Diaper Dermatitis: Etiology, Manifestations,Prevention, and Management

Georgios N. Stamatas, Ph.D.,* and Neena K. Tierney, Ph.D.

*Johnson & Johnson Sante Beaute France, Issy les Moulineaux, France, Johnson & Johnson Consumer CompaniesInc., Skillman, New Jersey

Abstract: Pediatricians and parents report diaper dermatitis (DD) to beone of the most common skin diseases that affects almost every child atsome point during the early months and years of life. Diapered skin isexposed to friction and excessive hydration, has a higher pH thannondiapered skin, and is repeatedly soiled with feces that containsenzymes with high irritation potential for the skin. The combination ofthese factors frequently results in skin damage, leading to visibleerythematous lesions that can be irritating and painful to the child.Behavioral changes such as increased crying and agitation and changesin eating and sleeping patterns indicate emotional distress. Appropriateskin care can help to prevent the occurrence of DD and to speed up thehealing of affected skin. This includes frequent diaper changes andaeration, gentle cleansing, and the use of a barrier cream. Mild tomoderate cases usually resolve after a few days of following this routine,but the use of harsh cleaning products can exacerbate DD.

MANIFESTATIONS AND ETIOLOGY OFDIAPER DERMATITIS

The predominant form of diaper dermatitis (DD) isirritant contact dermatitis, an inammation of theskin underneath the diaper manifested as erythema-tous dermatitis, which notably spares the inguinalfold. DD may worsen if left untreated and may recuruntil the infant stops wearing diapers (1). Areasaected are the buttocks, the perianal area, thegenitals, the inner thighs, and the waistline. In itsearly stages, DD appears as mild erythema in local-ized areas with minimal scaling. This may progress to

moderate erythema together with the appearance ofpapules aecting parts of the diapered area. This isfrequently associated with visible discomfort or pain(1). Severe cases exhibit papules, pustules, and skinerosion with open wounds. The severity of DD can beclinically evaluated using a scale such as the oneshown in Table 1 (2). Visual representation of DDseverity is also shown with the range of images inFig. 1AD. A common complication of DD is can-didiasis, which manifests with erythematous patches,plaques, and scales (3). For a precise diagnosis of DD,other types of dermatoses that can present witherythema and other lesions in the diaper area have

Address correspondence to Georgios N. Stamatas, Ph.D.,Johnson & Johnson Sante Beaute France, 1, rue Camille Desmo-ulins, 92787 Issy-les-Moulineaux, France, ore-mail: gstamata@its.jnj.com.

DOI: 10.1111/pde.12245

2013 Wiley Periodicals, Inc. 1

REVIEW

Pediatric Dermatology Vol. 31 No. 1 17, 2014

to be taken into consideration (e.g., intertrigo,seborrheic dermatitis, psoriasis) (3,4). Severe formsof DD require medical attention because they mayindicate a serious underlying condition, such asnutritional deciency, intestinal malabsorption syn-drome, congenital abnormalities of the urinary orlower gastrointestinal tract, or toxic reactions.

Reports on the frequency of DD show that themajority of children of both sexes are aected at somepoint in infancy (5,6). In recent studies, the percentageof children with DD at the time of evaluation rangedfrom 16% to 70% (5,7). The age of maximumfrequency reported in dierent studies varied, withpeaks at approximately 9 to 12 months (8,9) and 12 to24 months (5). Clinical signs of DD are absent at birthbut may appear as early as the rst month after birth(10). According to one study, by 4 weeks of age theincidence of DD was 25% (11). The incidence of DDin the general population may be underreportedbecause not all cases are brought to the attention ofa physician.

