med diagnosis and management of common dermatoses in children

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Clinical Pediatrics

DOI: 10.1177/00099228073094212008; 47; 332 originally published online Dec 5, 2007;Clin Pediatr (Phila)

Alan B. Fleischer, JrDermatitis

agnosis and Management of Common Dermatoses in Children: Atopic, Seborrheic, and Contac

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332

Diagnosis and Managementof Common Dermatoses in Children:

Atopic, Seborrheic, and ContactDermatitis

Alan B. Fleischer Jr, MD

also crucial to determine the appropriate therapeu-tic approach. This article will provide an overview of

AD, SD, and CD, with particular focus on how thesedermatoses manifest in infants and children, andwill discuss strategies to effectively manage thesedisorders in the pediatric population.

The Impact of Pediatric Dermatitis

Clinicians who treat dermatitis are beginning to

understand the effect these disorders have not onlyon the pediatric patient but also on the childs fam-ily. Dermatitis can be a significant source of physi-cal, psychologic, and economic burden for patients,siblings, and caregivers.4-7

As a result of pruritus, children with dermatitisoften experience disturbed sleep, with subsequentdiminishment of school performance and in somecases, behavioral problems.8,9 These children alsocan experience increased stress, anxiety, and lowself-esteem (due in part to bullying by other children)

and may not be able to take part in sports or other

Dermatitis comprises a group of diseasesinvolving inflammation of the skin, with ery-thematous and papulovesicular morphology

when acute, and erythema and scaling whenchronic. The most common pediatric dermatosesinclude atopic dermatitis (AD), seborrheic dermati-tis (SD, cradle cap), and contact dermatitis (CD,especially diaper dermatitis).1-3As there is no curefor dermatitis, a comprehensive long-term treatmentstrategy based on education, prevention, and phar-macologic therapy can provide patients with the

means by which to manage their disease. In addi-tion, considerations such as appropriately balancingsafety and efficacy in the pediatric population andtailoring treatment to the disease site and severity are

Atopic, seborrheic, and contact dermatitis can signifi-cantly reduce the quality of life of patients and their fam-ilies. Although differing in specific aspects of their

epidemiology, etiology, and pathobiology, all 3 dermatosesare common in the pediatric population, and they sharea common treatment approach. Although effective andwidely used to manage exacerbations of pediatric der-matitis, the use of topical corticosteroid remains a con-cern for some physicians and parents because of itspotential for systemic absorption and adverse eventsassociated with prolonged use. Newer additions to thedermatitis treatment algorithm, such as the topical

calcineurin inhibitors, may provide an effective steroid-sparing treatment option. Adjuvant treatments, such asantihistamines, antifungals, and antibiotics, also can pro-

vide benefit in appropriate circumstances. As there is nocure for dermatitis, a comprehensive, multipronged man-agement strategy of preventive measures, such as triggeravoidance and periodic pharmacologic treatment, willprovide patients and caregivers with the best opportunityto successfully control the disease.

Keywords: calcineurin inhibitor; eczema; skin disease;inflammation

From the Department of Dermatology, Wake Forest UniversitySchool of Medicine, Winston-Salem, North Carolina.

Editorial support provided by Novartis PharmaceuticalsCorporation.

Address correspondence to: Alan B. Fleischer Jr, MD, WakeForest University School of Medicine, Medical Center Boulevard,

Winston-Salem, NC 27157; e-mail: [email protected].

Clinical Pediatrics

Volume 47 Number 4

May 2008 332-346

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Managing Pediatric Dermatitis /Fleischer 333

social activities.10 Parents of children with dermati-tis also experience sleep disturbance and increasedfinancial stress due to frequent doctor visits, lostwages, diminished work productivity, home care,and medications.6 Considerable emotional stresswas reported in an Australian survey of families that

included 48 children with moderate to severe AD;caring for a child with AD was identified in this surveyas being significantly more stressful than caring fora child with insulin-dependent diabetes mellitus.11

In addition, the annual cost to the health care sys-tem due to AD alone is significant, estimated atbetween US$0.9 and US$3.8 billion.12 Thus, thetrue cost of dermatitis should be understood both interms of the financial burden and the negativeimpact on quality of life. Accordingly, effective treat-ment of pediatric dermatitis can benefit pediatric

patients, their caregivers, and society overall.

