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NEONATAL SKIN CARE - 06/09/11

Doi : 10.1016/S0031-3955(05)70239-X 
Gary L. Darmstadt, MD a, b, James G. Dinulos, MD a
a Departments of Pediatrics and Medicine, University of Washington School of Medicine, Seattle, Washington (GLD, JGD) 
b Department of International Health, School of Hygiene and Public Health, The Johns Hopkins Medical Institutions, Baltimore, Maryland (GLD) 

Riassunto

The skin acts as an interface between the internal milieu and the environment and provides many functions essential for human survival, including:

Modulation of transepidermal water fluxes, protection from dehydration and excessive water influx, and maintenance of electrolyte homeostasis
Thermoregulation and minimization of caloric losses
Antimicrobial defense
Protection from environmental toxins
Protection from trauma
Protection from ultraviolet radiation
Tactile sensation
Of principal importance, a competent epidermal barrier is necessary at the time of birth for maintaining fluid homeostasis in the extrauterine environment. The epidermal permeability barrier resides in the stratum corneum, the outermost layer of the skin. There, it is mediated by lamellar bilayers composed of hydrophobic lipids; principally fatty acids; cholesterol; and ceramides, located in extracellular spaces of multiple layers of tightly knit, anucleate corneocytes, which are girded with a protein-rich and keratin-rich cornified cell envelope.56 The barrier typically forms in utero during the third trimester. Developmental immaturity of the permeability barrier may include:
Structural immaturity
Stratum corneum and epidermis are thinner than in term infants.
Anchoring fibrils, anchoring filaments, and hemidesmosomes are fewer and smaller than in term infants, leading to decreased anchoring of the epidermis and increased susceptibility to shear forces.
Stratum corneum epidermal permeability barrier is underdeveloped, leading to increased transepidermal water loss, loss of heat, increased caloric demands, increased potential for absorption of environmental toxins, and compromised antimicrobial defense.
Expression of cationic antimicrobial peptides may be developmentally decreased.
Antibacterial acid mantle forms more slowly in neonates weighing less than 1 kg than in larger, more mature neonates.
Formation of a protective layer of vernix is underdeveloped.
Decreased numbers of melanocytes with immature melanosomes leads to increased susceptibility to ultraviolet light–induced damage.
A reduced subcutaneous fat supply limits thermoregulatory capabilities and buffering capacity against redistribution of fat-soluble drugs.
Developmental immaturity and a large surface area-to-body mass ratio can cause transepidermal water loss (TEWL), which correlates with epidermal barrier function,68 to be 10-fold to 15-fold greater in premature infants of 25 weeks' gestation compared with full-term infants.70 This may result in fluid losses of as much as 30% of total body weight in 24 hours and may be associated with:
Significant morbidity caused by dehydration and hypotension, increasing the risk for intraventricular hemorrhage and, possibly, necrotizing enterocolitis
Electrolyte imbalance, especially hyperosmolar hypernatremia, which also may place neonates at increased risk for intraventricular hemorrhage
Thermal instability
Increased caloric demands because skin evaporative losses (580 calories/mL) may comprise as much as 20% of the total energy expenditure of preterm infants born at less than 30 weeks' gestational age
Furthermore, rehydration of preterm infants may be fraught with difficulty and exacerbate or induce patent ductus arteriosus, congestive heart failure, pulmonary edema, and possibly necrotizing enterocolitis.

Another critical function of the skin is antimicrobial defenses, which include:

Stratum corneum: xeric environment, acidic pH (i.e., “acid mantle”), antimicrobial lipids (e.g., oleic acid, sphingosine, sphinganine, hydroxysphinganine; possibly serine protease activity of cholesterol sulfate), continual shedding of corneocytes
Cationic antimicrobial peptides: skin-derived antileukoprotease (elafin), secretory leukocyte protease inhibitor (SLPI; antileukoprotease), human β-defensin-2, LL-37
Cytokines: interleukin (IL)-1⍺, IL-1β, tumor necrosis factor-⍺, IL-10, and IL-12
Granzyme B
Fas ligand
Nitric oxide
Resident cutaneous flora (e.g., bacterial interference or bacteriocins) (not part of the innate immune system, but defense is intrinsic to the skin)
A developmentally mature and intact stratum corneum seems to effectively prevent infection of the skin and impedes microbial invasion mechanically and through its acidic pH; xeric environment; and the release of antibacterial products, including cytokines, lipid breakdown products and cationic antimicrobial peptides.48, 121 Neonates, especially preterm infants, are at high risk for infection, however, because of epidermal barrier immaturity; developmental defects in systemic immune function; and, possibly, disordered cutaneous immunoregulatory function in association with barrier perturbation or decreased cationic antimicrobial peptide expression.126, 127 As a result, infectious diseases and prematurity, together with birth asphyxia, are the major causes of neonatal deaths worldwide. Approximately one fourth of all very low birth weight (VLBW) infants weighing less than 1.5 kg in the United States who survive beyond the third day of life have at least one episode of sepsis.165 In developing countries, the prevalence of sepsis in premature infants is estimated at 30% to 60%, and the mortality rate is 40% to 70%; septicemia is the most prevalent cause of death, accounting for as much as 50% of neonatal mortality in premature infants.13, 164 Globally, an estimated 350,000 of neonates die each year because of septicemia and meningitis164; approximately half of these deaths occur in the first week of life, when epidermal barrier function is most highly compromised.

Postnatal age and gestational age are important considerations in assessing skin maturity and in determining skin-care practices because exposure of premature skin following birth to the dry, extrauterine environment accelerates development of an effective epidermal barrier.71, 74, 183 Barrier maturation following premature birth, however, typically requires approximately 2 to 4 weeks and may require as long as 8 weeks in extremely premature infants.74, 88 This suggests that, as more preterm infants survive at earlier gestational ages that approach the limits for interfollicular cornification and stratum corneum maturation at 22 to 24 weeks' gestational age, the stratum corneum responds more slowly to maturational signals expressed after birth.73, 182 During the neonatal period, although barrier function is developing, premature infants suffer significant morbidity and mortality, especially during the first week of life, when approximately two thirds of neonatal deaths occur.90

The importance of neonatal skin care is exemplified by survey results suggesting that nearly 80% of newborns develop a skin problem (i.e., “rash”) during the first month of life.42 But little information is available on which a rational approach to skin care in neonates may be based, and few instructions or recommendations for neonatal skin care are available in the literature.* This article reviews fundamental care and hygiene of neonatal skin, with particular reference to preterm infants born at less than 33 weeks' gestational age and hospitalized neonates who require intensive care, in whom these activities are of vital importance. Strategies for optimizing epidermal barrier integrity, including bathing and emolliation practices, preventing and managing infections and skin injury, and minimizing TEWL and heat or percutaneous absorption of toxins, are emphasized.

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 Address reprint requests to Gary L. Darmstadt, MD, Department of Pediatrics, Division of Dermatology, CH-25, Children's Hospital and Regional Medical Center, 4800 Sand Point Way NE, Seattle, WA 98105, e-mail: gdarms@chmc.org


© 2000  W. B. Saunders Company. Pubblicato da Elsevier Masson SAS. Tutti i diritti riservati.
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Vol 47 - N° 4

P. 757-782 - agosto 2000 Ritorno al numero
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