This chapter reviews the importance of thermoregulation and temperature monitoring in anesthetized children. It addresses the significance of keeping children normothermic and will help the trainee understand why pediatric anesthesiologists become apoplectic when faced with the possibility that the small infant they are caring for may become hypothermic. Important updates in this revision include new information and references regarding temperature control in neonates, and early detection of malignant hyperthermia with assiduous temperature monitoring that results in less morbidity and mortality from the disease.
Normal Temperature Physiology in Children
Body temperature is a result of the balance between heat production by the major organs and heat loss to the environment. There is no standard for normal body temperature; individuals exhibit different temperatures, which will be influenced by the time of day, activity, and so forth. Like adults, children’s bodies contain different compartments that exist at different temperatures. The core compartment is composed of the major organs and deep body tissues. The peripheral compartment is composed of the extremities. There is a normal temperature gradient between the core and peripheral compartments that is largely maintained by peripheral vasoconstriction. When the administration of general or regional anesthesia causes vasodilation, there is increased mixing of heat between the core and the peripheral compartments. This usually results in an overall decrease in core temperature after induction of general anesthesia.
As a homeotherm, when an infant is placed in a cooler than normal environment, it will consume oxygen and expend caloric energy in an attempt to maintain a normal body temperature. The neutral thermal environment (NTE) is defined as the environmental temperature range that is likely to result in a body temperature with the lowest metabolic heat production, measured as oxygen consumption. The clinical correlate of this is that if a small infant with lung disease has a preexisting defect in transfer of oxygen into the bloodstream and excretion of carbon dioxide, it is more likely to develop cellular hypoxemia during hypothermia, when the infant is increasing oxygen consumption and metabolic rate to maintain normothermia. Indeed, studies have documented differences in infant survival rates that were influenced by the temperature in the incubator. In one study, an increase in incubator temperature from 85 °F to 89 °F was associated with a 15% increase in survival.
Generally, the smaller and younger the infant, the higher the environmental temperature required to achieve the NTE. Graphs have been published that indicate the temperature required to maintain infants in the NTE based on weight and gestational age. For example, for newborns weighing between 1 and 3 kg, this temperature can exceed 85 °F (29.4°C). When anesthetizing small infants, you should attempt to replicate these conditions in the operating room in the area immediately surrounding the infant. For a naked infant lying supine on an open platform, it is estimated that the abdominal skin temperature should be between 36.5°C and 37°C to approximate the conditions required to be in an NTE.
Within an NTE, the human infant’s oxygen consumption is at its lowest, meaning that it is expending minimal amounts of energy to maintain normothermia. If the environmental temperature is lowered slightly, the infant can use compensatory mechanisms (vasoconstriction, brown fat oxidation) to maintain normothermia. However, when the infant’s thermal protective mechanisms can no longer sustain normothermia, its core temperature will drop. Eventually, oxygen consumption will also decrease because the temperature regulation center becomes impaired. Just because an infant’s temperature is relatively normal does not mean that it is still residing in the NTE. In fact, its thermal protective mechanisms may be very active and on the verge of failing to maintain normothermia. When the infant’s body temperature begins to fall, it is an indication that the thermal stress has been so severe that its normal thermal compensatory mechanisms are being overpowered. Furthermore, the presence of either hypoxemia or hypoglycemia impairs the metabolic response to hypothermia, resulting in a more dramatic decrease in body temperature.
The human infant is born with a well-developed temperature regulating system. However, small infants are prone to hypothermia in cold environments and hyperthermia in overly warm environments mainly because of their relatively large surface area-to-volume ratio. The body surface area-to-volume ratio of a tiny premature infant is three to five times higher than an adult’s, and the heat loss per unit body mass is about four times that of the adult. Because of less subcutaneous fat (i.e., less insulation), the range of the environmental temperature in which the infant is able to maintain normothermia is limited compared with the adult. For example, in a naked anesthesiologist, the lower limit of this control range is approximately 0°C (32 °F) whereas for the full-term infant it is 20 to 23°C (68 °F –73.4 °F). Therefore, the temperature within the infant’s immediate surrounding area in the OR should be maintained at a minimum of approximately 75 °F. Because subcutaneous fat is formed mainly in the third trimester of gestation, infants born prematurely are even more at risk for poikilothermic behavior.
Normal Compensation for Hypothermia
When body temperature begins to vary just slightly away (±0.2°C) from the physiologic set point, involuntary compensatory mechanisms will attempt to return the body’s temperature back to normal. There are a number of these compensatory mechanisms. Those that are most important in small children and that are most different from adults will be reviewed.
When most of us feel cold, we instinctively seek a warmer location, put on another layer of clothes, increase our muscle activity to generate heat, or cuddle with a loved one. Infants cannot do any of these (although it is often heard from neonatal intensive care unit [NICU] nurses that babies will instinctively find the warmest corner of their isolette).
Older children and adults have the capability to shiver, the high-intensity involuntary rhythmic muscle activity that is probably the most significant means by which adults produce heat. Young children do not have the capability of efficient shivering. Once anesthetized (even without muscle paralysis), efficient shivering is greatly attenuated until the process of awakening.