Atopic Dermatitis

Overview and Epidemiology

Atopic dermatitis is a chronic, highly pruritic, inflam-matory skin condition and is the most commonchronic skin disease13 affecting approximately 7% to17% of school-aged children in the United States.14

Onset of AD occurs in 45% of children by the age of6 months, in 60% of children by the age of 1 year,15

and in 85% of children by the age of 5 years.16As evi-denced by an international comparison of 463 801children aged 13 to 14 years, which evaluated therelative frequency of certain conditions over a 12-month period, the prevalence of AD was shown toincrease steadily in Western countries over the last 3decades, parallel to the increase in the prevalence ofasthma.17 The AD has also been linked to the develop-ment of allergic rhinitis. On the basis of these andother observations, it has been suggested that ADmay be the entry point for the atopic march, that is,the progressive development of systemic allergy.18,19

Diagnosis

Diagnosis of AD is based on the presence of severalessential and associated features (Table 1).20,21 Owingto the wide variety of clinical presentations and themultifactorial etiology of AD, diagnosis can be chal-lenging. The differential diagnosis for AD includeshyper-IgE syndrome, Wiskott-Aldrich syndrome,

Netherton syndrome, and juvenile dermatomyositis.22

Other conditions that also should be consideredinclude SD, psoriasis, and neurodermatitis, as wellas systemic illnesses such as malignancy, thyroid dis-orders, and hepatic or renal failure, all of which cancause pruritus and excoriations.23 Children with ADalso may present with disease variants or associated

conditions (eg, ichthyosis vulgaris, keratosis pilaris,nummular eczema, pityriasis alba, dermatophyteinfections, impetigo) that can confound the diagno-sis (Figure 1; Table 2).22-26

Pathobiology

The etiology of AD, although not fully understood, ishypothesized to be the result of dysregulation of theimmune system, particularly an imbalance of Thelper 1 and T helper 2 responses, dysfunction of

the skin barrier,27 and a combination of genetic andenvironmental factors. Recent studies have identi-fied a subset of the genes influencing developmentof AD in certain patients. Epidermal differentiationcomplex is expressed late during the maturation ofepidermal cells and has been linked to both AD andpsoriasis.28 In addition, the presence of 2 loss-of-function mutations in the filaggrin gene that resultin the development of ichthyosis vulgaris also areconsidered as strong predisposing factors for AD.29

Compared with the skin of healthy patients,

both the affected and the unaffected skin of patientswith AD exhibit xerosis, a key clinical characteristicof AD.27 Ceramides, whose concentrations arereduced in affected patients, are the major lipidpresent in the stratum corneum layer of the skin30

and are proposed to play a role in the pathobiologyof AD.31 As xerosis can enhance transepidermalwater loss, the skin of patients with AD often devel-ops microfissures and cracks that allow entry ofpathogens, antigens, and irritants, which may exacer-bate or complicate the condition. Consequently,

comprehensive, long-term management of ADshould address the immune and the skin barrier dys-functions that are characteristic of the disease.

Disease Management

Atopic dermatitis is a heterogeneous disease with aclinical course characterized by alternating periodsof remission (during which the patient is asympto-matic) and periodic exacerbations (flares). The goalsof AD treatment are both to lengthen the time

between flares and to reduce their severity.

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334 Clinical Pediatrics/ Vol. 47, No. 4, May 2008

Table 1. Guidelines for the Diagnosis of Atopic Dermatitisa

Essential Features Patient Must Have 3 or More Basic FeaturesPruritusTypical morphology and distribution

Flexural lichenification or linearity in adultsFacial and extensor involvement in infants and children

Chronic or chronically relapsing dermatitisPersonal or family history of atopy (asthma, allergic rhinitis, atopic dermatitis)

Associated Features Plus 3 or More Minor FeaturesXerosisIchthyosis/palmar hyperlinearity/keratosis pilarisImmediate (type I) skin-test reactivityElevated serum IgEEarly age of onsetTendency toward cutaneous infections (especiallyStaphylococcus aureus and herpes simplex)/impaired

cell-mediated immunityTendency toward nonspecific hand or foot dermatitisNipple eczemaCheilitis

Recurrent conjunctivitisDennie-Morgan infraorbital foldKeratoconus

Anterior subcapsular cataractsOrbital darkeningFacial pallor/facial erythemaPityriasis alba

Anterior neck-foldsItch when sweatingIntolerance to wool and lipid solventsPerifollicular accentuationFood intoleranceCourse influenced by environmental/emotional factors

