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DOI: 10.1542/neo.14-4-e1612013;14;e161Neoreviews

Steven A. RingerCore Concepts: Thermoregulation in the Newborn Part I: Basic Mechanisms

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Core Concepts: Thermoregulation in the NewbornPart I: Basic MechanismsSteven A. Ringer, MD, PhD

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AbstractSupport and regulation of the thermal environment of the newborn have long beenrecognized as critical aspects of newborn care, and they have become increasingly im-portant as smaller and less mature infants are able to survive. In this review, the foun-dational work done more than 50 years ago that defined the impact of hypothermia onmorbidity and mortality in infants is discussed, and the concept of the neutral thermalenvironment is described, as well as how the identification of a narrow range of bodytemperature in which metabolic and oxygen demands are at their lowest has ensuredsafety in infant care while facilitating growth and optimal outcome. Thermoregulationis discussed within the framework of a balance between heat production and loss. Theunique physiologic mechanisms that are available to the newborn to reduce loss andproduce extra heat when facing a cold stress are described. The relatively large amountof brown adipose tissue in the newborn is a key energy source for heat production,although the metabolic processes and control mechanisms surrounding nonshiveringthermogenesis differ between the more vulnerable premature infant and the term in-fant. In contrast to the means of heat production, the capacity of the newborn for self-protection against heat loss is limited. Without external support, newborns can readilylose heat and body temperature through all four mechanisms of heat loss, includingevaporation, conduction, radiation, and convection, although each plays a greateror lesser role at various times after birth. Unless measures are taken to minimize theselosses, 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.

IntroductionSupport and regulation of body temperature have long been recognized as central parts ofcaring for newborns, with some of the earliest observations by Soranus of Ephesus (98–138AD). Pierre Budin, a French obstetrician recognized as the father of perinatology, focusedon temperature and thermal regulation in his book The Nursling, which was published inEnglish in 1907. (1) He noted that the temperature of term infants at birth is actually slightlyhigher than that of the uterus, which he thought was due to “evaporation from the surface ofthe body, but more probably, it arises from the fact that the processes of respiration and com-bustion are not yet fully established and adjusted.” He noted that premature infants were atmuch greater risk of hypothermia, and that if these infants were “not placed under favourableconditions, the temperature not only falls considerably, but does not easily rise again,” es-pecially if they weighed less than 1,500 g. Without the use of incubators, the likelihoodof death was close to 100%, especially if the rectal temperature dropped to 32°C or less.

These observations have been echoed in conventional wisdom and experience both be-fore and after Budin, (1) but they were not better defined until the pioneering work of

Assistant Professor of Pediatrics, Harvard Medical School, Brigham and Women’s Hospital, Boston, MA.

Article core concepts

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Silverman et al (2)(3)(4) in the late 1950s and early1960s; they first defined the impact of temperatureand humidity on neonatal outcome. They found thathigher humidity also caused higher infant temperatures,and improved survival. When they controlled humidityand varied temperature alone, the use of incubators thatwere only w2°C warmer resulted in markedly highersurvival rates. Similar to the findings of Budin, the impacton mortality and morbidity was most pronounced in in-fants weighing less than 1,500 g. The risks have remainedreal even into this century. The EPICure study of ex-tremely low birth weight infants in the United Kingdomidentified hypothermia as an independent risk factor formortality, and 40% of the subjects born at less than 26weeks’ gestation had an admission temperature less than35ºC. (5)

Neutral Thermal EnvironmentThe critical importance of environmental temperature onoutcome and survival can be better understood by exam-ining the effects on infant metabolism. Human newbornsare homeotherms. Unlike poikilotherms such as reptiles,whose body temperature will mirror their environment,human or mammalian infants respond to decreased or in-creased temperature around them by attempting to main-tain their body temperature in the normal range of36.5ºC to 37.5ºC. The mechanisms responsible for thiscompensation require energy, and the infant must in-crease his or her consumption of calories and oxygen. Us-ing animal models, (6) Hill defined a set of thermalconditions under which oxygen consumption is minimaleven as body temperature is maintained in the normalrange. This neutral thermal environment (NTE) reflectsthe range of temperature over which metabolic demandsare minimal. Figure 1 (7) illustrates that within the neu-tral thermal zone, the metabolic demands of the infantare minimal, as reflected in the rate of oxygen consump-tion. As the environmental temperature rises above theNTE, the metabolic demands begin to rise, and ulti-mately the infant is unable to compensate for the elevatedtemperature (and accelerated water losses), and death canoccur. Similarly, as the environmental temperature dropsbelow the NTE, metabolic demands also increase, as theinfant attempts to compensate for the lower temperatureby increasing metabolism and oxygen consumption.There is a point at which the normal mechanisms areovercome, and the infant’s temperature begins to drop.As this happens, the metabolic rate actually diminishes,and this state can be exploited therapeutically (eg, forneuroprotection, during cardiac surgery). If the

