The most common eruptions of the neonatal period are sometimes difficult to distinguish from more serious rashes. Understanding common rashes is paramount to helping the clinician identify and differentiate them from rarer, more worrisome rashes. The timing, morphology, and distribution of miliaria, transient neonatal pustular melanosis (TNPM), neonatal cephalic pustulosis (NCP), and erythema toxicum neonatorum (ETN) are reviewed in Table 1. The text below reviews the key points in more detail.
Common Neonatal Eruptions
Both of the two major forms of miliaria, miliaria crystallina and miliaria rubra, occur due to occlusion of the sweat ducts with subsequent sweat outflow obstruction and entrapment within the skin. The types are only distinguished by the anatomic level of this obstruction. In miliaria crystallina (Figure 1), for example, the obstruction is more superficial, which leads to the formation of numerous pinpoint, noninflammatory vesicles; whereas in miliaria rubra, the obstruction is deeper in the dermis and small erythematous papules or papulovesicles appear. Miliaria occurs in about 1% to 5% of newborns, but the incidence may be as high as 40% during the first month of life.1–3
To distinguish miliaria crystallina from other vesicular or pustular eruptions, rupture of the vesicles should release clear sweat. Although the differential diagnosis of miliaria rubra includes folliculitis, the pustules of folliculitis are usually folliculocentric whereas the lesions of miliaria rubra are not. Viral exanthems, morbilliform drug eruptions, ETN, and seborrheic dermatitis in the skin folds may be considered in the differential diagnosis.
Miliaria in all forms is self-limited to a few days once the inciting occlusion (eg, tight clothing or tight swaddling) or overheating (eg, warm climates, febrile illnesses, or over-bundling) is eliminated. Treatment otherwise is not necessary, and topical medications or emollients may actually worsen the eruption by inciting additional duct obstruction. Cool baths, loose clothing, and keeping the neonate in a cool environment can decrease the development of miliaria.
Transient Neonatal Pustular Melanosis
TNPM most commonly occurs in patients with darker skin and is relatively rare, seen in 1% to 4% of newborns.4 The etiology is unknown.
TNPM typically presents at birth or within the first day or days of postnatal life. It is characterized by asymptomatic superficial sterile pustules that rupture easily, usually by day 3 of postnatal life, and leave behind hyperpigmented macules with a collarette of fine white scale. These macules may take weeks or months to resolve. Pustules sometimes rupture prior to birth, allowing for a varied presentation of both pustules and macules concurrently or even just hyperpigmented macules at the time of birth. To distinguish TNPM from other pustular eruptions, it is important to note that babies with TNPM are otherwise well-appearing.
Neonatal Cephalic Pustulosis
NCP is characterized by pustules on the head, neck, and occasionally the upper chest (Figure 2). It is thought to be due to colonization of the neonate by Malassezia, but the exact role of the yeast in the pathogenesis is not well understood.5,6
Neonatal cephalic pustulosis.
Although many practitioners use the terms NCP and neonatal acne interchangeably, NCP can technically be distinguished from neonatal acne as the former is a pustular eruption and the latter is a more comedonal eruption. Treatment is not necessary, but topical antifungal therapy or low-potency topical corticosteroids may be considered if treatment is desired. Exogenous oils such as baby oils, creams, and ointments may exacerbate the condition.
Erythema Toxicum Neonatorum
ETN appears during the first 3 to 4 days of postnatal life, although it can also present at birth or as late as age 10 days. Clinically, ETN presents with splotchy erythematous macules and patches of varying sizes with firm 1- to 3-mm white or pale yellow papulopustules that develop within the areas of erythema (Figure 3). Although individual lesions last anywhere from a few hours to a few days, the eruption overall can relapse and remit for the first 2 weeks of life but generally resolves without any residual scarring.
Erythema toxicum neonatorum.
