Antepartum period

The amount of heat generated increases 30% to 35% during pregnancy because of the thermogenic effects of progesterone, alterations in maternal metabolism and basal metabolic rate (see Chapter 16), and maternal dissipation of heat generated by the fetus.^30,91 As a result, many pregnant women develop an increased tolerance for cooler weather and decreased tolerance for heat. The additional heat is dissipated by peripheral vasodilation with a fourfold to sevenfold increase in cutaneous blood flow and increased activity of the sweat glands (see Chapter 14). Cutaneous vasodilation leads to skin warmth.

The maternal temperature usually increases by 0.5° C (0.3° F). Both core and skin temperature increase during pregnancy, with a slight decrease reported in late pregnancy. The core temperature peaks by midpregnancy.⁸⁵ The decrease in core temperature in late pregnancy may be related to decreases in progesterone and physical activity (which generates heat) during this time. The rise in skin temperature is particularly evident in the hands and feet, probably due to arteriovenous shunting in these areas.¹²⁹ In general, heat accumulation may be slower and heat dissipation faster in later pregnancy than before pregnancy or in early pregnancy. The increased plasma volume during pregnancy provides a greater area for heat storage and may enhance heat transfer from the fetus to the mother.⁸⁵ The pregnant woman has decreased vasoconstriction in response to cold during pregnancy. This may alter her ability to conserve heat during cold stress.⁸⁵

Body temperature increases with exercise due to heat generated by increased metabolic energy production. Some of this heat is dissipated by increased skin blood flow; the remainder is stored transiently, increasing the core temperature. Changes in temperature with exercise during pregnancy are moderate, as compared with changes in nonpregnant women, suggesting that the enhanced thermoregulatory capacity of the pregnant woman may help protect her against hyperthermia.⁸⁵ The increased plasma volume in pregnancy may assist in maintaining uterine and placental blood flow during exercise and in maximizing heat transfer from the fetus and heat dissipation in the mother. Aerobic exercise in water is associated with minimal changes in either core or skin temperature.^85,129 Exercise during pregnancy is discussed further in Chapters 9 and 10.

Intrapartum period

An increase in body temperature, averaging 1° C (1.7° F), may occur during labor as a result of physical activity with uterine contractions and the release of substances from the fetal-placental unit that may stimulate the maternal hypothalamic thermoregulatory center.^87,91,104 However, Bartholomew and colleagues reported that 95% of 147 women had temperatures between 36.2° C and 37.8° C (97.2° F and 100.0° F) during labor.¹¹ Diurnal variations were noted with a nadir at midday and peak in the evening.¹¹

In some women the increase in temperature during labor is high enough to generate concern that the mother is infected. Although this may sometimes be the case, the most common cause for maternal fever during labor is use of epidural analgesia, not infection.^1,11,134 Women with epidural analgesia are more likely to develop a fever during labor than women without this form of anesthesia.^{50,97,104,134} Epidural anesthesia in nonpregnant individuals is more likely to lead to a decreased rather than increased temperature. The fever seen with epidurals is usually characterized by a slow increase in temperature of approximately 0.07° C/hour, although the temperature may rise to greater than 37.5° C (99.5° F) or 38° C (100.4° F) in some women.^50,104 The basis for the increased temperature in pregnant women during the intrapartum period may be due to decreased heat dissipation (due to a decreased sweating threshold, alterations in ventilation, and altered hypothalamic responses) and an increase in heat production, possibly due to increased shivering.^{1,5,104,134,136} The autonomic block with epidural analgesia inhibits peripheral vasoconstriction and sweating in the lower body. The impairment of sweating and behavioral responses may decrease heat loss.^11,91 Maternal fever with epidural anesthesia is associated with an inflammatory state with increased cytokines, especially interleukin-6, but this state is rarely due to infection.^5,97,104,136 Prophylactic administration of acetaminophen has not been found to suppress the fever associated with epidurals.^69,104 Panzer and colleagues reported that women during labor do not show the same relationship between temperature, sweating, and shivering as nonpregnant individuals.⁹¹ In the parturient, shivering was not necessarily triggered by decreased temperature nor was sweating necessarily triggered by increased temperature; the woman might shiver and sweat simultaneously. Temperature increases can lead to an increased maternal heart rate, cardiac output, oxygen consumption, and catecholamine production.¹⁰⁴

