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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 up to 5 times greater than that of an adult, and the thickness of infant skin is 40% to 60% less.1 Attenuated rete ridges, formed from comparatively fewer stem cells at the basal layer, provide a relatively limited area of surface attachment to an immature dermis, resulting in relative skin fragility. 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 boys.

The most clinically significant difference between the skin of a premature 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.2 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.3 Benign clinical interventions such as barrier creams or ointments can dramatically decrease these losses. During this period, cutaneous contact with chemicals that can cause neurotoxicity, such as hexachlorophene, or alter thyroid function, such as povidone iodine, should be avoided.2,4 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 (eFig. 357.1). 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.5 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.

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