White dermographism/delayed blanch

a. Reproduced with permission from Hanifin JM and Rajka G.20

Table 2. Differential Diagnosis of Atopic Dermatitis23-26,a

Disease Distinguishing Features

Contact dermatitis Positive exposure history, rash in area of exposure, absence of family history Dermatitis herpetiformis Vesicles over extensor areas and associated enteropathyDermatophyte infections (including Serpiginous plaques with central clearing, positive potassium hydroxide preparation

tinea pedis/manuum)Immunodeficiency disorder History of recurrent infectionImpetigo Infection by streptococci or Staphylococcus aureus, infection often preceded by minor skin

injury (eg, insect bite), presents as small vesicles of blisters that rupture and leave behinda crust (sometimes honey-colored) on the surface of the lesion

Lichen planus Eruption appears over the course of several weeks, absence of family history, may beassociated or preceded by a stressful event, most common in the 30-60 year age group

Neurodermatitis Usually, a single patch in an area accessible to itching; absence of family history Psoriasis Localized patches on extensor surfaces, scalp, buttocks; pitted nailsScabies Papules, finger web involvement, positive skin scrapingSeborrheic dermatitis Greasy, scaly lesions, absence of family history Systemic diseases Findings on complete history and physical examination vary by disease

a. Adapted with permission from Correale et al.23



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Nonpharmacologic Approaches

Education and Prevention. Education plays an impor-tant role in management of all types of dermatitis.

With respect to patient and family education, it isimportant that clinicians anticipate parental anxietyabout dermatitis and its treatments. With propereducation, children and their caregivers will be ableto understand the chronic nature of the diseaseand have realistic expectations about its course andtreatment.

Trigger avoidance. Although the factors that triggerAD flares can vary between patients, conscientioustrigger avoidance and proper skin care help preventflares.32,33 Common triggers for AD flares includeexposure to harsh detergents or soaps, various chem-icals, and toiletries containing alcohol, fragrances,preservatives, and astringents.34 Data concerningthe significance of aeroallergens, such as dust mitesand animal dander, in AD are inconclusive and com-plete avoidance is not possible.34 Food allergies also

may trigger AD flares in some children, the offending

Figure 1. A variety of different conditions can initially present with morphology similar to that of atopic dermatitis.



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foods most often being milk, eggs, peanuts, soy, wheat,or fish.33 Parents should not overly restrict the dietsof children who have AD, because such practice hasresulted in malnutrition in some cases.35 Althoughtriggers can be difficult to pinpoint with currentlyavailable methods, allergy testing may be of benefit

in individuals with a clear allergic trigger or with der-matitis that is difficult to manage or refractory totreatment. Negative skin-prick or serum tests, in par-ticular, are valuable for their predictive ability in rul-ing out suspected allergens.34

Proper skin care. As mentioned previously, xerosis ischaracteristic of AD; thus, its prevention and treat-ment are essential. Bathing is generally consideredhelpful because it hydrates the skin and enhances pen-etration of topical therapies.36,37 However, children

with AD should not be bathed too frequently, as waterevaporation after bathing can dry the epidermal bar-rier and exacerbate xerosis. Lukewarm water and mildcleansers are recommended; it is best to avoid highlyfragranced soaps and bubble baths. Importantly, mois-turizers should be liberally applied within 3 minutesafter the bath to minimize water evaporation from theepidermis and maximize moisture retention.37

Ceramide-rich barrier repair mixtures and othermoisturizers, emollients, and hydrophilic ointmentsmay improve symptoms associated with AD by

enhancing moisture retention within the skin andproviding a mechanical barrier to irritants.30,37 Theseand other moisturizers should be applied 2 to 3 timesdaily for best effect. Ointments are more effectivethan creams, though lack of compliance, particularlyamong school-aged children, can limit their useful-ness. In these cases, ointments may be most success-fully applied while children are sleeping. In addition,hydrogels may provide relief from pruritus, burning,and pain associated with AD and other types of der-matitis. These devices are described in further detail

in the context of CD treatment.Disease flares, which can be triggered by seasonal

variation, vaccinations, respiratory illness, bacterialinfections, and allergies, among other factors, areoften unavoidable despite conscientious trigger avoid-ance and proper skin care.22 It is, therefore, importantthat children and their families understand and rec-ognize flares as short-term setbacks that may requirepharmacologic intervention.