The laboring woman is also at risk for hypothermia during the intrapartum period due to vasodilation (limiting usual vasoconstrictive responses to cold); administration of anesthetics, narcotics, and other pharmacologic agents; blood loss, rapid fluid replacement, especially if cool fluids are used; or other events that increase maternal heat loss (e.g., cold drafts, wet drapes or towels). Prolonged exposure to a cool environment can aggravate heat loss. Hypothermia can result in shivering, hypotension, and hemodynamic and cardiorespiratory instability.⁹¹

Postpartum period

Maternal temperature is monitored closely during the postpartum period because elevations may indicate infection or dehydration. A transient postpartum chill or shivering is often experienced about 15 minutes after birth of the infant or delivery of the placenta. The cause of this chill is unknown and various causes have been proposed. This phenomenon may represent muscular exhaustion or result from disequilibrium between the internal and external thermal gradients secondary to muscular exertion during labor and delivery, sudden changes in intraabdominal pressure with emptying of the uterus, or small amniotic fluid emboli. Most women who experience early postpartum shivering are normothermic, suggesting that this phenomenon is nonthermoregulatory in origin.⁹¹ Shivering is seen in about 20% of women who did not receive neuraxial analgesia and more frequently in women after epidural analgesia.⁹¹

Transient maternal temperature elevations up to 38° C (100.4° F) occur in up to 6.5% of vaginally delivering women during the first 24 hours after delivery. In most women this resolves spontaneously and is secondary to noninfectious causes such as dehydration or to a transient bacterial endometritis.⁴² Maternal fever in the postpartum period may be a sign of puerperal infection, mastitis, endometritis, or urinary tract infection, although these infections are usually the cause of fever after 24 hours. Any temperature elevation merits close monitoring, especially with increasingly early discharge.^3,30

Maternal hyperthermia and fever

Maternal fever has three potential detrimental effects on the fetus: (1) hypoxia secondary to maternal and fetal tachycardia and altered hemodynamics; (2) teratogenesis; and (3) preterm labor from the fever per se, from underlying infection, or from associated hemodynamic alterations.³⁰ Maternal intrapartum fever due to infection has been linked to a risk of cerebral palsy, cognitive defects, and neonatal seizures and encephalopathy, as well as later disorders such as schizophrenia and autism.^58,80,95,104 Maternal hyperthermia increases maternal oxygen consumption and shifts the oxygen-hemoglobin dissociation curve to the right. Although this latter change increases the oxygen supply to the placenta, fetal oxygen uptake becomes more difficult because of the altered thermal gradient.⁵⁷

Research regarding adverse fetal effects has focused primarily on maternal temperature elevations due to fever secondary to illness, exercise, and the use of saunas or hot tubs. Animal studies show specific effects of maternal hyperthermia, especially when the maternal core temperature increases to 2° C or more above baseline; the longer the temperature elevation is maintained or the higher the temperature, the greater the risk to the fetus.²⁴ Some of the human studies have been retrospective and suggestive but inconclusive, while other have demonstrated a clear association.^{7,23,24,39,85,89,120} A meta-analysis of studies, including both retrospective case-controlled and prospective cohort studies, reported an overall odds ratio of neural tube defects (NTDs) when associated with maternal hyperthermia of 1.92 (95% confidence interval, 1.16, 2.29).⁸⁹ Definitions of hyperthermia in the various studies ranged from temperature greater than 37.8° C (greater than 100.4° F) to temperature greater than 38.9° C (greater than 102.0° F). Most of the hyperthermia was due to maternal influenza or other febrile illness. Others have reported a twofold to fourfold increase in the risk for NTD with maternal first trimester hyperthermia for any reason.¹²⁰

