S. Humphrey, MD; J. N. Bergman, MD, FRCPC; S. Au, MD, FRCPC
Department of Dermatology and Skin Science, University of British Columbia,
Common diaper dermatitis is an irritant contact diaper dermatitis (IDD) created by the combined influence of moisture, warmth, urine, feces, friction, and secondary infection. It is difficult to completely eradicate these predisposing factors in a diapered child. Thus, IDD presents an ongoing therapeutic challenge for parents, family physicians, pediatricians, and dermatologists. This article will focus on practical management strategies for IDD.
diaper dermatitis, IDD
IDD is a common inflammatory eruption of the skin in the diaper area created by the presence of moisture, warmth, urine, feces, and friction, and is seen in 25% of children wearing diapers.1
Four key factors contribute to the development of IDD:2
- Wet diapers result in excessive hydration and maceration of the stratum corneum3 leading to impaired barrier function, enhanced epidermal penetration by irritants and microbes, and susceptibility to frictional trauma.4
- IDD is most commonly distributed in areas with the greatest skin-to-diaper contact.5
- Mechanical trauma disrupts the macerated stratum corneum, exacerbating barrier dysfunction.
Urine and feces
- Candida albicans (C. albicans) and, less commonly, Staphylococcus aureus (S. aureus) infections are associated with IDD.8
- The warm, humid, and high pH environment in the diaper provides the ideal milieu for microbial proliferation.
- Innate antimicrobial microflora cannot survive in a high pH environment.9
- There is a positive correlation between the clinical severity of IDD and the presence and level of C. albicans in the diaper, mouth, and anus of infants.8
- The interaction of urine and feces is key to the pathogenesis of IDD. Bacterial ureases in the stool degrade the urea that is found in urine, releasing ammonia and increasing local pH.6
- Fecal lipases and proteases are activated by the increased pH. They cause skin irritation and disruption of the epidermal barrier.7
- Ammonia does not irritate intact skin; it is thought to mediate irritation by contributing to the high local pH.6
IDD initially presents with localized asymptomatic erythema, and can progress to widespread painful, confluent erythema with maceration, erosions, and frank ulceration.10 IDD commonly spares the skin folds, and affects the convex skin surfaces in close contact with the diaper including the buttocks, genitalia, lower abdomen, and upper thighs. IDD complicated by Candida presents with beefy red intertriginous plaques and satellite papules and pustules in the diaper area. IDD complicated by S. aureus appears impetiginized, with erosions, honey-colored crust, and lymphadenopathy.
Granuloma gluteale infantum and Jacquet erosive diaper dermatitis are distinctive, severe variants of IDD. Granuloma gluteale infantum presents in the setting of IDD with violaceous papules and nodules on the buttocks and in the groin. The pathogenesis of granuloma gluteale infantum is not clear. Potential risk factors include treatment with topical steroids,11 candida infection, and occlusive plastic diaper covers.12 Granuloma gluteale infantum follows a self-limited course, resolving in weeks to months, often with residual scarring.5,11 The presence of punched-out erosions or ulcerations with heaped-up borders characterizes Jacquet erosive diaper dermatitis. This uncommon and severe presentation of IDD typically occurs in the context of frequent liquid stools, poor hygiene, infrequent diaper changes, or occlusive plastic diapers.12
|Granuloma gluteale infantum|
|Jacquet erosive diaper dermatitis|
|Allergic contact dermatitis|
|Langerhans cell histiocytosis|
|Table 1: Clinical features of diaper dermatoses.|
It is imperative to consider other conditions that may occur in the diaper area. Several excellent references are available that outline the differential diagnosis of IDD.5,13 Please see Table 1 for a review of the clinical features of relevant diaper dermatoses.
Fecal incontinence and diarrhea are risk factors for severe IDD because of prolonged and frequent skin contact with stool. Examples of at-risk children include those with Hirschsprung’s disease, fecal impaction and overflow, and anogenital malformations.14 Fecal proteases and lipases are also upregulated when gastrointestinal transit time is low.9 Increased bile acids in stool, seen in short gut syndrome and conjugated hyperbilirubinemia, also increase protease activity.12 Children with atopic dermatitis are prone to IDD because of their sensitivity to irritants and a greater susceptibility to secondary infection.
The continuous use of diapers is at the root of IDD. Maximizing “diaper-free” time is a widely recommended preventative strategy, but is not very practical. Frequent diaper changes are essential for maintaining dryness and keeping urine and feces separated. Diapers should be changed as soon as they are wet or soiled, at least every 3–4 hours and more frequently in the neonate due to increased skin fragility.15 Parents should forego tight-fitting diapers and consider a diaper slightly larger than the infant to minimize the contact between skin and urine or feces.5 Common IDD should resolve when children become toilet trained.