To understand the etiology of skin disorders,including DD, and to choose adequate preventive ortreatment measures, it is important to keep in mindthat infants have distinct skin physiology features thataect skin barrier function and water handlingproperties and that these continue to mature duringthe rst years of life (12). These include histologic,biochemical, and functional dierences, as well asdierences in the microbial population on the skin

(1317). Histologically, infant epidermis is made ofsmaller keratinocytes than those in adults, microreliefstructures are denser, the stratum corneum (SC) andthe epidermis are thinner, cell proliferation is greater,and collagen bers in the dermis are organizeddierently (17). The water handling properties ofinfant SC are also markedly dierent from those ofadults. Newborn skin is initially drier but subse-quently becomes more hydrated in older infants thanthe skin of adults. The concentration of the break-down products of laggrin proteolysis, collectivelyknown as natural moisturization factor (NMF), islower. A higher level of transepidermal water loss(TEWL) in some body areas of older infants, dierentwater-holding capacity, and a more alkaline pH areindicative of a developing skin barrier function (15).The composition of the skin microbiome is dierent,with infant skin being colonized primarily by Firmi-cutes, whereas adult skin is colonized primarily byActinobacteria (13).

Certain biophysical parameters of the diaperedarea of infants have site-specic dierences fromnondiapered regions, e.g., skin hydration is higher, asis the skin pH, and epidermal water handling prop-erties are dierent from those of nondiapered regions(18). Moreover, diapered areas with DD have higherTEWL rates, greater SC hydration, and higher pHthan healthy diapered skin (19). The microbial oracolonizing the skin surface in the buttocks area ofinfants is distinctly dierent from the microora in

TABLE 1. Clinical Evaluation Scale for Characterization of the Severity of DD

Score Degree Denition

0 None Skin is clear (may have some very slight dryness and/or a single papule but no erythema)0.5 Slight Faint to denite pink in a very small area (

other skin areas (13). In particular, bacteria that arenormally found in the gut are also present in thediaper area, which is explained by the skin coming infrequent contact with feces.

Figure 2 summarizes the factors involved in thepathophysiology of DD. DD occurs when prolongedexposure of the skin to factors that are characteristicof the diapered area, including excessive wetness,friction, high pH, and high enzymatic activity, com-promise the epidermal barrier function. The epider-mal barrier function resides in the outermostepidermal layer, the SC, which is the region ofterminal skin dierentiation and is composed ofcorneocytes (dierentiated keratinocytes) and anextracellular lipid matrix. Specialized proteins, thecorneodesmosomes, hold these cells, which containintracellular keratin laments with large water-hold-ing capacity that are linked to highly cross-linked,insoluble proteins of the cornied envelope (CE) thatsurrounds the corneocytes (20,21). On its exterior, theCE is linked to the lipid matrix that lls up theintercellular space. The hydrophobic components ofthe lipid matrix provide the epidermal permeabilitybarrier and protect against excessive water loss andirritant penetration, whereas the corneocytes and theCE provide mechanical strength to the SC. Water-soluble molecules of the NMF that are found insidethe corneocytes and are able to absorb water inuencethe water-holding capacity of the SC (22).

Central in the etiology of DD is excessive hydrationof the SC. Skin wetness and DD severity are corre-lated. Maceration of the SC increases susceptibility tofriction between the skin and the diaper fabric, whichcan cause physical damage to the SC and compromisethe epidermal barrier function (23). Furthermore,fecal ureases catalyze the breakdown of urea toammonia (24), which increases the pH of the skinsurface (18,23). This increase in pH contributes to theactivity of fecal enzymes, proteases, ureases, andlipases (23), which are highly irritating to the skin (25),

as the development of severe skin erythema andepidermal barrier breakdown under occlusive expo-sure of skin to fecal digestive enzymes demonstrates(26). These enzymes increase the permeability to bilesalts and other potential irritants (25). In turn, bilesalts potentiate the irritant activity of fecal enzymes(25). The reportedly benecial role of breastfeeding inthe prevention of DD (8,9) may be linked to the lowerirritation potential of the feces of exclusively breastfedbabies, which has a signicantly lower pH, lowerprotease and lipase activity, and lower urease contentthan that of formula-fed babies (23). The correlationbetween the number of bowel movements and thefrequency of DD supports the damaging role of feceson skin (8). Diarrhea is also a risk factor for DD (5),which may be due to the higher concentration ofresidual digestive enzymes related to shorter transittimes (27). Microorganisms present in the feces of theinfant can gain access through the damaged SC,leading to more severe DD with secondary infection.The most frequently isolated microbial species frominfected DD areas are Candida albicans (28) andStaphylococcus aureus (29).

