiesestimate 50% to 70% of all positive re-actions to be relevant in patients withsuspected ACD. Thus, the possibility ofACD should be considered in childrenwith unusual or difficult-to-control AD.


    Skin-directed therapies should be thefirst approach to management. Thisapproach has 4 main components, eachfocusing on a specific manifestation ofAD: (1) maintenance skin care, designedto repair and maintain a healthy skinbarrier; (2) topical antiinflammatorymedications, to suppress the inflam-matory response; (3) itch control; and(4) managing infectious triggers, rec-ognition and treatment of infection-related flares. Education of patientsand families is another critical factorthat should not be overlooked. AD isa frustrating disease because of itsrecurrent nature, even in the face ofexcellent care plans. When the primarycare provider is able to set realisticexpectations regarding outcomes, pa-rental compliance is better and frus-tration is decreased. It can be helpfulto discuss the prognosis of AD, be-cause most children will outgrow thesymptoms or at least the severity ofthe disease.27 Patients whose parentsreceive comprehensive education re-garding AD and its care have betterimprovement in AD severity than pa-tients whose parents do not receivethis education.33 Written action planshave been shown to improve adherencein children with asthma, and a similar

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  • model for patients with AD (see Fig 1 foran example), outlining specific indica-tions for different products and medi-cations, is likely to be helpful.34,35

    Maintenance Skin Care

    Maintenance skin care is the founda-tion of AD management; its goal is torepair and maintain a functional skinbarrier. Patients should be instructedto develop these habits and performthem daily. Preliminary evidence sup-ports the role of maintenance skincare in helping to reduce both thefrequency and severity of AD flares.The key facets of maintenance careinclude maintaining skin hydrationand avoiding irritants and triggers.

    The optimal frequency of bathing forchildren with AD has not been well

    studied and remains controversial.Soaking baths allow the skin to imbibemoisture, and a daily bath can bebeneficial in patients with AD as longas a moisturizer is applied after-ward.30,36 The specific frequency ofbathing should be titrated to theindividual patient and his or herresponse to bathing. The use oflukewarm water and limiting theduration of the bath can prevent skindehydration. Cleansing may also re-move bacteria from the skin surface.A mild synthetic detergent withoutfragrance can be used to cleansesoiled areas without fear of exac-erbating the skin disease. Additivesare not proven to be effective, al-though dilute bleach can be helpfulfor patients who are prone to infection

    and flares (see Managing InfectiousTriggers).

    A second and extremely importantcomponent of maintaining skin hydra-tion is lubrication of the skin, commonlyreferred to as moisturization. Frequentmoisturization alleviates the discomfortassociated with xerosis, helps to repairthe skin barrier, and reduces the quan-tity and potency of pharmacologic inter-ventions.37,38 In a British study evaluating51 children with AD, parents were ed-ucated on the proper use of moistur-izers and topical treatments by a nursespecialist. During the study period, thequantity of moisturizer used increased800% (average use of 426 g per weekper patient) while the severity of ADdecreased and the percentage of pa-tients having to use moderate or po-tent topical steroids decreased.39

    Studies comparing the relative effec-tiveness of specific moisturizers arelacking, and the plethora of productscan make the task of choosing amoisturizer daunting. Simplistically,all moisturizers are mixtures of lipid(liquid or semisolid) and water. Oint-ments have the highest proportion oflipid (for example, petroleum jelly is100% lipid) and likewise feel greasywhen applied to the skin. Creams areemulsions of water in lipid (oil>water)and contain preservatives and stabi-lizers to keep these ingredients fromseparating. Although creams can beless greasy than ointments, the addedingredients can sometimes burn orsting atopic skin. Similarly, lotions arealso emulsions with a higher pro-portion of water to lipid than creams.Frequent reapplication of lotions isneeded to maintain skin hydration. Ingeneral, ointments tend to have thegreatest moisturizing effect, followedby creams, and then lotions. The bestmoisturizers for patients with AD arefragrance free and have the leastpossible number of preservatives, be-cause these are potential irritants.

    FIGURE 1An action plan for the management of AD.

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  • Moisturizers should be applied at leastonce daily to the entire body, regard-less of whether dermatitis is present.

    There are a handful of prescription bar-rier creams marketed for the treat-ment of AD. These products do not haveactive pharmacologic ingredients. A smallstudy compared 2 of these productswith an over-the-counter ointment andrevealed no significant difference in ef-ficacy for patients with mild-to-moderateAD, as defined by investigator globalassessment.40 Although no major ad-verse effects have been reported withthese products, they are considerablymore expensive and may, therefore,be less cost effective than standardmoisturizers.