Maternal febrile illness is thought to pose the greatest hyperthermic risk; however, susceptibility may be modified by genotype.²⁰ Elevated maternal temperature secondary to illness-induced fever during early pregnancy has been associated with increased risk of anencephaly and spina bifida (especially around the time of neural tube closure (22 to 28 days), microcephaly, and other central nervous system disorders; alterations in growth; cleft lip; and facial dysmorphogenesis in humans.^10,23,51 In a prospective study, Chambers and colleagues reported a 10-fold increase in NTDs in women who had a temperature of 38.9° C (102° F) or greater lasting for more than 24 hours in the first month of pregnancy.²³ Whether these disorders are primarily due to the elevated temperature, the underlying infection, or a combination of these events has been debated. Most human and animal studies suggest that the increased risk is correlated to the maternal fever and not the viral illness per se.^39,89 Several investigators have reported increased cleft lip and palate, NTDs, and cardiovascular disorders in women with influenza accompanied by high temperature in the first trimester with a reduction in risk with treatment of the fever with antipyretics.^16,120 Reductions in risk have also been reported with folic acid supplementation.¹⁶ Antifever medications and folic acid may reduce the risk of vascular disruption and apoptosis leading to congenital anomalies.^16,39

Several studies have reported an increase in neural tube defects and oral clefts in infants born to women with an extended heat exposure secondary to sauna or hot tub use in the first trimester, suggesting that an elevated temperature may be the critical factor.^23,24,120 Milunsky and colleagues found that the hot tub exposure, especially in the first two months of pregnancy (and the risk increased with number of exposures during this time), posed a greater risk than sauna use, with no risk from electric blanket use.⁸⁸ Prospective studies from Finland of sauna use in pregnancy have not shown an increased risk. However, in these studies, maximal temperature was 38.1° C (100.6° F), below the value of 38.9° C (102° F) thought to be critical.⁸⁵ 

Maternal exercise and temperature elevations

Maternal exercise is associated with increased heat production and body temperature increases that may alter the maternal-fetal thermal gradient and fetal heat dissipation. Uterine blood flow decreases during exercise, further altering the ability of the mother to dissipate fetal heat.^57,118 However, most women seem to be able to tolerate moderate intensity exercise without significant changes in core temperature.¹¹⁸ Low-impact aerobic exercise (to 70% of maximal heart rate) has not been associated with hyperthermia.^72,78 The ability of the mother to dissipate the heat generated by exercise may improve as pregnancy progresses.^85,118 The risks from temperature changes during exercise in late pregnancy are related to decreased uterine blood flow, which can be potentiated by dehydration. Prolonged exercise or exercise in heat (increased ambient heat reduces the thermal gradient between the skin and environment) or high humidity (decreases evaporative heat loss) may result in a higher maternal temperature than exercise in a cool, dry environment or water environment (e.g., aerobic exercise in water).^85,93,129 Physical conditioning before pregnancy can improve thermoregulatory capacity and may decrease the effect of heat stress.^85,93

Transitional events

With birth the fetus moves from the warm, moist intrauterine environment to the colder, drier extrauterine environment. The infant’s temperature falls after birth, triggering cold-induced metabolic responses and heat production.^14,18,103 Because fetal thermoregulation is linked to the mother, thermoregulatory processes are suppressed in the fetus. These processes, especially initiation of nonshivering thermogenesis (NST), must be activated rapidly after birth if the infant is to survive the transition to extrauterine life. Stimulation of cutaneous cold receptors and spinal cord and hypothalamic thermal receptors at birth activates the sympathetic nervous system. This leads to the release of norepinephrine and a twofold to threefold increase in metabolic rate, oxygen consumption, and heat production.^47,94 Occlusion of the umbilical cord, which removes placental factors that suppress NST, increases a brown adipose tissue (BAT)-specific uncoupling protein with a rapid increase in BAT metabolism (see Brown Adipose Tissue Metabolism) and heat production.^94,99 Thermal transition at birth and BAT metabolism are interrelated with changes in thyroid function (see Chapter 19).

