Are You Confident of the Diagnosis?

What you should be alert for in the patient’s history


  • –Disposable diapers: cellulose-core diapers, absorbent gelling material (AGM) diapers (extra-absorbent)—prevent irritant-based diaper dermatitis by reducing wetness

  • –Dye vs dye-free diapers: Patients may experience allergic contact dermatitis from the dyes within the diaper.

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  • –Cloth diapers consist of cotton weave and may not wick away moisture as well as disposable diapers.

  • –Weather: Hot weather can contribute to intertrigo.

  • –Infant being overdressed—can contribute to intertrigo.

  • –Recent antibiotic use—can increase Candida colonization.

Dermatitis with

–Painful or difficult urination (could indicate a Jacquet’s dermatitis)

–Perianal pseudoverrucous papules and nodules (can correlate with a history of Hirschsprung disease, encopresis, or urinary incontinence)

–Diarrhea, failure to thrive, alopecia (consistent with acrodermatitis enteropathica)

–Lymphadenopathy, anemia, hepatosplenomegaly (suggests Langerhans cell histiocytosis)

–Fever, pustular drainage, lymphangitis (consider bacterial diaper dermatitis)

Differential diagnosis and characteristic findings on physical examination

Chafing dermatitis: mild erythema and scaling that comes and goes, appearing in areas of friction, i.e. abdomen, inner thighs, buttocks, and genitalia (Figure 1).

Figure 1.

Chafing dermatitis with secondary contact dermatitis

Atopic Dermatitis (AD): erythematous, scaly papules and plaques, often pruritic and excoriated. Thickening, hyperpigmentation, and lichenification can be observed with a chronic course.

Irritant contact dermatitis (ICD): erythema and scaling of the diaper region; a key to diagnosis is that ICD routinely spares the intertriginous creases (Figure 2).

Figure 2.

Irritant contact dermatitis

Allergic contact dermatitis (ACD): eczematous-like eruption often with geometric patterns consistent with distribution of the contactant, but often spreads beyond. It may also include the creases.

Diaper candidiasis: “beefy” red erythema with a raised, white scaly, sharply demarcated edge. The diagnostic hallmark is the presence of satellite lesions, both pustules and vesicles. Oral thrush may also be present (Figure 3).

Figure 3.

Diaper candidiasis

Seborrheic dermatitis: yellowish, scaly, greasy plaques, which tends to involve the intertriginous creases and may also be found on the scalp, face and neck.

Psoriasis: persistent erythematous, well-demarcated plaques with dry, silvery scale that often spares the diaper area and is most commonly found elsewhere on the body, such as the scalp. It may be accompanied by nail changes, and scale may be revealed with gentle scraping on the skin. Family history is also a helpful clue (Figure 4).

Figure 4.


Intertrigo: bright red erythema with a potential overlying white to yellow exudate that has a predilection for creases, such as inguinal region and thigh, as well as the intergluteal cleft. The anterior neck fold and axillae may also be affected.

Jacquet’s dermatitis (dermatitis syphiloids posterosiva): ulcerated papules and nodules that can affect the glans penis and urinary meatus in males and can be present in females as well.

Perianal pseudoverrucous papules and nodules: may also occur in the suprapubic region.

Perianal streptococcal dermatitis: pruritic, sharply demarcated erythema and edema of perianal region, sometimes also involving the vulva, vagina, or penis.

Acrodermatitis enteropathica: erythematous pustular or erosive dermatitis appearing in intertriginous and/or acral sites and may appear in a periorificial pattern that can include the perioral face.

Bacterial dermatitis: edema, erythema, tenderness to palpation, and possible purulent drainage.

Langerhans cell histiocytosis (LCH): yellowish to red-brown papules with possible erosion or purpura and severe hemorrhage, unresponsive to any treatment. It is important to look for additional areas of involvement, such as the scalp and retroauricular areas; the infant may also clinically have diarrhea. This disease can be fatal.

Granuloma gluteale infantum: purple-red nodules located on the lower abdomen, groin, and inner thighs that can resolve spontaneously after a few months.

Scabies: acute onset of pruritic, often excoriated, erythematous serpiginous papules, vesicles, and/or burrows that favor the intertriginous regions, ie, inguinal folds, axillae, and web spaces. Infants may display acropustulosis (palms and soles) and scalp involvement as well.

Miliaria: pruritic, discrete, erythematous papules, vesicles, or pustules found in the diaper distribution, but also may be present on the face, neck, and axillae.

