Common Skin Problems During the First Year of Life

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CARE OF THE INFANT

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COMMON SKIN PROBLEMS DURING THE FIRST YEAR OF LIFE Elizabeth J. LaVoo, MD, and Amy S. Paller, MD

This article reviews the most common skin problems encountered in the first year of life, not necessarily the most extensive or severe, and it is not meant to be all inclusive of problems that can be seen at this age. The spectrum of common skin problems in the first year of life includes congenital disorders, infections, infestations, and disorders that may occur in adults as well. 6 , 12, 15

TRANSIENT, BENIGN NEONATAL DISORDERS

The most common transient cutaneous abnormality in the neonate is erythema toxicum neonatorum, a disorder of unknown cause characterized by erythematous macules, papules, vesicles, and pustules (Table 1).14 This disorder occurs in approximately 50% of newborns and is less common in premature neonates, The lesions usually appear at 2 to 3 days of age and clear spontaneously at the end of the first week of life; however, erythema toxicum may appear as late as 3 weeks of age, The face, trunk, and extremities are usually affected, and the palms and soles are almost always spared, The diagnosis may be confirmed by performing a smear of the contents of a vesicle or pustule which shows eosinophils with rare polymorphonuclear leukocytes, Blood eosinophilia (up to 18%) may be associated. In contrast, transient neonatal pustular melanosis is usually noted at birth or within the first 24 hours of life. It occurs in fewer than 5% of newborns, primarily in black neonates. The typical lesions are pustules and vesicles with a collarette of scale (Fig. 1); hyperpigmented

From the Departments of Pediatrics and Dermatology, The Children's Memorial Hospital, Northwestern University Medical School, Chicago, Illinois

PEDIATRIC CLINICS OF NORTH AMERICA VOLUME 41· NUMBER 5· OCTOBER 1994

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Table 1. VESICULOPUSTULAR DISORDERS OF THE NEONATE AND INFANT Disorder

Confirming Diagnostic Test'

Erythema toxicum neonatorum Transient neonatal pustular melanosis

Wright's stain

Herpes simplex

Tzanck smear Rapid antigen immunoassay Viral culture KOH preparation Fungal culture

Candidiasis Folliculitis

Wright's stain Gram stain

Scabies

Gram-stain Wright's stain Bacterial culture Mineral oil preparation

Miliaria

Wright's stain

Expected Findings Many eosinophils, rare neutrophils Many neutrophils, rare eosinophils No organisms Multinucleated giant cells Positive for herpes simplex Growth of herpes simplex Pseudohyphae and spores Growth of Candida albicans Gram-positive cocci Neutrophils Growth of S. aureus Mites, eggs, and feces identified Mainly lymphocytes

·Biopsies can be done for any of these disorders if tests are not characteristic and the clinical situation warrants. If a secondary pyoderma is suspected, Gram stain and culture should be added. Data from Schachner LA, Press S: Vesicular, bullous, and pustular disorders in the neonate and infant. In Schachner LA, Hanson RC (eds): Pediatric Dermatology, Vol 1. New York, Churchill-Livingstone, 1988, p 820.

Figure 1. Multiple lesions of transient neonatal pustular melanosis on the back of a black neonate. Note the discrete pustules and also many "collarettes of scale" on the lower back of the baby.

