Therapeutic hypothermia

Hypothermia is common during anaesthesia and surgery owing to anaesthetic-induced inhibition of thermoregulatory control. Perioperative hypothermia is associated with numerous complications. However, for certain patient populations, and under specific clinical conditions, hypothermia can provide substantial benefits. Lowering core temperature to 32–34 °C may reduce cell injury by suppressing excitotoxins and oxygen radicals, stabilizing cell membranes, and reducing the number of abnormal electrical depolarizations. Evidence from animal studies indicates that even mild hypothermia provides substantial protection against cerebral ischaemia and myocardial infarction. Mild hypothermia has been shown to improve outcome after cardiac arrest in humans. Randomized trials are in progress to evaluate the potential benefits of mild hypothermia during aneurysm clipping and after stroke or acute myocardial infraction. However, as hypothermia can cause unwanted side-effects, further research is needed to better quantify the risks and benefits of therapeutic hypothermia.     

Intraoperative Wärmekonservierung Viel Lärm um heiße Luft?

Thermoregulation and its impairment by anaesthesia and surgery has recently been brought back into focus by researchers and clinicians. All volatile and IV anaesthetics, opioids, as well as spinal and epidural anaesthesia increase the inter-threshold range of thermoregulation from 0.2°?C to 4°?C between vasodilation and vasoconstriction. Thermoregulatory vasoconstriction and shivering occurs in anaesthetized patients at lower core temperatures than in awake subjects. Following induction of general or spinal/epidural anaesthesia, core temperature decreases significantly due to internal redistribution of body heat from the core thermal compartment to peripheral tissues. About 1?h after induction of general anaesthesia and initial redistribution hypothermia, a real reduction in body heat occurs as heat loss exceeds metabolic heat production. Heat loss is further increased due to low operating room temperatures, evaporation from open body cavities, and cold IV fluids. Peripheral thermoregulatory vasoconstriction is triggered by core temperatures between 33°?C and 35°?C, and is able to slow heat loss. However, body heat content continues to decrease even though core temperatures remain nearly constant. During spinal or epidural anaesthesia thermoregulation remains intact in the unblocked body segments, leading to reduced real heat loss when compared to general anaesthesia. Inadvertent hypothermia markedly decreases drug metabolism. Coagulation is impaired by cold-induced defects of platelet function. Hypothermia reduces neutrophil phagocytosis and oxidative killing capacity, causing wound infections. Postoperative hypothermia represents an unnecessary stress for the circulatory system, elevating plasma catecholamines and leading to myocardial ischaemia and arrhythmias. These hypothermia-related morbidities therefore have consequences reaching fare into the postoperative period. Prevention of inadvertent hypothermia is always indicated. Forced-air warming is the most effective and safest method to prevent perioperative hypothermia.     

Prevention and treatment of perioperative hypothermia

Less than 10% of metabolic heat is lost via respiration, even when patients are ventilated with dry, cool gas. Passive or active airway heating and humidification, therefore, contributes little to perioperative thermal management. Each litre of intravenous (i.v.) fluid infused into adult patients at ambient temperature, or each unit of blood infused at 4°C, decreases mean body temperature approximately 0.25°C. Administration of sufficient unwarmed fluid can thus markedly decrease body temperature. Heating fluids to near 37°C prevents this hypothermia, and is appropriate when large volumes are administered.Cutaneous heat loss predominates during surgery, although evaporation from large surgical incisions may also contribute significantly. Cutaneous heat loss can be passively decreased by covering skin with surgical drapes, blankets, plastic bags etc. A single layer of each insulator reduces heat loss by approximately 30%; unfortunately, adding additional layers does not proportionately increase the benefit. In most patients, some form of active warming is required to prevent intraoperative hypothermia. Among available active heaters, forced-air warming is generally most effective.Perioperative hypothermia is associated with numerous adverse outcomes. Consequently, body temperature should be measured in most surgical patients. Unless hypothermia is specifically indicated (e.g. for protection against ischaemia), intraoperative core temperature should be maintained above 36°C. Any method or combination of methods that maintains core temperature above 36°C is adequate.     

