Papules and Pustules—Diffuse or Scattered

Erythema toxicum is a benign condition that occurs in 30-70% of white full-term infants. Erythema toxicum occurs less frequently in premature infants. The eruption is characterized by blotchy, erythematous macules or patches with central papules, pustules, or vesicles that give the infant a “flea-bitten” appearance ( Fig. 47.1 ). The lesions develop most commonly between the 2nd and 4th days after birth; however, they may appear during the 1st 2-3 weeks. They are self-limiting and usually resolve within several days. Typical sites of involvement include the face, trunk, and proximal extremities. There may be very few to hundreds of lesions.

Papules surrounded by erythema are characteristic of erythema toxicum. Typically it is located on the trunk, but can be on the extremities as well.

A Giemsa or Wright stain of the intralesional contents reveals sheets of eosinophils with a relative absence of neutrophils. Peripheral eosinophilia may be present in up to 20% of affected infants. Erythema toxicum is occasionally confused with transient neonatal pustular melanosis, congenital cutaneous candidiasis, impetigo neonatorum, milia, herpes simplex, or miliaria rubra (prickly heat).

Transient neonatal pustular melanosis , seen in up to 4% of neonates, occurs more often in African-American infants. Typically present at birth, the initial lesions are 2- to 5-mm pustules distributed over the face, neck, and upper chest and, less often, on the sacrum, trunk, thighs, palms, and soles ( Fig. 47.2 ). In contrast to the lesions of erythema toxicum, there is no erythema surrounding each pustule, and Wright stain of pustular contents reveals many neutrophils. In both disorders, the pustules are sterile and should be distinguished from those seen in potentially serious infections caused by herpes simplex virus (HSV), Staphylococcus aureus , or Candida species.

Transient neonatal pustular melanosis. Papules and papulopustules that rupture to leave a collarette of fine scales and eventual hyperpigmentation.

(From Paller AS, Mancini AJ. Cutaneous disorders of the newborn. In: Paller AS, Mancini AJ, eds. Hurwitz Clinical Pediatric Dermatology . 4th ed. Philadelphia: Elsevier; 2011:18.)

The superficial pustules of transient neonatal pustular melanosis rupture spontaneously within the 1st few days after birth, leaving hyperpigmented macules that have collarettes of fine scale. It is common to see only the hyperpigmented macules at birth. These brown spots slowly fade over several weeks to months.

Miliaria results from sweat retention and is exacerbated by heat and humidity. Affected newborns are frequently in incubators or receiving phototherapy. Keratinous plugging of the eccrine ducts and subsequent release of eccrine sweat into the surrounding skin produces 2 distinct clinical manifestations with different sites of eccrine duct obstruction. In miliaria crystallina, obstruction occurs just below the stratum corneum, resulting in superficial, noninflammatory 1- to 2-mm vesicles. In miliaria rubra, or “prickly heat,” obstruction occurs in the mid-epidermis. This is associated with an inflammatory response exhibited by vesicles, papules, or papulovesicles surrounded by a rim of erythema. The lesions occur in clusters on the trunk, face, scalp, and intertriginous regions. Neither type of miliaria warrants therapy, but improvement occurs with cooling of the skin and avoidance of excessive warmth and moisture.

Eosinophilic pustular folliculitis is another disorder of infancy characterized by recurrent crops of vesicles and pustules, beginning in the 1st year of life. Lesions are often present on the forehead and scalp. The condition tends to occur in a cyclic pattern and is very pruritic. Scraped material from the pustules subjected to Wright stain demonstrates a large number of eosinophils but no evidence of infectious organisms. A complete blood cell count may show peripheral eosinophilia. In rare cases, skin biopsy may be necessary. Histopathologic study demonstrates a perifollicular and dermal infiltrate of eosinophils, as well as lymphocytes and histiocytes. Because the clinical condition is very similar to infantile acropustulosis, some authors contend that eosinophilic pustular folliculitis may be part of the same clinical spectrum. This condition is not associated with systemic disease, and the 1st-line treatment is symptomatic with topical corticosteroids and antihistamines. Oral and topical indomethacin has been effective in recalcitrant cases. Eosinophilic pustular folliculitis usually resolves spontaneously by 2-3 years of age.

Acropustulosis of infancy is a condition that may present at birth or during the 1st few weeks or months afterward. The disorder is characterized by recurrent eruptions of pruritic pustules or vesicles involving the hands and feet ( Fig. 47.3 ). On occasion, involvement includes other sites such as the trunk or abdomen. The lesions frequently begin in crops, which typically last approximately 1 week, and resolve with desquamation, followed by postinflammatory hyperpigmentation.

Acropustulosis of infancy. Multiple tense erythematous papules and pustules on the palm of this 4-month-old girl.

(From Paller AS, Mancini AJ. Cutaneous disorders of the newborn. In: Paller AS, Mancini AJ, eds. Hurwitz Clinical Pediatric Dermatology . 4th ed. Philadelphia: Elsevier; 2011:19.)