    Multiple patient-specific factors, com-monly referred to as triggers, mayexacerbate AD. Triggers may be un-avoidable, but minimizing exposure tothem can be helpful. Common triggersmay include aeroallergens or environ-mental allergens, infections (particu-larly viral illnesses), harsh soaps anddetergents, fragrances, rough or non-breathable clothing fabrics, sweat, ex-cess saliva, and psychosocial stress.

    Topical AntiinflammatoryMedications

    The eczematous dermatitis seen in ADis the manifestation of an inflam-matory immune response in the skin.Flares of dermatitis are unlikely torespond to moisturization alone, andduring these times, treatment is fo-cused on suppressing the inflam-matory response. Topical steroids arethe first-line, most commonly usedmedications to treat active AD andhave been used for the last 40 to 50years.30 When used appropriately, theyare effective and safe.41 However,when used inappropriately, there arepotential risks of cutaneous atrophy,striae, telangiectasia, and systemic ab-sorption with resulting adrenal sup-pression. There are also other potential

    local effects when used around the eyes(intraocular hypertension, cataracts)or mouth (periorificial dermatitis). Be-cause of these potential risks, there isa real phenomenon of steroid phobiaon the part of both parents and healthcare providers. Although this phobiadoes not correlate with AD severity, itdoes lead to undertreatment of theskin disease.42,43

    Topical steroids are classified accord-ing to their potency, ranging from classVII (low potency) to class I (super po-tent; Table 2). Class I medications are1800 times more potent than the leastpotent class VII medications. Risk ofadverse effects directly correlates withpotency, with high-potency and super-potent topical steroids carrying thegreatest risk. When treating most casesof AD, high-potency medications aregenerally not needed. Patients treatedwith higher-potency topical steroids areat risk for developing the aforemen-tioned adverse effects, making closefollow-up necessary. Choosing an ap-propriate topical steroid can be dif-ficult, given the number of differentmedications, and health care pro-viders are advised to rely on 2 or 3medications from the low- (classes VIand VII) and moderate-potency groups(classes III, IV, and V) as go-to medi-cations for everyday practice. Thesechoices may be based on regionalprescribing practices and insurancecoverage or cost. Inexpensive low-and moderate-potency generic topicalsteroids are hydrocortisone and tri-amcinolone, respectively. Acceptablelimits of topical steroid potency in aprimary care practice are low-potencytopical steroids for the face, neck,and skin folds and moderate-potencytopical steroids for the trunk andextremities.

    For acute flares and moderate to se-vere cases, wet wrap therapy (alsocalled wet dressings) can be used inconjunction with topical steroids to

    quickly control the dermatitis.44 Wetdressings increase penetration of top-ical steroids into the skin, decrease

    TABLE 2 Topical Steroid Medications byClass

    Class I: SuperpotentClobetasol propionate 0.05% ointment, cream,

    solution, and foamDiflorasone diacetate 0.05% ointmentFluocinonide 0.1% creamHalobetasol propionate 0.05% ointment

    and creamClass II: High potencyBetamethasone dipropionate 0.05% ointment

    and creamBudesonide 0.025% creamDesoximetasone 0.25% ointment and creamDiflorasone diacetate 0.05% creamFluocinonide 0.05% ointment, cream, and gelHalcinonide 0.1% cream and ointmentMometasone furoate 0.1% ointment

    Class III: Moderate potencyBetamethasone valerate 0.1% ointment, foamDesoximetasone 0.05% creamDiflorasone diacetate 0.05% creamFluticasone propionate 0.005% ointmentTriamcinolone acetonide 0.1% ointmentTriamcinolone acetonide 0.5% cream

    Class IV: Moderate potencyBetamethasone valerate 0.12% foamClocortolone pivalate 0.1% creamFlurandrenolide 0.05% ointmentFluocinolone acetonide 0.025% ointmentHalcinonide 0.025% creamHydrocortisone valerate 0.2% ointmentMometasone furoate 0.1% cream and lotionTriamcinolone acetonide 0.1% cream