Pharmacologic Management

Mild or moderate (minor) AD flares involve itchingand moderate erythema with few or no excoriations,

papules, or lichenification, but can quickly progress tosevere (major) AD flares involving persistent, intenseitching, erythema with extensive excoriations, oozingand crusting, and pronounced lichenification. In treat-ing children with severe flares, it can be challengingto balance caution and effective treatment. Topical

agents that inhibit the inflammatory response aremainstays of therapy, with appropriate managementtailored to the site and severity of the flare and theage of the patient. Although families of childrenexperiencing severe flares can be understandablyanxious, some of their concerns can be alleviated byclear, detailed explanations of treatment agents andtheir use. An open dialogue on these subjectsencourages children to take an active role in theirown treatments and may improve patient and familycompliance.

Topical corticosteroids. Topical corticosteroids (TCSs)have been used for the treatment of AD flares forseveral decades. The anti-inflammatory effects ofTCSs include diminishment of dermal edema andcapillary dilation, attenuation of the humoralinflammation process, and reduced movement ofinflammatory cells within the skin.38 In a classicclinical trial, hydrocortisone acetate effectivelyresolved long-standing symptoms of AD in 66% ofchildren and adults evaluated, although beneficial

results diminished 4 to 5 days after hydrocortisonewas discontinued.39 Despite widespread use ofTCSs, the results of a large meta-analysis indicatethat existing clinical trials do not adequately com-pare their efficacy and do not provide a clear con-sensus on appropriate dosing regimens.40

Topical corticosteroids are grouped according totheir potency and are selected based on diseaseseverity, area of the body affected, and age of thepatient. A stepwise approach to treatment is appro-priate, beginning with the lowest-potency steroid

likely to be effective and avoiding underdosing tominimize the risk of flare rebound.40 Table 3 listssome commonly available corticosteroid agentsaccording to potency.41Application frequency can bedecreased from twice daily to several times weeklyafter flare symptoms are controlled and a less potentTCS can be used. Available data do not support theefficacy of short-term bursts of more potent cortico-steroids versus long-term use of mild agents forchildren with mild to moderate AD.42

Although TCSs offer effective treatment for AD,

adverse events (AEs) associated with long-term uselimit their clinical use.40 Three weeks of continuous



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or intermittent TCS treatment has been shown tosubstantially decrease collagen synthesis in theskin,43 causing local AEs such as skin atrophy, striae,telangiectasias, hypopigmentation, rosacea, perioraldermatitis, and acne.40,44 Topical corticosteroids therapy

should, therefore, be used conservatively and shouldbe limited to 3 to 7 days in patients with acute AD, andto 2 to 3 weeks in those with chronic symptoms.45

Topical corticosteroids also may be absorbed sys-temically when used on thin, highly absorptive skinareas, such as the face and groin, and they are asso-ciated with greater potential for AEs.46,47 Rare butsignificant AEs can include suppression of thehypothalamic-pituitary-adrenal axis, growth retardation,and reduced bone density, all of which are of particularconcern in the pediatric population.40,46 Cushings

syndrome, cataract formation, and glaucoma also may

occur.46 Prolonged use of TCSs, particularly on highlyabsorptive skin areas, is therefore contraindicated.46

Step-down to nonsteroid pharmacotherapy. Becauseof the potential for AEs related to TCS treatment,

parents and physicians should routinely monitortheir childrens treated skin for potential AEs and togauge therapeutic response. As an alternative tolong-term steroid therapy, patients can be steppeddown to nonsteroid pharmacotherapies, such as top-ical calcineurin inhibitors (TCIs), after initial treat-ment with appropriate TCSs (Figure 2). Alternativesto TCS therapy are valuable for a variety of situa-tions, including symptom relapse after TCS therapy,steroid insensitivity, steroid allergy, and the so-calledsteroid phobia, in which parents refuse TCS therapy

out of concern about potential AEs.48

In such cases,

Table 3. Relative Potency of Select Topical Corticosteroidsa

Potency Topical Corticosteroid

Class 1 (superpotent) Betamethasone dipropionate 0.05% ointment/gelClobetasol propionate 0.05% ointment/creamDiflorasone diacetate 0.05% ointment

Halobetasol propionate 0.05% ointment/creamClass 2 (potent) Amcinonide 0.1% ointmentBetamethasone dipropionate 0.05% ointmentDesoximetasone 0.25% ointment/cream; 0.05% gelFluocinonide 0.05% ointment/creamHalcinonide 0.1% cream

