Core Concepts: Thermoregulation in the Newborn Part I: Basic Mechanisms Steven A. Ringer Neoreviews 2013;14;e161 DOI: 10.1542/neo.

14-4-e161

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Neoreviews is the official journal of the American Academy of Pediatrics. A monthly publication, it has been published continuously since . Neoreviews is owned, published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois, 60007. Copyright 2013 by the American Academy of Pediatrics. All rights reserved. Print ISSN: .

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Article

core concepts

Thermoregulation in the Newborn Part I: Basic Mechanisms

Steven A. Ringer, MD, PhD

Core Concepts:
Author Disclosure Dr Ringer has disclosed no nancial relationships relevant to this article. This commentary does not contain a discussion of an unapproved/ investigative use of a commercial product/ device.

Abstract
Support and regulation of the thermal environment of the newborn have long been recognized as critical aspects of newborn care, and they have become increasingly important as smaller and less mature infants are able to survive. In this review, the foundational work done more than 50 years ago that dened the impact of hypothermia on morbidity and mortality in infants is discussed, and the concept of the neutral thermal environment is described, as well as how the identication of a narrow range of body temperature in which metabolic and oxygen demands are at their lowest has ensured safety in infant care while facilitating growth and optimal outcome. Thermoregulation is discussed within the framework of a balance between heat production and loss. The unique physiologic mechanisms that are available to the newborn to reduce loss and produce extra heat when facing a cold stress are described. The relatively large amount of brown adipose tissue in the newborn is a key energy source for heat production, although the metabolic processes and control mechanisms surrounding nonshivering thermogenesis differ between the more vulnerable premature infant and the term infant. In contrast to the means of heat production, the capacity of the newborn for selfprotection against heat loss is limited. Without external support, newborns can readily lose heat and body temperature through all four mechanisms of heat loss, including evaporation, conduction, radiation, and convection, although each plays a greater or lesser role at various times after birth. Unless measures are taken to minimize these losses, severe physiologic derangements may result.

Objectives

After completing this article, readers should be able to:

1. Understand the balance of heat production and transfer in the fetus and how it changes at the time of birth. 2. Explain the concept of the neutral thermal environment and how it can be used to appropriately gauge and support the thermal needs of an infant. 3. Understand how the neonate responds to cold stress and the mechanism of thermogenesis and reduction in heat losses, including the four basic avenues of heat loss.

Introduction
Support and regulation of body temperature have long been recognized as central parts of caring for newborns, with some of the earliest observations by Soranus of Ephesus (98138 AD). Pierre Budin, a French obstetrician recognized as the father of perinatology, focused on temperature and thermal regulation in his book The Nursling, which was published in English in 1907. (1) He noted that the temperature of term infants at birth is actually slightly higher than that of the uterus, which he thought was due to evaporation from the surface of the body, but more probably, it arises from the fact that the processes of respiration and combustion are not yet fully established and adjusted. He noted that premature infants were at much greater risk of hypothermia, and that if these infants were not placed under favourable conditions, the temperature not only falls considerably, but does not easily rise again, especially if they weighed less than 1,500 g. Without the use of incubators, the likelihood of death was close to 100%, especially if the rectal temperature dropped to 32C or less. These observations have been echoed in conventional wisdom and experience both before and after Budin, (1) but they were not better dened until the pioneering work of

Assistant Professor of Pediatrics, Harvard Medical School, Brigham and Womens Hospital, Boston, MA.