environmental temperature is decreased further suchthat the infant’s hypothermia worsens, metabolic func-tion becomes deranged and ultimately ceases as deathoccurs.

The upper graph in Fig 1 illustrates and reiterates an-other important point related to efforts to regulate andmaintain body temperature. As homeotherms, human in-fants are able to maintain a normal body temperatureover a range of environmental temperatures that extendsoutside the NTE, but this requires energy, as noted ear-lier. There is some capacity to increase heat loss to accom-modate higher temperatures or to increase metabolism tocounteract cold. This means that one cannot rely on themeasurement of body temperature alone to determine ifan infant is not being subjected to thermal stress, nor canit reveal if the infant is near the point at which the capacityof the infant to respond and maintain a normal temper-ature will be overwhelmed. Monitoring must thereforeinclude vigilance for other signs of stress, such as in-creased oxygen requirement or changes in heart rate.In practice, there is little margin for error in ensuringthermal neutrality in newborns, especially in those whoare small or premature. The actual range of environmen-tal temperature that constitutes the NTE depends on theweight, gestational age, and postnatal age of the particu-lar infant, but the size of these ranges of thermal neutral-ity is on the order of 1.5ºC or less when the infant weighsless than 2,500 g. (8)(9) The Table presents a compilationof values for use in setting clinical parameters for specificinfants. The data were originally derived by using singlewall incubators in which the incubator wall temperaturewas maintained within 1° of the incubator air tempera-ture. If the temperature difference is greater becausethe nursery air is colder, the incubator temperature mustbe increased 1° for every 7° of difference. In modernpractice, such a table is rarely used because incubatorsare commonly double-walled, and both they and radiantwarmers can be set to regulate their output to ensurea normal body temperature for the infant.

Thermoregulation in the Fetus and NewbornBody temperature results from a balance between theprocesses that result in heat loss and those that createheat. The latter can be divided into mechanisms of heatproduction, or heat produced as a byproduct of normalmetabolism, and mechanisms of thermogenesis (specificmetabolic reactions whose primary purpose is the gener-ation of heat). Our understanding of these factors and re-sultant temperature control in fetuses is based primarilyon a number of studies performed by using a chronicallyinstrumented sheep model.

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The fetus resides inside the warm body of its mother,but fetal warmth is not dependent on the flow of heatfrommother to fetus. (10) The fetus has an elevated met-abolic rate, resulting in heat production between 3 and 4W/kg, approximately double the rate of adults. As a re-sult, the net flow of heat is actually from fetus to mother.Most (w85%) of this exchange occurs through the pla-centa, with the remainder being lost through the fetalskin. (11) In the equilibrium state, fetal temperature isw0.5ºC higher than the maternal temperature, and inthe presence of a maternal fever, the fetus may be as muchas 1ºC warmer (12). The maintenance of fetal tem-perature depends on the balance between basal fetal heatproduction from normal metabolism and the rate of um-bilical blood flow, with only the latter being potentiallyvariable. (8) As a result, there is no capacity for the fetus

to regulate its own temperature bytriggering specific thermogenesis inresponse to a cold stress. Such a pro-cess would require a simultaneous in-crease in heat production throughadditional or augmented metabolicpathways (which would require in-creased oxygen supply and consump-tion) and a decrease in the rate ofumbilical flow and oxygen supply.In essence, thermogenesis in the fe-tus is a physiologic impossibility. (13)

