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SUMMARY

Body temperature is normally controlled by a negative feedback system in the hypothalamus, which integrates thermal information from most tissues. Approximately 80% of this thermal input is derived from core body temperature, which can be measured with distal esophageal, nasopharyngeal, or tympanic membrane thermometer probes. The hypothalamus coordinates increases in heat production (nonshivering thermogenesis and shivering), increases in environmental heat loss (sweating), and decreases in heat loss (vasocon-striction) as needed to maintain normothermia.

Thermal steady state requires that heat loss to the environment equal metabolic heat production; hypothermia occurs when heat loss exceeds production. Mild core hypothermia is common during surgery and anesthesia and results initially from redistribution of body heat from the core to peripheral tissues and subsequently from heat loss exceeding metabolic heat production. Clinical doses of all tested general anesthetics decrease the threshold for response to hypothermia from approximately 37°C (normal) to 33°C to 35°C. Thus, anesthetized patients with core temperatures exceeding these temperatures are usually poikilothermic and do not actively respond to thermal perturbations. Patients becoming sufficiently hypothermic do trigger thermoregulatory vasoconstriction, and the vasoconstriction is remarkably effective in minimizing further core hypothermia.

Mild intraoperative hypothermia provides significant protection against tissue ischemia and hypoxia. It also decreases triggering of malignant hyperthermia and reduces the severity of the syndrome once triggered. However, most consequences of inadvertent hypothermia are harmful. Major adverse effects include morbid myocardial outcomes, reduced resistance to surgical wound infections, impaired coagulation, prolonged duration of drug action, shivering, and decreased postoperative thermal comfort.

Little metabolic heat is lost through the respiratory tract. Consequently, even active airway heating and humidification are of little benefit and virtually never indicated. Administration of sufficient volumes of cold intravenous fluid can produce substantial hypothermia. Fluids should therefore be warmed for patients requiring intravenous administration of more than several liters per hour. Among the clinically available active systems, forced-air heating and resistive heating (electric blankets) are the most effective and can usually maintain normothermia even during the largest operations.

Regional anesthesia produces both peripheral and central inhibition of thermoregulatory control. Peripheral inhibition results when local anesthetics block nerves that are required for thermoregulatory defense. Hypothermia during neuraxial anesthesia results initially from core-to-peripheral redistribution of body heat and subsequently from heat loss exceeding heat production. Hypothermia during major conduction anesthesia may be as severe as that during general anesthesia.

Increased core temperature can result from augmented thermogenesis (malignant hyperthermia), excessive heating (passive hyperthermia), or a specific increase in the thermoregulatory target temperature (fever). Because the causes of hyperthermia are varied and often serious, the etiology of observed increases in core temperature should be sought and appropriate treatments instituted.

A reasonable strategy for detecting and preventing thermal disturbances is to monitor core temperature in patients subjected to general anesthesia lasting longer than 30 minutes and in those undergoing major surgery with regional anesthesia. Unless hypothermia is specifically indicated (i.e., for protection against cerebral ischemia), core temperature should be maintained above 36°C.