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core concepts

Silverman et al (2)(3)(4) in the late 1950s and early 1960s; they rst dened the impact of temperature and humidity on neonatal outcome. They found that higher humidity also caused higher infant temperatures, and improved survival. When they controlled humidity and varied temperature alone, the use of incubators that were only w2C warmer resulted in markedly higher survival rates. Similar to the ndings of Budin, the impact on mortality and morbidity was most pronounced in infants weighing less than 1,500 g. The risks have remained real even into this century. The EPICure study of extremely low birth weight infants in the United Kingdom identied hypothermia as an independent risk factor for mortality, and 40% of the subjects born at less than 26 weeks gestation had an admission temperature less than 35C. (5)

Neutral Thermal Environment

The critical importance of environmental temperature on outcome and survival can be better understood by examining the effects on infant metabolism. Human newborns are homeotherms. Unlike poikilotherms such as reptiles, whose body temperature will mirror their environment, human or mammalian infants respond to decreased or increased temperature around them by attempting to maintain their body temperature in the normal range of 36.5C to 37.5C. The mechanisms responsible for this compensation require energy, and the infant must increase his or her consumption of calories and oxygen. Using animal models, (6) Hill dened a set of thermal conditions under which oxygen consumption is minimal even as body temperature is maintained in the normal range. This neutral thermal environment (NTE) reects the range of temperature over which metabolic demands are minimal. Figure 1 (7) illustrates that within the neutral thermal zone, the metabolic demands of the infant are minimal, as reected in the rate of oxygen consumption. As the environmental temperature rises above the NTE, the metabolic demands begin to rise, and ultimately the infant is unable to compensate for the elevated temperature (and accelerated water losses), and death can occur. Similarly, as the environmental temperature drops below the NTE, metabolic demands also increase, as the infant attempts to compensate for the lower temperature by increasing metabolism and oxygen consumption. There is a point at which the normal mechanisms are overcome, and the infants temperature begins to drop. As this happens, the metabolic rate actually diminishes, and this state can be exploited therapeutically (eg, for neuroprotection, during cardiac surgery). If the
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environmental temperature is decreased further such that the infants hypothermia worsens, metabolic function becomes deranged and ultimately ceases as death occurs. The upper graph in Fig 1 illustrates and reiterates another important point related to efforts to regulate and maintain body temperature. As homeotherms, human infants are able to maintain a normal body temperature over a range of environmental temperatures that extends outside the NTE, but this requires energy, as noted earlier. There is some capacity to increase heat loss to accommodate higher temperatures or to increase metabolism to counteract cold. This means that one cannot rely on the measurement of body temperature alone to determine if an infant is not being subjected to thermal stress, nor can it reveal if the infant is near the point at which the capacity of the infant to respond and maintain a normal temperature will be overwhelmed. Monitoring must therefore include vigilance for other signs of stress, such as increased oxygen requirement or changes in heart rate. In practice, there is little margin for error in ensuring thermal neutrality in newborns, especially in those who are small or premature. The actual range of environmental temperature that constitutes the NTE depends on the weight, gestational age, and postnatal age of the particular infant, but the size of these ranges of thermal neutrality is on the order of 1.5C or less when the infant weighs less than 2,500 g. (8)(9) The Table presents a compilation of values for use in setting clinical parameters for specic infants. The data were originally derived by using single wall incubators in which the incubator wall temperature was maintained within 1 of the incubator air temperature. If the temperature difference is greater because the nursery air is colder, the incubator temperature must be increased 1 for every 7 of difference. In modern practice, such a table is rarely used because incubators are commonly double-walled, and both they and radiant warmers can be set to regulate their output to ensure a normal body temperature for the infant.

Thermoregulation in the Fetus and Newborn

Body temperature results from a balance between the processes that result in heat loss and those that create heat. The latter can be divided into mechanisms of heat production, or heat produced as a byproduct of normal metabolism, and mechanisms of thermogenesis (specic metabolic reactions whose primary purpose is the generation of heat). Our understanding of these factors and resultant temperature control in fetuses is based primarily on a number of studies performed by using a chronically instrumented sheep model.