Heat ProductionBeginning at birth, the infant facesnew environmental challenges andnew means of coping with a cold en-vironment.When an infant is exposedto cold or heat, the temperature issensed through peripheral thermal re-ceptors found over the entire surfaceof the skin, (14) which then send in-creased signals to the hypothalamicregulatory center. (15) Signals arealso sent via the thalamus to the cere-bral cortex, resulting in consciousperception of the change in environ-ment, leading to changes in behaviorand increased movement. (16) Thisprocess can increase heat production,but the ill or extremely premature in-fant will have diminished tone andlittle movement. The signaling path-ways are the same as those found inadults, but the physiologic response

in the newborn is distinctly different.The hypothalamic regulatory center is in the preoptic

and anterior nuclei of the hypothalamus. It is here thatsignals from both peripheral and central thermoreceptorsare integrated together, triggering mechanisms to con-serve and produce heat. Efferent signals from the hypo-thalamic nuclei result in an increase in sympatheticactivity. In the adult, this leads to heat production andconservation via shivering, peripheral vasoconstriction,and diminished sweating. Other than vasoconstriction,however, these factors play a minimal role in newborns.Sympathetic stimulation of skeletal muscle is minimal,and shivering plays little role in the response to cold.(17) Instead, the newborn response depends largely onnonshivering thermogenesis or direct heat productionthrough the metabolism of brown adipose tissue. (18)

Figure 1. Neutral thermal environment: effects of heat and cooling on metabolic rate andbody temperature. Adapted with permission from Baumgart S. Incubation of the humannewborn infant. In: Pommerance J, Richardson CJ, eds. Issues in Clinical Neonatology.Norwalk, CT: Appleton & Lange; 1992:139–150. (7)

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Brown adipose tissue was originally regarded as a partof the thymus and later considered to be either an endo-crine tissue or modified form of adipose tissue. Some ofthis tissue is found in adults, but it is prominent in thefetus and newborn, with increasing amounts found asgestation approaches term. The peak amount is foundin the term newborn, and after birth, the tis-sue substantially disappears over 9 months. (19) Brown

adipose tissue is found in severalsites in the body, primarily in theintrascapular regions and surround-ing vasculature and major organs.When it is metabolized, heat is pro-duced that directly warms the bloodand organs. Brown adipose tissue ishighly vascularized, on the orderof four to six times the vascularityof white adipose tissue, (20) and itis highly innervated as well. Thesecharacteristics make it well suitedto serve as the fuel for heat produc-tion when a need arises.

When the hypothalamic nucleireceive signals indicating a decreasein skin temperature, signals are sentto the sympathetic nervous system,triggering an increase in activity.As shown in Fig 2, this action simul-taneously results in the release ofnorepinephrine from the diffuse in-nervation at the surface of brownadipose tissue and the stimulationof thyroid-stimulating hormone re-lease, which in turn stimulates a risein thyroxine levels from the thyroidgland. The released norepinephrineactivates 5939-monodeiodinase, whichconverts thyroxine to triiodothyronine,which upregulates the productionof an uncoupling protein (thermo-genin) in the brown adipose tissue.(21) The uncoupling of mitochon-drial oxidation from phosphoryla-tion results in heat productionfrom oxidation of free fatty acids,and the uncoupling of adenosine tri-phosphate synthesis means that noneof the produced energy is stored,thereby raising the body temperature.

Contrary to earlier beliefs, brownadipose tissue is in fact present and

well developed even in extremely premature infants asearly as 25 weeks’ gestation, (22) albeit in lesser amountsthan at term. Nonshivering thermogenesis is much lessefficient in these less-mature infants because the adiposetissue is only one part of the mechanism. In prematureinfants, the levels of an uncoupling protein (thermogenin)are less than one-half those at term, (23) and the levels of5939-monodeiodinase are low as well. Both of these

Table 1. Neutral Thermal EnvironmentTemperature Ranges

PostnatalAge/Weight

TemperatureRange (ºC)

PostnatalAge/Weight

TemperatureRange (ºC)

0–6 h 72–96 h<1,200 g 34.0–35.4 <1,200 g 34.0–35.01,200–1,500 g 33.9–34.4 1,200–1,500 g 33.0–34.01,501–2,500 g 32.8–33.8 1,501–2,500 g 31.1–33.2>2,500 g(and >36 wk)

32.0–33.8 >2,500 g(and >36 wk)

29.8–32.8

6–12 h 4–12 d<1,200 g 34.0–35.4 <1,500 g 33.0–34.01,200–1,500 g 33.5–34.4 1,501–2,500 g 31.0–33.21,501–2,500 g 32.2–33.8 >2,500 g