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macules also may occur. The vesicles and papules clear spontaneously by 3 days of age, and the hyperpigmented macules by 3 months. Scrapings from the vesicles or pustules show neutrophils with rare eosinophils. The lesions of erythema toxicum and transient neonatal pustular melanosis are benign and require no therapy. Miliaria rubra and miliaria crystallina result from obstruction and rupture of the eccrine sweat ducts. Miliaria crystallina (sudamina) is an asymptomatic eruption characterized by crops of 1- to 2-mm clear vesicles that rupture easily. This eruption is not uncommon in neonates, particularly if overheating occurs. The duct obstruction in miliaria crystallina is superficial, and the vesicle forms beneath the horny layer. Miliaria rubra (heat rash) is a pruritic eruption in response to heat and sweating that is often found on areas of skin covered by clothing and is characterized by erythematous papulovesicles and rarely pustules. The sweat duct obstruction is deeper than in miliaria crystallina. Spontaneous resolution can be hastened by controlling ambient temperature and humidity and by removing excess clothing. If the clinical diagnosis is not apparent, fluid from the lesions can be stained; vesicular fluid of miliaria crystallina should be free of cells, whereas lesions of miliaria rubra may contain lymphocytes. Approximately one half of all newborns have milia. Milia are minute epidermal cysts limited to the epidermis. They appear as single or multiple 0.5- to 2.0-mm white or yellow firm papules, primarily on the face. Milia tend to clear spontaneously over several weeks. Suction blisters result from the friction of repeated sucking in utero or in early infancy, particularly on a finger, hand, or lip. Self-healing occurs. The location, noninflammatory nature of the clear blister, and lack of associated blisters or vesicles is reassuring. Neonatal acne occurs in response to the maternal hormones and usually resolves spontaneously within 1 to 3 months. Most commonly, the face is affected with pustules, papules, and comedones. Two-percent topical erythromycin solution or 2.5% to 5% benzoyl peroxide preparations may hasten resolution. Infantile acne appears after 3 months of life and not uncommonly may have a wider distribution involving nonfacial areas. The severity is variable, but cysts may occur. The process can persist for months to several years. Oral erythromycin might be added to topical agents, especially if scarring or cysts occur. The pathogenesis is unknown, but most commonly, boys with a family history of severe acne are affected. Only unusually severe or persistent acne or an associated virilization should prompt a search for an abnormal endogenous source of androgens.

CUTANEOUS INFECTIONS AND INFESTATIONS

Staphylococcus aureus is the most common cause of honey-crusted impetigo, occasionally coinfected with group A J3-hemolytic streptococcus. Folliculitis, furunculosis, and secondary infection of abnormal skin,

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as in atopic dermatitis, insect bite reactions, and scabies, are the other most common forms of staphylococcal infections. Staphylococcal scalded skin syndrome, bullous impetigo, and staphylococcal scarlet fever result from production by the organism of exfoliatin, an epidermolytic toxin. Staphylococcal scalded skin syndrome has its highest incidence during infancy because of poor metabolism and excretion of the exfoliatin. Infants usually present with cutaneous tenderness, even before any visible skin change. Within 1 to 2 days after onset of cutaneous erythema, superficial crusting of periorificial sites is noted. Superficial desquamation follows before resolution. The staphylococcal organism is usually cultured from the nasopharynx and not from skin. Staphylococcal infections in the neonate should be treated with intravenous antibiotics and isolation to avoid spread in the nursery. Older infants may be treated with oral antistaphylococcal antibiotics. Neonatal candidal infections, acquired by passage through the infected genital area, present as moist red dermatitis in the diaper area, often with satellite pustules at the borders. Other intertriginous folds also may be affected, and thrush may be associated. Recurrent episodes of candidal infection tend to accompany usage of antibiotic therapy in affected infants. A potassium hydroxide preparation shows the presence of pseudohyphae and spores, and confirmatory cultures yield Candida albicans. Congenital cutaneous candidiasis, a rare condition, presents within the first 24 hours of life as a widespread papulovesicular eruption due to ascending transplacental infection, usually without visceral involvement. Both neonatal and congenital cutaneous candidiasis are treated with topical anticandidal therapy, with the addition of nystatin oral suspension for thrush. Herpes simplex infection in the newborn infant is the most devastating of the vesiculopustular eruptions.3, 13, 17 Lesions may be single or grouped. Tzanck smears of lesional contents may show multinucleated epidermal cells and occasionally intracytoplasmic inclusion bodies. Rapid antibody tests for herpes simplex are usually positive. Viral cultures are confirmatory. Administration of intravenous acyclovir should be initiated if the diagnosis of herpes simplex is suspected. Primary herpetic stomatitis also may develop during the first year of life with associated fever and adenopathy. Roseola (exanthem subitum), a viral infection caused by human herpesvirus 6, is now known to have a wide spectrum of presentations and complications. 1O,18 Roseola commonly presents as a fever for 3 to 5 days followed by a maculopapular erythematous rash on the face, neck, and trunk lasting 1 to 2 days. Most infants acquire this infection in the first year of life, especially after the first 6 months of age as maternal antibodies begin to diminish. Either isolated fever or rash may occur. Rare clinical findings include mild respiratory signs and symptoms, lymphadenopathy, especially suboccipital, mild diarrhea, fatigue, and hepatosplenomegaly with hepatitis. Encephalitis and thrombocytopenic purpura have been reported.

