Overview
Body temperature is a critical part of the homeostasis that allows for normal functioning of the human body. Alterations in body temperature can affect a wide array of physiologic processes, from vital chemical reactions catalyzed by enzymes to the optimal functioning of white blood cells and platelets.
Humans maintain body temperature by balancing heat production, primarily by metabolism, with heat loss mainly through a variety of physiologic mechanisms as well as environmental factors. The human body has a complex system in place to regulate body temperature in the awake state. However, during anesthesia many of these temperature-regulating pathways are interrupted or inhibited. This underscores the need for temperature monitoring during anesthesia.
As it relates to anesthesia and the perioperative period, the goal of the anesthesia provider is to minimize deviations in body temperature—unless indicated for specific reasons, such as organ protection—and to determine reasons for any observed deviations in body temperature.
Beginning in the 1960s, a major concern related to body temperature during or immediately following anesthesia was the marked hyperthermia characteristic of the malignant hyperthermia (MH) syndrome. This potentially fatal pharmacogenetic disorder of anesthesia had a marked influence on how the anesthesia community viewed the importance of temperature measurement and regulation.
However, studies conducted more recently have pointed out that even mild hypothermia, as is often noted during anesthesia, carries physiologic risks. Core temperature in the range of 35° C to 36° C triples the incidence of morbid cardiac outcomes, triples the risk of surgical wound infection, and significantly increases blood loss and the need for allogeneic transfusion. In the pediatric population, hypothermia poses additional dangers in terms of acid-base balance and cardiovascular physiology.
This chapter provides an in-depth understanding of perianesthetic thermoregulation in terms of effects of anesthetic agents and techniques, use of monitoring devices, and techniques for maintenance of normothermia. It also provides current recommendations for management of core temperature during surgery and in the recovery period.
Thermoregulation
Temperature regulation has three components: 1) an afferent input, 2) a central control, and 3) an efferent response. The afferent component is composed of both heat and cold receptors, which are widely distributed in the body. Heat and warmth receptors travel primarily through unmyelinated C fibers, whereas cold receptors travel along A-δ nerve fibers, although some overlap does occur.
Ascending sensory thermal input is then transmitted to the hypothalamus, the primary thermoregulatory control center of mammals, via the spinal thalamic tracts in the anterior spinal cord. Although most thermal information is integrated by the hypothalamus, some processing and response occurs within the spinal cord itself. For example, patients with high spinal cord transections have better than expected thermoregulation.
Each thermoregulatory response can be characterized by the threshold, gain, and response. The threshold is the temperature at which a response will occur. The gain represents the intensity of that response. The threshold for responses to warmth (sweating and vasodilation) normally exceeds the threshold for the first response to cold (vasoconstriction) by 0.2° C to 0.4° C ( Fig. 14-1 ). Temperatures within this interthreshold range—0.2° C to 0.4° C, the range in between the threshold for response to cold and the threshold for response to warmth—do not trigger any thermoregulatory responses. However, temperatures outside the interthreshold range do trigger a response.
Efferent responses are the activation of effector mechanisms, which either increase metabolic heat production or alter environmental heat loss. The intensity of the response is proportional to the need, or afferent input, and the order in which the responses are used is progressive. Energy-efficient effectors, such as vasoconstriction, are first maximally used before the energy-costly ones, such as shivering, occur. Quantitatively, the most effective responses are behavioral ones: dressing appropriately, moving voluntarily, or adjusting ambient temperature. However, behavioral responses are not relevant for patients under general anesthesia, who are unconscious and often paralyzed.
The major autonomic responses to heat are sweating and active cutaneous vasodilation. Sweating is mediated by postganglionic cholinergic (acetylcholine [ACh]) nerves, and sweat essentially is an ultrafiltrate of plasma. Sweating is the only mechanism by which the body can dissipate heat in an environment in which ambient temperature exceeds core temperature. The body is highly efficient at doing so: 0.58 kcal of heat is dissipated per gram of evaporated sweat. It is also believed that sweat glands release an unidentified substance that mediates cutaneous vasodilation. Cutaneous vasodilation, a unique effector mechanism of humans, diverts blood to the periphery, where heat can be dissipated by the environment more easily and ultimately can lower core temperature.
