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Neonatal Skin: Back to Nature?

  • Authors: Laura A Stokowski, RN, MS
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Target Audience and Goal Statement

This activity is intended for neonatal nurses, neonatal nurse practitioners, and other clinicians who care for newborns.

The goal of this activity is provide participants with a review and update in 3 important areas of neonatal care. Topics include neonatal skin, implementation of guidelines for hyperbilirubinemia, and the use of selective cooling to reduce brain injury in infants.

Upon completion of this activity, participants will be able to:

  1. Describe the pathogenesis of cerebral injury-reperfusion injury in the full-term infant with hypoxic-ischemic encephalopathy.
  2. Discuss modest hypothermia, including infants most likely to benefit and the therapeutic window for this procedure.
  3. List reasons that neonates with hyperbilirubinemia might benefit from direct admission to the NICU rather than admission via the emergency department.
  4. Identify the properties of vernix and their importance to normal development of the skin in term and preterm infants.


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  • Laura A Stokowski, RN, MS

    Staff Nurse, Inova Fairfax Hospital for Children, Falls Church, Virginia; Editor, Medscape Ask the Experts Advanced Practice Nurses


    Disclosure: Laura A. Stokowski, RN, MS, has disclosed no relevant financial relationships.

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Neonatal Skin: Back to Nature?

Authors: Laura A Stokowski, RN, MSFaculty and Disclosures


Skin and Brains

Earthworms have a simple membrane. Fish have scales. Birds, of course, have feathers, and mammals have fur. And humans? Well, humans are "naked apes."[1] Unlike all other primates, we are unique in having little body fur and a thick, stratified, interfollicular epidermis with a well-developed stratum corneum. Steven B. Hoath, MD, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, began his presentation about neonatal skin by reminding us that our skin has co-evolved with our large, versatile, and highly organized brains.[2]

The skin and the brain are both of embryonic ectodermal origin, so developmentally, the skin is the surface of the brain. The skin "closes the loop," so to speak, preventing nerve endings from being exposed, yet providing the all-important interface between the central nervous system and the environment.

The formation of a barrier to water loss and infection is critical for survival in the extrauterine environment. Somehow, after 9 months in the fluid-filled uterus, the term neonate emerges with a well-developed skin and stratum corneum. How does the newborn skin become such a superb, highly organized water-retentive envelope? The answer lies in the slippery white substance that coats the skin of newborn infants before birth.

Rethinking Vernix

Many people view vernix, like blood, meconium, or amniotic fluid, as one of the soils of the birth process that should be removed as thoroughly as possible after birth. Some babies have an abundance of vernix -- in every crack and crevice -- and quite a lot of energy is expended to present the parents with a clean newborn baby. The myth about why babies have vernix -- as a sort of "grease" to facilitate the birth process -- doesn't really make sense, given that the largest, term infants seem to have the least amount of the stuff.

Dr. Hoath and his colleagues at the Skin Sciences Institute, Cincinnati Children's Hospital Medical Center, have been studying the composition and properties of vernix and its role in adaptation of the neonate to the extrauterine, or dry, environment. Their research suggests that rather than being a soil, vernix is a natural skin cleanser. It may also be an anti-infective, an anti-oxidant, a moisturizer, and a wound-healing agent. Perhaps instead of rubbing vernix off of the newborn infant's skin, we should be rubbing it in![2]

The Biology of Vernix

Vernix caseosa is unique to humans. Structurally, it is similar to the outermost layer of the epidermis, the stratum corneum. Vernix is made up of hydrated fetal corneocytes embedded in a rich lipid matrix. It is the ability of these corneocytes to hold a large volume of water that gives vernix its water-retentive properties.

Vernix is synthesized during the last trimester of pregnancy. At that time, a surge in sebaceous gland activity and increased desquamation of fetal corneocytes combine to create a proteolipid film that covers the fetal skin surface during the critical period of adaptation before birth.[3]

Vernix is believed to interact with the developing epidermis and facilitate the in utero formation of the stratum corneum.[4] By covering the developing stratum corneum and waterproofing its surface, vernix allows cornification of the skin to occur. With advancing gestational age, vernix on the skin surface detaches into the surrounding amniotic fluid.[3] Evidence suggests that pulmonary surfactant produced by the fetal lung has a role in detaching vernix from the skin surface.[3] The detached vernix mixes with the amniotic fluid, causing turbidity of the fluid, a recognized marker of lung maturity.

Neonatal Adaptation and the Skin

The neonate faces numerous physiologic challenges during the transition from the aqueous surroundings of the womb to the dry, terrestrial environment at birth. Challenges include adaptation to air breathing and enteral nutrition, elimination of wastes, and maintenance of body temperature and water balance.