Perioperative heat balance

Hypothermia during general anesthesia develops with a characteristic three-phase pattern. The initial rapid reduction in core temperature after induction of anesthesia results from an internal redistribution of body heat. Redistribution results because anesthetics inhibit the tonic vasoconstriction that normally maintains a large core-to-peripheral temperature gradient. Core temperature then decreases linearly at a rate determined by the difference between heat loss and production. However, when surgical patients become sufficiently hypothermic, they again trigger thermoregulatory vasoconstriction, which restricts core-to-peripheral flow of heat. Constraint of metabolic heat, in turn, maintains a core temperature plateau (despite continued systemic heat loss) and eventually reestablishes the normal core-to-peripheral temperature gradient. Together, these mechanisms indicate that alterations in the distribution of body heat contribute more to changes in core temperature than to systemic heat imbalance in most patients. Just as with general anesthesia, redistribution of body heat is the major initial cause of hypothermia in patients administered spinal or epidural anesthesia. However, redistribution during neuraxial anesthesia is typically restricted to the legs. Consequently, redistribution decreases core temperature about half as much during major conduction anesthesia. As during general anesthesia, core temperature subsequently decreases linearly at a rate determined by the inequality between heat loss and production. The major difference, however, is that the linear hypothermia phase is not discontinued by reemergence of thermoregulatory vasoconstriction because constriction in the legs is blocked peripherally. As a result, in patients undergoing large operations with neuraxial anesthesia, there is the potential of development of serious hypothermia. Hypothermic cardiopulmonary bypass is associated with enormous changes in body heat content. Furthermore, rapid cooling and rewarming produces large core-to-peripheral, longitudinal, and radial tissue temperature gradients. Inadequate rewarming of peripheral tissues typically produces a considerable core-to-peripheral gradient at the end of bypass. Subsequently, redistribution of heat from the core to the cooler arms and legs produces an afterdrop. Afterdrop magnitude can be reduced by prolonging rewarming, pharmacologic vasodilation, or peripheral warming. Postoperative return to normothermia occurs when brain anesthetic concentration decreases sufficiently to again trigger normal thermoregulatory defenses. However, residual anesthesia and opioids given for treatment of postoperative pain decreases the effectiveness of these responses. Consequently, return to normothermia often needs 2-5 h, depending on the degree of hypothermia and the age of the patient.     

Thermal care in the perioperative period

Perioperative hypothermia is, even today, 15 years after the development of active warming devices, a common complication of anesthesia and surgery.The combination of anesthetic-induced thermoregulatory impairment and exposure to cold operating room environments makes most surgical patients hypothermic. Hypothermia results initially from a core-to-peripheral redistribution of body heat, and subsequently from heat loss exceeding heat production. Patients becoming sufficiently hypothermic during general anesthesia develop a core-temperature plateau when arterio-venous shunt tone is re-established.General anesthesia produces marked and dose-dependent inhibition of thermoregulatory control, typically increasing the sweating and vasodilation thresholds by approximately 1 °C and reducing the vasoconstriction and shivering thresholds by approximately 3 °C. As a result, the inter-threshold range increases roughly 20-fold, leaving patients poikilothermic over an approximately 4 °C range of core temperatures. Regional anesthesia also impairs thermoregulatory control, producing both peripheral and central inhibition.Even mild perioperative hypothermia, which can easily be prevented, is associated with adverse outcomes including morbid cardiac events, coagulopathy, surgical wound infections, and prolonged hospitalization. Consequently, body temperature should be measured in most surgical patients. Unless hypothermia is specifically indicated (e.g. for protection against ischemia), intraoperative core temperature should be maintained above 36 °C.     