Acropustulosis is often confused with infantile scabies . Family history and examination of scrapings of the involved area may help differentiate between these 2 diagnoses. However there is some thought that it may occur after a previous scabies infection. Scrapings of lesions in acropustulosis often demonstrate neutrophils. Bacterial infection should also be ruled out by wound cultures. Treatment is symptomatic and consists of control of pruritus with low- to mid-potency topical corticosteroids and antihistamines. Parents should be advised that lesions tend to occur episodically until approximately 2-3 years of age.

Neonatal cephalic pustulosis (neonatal acne) develops in approximately 20% of newborns. Typically, it is not present at birth, but appears during the 1st few weeks after birth. Characterized by papules and pustules located on the face or trunk, this condition usually resolves within the 1st several months of life ( Fig. 47.4 ). Neonatal acne is a misnomer as neonatal cephalic pustulosis is likely caused by Malassezia yeast species. Therapeutic intervention is rarely required, but ketoconazole 2% cream may be of some use.

Neonatal acne (cephalic pustulosis) is usually found on the cheeks and scalp in the 1st 2-4 weeks of life; small red papules and pustules without comedones are evident.

(Modified from Eichenfield LF, Frieden IJ, Esterly NB. Textbook of Neonatal Dermatology . Philadelphia: Saunders; 2001:94.)

Langerhans cell histiocytosis (LCH) is a rare disorder, affecting about 5 per 1 million children, which is characterized by a proliferation of clonal dendritic cells, called Langerhans cells. There are 4 main types, 2 of which are most frequently seen in neonates and infants, though there is substantial overlap among the types.

Congenital self-healing reticulohistiocytosis (Hashimoto–Pritzker disease) typically presents at birth or within the 1st few days of life and is limited to the skin. There is a diffuse eruption of red to purple-brown papules and nodules that will crust and remit after several weeks. While it is considered a benign, self-limited condition, it can rarely progress to other more aggressive forms of LCH.

Letterer–Siwe disease is the more acute, diffuse form of LCH that has multisystem involvement. It commonly presents before 1 year of age with the majority of patients having skin findings of small 1- to 2-mm papules, pustules, and vesicles, typically on the scalp, intertriginous areas, and trunk. The lesions are often crusted and may have secondary bacterial infections. Fissures and confluence of papules can be seen. It can be confused with seborrheic dermatitis, and other forms of diaper dermatitis ( Table 47.1 ).

Patches and Plaques

Patches are confluent, flat lesions over 1 cm in size, while plaques are slightly raised lesions over 1 cm in size. Many of these conditions have overlapping features but can often be distinguished by their location, distribution, and response to certain treatments ( Table 47.1 ).

Neonatal lupus erythematosus is a unique annular erythematous eruption during the neonatal period. Lesions of neonatal lupus are often scaly, annular plaques that usually occur on the face and scalp and may affect the periorbital and malar areas, creating a “raccoon eyes” appearance ( Fig. 47.5 ). Other manifestations may include transient hypopigmentation with epidermal atrophy or telangiectasia. Cutaneous lesions may be present at birth but often appear within the 1st 2-3 months of life. The lesions are usually exacerbated by sun exposure and are typically photodistributed. The majority of skin findings are transient, lasting up to 6-9 months.

“Raccoon eyes” eruption of neonatal lupus erythematosus.

(From Eichenfield LF, Frieden IJ, Esterly NB. Textbook of Neonatal Dermatology . Philadelphia: Saunders; 2001:297.)

(See Nelson Textbook of Pediatrics, p. 1176.)

Cutaneous findings or congenital heart block are each present individually in approximately 50% of affected infants; some studies have shown congenital heart block to be much less common. An overlap of both is present in approximately 10% of affected infants. The major morbidity and mortality of neonatal lupus result from congenital heart block.

The diagnosis of neonatal lupus includes examination of anti-Ro, anti-La, and anti-U1RNP autoantibodies in both the infant and mother. Ninety-five percent of mothers of infants with neonatal lupus have anti-Ro antibodies. Skin biopsy is usually not necessary. Work-up should include an electrocardiogram (ECG), platelet count, and liver function tests because approximately 5-10% of affected infants have liver disease or thrombocytopenia. Rare reports of multisystem involvement, including neurologic and respiratory findings have been reported.

Mothers with high titers of anti-Ro antibodies or with systemic lupus erythematosus have a higher risk of delivering an infant with neonatal lupus and should be counseled appropriately. Despite high antibody titers, fewer than half of mothers of affected infants are symptomatic at the time of delivery. In most of these mothers, evidence of connective tissue disease, usually Sjögren syndrome or subacute cutaneous lupus, develops over time.

Differential diagnosis should include annular erythema of infancy, tinea corporis, and cutis marmorata telangiectatica congenita (CMTC). Treatment consists of photoprotection and topical steroids. Most cutaneous changes resolve spontaneously by 6-9 months of age as a result of a gradual decrease in maternal antibodies.