Although the etiology of ETN is not well established, it is hypothesized to represent an immune response to microbial colonization of the hair follicle.7 The incidence is estimated to be about 20%4,8 but may be even higher. White ancestry, male gender, higher birth weight, later gestational age, and vaginal delivery are risk factors.4,8
In distinguishing ETN from other eruptions, it is important to note that patients are otherwise well-appearing. The differential diagnosis of ETN includes NCP, TNPM, miliaria, and infections (bacterial, viral, and fungal). Compared to ETN, NCP features acneiform pustules on the cheeks, forehead, and chin, and these pustules are not evanescent like those of ETN. TNPM occurs most commonly in infants with darker skin types and features pustules without splotchy erythema that resolve, leaving hyperpigmented macules. Miliaria rubra also presents with red papules and pustules but tends to have a predilection for intertriginous and occluded sites. Bacterial infections often feature somewhat similar pustules on a background of erythema, but crusting is common in bacterial infections and not a feature of ETN. Viral infections of the newborn, such as herpes simplex and varicella zoster, tend to have more vesicles rather than pustules, and the patients are often unwell. Cutaneous candidiasis may involve the palms and soles, which are spared in ETN.
When the diagnosis is in doubt, Wright or Giemsa staining of fluid expressed from a pustule demonstrating a predominance of eosinophils can quickly differentiate ETN from other, more serious newborn pustular conditions. Laboratory testing, which is not normally performed for ETN, may reveal peripheral eosinophilia.
Treatment is not necessary given the benign and self-limited nature of ETN. Gentle cleaning of any purulence or scale is sufficient.
Diaper dermatitis is one of the most common, yet challenging, dermatologic conditions seen in the neonatal and infant periods. Although diaper dermatitis is frequently encountered by the pediatrician, correctly diagnosing the underlying cause can be extremely difficult. Erythema in the diaper area is best viewed as a symptom and not a diagnosis. The three most common types of diaper dermatitis are chafing/frictional dermatitis, irritant contact dermatitis, and diaper candidiasis. Many different conditions can cause a “diaper dermatitis,” including seborrheic dermatitis, allergic contact dermatitis, Jacquet's dermatitis, granuloma gluteale infantum, psoriasis, intertrigo, acrodermatitis enteropathica, and Langerhans cell histiocytosis.
Chafing, or frictional dermatitis, presents as mild redness and usually scaling in areas where friction from diapers is most pronounced, such as the inner thighs, buttocks, abdomen, and genitalia.
Irritant contact diaper dermatitis presents as erythematous patches and papules with relative sparing of the creases such as the inguinal and intergluteal folds.9 When severe, vesicles and erosions may also be seen. It is usually caused by prolonged contact with urine and feces in a damp diaper environment, although it may also be caused by irritating soaps, topical preparations, or detergents.10 In female infants, the rash may be more severe posteriorly whereas in male infants it may be more severe anteriorly, as this is where urine accumulates more readily in the diaper.
Treatment for both chafing/frictional and irritant contact diaper dermatitis focuses on keeping the diaper area as dry as possible. Frequent diaper changes, gentle cleansing with a moist cloth or fragrance-free wipes, and the use of zinc oxide or petrolatum-based topical preparations to form a skin barrier against further contact with urine or feces are essential. Low-strength topical steroid ointments, such as hydrocortisone 1% to 2.5%, may be applied 2 to 3 times daily under the barrier cream when acute dermatitis is present.
Allergic contact diaper dermatitis is increasingly being recognized in pediatric patients, either to the diaper components themselves or to skin care products (eg, “wet wipes”). Symmetric scaly pink papules or plaques on the lateral buttocks, hips, or inner thighs should raise suspicion for allergic contact dermatitis to the diaper itself. Diapers contain numerous culprits including fragrances, mercapto compounds found in the elastic, and disperse colored dyes. Disperse dyes are used in many synthetic fabrics and loosely adhere to the fabric allowing leeching from the fabric onto skin.10 A colored lining inside the diaper, often blue or green, can help identify these dyes. If allergic contact dermatitis is suspected, the patient should switch to diapers and wipes made for sensitive skin and a mild topical steroid can be applied until the area heals. In recalcitrant cases, the patient should be referred to a pediatric dermatologist for possible patch testing. Regardless of the etiology, good diaper hygiene should be stressed. Figure 4 has several tips for caregivers.