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SCABIES

Infestations with scabies in the first year of life differ from scabies in later lifeY, 16 The typical intertriginous burrows may be less apparent than associated papules (Fig. 2) and even vesicles, especially on the palms and soles. The scalp and face are often involved and must be treated. Pruritus may not be apparent in infancy, and secondary eczematization and bacterial infection are common. Nodular hypersensitivity reactions may persist for weeks after treatment. The illite, ova and, feces may be demonstrated on mineral oil preparation of skin scrapings. All members of the household must be treated as well as frequent visitors who have physical contact. Bedding, towels, and clothing must be washed. A single 8 to 12 hour application of permethrin cream 5% is the treatment of choice for infants, although use of lindane is also effective and safe for older children and adults. DIAPER DERMATITIS

Diaper dermatitis is the most common skin condition in infancy, particularly irritant dermatitis due to exposure to stool and urine. Emollients such as white petrolatum and zinc oxide ointment used regularly, and even prophylactically, can be helpful. Simple irritant dermatitis without secondary infection often responds to a short course of 1% to 2.5% hydrocortisone preparations, topped with protective emollients. It is important to recognize superimposed candidal, staphylococcal, and streptococcal infections. Perianal streptococcal infections caused by group A l3-hemolytic streptococcus tend to involve the immediate perianal skin with bright erythema and may cause pain on defecation and occasionally bloody stools. Although perianal streptococcal cellulitis is

Figure 2. Multiple nodules in the axillary area of an infant with scabies.

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rare during infancy, a culture will confirm the diagnosis. Oral penicillin should be given for 10 days with local antibiotic ointments. ATOPIC DERMATITIS

Atopic dermatitis is a chronic, severely pruritic disorder characterized by dry skin, eczematous patches, lichenification, and a predisposition to staphylococcal pyodermas.7,8 The term "atopic" refers to the fact that affected children frequently have elevated IgE levels and a family or personal history of other atopic disorders, especially allergic rhinitis and asthma. The disorder usually begins in infancy and affects up to 10% of 1-year-old children. The diagnosis is made by the characteristic distribution and clinical features of the rash. The lesions of atopic dermatitis are typically intensely pruritic, dry, scaling, erythematous patches, often characterized by edema and linear excoriations. The lesions are poorly defined, and their borders fade gradually into the surrounding normal skin sites. In infants, the rash is frequently exudative (Fig. 3), even without secondary infection. Well-circumscribed patches of eczema (nummular eczema) are less common during the first year of life than in older children. With persistent disease, evidence of chronicity may be present, including thickened skin with exaggerated skin markings (lichenification) and hyperpigmentation. In infancy, the eruption may be widespread or limited to areas with maximal irritation, such as the perioral area and cheeks. By the second half of the first year of life, the crawling infant is most severely affected on the extensor surfaces of the arms, wrists, and legs. The most common complication of atopic dermatitis is secondary bacterial infection of affected areas of skin by Staphylococcus aureus, especially at excoriated sites. Patients with secondary infection will often not respond to appropriate therapy for the underlying eczema unless the infection is cleared with systemic antibiotics. Eczema herpeticum (Kapo-

Figure 3. Exudative facial dermatitis in an infant with atopic dermatitis.