Clonidine produces a dose-dependent impairment of baroreflex-mediated thermoregulatory responses to positive end-expiratory pressure in anaesthetized humans

Background. Perioperative hypothermia is common and resultsfrom anaesthesia-induced inhibition of thermoregulatory control.Hypothermia is blunted by baroreceptor unloading caused by positiveend-expiratory pressure (PEEP), and is mediated by an increasein the vasoconstriction threshold. Premedication with clonidineimpairs normal thermoregulatory control. We therefore determinedthe effect of clonidine on PEEP-induced hypothermia protection. Methods. Core temperature was evaluated in patients undergoingcombined general and epidural anaesthesia for lower abdominalsurgery. They were assigned to an end-expiratory pressure ofzero (ZEEP) or 10 cm H₂O PEEP. The PEEP group was divided intothree blinded subgroups that received placebo (Cl-0), clonidine150 µg (Cl-150) and clonidine 300 µg (Cl-300) respectively.Placebo or clonidine was given orally 30 min before surgery.We evaluated core temperature and thermoregulatory vasoconstriction.We also determined plasma epinephrine, norepinephrine, angiotensinII concentrations and plasma renin activity. Results. Core temperature after 180 min of anaesthesia was 35.1(0.4)°C in the ZEEP group. PEEP significantly increasedfinal core temperature to 35.8 (0.5)°C (Cl-0 group). Clonidineproduced a linear, dose-dependent impairment of PEEP-inducedhypothermia protection: final core temperatures were 35.4 (0.3)°Cin the Cl-150 group and 35.0 (0.6)°C in the Cl-300 group.Similarly, clonidine produced a linear and dose-dependent reductionin vasoconstriction threshold: Cl-0, 36.4 (0.3)°C; Cl-150,35.8 (0.3)°C; Cl-300, 35.4 (0.6)°C. Plasma norepinephrine,angiotensin II concentrations and renin activity were consistentwith the thermoregulatory responses. Conclusion. Baroreceptor unloading by PEEP normally moderatesperioperative hypothermia. However, clonidine premedicationproduces a linear, dose-dependent reduction in this benefit.     

Consequences of hypothermia

Virtually all anaesthetics render patients poikilothermic and body temperature invariably decreases during surgery. For selected surgical procedures, hypothermia can protect vital organs from ischaemic injury. Hypothermia, however, is not without consequences as hypothermia-related complications are well known. As little as 2°C of core hypothermia impairs coagulation and predisposes to bleeding. Hypothermia slows emergence from general anaesthesia by both pharmacokinetic and pharmacodynamic mechanisms. Thermal discomfort is another commonly recognized perioperative problem. In the postoperative setting, even mild hypothermia exacerbates the stress response by activation of the sympathetic nervous system resulting in increased catecholamines. By this mechanism, hypothermia can precipitate myocardial ischaemia and cardiac morbidity in awake patients. In surgical patients, body temperature should be carefully monitored and controlled with the same level of attention that is given to the other vital signs. By controlling body temperature in the perioperative period, improved outcomes can be achieved.     

Trauma and hypothermia

Hypothermia occurs commonly in patients sustaining injury and may result in morbidity and mortality due to impaired cardiorespiratory function, peripheral vasoconstriction, bleeding diathesis, metabolic acidosis, diminished hepatorenal function, and impaired immune response. Hypothermia decreases metabolic function of the body and is neuroprotective. However, injured patients in whom hypothermia develops have a higher mortality than do patients with a similar injury severity who remain normothermic. Also, post-injury life-threatening coagulopathy is predicted by persistent hypothermia in patients receiving massive transfusion. Treatment of hypothermia in the trauma patient should begin with the ABCs (airway with cervical spine protection, breathing, circulation and control of bleeding). Prevention of further heat loss is achieved by maintaining the patient in a thermoneutral environment at high ambient temperature and use of warmed intravenous (i.v.) fluids. The thermal stress from cold fluid resuscitation can substantially decrease core temperature mandating the use of effective fluid and blood warming devices in all severely injured patients. Several non-invasive and invasive rewarming methods are available. Of the various non-invasive treatment modalities, convective warming appears to be most effective for mild (32–35°C) and mild–moderate (30–32°C) hypothermia. Continuous arteriovenous rewarming may be used in the patient with moderate–severe (28–32°C) and severe (<30°C) hypothermia provided there is an adequate perfusing rhythm. Cardiopulmonary bypass or body cavity lavage may be indicated for severe hypothermia in the absence of a perfusing cardiac rhythm.     