Syphilis: reddish-brown papules present in the diaper area, with possible desquamation of palms and soles, appearing symmetrically.

Expected results of diagnostic studies

–Allergic contact dermatitis (ACD)

Comprehensive patch testing is also employed as a diagnostic tool when suspected allergens are not included on the T.R.U.E. test. Furthermore, the diaper itself, as well as the creams, salves, and powders used in the afflicted area can themselves be tested to discern whether they contain a potential contact allergen to which the infant reacts.

–Diaper candidiasis: Potassium hydroxide microscopic examination of skin scrapings: egg-shaped budding yeast with pseudohyphae. Sabouraud’s medium with skin scrapings: growth of yeast 48 to 72 hours.

–Acrodermatitis enteropathica: zinc level less than 50mcg/dL.

–Impetigo/bacterial dermatitis (severe or recalcitrant): bacterial Gram stain/culture from vesicular fluid or purulent drainage and sensitivity. Complete blood count (CBC): white blood cell elevation could indicate a bacterial infection in the presence of a fever.

–Langerhans cell histiocytosis: skin biopsy with hematoxylin-eosin stain will show a pink granular cytoplasm within the Langerhans cells, which on electron microscopy reveals Birbeck granules (which are tennis racket and rod-shaped). Immunoperoxidase studies positive for S-100 and CD1a have supplanted electron microscopy in diagnosis confirmation. Anemia in conjunction with hepatosplenomegaly may suggest Langerhans cell histiocytosis or congenital syphilis.

–Congenital syphilis: serology includes initial nontreponemal tests, such as venereal disease research laboratory (VDRL) and rapid plasma reagin (RPR), and confirmation with treponemal tests, such as treponemal pallidum particle agglutination (TPHA) or fluorescent treponemal antibody absorption test (FTA-Abs). Dark field microscopy may also show the presence of spirochetes.

–Granuloma gluteale infantum: skin biopsy showing a histologic dermal infiltration of neutrophils, lymphocytes, histiocytes, plasma cells, eosinophils, and occasional giant cells. Electron microscopy shows three different types of giant cells: those that can mimic histiocytes with vesicles and granules, those with large endoplasmic reticulum, and those that phagocytize erythrocytes.

–Scabies: Mineral oil preparation of scraping from a burrow showing mites, ova, or feces.

–Perianal streptococcal dermatitis: swab the skin for bacterial culture

Patch testing is the gold standard for diagnosis. A positive reaction is indicated by erythema, induration, papules, or vesicles at the site of the patch test application. Notably, flare-reactions can occur at previous sites of involvement. The Thin-layer Rapid Use Epicutaneous (T.R.U.E.) Test (Mekos Laboratories ApS, Hillerod, Denmark) is a commercially available, convenient, pre-made, FDA- approved patch test, consisting of 3 panels of allergens containing a total of 29 chambers, one being a negative control. This test contains some of the allergens frequently associated with diaper dermatitis, indicated below.

Who is at Risk for Developing this Disease?

Diaper dermatitis occurs regularly, but its severity and overall incidence has declined, estimated between 7% and 35% and peaking at 9 to 12 months of age.

The infant’s anatomy can place them at higher risk, as many folds and creases in the diaper distribution can create a problem due to difficulty cleansing and a moist environment.

What is the Cause of the Disease?
  • –Chafing dermatitis: due to friction, often in the presence of urine and feces.

  • –Atopic dermatitis (AD): due to intrinsic defects in the epidermal barrier function, leading to a TH2 immune response and subsequent inability to retain moisture and protect against the pathogens and allergens.

  • –Irritant contact dermatitis (ICD) is a non-immunologic reaction that is the most common form of contact dermatitis. Risk factors include prolonged exposure to urine or feces, skin wetness, and biochemical irritants.

  • –Allergic contact dermatitis (ACD): an immunologic reaction that is the second most common form of contact dermatitis. Potential allergens include diaper constituents as well as topical personal care products/medicaments used in the diaper distribution. Moreover, the risk of sensitization to these allergens is increased due to the wet, occluded environment created with diaper use. Reported allergen sources include:

    Disperse dyes: used on synthetic fabrics, and are easily leached out onto skin when exposed to moisture and friction. Sensitization has been reported to disperse red 1/17, disperse blue 106/124, and disperse orange.