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si's varicelliform eruption) is a severe complication of atopic dermatitis, characterized by the abrupt development and rapid spread of the vesicles of herpes simplex. The lesions are usually multiple groups of intact or umbilicated vesicles and pustules overlying erythematous bases. The diagnosis may be further classified by the finding of multinucleated giant epithelial cells by Tzanck smear or a positive rapid antibody test for herpes simplex, and confirmed by culture. Infants with atopic dermatitis also have an increased risk of the development and spread of molluscum contagiosum. The major components of treatment for infants with atopic dermatitis are good emollients, especially following baths, and appropriate topical corticosteroid preparations, usually hydrocortisone. Parents should understand that atopic dermatitis is a chronic condition, and that quick cures do not exist. They should be reassured, however, that therapy can result in dramatic improvement. If bacterial infection is suspected and involves more than a small area, the patient should be treated with systemic antistaphylococcal antibiotics, such as cephalexin. Infants with herpetic infections should be treated with systemic acyclovir, in addition to compresses and topical antibiotics. Infants with significant involvement require hospitalization for intravenous therapy. Secondary bacterial infection of herpetic lesions should be treated with systemic antistaphylococcal antibiotics. Manipulation of diet through changing formula to casein hydrolysate or restriction of maternal ingestion of allergens for breast-fed babies helps some patients. SEBORRHEIC DERMATITIS

Seborrheic dermatitis of the infant often develops between 2 and 10 weeks of life. Redness and greasy scaling most commonly involves the scalp, but the face, neckfolds, axillae, and diaper area may be affected as well. The pathogenesis is unknown, but investigators have recently linked seborrheic dermatitis to overgrowth of pityrosporum yeast. Resolution is hastened by the use of topical antifungal agents and by nonfluorinated topical corticosteroid creams. Softening of scalp scales with mineral oil overnight followed by a antiseborrheic shampoo applied at least every other day is often effective. In some patients, it may be difficult to differentiate seborrheic dermatitis from early atopic dermatitis. Recurrence of seborrheic dermatitis after clearing, dry white scaling, more widespread involvement, pruritus, or a strong family history of atopy should prompt consideration of atopic dermatitis. VASCULAR LESIONS

Vascular disorders occur in 20% to 40% of newborn infants. Telangiectasias are ectatic vessels, and hemangiomas are collections of proliferating endothelium-lined vessels. Although usually confined to the skin,

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vascular lesions may occur in other organs and are occasionally associated with systemic complications or as a feature of a variety of syndromes. The most common form of hemangioma is the superficial (capillary, "strawberry") hemangioma which is a raised, red, firm, well-circumscribed, partially compressible lesion.4,s, 6,9 Deep (cavernous) hemangiomas are characteristically red-blue, soft, poorly demarcated, compressible lesions. The depth of the vascular lesion imparts the blue color. Often a combination of superficial and deep elements occurs, the mixed hemangioma (Fig. 4). Overall, 10% of infants have hemangiomas at 1 year of age, although hemangiomas are more common in premature infants. Most hemangiomas are not present at birth, but appear within the first weeks after birth. The face, scalp, and thorax are the usual sites. The initial lesion may appear as fine telangiectasias surrounded by pallor or as an erythematous patch that resembles nevus flammeus. The surface often develops a lobulated texture as the lesion expands and becomes more elevated during the first few months of life. Superficial hemangiomas may be confused with pyogenic granulomas, common vascular lesions that are bright red, firm, raised, slightly pedunculated papules. Pyogenic granulomas grow rapidly and bleed easily, but may clear spontaneously. They usually respond well to shave and electrodessication or laser therapy. Hemangiomas grow rapidly during the first 6 months of life, but usually do not more than double in size. During this period of rapid growth, complications may occur. Larger lesions, especially those that are subject to trauma, may ulcerate. Ulcerated lesions do not tend to bleed significantly, but may become secondarily infected and result in scarring. A more serious complication that may occur during the period of rapid expansion is the development of thrombocytopenia, microangiopathic anemia, and disseminated intravascular coagulation, which is thought to be caused by platelet trapping within the growing hemangioma (Kasabach-Merritt syndrome). Disseminated eruptive hemangiomas de-

Figure 4. Mixed hemangioma on the labial area. These hemangiomas often develop surface erosion with secondary infection, and healing is made difficult by frequent irritancy in the diaper area.