Hypothermie modérée et protection cérébrale

To define the part played by mild-to-moderate hypothermia in neuroprotection, it is necessary to take into account the thermoregulatory responses that occur in the normal human as the change in central temperature exceeds 0.2 °C. The mechanisms induced by cold are cutaneous vasoconstriction and shivering. They must be suppressed before starting controlled hypothermia. In these conditions, controlled moderate hypothermia between 32 and 35 °C dœs not seem to have deleterious side-effects, especially on coagulation. Caution is needed with the analysis of the numerous papers reporting experiments concerning the effects of moderate hypothermia in animals with induced cerebral ischaemia because of significant differences in the study designs. These differences concern mainly the time of onset of hypothermia, viz before or after ischaemia, the fact that the ischaemia is either global or focal, that it is caused by vascular occlusion posttraumatic or initiated by hypo or hyperglycemia. Some differences are also existing in the criteria used to appreciate the neuronal damage, as well as in the level of temperature and the site where it is measured. The mechanism of neuroprotectionfrom moderate hypothermia seems to be not only a decrease in cerebral metabolism, but also involves a specific action on some intra-cellular events such as the blocking of the release of glutamate and of lipid peroxydation in brain tissue. An indirect proof of the neuroprotective effect of moderate hypothermia is the increase in the neuronal damage induced by moderate hyperthermia. It is conceivable that moderate hypothermia could exert a better neuroprotective effect than the drugs having this reputation, such as barbiturates, isoflurane and propofol. The possible induction of hypothermia into experiments concerning barbiturate or isoflurane protection could even explain the protection observed, as this has been proven for anti NMDA, MK-801. The few clinical studies already published do not show obvious differences allowing to recommend moderate hypothermia as a standard technique among the therapeutic modalities used for cerebral protection for intracerebral vascular surgery or cerebral resuscitation after severe head trauma. However, the experimental results are strong enough to justify futur controlled clinical studies. The prevention of brain hyperthermia may also emerge as a major objective of resuscitative intervention.     

Isoflurane-induced vasodilation minimally increases cutaneous heat loss

Central body temperature, which usually is well controlled, typically decreases more than 1 degree C during the 1st h of general anesthesia. This hypothermia has been attributed partially to an anesthetic-induced peripheral vasodilation, which increases cutaneous heat loss to the environment. Based on the specific heat of humans, heat loss would have to increase more than 70 W for 1 h (in a 70-kg person) to explain hypothermia after induction of general anesthesia. However, during epidural anesthesia, sympathetic blockade increases heat loss only slightly. Furthermore, thermoregulatory vasoconstriction in unanesthetized humans decreases heat loss to the environment only 15 W. Therefore, we tested the hypothesis that the hypothermia that follows induction of general anesthesia does not result from increased cutaneous heat loss. Heat loss and skin-surface and tympanic membrane temperatures, before and after induction of isoflurane anesthesia, were measured in five minimally clothed volunteers. Peripheral skin blood flow was evaluated with venous-occlusion volume plethysmography and skin-surface temperature gradients. Cutaneous heat losses in watts were summed from ten area-weighted thermal flux transducers. Tympanic membrane temperature, which was stable during the 30-min control period preceding induction, decreased 1.2 +/- 0.2 degrees C in the 50 min after induction. Isoflurane anesthesia decreased mean arterial blood pressure approximately 20%. Average skin-surface temperature increased over 15 min to 0.5 degree C above control. Heat loss from the trunk, head, arms, and legs decreased slightly, whereas loss from the hands and feet (10.5% of the body surface area) doubled (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Perioperative thermoregulation and temperature monitoring