Diaper care tips for caregivers.
Diaper candidiasis should be considered whenever a diaper rash fails to respond to good diaper hygiene and mild topical steroids or when a diaper rash occurs in the context of recent antibiotic use. Candidal “diaper dermatitis” presents as beefy-red erythema on the lower abdomen, genitals, and buttocks, and typically involves the inguinal folds. Pinpoint satellite papules or pustules may be present. A potassium hydroxide preparation or fungal culture can confirm the diagnosis. Treatment consists of topical antifungal and barrier creams to address any skin breakdown that may serve as a nidus for infection. Azoles are generally preferred over nystatin.
Jacquet's dermatitis is a rare but severe erosive dermatitis. It is important to recognize the erosive lesions early before they become severe as they are painful, prone to infection, and difficult to heal. In addition to meticulous diaper care, low-to-mid potency topical steroids may be needed.
Granuloma gluteale infantum presents with purple-red papulonodules in the groin, lower abdomen, and inner thigh. It likely occurs from an unusually robust, unique inflammatory response to chronic irritation or candidiasis. Additionally, the underlying etiology may be associated with higher-potency fluorinated topical steroids, and these should be tapered if they are being used.
Finally, psoriasis and Langerhans cell histiocytosis are infrequent causes of “diaper dermatitis” and must be considered in recalcitrant cases. Psoriasis may initially present in the diaper region with sharply demarcated erythematous scaly plaques, although the scale may be absent in a moist region such as the diaper. Dermatology should be involved in managing these patients as the disease is often chronic.
Seborrheic dermatitis is a self-limiting erythematous, scaly eruption. The etiology of infantile seborrheic dermatitis remains poorly understood, but its localization to areas of high sebaceous gland density may indicate a relation to sebum production and sebaceous gland activity. The commensal Malassezia yeast, which has been implicated as the causative organism in adult and adolescent seborrheic dermatitis, is of uncertain significance in infants.11–13
Infantile seborrheic dermatitis appears between the second and twelfth week of life.14 The eruption typically begins on the scalp (eg, “cradle cap”) (Figure 5) or with mild erythema in the diaper area and can spread to the forehead, eyebrows, nose, and retroauricular area. In more widespread cases, erythematous patches appear diffusely but are most heavily concentrated in intertriginous areas such as the folds of the neck, axillae, groin, ankles and wrists, around the umbilicus, and in the anogenital area (Figure 6). Pruritus is minimal or absent.
Infantile seborrheic dermatitis on the scalp.
Infantile seborrheic dermatitis in intertriginous areas.
Scalp seborrheic dermatitis typically lacks oozing and alopecia, which help in differentiating it from tinea capitis. Infantile seborrheic dermatitis and infantile atopic dermatitis (AD) may have similar sites of involvement including the face, ears, and trunk; however, the occluded diaper area is usually spared in AD and involved in seborrheic dermatitis. Additionally, involvement of the anterior neck and axillary regions, as well as an absence of pruritus and oozing, may also favor seborrheic dermatitis. Seborrheic dermatitis and AD often initially overlap and a formal diagnosis of AD may be made once the seborrheic dermatitis resolves. More important than distinguishing seborrheic dermatitis from AD is distinguishing it from psoriasis and Langerhans cell histiocytosis, which will have a sluggish or absent response to topical steroids. As such, any recalcitrant cases of clinically diagnosed seborrheic dermatitis should be referred for evaluation by a dermatologist.