Diaper dermatitis causes emotional stress forinfants, as indicated in a study on infant behaviorduring and after an episode of DD (unpublisheddata). Parents reported an increase in the frequency ofcrying as the rst symptom of pain together withagitation. Other behavioral indicators of distress, suchas facial expressions (eyes squeezed shut, deepening ofthe nasolabial furrow), were more prevalent, normaleating habits and sleeping patterns were disrupted,and the frequency of urination and defecation dimin-ished. Levels of salivary cortisol, a molecular indica-tor of stress (30), also increased in some infants duringthe period with DD.

PREVENTION AND MANAGEMENT

A number of good reviews have been published toaddress optimal management strategies and treatmentalgorithms for DD (4,3133). In this section we willreview common practices and present new data on theecacy of routines relating to DD prevention andtreatment.

The key to DD treatment lies in its prevention (33).The most eective routine to prevent DD involvesfrequent diaper changes to reduce exposure to urineand feces under occlusion. Exposure of the buttocksto air for as long as possible reduces the duration ofdirect contact of the skin with the wet fabric surfaceand reduces friction. A fresh diaper should be put onafter each urination or defecation. For newborns with

Figure 2. Physical and biochemical factors involved inthe pathophysiology of DD.

Stamatas and Tierney: Diaper Dermatitis 3

a high wetting frequency, this means a diaper changeideally approximately every 2 hours during the day,whereas for older infants, every 34 hours should besucient (34).

To help reduce the risk of DD onset or furtherdegradation, if the skin barrier is already compro-mised, aggressive approaches such as the use of harshcleansers and scrubbing of the delicate skin should beavoided. Routine bathing of infants should beperformed with warm water (37C40C) and asmall amount of a mild (nonirritating) cleanser withslightly acidic to neutral pH that respects the acidmantle of the skin (35,36). Traditional soaps withtheir alkaline pH are too harsh, increasing the skinpH and reducing the epidermal fat content (37,38).By comparison, synthetic cleansers aect the skin pHto a lesser degree and provoke less lipid depletion,less erythema, and a lower TEWL rate (38,39).Clinical studies on routine bathing in infants haveshown that neither water alone nor the addition of amild cleanser causes any physiologically aberrantchanges in skin barrier function (TEWL, hydration,pH), skin condition (erythema, dryness, scaling), ormicrobial colonization (4042), but water alone maynot be sucient for the removal of feces because ofits fat content. Instead, water should be combinedwith a gentle cleanser (3). Cleansing with appropri-ately formulated diaper wipes is also an option (35).Evidence from one large assessor-blinded, random-ized clinical trial (43) and another double-blind study(44) suggests that appropriately formulated wipes aresafe for use on infant skin in the diaper area.Fragrance-free baby wipes impregnated with a mildsurfactant system (Johnsons Baby; Johnson &Johnson Ltd., Maidenhead, UK) have been shownto have an eect on skin hydration equivalent to thatof cotton wool and water, and they did not adverselyaect infant skin (43). Moreover, it has beensuggested that alcohol-free and fragrance-free wipesformulated with emollient cleansers and acidic pHprotect the barrier function better than washing witha cloth and water alone (45). In cases in which theskin is severely damaged, gently patting dry ratherthan rubbing is advised.

