Chapter 7

Newborn skin is thinner, it is less hairy, it has less pigment, it has a weaker attachment of the epidermis to the dermis, and newborns may have brown fat. ^∗

The skin of premature infants is immature and has compromised barrier function ( Fig. 7-1). Clinical consequences include increased transepidermal water loss; fluid and electrolyte disturbances; temperature instability; infection (cutaneous and systemic); absorption of substances applied to the skin; and susceptibility to mechanical, chemical, and thermal stresses.

Most premature infants exhibit rapid maturation of skin barrier function over the first 2 to 3 weeks of life. In infants born before 25 weeks’ gestation, skin barrier function may require 8 weeks or longer after birth to mature.

Prilocaine, resorcinol, aniline dyes, and methylene blue can lead to methemoglobinemia. ^∗

Hypothyroxinemia and goiter have been reported. ^∗

Skin injury may accompany routine care of very premature infants. Anetoderma of prematurity is the term for focal depressions or outpouchings, which are presumed to be a response to mechanical or thermal injury to the skin.

Although bacteria, especially Staphylococcus and Streptococcus species, should always be considered as a cause of cutaneous pustules, tape sites have been associated with opportunistic fungal infections of the skin, especially involving Aspergillus species. Other fungi and yeast, including Rhizopus and Candida organisms, should also be considered. Performing a biopsy and culture is a standard approach to diagnosis. ^∗

Infants that receive numerous heel sticks may develop calcinosis cutis over the heel. This seldom shows up until several months after discharge. The presenting symptoms are small yellow or white papules that can be mistaken for warts. They are generally not symptomatic and will often resolve by 30 months of age. If they become problematic, they can be treated with curettage.

Subcutaneous fat necrosis of the newborn usually appears within the first weeks of life with red to violaceous mobile plaques, especially on the back, thighs, and cheeks. The cause of subcutaneous fat necrosis is not definitively known.

Subcutaneous fat necrosis may occur in cases of fetal distress, birth trauma, infection, or cold stress. It is increasingly being seen after the use of whole body cooling for the treatment of hypoxic-ischemic birth injury. ^∗

Although the disorder is most often benign and self-limited, in some cases subcutaneous fat necrosis of the newborn may be associated with hypercalcemia and death. Therefore serum calcium levels must be monitored, and caregivers must be vigilant for clinical signs and symptoms of hypercalcemia.

Findings of sclerema usually appear in the first 2 weeks of life but can begin as late as 4 months. Infants who are poorly nourished, dehydrated, hypothermic, or septic are most commonly affected. Sclerema neonatorum begins in the lower extremities with the appearance of hard, cool skin and decreased mobility and subsequently ascends to involve the trunk and face. Palms, soles, and genitalia are usually not involved. Joints become immobile, and the face appears masklike. Sclerema may be associated with necrotizing enterocolitis, pneumonia, intracranial hemorrhage, hypoglycemia, and electrolyte disturbances. ^∗

Sclerema is likely a result of lipoenzyme dysfunction and occurs in infants who are stressed with severe illnesses. More specifically, dysfunction of enzymes regulating the conversion of saturated fatty acids to unsaturated fatty acids results in an excess of saturated fatty acids. This dysfunction promotes fat solidification. The incidence of sclerema has decreased significantly in recent years because events such as malnutrition, dehydration, and hypothermia occur less commonly in modern nurseries. Treating the underlying condition can result in resolution of sclerema. Some authors also propose systemic steroids or therapy with exchange transfusions.

Cutis marmorata is a reticulated (i.e., netlike) mottling of the skin seen in most infants. It is seen most often when the environment is cooler and will usually improve if the infant is warmed. It usually improves in childhood, but can be persistent in patients with Down syndrome, trisomy 18, and Cornelia de Lange syndrome.