Seborrheic dermatitis usually resolves spontaneously around age 6 months, but some cases last until age 2 years.14 Mild cases of scalp-limited seborrheic dermatitis can be treated with gentle shampooing and scrubbing of any thicker or more adherent scales. Scales may be softened with mineral oil before gentle brushing. Anti-seborrheic shampoos are not considered first-line treatments due to the potential for eye irritation and drying of the skin. In cases with a significant inflammatory component, a mild topical steroid (eg, hydrocortisone 1% or 2.5%) in a lotion, solution, or oil formulation for the scalp, and cream or ointment for the body, may be applied twice a day until the eruption clears. Topical antifungal agents are another option.
AD is one of the most common skin disorders seen in pediatric populations. Epidermal barrier dysfunction, immune dysregulation, and environmental exposures play a role in the pathogenesis.15 Children with AD are at a 3-fold increased risk for developing asthma and allergic rhinitis compared to children without AD.16 Please note that this review is limited to infantile AD and forgoes a detailed discussion on childhood or adult disease.
Infantile AD commonly develops between ages 3 and 6 months. Approximately 60% of all AD develops within the first year of life.17 It is characterized by erythema, edema, papules, vesicles, oozing, and crusting. Pruritus is a hallmark feature. The eruption usually begins on the cheeks, forehead, or scalp before extending onto the trunk and extensor extremities. The diaper area is relatively spared as the diaper creates a humid environment and protects against allergen entry and scratching. Young infants can often be seen scissoring the legs (Figure 7) or scooting to scratch as they cannot yet localize itch.
Atopic dermatitis. Note the baby scissoring his legs while scratching.
The differential diagnosis of AD in infancy includes seborrheic dermatitis, irritant contact dermatitis, psoriasis, and ichthyosis vulgaris. Seborrheic dermatitis may be differentiated from AD by the presence of greasy yellow scale, involvement of intertriginous areas as well as the diaper area, and minimal to no pruritus. Additionally, seborrheic dermatitis tends to have an earlier onset in the first 3 months of life and tends to improve by age 6 months, whereas AD tends to occur around or after age 3 months and often persists. Irritant contact dermatitis can present on the cheeks and chin due to irritation from saliva, on the trunk and extensor surfaces due to irritation from crawling or harsh personal care products, and in the diaper area due to irritation from urine and feces. Irritant contact dermatitis, however, tends to be more localized than AD. In contrast to the poorly defined, erythematous, edematous papules or plaques of AD, the lesions of infantile psoriasis tend to be bright red, sharply demarcated, and covered in a gray-silver scale. Ichthyosis vulgaris presents with dry, fine, scaling skin that often forms a network of “fish-like” scale on the extensor extremities and usually does not have the erythema or pruritus of AD, although the two diseases often occur simultaneously.
Parent education is a major cornerstone in the management of AD given the chronic nature of the disease and the commitment necessary to provide regular skin care even when the eruption is quiescent. Counseling should include a discussion about the avoidance of irritant and allergic triggers, liberal and frequent emollient use, bathing suggestions, and the proper use of topical treatments when prescribed. In general, ointments are ideal emollients for patients with AD; however, they are greasy and sometimes not acceptable to either the patient or caregiver. In such cases, we usually recommend a thick cream. Sunflower and coconut oil may be helpful for patients who prefer to use oil formulations on their skin rather than ointments or creams; however, other oils such as olive oil, mustard oil, and soybean oil are detrimental to the management of AD.18,19 See Figure 8 for management suggestions for caregivers.
Management suggestions for caregivers in cases of atopic dermatitis.