Class 3 (upper midstrength) Betamethasone dipropionate 0.05% creamBetamethasone valerate 0.1% ointmentFluticasone propionate 0.005% ointmentMometasone furoate 0.1% ointmentTriamcinolone acetonide 0.5% cream

Class 4 (midstrength) Betamethasone valerate 0.12% foamClocortolone pivalate 0.1% cream

Desoximetasone 0.05% creamFluocinolone acetonide 0.025% ointment; 0.2% creamFlurandrenolide 0.05% ointmentTriamcinolone acetonide 0.1% ointment/cream

Class 5 (lower midstrength) Betamethasone dipropionate 0.05% lotionBetamethasone valerate 0.1% cream/lotionFluocinolone acetonide 0.025% creamFlurandrenolide 0.05% creamFluticasone propionate 0.05% creamHydrocortisone butyrate 0.1% creamHydrocortisone valerate 0.2% creamPrednicarbate 0.1% creamTriamcinolone acetonide 0.1% cream/lotion

Class 6 (mild strength) Alclometasone dipropionate 0.05% ointment/creamDesonide 0.05% creamFluocinolone acetonide 0.01% cream/solution/oil

Class 7 (least potent) Topicals with hydrocortisone, dexamethasone, flumethasone, methylprednisolone, and prednisolone

a. Adapted with permission from Del Rosso and Friedlander.41



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parents fears about AEs have implications for treat-ment compliance. In a recent investigation, 72.5%of the respondents worried about TCS use on theirown or their childrens skin, and 24% of the respon-dents reported noncompliance with therapy as aresult.48Additionally, the results of the InternationalStudy of Life with Atopic Eczema (ISOLATE)underscore the need not only for accurate familyeducation about safety, potency, and appropriate use

of TCSs,48 but also for steroid-sparing treatmentalternatives.

Topical calcineurin inhibitors. Recent findings indi-cate that 62% of patients (aged >13 years) and 74% ofcaregivers would prefer to prevent an AD flare fromoccurring or getting worse through use of a non-steroidal treatment.7 The TCIs tacrolimus and pimecro-limus offer an alternative to steroid treatment andhave become part of an effective long-term treatmentstrategy for many patients. These agents inhibit the

action of calcineurin and block T-cell activation and

the production of inflammatory cytokines,49,50 a moreselective mechanism of action than that of the TCSs.

Tacrolimus and pimecrolimus have been effectiveand well tolerated as short-term and intermittent long-term treatment in clinical trials of adults and children.The most common AE noted during clinical trials ofTCIs was a transient burning sensation at the applica-tion site that diminished during further treatment.51

In one clinical comparison, the efficacy of 0.1%

tacrolimus ointment was comparable to that of 0.1%hydrocortisone butyrate ointment in the treatmentof 570 adults with moderate to severe AD.52 Skinburning and pruritus were the only AEs with a sig-nificantly higher incidence in the tacrolimus groupthan in the hydrocortisone group.52Additional clini-cal trial data have shown that tacrolimus enhancesquality of life, reduces flare incidence, and providessafe, effective treatment of cutaneous symptoms andpruritus in patients aged 2 years with moderate tosevere AD.51,53A retrospective chart review has also

suggested that tacrolimus is effective in children

Figure 2. The management of atopic dermatitis. Long-term management requires daily preventive care and pharmacologictreatment with topical corticosteroids, topical calcineurin inhibitors, and adjunctive therapies (when appropriate). TCI = topicalcalcineurin inhibitor; TCS = topical corticosteroid.



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aged


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Cradle cap is characterized by nonpruritic, thick,greasy scales (white, off-white, or yellow) on the ver-tex of the scalp. Although the center of the face,ears, and forehead may have fine scaling, general-ized SD (ie, SD appearing on the flexural folds) isuncommon in healthy children and is usually asso-

ciated with immunodeficiencies. Therefore, infantswith generalized SD should be evaluated for moreserious disease.84 Dandruff typically appears duringpuberty when sebaceous glands have matured.Pubescent scaling in the nasolabial creases, pinnae,eyebrows, retroauricular areas, glabella, eyelids, andaural canals may also occur.1

In a survey of 1116 Australian children, the over-all prevalence of SD was 10% in boys and 9.5% ingirls.88 In most children (72%), SD was minimal ormild, and the highest prevalence occurred in the first

