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.
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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