Harlequin color change is a demarcated erythema forming on the dependent half of the body of newborns. In some cases the baby appears as if a line were drawn right down the midline. The more superior half of the body appears pale. This appearance can occur in any position and commonly lasts from seconds up to 20 minutes. It is rarely seen after 10 days of life. Harlequin color change is explained by immature autonomic vasomotor control because it is more common in premature infants and is reversible. If the baby is flipped over during an episode, the newly dependent portion will become erythematous.

All three forms represent cystic retention of keratin, appear and resolve in the first month, and can be present at birth. They are white, 1- to 2-mm papules that can be found singularly or in clusters.

Aplasia cutis congenita results from failure of the development of the normal layers of skin. It occurs most often on the scalp and may present clinically as an ulcer, healed erosion, or well-formed scar. Therefore it is often mistaken for trauma caused by a scalp pH probe. In cases of large lesions or lesions overlying the midline neurocranial axis, imaging should be considered because aplasia cutis congenita may be associated with underlying malformations of bone or may extend deeply to the meninges. Large and irregular lesions can also be associated with Adams–Oliver syndrome and chromosomal abnormalities.

Dermoid cysts form along embryonic fusion lines. They are congenital but may not be seen until childhood, when they begin to enlarge. They commonly occur along the orbital ridge. Surgical removal is recommended because they can become infected. When they are located along the lateral eyebrow, they do not require specific imaging. Other locations, especially midline, can have a connection to the central nervous system and should be imaged before surgery.

This description fits a dermoid sinus. Midline lesions should always raise the possibility of a developmental defect. The presence of a hair coming out of the sinus is especially significant because it is considered a marker for a connection with the central nervous system. The baby should be imaged before the defect is repaired.

Preauricular skin tags, also called accessory tragi, are embryonic remnants of the first branchial arch ( Fig. 7-3). The formation of the first branchial arch occurs during the fourth week of fetal development. Because this may be associated with hearing abnormalities, patients should have their hearing screened before they are discharged from the hospital. The evidence for associated renal problems in patients with no other associated abnormalities is controversial. Renal ultrasound should be considered for patients with additional dysmorphic features or a family history of deafness or renal malformations. ^∗

Accessory nipples, also called supernumerary nipples ( Fig. 7-4), are embryonic remnants of the mammary line that extend from the axilla to the inner thigh. They appear as pink or brown papules, with or without surrounding areola, anywhere along the mammary line. There have been conflicting reports about an association with urinary tract abnormalities. Current studies, however, have not found an association in patients who have no other anomalies.

A CMN is usually defined as a melanocytic lesion that is present at birth. The incidence is reported to be 0.5% to 2%.

Most CMNs do not have any associated complications. CMNs are often subdivided according to their size. A common classification is that a CMN greater than 20 cm in adulthood is considered to be large. Melanoma has been reported to arise within congenital lesions, but the exact risk for this complication is unclear. It is known that large lesions carry the greatest risk and that melanoma, when it occurs, does so earlier in life. Leptomeningeal melanosis is a rare complication that may occur in association with a giant congenital nevus with numerous satellite nevi. ^∗

The cause and nomenclature of these conditions remain somewhat controversial. Some neonatal outbreaks, although commonly called neonatal acne, are not composed of distinct pimples (i.e., comedones) but rather superficial pustules.

Erythema toxicum is a benign condition ( Fig. 7-5). Erythema toxicum is no alien to the nursery; it is present in 50% of term newborns. It is much less prevalent in premature infants, however, occurring in only approximately 5%.

Erythema toxicum usually begins between 24 and 48 hours of life and spontaneously resolves in 4 to 5 days; however, new lesions can occur up to day 10 of life. Exacerbations and remissions may occur in the first 2 weeks of life. Erythema toxicum lesions are irregularly bordered, erythematous macules, 2 to 3 cm in diameter, with central yellowish vesicopustules. They are mostly discrete, but some erythematous macules become confluent. Lesions do not involve the palms or soles.

Wright-Giemsa stains of pustule scrapings show mostly eosinophils. Up to 15% of affected infants demonstrate peripheral eosinophilia as well.

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Fetal _ Neonatal Secrets 3e