(and >36 wk)29.0–32.6

>2,500 g(and >36 wk)

31.4–33.8

12–24 h<1,200 g 34.0–35.4 12–14 d1,200–1,500 g 33.3–34.3 <1,500 g 32.0–34.01,501–2,500 g 31.8–33.8 1,501–2,500 g 31.0–33.2>2,500 g(and >36 wk)

31.0–33.7 >2,500 g(and >36 wk)

29.0–30.8

24–36 h 2–3wk<1,200 g 34.0–35.0 <1,500 g 32.2–34.01,200–1,500 g 33.1–34.2 1,501–2,500 g 30.5–33.01,501–2,500 g 31.6–33.6>2,500 g(and >36 wk)

30.7–33.53–4 wk<1,500 g 31.6–33.6

36–48 h 1,501–2,500 g 30.0–32.7<1,200 g 34.0–35.01,200–1,500 g 33.0–34.1 4–5 wk1,501–2,500 g 31.4–33.5 <1,500 g 31.2–33.0>2,500 g(and >36 wk)

30.5–33.3 1,501–2,500 g 29.5–32.2

48–72 h 5–6 wk<1,200 g 34.0–35.0 <1,500 g 30.6–32.31,200–1,500 g 33.0–34.0 1,501–2,500 g 29.0–31.81,501–2,500 g 31.2–33.4>2,500 g(and >36 wk)

30.1–33.2

Data are based on single wall incubators with wall temperature within 1ºC of incubator air temperature.

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important effectors increase significantly starting at w32weeks’ gestation, and the effectiveness of nonshivering ther-mogenesis increases after that point.

Perhaps mediated by the sympathetic stimulation thatoccurs, changes in infant behavior may also contribute toheat production and preservation. Irritability and excessmovement by the infant will generate heat and will gainthe attention of parents, who will instinctively interveneby drying, cuddling, or swaddling the infant, each ofwhich will reduce heat loss. (24)(25)

Although the capacity for heat production is impor-tant, newborns are not able to maintain their own bodytemperature without some means of thermal protection.In part this is true because the zone of thermal neutralityis so narrow and the range of tolerable body temperatureis small, but in large part it is because the protectionagainst heat loss is so markedly diminished comparedwith the adult. For example, a naked newborn ina 23ºC environment (warmer than many delivery rooms)suffers the same cold stress that a naked adult would ex-perience at 0ºC, (26) and protective mechanisms are di-minished or overwhelmed in the presence of hypoxia.Unless heat loss or excess can be prevented or controlled,the newborn, and especially the premature newborn, isfunctionally poikilothermic, (24) and their body temper-ature will vary with their environment. The protectivemechanisms and homeothermic response can be quickly

overwhelmed, and with rapid environmental cooling,a newborn’s body temperature will drop at a rate of0.2°C to 1.0°C per minute. As discussed in detail inthe following text, one of the most vulnerable times is im-mediately after birth when a wet newborn can lose heat ata rate of 200 kcal/kg per minute or greater. (27)

Heat LossThe newborn faces greater risks of heat loss than do olderchildren or adults, and many of the factors responsible areexacerbated by prematurity and low birth weight. Thenewborn has a higher skin surface area to weight (vol-ume) ratio than the older child or adult, a ratio that in-creases dramatically in smaller infants. The shape of theextremely preterm infant can be roughly approximatedby 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 thenewborn skin, and the diminished amount of subcutane-ous fat provides little help as an insulating barrier. Atgreater degrees of prematurity, the skin is increasinglypermeable, and the transdermal loss of water and heatis similarly increased.

Normal newborn body temperature is defined by theWorld Health Organization as within the rangeof 36.5ºC to 37.5ºC, (26) and hypothermia is definedas a body temperature below this range. Mild hypother-

mia (36ºC–36.5ºC) is caused bycold stress and should lead to eval-uation and corrective action be-cause it indicates that the infant islosing more heat than can be pro-duced. (15) A temperature of32ºC to 36ºC indicates a dangerouscondition of moderate hypother-mia, one that requires steps for im-mediate warming. Whenhypothermia is severe and the tem-perature falls to less than 32ºC, it isan emergency situation. The ther-moregulatory system becomes para-lyzed, and metabolic processes beginto fail. As a result, the risk of death orserious morbidity exists.