Newborns lose heat rapidly after birth, especially through evaporative losses (0.58 kcal/mL [2.4 J/mL] of water loss) from their moist body surface, as well as via convection to cooler room air and radiation to cooler room walls. A newborn’s temperature may fall 0.2° C to 1° C/min (0.5° F to 1.7° F/min) if thermal interventions are not initiated.^25,47,62 Rutter estimated that in a cool room, the body temperature of a 1000-g preterm infant falls 1° C (1.7° F) every 5 minutes.¹⁰⁰ Initial temperatures of infants born by cesarean birth are on average 0.3° C (0.5° F) lower than infants born vaginally, perhaps due to slightly lower levels of sympathetic activity, catecholamines, and thyroid activity.⁹⁴ Interventions in the delivery room to reduce evaporative and other losses support transition, reduce cold stress, and have been associated with a higher PO₂ at 1 hour of age, lower mortality, and decreased morbidity.⁶² Since much of the heat loss immediately after birth is due to evaporative losses, infants should be quickly dried and wrapped in a warm, dry towel and either given to the mother for skin-to-skin contact or placed under a radiant warmer or in a prewarmed incubator.^47,48 A polyethylene bag or wrap can be used with VLBW infants to reduce heat loss after birth (see Methods of Promoting Thermal Stability).^14,29,64 Heat loss in VLBW infants immediately after birth can also be reduced by maintaining adequate ambient temperatures and humidity in the delivery and stabilization room.¹²² Bissinger and Annibale recommend 50% humidity and room temperatures of 78° F to 80° F (25.5° C to 26.6° C) for infants less than or equal to 28 weeks’ gestation (less than or equal to 1000 g) and greater than or equal to 72° F (22.2° C) with a goal of 75° F (23.8° C) for infants 29 to 32 weeks’ gestation (1001-1500 g).¹⁴ Other interventions to reduce evaporative, radiant, conductive, and convective losses are listed in Table 20-2.

Heat transfer

Heat transfer involves two interrelated processes: the internal and external gradients. The internal gradient involves transfer of heat from within the body to the surface and relies primarily on blood flow within an extensive capillary and venous plexus. Tissue insulation (subcutaneous fat) and convective movement of heat through blood influence efficiency of heat conduction. Heat conduction can be altered by vasomotor control processes mediated by the sympathetic nervous system that change skin blood flow with peripheral vasoconstriction to conserve heat and vasodilatation to eliminate heat.

Heat transfer through the internal gradient is increased in neonates because of their thinner layer of subcutaneous fat (i.e., less insulation) and a larger surface area–to–body mass ratio, especially in preterm infants. The subcutaneous layer of insulating fat accounts for only 16% of body fat in infants compared with 30% to 35% in adults.³⁴ The body mass of the neonate is about 5% of adult mass, whereas the surface area is 15%. In term infants, the surface area–to–body mass ratio may be three times, and in preterm infants five times, greater than that of adults.¹⁰¹ This ratio is even higher in ELBW infants. For example, the surface area–to–body mass ratio of a 500-g infant may be six times greater than that of an adult and twice as great as that of a 1500-g infant.⁵⁵

The external gradient involves transfer of heat from the body surface to the environment. The rate of heat loss is directly proportional to the magnitude of the difference between skin temperature and the environmental temperature and can be expressed as follows: heat loss = h (skin temperature − environmental temperature) × (surface area), where h is the thermal transfer coefficient (the rate at which heat leaves the body surface) and is influenced by body size, tissue conductance, skin blood flow, and vasoactivity.^18,103 Heat loss per unit of body mass is inversely proportional to body size.¹⁸ As noted above, the mechanisms by which heat is transferred from the body surface are conduction, convection, radiation, and evaporation (see Prevention of Excessive Heat Loss or Heat Gain).

Heat transfer by the external gradient is also increased in the neonate because of increased surface area and an increased thermal transfer coefficient.¹⁰³ In terms of heat loss, the amount of exposed surface area is most critical; thus an infant who is not in an incubator or radiant warmer will lose less heat if he or she is clothed or swaddled. Factors that increase the thermal transfer coefficient (and thus heat loss), such as decreased skin thickness and altered conductance, are present in the neonate. The threshold for heat production in the newborn is more closely linked to skin temperature than in the adult. As a result, cold responses, especially in preterm infants, are related primarily to skin rather than core temperature changes.¹⁸