The major autonomic response to cold is cutaneous vasoconstriction, mediated by α 1 -adrenergic receptors and synergistically augmented by hypothermia-induced α 2 -adrenergic receptors. Cutaneous vasoconstriction reduces the amount of blood vulnerable to heat loss from the skin surface through convection and radiation. The other major response to cold is shivering, an involuntary muscular activity that increases metabolic heat production by 50% to 100%. Metabolic heat production can be estimated from oxygen consumption or from carbon dioxide production. The response of shivering is absent in the newborn and is probably not fully functional for several years. Infants therefore rely on nonshivering thermogenesis, an important thermoregulatory response that doubles heat production in infants, although it raises temperature only slightly in adults. Nonshivering thermogenesis is mediated by β 3 -adrenergic receptors found on brown fat, which contains a unique uncoupling protein that allows the direct transformation of substrate into heat.
Effects of Anesthesia
General anesthesia is associated with an initial decrease in core temperature of approximately 0.5° C to 1.5° C over approximately 30 minutes followed by a slower linear decrease of about 0.3° C per hour until a plateau finally is reached ( Fig. 14-2 ). The initial temperature drop is due in part to increased heat loss during prepping and draping but primarily reflects redistribution of body heat from the core to cooler peripheral tissues with anesthesia-induced vasodilation ( Fig. 14-3 ). The periphery may be 3° C cooler than the core, but body temperature is maintained because of vasoconstriction. With general anesthesia, the vasoconstriction is reduced, leading to mixing of warm core blood with the cooler periphery. The slower linear decrease in temperature occurs as a result of heat loss that exceeds metabolic heat production. General anesthesia completely eliminates any behavioral responses to temperature change. In addition, vasoconstriction is impaired by most anesthetic agents, and muscle relaxants reduce heat production from resting tone in muscles and prevent shivering. Although central regulation of temperature is likely to be depressed, regulation still occurs, albeit at a lower temperature. Sessler and colleagues found that with potent inhaled agents and intravenous (IV) agents, the threshold for the vasoconstrictive response to hypothermia decreases and is dose related ( Fig. 14-4 ) but nevertheless occurs.
Major conduction anesthesia has its own implications on body temperature and is almost as severe as general anesthesia. There is still an initial drop in core temperature caused by neuraxial blockade–induced vasodilation, resulting in redistribution of perfusion from the core to the periphery. As with general anesthesia, subsequent heat loss exceeds metabolic production owing to a slow linear decline. In contrast to general anesthesia, a plateau may not be reached for two reasons: the vasoconstriction threshold is centrally altered, decreasing the threshold about 0.6° C 21 ; more importantly, however, vasoconstriction in the lower extremities is directly inhibited by the nerve block ( Fig. 14-5 ). Because the lower extremities represent a major thermal compartment, it is difficult to reach an effective plateau without vasoconstriction in the lower extremities, which would minimize cutaneous heat loss. Both spinal and epidural anesthesia alter the central control of thermoregulation to a similar degree.
The effects of general and regional anesthesia on temperature are additive. The threshold for vasoconstriction during combined regional/general anesthesia is centrally decreased by 1° C more than with general anesthesia alone. Core temperature during regional/general anesthesia continues to decrease throughout the surgery ; thus it is especially crucial to monitor temperature during combined regional/general anesthesia.
Mechanisms of Intraoperative Heat Loss
The four physical processes of heat transfer of interest are radiation, conduction, evaporation, and convection. Radiation is the most significant route for intraoperative heat loss, but any one of these processes can overwhelm regulating mechanisms.
Radiant heat transfer likely accounts for the majority of heat loss to the environment. It occurs via infrared radiation and is a function of the body surface area exposed to the environment. Radiant heat transfer is proportional to the fourth power of the absolute temperature difference between the surfaces. Infants have a high surface area/body mass ratio and therefore are especially vulnerable to heat loss by radiation.
Conductive heat transfer occurs from direct contact of body tissues or fluids to a colder material. This may be direct contact between the skin and the operating table or between the intravascular compartment and the infusion of cold fluid. For example, 1 L of crystalloid fluid infused at 21° C to a body temperature of 37° C will decrease mean body temperature by 0.25° C/L, and the infusion of 2 units of cold blood can result in a core temperature decrease of 1° C.