Traditionally, hypothermia has been thought of and used perioperatively as a presumptive strategy to reduce cerebral and myocardial tissue sensitivity to ischemia. Evidence, however, is mounting that maintenance of perioperative normothermia is associated with improved outcomes in patients undergoing all types of surgery, even cardiac surgery. Ambient environmental temperature is sensed by free nerve endings in the dermal and epidermal layers of the skin, which are the axonal extensions of thermosensitive neurons found in the dorsal root ganglia. Free nerve endings in the skin, by means of transient receptor ion channels that are specifically thermosensitive, also may directly sense environmental temperature. This information is transmitted to the preoptic/anterior hypothalamic region of the brainstem, which coordinates efferent responses to abnormal temperature deviation. People have evolved a highly integrated thermoregulatory system that maintains core body temperature in a relatively narrow temperature range. This system, though, is impaired by the stress of regional and general anesthesia, and the added exposure that occurs during the surgical procedure. When combined, these factors can lead to unwanted thermal disturbances. In a cold operating room environment, hypothermia is the usual perioperative consequence; however, hyperthermia is more dangerous and demands immediate diagnosis. Intraoperative hypothermia usually develops in three phases. The first is a rapid decrease in core temperature following anesthetic induction, which mostly results from redistribution of heat from the core thermal compartment to the outer shell of the body. This is followed by a slower, linear reduction in the core temperature that may last several hours. Finally, a core temperature plateau is reached, after which core temperature remains virtually unchanged for the remainder of the procedure. The plateau can be passive or result from re-emergence of thermoregulatory control in patients becoming sufficiently hypothermic. Mild hypothermia in the perioperative period has been associated with adverse outcomes, including impaired drug metabolism, prolonged recovery from anesthesia, cardiac morbidity, coagulopathy, wound infections, and postoperative shivering. Perioperative temperature monitoring devices vary by transducer type and site monitored. More important than the specific device is the site of temperature monitoring. Sites that are accessible during surgery and give an accurate reflection of core temperature include esophageal, nasopharynx, bladder, and rectal sites. Core temperature also may be estimated reasonably using axillary temperature probes except under extreme thermal conditions. Rather than taking a passive approach to thermal management, anesthesiologists need to be proactive in monitoring patients in cold operating rooms and use available technology to prevent gross disturbances in the core temperature. Various methods are available to achieve this. Prewarming patients reduces redistribution hypothermia and is an effective strategy for maintaining intraoperative normothermia. Additionally, forced-air warming and circulating water garments also have been shown to be effective. Heating intravenous fluids does not warm patients, but does prevent fluid-induced hypothermia in patients given large volumes of fluid. This article examined the evolutionary adaptations people possess to combat inadvertent hypothermia and hyperthermia. Because thermal disturbances are associated with severe consequences, the standard of care is to monitor temperature during general anesthesia and to maintain normothermia unless otherwise specifically indicated.     

Heat Flow and Distribution during Induction of General Anesthesia

Background: Core hypothermia after induction of general anesthesia results from an internal core-to-peripheral redistribution of body heat and a net loss of heat to the environment. However, the relative contributions of each mechanism remain unknown. The authors evaluated regional body heat content and the extent to which core hypothermia after induction of anesthesia resulted from altered heat balance and internal heat redistribution.

Methods: Six minimally clothed male volunteers in an [nearly equal] 22 degrees Celsius environment were evaluated for 2.5 control hours before induction of general anesthesia and for 3 subsequent hours. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Arm and leg tissue heat contents were determined from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. To separate the effects of redistribution and net heat loss, we multiplied the change in overall heat balance by body weight and the specific heat of humans. The resulting change in mean body temperature was subtracted from the change in distal esophageal (core) temperature, leaving the core hypothermia specifically resulting from redistribution.

Results: Core temperature was nearly constant during the control period but decreased 1.6 plus/minus 0.3 degrees Celsius in the first hour of anesthesia. Redistribution contributed 81% to this initial decrease and required transfer of 46 kcal from the trunk to the extremities. During the subsequent 2 h of anesthesia, core temperature decreased an additional 1.1 plus/minus 0.3 degrees Celsius, with redistribution contributing only 43%. Thus, only 17 kcal was redistributed during the second and third hours of anesthesia. Redistribution therefore contributed 65% to the entire 2.8 plus/minus 0.5 degrees Celsius decrease in core temperature during the 3 h of anesthesia. Proximal extremity heat content decreased slightly after induction of anesthesia, but distal heat content increased markedly. The distal extremities thus contributed most to core cooling. Although the arms constituted only a fifth of extremity mass, redistribution increased arm heat content nearly as much as leg heat content. Distal extremity heat content increased [nearly equal] 40 kcal during the first hour of anesthesia and remained elevated for the duration of the study.     