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velop in crops of up to hundreds of hemangiomas during the first 3 months of life. Visceral hemangiomas, especially of the liver, gastrointestinal tract, spleen, lungs, eyes, and central nervous system, may be associated. Most hemangiomas do not enlarge after 12 months of life and subsequently begin to involute spontaneously. In the process of involution, capillary hemangiomas become pale centrally with lacy gray regions within the lesion. Clinical regression is complete in 60% of children by the time that they begin school and in more than 90% of children by 9 years of age. The superficial and deep hemangiomas follow a similar course. In general, no treatment is indicated for hemangiomas. The longterm cosmetic result of spontaneous involution is usually superior to that of treatment with cryotherapy, sclerosing agents, surgery, or radiation, all of which often lead to scarring or atrophy; in contrast, treatment of the superficial component of selected hemangiomas with the pulsed dye laser is extremely effective without residual scarring and is particularly useful for facial and diaper area hemangiomas. Occasionally, hemangiomas require intervention because their location or size compromise vital structures, especially the eyes and airway. When therapy is needed, prednisone is usually the most effective agent, in a dosage of 2 to 3 mg/ kg/ d for at least the first month, followed by gradual withdrawal as tolerated. Involution usually begins by the second or third week. Intralesional injections of corticosteroids are most useful for periorbital hemangiomas and ulcerating hemangiomas in the diaper area. Interferon-a is now considered by many investigators to be the treatment of choice for patients with Kasabach-Merritt syndrome. The salmon patch, the most common vascular lesion of infancy, is a congenital telangiectatic nevus. It occurs in 40% of infants, most commonly as a flat pink macule on the nape of the neck ("stork bite"); glabellar or upper eyelid ("angel kiss") sites may be associated or occur separately. Ninety-five percent of salmon patches on the glabella and eyelids disappear within the first years of life, and 50% of the nuchal lesions clear spontaneously. Cutis marmorata is a normal physiologic response of transient vascular mottling that occurs in response to chilling during the first weeks of life in neonates. Cutis marmorata telangiectatica congenita is a congenital vascular disorder with persistent, prominent venules and capillaries, resulting in a deep red mottling of skin. Affected patients may have associated abnormalities, particularly limb asymmetry, macrocephaly, and mental and psychomotor retardation. The port wine stain (nevus flammeus) is a permanent vascular lesion of dilated mature capillaries that is present at birth. It grows in proportion to the growth of the child, and may thicken with age (Fig. 5). The lesions are flat and pink to reddish-purple. The vascular lesions may be treated with pulsed dye laser therapy as early as the first weeks of life. The KlippelTrenaunay- Weber syndrome combines the triad of nevus flammeus, associated hypertrophy or hypotrophy of the soft tissue and bone, and venous varicosities of an extremity. The Sturge-Weber syndrome (encephalotrigeminal angiomatosis) is a congenital vascular disorder characterized by

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Figure 5. Extensive nevus flammeus in an infant. With such extensive involvement, the possibility of Sturge-Weber syndrome, ophthalmic involvement, and/or Klippel-Trenaunay-Weber syndrome must be considered.

vascular malformation of the vessels of the leptomeninges over the cerebral cortex (usually the posterior parietal and occipital lobes) in association with an ipsilateral nevus flammeus in the distribution of the first trigeminal nerve. Patients usually have seizures at an early age with cerebral atrophy. Ocular abnormalities, especially glaucoma, are more prevalent in infants with involvement of both the first and second trigeminal branches. PIGMENT ABNORMALITIES

Mongolian spots are flat, blue-gray, often poorly circumscribed lesions that are usually found on the buttocks, lumbosacral area and shoulders of infants, especially in black, oriental, and hispanic infants. The lesions are thought to represent melanocytes that have failed to migrate to the epidermis. The blue color results from the depth of the pigmentation and the reflection of blue light (Tyndall effect). Mongolian spots usually disappear within the first 5 years of life. In contrast with the disappearance of Mongolian spots, nevus of Ota and nevus of Ito persist and often darken with increasing age. The nevus of Ota is usually found