Topical anti-inflammatory medications are often employed to help control infantile AD. Most cases respond to low-potency topical corticosteroids, preferably in an ointment formulation. Parents should be assured that side effects of low-potency topical corticosteroids almost never occur and are safe when patients are using the appropriate strength of medication under physician supervision. Care should be taken when using topical steroids in flexural areas and skin folds as the occlusive nature of those areas will cause the medication to concentrate and increase in potency, leading to a greater risk of side effects. The main side effects of topical steroids that the physician should look for include epidermal atrophy, skin thinning, striae, telangiectasias, and acneiform lesions. If topical steroids are to be used in a chronic manner, steroid-sparing agents such as topical calcineurin inhibitors or topical phosphodiesterase-4 inhibitors may be considered. Parents should be counseled on using topical medications only when the dermatitis is active in addition to emollients and using emollients alone when the dermatitis is quiescent. Other treatment modalities such as phototherapy and systemic immunosuppressants (eg, cyclosporine, methotrexate, and dupilumab) should be considered early for patients with disease refractory to topical medications, but these treatments generally should not be initiated without evaluation by a pediatric dermatologist as refractory cases are rare and other causes of dermatitis must be excluded.20
The newborn and infant skin conditions discussed here, including miliaria, TNPM, NCP, ETN, diaper dermatitis, seborrheic dermatitis, and AD, are often encountered by the pediatrician in daily practice. We hope our discussion highlighted salient features of each condition that will aid in their diagnosis and help in differentiating them from more serious newborn and infant skin conditions.
- Reginatto FP, DeVilla D, Muller FM, et al. Prevalence and characterization of neonatal skin disorders in the first 72h of life. J Pediatr (Rio J). 2017;93(3):238–245. doi:. doi:10.1016/j.jped.2016.06.010 [CrossRef]
- Haas N, Henz BM, Weigel H. Congenital miliaria crystallina. J Am Acad Dermatol. 2002;47(5 Suppl):S270–S272. doi:10.1067/mjd.2002.108489 [CrossRef]
- Feng E, Janniger CK. Miliaria. Cutis.1995;55(4):213–216.
- Reginatto FP, Muller FM, Peruzzo J, Cestari TF. Epidemiology and predisposing factors for erythema toxicum neonatorum and transient neonatal pustular: a multicenter study. Pediatr Dermatol. 2017;34(4):422–426. doi:. doi:10.1111/pde.13179 [CrossRef]
- Ayhan M, Sancak B, Karaduman A, Arikan S, Sahin S. Colonization of neonate skin by Malassezia species: relationship with neonatal cephalic pustulosis. J Am Acad Dermatol.2007;57(6):1012–1018. doi:. doi:10.1016/j.jaad.2007.02.030 [CrossRef]
- Bernier V, Weill FX, Hirigoyen V, et al. Skin colonization by Malassezia species in neonates: a prospective study and relationship with neonatal cephalic pustulosis. Arch Dermatol. 2002;138(2):215–218. doi:10.1001/archderm.138.2.215 [CrossRef]
- Marchini G, Nelson A, Edner J, Lonne-Rahm S, Stavreus-Evers A, Hultenby K. Erythema toxicum neonatorum is an innate immune response to commensal microbes penetrated into the skin of the newborn infant. Pediatr Res. 2005;58(3):613–616. doi:. doi:10.1203/01.pdr.0000176836.27156.32 [CrossRef]
- Monteagudo B, Labandeira J, Cabanillas M, Acevedo A, Toribio J. Prospective study of erythema toxicum neonatorum: epidemiology and predisposing factors. Pediatr Dermatol. 2012;29(2):166–168. doi:. doi:10.1111/j.1525-1470.2011.01536.x [CrossRef]
- Folster-Holst R. Differential diagnoses of diaper dermatitis. Pediatr Dermatol. 2018;35(Suppl 1):S10–S18. doi:. doi:10.1111/pde.13484 [CrossRef]
- Klunk C, Domingues E, Wiss K. An update on diaper dermatitis. Clin Dermatol.2014;32(4):477–487. doi:. doi:10.1016/j.clindermatol.2014.02.003 [CrossRef]
- Broberg A. Pityrosporum ovale in healthy children, infantile seborrhoeic dermatitis and atopic dermatitis. Acta Derm Venereol Suppl (Stockh). 1995;191:1–47.