A novel thermoregulatory system maintains perioperative normothermia in children undergoing elective surgery

BACKGROUND: Body heat loss during anaesthesia may result in increased morbidity, particularly in high-risk populations such as children. To avoid hypothermia, a novel thermoregulatory system (Allon) was devised. We tested the safety and efficacy of this system in maintaining normothermia in children undergoing routine surgical procedures. METHODS: The system consists of a computerized body, which receives continuous afferent data, i.e. core (rectal) temperature. These data are then compared with a preset temperature (37 degrees C) and a microprocessor heating/cooling unit warms/cools the temperature of circulating water in a garment that is specially designed to allow maximal coverage of body surface area, without impingement on the surgical field. Water temperature to the garment was limited to a maximum of 39.5 degrees C. Continuous perioperative monitoring of skin and rectal temperature, heart rate and blood pressure was performed. Postoperative shivering and adverse effects were also assessed. RESULTS: The Allon system was used in 38 patients aged 3 months to 14 years undergoing surgery under general anaesthesia lasting more than 30 min. Fifty to 80% body surface area was covered by the garment. Mean operative and postoperative core temperatures were 36.9 +/- 0.5 degrees C and 36.7 +/- 0.5 degrees C, respectively. Intraoperative skin temperatures were maintained at 34.4 +/- 2.7 degrees C. The average core- to-periphery intraoperative gradient was 2.9 +/- 4.9 degrees C. Postoperative shivering was absent in 36 cases and mild in two cases. No device-related adverse effects were observed. CONCLUSIONS: Perioperative thermoregulation using the Allon system is safe and effective in maintaining body temperature within a narrow range in children undergoing brief surgical procedures.     

Body temperature and its regulation

Humans are homeotherms, i.e. they fix their temperature regardless of their environment. This is vital for normal cellular function and for metabolism to be independent of external temperature. The body has a warm ‘core’ and a cooler peripheral ‘shell’ whose role is to regulate heat transfer in and out of the core. Body temperature is controlled by a feedback system with both peripheral and central sensors, and an integrator located in the hypothalamus. Anaesthesia exposes patients to thermoregulatory challenges due to enhanced heat loss from the core to the shell to the environment, and interference with the hypothalamic temperature ‘set-point’. In extreme circumstances, deliberate hypothermia may provide benefits that outweigh the risks.     

Body temperature and its regulation

Humans are homeotherms, i.e. they fix their temperature regardless of their environment. This is vital for normal cellular function and for metabolism to be independent of external temperature. The body has a warm ‘core’ and a cooler peripheral ‘shell’ whose role is to regulate heat transfer in and out of the core. Body temperature is controlled by a feedback system with both peripheral and central sensors, and an integrator located in the hypothalamus. Anaesthesia exposes patients to thermoregulatory challenges due to enhanced heat loss from the core to the shell to the environment, and interference with the hypothalamic temperature ‘set-point’. In extreme circumstances, deliberate hypothermia may provide benefits that outweigh the risks.     

Effect of preoperative amino acid infusion on thermoregulatory response during spinal anaesthesia

Background. Intravenous amino acid infusion during general anaesthesiaprevents decreases in core temperature resulting from increasedenergy expenditure and heat accumulation. Methods. We investigated whether such stimulation also occursduring spinal anaesthesia, which blocks sympathetic nervousactivity. We examined the effect of i.v. amino acid infusionon changes in core temperature during spinal anaesthesia. Thirty-fivepatients were divided into two groups: an i.v. amino acid infusiongroup (4 kJ kg^–1 h^–1 starting 2 hbefore surgery); and a saline infusion group. Tympanic membranecore temperature, forearm–fingertip temperature gradient(an index of peripheral vasoconstriction) and mean skin temperaturewere measured for 90 min after the onset of spinal anaesthesia. Results. Changes in mean arterial pressure and heart rate didnot differ significantly between the groups during the studyperiod. Mean final core temperature 90 min after inductionof spinal anaesthesia was 35.8 (SEM 0.1)°C in the salinegroup and 36.6 (0.1)°C in the amino acid group (P<0.05).The increased level of oxygen consumption in the amino acidgroup compared with the saline group was preserved even afterthe onset of spinal anaesthesia. The thermal vasoconstrictionthreshold, defined as the tympanic membrane temperature thattriggered a rapid increase in forearm–fingertip temperaturegradient, was increased in the amino acid group [36.8 (0.1)°C]compared with the saline group [36.5 (0.1)°C] (P<0.05). Conclusions. Preoperative infusion of amino acids effectivelyprevents spinal anaesthesia-induced hypothermia by maintaininga higher metabolic rate and increasing the threshold core temperaturefor thermal vasoconstriction. Br J Anaesth 2003; 90: 58–61     