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core concepts

to regulate its own temperature by triggering specic thermogenesis in response to a cold stress. Such a process would require a simultaneous increase in heat production through additional or augmented metabolic pathways (which would require increased oxygen supply and consumption) and a decrease in the rate of umbilical ow and oxygen supply. In essence, thermogenesis in the fetus is a physiologic impossibility. (13)

Heat Production
Beginning at birth, the infant faces new environmental challenges and new means of coping with a cold environment. When an infant is exposed to cold or heat, the temperature is sensed through peripheral thermal receptors found over the entire surface of the skin, (14) which then send increased signals to the hypothalamic regulatory center. (15) Signals are also sent via the thalamus to the cerebral cortex, resulting in conscious perception of the change in environment, leading to changes in behavior and increased movement. (16) This process can increase heat production, Figure 1. Neutral thermal environment: effects of heat and cooling on metabolic rate and but the ill or extremely premature inbody temperature. Adapted with permission from Baumgart S. Incubation of the human fant will have diminished tone and newborn infant. In: Pommerance J, Richardson CJ, eds. Issues in Clinical Neonatology. little movement. The signaling pathNorwalk, CT: Appleton & Lange; 1992:139150. (7) ways are the same as those found in adults, but the physiologic response in the newborn is distinctly different. The fetus resides inside the warm body of its mother, The hypothalamic regulatory center is in the preoptic but fetal warmth is not dependent on the ow of heat and anterior nuclei of the hypothalamus. It is here that from mother to fetus. (10) The fetus has an elevated metsignals from both peripheral and central thermoreceptors abolic rate, resulting in heat production between 3 and 4 W/kg, approximately double the rate of adults. As a reare integrated together, triggering mechanisms to consult, the net ow of heat is actually from fetus to mother. serve and produce heat. Efferent signals from the hypothalamic nuclei result in an increase in sympathetic Most (w85%) of this exchange occurs through the plaactivity. In the adult, this leads to heat production and centa, with the remainder being lost through the fetal conservation via shivering, peripheral vasoconstriction, skin. (11) In the equilibrium state, fetal temperature is and diminished sweating. Other than vasoconstriction, w0.5C higher than the maternal temperature, and in however, these factors play a minimal role in newborns. the presence of a maternal fever, the fetus may be as much Sympathetic stimulation of skeletal muscle is minimal, as 1C warmer (12). The maintenance of fetal temperature depends on the balance between basal fetal heat and shivering plays little role in the response to cold. production from normal metabolism and the rate of um(17) Instead, the newborn response depends largely on nonshivering thermogenesis or direct heat production bilical blood ow, with only the latter being potentially through the metabolism of brown adipose tissue. (18) variable. (8) As a result, there is no capacity for the fetus
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core concepts