Heat loss occurs via a combina-tion of four different phenomena:evaporation, conduction, radiation,and convection. The most commonroute right at the time of birth isevaporation. As the fluid coveringa wet infant evaporates, heat loss

Figure 2. Nonshivering thermogenesis in the newborn. T3[triiodothyronine; T4[thyroxine;UCP[uncoupling protein.

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will occur at a rate of 0.58 kcal/mL of fluid (15) and caneasily total 200 kcal/kg per minute, as the infant’s envi-ronment suddenly changes from the 37ºC of the womb toan external room with a temperature 15º or more cooler.Even after birth, baths may represent a period of in-creased risk, but it must be recognized that evaporativeheat loss continues even when the infant is dry, especiallyin low humidity environments. This mode of heat loss ishigh in extremely premature infants because of the imma-turity of their skin, such that these infants can lose asmuch as 15 times more water per kilogram of bodyweight than term infants. (28) As their skin matures overthe first several days after birth, these losses and the asso-ciated heat loss gradually diminish.

Conductive heat loss occurs when an unclothed infantis placed on a cold surface, such as a procedure table ora scale. (16) The rate of loss is proportional to the tem-perature differential between the infant and the object,and this differential may still be as large as 15ºC evenwhen the equipment is kept in a comfortably warm roomat 23ºC to 24 ºC. The magnitude of these losses can beminimized by “prewarming” the equipment surfaces andlinen or by using exothermic chemical mattresses.

Radiational heat loss is more difficult to control becausethe heat is lost via the radiation of infrared energy from in-fant to nearby cold surfaces, such as a wall or a window,and the rate of loss is again proportional to the temperaturedifferential between the infant and the object. Even if the airin the neonatal unit is kept warm, losses may occur evento the internal walls that abut air-conditioned hallways orrooms. In term and larger premature infants, radiationallosses represent the major route of heat loss. (29)

Convective loss occurs when the infant is in contactwith moving air or water that is cooler than body temper-ature and is again proportional to the temperature differ-ential between the fluid and the infant. (16) The lossesmay occur as cooler fluid moves around the infant suchas air movement from a ventilation system, but they cansimilarly result from moving the infant through coolerair, as occurs when the newborn is moved from his orher mother to a warming table at the time of birth or backagain to the parents. As noted earlier, this route of loss canbe minimized by keeping the room temperature higher.

ConclusionsThe control and support of the newborn’s temperatureare of critical importance, beginning right at the momentof birth. Fundamentally, temperature control representsa balance between the competing processes of produc-tion/conservation and excess losses. Newborns do havemechanisms, including nonshivering thermogenesis, to

produce extra heat and to conserve it, and these are de-velopmentally regulated, becoming increasingly effectiveas gestation approaches term. They are often inadequate,however, to overcome the increased susceptibility of thenewborn to heat loss through a host of mechanisms. Carepractices must focus on preventing or eliminating excesslosses while avoiding overheating.

References1. Budin P. The Nursling. London, United Kingdom: Caxton;19072. Silverman WA, Balnc WA. The effect of humidity on survival ofnewly born premature infants. Pediatrics. 1957;20(3):477–4863. Silverman WA, Fertig JW, Berger AP. The influence of thethermal environment upon the survival of newly born prematureinfants. Pediatrics. 1958;22(5):876–8864. Silverman WA, Agate FJ Jr, Fertig JW. A sequential trial of thenonthermal effect of atmospheric humidity on survival of newborninfants of low birth weight. Pediatrics. 1963;31:719–7245. Costeloe K, Hennessy E, Gibson AT, Marlow N, Wilkinson AR.The EPICure study: outcomes to discharge from hospital forinfants born at the threshold of viability. Pediatrics. 2000;106(4):659–6716. Hill JR. The oxygen consumption of new-born and adultmammals. Its dependence on the oxygen tension in the inspired airand on the environmental temperature. J Physiol. 1959;149:346–3737. Baumgart S. Incubation of the human newborn infant. In:Pommerance J, Richardson CJ, eds. Issues in Clinical Neonatology.Norwalk, CT: Appleton & Lange; 1992:139–1508. Scopes JW, Ahmed I. Range of critical temperatures in sick andpremature newborn babies. Arch Dis Child. 1966;41(218):417–4199. Hey EN, Katz G. The optimum thermal environment for nakedbabies. Arch Dis Child. 1970;45(241):328–33410. Power GG, Schröder H, Gilbert RD. Measurement of fetalheat production using differential calorimetry. J Appl Physiol. 1984;57(3):917–92211. Gilbert RD, Schröder H, Kawamura T, Dale PS, Power GG.Heat transfer pathways between fetal lamb and ewe. J Appl Physiol.1985;59(2):634–63812. Schröder HJ, Power GG. Engine and radiator: fetal andplacental interactions for heat dissipation. Exp Physiol. 1997;82(2):403–414