The advent of disposable diapers and the ongoing development of new diaper technology has radically changed the face of IDD. Early cellulose-core containing disposable diapers were dramatically improved by the addition of cross-linked sodium polyacrylate polymers to the diaper core.10,16,17 These polymers, also called absorbent gelling materials, bind water in a gel matrix when hydrated.16,17 This gel effectively traps moisture away from the skin surface. It controls pH through its buffering capacity, and by separating urine from feces.17 These diapers are referred to as superabsorbent diapers.16 In a study of 1,614 infants, superabsorbent diapers were associated with reduced skin wetness, superior
pH control, and less diaper dermatitis compared with cellulose-core disposable and cloth diapers.17 Originally, these diapers were developed with an impenetrable backsheet (outer cover) to prevent leaks, but this led to increased humidity and skin maceration. A “breathable” diaper was subsequently developed with a backsheet that is permeable to air and vapor but still impenetrable to leaks.16 This backsheet is readily identified by its cloth-like, rather than plastic, texture. The “breathable” superabsorbent diaper has been shown to reduce the prevalence of severe IDD by up to 50%.10 Nearly all commercially available disposable diapers in North America now use polyacrylate gel-core technology, and many use the breathable backsheet (e.g., Pampers®, Procter & Gamble; Huggies®, Kimberly-Clark). A novel diaper has recently been developed that transfers a petrolatum and zinc oxide-based formula to the child’s skin.18 In a double-blinded, randomized trial, infants using this diaper had consistently less skin erythema and diaper rash compared with those using a superabsorbent diaper alone over a 4-week period of use.1 Cloth diapers are not recommended for patients with IDD. They increase skin wetness, promote mixing of urine and feces, and are associated with Jacquet erosive diaper dermatitis.12
Application of a suitable barrier preparation is the cornerstone of prevention and treatment of IDD. There is a notable absence of controlled trials to support and guide the use of barrier preparations for IDD. Anecdotal evidence is abundant and suggests a barrier preparation should be applied to the diaper area after every diaper change and bath. A suitable barrier preparation should minimize transepidermal water loss (TEWL) and decrease permeability to irritants.9 The barrier corrects these deficits by forming a lipid barrier over the skin surface, or by penetrating the stratum corneum and assuming the role of endogenous intercellular lipids.5,19 The barrier also minimizes cutaneous friction. The barrier must be lipid-rich, long-lasting and adherent to the macerated and eroded diapered skin.
Pastes are the most hardy and desirable barriers, followed by ointments. Ointments are superior to creams and lotions, which are poorly adherent, minimally occlusive, and contain preservatives. Diaper pastes are tenacious semisolid compounds containing a high
proportion (usually >10%)9 of a fine powder such as zinc oxide, titanium dioxide, and starch or talc.20 Pastes should be applied thickly, like “icing on a cake”, and can be covered by petroleum jelly to avoid sticking to the diaper.14 Products containing fragrance, preservatives, and other ingredients with irritant or allergic potential should be avoided. Products containing boric acid, camphor, phenol, and salicylates should be avoided due to potential systemic toxicity.21 The local ostomy nurse may also be a valuable resource in identifying suitable barrier preparations in severe IDD.
Children predisposed to IDD should be bathed daily in a lukewarm bath using an irritant-free and fragrance free soap or cleanser followed by liberal application of a barrier preparation to the diaper area. The diaper area should be cleaned gently and dried by patting with a towel to avoid any undue friction. Aggressive wiping at diaper changes should be avoided. Residual adherent barrier paste does not need to be wiped off along with the urine and stool at each diaper change. Mineral oil can help facilitate paste removal, if required.5,14
It is a commonly held belief that baby wipes contribute to IDD; however an investigator-blinded, parallelcomparison study of 102 infants found no difference between skin cleaned with an alcohol-free, nonwoven disposable wipe, and skin cleaned with water and a cleanser.22 Moreover, skin cleaned with wipes had statistically better rash scores in the intertriginous areas, suggesting that wipes may help parents access hardto- reach areas. These wipes were found to be safe and well tolerated in infants with atopic dermatitis. Baby wipes can cause an allergic contact hand dermatitis in caregivers, in a “grip-like” distribution.23 It is prudent to choose wipes without fragrance and preservatives to avoid allergic sensitization.