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in black or oriental female patients and is characterized by patchy blue discoloration of the periorbital area, forehead, upper cheek, and sclera. The nevus of Ito shares the clinical characteristics of the nevus of Ota, but involves the shoulder, upper arms, scapula, and supraclavicular regions. Blue nevi are small, round, well-circumscribed melanocytic nevi that are blue in color; they are rarely congenital. Cafe-au-Iait spots are well-circumscribed, homogeneously light brown macules that are usually present at birth or noticed during the first year.! Ten percent of all people have one cafe-au-Iait spot, although the presence of greater than two cafe-au-Iait spots is unusual (less than 0.75%). Cafe-au-Iait spots are associated with polyostotic fibrous dysplasia (large, usually solitary cafe-au-Iait spot) and neurofibromatosis (greater than five, may have associated axillary freckling). White spots, or hypopigmented macules, occur in 0.2% to 0.3% of all neonates. Although of no clinical significance in most neonates, one or more white spots may be an additional sign of tuberous sclerosis in a neonate with seizures, or cardiac obstructive abnormalities due to a rhabdomyoma. The term congenital nevus refers to a nevocellular (melanocytic) nevus present at birth (or noted within a few months of life).!' 6 The proper management of congenital nevus remains unclear and awaits the results of prospective trials, which are in progress. Infants with giant congenital nevi have a lifetime risk of melanoma of 4.6% to 6.3%, particularly during the first decade of life. For small or mid sized congenital nevi, however, the risk of malignant transformation is estimated to be much lower than that of giant congenital nevi. In general, most physicians recommend excision of giant congenital nevi during infancy, often using tissue expansion techniques. 2 Smaller nevi should be examined periodically, and parents should be instructed about changes that suggest transformation (irregular borders, variegate pigmentation, abnormal topography). The medical necessity for prophylactic excision of smaller to midsized congenital nevi (Fig. 6) has not been established, but most dermatologists recommend periodic reevaluation and removal by puberty because of the increased risk after that time of melanoma.

NEVUS SEBACEUS

Nevus sebaceus of Jadassohn is a congenital lesion with excessive sebaceous glands and malformed hair follicles.! Usually a single, yellowish-orange, slightly raised, hairless plaque is located on the scalp (Fig. 7) or less commonly on the face. Verrucoid thickening develops at puberty, because the glands respond to androgens. Benign and malignant tumors develop in 20% of patients as a lifetime risk. Slow-growing basal cell carcinomas are by far the most common, but aggressive metastasizing tumors of a variety of cell types have been reported in adults. Fullthickness excision at or before puberty is advised. Timing may depend on the location of the tumor and cosmetic needs of the patient.

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Figure 6. Medium-sized congenl-

tai pigmented nevus. Luxuriant, darker hair within the nevus is a frequent and benign finding.

JUVENILE XANTHOGRANULOMAS

Juvenile xanthogranulomas (JXGs) are often present at birth and commonly appear during the first year of life (Fig. 8). JXGs may be single or multiple, dome-shaped or flattened. Lesions may be red initially, and gradually become the typical yellow-orange color. Biopsy of the lesion, if necessary, shows lipidized dermal cells with Touton-type giant cells.

Figure 7. Nevus sebaceus is most commonly located on the . scalp as a hairless patch which is often yellow and pebbly during the first months of life.

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Figure 8. Juvenile xanthogranuloma most often is noted at birth or develops during the first year of life as a yellow papulonodule.

Rarely, cutaneous JXGs are associated with extracutaneous involvement, the most serious being the ocular complications of glaucoma and hyphema; screening ophthalmologic examination should be performed in any patient with a JXG. JXGs tend to clear spontaneously within a few years, sometimes leaving localized atrophy. They are most likely to be confused in appearance with mastocytomas (see following section).

MASTOCYTOSIS

The group of disorders characterized by mast cell infiltration of skin is called mastocytosis. In the neonate and young infant, collections of

mast cells usually manifest as mastocytomas, usually solitary, slightly elevated, red-brown nodules that are most frequently located on the trunk or arms (Fig. 9). In older infants, urticaria pigmentosa is the most common form. Urticaria pigmentosa is characterized by solitary or mul-

Mastocytomas are collections of excessive numbers of mast cells. Stroking of lesions usually leads to erythema, swelling, or frank blister formation due to the release of mast cell contents. Figure 9.