3 months of life and decreased rapidly by the age of 1year. Cradle cap (mostly minimal to mild) was evidentin 42% of children.88Although SD is reported to berare between infancy (ie, resolution of cradle cap) andadolescence (ie, appearance of dandruff) due to theimmaturity of sebaceous glands,89 a recent, cross-sectional study of 300 children found that SD waspresent in 6% of children between the ages of 2 and10 years (roughly 3 times less prevalent in childrenless than the age of 2 years).90 The SD in the 2-year-old to 10-year-old children appeared as both the

greasy-scale SD characteristic of cradle cap as well asthe fine, nongreasy scale seen in dandruff.90Althoughmore study is needed to confirm the prevalence of SDbetween infancy and puberty, physicians should notethat SD in this age group may occur.

Diagnosis

Diagnosis of SD in children involves an evaluationof patient history (onset of SD, attempts by family oftreatment) and physical examination of the type,

location, configuration, and pattern of scales.3 Asmentioned, cradle cap (greasy, nonpruritic white, off-white, or yellow scales) appears predominantly on the

vertex of the scalp. Differential diagnosis includesAD, tinea capitis (rare in infancy), and psoriasis.3 Inadolescents, the appearance and the distribution ofscales render diagnosis straightforward. Differentialdiagnosis includes the same conditions listed for dif-ferential diagnosis of cradle cap, with the addition ofhistiocytic disorders and dermatomyositis. Theappearance of SD in adolescents is rarely confused

with other dermatoses, with the exception of psoriasis.In psoriasis, however, lesions may extend onto theforehead, whereas SD is confined to the scalp.1

Disease Management

The treatment of childhood SD involves parent andpatient education, as well as nonpharmacologic(hygienic) and pharmacologic strategies.

Education

Parents who seek medical attention for their childscradle cap should be informed that the cause isunknown and should receive brief explanations ofthe existing theories. The main message to parents isthat cradle cap can be easily and effectively treated

and that it usually resolves within the first year oflife. Possible regimens for treatment and care shouldbe discussed and should be accompanied by printedinstructions that parents can take home. Similarly,parents and adolescent patients should be educatedregarding treatment regimens for adolescent SD.

Treatment of Cradle Cap

The treatment of cradle cap is very straightforwardand consists of a combination of scale loosening and

shampooing. In mild cases, daily shampooing with anonmedicated shampoo for 1 week may be effectivein loosening and removing scales, and emollientscan be applied to loosen scales should simple sham-pooing prove ineffective. Emollients can be left onthe scalp overnight and white petrolatum or slightlywarmed mineral or olive oil can be applied to thescalp for a minimum of 20 minutes. Subsequent tothe emollients, the scales can be gently removedwith an infant hairbrush or fingertips, followed by anonmedicated shampoo.3,91

Treatment of Adolescent SD

The management of adolescent SD involves a com-bination of nonpharmacologic and pharmacologicapproaches. Emollients help relieve xerosis23 andfrequent cleansing of the affected area removesexcess oil from the skin and is part of a preventivestrategy.91Antifungal creams, such as ketoconazole,and antifungal or antidandruff shampoos are part offirst-line pharmacologic therapy81,92 and are used to



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decrease colonization by yeasts.93 The recently approved2% ketoconazole gel, Xolegel, has been shown toimprove erythema and scaling scores, as well as theInvestigators Global Assessment score in childrenaged 12 years and older.94 The product is applied oncedaily to the affected area for 2 weeks.94 The most com-

mon adverse reactions are application-site burningand headache.94 Short courses of low-potency TCSsaid in resolution of erythema and itching and are acommon treatment. The TCIs have been proposed asa steroid-sparing therapy for SD,84 and several small-scale studies and case reports have suggested thattacrolimus and pimecrolimus may be useful in adultswith this condition.93,95-100 The most common sideeffects are mild local burning and irritation.93,95,98

Further study is needed in adolescent patients withSD to evaluate the utility of this treatment option.