    Class V: Moderate potencyBetamethasone valerate 0.1% creamClocortolone pivalate 0.1% creamFlurandrenolide 0.025% ointmentFlurandrenolide 0.05% creamFluocinolone acetonide 0.01% creamFluocinolone acetonide 0.025% creamHydrocortisone butyrate 0.1% ointment,

    cream, and lotionHydrocortisone probutate 0.1% creamHydrocortisone valerate 0.2% creamPrednicarbate 0.1% creamTriamcinolone 0.025% ointment

    Class VI: Low potencyAlclometasone dipropionate 0.05% ointment

    and creamDesonide 0.05% ointment, cream, lotion,

    hydrogel, and foamFluocinolone acetonide 0.01% oilFlurandrenolide 0.025% creamTriamcinolone acetonide 0.025% cream

    Class VII: Low potencyHydrocortisone 0.5% and 1% ointment

    and cream (over the counter)Hydrocortisone 2.5% ointment, cream,

    and lotion

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  • itch, and serve as an effective deter-rent to scratching. The technique isstraightforward: after a soaking bath,topical steroid is applied to affectedareas followed by application of mois-turizer to the rest of the skin; moistgauze or cotton clothing that has beendampened with warm water is thenapplied; the wet layer is covered withdry cotton clothing. Blankets and awarm room keep the child comfort-able. The dressings can be left in placefor 3 to 8 hours before being changed.Wet dressings can be used continu-ously for 24 to 72 hours or overnightfor up to 1 week at a time.

    Another consideration when prescrib-ing topical steroids is the vehicle orform of product by which the activeingredient is delivered. Ointments areless likely to produce a burning orstinging sensation and are better tol-erated by infants and younger children.When comparing the same active in-gredient and concentration, ointmentsare more effective than creams orlotions, because their occlusive effectresults in a higher relative potency.Topical steroids should be applied asa thin layer once or twice daily to af-fected areas until these areas aresmooth to touch and no longer red oritchy. Traditionally, topical steroids areheld when dermatitis is quiescent andrestarted when the eruption recurs.Placing an absolute limit on the dura-tion of topical steroid use can beconfusing for families, leads to un-satisfactory outcomes, and conflictswith the relapsing nature of the diseaseitself. However, if AD is not respondingafter 1 to 2 weeks of treatment, re-evaluation to consider other diagnosesor treatment plans is indicated. Whenthese general guidelines are followed,the risk of adverse effects from the useof topical steroids is extremely low.

    Topical calcineurin inhibitors (TCIs) area newer treatment of AD. These medi-cations are topical immunosuppressive

    agents that inhibit T-cell function.There are currently 2 forms: tacrolimusointment (available in 0.03% and 0.1%)and pimecrolimus 1% cream. Both areapproved as second-line therapy formoderate-to-severe AD. A recent meta-analysis in pediatric patients with ADdemonstrated that both tacrolimus andpimecrolimus are effective; tacrolimusis more effective than pimecrolimus,but both reduce the inflammation andpruritus associated with AD.45

    TCIs have a different adverse effectprofile than topical steroids and do notcause atrophy, striae, telangiectasia, andadrenal suppression. Thus, they arehighly beneficial to treat AD in patientsfor whom concerns for adverse effectsfrom long-termuse of topical steroids arehighest (eg, face, eyelids). The negatives,however, are a higher relative cost andthe potential adverse effects of burningand stinging (tacrolimus>pimecrolimus).In addition, the Food and Drug Adminis-tration has issued a so-called blackbox or boxed warning for TCIs, citinga potential cancer risk with the medi-cation, on the basis of the observationthat laboratory animals exposed to highdoses of systemic calcineurin inhibitorsdeveloped malignancies more frequentlyand on rare case reports of adult pa-tients using TCIs who developed lym-phoma and skin cancers.46 However, thecause-and-effect relationship betweenTCI use and malignancy in these casereports is unclear. Reassuringly, TCIs havebeen used in children for more than 15years, there have been no reports ofmalignancy in children, and there is littleto no concern for systemic absorptionor systemic immunosuppression.47

    Indeed, in 1 adult study, there was alower rate of nonmelanoma skin can-cer in patients with AD who used TCIsto treat their inflammatory disease.48

    Proactive Treatment

    Although traditional AD managementconsists of treating active disease andflares with topical steroids and/or TCIs,

    emerging data suggest that use ofthese medications when a patient is nothaving active disease may be helpfulas well. In 1 study, patients used twice-daily antiinflammatory medications totreat active AD and were then randomlyassigned to receive proactive twice-weekly treatment with topical tacrolimusor placebo. Patients who received top-ical tacrolimus had significantly lessAD flares and increased time to newflare development when compared withthose who received placebo.49 A sim-ilar effect may also be true with top-ical steroids (fluticasone propionateand methylprednisolone aceponate havebeen studied),50 although none of thesestudies have evaluated the long-termsafety of this treatment regimen. Thechoice of medication used for flareprevention may depend on patient age,location of involvement, and cost.