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tiple, red-brown macules, papules and nodules. The lesions are usually 1 to 3 ern in diameter and most commonly are located on the trunk. When mastocytomas or lesions of urticaria pigmentosa are stroked, they usually become erythematous and edematous (Oarier's sign); often they become urticarial or frankly bullous. The reaction is thought to relate to the release of mast cell contents, especially histamine. Histopathologic examination of skin biopsy samples shows large numbers of mast cells in the dermis and subcutaneous tissues. Mastocytomas usually clear by school age and often fail to urticate after 1 year of age because of progressive mast cell depletion. Patients with urticaria pigmentosa usually show significant clearance of lesions spontaneously by puberty. Systemic involvement is rare in children who develop the disorder before 10 years of age. Most infants with mastocytosis are asymptomatic and require no therapy. Patients with pruritus, urticaria, flushing, or more severe symptoms are best managed by antihistamine administration and the avoidance of exacerbating factors. Parents should be aware that a variety of drugs, toxins, radiographic dyes, and agents used during general anesthesia in addition to local physical stimulation can precipitate mast cell degranulation and symptoms. TOPICAL THERAPY

Because many chemicals can be absorbed transcutaneously and some can produce systemic toxicity, it is important to carefully consider any topical application to an infant. Active ingredients as well as all components of the vehicle are potentially absorbed. The degree of absorption is increased in the preterm infant because of the thinner epidermis and stratum corneum, and also because of a lack of detoxifying enzyme activity, normally found in adult epidermis. Preterm infant skin is more fragile and has a tendency for hypohidrosis, because of immature sweat glands. If topical preparations are used, they should be limited to bland emollients and specifically required drugs in the newborn and especially the preterm infant. References 1. Alper J, Holmes LB, Mihm MC: Birthmarks with serious medical Significance: Nevocel-

lular nevi, sebaceous nevi, and multiple cafe au lait spots. J Pediatr 95:696,1979 2. Bauer BS, Vicari FA: An approach to excision of congenital giant pigmented nevi in infancy and early childhood. Plast Reconstr Surg 2:1012,1988 3. Brown ZA, Benedetti J, Ashley R: Neonatal herpes simplex virus infection in relation to asymptomatic maternal infection at the time of labor. N Engl J Med 324:1247, 1991 4. Esterly NB: Cutaneous hemangiomas, vascular stains, and associated syndromes. Curr Probl Pediatr 17:1, 1987 5. Esterly NB: Hemangiomas in infants and children: Clinical observations. Pediatr Dermatol 9:353,1992. 6. Esterly NB, Solomon LM: Neonatal dermatology, III: Pigmentary lesions and hemangiomas. Pediatrics 81:1003, 1972

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7. Hanifin JM: Atopic dermatitis in infants and children. Pediatr Clin North Am 38:763, 1991 8. Hanifin JM: Atopic dermatitis: New therapeutic considerations. J Am Acad Dermatol 24:1097, 1991 9. Hurvitz C, Alkalay A: Managing hemangiomas. Pediatrics 87:582,1991 10. Irving WL, Chang J, Raymond DR, et al: Roseola infantum and other syndromes associated with acute HHV6 infection. Arch Dis Child 65:1297, 1990 11. Paller AS: Scabies in infants and small children. Semin Dermatol12:3, 1993 12. Rivers JK, Frederiksen pc, Dibdin C: A prevalence survey of dermatoses in the Australian neonate. J Am Acad Dermatol23:77, 1990 13. Sarkell B, Blaylock WK, Vernon H: Congenital neonatal herpes simplex virus infection. J Am Acad Dermatol 27:817, 1992 14. Schachner LA, Press S: Vesicular, bullous, and pustular disorders in the neonate and infant. In Schachner LA, Hansen RC (eds): Pediatric Dermatology, vol 2. New York, Churchill-Livingstone, 1988, p 820 15. Solomon LM, Esterly NB: Neonatal dermatology, I: The newborn skin. J Pediatr 77:888, 1970 16. Taplin D, Meinking T: Scabies. In Schachner LA, Hansen RC (eds): Pediatric Dermatology, vol 2. New York, Churchill-Livingstone, 1988, p 1065 17. Whitley R, Arvin A, Prober C, et al: Predictors of morbidity and mortality in neonates with herpes simplex virus infections. N Engl J Med 324:450, 1991 18. Yamanashi K, Shiraki K, Kondo T, et al: Identification of human herpesvirus-6 as a causal agent for exanthem subitum. Lancet 1:1065,1988

Address reprint requests to Amy S. Paller, MD Division of Dermatology #107 Children's Memorial Hospital 2300 Children's Plaza Chicago, IL 60614