The etiology and management of inadvertent perioperative hypothermia

Mild perioperative hypothermia is a frequent complication of anesthesia and surgery. Core temperature should be monitored during general anesthesia and during regional anesthesia for large operations. Reliable sites of core temperature monitoring include the tympanic membrane, nasopharynx, esophagus, bladder, rectum, and pulmonary artery. The skin surface is not an acceptable site for monitoring core temperature. Anesthetic-induced vasodilation initially rapidly decreases core temperature secondary to an internal redistribution of heat rather than an increased heat loss to the environment. Both general and regional anesthetics impair thermoregulation, increasing the interthreshold range; that is, the range of core temperatures over which no autonomic respose to cold or warmth occurs. Preinduction skin surface warming is the only means to prevent this initial redistribution hypothermia. Forced-air warming is the most effective method of rewarming hypothermic patients intraoperatively.     

Body temperature and its regulation

Humans are homeotherms, i.e. they fix their temperature regardless of their environment. This is vital for normal cellular function and for metabolism to be independent of external temperature. The body has a warm ‘core’ and a cooler peripheral ‘shell’ whose role is to regulate heat transfer in and out of the core. Body temperature is controlled by a feedback system with both peripheral and central sensors, and an integrator located in the hypothalamus. Anaesthesia exposes patients to thermoregulatory challenges due to enhanced heat loss from the core to the shell to the environment, and interference with the hypothalamic temperature ‘set-point’. In extreme circumstances, deliberate hypothermia may provide benefits that outweigh the risks.     

Thermoregulatory Vasoconstriction Impairs Active Core Cooling

Background: Many clinicians now consider hypothermia indicated during neurosurgery. Active cooling often will be required to reach target temperatures < 34 degrees Celsius sufficiently rapidly and nearly always will be required if the target temperature is 32 degrees Celsius. However, the efficacy even of active cooling might be impaired by thermoregulatory vasoconstriction, which reduces cutaneous heat loss and constrains metabolic heat to the core thermal compartment. The authors therefore tested the hypothesis that the efficacy of active cooling is reduced by thermoregulatory vasoconstriction.

Methods: Patients undergoing neurosurgical procedures with hypothermia were anesthetized with either isoflurane/nitrous oxide (n = 13) or propofol/fentanyl (n = 13) anesthesia. All were cooled using a prototype forced-air cooling device until core temperature reached 32 degrees Celsius. Core temperature was measured in the distal esophagus. Vasoconstriction was evaluated using forearm minus fingertip skin-temperature gradients. The core temperature triggering a gradient of 0 degree Celsius identified the vasoconstriction threshold.

Results: In 6 of the 13 patients given isoflurane, vasoconstriction (skin-temperature gradient = 0 degree Celsius) occurred at a core temperature of 34.4 plus/minus 0.9 degree Celsius, 1.7 plus/minus 0.5 h after induction of anesthesia. Similarly, in 7 of the 13 patients given propofol, vasoconstriction occurred at a core temperature of 34.5 plus/minus 0.9 degree Celsius, 1.6 plus/minus 0.6 h after induction of anesthesia. In the remaining patients, vasodilation continued even at core temperatures of 32 degrees Celsius. Core cooling rates were comparable in each anesthetic group. However, patients in whom vasodilation was maintained cooled fastest. Patients in whom vasoconstriction occurred required nearly an hour longer to reach core temperatures of 33 degrees Celsius and 32 degrees Celsius than did those in whom vasodilation was maintained (P < 0.01).