    Fragrances: fragrance mix 1* and balsam of Peru* have also been associated with ACD, as they are used in the diapers to impart pleasant scents and are in some creams and salves to treat and prevent diaper dermatitis (A&D, Vaseline baby, and butt balm).

    Emulsifier: sorbitan sesquioleate is included in many topical creams and some ointments, including medicaments.

    Preservatives: iodopropynyl carbamate and bronopol are used in baby wipes and have been reportedly associated with diaper dermatitis as well.

*Included on the T.R.U.E. Test

  • –Diaper candidiasis: the primary source is infected feces along with alterations in skin microbial flora and skin pH, often developing during or shortly after antibiotics.

  • –Intertrigo: due to friction, heat, and moisture. Superinfection with bacteria, Candida or viruses may be also be present.

  • –Perianal streptococcal dermatitis: caused by group A beta-hemolytic streptococcal bacteria.


–Chafing dermatitis: due to friction, often in the presence of urine and feces, which can cause maceration of the stratum corneum and alter the skin’s pH. The pH of normal skin ranges from ~4.5 to 6.0, closer to 6.0 at birth, but the pH of atopic skin is reportedly higher. Given the barrier defects associated with atopic dermatitis and the increased pH values noted, it has been suggested that pH may have a role in lipid turnover and barrier function. An instance of pH being indirectly involved with impairment of the skin’s barrier is when pH is increased due to the formation of ammonia upon exposing feces to ureases in urine.

The elevated pH can activate proteases and lipases within feces, placing the stratum corneum at risk for damage. Defects in the stratum corneum can also result from increased skin hydration, as the observed higher coefficient of friction causes more susceptibility to mechanical chafing. Once the skin’s natural barrier has been damaged, irritants can more easily penetrate the epidermis. The pH of personal hygiene products, such as cleansing products, can alter the skin’s flora. In addition, soaps with high pH can contribute to growth of propionibacteria.

–Irritant contact dermatitis (ICD): secondary to contact with an irritating substance, such as urine, feces, balms, and often enhanced by certain conditions, such as prolonged exposure or high concentration, sensitive skin, and increased moisture.

–Allergic contact dermatitis (ACD): secondary to a delayed type IV hypersensitivity reaction, generally occurring between 48 and 96 hours. Defects in the epidermis allow for allergen entry and subsequent processing by dendritic cells, which then present them to naïve T-cells. This phase is called sensitization, and ends with clonal expansion of memory T-cells. After repeated exposure to a particular allergen, the second phase of ACD (elicitation) occurs.

–Diaper candidiasis: the primary source is infected feces, as C albicans resides in the lower intestines of infants. Alterations in skin microbial flora and skin pH can also contribute to diaper dermatitis caused by infections, such as C albicans.

–Psoriasis: may occur in this region due to the Koebner phenomenon, meaning that the friction from the diaper rubbing against the skin, often in a damp environment, can induce expression of the underlying condition.

–Intertrigo: friction, heat, and moisture can cause maceration and predispose to infection with bacteria or candida.

–Miliaria: prolonged exposure of the stratum corneum to moisture can cause edema and subsequent obstruction of the eccrine sweat glands.

–Perianal pseudoverrucous papules and nodules: may be a reaction to severe, chronic ICD.

–Acrodermatitis enteropathica: due to zinc deficiency.

–Granuloma gluteale infantum: may be a response to inflammation, maceration, and possibly superimposed infection.

Systemic Implications and Complications

Secondary Infection

Impetigo: diaper dermatitis can predispose an infant to developing this superficial skin infection, marked by vesicles that contain cloudy yellow fluid that when dry, form honey-colored crusts. This often occurs in the first 6 months of life and follows a seasonal (summer) pattern. Either staphylococci or less commonly, streptococci are usually the causative bacteria in this condition, with the perineum being an important reservoir for staphylococci. Enterobacteriaceae bacteria and anaerobes can also be involved in impetigo. It can lead to both fever and lymphadenopathy, with more severe sequelae being sepsis and osteomyelitis. Cultures of the vesicular fluid may be obtained but are not necessary in all cases, before topical or systemic antibiotics are started.

Diaper candidiasis: infants can also be predisposed to secondary infection by C albicans.

Treatment Options

Identify the etiology for the diaper dermatitis



–Zinc oxide (barrier)

–Petrolatum preparations (barrier)


–Antibiotics (severe impetigo):

Macrolides: erythromycin

Penicillinase-resistant penicillins: cloxacillin, dicloxacillin

Amoxicillin and clavulanic acid

Cephalosporins: first or second generation


–Antifungal preparations (C albicans): nystatin, fluconazole, clotrimazole, miconazole, ketoconazole

Surgical options: not applicable.