Application of barrier creams or ointments at eachdiaper change is recommended as an additionalprotective or preventive measure and for the treat-ment of mild to moderate DD. They form a lipid lmon the skin surface and protect it from contact withmoisture and irritants. Most products contain zincoxide (ZnO), petrolatum (petroleum jelly), or both asactive ingredients. Underneath this protective lm,injured skin is allowed to heal and is protected from

contact with urine and feces and irritation. Duringdiaper changes, complete removal of the barrier creamor ointment is not necessary to prevent additionalinjury to the skin; the skin in the diaper area should begently patted, not rubbed. A benecial eect may alsobe associated with reduced skin hydration afterapplication of a barrier cream (46). Other ingredientsin use are cod liver oil, aloe barbadensis, dimethicone,and dexpanthenol (47). In some European countries,application of an aqueous solution of 2% eosin afterdiaper changes is used for DD treatment (48). Thelack of barrier cream use and a low frequency ofdiaper changes are among the factors associated withrecurrent DD (5,8).

The ecacy of ZnO- or petrolatum-based creams,pastes, and ointments has been demonstrated intreating diaper rash (27,35,49). In an evaluator-blinded, randomized study, 112 diaper-wearinginfants ages 2 to 36 months with mild to moderateDD (diaper rash severity score 1.5 or greater) wererandomized to receive one of two ZnO-containingtopical products in a petrolatum base (DES13 with13% ZnO and DES40 with 40% ZnO; Desitin,Johnson & Johnson Consumer Products, Skillman,NJ) at each diaper change and after bathing (2). Theywere evaluated after 12 and 24 hours of treatmentapplication by a trained evaluator. The data for the111 evaluable infants showed clinically signicantimprovement of DD at both time points in all veassessed anatomic areas (buttocks, abdomen, sacrum,inner thighs, and anogenital area). The global meanDD score attributed to the two treatment groupsdecreased signicantly from 1.7 at baseline (bothtreatment groups) to 1.1 and 1.0, respectively, at12 hours and to 0.9 (both treatment groups) at24 hours. In parallel, the parents of the evaluatedinfants conrmed alleviation of the DD symptomsand reported signicant improvement in 79% and96% of the cases, respectively, at 12 hours and in 84%and 87%, respectively, at 24 hours. ZnO-based top-ical products have also been shown to provide rapidimprovement in the signs of diaper rash, such aserythema, which can be comforting to parents ofbabies with DD (observations by NKT). In a double-blinded clinical study, 60 diaper-wearing infants (ages336 months) with mild to moderate DD (overalldiaper rash severity score 0.52.0) were randomized toreceive one of two ZnO-containing products (DES13and DES40) and were asked to apply one applicationof the test product to the diaper area and to rediapertheir infant. After 3 hours (1 hour), the test productwas gently removed and a trained evaluator and theparent reevaluated the diaper area. The data showed

4 Pediatric Dermatology Vol. 31 No. 1 January/February 2014

clinically signicant improvement in erythema afterone application, evaluated on a visual scale (Fig. 1).The erythema score decreased by 20% (p < 0.001),from 1.61 (treatment 1) and 1.93 (treatment 2) atbaseline to 1.29 and 1.55, respectively, at 3 hours. Theparents of the evaluated infants conrmed theimprovement in erythema and reported signicantimprovement in 64% (treatment 1) and 65% (treat-ment 2) of cases.

ZnO- or petrolatum-based diapering productsexert their protective and preventive propertiesthrough the formation of a suitable protective lmon the skin surface. In a study conducted on 36adults, the overnight use of two ZnO-containingtopical products (DES13 and DES40) prevented thepenetration of a dye into the treated skin (unpub-lished data). The 36 participants received one testproduct on one site on one arm and the other testproduct on one site on the other arm through randomassignment, whereas one site on each arm served asan untreated control. The treated areas were imme-diately covered with mini-diapers for 12 hours over-night. All four areas were then exposed to stainingwith crystal violet and the extent of staining wascompared with that of an unstained area using acolorimetric technique. The results showed markedstaining of the untreated areas, whereas the areastreated with either of the two test products com-pletely protected the skin from the applied stain.Similarly, when skin barrier function was measuredusing in vivo Raman microspectroscopy, skin treat-ment using a ZnO-containing barrier cream (DES13)blocked externally applied caeine penetration,unlike the untreated control (49). These resultsconrm the protective action of ZnO against thepenetration of skin irritants. Petrolatum-based prod-ucts also have the ability to prevent skin macerationand irritant penetration (50). The ability of petrola-tum to penetrate deep into the SC (~30 m), where itincreases the lipid content and provides skin occlu-sion, as indicated by greater SC thickness in adultsand infants, probably explains this (51).

