A 2-week-old infant is brought to the office for her first well-baby check. The parents noticed a rash on the face. You diagnose the white spots on the bridge of the nose as milia and neonatal acne on the cheeks. The parents are happy to hear that the neonatal acne and milia will go away without treatment (Figures 92-1 and 92-2).
FIGURE 92-2
Neonatal acne on the same infant as in Figure 92-1. (Used with permission from Richard P. Usatine, MD.)
Rashes are common in newborns. Physicians will be consulted frequently as they are a common parental concern. Almost all newborn rashes are benign; however, a few are associated with more serious conditions. A newborn’s skin shows a variety of changes during the first 2 months of life and most are self-limited. Physicians must be prepared to identify common rashes and provide advice to parents.1
Milia are inclusion cysts that appear as tiny white papules in the skin (Figure 92-1) or on the roof of the mouth.
Neonatal acne is an acneiform eruption appearing as small red papules or whiteheads with surrounding erythema on the skin of newborns (Figure 92-2).
A mongolian spot is a hereditary, congenital macule of bluish-black or bluish-gray pigment usually in the sacral area, back, and buttocks of infants (Figures 92-3 and 92-4).
Erythema toxicum neonatorum (ETN) is a benign, self-limited skin eruption appearing as small yellow-white papules or vesicles with surrounding skin erythema (Figures 92-5 and 92-6).
Approximately 40 percent of newborn infants in the US develop milia.2 This condition is mainly associated with newborns carried to full term or near term.
Neonatal acne occurs in up to 20 percent of the newborns. It typically consists of close comedones of the forehead, nose, and cheeks, although other locations are possible. It is most frequent in boys in the first week of life and is 5 times more common in boys than girls.3
The prevalence of mongolian spots varies among different ethnic groups. They have been reported in approximately 96 percent of black infants, 90 percent of Native American infants, 81 to 90 percent of Asian infants, 46 to 70 percent of Hispanic infants, and 1 to 10 percent of white infants.2,4,5
ETN occurs in 30 to 70 percent of full-term infants and in 5 percent of premature infants. The incidence rises with increasing gestational age and birth weight.6,7
In one case series of infants in the first 48 hours of life in San Diego (N = 594), the incidence of milia was 8 percent and ETN, 7 percent.8 A prevalence rate of ETN of 16.7 percent was found within the first 72 hours in 1,000 Spanish infants.9
Milia are inclusion cysts that contain trapped keratinized stratum corneum surrounded by a dense lymphocytic infiltrate. Milia are caused by retention of keratin within the dermis. They may rarely be associated with other abnormalities in syndromes such as epidermolysis bullosa and the orofacial digital syndrome (type 1).2,10
Neonatal acne was thought to be due to maternal androgenic hormones stimulating sebaceous glands; more recently it is theorized that neonatal acne is caused by an increase in dehydroepiandrosterone (DHEA) production causing enlargement and possibly hyperactivity of the fetal adrenal gland.3
Histologic examination shows hyperplastic sebaceous glands with keratin-plugged orifices.
The mongolian spot is a hereditary, congenital, developmental condition exclusively involving the skin. It results from entrapment of melanocytes in the dermis during their migration from the neural crest into the epidermis.
Mongolian spots are associated with cleft lip, spinal meningeal tumor, melanoma, and phakomatosis pigmentovascularis types 2 and 5.2,11
A few cases of extensive mongolian spots have been reported with inborn errors of metabolism, the most common being Hurler syndrome, followed by gangliosidosis type 1, Niemann-Pick disease, Hunter syndrome, and mannosidosis. In such cases, they are likely to persist rather than resolve.2,4
The etiology of ETN is not known. ETN is thought to be an immune system reaction; the condition is associated with increased levels of immunologic and inflammatory mediators (e.g., interleukins 1 and 8, eotaxin).12
The eosinophilic infiltrate of ETN suggests an allergic-related or hypersensitivity-related etiology, but no allergens have been identified. Newborn skin appears to respond to any injury with an eosinophilic infiltrate.
Because ETN rarely is seen in premature infants, it is believed that mature newborn skin is required to produce this reaction pattern.