adipose tissue is found in several sites in the body, primarily in the intrascapular regions and surrounding vasculature and major organs. Postnatal Temperature Postnatal Temperature When it is metabolized, heat is proAge/Weight Range (C) Age/Weight Range (C) duced that directly warms the blood 06 h 7296 h and organs. Brown adipose tissue is <1,200 g 34.035.4 <1,200 g 34.035.0 highly vascularized, on the order 1,2001,500 g 33.934.4 1,2001,500 g 33.034.0 of four to six times the vascularity 1,5012,500 g 32.833.8 1,5012,500 g 31.133.2 of white adipose tissue, (20) and it >2,500 g 32.033.8 >2,500 g 29.832.8 (and >36 wk) (and >36 wk) is highly innervated as well. These 612 h 412 d characteristics make it well suited <1,200 g 34.035.4 <1,500 g 33.034.0 to serve as the fuel for heat produc1,2001,500 g 33.534.4 1,5012,500 g 31.033.2 tion when a need arises. 1,5012,500 g 32.233.8 >2,500 g 29.032.6 When the hypothalamic nuclei (and >36 wk) >2,500 g 31.433.8 receive signals indicating a decrease (and >36 wk) in skin temperature, signals are sent 1224 h to the sympathetic nervous system, <1,200 g 34.035.4 1214 d triggering an increase in activity. 1,2001,500 g 33.334.3 <1,500 g 32.034.0 As shown in Fig 2, this action simul1,5012,500 g 31.833.8 1,5012,500 g 31.033.2 >2,500 g 31.033.7 >2,500 g 29.030.8 taneously results in the release of (and >36 wk) (and >36 wk) norepinephrine from the diffuse in2436 h 23wk nervation at the surface of brown <1,200 g 34.035.0 <1,500 g 32.234.0 adipose tissue and the stimulation 1,2001,500 g 33.134.2 1,5012,500 g 30.533.0 of thyroid-stimulating hormone re1,5012,500 g 31.633.6 >2,500 g 30.733.5 lease, which in turn stimulates a rise (and >36 wk) 34 wk in thyroxine levels from the thyroid <1,500 g 31.633.6 gland. The released norepinephrine 3648 h 1,5012,500 g 30.032.7 activates 59 39 -monodeiodinase, which <1,200 g 34.035.0 converts thyroxine to triiodothyronine, 1,2001,500 g 33.034.1 45 wk 1,5012,500 g 31.433.5 <1,500 g 31.233.0 which upregulates the production >2,500 g 30.533.3 1,5012,500 g 29.532.2 of an uncoupling protein (thermo(and >36 wk) genin) in the brown adipose tissue. 4872 h 56 wk (21) The uncoupling of mitochon<1,200 g 34.035.0 <1,500 g 30.632.3 drial oxidation from phosphoryla1,2001,500 g 33.034.0 1,5012,500 g 29.031.8 1,5012,500 g 31.233.4 tion results in heat production >2,500 g 30.133.2 from oxidation of free fatty acids, (and >36 wk) and the uncoupling of adenosine triphosphate synthesis means that none Data are based on single wall incubators with wall temperature within 1C of incubator air temperature. of the produced energy is stored, thereby raising the body temperature. Contrary to earlier beliefs, brown adipose tissue is in fact present and well developed even in extremely premature infants as Brown adipose tissue was originally regarded as a part early as 25 weeks gestation, (22) albeit in lesser amounts of the thymus and later considered to be either an endothan at term. Nonshivering thermogenesis is much less crine tissue or modied form of adipose tissue. Some of efcient in these less-mature infants because the adipose this tissue is found in adults, but it is prominent in the fetus and newborn, with increasing amounts found as tissue is only one part of the mechanism. In premature gestation approaches term. The peak amount is found infants, the levels of an uncoupling protein (thermogenin) are less than one-half those at term, (23) and the levels of in the term newborn, and after birth, the tis59 39 -monodeiodinase are low as well. Both of these sue substantially disappears over 9 months. (19) Brown
Table 1.

Neutral Thermal Environment Temperature Ranges

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The newborn faces greater risks of heat loss than do older children or adults, and many of the factors responsible are exacerbated by prematurity and low birth weight. The newborn has a higher skin surface area to weight (volume) ratio than the older child or adult, a ratio that increases dramatically in smaller infants. The shape of the extremely preterm infant can be roughly approximated by two large spheres (the head and the chest/abdomen), resulting in the highest possible surface area for volume. Heat loss is exacerbated by the relative thinness of the newborn skin, and the diminished amount of subcutaneous fat provides little help as an insulating barrier. At greater degrees of prematurity, the skin is increasingly permeable, and the transdermal loss of water and heat is similarly increased. Normal newborn body temperature is dened by the World Health Organization as within the range of 36.5C to 37.5C, (26) and hypothermia is dened as a body temperature below this range. Mild hypothermia (36C36.5C) is caused by cold stress and should lead to evaluation and corrective action because it indicates that the infant is losing more heat than can be produced. (15) A temperature of 32C to 36C indicates a dangerous condition of moderate hypothermia, one that requires steps for immediate warming. When hypothermia is severe and the temperature falls to less than 32C, it is an emergency situation. The thermoregulatory system becomes paralyzed, and metabolic processes begin to fail. As a result, the risk of death or serious morbidity exists. Heat loss occurs via a combination of four different phenomena: evaporation, conduction, radiation, and convection. The most common route right at the time of birth is Figure 2. Nonshivering thermogenesis in the newborn. T3[triiodothyronine; T4[thyroxine; evaporation. As the uid covering a wet infant evaporates, heat loss UCP[uncoupling protein.
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important effectors increase signicantly starting at w32 weeks gestation, and the effectiveness of nonshivering thermogenesis increases after that point. Perhaps mediated by the sympathetic stimulation that occurs, changes in infant behavior may also contribute to heat production and preservation. Irritability and excess movement by the infant will generate heat and will gain the attention of parents, who will instinctively intervene by drying, cuddling, or swaddling the infant, each of which will reduce heat loss. (24)(25) Although the capacity for heat production is important, newborns are not able to maintain their own body temperature without some means of thermal protection. In part this is true because the zone of thermal neutrality is so narrow and the range of tolerable body temperature is small, but in large part it is because the protection against heat loss is so markedly diminished compared with the adult. For example, a naked newborn in a 23C environment (warmer than many delivery rooms) suffers the same cold stress that a naked adult would experience at 0C, (26) and protective mechanisms are diminished or overwhelmed in the presence of hypoxia. Unless heat loss or excess can be prevented or controlled, the newborn, and especially the premature newborn, is functionally poikilothermic, (24) and their body temperature will vary with their environment. The protective mechanisms and homeothermic response can be quickly