Finally, diaper rash formulations have been shownto be well tolerated in the diaper area, with no adverseevents reported with their use. This was demonstratedin the infant study mentioned above regarding treat-ment with two ZnO-containing products for 24 hours(2). Similar tolerability was observed in a double-blind study conducted on 72 diaper-wearing 3- to 24-month-old infants with healthy skin (group 1) orslight (diaper rash severity score of 0.5) to mild tomoderate (diaper rash severity score of 1.5) DD(group 2) who were treated using a ZnO-containing

product (DES13) under normal use conditions for4 weeks, with 65 participants completing the study(unpublished data).

Diaper dermatitis can be successfully treated usingthe measures outlined above. If conventional mea-sures fail for moderate to severe cases, topicalcorticosteroids and topical antifungal medicationsmay be prescribed for treatment and applied under thebarrier cream. Nystatin, clotrimazole, and ketoconaz-ole are frequently prescribed antifungal drugs tocontrol fungal growth when candidal infection issuspected, especially in DD that lasts for longer than afew days, and mild topical corticosteroids such ashydrocortisone are used to reduce inammation (6).Creams containing mid- and high-potency corticos-teroids in combination with antifungal treatment(nystatintriamcinolone, clotrimazolebetamethasonedipropionate) are among those most frequently pre-scribed by pediatricians for the treatment of DD in theUnited States (6), but they are not considered appro-priate for mild to moderate DD treatment and shouldbe avoided to prevent possible side eects (52). If asecondary infection involving bacteria is expected,topical antibiotics may be considered (3).

CONCLUSION

In summary, DD is a common skin condition fornewborn and young infants. The diaper occlusioncreates an environment conducive to skin irritationbeginning with damage to the skin barrier caused bycomponents of urine and feces. Supporting the skinbarrier with barrier creams coupled with frequentdiaper changes is an eective preventive strategy.

ACKNOWLEDGMENTS

The authors would like to thank Dr. Beate Gerstbreinof Ascopharm (Paris, France) for editorial assistance.

CONFLICT OF INTEREST

The authors are employees of Johnson & JohnsonFamily of Consumer Companies.

REFERENCES

1. Berg RW. Etiology and pathophysiology of diaperdermatitis. Adv Dermatol 1988;3:7598.

2. Brown WM, Berg JE, Li Q et al. A clinical study toevaluate the ecacy of two marketed zinc oxide-baseddiaper rash ointments in children with diaper dermati-tis. Clinical Dermatology Conference. Las Vegas, NV,2006.

Stamatas and Tierney: Diaper Dermatitis 5

3. Shin HT. Diaper dermatitis that does not quit. Derma-tol Ther 2005;18:124135.

4. Boiko S. Treatment of diaper dermatitis. Dermatol Clin1999;17:235240.

5. Adalat S, Wall D, Goodyear H. Diaper dermatitisfrequency and contributory factors in hospital attend-ing children. Pediatr Dermatol 2007;24:483488.

6. Ward DB, Fleischer AB Jr, Feldman SR et al. Charac-terization of diaper dermatitis in the United States.Arch Pediatr Adolesc Med 2000;154:943946.

7. Liu N, Wang X, Odio M. Frequency and severity ofdiaper dermatitis with use of traditional Chinese clothdiapers: observations in 3- to 9-month-old children.Pediatr Dermatol 2011;28:380386.

8. Jordan WE, Lawson KD, Berg RW et al. Diaperdermatitis: frequency and severity among a generalinfant population. Pediatr Dermatol 1986;3:198207.

9. Benjamin L. Clinical correlates with diaper dermatitis.Pediatrician 1987;14(Suppl 1):2126.

10. Visscher MO, Chatterjee R, Munson KA et al. Devel-opment of diaper rash in the newborn. Pediatr Derma-tol 2000;17:5257.