Nonshivering thermogenesis describes a cold-induced increase in oxygen consumption and heat production that is not inhibited by muscle relaxants. In small infants, nonshivering thermogenesis is probably the most important means of heat production in a cool environment. The thermogenic effector organ—brown fat—is the most significant contributor to nonshivering thermogenesis in the small infant. In the human infant, brown fat accounts for 2% to 6% of total bodyweight and is located in the abdominal cavity surrounding the kidneys and adrenal glands, in the mediastinum, and between the scapulae. As opposed to the more abundant white fat, brown fat cells are rich in mitochondria, contain a dense capillary network, and are richly innervated with sympathetic nerve endings. When norepinephrine release is stimulated by sympathetic activity, triglycerides are hydrolyzed to free fatty acids and glycerol, with heat production resulting from enhanced oxygen consumption and uncoupling of the electron transport chain mediated by the protein thermogenin. Immediately after an infant is exposed to a cold stimulus the metabolic rate begins to increase, even before core body temperature decreases. Even a mild cold stimulus such as unheated preoxygenation can trigger the onset of an increase in metabolic heat production. In infants exposed to a cold environment, nonshivering thermogenesis is capable of doubling the metabolic rate. However, the decrease in temperature required to initiate nonshivering thermogenesis is unknown. In one study of infants anesthetized with propofol and fentanyl, there was a lack of nonshivering thermogenesis with a temperature drop of 2°C.
Thermoregulatory vasoconstriction occurs in the peripheral compartments in response to cold receptors on the skin. It serves to limit heat loss to the environment. In children undergoing abdominal surgery with isoflurane anesthesia, thermoregulatory vasoconstriction is attenuated by an average of about 2.5°C less than the unanesthetized state. This is similar to the values found in anesthetized adults.
Complications of Hypothermia in Infants
Hypothermia sets into motion a variety of physiologic compensation mechanisms that increase oxygen consumption and may adversely affect normal physiology. Cooling results in release of norepinephrine. This, along with the direct effects of hypothermia, results in widespread vasoconstriction. Peripheral vasoconstriction may restrict oxygen delivery to tissues and cause cellular hypoxia that manifests as a metabolic acidosis. Pulmonary vasoconstriction will increase pulmonary arterial pressures and cause increased susceptibility to right-to-left shunting at the atrial level through a patent foramen ovale and through a patent ductus arteriosus. This will result in additional peripheral tissue hypoxia. NICU patients with hypothermia require more respiratory and cardiac interventions.
Mild hypothermia (34°C–36°C) in healthy infants and children during peripheral procedures probably does not result in adverse effects, and does not influence postoperative recovery indices. Postoperative shivering is uncommon in children. In an audit of 1507 children, 3.5% experienced shivering. Risk factors included use of intravenous induction agents, age older than 6 years, and prolonged duration of surgery. Clonidine has been shown to decrease occurrence of postoperative shivering.
Heat Loss During Anesthesia
After induction of general anesthesia, an initial decrease in core temperature results from the redistribution of heat from the core to the periphery. This is largely caused by a combination of direct vasodilation by the anesthetic agents and an anesthetic-induced inhibition of thermoregulatory vasoconstriction that occurs at a lower than normal core temperature. In children the administration of general anesthesia blunts the ability of the central nervous system to trigger compensatory vasoconstriction by approximately 2.5°C, compared with approximately 0.2°C in the unanesthetized state. This threshold is similar to that of adults. Because infants and small children have a relatively greater proportion of their body mass contained in the core compartment, they may, at least initially, lose proportionately less heat because of redistribution of core heat to the periphery. Their relatively small extremities will not absorb as much heat from the core compared with an adult.
After this initial decrease in core temperature from redistribution, infants will likely continue to lose heat to the environment at a faster pace than older children and adults. This is mainly caused by their relatively large surface area-to-volume ratio, paucity of subcutaneous fat, immature epidermal barrier, and limited capacity for metabolic heat production. In addition, there is a relatively greater contribution to body cooling from unwarmed intravenous solutions and sterile irrigating solutions.
Mechanisms of Heat Loss to the Environment
Radiation is the process by which heat is lost from the child to any colder surrounding structures (e.g., walls in the operation room [OR]) by the transfer of photons and is not influenced by the temperature of the surrounding air. Radiation normally accounts for the greatest percentage of heat lost during anesthesia. During transport of a neonate to and from the operating room, heat lost through radiation can be decreased by use of a double-shelled incubator, or another type of barrier between the infant and the surrounding incubator walls, such as a blanket.
Conduction refers to the direct transfer of heat between contiguous structures. Examples include loss of heat from the child to the operating room table, or the hypothermic effect of infusion of cool intravenous fluids. Because of the relatively larger surface area-to-volume ratio of infants, conduction may influence heat loss more in infants than in older children or adults. Heat lost by conduction is reduced by using a warming mattress beneath the child, increasing the ambient temperature in the operating room, use of a forced warm air blanket on nonsurgical areas of the body, and warming infused intravenous fluids and sterile prep solutions.
Convection is the loss of heat by the movement of air flowing past the surface of the skin. The best way to minimize heat lost through convection is to cover all exposed parts of the child with a sheet or blanket.
Evaporation is the loss of heat by the energy depleted when water dissipates from exposed surfaces of the body, such as the skin, visceral organs, and respiratory epithelium. Evaporative heat loss is minimized by humidification of inspired gases, covering exposed skin surfaces, and using warmed sterile prep solutions.
Prevention and Treatment of Perioperative Hypothermia
Preoperative warming of the extremities is perhaps the most effective method for prevention of the initial decrease in temperature as a result of redistribution. However, this is not practical in most children. Therefore, more effective means must be used to prevent large decreases in temperature. Every attempt should be made to achieve cutaneous warming by covering all exposed areas with sheets or blankets. This will significantly decrease radiant, convective, and evaporative heat losses. Many institutions use radiant warmers, which are kept over the infant during induction of anesthesia and placement of lines and monitors ( Fig. 16.1 ). These devices may help prevent heat loss via evaporation and conduction of heat to the surrounding cold air.