Physical modalities

–Frequent diaper changes (to avoid chafing and irritant contact dermatitis)

–Disposable diapers (to prevent ICD or Candida albicans)

–Diapers containing petrolatum (to prevent ICD)

–pH buffered disposable baby wipes

–Syndets (synthetic detergents)

–Dye-free diapers (to avoid ACD to dyes)

–Fragrance-free products (to avoid ACD to fragrance)

–Cloth (cotton) diapers (to avoid ACD to rubber accelerators, such as mercaptobenzothiazole, or to the adhesive, p-tert-butyl phenol formaldehyde resin)

–Lipid ointments contain lanolin (Aquaphor) or ceramides (ie, Cerave, Cetaphil, Keri)

–Lassar’s paste contains zinc oxide, salicylic acid, Vaseline

–Corticosteroids: low-potency, nonfluorinated, such as 1% hydrocortisone, applied 2 to 3 times per day

–Calcineurin inhibitors: ie, tacrolimus or pimecrolimus

–Antifungal preparations (C albicans): ie, nystatin, clotrimazole, miconazole

–Antiseptic preparations: ie, Burow’s solution

–Antibiotics: Mild, localized impetigo or intertrigo: bacitracin, polymyxin, neomycin; Moderate impetigo: mupirocin.

–Vitamin A&D ointment (barrier)

Optimal Therapeutic Approach for this Disease

Frequent diaper changes help to prevent chafing or frictional dermatitis as well as ICD, as common irritants, such as urine and feces, are removed. The goal is to keep the skin clean and dry, meaning that exposure to air is important as well. Generally, for uncomplicated ICD, miliaria, or intertrigo, response to treatment takes a few days.

Disposable wipes provide an advantage over wash cloths both hygienically, as wash cloths can be reused, and mechanically, as the cloths may also contribute to irritation, especially in already compromised skin. Wipes are considered mild enough to be used on newborn, irritated, or atopic skin. Some disposable wipes also contain a pH buffering system to help the skin maintain its normal physiologic pH after cleansing.

These wipes are soaked in a watery emulsion or mineral oil, often with fragrances, additives (chamomile, aloe, panthenol), and/or preservatives added (such as bronopol, iodopropynyl carbamate, sodium hydroxymethylglycinate and quaternium 15). While disposable wipes are attractive in many ways for their prevention and improvement of diaper dermatitis, the chemical constituents mentioned above can also pose the threat of allergic contact diaper dermatitis. In addition, mineral oil wipes may not be the most effective cleansing tool.

Classic soaps are alkali salts of fatty acids and have high pH values (10), altering the skin’s normal pH (4.5 to 6.0) and leaving calcium and magnesium salts behind after washing, which can contribute to ICD. Syndets are synthetic detergents that contain surfactants and have a lower pH (5.5) than soaps; they are less likely to alter the skin’s microflora. They have, however, been associated with delipidization; thus, in order to prevent this, petrolatum or rice starch can be added.

With ACD as the cause of “diaper rash,” avoidance is the most effective treatment measure. This means using diapers or personal care products free of dye, fragrance, rubber accelerators, adhesives/resins, or certain preservatives, depending on the particular contact allergy.

Barrier creams and ointments, such as zinc oxide or petrolatum preparations as well as lipid-based moisturizers should be used frequently at each diaper change when dermatitis is present. A low-potency corticosteroid, such as 1% hydrocortisone, can be applied per the instructions of the healthcare provider, usually no longer than 2 weeks, but should be stopped once improvement is observed.

Generally, high-potency corticosteroids are avoided due to both local and systemic side effects; however, one’s healthcare provider may prescribe a short course of mid-potency corticosteroids for severe involvement. Absorption may be enhanced due to diaper occlusion. For this reason, steroid-sparing agents, such as calcineurin inhibitors, are often employed.

Antifungal topical preparations may be used with fungal infection, such as C albicans, with resolution occurring after a few weeks. If severe cutaneous candidiasis is present, oral fluconazole may be used, and if thrush is present, oral nystatin may supplement a topical anti-fungal agent.

Antibiotics are used with evidence of impetigo; topical antibiotics should be sufficient for mild infection caused by Staphylococcus aureus, but systemic antibiotics are reserved for more severe cases of impetigo caused by either S aureus or group A beta-hemolytic streptococci (GABHS). Of note, mupirocin is a topical antibiotic that possesses a high level of bactericidal activity against both S aureus and GABHS.