American Board of Pediatrics Neonatal-PerinatalContent Specifications

• Know the mechanisms of heat gain andloss.

• Know the definition and physiologicimplications of a neutral thermalenvironment.

• Know the various types and mechanisms ofaction of devices to maintain a neutral thermal environment.

• Know the causes, metabolic consequences, and treatment ofinfants with hypothermia.

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13. Schröder H, Gilbert RD, Power GG. Computer model offetal-maternal heat exchange in sheep. J Appl Physiol. 1988;65(1):460–46814. Widmaier J, Raff H, Strang K. Vander’s Human Physiology: TheMechanisms of Body Function. 9th ed. New York, NY: McGraw-Hill; 200515. Knobel R, Holditch-Davis D. Thermoregulation and heat lossprevention after birth and during neonatal intensive-care unitstabilization of extremely low-birthweight infants. J Obstet GynecolNeonatal Nurs. 2007;36(3):280–28716. Nadel E. Regulation of body temperature. In: Born W,Boulpaep E, eds. Medical Physiology. Philadelphia, PA: Saunders;2003:1231–124117. Tourneux P, Libert JP, Ghyselen L, et al. Heat exchanges andthermoregulation in the neonate [in French]. Arch Pediatr. 2009;16(7):1057–106218. Janský L. Non-shivering thermogenesis and its thermoregula-tory significance. Biol Rev Camb Philos Soc. 1973;48(1):85–13219. Lean ME, James WP, Jennings G, Trayhurn P. Brown adiposetissue uncoupling protein content in human infants, children andadults. Clin Sci (Lond). 1986;71(3):291–29720. Hausberger FX, Widelitz MM. Distribution of labeled eryth-rocytes in adipose tissue and muscle in the rat. Am J Physiol. 1963;204:649–65221. Mostyn A, Pearce S, Stephenson T, Symonds ME. Hormonal andnutritional regulation of adipose tissue mitochondrial development

and function in the newborn. Exp Clin Endocrinol Diabetes. 2004;112(1):2–922. 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 WeightNeonates. Berlin, Germany: Springer-Verlag; 1995:9–2023. Houstĕk J, Vízek K, Pavelka S, et al. Type II iodothyronine59-deiodinase and uncoupling protein in brown adipose tissueof human newborns. J Clin Endocrinol Metab. 1993;77(2):382–38724. Baumgart S. Iatrogenic hyperthermia and hypothermia in theneonate. Clin Perinatol. 2008;35(1):183–197, ix–x25. Winberg J. Mother and newborn baby: mutual regulation ofphysiology and behavior—a selective review. Dev Psychobiol. 2005;47(3):217–22926. World Health Organization. Thermal Protection of the New-born: A Practical Guide. Geneva, Switzerland: Maternal andNewborn Health/Safe Motherhood Unit, Division of Reproduc-tive Health, World Health Organization; 199727. Nalepka CD. Understanding thermoregulation in newborns.JOGN Nurs. 1976;5(6):17–1928. Hammarlund K, Sedin G. Transepidermal water loss innewborn infants. III. Relation to gestational age. Acta PaediatrScand. 1979;68(6):795–80129. Sedin G. Neonatal heat transfer, routes of heat loss and heat gain.In: Okken A, Koch J, eds. Thermoregulation of Sick and Low BirthWeight Neonates. Berlin, Germany: Springer-Verlag; 1995:21–36

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DOI: 10.1542/neo.14-4-e1612013;14;e161Neoreviews

Steven A. RingerCore Concepts: Thermoregulation in the Newborn Part I: Basic Mechanisms

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