Contact Dermatitis

Overview

The CD is caused by direct skin exposure to an allergenor irritant101 and is categorized into 2 common sub-types: irritant CD (ICD) and allergic CD (ACD).101

Environmental factors are primarily responsible forthese dermatoses, especially in the case of ICD. The

ICD is a result of cellular injury caused by directchemical contact with common triggers, such assoaps, detergents, solvents, acids, and alkali. TheICD may occur minutes to hours after exposure to astrong irritant (acute reactions), or after repeatedexposure to milder agents (cumulative insult reac-tions). The ACD occurs in individuals previouslyexposed and immunologically sensitized to a partic-ular chemical, such as nickel sulfate (commonlyfound in everyday items such as keys, buttons, andclothing), or pentadecylcatechols (the active agent

in poison ivy, poison oak, and poison sumac).101

TheACD is similar to AD in that the disease is manifestedthrough immune-mediated mechanisms, specificallya type IV (delayed-type) hypersensitivity reaction.101

Contact Dermatoses in Children

In infants and children, the most common forms of ICDare lip-licking or drooling and diaper dermatitis.102,103

Other forms of ICD in children are uncommon.102

Nickel allergy (from snaps on clothing or on belt

buckles) is the most common form of pediatric ACD,but is still relatively rare.102

Lip-Licking or Drooling

Lip-licking is localized to the area around the

mouth; saliva and air mix to cause a dryness that canbecome inflamed.102 The drool of teething infantsmay cause ICD of the perioral area, neck, andchest.22 First-line treatment of these straightforwardICDs involves minimizing trigger exposure by use ofprotective barriers as complete trigger avoidance inchildren and infants in these cases is difficult. Forexample, in the case of teething infants who developICD of the perioral area, neck, and chest because ofchronic skin exposure to saliva, food, and saturatedbibs, a thick emollient may act as an effective barrier

when applied before and after meals.22 Similarly,emollients for the perioral area of children who licktheir lips (especially in the winter months) can pro-

vide an effective barrier.

Diaper Dermatitis

Diaper dermatitis, the most common dermatologicproblem in infancy,103 results directly from the irri-tation caused by diapers.3 Prevalence is estimated tobe between 7% and 35% but is almost certainly

underreported.3,104 Diaper dermatitis most com-monly occurs in infants 9 to 12 months of age, andalmost half of all diaper-wearing infants and chil-dren seen by pediatricians will experience diaperdermatitis.2 The warmth and wetness of the diaperarea create an impairment of the barrier function ofthe skin.103 Moisture renders the skin more fragileand thereby makes the skin more vulnerable to dam-age caused by friction, which occurs in the areascovered by diapers (abdomen, buttocks, genitals).2

Exposure of the skin to urine and feces also com-

promises the skin and increases the permeability ofirritants. Although the pathogenic significance ofCandida albicans in the induction of diaper dermati-tis remains unclear, extensive colonization increasesseverity of the dermatitis.2,103

Diaper dermatitis, which is self-limiting with amean duration of 2 to 3 days per episode,2 most com-monly presents as erythema and mild scaling of thebuttocks, thighs, lower abdomen, and gluteal creasebut may also present as shiny plaques or erosionswith a macular, papular, or vesicular composition.3,103



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Differential diagnosis includes AD, psoriasis, and SD.The childs hygienic routine should be discussed withparents, and potential irritating agents used for thechilds cleansing routine should be identified. First-line treatment includes hygienic measures, such asincreasing the frequency of diaper changes, ensuring

adequate airflow into diapers (ie, fastening diapersloosely), or, when possible, allowing the infant orchild to remain diaper-free. The use of disposable dia-pers designed to be superabsorbant that provide a bar-rier between wetness and the skin should be usedinstead of cloth diapers. Water-repellant barriercreams (eg, zinc oxide) should be applied to areasprone to wetness and friction, and frequent bathing(once or twice daily) is also recommended. The use ofbaby wipes that contain fragrances or alcohol shouldbe avoided, as they may further irritate the skin.2,103

If diaper dermatitis persists after these conserv-ative measures, a short course of 1% hydrocortisonecream (twice daily for a maximum of 2 weeks) canbe applied to decrease inflammation, alone or, ifC albicans colonization is extensive, in combinationwith an antifungal cream. Until recently, no topicalantifungal was indicated for the treatment of diaperdermatitis in infants. In 2006, however, an ointmentcontaining 0.25% miconazole nitrate in a base ofzinc oxide and white petrolatum was approved by theUS Food and Drug Administration for the adjunctive

treatment of diaper dermatitis specifically compli-cated by C albicans.105 Although not indicated forthe treatment of diaper dermatitis in the UnitedStates, short courses of low-potency, nonhalo-genated TCSs are often prescribed. Higher-potencyTCSs (both alone and when used in combinationproducts) should be avoided for the treatment ofdiaper dermatitis due to the AEs covered in the sec-tion on AD.2When a secondary bacterial infection issuspected due to the decreased integrity of the skin,a topical antibiotic is appropriate.2