Candida infection is often associated with moderatesevere cases of IDD. C. albicans is present in the mouth, inguinal and perianal skin more frequently in patients with IDD.8 The azoles, nystatin, and ciclopirox are all appropriate topical anticandidal agents,5,24 but few well-designed comparative trials are available to guide clinical practice. Twice-daily
application is recommended until resolution. In a National Ambulatory Medical Care Survey (NAMCS), more than 200,000 visits for diaper dermatitis in the US were reviewed; nystatin and clotrimazole were the most commonly prescribed topical antifungals (27% and 16% respectively).1 A prospective, randomized study compared topical nystatin with mupirocin in the treatment of IDD complicated by C. albicans infection. Treatment with both agents resulted in mycological cure; however, resolution of IDD was observed in all patients treated with mupirocin compared with only 30% treated with nystatin.25 Application of miconazole nitrate 0.25% in a zinc oxide and petrolatum base has demonstrated efficacy and safety in vehicle-controlled, randomized, double-blinded trials.26,27 In an open trial, ciclopirox 0.77% topical suspension demonstrated significant improvement in rash severity and superior mycological cure by 7 days in patients with IDD and C. albicans infection.28 There is little evidence to support the addition of an oral antifungal to topical therapy in IDD.29 Patients with concomitant oral thrush, however, may benefit from a course of systemic antifungal therapy.5
A short course of a mild topical corticosteroid is frequently necessary in moderate-to-severe IDD. Hydrocortisone 1% ointment can be applied to affected areas twice daily for a limited duration. Mid-to-high potency corticosteroids should never be used in the diaper area. The NAMCS documented a surprisingly high rate of moderate-to-high potency halogenated topical corticosteroid use in IDD. Triamcinolone acetonide or betamethasone dipropionate use, either alone or in combination with antifungals, was documented in a staggering 24.3% of visits for diaper dermatitis.1 Atrophy, systemic absorption, candidiasis, and granuloma gluteale infantum are all associated with mid-to-high potency corticosteroid use in the diaper area. The topical calcineurin inhibitors, tacrolimus and pimecrolimus, have not been studied for the treatment of IDD. These agents have been studied for efficacy and safety as a steroid-sparing treatment for atopic dermatitis in infants < 2 years old.30 Although they are not approved for use in this age group, they may be a useful off-label alternative for IDD in the appropriate clinical setting.
A number of other agents have been reported to be efficacious in the treatment of IDD. A recent pilot study found clinical and mycological benefits using a 1:1:1 mixture of honey: olive oil: beeswax to treat IDD.31 Eosin, an orange-red dye derived from coal tar, is a common agent used for IDD in Europe. It was found to have a greater rate of clearance of IDD within 5 days compared with zinc oxide and a moderate-potency topical corticosteroid ointment.32 In a randomized, vehicle-controlled study, topical vitamin A cream did not improve the outcome of IDD.33
IDD is a common dermatosis afflicting diapered children. It is caused by wetness, friction, urine, stool, and microorganisms. A proactive approach targeting predisposing factors is the best defence against IDD.
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- Atherton DJ. The aetiology and management of irritant diaper dermatitis. J Eur Acad Dermatol Venereol 15 Suppl 1:1-4 (2001).
- Willis I. The effects of prolonged water exposure on human skin. J Invest Dermatol 60(3):166-71 (1973 Mar).
- Zimmerer RE, Lawson KD, Calvert CJ. The effects of wearing diapers on skin. Pediatr Dermatol 3(2):95-101 (1986 Feb).
- Shin HT. Diaper dermatitis that does not quit. Dermatol Ther 18(2):124-35 (2005 Mar-Apr).
- Berg RW, Buckingham KW, Stewart RL. Etiologic factors in diaper dermatitis: the role of urine. Pediatr Dermatol 3(2):102-6 (1986 Feb).
- Andersen PH, Bucher AP, Saeed I, Lee PC, Davis JA, Maibach HI. Faecal enzymes: in vivo human skin irritation. Contact Dermatitis 30(3):152-8 (1994 Mar).
- Ferrazzini G, Kaiser RR, Hirsig Cheng SK, et al. Microbiological aspects of diaper dermatitis. Dermatology 206(2):136-41 (2003).
- Atherton DJ. A review of the pathophysiology, prevention and treatment of irritant diaper dermatitis. Curr Med Res Opin 20(5):645-9 (2004 May).