- Tollesson A, Frithz A, Stenlund K. Malassezia furfur in infantile seborrheic dermatitis. Pediatr Dermatol. 1997;14(6):423–425. doi:10.1111/j.1525-1470.1997.tb00680.x [CrossRef]
- Wananukul S, Chindamporn A, Yumyourn P, Payungporn S, Samathi C, Poovorawan Y. Malassezia furfur in infantile seborrheic dermatitis. Asian Pac J Allergy Immunol. 2005;23(2–3):101–105.
- Elish D, Silverberg NB. Infantile seborrheic dermatitis. Cutis. 2006;77(5):297–300.
- Leung DY, Guttman-Yassky E. Deciphering the complexities of atopic dermatitis: shifting paradigms in treatment approaches. J Allergy Clin Immunol. 2014;134(4):769–779. doi:. doi:10.1016/j.jaci.2014.08.008 [CrossRef]
- Dharma C, Lefebvre DL, Tran MM, et al. Patterns of allergic sensitization and atopic dermatitis from 1 to 3 years: effects on allergic disease. Clin Exp Allergy. 2018;48(1):48–59. doi:. doi:10.1111/cea.13063 [CrossRef]
- Kay J, Gawkrodger DJ, Mortimer MJ, Jaron AG. The prevalence of childhood atopic eczema in a general population. J Am Acad Dermatol. 1994;30(1):35–39. doi:10.1016/S0190-9622(94)70004-4 [CrossRef]
- Darmstadt GL, Mao-Qiang M, Chi E, et al. Impact of topical oils on the skin barrier: possible implications for neonatal health in developing countries. Acta Paediatr. 2002;91(5):546–554. doi:10.1111/j.1651-2227.2002.tb03275.x [CrossRef]
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Common Neonatal Eruptions
||Prognosis and Treatment
||Sweat duct obstruction in the superficial epidermis
||Anytime, especially under conditions of warmth (eg, fevers and over-bundling) and tight clothing/swaddling
||Clear thin-walled pinpoint vesicles
||Intertriginous areas (eg, neck and skin folds)
||Self-limited; eliminate inciting factor; cool baths; loose clothing; cool environment; and avoid thick emollients
||Sweat duct obstruction deeper in the dermis
||Anytime, especially under conditions of warmth (eg, fevers and over-bundling) and tight clothing/swaddling
||Small erythematous non-follicularly based papulovesicles
||Chest, abdomen, back, arms, and intertriginous areas
||Self-limited; eliminate inciting factor; cool baths; loose clothing; cool environment; and avoid thick emollients
|Transient neonatal pustular melanosis
||Present at birth or occurs during first day of life
||Asymptomatic superficial sterile pustules that rupture by day 3 of life, leaving behind hyperpigmented macules and collarettes of scale
||Forehead, chin, neck, lower back, and shins; can be generalized in severe cases
||Self-limited; gentle exfoliation of scale; hyperpigmented macules can take weeks to months to fade
|Neonatal cephalic pustulosis
||Not well understood; thought to be due to colonization by Malassezia species
||Age 5 days to 5 weeks
||Small, minimally erythematous pustules
||Head, neck, and upper chest
||Self-limited; may use topical antifungal creams and avoid thick emollients and oils
|Erythema toxicum neonatorum
||Not well understood; thought to be an immune response to bacterial colonization of hair follicles
||Usually within the first 4 days of life, but can present as late as 10th day of life; can also be present at birth
||Well-appearing baby with splotchy erythematous macules and patches that then develop small, firm white or pale-yellow papules or pustules
||Face, forehead, trunk, buttocks, and proximal extremities
||Individual lesions may be evanescent; eruption can last for first 2 weeks of life; gentle cleaning of any purulence or scale