overwhelmed, and with rapid environmental cooling, a newborns body temperature will drop at a rate of 0.2C to 1.0C per minute. As discussed in detail in the following text, one of the most vulnerable times is immediately after birth when a wet newborn can lose heat at a rate of 200 kcal/kg per minute or greater. (27)

Heat Loss

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core concepts

will occur at a rate of 0.58 kcal/mL of uid (15) and can easily total 200 kcal/kg per minute, as the infants environment suddenly changes from the 37C of the womb to an external room with a temperature 15 or more cooler. Even after birth, baths may represent a period of increased risk, but it must be recognized that evaporative heat loss continues even when the infant is dry, especially in low humidity environments. This mode of heat loss is high in extremely premature infants because of the immaturity of their skin, such that these infants can lose as much as 15 times more water per kilogram of body weight than term infants. (28) As their skin matures over the rst several days after birth, these losses and the associated heat loss gradually diminish. Conductive heat loss occurs when an unclothed infant is placed on a cold surface, such as a procedure table or a scale. (16) The rate of loss is proportional to the temperature differential between the infant and the object, and this differential may still be as large as 15C even when the equipment is kept in a comfortably warm room at 23C to 24 C. The magnitude of these losses can be minimized by prewarming the equipment surfaces and linen or by using exothermic chemical mattresses. Radiational heat loss is more difcult to control because the heat is lost via the radiation of infrared energy from infant to nearby cold surfaces, such as a wall or a window, and the rate of loss is again proportional to the temperature differential between the infant and the object. Even if the air in the neonatal unit is kept warm, losses may occur even to the internal walls that abut air-conditioned hallways or rooms. In term and larger premature infants, radiational losses represent the major route of heat loss. (29) Convective loss occurs when the infant is in contact with moving air or water that is cooler than body temperature and is again proportional to the temperature differential between the uid and the infant. (16) The losses may occur as cooler uid moves around the infant such as air movement from a ventilation system, but they can similarly result from moving the infant through cooler air, as occurs when the newborn is moved from his or her mother to a warming table at the time of birth or back again to the parents. As noted earlier, this route of loss can be minimized by keeping the room temperature higher.

produce extra heat and to conserve it, and these are developmentally regulated, becoming increasingly effective as gestation approaches term. They are often inadequate, however, to overcome the increased susceptibility of the newborn to heat loss through a host of mechanisms. Care practices must focus on preventing or eliminating excess losses while avoiding overheating.

American Board of Pediatrics Neonatal-Perinatal Content Specications

Know the mechanisms of heat gain and loss. Know the denition and physiologic implications of a neutral thermal environment. Know the various types and mechanisms of action of devices to maintain a neutral thermal environment. Know the causes, metabolic consequences, and treatment of infants with hypothermia.