- Akin F, Spraker M, Aly R, Leyden J, Raynor W, Landin W. Effects of breathable disposable diapers: reduced prevalence of Candida and common diaper dermatitis. Pediatr Dermatol 18(4):282-90 (2001 Jul-Aug).
- Bluestein J, Furner BB, Phillips D. Granuloma gluteale infantum: case report and review of the literature. Pediatr Dermatol 7(3):196-8 (1990 Sep).
- Fiorillo L. Therapy of pediatric genital diseases. Dermatol Ther 17(1):117-28 (2004).
- Kazaks EL, Lane AT. Diaper dermatitis. Pediatr Clin North Am 47(4):909-19 (2000 Aug).
- Borkowski S. Diaper rash care and management. Pediatr Nurs 30(6):467-70 (2004 Nov-Dec).
- Lane AT, Rehder PA, Helm K. Evaluations of diapers containing absorbent gelling material with conventional disposable diapers in newborn infants. Am J Dis Child 144(3):315-8 (1990 Mar).
- Odio M, Friedlander SF. Diaper dermatitis and advances in diaper technology. Curr Opin Pediatr 12(4):342-6 (2000 Aug).
- Campbell RL, Seymour JL, Stone LC, Milligan MC. Clinical studies with disposable diapers containing absorbent gelling materials: evaluation of effects on infant skin condition. J Am Acad Dermatol 17(6):978-87 (1987 Dec).
- Baldwin S, Odio MR, Haines SL, O’Connor RJ, Englehart JS, Lane AT. Skin benefits from continuous topical administration of a zinc oxide/petrolatum formulation by a novel disposable diaper. J Eur Acad Dermatol Venereol 15 Suppl 1:5-11 (2001 Sep).
- Clark C, Hoare C. Making the most of emollients. Pharm J 266:227-229 (2001).
- Juch RD, Rufli T, Surber C. Pastes: what do they contain? How do they work? Dermatology 189(4):373-7 (1994).
- Farrington E. Diaper dermatitis. Pediatr Nurs 18(1):81-2 (1992 Jan-Feb).
- Ehretsmann C, Schaefer P, Adam R. Cutaneous tolerance of baby wipes by infants with atopic dermatitis, and comparison of the mildness of baby wipe and water in infant skin. J Eur Acad Dermatol Venereol 15 Suppl 1:16-21 (2001 Sep).
- Guin JD, Kincannon J, Church FL. Baby-wipe dermatitis: preservative-induced hand eczema in parents and persons using moist towelettes. Am J Contact Dermat 12(4):189-92 (2001 Dec).
- Gupta AK, Skinner AR. Management of diaper dermatitis. Int J Dermatol 43(11):830-4 (2004 Nov).
- de Wet PM, Rode H, van Dyk A, Millar AJ. Perianal
- candidosis—a comparative study with mupirocin and nystatin. Int J Dermatol 38(8):618-22 (1999 Aug).
- 26. Concannon P, Gisoldi E, Phillips S, Grossman R. Diaper dermatitis: a therapeutic dilemma. Results of a double-blind placebo controlled trial of miconazole nitrate 0.25%. Pediatr Dermatol 18(2):149-55 (2001 Mar-Apr).
- Spraker MK, Gisoldi EM, Siegfried EC, et al. Topical miconazole nitrate ointment in the treatment of diaper dermatitis complicated by candidiasis. Cutis 77(2):113-20 (2006 Feb).
- Gallup E, Plott T, Ciclopirox TS Investigators. A multicenter, open-label study to assess the safety and efficacy of ciclopirox topical suspension 0.77% in the treatment of diaper dermatitis due to Candida albicans. J Drugs Dermatol 4(1):29-34 (2005 Jan- Feb).
- Hoppe JE. Treatment of oropharyngeal candidiasis and candidal diaper dermatitis in neonates and infants: review and reappraisal. Pediatr Infect Dis J 16(9):885-94 (1997 Sep).
- Patel RR, Vander Straten MR, Korman NJ. The safety and efficacy of tacrolimus therapy in patients younger than 2 years with atopic dermatitis. Arch Dermatol 139(9):1184-6 (2003 Sep).
- Al-Waili NS. Clinical and mycological benefits of topical application of honey, olive oil and beeswax in diaper dermatitis. Clin Microbiol Infect 11(2):160- 3 (2005 Feb).
- Arad A, Mimouni D, Ben-Amitai D, Zeharia A, Mimouni M. Efficacy of topical application of eosin compared with zinc oxide paste and corticosteroid cream for diaper dermatitis. Dermatology 199(4):319-22 (1999).
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