Also critical to neonatal adaptation is the development of a relatively impermeable cutaneous barrier, the stratum corneum. In the transition to the extrauterine environment, the stratum corneum immediately performs many functions vital to the neonate's survival.[4] Among these are maintaining a barrier to water loss, infection control, immunosurveillance, acid mantle formation, antioxidant functions, thermoregulation, and protection from ultraviolet light and other chemicals. If left intact, vernix contributes considerably to these critical functions.

At birth, the skin surface is relatively neutral (pH about 6.5) and gradually becomes more acidic over the first few postnatal weeks.[4] The acid mantle forms as a result of changes on the skin surface following birth (sweat, sebum, microorganisms) and lactic acid and free fatty acids from metabolic processes within the stratum corneum. The skin pH falls to about 5.5, a level that is beneficial for antimicrobial defense by inhibiting the growth of pathogenic bacteria. Acidification also maintains epidermal barrier integrity by stabilizing the double-lamellar structure of intracellular lipids.

Early routines in newborn care, however well intentioned, can disrupt the formation of the acid mantle. A prime example is the use of alkaline soaps for newborn bathing.

Acid mantle development is delayed in extremely preterm infants. Even in the term infant, the acid mantle is slow to develop on areas of occluded skin, such as the diaper area. It has been demonstrated that leaving vernix on the skin of the newborn produces earlier skin acidification.[5] World Health Organization guidelines for newborn care specify that vernix should not be removed from the skin of newborn infants and bathing should be delayed for at least 6 hours after birth.[6]

Innate Defense

Colonization of the skin after birth is an essential part of the neonate's defense against infection. The innate component of the immune system is the first line of host defense. The skin of the term newborn has a well-developed immune system.[4] Defense mechanisms include the anatomical barrier presented by the stratum corneum, the acid environment, commensal microflora, antimicrobial peptides, and phagocytes. The epidermis itself contributes by internalizing bacteria and containing infection, and harboring the bone-marrow-derived Langerhans cells, which function as sentinels for the immune system.

Sandwiched between the fetal skin and the amniotic fluid, vernix appears to be strategically located to contribute to host defense.[6] The protein components of vernix contain several antibacterial polypeptides that are active against common bacterial and fungal pathogens.[7] The innate immune proteins found in vernix are similar to antimicrobial peptides in breast milk. It is possible that an important prenatal function of vernix is to protect the fetus from acute or subacute chorioamnionitis.[5]

The Preterm Infant and Immature Skin

The immature skin of the preterm infant undergoes a marked acceleration of barrier maturation when exposed to the extrauterine environment.[4] Birth triggers lipid and DNA synthesis followed by cornification of the epidermal keratinocytes. Rapid formation of the stratum corneum is responsible for the excessive desquamation and scaliness that are characteristic of the very low birthweight infant's skin.[4] This dry scaly skin is a poor barrier: susceptibility to infection and penetration of exogenous agents are increased. Furthermore, transepidermal water loss from the preterm infant's skin remains elevated compared to full-term infants, even as late as the 28th postnatal day.

Figure 1. External variables affecting newborn skin.


Neonatal care involves near constant interaction with newborn skin as a primary care interface (Figure 1). Protecting the integrity of the skin under these circumstances can be challenging. Very few successful epidermal protection and repair strategies have been developed for neonates. Research to date indicates that one of the best strategies may be the simplest, yet the most widely ignored -- nature's own moisturizer, vernix.


  1. Morris D. The Naked Ape: A Zoologist's Study of the Human Animal. New York: Random House; 1999.
  2. Hoath SB. The skin and neonatal nursing -- from the biology of vernix to neonatal adaptation. Program and abstracts of the 21st Annual Conference of the National Association of Neonatal Nurses; September 28-October 1, 2005; Anaheim, California.
  3. Narendran V, Wickett RR, Pickens WL, Hoath SB. Interaction between pulmonary surfactant and vernix: a potential mechanism for induction of amniotic fluid turbidity. Pediatr Res. 2000;48:120-124. Abstract
  4. Hoath SB. Physiologic development of the skin. In: Polin RA, Fox WW, Abman SH, eds. Fetal and Neonatal Physiology. Philadelphia, Pa: Elsevier; 2004.
  5. Visscher MO, Narendran V, Pickens WL, et al. Vernix caseosa in neonatal adaptation. J Perinatol. 2005;25:440-446. Abstract
  6. World Health Organization. Pregnancy, Childbirth, Postpartum and Newborn Care. 2003. Available at: Accessed October 8, 2005.
  7. Akinbi HT, Narendran V, Pass AK, Markart P, Hoath SB. Host defense proteins in vernix caseosa and amniotic fluid. Am J Obstet Gynecol. 2004;191:2060-2096.