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

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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Article core concepts

Core Concepts: Thermoregulation in the Newborn Part I: Basic Mechanisms

Steven A. Ringer, MD, PhD

Author Disclosure Dr Ringer has disclosed no financial 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 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 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 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 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 (98 138 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 com- bustion 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,es- pecially 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 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 de ned until the pioneering work of

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

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Silverman et al (2)(3)(4) in the late 1950s and early 1960s; they rst de ned 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 w 2°C warmer resulted in markedly higher survival rates. Similar to the ndings of Budin, the impact on mortality and morbidity was most pronounced in in- fants weighing less than 1,500 g. The risks have remained real even into this century. The EPICure study of ex- tremely low birth weight infants in the United Kingdom identi ed 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 35ºC. (5)

Neutral Thermal Environment

The critical importance of environmental temperature on outcome and survival can be better understood by exam- ining 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 in- creased temperature around them by attempting to main- tain their body temperature in the normal range of 36.5ºC to 37.5ºC. The mechanisms responsible for this compensation require energy, and the infant must in- crease his or her consumption of calories and oxygen. Us- ing animal models, (6) Hill de ned 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) re ects the range of temperature over which metabolic demands are minimal. Figure 1 (7) illustrates that within the neu- tral thermal zone, the metabolic demands of the infant are minimal, as reected in the rate of oxygen consump- tion. As the environmental temperature rises above the NTE, the metabolic demands begin to rise, and ulti- mately 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 infant s hypothermia worsens, metabolic func- tion becomes deranged and ultimately ceases as death occurs. The upper graph in Fig 1 illustrates and reiterates an- other important point related to efforts to regulate and maintain body temperature. As homeotherms, human in- fants 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 ear-

lier. There is some capacity to increase heat loss to accom- modate 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 temper- ature will be overwhelmed. Monitoring must therefore include 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 ensuring thermal neutrality in newborns, especially in those who are small or premature. The actual range of environmen- tal temperature that constitutes the NTE depends on the weight, 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 weighs less than 2,500 g. (8)(9) The Table presents a compilation

of values for use in setting clinical parameters for speci c 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 tempera- ture. 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 (speci c metabolic reactions whose primary purpose is the gener- ation of heat). Our understanding of these factors and re- sultant 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

core concepts Figure 1. Neutral thermal environment: effects of heat and cooling on metabolic rate and

Figure 1. Neutral thermal environment: effects of heat and cooling on metabolic rate and body temperature. Adapted with permission from Baumgart S. Incubation of the human newborn infant. In: Pommerance J, Richardson CJ, eds. Issues in Clinical Neonatology .

Norwalk, CT: Appleton & Lange; 1992:139–150. (7)

The fetus resides inside the warm body of its mother, but fetal warmth is not dependent on the ow of heat from mother to fetus. (10) The fetus has an elevated met- abolic rate, resulting in heat production between 3 and 4 W/kg, approximately double the rate of adults. As a re- sult, the net ow of heat is actually from fetus to mother. Most (w 85%) of this exchange occurs through the pla- centa, with the remainder being lost through the fetal skin. (11) In the equilibrium state, fetal temperature is w 0.5ºC higher than the maternal temperature, and in the presence of a maternal fever, the fetus may be as much as 1ºC warmer (12). The maintenance of fetal tem- perature depends on the balance between basal fetal heat production from normal metabolism and the rate of um- bilical blood ow, with only the latter being potentially variable. (8) As a result, there is no capacity for the fetus

to regulate its own temperature by triggering specic thermogenesis in response to a cold stress. Such a pro- cess would require a simultaneous in- crease in heat production through additional or augmented metabolic pathways (which would require in- creased oxygen supply and consump- tion) and a decrease in the rate of umbilical ow and oxygen supply. In essence, thermogenesis in the fe- tus is a physiologic impossibility. (13)

Heat Production

Beginning at birth, the infant faces new environmental challenges and new means of coping with a cold en- vironment. When an infant is exposed to cold or heat, the temperature is sensed through peripheral thermal re- ceptors found over the entire surface of the skin, (14) which then send in- creased signals to the hypothalamic regulatory center. (15) Signals are also sent via the thalamus to the cere- bral cortex, resulting in conscious perception of the change in environ- ment, leading to changes in behavior and increased movement. (16) This process can increase heat production, but the ill or extremely premature in- fant will have diminished tone and little movement. The signaling path-

ways are the same as those found in adults, 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 that signals from both peripheral and central thermoreceptors are integrated together, triggering mechanisms to con- serve and produce heat. Efferent signals from the hypo- thalamic nuclei result in an increase in sympathetic activity. In the adult, this leads to heat production and conservation 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 on nonshivering thermogenesis or direct heat production through the metabolism of brown adipose tissue. (18)

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Table 1. Neutral Thermal Environment Temperature Ranges

 

Postnatal

Temperature

Postnatal

Temperature

Age/Weight

Range (ºC)

Age/Weight

Range (ºC)

0–6 h

72–96 h

<1,200 g

34.0–35.4

< 1,200 g

34.0–35.0

1,200–1,500 g

33.9–34.4

1,200–1,500 g

33.0–34.0

1,501–2,500 g

32.8–33.8

1,501–2,500 g

31.1–33.2

>2,500 g 36 wk)

(and >

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

33.0–34.0

1,200–1,500 g

33.5–34.4

1,501–2,500 g

31.0–33.2

1,501–2,500 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 d

1,200–1,500 g

33.3–34.3

< 1,500 g

32.0–34.0

1,501–2,500 g

31.8–33.8

1,501–2,500 g

31.0–33.2

>2,500 g 36 wk)