11. Philipp R, Hughes A, Golding J. Getting to the bottomof nappy rash. ALSPAC Survey Team. Avon Longitu-dinal Study of Pregnancy and Childhood. Br J GenPract 1997;47:493497.

12. Stamatas GN, Nikolovski J, Mack MC et al. Infantskin physiology and development during the rst yearsof life: a review of recent ndings based on in vivostudies. Int J Cosmet Sci 2011;33:1724.

13. Capone KA, Dowd SE, Stamatas GN et al. Diversity ofthe human skin microbiome early in life. J InvestDermatol 2011;131:20262032.

14. Giusti F, Martella A, Bertoni L et al. Skin barrier,hydration, and pH of the skin of infants under 2 yearsof age. Pediatr Dermatol 2001;18:9396.

15. Nikolovski J, Stamatas GN, Kollias N et al. Barrierfunction and water-holding and transport properties ofinfant stratum corneum are dierent from adult andcontinue to develop through the rst year of life.J Invest Dermatol 2008;128:17281736.

16. Saijo S, Tagami H. Dry skin of newborn infants:functional analysis of the stratum corneum. PediatrDermatol 1991;8:155159.

17. Stamatas GN, Nikolovski J, Luedtke MA et al. Infantskin microstructure assessed in vivo diers from adultskin in organization and at the cellular level. PediatrDermatol 2010;27:125131.

18. Visscher MO, Chatterjee R, Munson KA et al. Changesin diapered and nondiapered infant skin over the rstmonth of life. Pediatr Dermatol 2000;17:4551.

19. Stamatas GN, Zerweck C, Grove G et al. Documenta-tion of impaired epidermal barrier in mild and moderatediaper dermatitis in vivo using noninvasive methods.Pediatr Dermatol 2011;28:99107.

20. Elias PM, Menon GK. Structural and lipid biochemicalcorrelates of the epidermal permeability barrier. AdvLipid Res 1991;24:126.

21. Madison KC. Barrier function of the skin: la raisondetre of the epidermis. J Invest Dermatol 2003;121:231241.

22. Rawlings AV, Harding CR. Moisturization and skinbarrier function.DermatolTher2004;17(Suppl1):4348.

23. Berg RW, Buckingham KW, Stewart RL. Etiologicfactors in diaper dermatitis: the role of urine. PediatrDermatol 1986;3:102106.

24. Cooke JV. The etiology and treatment of ammoniadermatitis of the gluteal region of infants. Am J DisChild 1921;22:481492.

25. Buckingham KW, Berg RW. Etiologic factors in diaperdermatitis: the role of feces. Pediatr Dermatol1986;3:107112.

26. Andersen PH, Bucher AP, Saeed I et al. Faecalenzymes: in vivo human skin irritation. Contact Der-matitis 1994;30:152158.

27. Atherton DJ. The aetiology and management of irritantdiaper dermatitis. J Eur Acad Dermatol Venereol2001;15(Suppl 1):14.

28. Ferrazzini G, Kaiser RR, Hirsig Cheng SK et al.Microbiological aspects of diaper dermatitis. Derma-tology 2003;206:136141.

29. Brook I. Microbiology of secondarily infected diaperdermatitis. Int J Dermatol 1992;31:700702.

30. Schmidt NA. Salivary cortisol testing in children. IssuesCompr Pediatr Nurs 1998;20:183190.

31. Boiko S. Diapers and diaper rashes. Dermatol Nurs1997;9:3339.

32. Friedlander SF, Eicheneld LF, Leyden J et al. Diaperdermatitis: appropriate evaluation and optimal manage-ment strategies. Contemp Pediatr 2009;April(Suppl).

33. Heimall LM, Storey B, Stellar JJ et al. Beginning at thebottom: evidence-based care of diaper dermatitis. MCNAm J Matern Child Nurs 2012;37:1016.