Seborrheic dermatitis , common during infancy, typically manifests within the 1st several weeks after birth. Characterized by erythema and a yellow, greasy scale, it usually resolves spontaneously within several months. The eruption occurs at sites where sebaceous glands are concentrated, such as the face, chest, posterior auricular scalp, and intertriginous areas. Malassezia colonization plays a part in the development of seborrheic dermatitis. “Cradle cap” is seborrhea that is confined to the scalp. Involvement of the diaper area is characterized by salmon-colored patches that arise in skin folds and spread to the genitalia, suprapubic area, and upper medial thighs. Scale may not be as apparent in intertriginous areas. Unlike atopic dermatitis, this eruption is not very pruritic. Secondary candidal or bacterial infection is common, particularly if erosions or fissures are seen.

The diagnosis is established clinically. The presence of greasy yellow scales and salmon-colored patches, involvement of the scalp and intertriginous areas, early onset, and lack of pruritus or atopic history help distinguish seborrheic from atopic dermatitis. However, some infants have an overlap of seborrheic dermatitis and atopic dermatitis. Seborrheic dermatitis should also be differentiated from LCH, in which the lesions are typically purpuric, erosive, or crusted; and from psoriasis (see Chapter 48 ). Skin biopsy findings, as well as hepatosplenomegaly, purpura, lymphadenopathy, anemia, thrombocytopenia, external otitis, interstitial pneumonia, and osseous lesions, further distinguish LCH from seborrheic dermatitis.

Treatment of the scalp consists of mild keratolytic shampoos, such as those containing selenium sulfide or zinc pyrithione. Ketoconazole 2% shampoo can be efficacious, particularly with controlling overgrowth of the yeast. Mineral oil may be helpful in removing thick, adherent scales. The scalp and diaper dermatitis may be treated with low-potency topical corticosteroids and barrier ointments. Topical antifungal or antibacterial agents should be used for coexisting candidiasis or impetigo.

Diaper dermatitis is 1 of the most common dermatologic disorders of infants and toddlers ( Table 47.2 ). It comprises a group of inflammatory conditions that involve the lower abdomen, genitalia, upper thighs, and buttocks. Clinical manifestations include erythema, edema, erosions, vesicles, and pustules. Secondary changes of postinflammatory hyperpigmentation or hypopigmentation are common.

TABLE 47.2

Diaper Dermatitis

Disease	Clinical Manifestation	Other Features	Treatment
Friction	Inner surface of thighs, genitalia, buttocks, abdomen.	Course waxes and wanes. Aggravated by talc.	Responds well to diaper changes. Avoidance of diapers.
Irritant	Mild erythema with shiny surface and occasional papules. Confined to convex surfaces. Spares intertriginous areas.	Exacerbated by heat, moisture, and sweat retention.	Gentle cleansing. Regular diaper changes. Barrier creams (zinc oxide, Vaseline). Low-potency topical steroids can help.
Allergic contact	Typically confined to convex surfaces. Skin involved is in direct contact with offending agent. Mild cases: diffuse erythema, papules, vesicles, scaling. Severe cases: papules, plaques, psoriasiform lesions, ulcerations, infiltrative nodules.	Often related to topical antibiotics (neomycin, bacitracin). Certain emulsifiers in topical products. Preservatives in wet wipes can be an offender.	Remove offending agent. Judicious use of low-potency topical steroids. Barrier creams/ointments.
Seborrheic dermatitis	Salmon-colored patches. Often have yellow, greasy scale. Fissures, erosions, maceration, and weeping can be seen.	Axillae, ear creases, and neck are often involved. “Cradle cap” on scalp. Hypopigmentation often seen in patients with darker skin tones.	Low-potency topical steroids. If coexistent infection–antifungal or antibacterial agents.
Candidiasis	Usually involves intertriginous areas and convex surfaces. Bright-red papules and plaques. Satellite lesions on abdomen and thighs.	Oral thrush may be present. Often occurs after treatment with systemic antibiotics or local topical steroid use.	Topical anticandidal agent, including nystatin.
Intertrigo	Well-demarcated, macerated plaques with weeping. Gluteal cleft and fleshy folds of thighs.	May be associated with miliaria.	Avoiding excessive heat. Cool clothing.
Psoriasis	Bright red, scaly, well-demarcated plaques. Can persist for months. Less responsive to topical treatment.	Red, sometimes scaly. Can be present on extremities or trunk. Nail changes seen. Family history.	Low-potency topical steroids. Moisturizers.
Staphylococcal infection	Many thin-walled pustules with pink-red base. Collarette of scale after rupturing.		Antistaphylococcal therapy.
Acrodermatitis enteropathica (zinc deficiency)	Early lesions are vesicular and pustular. Become confluent, pink, dry, scaly, crusty plaques.	Perioral skin typically also involved. Irritability or listlessness. Failure to thrive, alopecia, diarrhea.	Secondary to zinc deficiency or inborn error of zinc transporter. Treat with zinc replacement.
Langerhans cell histiocytosis	May mimic candidiasis or seborrheic dermatitis. Persistent, does not improve with standard treatments. Clusters of infiltrative, crusted, hemorrhagic papules. Ulceration can be seen.	Involvement of groin, axillae, periauricular skin, hairline, and scalp. Anemia, thrombocytopenia, hepatosplenomegaly, and osseous lesions.	Chemotherapy.

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