    Itch Control

    Pruritus is another important com-ponent of AD. AD is commonly referredto as the itch that rashes; the asso-ciated pruritus may be significant,even in the absence of significant rash.Often, parents may be unaware of howmuch their child scratches, becauseitching is generally worse at night. Thepathophysiology behind pruritus iscomplex, and both peripheral andcentral factors are involved.51 Exam-ples of peripheral factors are irritantentry through a defective epidermalbarrier, transepidermal water loss,and protease activity in the skin.52

    Centrally, there is a complex interplayof multiple different mediators, al-though histamine seems to havea limited role, if any.52,53 Clinical fac-tors can also promote itch, includingscratching (the itch-scratch cycle),xerosis, psychological stress, sweat,and contact with irritants such as wooland aeroallergens.

    It is often challenging to remove itch,even when a patients skin is improving.Management of itch initially focuses on

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  • minimizing triggers and continuing theskin-directed treatments of restoring theskin barrier and suppressing inflam-mation. Adjunctive systemic therapy canbe added to help manage itch. Oralantihistamines do not have a direct ef-fect on the dermatitis, but can help re-duce the sensation of itching and,thus, decrease scratching and traumato the skin in patients with ADflares.54 Sedating antihistamines (suchas diphenhydramine or hydroxyzine)should be used with caution in infants,who may be more prone to adverseeffects of these agents. In addition,paradoxical effects of agitation insteadof sedation may occur in some children.Nonsedating antihistamines (such ascetirizine and loratadine) are less effec-tive on pruritus but can be helpful forpatients who have environmental allergictriggers.54 Topical antihistamines arenot effective in the treatment of AD-associated pruritus and contain poten-tial irritants and allergens that mayworsen dermatitis.

    Managing Infectious Triggers

    Both bacterial and viral skin infectionsare associated with flares in childrenwith AD. Affected patients, particularlythose with poorly controlled AD, havea higher risk of cutaneous infections.The skin of patients with AD has anabnormal expression of antimicrobialpeptides responsible for responding tobacteria or skin barrier compromise,toll-like receptor defects, and immunedysregulation in the form of diminishedimmune cell recruitment.55 This com-bination of factors puts patients withAD at higher risk of skin infection.

    Ninety percent of patients with AD arecolonized with S aureus.56 Pruritusmay occur even in patients who arecolonized but not actively infected.Many patients with AD have suddenexacerbations of their disease that canbe attributed to active infection withbacteria, most commonly S aureus,

    and active treatment of the infectionsubsequently improves the skin.56 Clin-ical signs of infection, such as pustules,oozing and honey-colored crusts, andless commonly fever and cellulitis, maylead the primary care provider toprescribe antibacterial treatment. Sec-ondary infection of AD is a clinicaldiagnosis and is often associated withflare of the underlying AD. Obtainingskin cultures, particularly of pustulesand draining lesions, before treat-ment can be helpful in determiningthe causative pathogen but is not al-ways necessary. The rate of methicillin-resistant S aureus (MRSA) colonizationin patients with AD varies dependingon the community in which the pa-tient resides.57 Streptococcal infec-tions may also occur in patients withAD. Signs of streptococcal infectioninclude pustules, painful erosions, andfever. In addition, patients may havefacial or periorbital involvement andinvasive infections.58

    There are multiple synergistic com-ponents involved in treating active Saureus and streptococcal infection inAD. Topical, oral, or intravenous anti-biotic therapy may be needed depend-ing on the extent and severity ofinfection. The specific medication usedshould be directed at S aureus andStreptococcus. Topical mupirocin canbe used for limited skin lesions.Cephalexin is a common first-choicewhen oral antibiotics are needed andMRSA is not suspected. Repair of theskin barrier is continued simultaneously:bathing, moisturization, and topical anti-inflammatory therapies are all usuallyindicated. MRSA or other etiologies maybe considered in patients who remainrefractory to treatment.