34. Wolf R, Wolf D, Tuzun B et al. Diaper dermatitis. ClinDermatol 2000;18:657660.

35. LundCH,KullerJ,RainesDAet al.Neonatalskincareevidence-based clinical practice guideline, 2nd ed.Wash-ington, DC: Association of Womens Health, Obstetricand Neonatal Nurses and the National Association ofNeonatal Nurses, 2007.

36. Blume-Peytavi U, Cork MJ, Faergemann J et al.Bathing and cleansing in newborns from day 1 to rstyear of life: recommendations from a European roundtable meeting. J Eur Acad Dermatol Venereol2009;23:751759.

37. Gelmetti C. Skin cleansing in children. J Eur AcadDermatol Venereol 2001;15(Suppl 1):1215.

38. Gfatter R, Hackl P, Braun F. Eects of soap anddetergents on skin surface pH, stratum corneumhydration and fat content in infants. Dermatology1997;195:258262.

39. Strube DD, Koontz SW, Murahata RI et al. The exwash test: a method for evaluating the mildness ofpersonal washing products. J Soc Cosmet Chem1989;40:297306.

40. Dizon MV, Galzote C, Estanislao R et al. Tolerance ofbaby cleansers in infants: a randomized controlled trial.Indian Pediatr 2010;47:959963.

41. Garcia Bartels N, Scheufele R, Prosch F et al. Eect ofstandardized skin care regimens on neonatal skinbarrier function in dierent body areas. PediatrDermatol 2010;27:18.

42. Lavender T, Bedwell C, OBrien E et al. Infant skin-cleansing product versus water: a pilot randomized,assessor-blinded controlled trial. BMC Pediatr 2011;11:35.

6 Pediatric Dermatology Vol. 31 No. 1 January/February 2014

43. Lavender T, Furber C, Campbell M et al. Eect on skinhydration of using baby wipes to clean the napkin areaof newborn babies: assessor-blinded randomised con-trolled equivalence trial. BMC Pediatr 2012;12:59.

44. Ehretsmann C, Schaefer P, Adam R. Cutaneous toler-ance of baby wipes by infants with atopic dermatitis,and comparison of the mildness of baby wipe and waterin infant skin. J Eur Acad Dermatol Venereol 2001;15(Suppl 1):1621.

45. Visscher M, Odio M, Taylor T et al. Skin care in theNICU patient: eects of wipes versus cloth and wateron stratum corneum integrity. Neonatology 2009;96:226234.

46. Xhauaire-Uhoda E, Henry F, Pierard-Franchimont Cet al. Electrometric assessment of the eect of a zincoxide paste in diaper dermatitis. Int J Cosmet Sci2009;31:369374.

47. Adam R. Skin care of the diaper area. Pediatr Dermatol2008;25:427433.

48. Arad A, Mimouni D, Ben-Amitai D et al. Ecacy oftopical application of eosin compared with zinc oxide

paste and corticosteroid cream for diaper dermatitis.Dermatology 1999;199:319322.

49. Stamatas GN, Boireau-Adamezy E. Development of anon-invasive optical method for assessment of skinbarrier to external penetration. In: Biomedical Opticsand 3-D Imaging. OSA Technical Digest, paperJM3A.42. Miami, FL: Optical Society of America,2012.

50. Hoggarth A, Waring M, Alexander J et al. A con-trolled, three-part trial to investigate the barrierfunction and skin hydration properties of six skinprotectants. Ostomy Wound Manage 2005;51:3042.

51. Stamatas GN, de Sterke J, HauserM et al. Lipid uptakeand skin occlusion following topical application of oilson adult and infant skin. J Dermatol Sci 2008;50:135142.

52. Railan D, Wilson JK, Feldman SR et al. Pediatricianswho prescribe clotrimazole-betamethasone dipropio-nate (Lotrisone) often utilize it in inappropriate settingsregardless of their knowledge of the drugs potency.Dermatol Online J 2002;8:3.

Stamatas and Tierney: Diaper Dermatitis 7