Evaporative heat transfer is attributed to the latent heat of vaporization of water from open body cavities and the respiratory tract. Sweating increases evaporative heat loss but is uncommon during anesthesia. Evaporative heat loss through the skin is usually less than 10% of metabolic heat production.
Convective heat transfer is defined as heat loss as a result of moving fluid (air). This is likely the second most significant route for intraoperative heat loss. Convective heat transfer is proportional to the square root of the air speed and occurs as a result of the ambient air circulation that removes the air warmed by skin and viscera. Clothing or drapes are very effective in decreasing convective heat loss by trapping air near the skin.
Effects of Mild Hypothermia
Inadvertent mild hypothermia is a common occurrence during anesthesia. This is due primarily to anesthesia-induced redistribution and partly due to exposure to a cold operating room. The effects of mild hypothermia may be even greater than once thought, and many studies have examined the effects of mild intraoperative hypothermia.
Coagulation is impaired by mild hypothermia; a cold-induced defect in platelet function occurs, and activity of enzymes involved in the coagulation cascade is impaired. Randomized clinical trials have shown that mild hypothermia significantly increases blood loss during hip arthroplasty and increases allogeneic transfusion requirements.
Wound infections are another consequence of mild intraoperative hypothermia. Immune function is directly impaired, and cold-induced vasoconstriction decreases oxygen delivery to the wound site. Mild intraoperative hypothermia (<1° C decrease in core temperature) triples the risk for surgical wound infection in patients undergoing colon surgery. It also delays wound healing and prolongs hospitalization by 20%, even in noninfected patients.
The most serious complication of hypothermia is a threefold increase in morbid myocardial outcomes. This might be due to the elevated blood pressure and heart rate and increased plasma catecholamine levels found in hypothermic patients.
Shivering is uncomfortable for patients and also is potentially harmful because it can increase oxygen requirements by 135% to 468%, although an increase of oxygen consumption above 100% usually is not sustained. This can be especially problematic in the elderly or patients with preexisting cardiac disease who cannot afford acute increases in oxygen demand. However, myocardial infarction is poorly correlated with shivering. Postanesthetic shivering can be effectively treated with meperidine (12.5 to 25 mg IV).
Drug metabolism is decreased by hypothermia. For example, the duration of action for vecuronium is more than doubled by a 2° C reduction in core temperature. During a constant infusion of propofol, the plasma concentration is approximately 30% greater than normal in hypothermic patients. Extra caution should be taken to ensure that residual paralysis and sedation have satisfactorily been reversed or have otherwise worn off.
Hyperthermic States
Only a limited number of conditions predispose to intraoperative hyperthermia because anesthesia tends to lower body temperature and blunt the response to interleukins that produce fever. Even patients who are febrile at the onset of anesthesia generally cool down during surgery.
The most common reason for intraoperative hyperthermia is iatrogenic overwarming, particularly in children. The typical scenario is the use of a full-body convective warmer, often accompanied by a warming blanket during surgery on a peripheral body part, such as the hand or the neck. The excess heat is not dissipated because the patient is covered; hence hyperthermia may occur. This condition is best diagnosed based on the clinical condition and the resolution of hyperthermia upon uncovering the patient. Such hyperthermia may be accompanied by mild respiratory acidosis and an increase in carbon dioxide production as a result of an increased metabolic rate secondary to patient warming. In rare cases, a reaction to mismatched blood may be accompanied by intraoperative hyperthermia.
Not to be overlooked is equipment malfunction that may lead to spuriously elevated temperature. An unusual cause of a spuriously elevated body temperature is when a patient’s temperature is monitored by a liquid crystal temperature strip on the forehead, and the patient is given a medication that leads to peripheral vasodilation and flushing. In some cases these temperature strips have a built-in 2° C offset to account for the normally cool skin temperature. In that case, when flushing occurs, the temperature strip reads several degrees higher than core temperature.
MH syndrome is the most feared complication of anesthesia accompanied by hyperthermia. This syndrome may be easily diagnosed if muscle rigidity and hypercarbia are noted despite normal minute ventilation. However, a more insidious onset of MH may also occur, marked first by slowly rising, then rapidly rising, end-tidal carbon dioxide (ETCO 2 ). Hyperkalemia and acidosis, both respiratory and metabolic, often are accompanying signs of MH. By the time MH has developed, the syndrome will have been in progress for many minutes.
