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The skin of a newborn infant differs from adult skin in several ways that place infants at increased risk for thermal instability, skin damage, percutaneous infection, and percutaneous toxicity from topically applied agents. The neonatal body surface area–to–weight ratio is far greater than that of an adult with thinner skin overall. Sebaceous glands are hypertrophic for several weeks after birth, under the influence of fetal and maternal androgens, but eccrine function does not mature until after term, placing newborns at risk for hyperthermia with overbundling. The vernix caseosa is composed of sloughed keratinocyte and sebaceous gland lipids, with a higher proportion of glandular lipids in males.

The most clinically significant difference between the skin of a premature infant and that of a term infant is the barrier function of the most superficial layer of the epidermis, the stratum corneum. Infants born before 32 weeks of gestation have a very thin stratum corneum. Although even in premature neonates the stratum corneum matures within 2 weeks after birth, premature infants suffer from significant transepidermal water loss with associated hypothermia and fluid and electrolyte disturbances. These problems are proportional to the degree of prematurity. Transepidermal water loss is 10 times higher for an infant born at 24 weeks of gestation than for a term neonate. Barrier function rapidly improves during the first 2 weeks after birth, but infants born at 25 weeks or less can have increased transepidermal water loss for significantly longer than 4 weeks after gestation. Benign clinical interventions such as barrier creams or ointments can dramatically decrease these losses. During this period, medications with the potential for systemic toxicity such as hexachlorophene or povidone iodine should be avoided. Desiccated skin is even more susceptible to injury, providing a portal of entry for invading microbes and increasing the risk of disseminated infection.


Aplasia Cutis Congenita

The congenital absence of skin is a cutaneous anomaly most often seen at the scalp vertex. Sharply marginated lesions may present either singly or as multiple ulcers, bullae, or scars that measure up to several centimeters in diameter (Fig. 352-1). Aplasia cutis can have underlying skull defects, and larger irregular defects may extend to the dura or meninges. These larger lesions are more often familial and may be complicated by meningitis, hemorrhage (which can be fatal), or sagittal sinus thrombosis. Aplasia cutis of the trunk and extremities is often strikingly symmetric in distribution. Histologically, aplasia cutis is characterized by absent epidermis, diminished dermis and adnexal structures, or, in full-thickness lesions, the absence of all skin layers.

Figure 352-1

Aplasia cutis with a “hair collar sign” on the superior scalp.

Several distinct subtypes of aplasia cutis have been described on the basis of distribution, mode ...

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