Patient Management

Monitoring: Depending on the severity of the dermatitis and its response to treatment, a follow-up visit will often be scheduled.

Maintenance therapy: Once the dermatitis has been controlled, maintenance therapy should include proper barrier protection with creams and emollients at each diaper change. Diaper changes should be frequent, utilizing disposable, absorbent diapers, and pH buffered disposable baby wipes.

Recalcitrant: If the infant’s diaper dermatitis is recalcitrant to treatment the differential diagnosis should be considered in depth. Treatment with steroids can at times be associated with an ensuing candidal infection for which an antifungal would need to be started. Bacterial infection must also be suspected in cases of recalcitrant diaper dermatitis, and a trial of antibiotics begun. Resistance to all of the above could indicate granuloma gluteal infantum or psoriasis. Langerhans cell histiocytosis can also be considered, for which a biopsy could be performed. Zinc levels can be obtained to rule out acrodermatitis enteropathica as well. Allergic contact dermatitis should also be considered.

Risk/benefit: Treatment with steroids poses certain risks. In regard to diaper dermatitis, however, low-potency topical corticosteroids are used in order to prevent adverse events in a delicate area. Risks include cutaneous atrophy, striae, telangiectasia, hirsutism, acne, and changes in pigmentation.

Unusual Clinical Scenarios to Consider in Patient Management

Most people diagnose diaper dermatitis by history; however, in refractory cases, a more extensive workup is indicated. This may include blood work, such as a CBC to check for leukocytosis and anemia, VDRL or RPR, and zinc levels. Gram stain/culture and skin biopsies are also options given the appropriate case. In addition, admission to the hospital should be considered with febrile neonates or with infants that appear to have a systemic bacterial infection with possible sepsis.

When treating diaper dermatitis with corticosteroids, it is important to keep the occlusive diaper environment in mind, as this may increase steroid potency.

A single dose of intramuscular penicillin G can treat congenital syphilis.

What is the Evidence?

Rietschel, RL, Fowler, JF. “Role of age, sex, color of skin, and atopic status”. Fisher’s Contact Dermatitis. 2008. pp. 38-65. (This chapter discusses contact dermatitis in childhood, with diaper dermatitis as an example. Few additional forms of diaper dermatitis are also mentioned in the differential.)

Smith, WJ, Jacob, SE. “The role of allergic contact dermatitis in diaper dermatitis”. Pediatr Dermatol. vol. 26. 2009. pp. 369-70. (This letter to the editor comments on the below article by Dr Adam, "Skin care of the diaper area." It highlights allergic contact dermatitis as yet another cause of diaper dermatitis, describing potential allergen sources and testing.)

Roul, S, Ducombs, G, Leaute-Labreze, C. “"Lucky Luke" contact dermatitis due to rubber components of diapers”. Contact Dermatitis. vol. 38. 1998. pp. 363-364. (This article discusses the details of "Lucky Luke" contact dermatitis, i.e. the clinical distribution and potential causative allergens.)

Alberta, L, Sweeney, SM, Wiss, K. “Diaper dye dermatitis”. Pediatrics. vol. 116. 2005. pp. e450-e452. (This article discusses the role of dyes as a cause of allergic contact diaper dermatitis.)

Adam, R. “Skin care of the diaper area”. Pediatr Dermatol. vol. 25. 2008. pp. 427-433. (This article explains the anatomy and physiology of newborn skin and discusses factors that may contribute to diaper dermatitis, illustrating a "diaper rash model." It also describes different cleansing regimens.)

Paller, AS, Mancini, AJ. Hurwitz clinical pediatric dermatology. 2006. pp. 27-30. (This text describes the different clinical manifestations of diaper dermatitis, discusses some of the etiologies, available testing, as well as some treatment options.)

Nijhawen, RI, Matiz, C, Jacob, SE. “Contact dermatitis: From basics to allergodromes”. Pediatr Ann. vol. 38. 2009. pp. 99-108. (This article discusses the pathophysiology of ACD, as well as differentiates between ICD and ACD.)

Jacob, SE, Castenedo-Tardan, MP. “Pharmacotherapy for allergic contact dermatitis”. Expert Opin Pharmacother. vol. 8. 2007. pp. 2757-74. (This reference describes a thorough treatment algorithm for allergic contact dermatitis.)