The treatment must be geared first to discontinuing the triggering anesthetic gases with hyperventilation and immediate parenteral administration of dantrolene, starting with 2.5 mg/kg. Because the syndrome may recrudesce, dantrolene must be continued for at least 36 hours in an intensive care unit (ICU) setting. More information about MH is available from the Malignant Hyperthermia Association of the United States ( www.mhaus.org ) and in standard anesthesia textbooks.
Of note, MH has not been reported to occur later than 40 minutes after discontinuation of anesthesia. In cases of marked hyperthermia in the postanesthesia care unit (PACU), the cause generally is infection. Marked hyperthermia may therefore develop postoperatively in patients undergoing urologic procedures, dental rehabilitation, surgery on body cavities that are “dirty,” or drainage of an abscess. In addition, preexisting pneumonia or intraoperative aspiration may lead to postoperative febrile reactions. Rigors sometimes develop at the onset of the fever that are mistaken for the muscle rigidity of MH. Such fevers respond promptly to antipyretics, antibiotics, and surface cooling. However, if there is any doubt as to the cause of the fever, administration of dantrolene is appropriate. A prompt response to dantrolene, however, does not prove that the fever was related to MH.
Perioperative Temperature Management
The importance of temperature regulation within the human body underscores the importance of temperature monitoring during anesthesia. With the normal temperature-regulating pathways being inhibited under anesthesia comes a need for temperature management devices. Because inadvertent mild hypothermia is the most common temperature-related complication, a multitude of patient warming devices are available.
During anesthesia, the initial 0.5° C to 1.5° C reduction in core temperature, reflecting redistribution of blood from the core to cooler peripheral tissues, is difficult to prevent. However, warming the skin surface prior to induction results in less redistribution hypothermia because heat can only flow down a temperature gradient ( Fig. 14-6 ). Active prewarming for as little as 30 minutes likely prevents considerable redistribution. This approach is gaining popularity because it is safe, easy to implement, and inexpensive if the same warming device is used intraoperatively.
Two types of devices attempt to maintain normothermia by affecting respiratory air exchange. One preserves heat by preventing evaporative losses and is often referred to as an artificial nose, a passive device that prevents some degree of heat loss but does not compare with active warming devices to maintain normothermia. The other type of device uses heating and humidification of inspiratory airway gases to maintain normothermia. Such devices are inserted in the inspiratory limb of the anesthesia machine, but they are cumbersome and require installation and setup. Because only a small amount of heat is lost through respiratory gases, active heating and humidification only minimally influence core temperature. Most of the heat loss occurs from evaporation rather than gas exchange; devices therefore are only minimally beneficial in preventing heat loss. Furthermore, to avoid airway burns, the temperature of the heated gases must be carefully monitored.
Heat loss from administration of cold IV fluids can become significant when large volumes of fluid are being administered. A number of devices are available that warm the IV fluid pathway to deliver heat. A unit of refrigerated blood or 1 L of crystalloid solution administered at room temperature decreases mean body temperature approximately 0.25° C. When massive transfusion occurs, such as during rapid blood loss from trauma, these devices are helpful in maintaining body temperature.
A variety of devices warm IV fluids. Some, such as the standard Ranger blood/fluid warming system ( Fig. 14-7 ; Arizant Healthcare, Inc., now a part of 3M, Eden Prairie, MN) and the Medi-Temp blood/fluid warming system (Gaymar Industries, Inc., Orchard Park, NY), incorporate a fluid pathway in a cassette device that sits in or fits into a warming dock. Others, such as the Hotline (Smiths Medial, St. Paul, MN), are coaxial systems, in which the administered fluid flows through the inner lumen and is warmed using a counterflow of fluid traveling from a warming device along the outer lumen. Yet another device, the Astotherm Plus ( Fig. 14-8 ; Futuremed America, Granada Hills, CA) warms the fluid pathway by inserting the tubing in a series of grooves in a drum-like device that delivers heat to the fluid as it courses through the tubing. Devices such as the Bair Hugger (Arizant Healthcare) warm the fluid by warm air diverted to an accessory device containing the IV fluid line.