(and >

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

32.2–34.0

1,200–1,500 g

33.1–34.2

1,501–2,500 g

30.5–33.0

1,501–2,500 g

31.6–33.6

>2,500 g (and > 36 wk)

30.7–33.5

3–4 wk

 

< 1,500 g

31.6–33.6

36–48 h

1,501–2,500 g

30.0–32.7

<1,200 g

34.0–35.0

1,200–1,500 g

33.0–34.1

4–5 wk

1,501–2,500 g

31.4–33.5

< 1,500 g

31.2–33.0

>2,500 g 36 wk)

(and >

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

30.6–32.3

1,200–1,500 g

33.0–34.0

1,501–2,500 g

29.0–31.8

1,501–2,500 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.

adipose tissue is found in several sites in the body, primarily in the intrascapular regions and surround- ing vasculature and major organs. When it is metabolized, heat is pro- duced that directly warms the blood and organs. Brown adipose tissue is highly vascularized, on the order of four to six times the vascularity of white adipose tissue, (20) and it is highly innervated as well. These characteristics make it well suited to serve as the fuel for heat produc- tion when a need arises. When the hypothalamic nuclei receive signals indicating a decrease in skin temperature, signals are sent to the sympathetic nervous system, triggering an increase in activity. As shown in Fig 2, this action simul- taneously results in the release of norepinephrine from the diffuse in- nervation at the surface of brown adipose tissue and the stimulation of thyroid-stimulating hormone re- lease, which in turn stimulates a rise in thyroxine levels from the thyroid gland. The released norepinephrine activates 5 9 3 9 -monodeiodinase, which converts thyroxine to triiodothyronine, which upregulates the production of an uncoupling protein (thermo- genin) in the brown adipose tissue. (21) The uncoupling of mitochon- drial oxidation from phosphoryla- tion results in heat production from oxidation of free fatty acids, and the uncoupling of adenosine tri- phosphate synthesis means that none

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 early as 25 weeksgestation, (22) albeit in lesser amounts than at term. Nonshivering thermogenesis is much less efcient in these less-mature infants because the adipose tissue is only one part of the mechanism. In premature infants, the levels of an uncoupling protein (thermogenin) are less than one-half those at term, (23) and the levels of 5 9 3 9 -monodeiodinase are low as well. Both of these

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

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important effectors increase signicantly starting at w 32 weeksgestation, and the effectiveness of nonshivering ther- mogenesis 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 impor- tant, 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 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, is functionally poikilothermic, (24) and their body temper- ature 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

0.2°C to 1.0°C per minute. As discussed in detail in the following text, one of the most vulnerable times is im-

mediately after birth when a wet newborn can lose heat at

a rate of 200 kcal/kg per minute or greater. (27)

Heat Loss

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 (vol- ume) ratio than the older child or adult, a ratio that in- creases 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 subcutane- ous 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 de ned by the

World Health Organization as within the range of 36.5ºC to 37.5ºC, (26) and hypothermia is de ned

as

a body temperature below this range. Mild hypother- mia (36ºC36.5ºC) is caused by cold stress and should lead to eval- uation and corrective action be- cause it indicates that the infant is losing more heat than can be pro- duced. (15) A temperature of 32ºC to 36ºC indicates a dangerous condition of moderate hypother- mia, one that requires steps for im- mediate warming. When hypothermia is severe and the tem- perature falls to less than 32ºC, it is an emergency situation. The ther- moregulatory system becomes para- lyzed, and metabolic processes begin

to fail. As a result, the risk of death or

serious morbidity exists. Heat loss occurs via a combina- tion of four different phenomena:

evaporation, conduction, radiation, and convection. The most common

route right at the time of birth is evaporation. As the uid covering

a wet infant evaporates, heat loss

As the fl uid covering a wet infant evaporates, heat loss Figure 2. Nonshivering thermogenesis in
As the fl uid covering a wet infant evaporates, heat loss Figure 2. Nonshivering thermogenesis in
As the fl uid covering a wet infant evaporates, heat loss Figure 2. Nonshivering thermogenesis in
As the fl uid covering a wet infant evaporates, heat loss Figure 2. Nonshivering thermogenesis in
As the fl uid covering a wet infant evaporates, heat loss Figure 2. Nonshivering thermogenesis in
As the fl uid covering a wet infant evaporates, heat loss Figure 2. Nonshivering thermogenesis in

Figure 2. Nonshivering thermogenesis in the newborn. T 3 [triiodothyronine; T 4 [thyroxine; UCP[uncoupling protein.

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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 envi- ronment suddenly changes from the 37ºC of the womb to an 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 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 imma- turity 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 asso- ciated 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 tem-

perature differential between the infant and the object, and this differential may still be as large as 15ºC even when the equipment is kept in a comfortably warm room at 23ºC to 24 ºC. 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 in- fant 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 temper- ature and is again proportional to the temperature differ- ential 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.

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 produc-

tion/conservation and excess losses. Newborns do have

mechanisms, including nonshivering thermogenesis, to

e166 NeoReviews Vol.14 No.4 April 2013

produce extra heat and to conserve it, and these are de- velopmentally 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 Specifications

• Know the mechanisms of heat gain and loss.

• Know the definition 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.

a neutral thermal environment. • Know the causes, metabolic consequences, and treatment of infants with hypothermia.

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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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