    Dilute bleach baths may have a usefulrole in the management of patientswith AD, particularly those prone torecurrent infection and AD flares. Arecent placebo-controlled, blinded studyexamined the effects of 0.005% bleach

    baths plus intranasal mupirocin versusplacebo in children with moderate tosevere AD. Patients bathed for 5 to 10minutes twice weekly with the in-tervention. Those in the treatmentgroup had significant improvement intheir AD severity scores versus thosein the placebo group.56 Areas of thebody that were not submerged in thebleach-containing water, specificallythe head and the neck, revealed nodifference in AD severity scores be-tween the 2 groups. The treatment waswell tolerated, without any adverse ef-fect, and without any increase in re-sistant strains of S aureus. Althougha relatively small study, the resultsprovide support for the practice ofusing dilute bleach baths as one mo-dality in the treatment of patients withAD. A concentration of 0.005% bleach ismade by adding 120 mL (1/2 cup) of6% household bleach to a full bathtub(estimated to be 40 gallons) of water.The amount of bleach should be ad-justed based on the size of the bathtuband the amount of water in the tub.

    Patients with AD are also at greaterrisk of viral skin infections. These in-clude molluscum contagiosum, eczemaherpeticum, the recently describedatypical enteroviral infection attrib-utable to Coxsackie virus A6 (the so-called eczema coxsackieum),59 andvaccinia virus (the virus used insmallpox vaccine). Patients with eczemaherpeticum present with shallow,punched-out erosions in areas of skinaffected with or prone to AD. Similarly,the lesions seen with hand, foot, andmouth disease caused by Coxsackievirus A6 tend to localize to AD skin. Incases in which the diagnosis is notclear, viral studies are indicated.

    Eczema herpeticum can be potentiallylife threatening and requires systemictreatment with acyclovir. In addition,adequate analgesia, skin care, andtopical antiinflammatory medicationsare used. Secondary bacterial infection

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  • often coexists with eczema herpeticumand should be treated appropriately aswell. Herpetic keratitis is associatedwith periocular eczema herpeticum.60

    Smallpox vaccine uses a live vacciniavirus, and its use was resumed by themilitary in 2002. Although it is con-traindicated for those with AD and inthose who have a close contact withAD, rare cases of eczema vaccinatumhave been reported. Eczema vaccinatummanifests as a rapidly developing pap-ular, pustular, or vesicular eruptionwith a predilection for areas of AD,following inadvertent transmission ofvaccinia virus from the unhealed in-oculation site of the immunized personto a close contact with AD. Systemicdissemination may follow, and casefatality rates range from 5% to 40%. Ifeczema vaccinatum is suspected, infec-tious disease experts should be con-sulted, because treatment with cidofovirmay be necessary.61

    Final Points

    Using this information, the pediatricprimary care provider should be wellequipped to treat most children withAD. If patients with suspected AD do notrespond to these treatments, referral

    to a pediatric medical subspecialist,such as a pediatric dermatologist, maybe useful. Other reasons for referralinclude poorly controlled or gen-eralized AD with consideration forsystemic immunosuppressive therapy,recurrent infections (viral or bacterial)in the setting of AD, suspected ACD, andthe presence of atypical features orphysical examination findings. In casesof persistent, refractory, and/or gen-eralized AD, systemic treatment, suchas phototherapy or immunosuppres-sive medications, may be indicated. Oralsteroids are generally not indicatedbecause of their adverse side effectprofile and a high likelihood of rebounddermatitis, making ongoing manage-ment difficult.


    AD can be a challenging and frustratingchronic disease for pediatric patients,parents, and primary care providers.Although the pathogenesis of AD iscomplex, recent research advancessupport the role of an abnormal skinbarrier. The clinical corollary to thesediscoveries is a greater focus on skin-directed therapies as the first-linetreatment of children with AD. This

    includes maintenance skin care andthe use of topical steroids for activedisease. Low- and moderate-potencytopical steroids are safe and effec-tive for children when used appro-priately. Early recognition and treatmentof infectious complications can lead toimproved patient outcomes. Patientand family education and counselingby the health care provider regardingthe pathogenesis, specific treatment,and prognosis of the disease play anextremely important role in the man-agement of AD.

    SECTION ON DERMATOLOGYEXECUTIVE COMMITTEE, 20132014Bernard A. Cohen, MD, FAAP, ChairpersonRichard Antaya, MD, FAAPAnna Bruckner, MD, FAAPKim Horii, MD, FAAPNanette B. Silverberg, MD, FAAPTeresa Wright, MD, FAAP


    EX OFFICIOMichael L. Smith, MD, FAAP

    STAFFLynn M. Colegrove, MBA


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