References
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Conclusions
The control and support of the newborns temperature are of critical importance, beginning right at the moment of birth. Fundamentally, temperature control represents a balance between the competing processes of production/conservation and excess losses. Newborns do have mechanisms, including nonshivering thermogenesis, to
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13. Schrder H, Gilbert RD, Power GG. Computer model of fetal-maternal heat exchange in sheep. J Appl Physiol. 1988;65 (1):460468 14. Widmaier J, Raff H, Strang K. Vanders Human Physiology: The Mechanisms of Body Function. 9th ed. New York, NY: McGrawHill; 2005 15. Knobel R, Holditch-Davis D. Thermoregulation and heat loss prevention after birth and during neonatal intensive-care unit stabilization of extremely low-birthweight infants. J Obstet Gynecol Neonatal Nurs. 2007;36(3):280287 16. Nadel E. Regulation of body temperature. In: Born W, Boulpaep E, eds. Medical Physiology. Philadelphia, PA: Saunders; 2003:12311241 17. Tourneux P, Libert JP, Ghyselen L, et al. Heat exchanges and thermoregulation in the neonate [in French]. Arch Pediatr. 2009; 16(7):10571062 18. Jansk L. Non-shivering thermogenesis and its thermoregulatory signicance. Biol Rev Camb Philos Soc. 1973;48(1):85132 19. Lean ME, James WP, Jennings G, Trayhurn P. Brown adipose tissue uncoupling protein content in human infants, children and adults. Clin Sci (Lond). 1986;71(3):291297 20. Hausberger FX, Widelitz MM. Distribution of labeled erythrocytes in adipose tissue and muscle in the rat. Am J Physiol. 1963; 204:649652 21. Mostyn A, Pearce S, Stephenson T, Symonds ME. Hormonal and nutritional regulation of adipose tissue mitochondrial development

and function in the newborn. Exp Clin Endocrinol Diabetes. 2004;112 (1):29 22. Sauer P. Metabolic background of neonatal heat production, energy balance, metabolic response to heat and cold. In: Okken A, Koch J, eds. Thermoregulation of Sick and Low Birth Weight Neonates. Berlin, Germany: Springer-Verlag; 1995:920 23. Houstk J, Vzek K, Pavelka S, et al. Type II iodothyronine 59 -deiodinase and uncoupling protein in brown adipose tissue of human newborns. J Clin Endocrinol Metab. 1993;77(2):382387 24. Baumgart S. Iatrogenic hyperthermia and hypothermia in the neonate. Clin Perinatol. 2008;35(1):183197, ixx 25. Winberg J. Mother and newborn baby: mutual regulation of physiology and behaviora selective review. Dev Psychobiol. 2005; 47(3):217229 26. World Health Organization. Thermal Protection of the Newborn: A Practical Guide. Geneva, Switzerland: Maternal and Newborn Health/Safe Motherhood Unit, Division of Reproductive Health, World Health Organization; 1997 27. Nalepka CD. Understanding thermoregulation in newborns. JOGN Nurs. 1976;5(6):1719 28. Hammarlund K, Sedin G. Transepidermal water loss in newborn infants. III. Relation to gestational age. Acta Paediatr Scand. 1979;68(6):795801 29. Sedin G. Neonatal heat transfer, routes of heat loss and heat gain. In: Okken A, Koch J, eds. Thermoregulation of Sick and Low Birth Weight Neonates. Berlin, Germany: Springer-Verlag; 1995:2136

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Core Concepts: Thermoregulation in the Newborn Part I: Basic Mechanisms Steven A. Ringer Neoreviews 2013;14;e161 DOI: 10.1542/neo.14-4-e161

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including high resolution figures, can be found at: http://neoreviews.aappublications.org/content/14/4/e161 This article cites 22 articles, 12 of which you can access for free at: http://neoreviews.aappublications.org/content/14/4/e161#BIBL This article, along with others on similar topics, appears in the following collection(s): Fetus and Newborn Infant http://neoreviews.aappublications.org/cgi/collection/fetus_newb orn_infant Information about reproducing this article in parts (figures, tables) or in its entirety can be found online at: /site/misc/Permissions.xhtml Information about ordering reprints can be found online: /site/misc/reprints.xhtml

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