Heat production and conservation

Heat production is a result of metabolic processes that generate energy by oxidative metabolism of glucose, fats, and proteins. The amount of metabolic heat produced varies with activity, feeding (calorigenic or specific dynamic action), state (greater heat is produced in awake infants than in sleeping infants and in active versus quiet (deep) sleep), health status, and environmental temperature.^18,26,35 Organs that generate the greatest amount of metabolic energy are the brain, heart, and liver. To maintain a constant body temperature, heat production must equal heat loss from the body surface over a given time. Basal heat production to maintain this stability is generated by body metabolic processes. In the event of cold stress, heat above basal needs can be generated by physical or chemical mechanisms. Because of their surface area–to–body mass ratio (which is an important determinant of heat loss), heat production in infants is low relative to heat loss.¹⁰⁰ In the term infant, heat production at rest (estimated by oxygen consumption) in a thermoneutral environment is similar to that of adults per unit of weight, but approximately half that of the adult per unit of surface area. This is further decreased in preterm infants, who have an even greater surface area–to–body mass ratio and are less likely to spontaneously lie in a flexed position.¹⁰⁰ Prone positioning in low–birth weight (LBW) infants has been reported to increase central and peripheral body temperature in spite of the lower metabolic rates seen in this position.⁴ In term infants the maximal heat production increases from 20% to 75% of adult values over the first postbirth week; this change takes longer in preterm infants.¹⁰³

Physical mechanisms to generate include involuntary (shivering) and voluntary muscular activity. Shivering is the most important mechanism for the generation of additional heat in adults. The neonate uses physical methods (shivering and increased muscular activity) to some extent to generate additional heat. Shivering, which is controlled via the somatomotor system, is not as important in the neonate as in the adult, and the shivering threshold is probably at a lower body temperature.¹⁰¹ Shivering in neonates is primarily seen as a late event associated with decreased spinal cord temperature after prolonged cold exposure. The cervical spinal region is protected from cold stress and preferentially receives heat generated by NST through metabolism of BAT in the intrascapular area. If NST is blocked or the infant is unable to generate adequate heat to compensate for severe or prolonged cold stress, the temperature of the spinal cord eventually decreases.¹⁸

Infants, primarily term or late preterm infants, produce some heat by increasing muscular activity with restlessness, hyperactivity, or crying. This increases heat production in skeletal muscles with breakdown of glycogen and glucose oxidation.^13,25 Infants may try to conserve heat by postural changes such as flexion that reduce the surface area and heat loss through the internal gradient. The ability to produce heat by physical methods can be markedly reduced or obliterated with the use of anesthetics, muscle relaxants, sedatives, or tight restraints and in infants with brain injury.^18,34,47,103

Heat can be generated by chemical mechanisms or NST through changes in the metabolic rate and, primarily in neonates, by BAT metabolism. These changes are mediated by the sympathetic nervous system. Both infants and adults can generate heat by increasing their metabolic rate above basal levels. An adult can increase heat production by 10% to 15% by NST; in the neonate, this increase can be 100% or more.⁵³ NST is mediated by epinephrine in the adult and by norepinephrine in the neonate.^21,119 This results in activation of an adipose tissue lipase and splitting of triglycerides into glycerol and nonesterified fatty acids (NEFA), which are oxidized to produce heat, esterified to form triglycerides, or released into the circulation.^21,115,119 NST is triggered when the mean skin temperature falls to 35° C to 36° C (95° F to 96.8° F).¹¹⁵

NST is the major mechanism through which the infant produces heat above basal needs. Increasing the metabolic rate may lead to further problems in immature or compromised neonates, because any increase in metabolic rate increases oxygen consumption. Stressed infants may be unable to provide enough oxygen; oxygen debt with lactic acidosis from anaerobic metabolism and finally exhaustion can result. The ability to generate heat by NST is limited in ELBW infants.⁶⁵

Thermal receptors in the skin are important mediators of the hypothalamic thermal center’s response to temperature changes or cold stress. Stimulation of these receptors initially leads to heat-conserving responses with peripheral vasoconstriction.⁶⁴ This may result in acrocyanosis in the neonate. In the infant, thermal receptors are most prominent and sensitive over the trigeminal area of the face. For example, cooling the face of an infant who is normothermic causes a rise in metabolic rate. Conversely, warming the facial skin (i.e., use of warmed oxygen in an oxygen hood) when the infant’s body is cold may suppress the usual increase in metabolic rate and other heat-generating mechanisms and can be dangerous.¹⁰³ A recent study of ELBW found that these infants did not demonstrate peripheral vasoconstriction the first 12 hours after birth even with a low body temperature.⁶⁵ Other studies have found minimal or no peripheral vasoconstriction with poor vasomotor control in infants weighing less than 1000 g, increasing their risk of thermoregulatory problems.⁶⁵