Nickel ACD

Nickel ACD, the most common ACD in infants, pro-duces a pruritic dermatitis that is difficult to distinguishfrom AD. The location and pattern of exposure is help-ful in differentiating nickel ACD from AD; the areawhere the child has exposure to nickel snaps or buttonsis the most frequent area of presentation. The only cureis to remove the allergen; inflammation can be con-trolled with a short course of a nonhalogenated TCS.1

Contact Dermatoses in Adolescents

Adolescents also suffer ICD and ACD. Due to theadolescents mobility and independence, the range ofirritating substances and potential allergens isincreased. As with ICD or ACD in infancy and child-

hood, trigger recognition and avoidance are para-mount, and conservative measures should be used asa first-line treatment. During an outbreak of ICD or

ACD, skin should be cleansed with minimal use ofsoap, relying instead on plain water to remove dry par-ticulates from the skin, and a slurry of fine cornmealand water to remove soil or grease. Mild soaps withneutral pH can be used as needed to fight microbialcontamination. Skin hydration and emollients may beuseful in treating ICD. Wet compresses with Burowssolution help reduce the discomfort of ACD lesions

and have a mild antimicrobial effect.

101

Other treat-ments, such as TCSs, antihistamines, phototherapy,and systemic agents, may be useful, depending on theseverity of the disease and the age of the patient. TheTCIs may offer a steroid-sparing treatment for someforms of CD.106-111 Evaluation of tacrolimus ointmenthas shown a treatment benefit in nickel allergy,107,109

protein contact dermatitis,106 and eyeglass frame der-matitis.107 Similarly, pimecrolimus has exhibited effi-cacy in the treatment of nickel110 and chronic handdermatitis.111 Further study in pediatric populations iswarranted to fully evaluate these treatments.

Hydrogels, which can consist of a water-solublenetwork of polymer chains, a colloidal gel in anaqueous dispersion medium, or superabsorbent nat-ural or synthetic polymers, are recently introducedmedical devices that may speed lesion healing insome patients with CD. In a clinical trial of 20 menand women aged 18 to 65 years, the efficacy of anonsteroid hydrogel compound was demonstrated intreatment of ICD induced by exposure to sodiumlaurel sulfate.112 Further data are needed to deter-mine whether hydrogels will prove superior to high-quality moisturizers in the treatment of CD and totest these treatments in children.

Conclusion

The AD, SD, and CD comprise a group of chronicdiseases that can significantly affect quality of life forchildren and their families. Comprehensive treat-ment of these conditions requires the integration of



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appropriate nonpharmacologic and pharmacologictherapies.

With respect to AD, 75% of patients and caregiversindicate that effectively controlling their disease wouldbe the single most important improvement to theirquality of life.7 Proper skin care and trigger avoidance

are key components in preventing exacerbations, butmost patients will experience periodic disease flaresand recalcitrant dermatoses that require pharmaco-logic treatment. The TCSs are a mainstay of therapy,but their clinical utility is limited by AEs associatedwith long-term use. The TCIs provide a means ofstepping down to nonsteroidal pharmacotherapy afterinitial treatment with TCSs.

The occurrence of SD typically exhibits abimodal pattern, with peaks during infancy and afterpuberty. Although SD is considered rare between

infancy and adolescence, clinicians should remainalert to the possibility of the disease among childrenin this age group. Antifungals and low-potency TCSsare commonly used to treat this condition and itssymptoms, and emerging data suggest that TCIs maybe useful as steroid-sparing therapy.

The optimal management of irritant and allergicforms of CD requires collaboration between clini-cians and parents or patients to identify triggers andimplement strategies for minimizing or avoidingexposure to these factors. A variety of barrier treat-

ments and topical therapies may be beneficial.As therapies for common dermatoses continue to

evolve, clinicians are being presented with broaderoptions that may enhance prospects for tailoringtreatment to the individual patient. Pediatric studiesof newer therapies such as the TCIs will help clini-cians determine how to integrate assorted treatmentsinto comprehensive strategies to help children andparents effectively and safely manage these diseases.

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