To the Editor:-The last decade has seen publication of hundreds of articles about perioperative thermoregulation, heat balance, and consequences of thermal disturbances. We thus know far more about control of body temperature and the effects of thermal perturbations than when the original Temperature Monitoring Standards of the American Society of Anesthesiologists were introduced. More importantly, four major outcome studies were published in recent years; these studies indicate that even small reductions in intraoperative body temperature produce substantial morbidity in selected patient populations.

We must therefore consider whether revision of the current Temperature Monitoring Standards might be appropriate. To that end, I would like to summarize major recent studies relevant to patient temperature monitoring and thermal management, and their clinical implications. I will then propose a revised set of guidelines based on our current understanding of perioperative temperature control.

Normal core temperature varies between 36.5 and 37.5 [degree sign]C. Core temperature usually decreases 0.5-1.5 [degree sign]C in the first 30 min after induction of general anesthesia. Hypothermia results from internal redistribution of heat and various factors, the importance of which is hard to predict in individual patients. [1]As a result, core temperature perturbations during the first 30 min of anesthesia are difficult to interpret.

Significant subsequent decreases in core temperature are most likely in patients undergoing abdominal or thoracic surgery, but malignant hyperthermia-and hyperthermia from other causes-remains a risk in all patients. Consequently, body temperature should be monitored in most patients undergoing general anesthesia that exceeds 30 min. Body temperature ideally might be monitored continuously; however, 15-min intervals probably are sufficient in most patients.

The drugs used during intravenous sedation or regional anesthesia do not trigger malignant hyperthermia. However, core hypothermia occurs during conduction anesthesia, [2]especially when surgery involves major body cavities, [3]and often is manifested as shivering. Core temperature should therefore be measured during spinal or epidural anesthesia in patients who clinicians believe are likely to become hypothermic.

The core thermal compartment is composed of highly perfused tissues, the temperature of which is uniform and high compared with the rest of the body. Temperature in this compartment can be evaluated in the pulmonary artery, the distal esophagus, the tympanic membrane, or the nasopharynx. Even during rapid thermal perturbations (e.g., cardiopulmonary bypass), these temperature monitoring sites remain reliable.* Core temperature can be estimated with reasonable accuracy using oral, axillary, and bladder temperatures, except during extreme thermal perturbations. [4,5] 

Skin surface temperatures are considerably lower than core temperature. Skin surface temperatures, when adjusted with an appropriate offset, nonetheless reflect core temperature reasonably well. [6]However, skin temperatures fail to reliably confirm the clinical signs of malignant hyperthermia (tachycardia and hypercarbia) in swine [7]and have not been evaluated for this purpose in humans. Rectal temperature also normally correlates well with core temperature [4]but fails to increase rapidly during malignant hyperthermia crises [7]and during other documented situations. [8]Consequently, rectal and skin surface temperatures must be used with some caution.

Thermoregulatory responses are impaired by general anesthesia. [9]Intra-operative core body temperature changes are thus largely determined by patient environment. Because the typical operating room is cold and because factors associated with surgery increase heat loss, [10]perioperative hypothermia is common. Mild hypothermia (33-35 [degree sign]C) provides substantial protection from tissue ischemia [11,12]and hypoxemia. [13]It also slows triggering of malignant hyperthermia, and the syndrome is less severe after being triggered in hypothermic swine. [14,15] 

In contrast, mild hypothermia ([almost equal to] 2 [degree sign]C below normal) prolongs drug action [16,17]by decreasing metabolism, [18]causes protein wasting, [19]impairs platelet [20]and clotting-cascade enzyme function, [21,22]and triggers postanesthetic shivering [23,24]and thermal discomfort. [24,25]More importantly, core temperatures that are only 1-2 [degree sign]C below normal are associated with adverse patient outcomes. Two groups have shown that mild hypothermia in selected patient populations prolongs postanesthetic recovery, [26]augments bleeding and transfusion requirements, [27]increases morbid myocardial outcomes, [28]and reduces resistance to surgical wound infections and prolonged hospital stay. [29] 

The minor and major complications of hypothermia are thus well documented. In some patients mild hypothermia is likely to be dangerous. In others it will be an uncomfortable and slow recovery. I therefore propose that intraoperative core temperatures should usually be maintained at more than 36 [degree sign]C unless hypothermia is specifically indicated.


To detect thermal disturbances and maintain appropriate body temperature during anesthesia.


1. Core body temperature should be measured or reliably estimated in most patients given general anesthesia for more than 30 min.

2. Temperature should also be measured or reliably estimated during regional anesthesia when changes in body temperature are intended, anticipated, or suspected.

3. Unless hypothermia is specifically indicated (e.g., for protection against ischemia), efforts should be made to maintain intraoperative core temperature at more than 36 [degree sign]C.

Daniel I. Sessler, M.D.

Professor; Department of Anesthesia; University of California; San Francisco, California; Professor; Ludwig Boltzmann Institute for Clinical Anesthesia and Intensive Care; Director, Outcomes Research [trade mark sign] and Vice Chair; Department of Anesthesia and General Intensive Care; University of Vienna; Vienna, Austria;

(Accepted for publication August 6, 1998.)

*Stone JG, Yound WL, Smith CR, Solomon RA, Ostapkovich N, Reeg T, Wang A: Do temperature recorded at standard monitoring sites reflect actual brain temperature during deep hypothermia? Anesthesiology 1991; 75:A483

Matsukawa T, Sessler DI, Sessler AM, Schroeder M, Ozaki M, Kurz A, Cheng C: Heat flow and distribution during induction of general anesthesia. Anesthesiology 1995; 82:662-73
Frank SM, Beattie C, Christopherson R, Norris EJ, Rock P, Parker S, Kimball AW: Epidural versus general anesthesia, ambient operating room temperature, and patient age as predictors of inadvertent hypothermia. Anesthesiology 1992; 77:252-7
Hendolin H, Lansimies E: Skin and central temperatures during continuous epidural analgesia and general anaesthesia in patients subjected to open prostatectomy. Ann Clin Res 1982; 14:181-6
Cork RC, Vaughan RW, Humphrey LS: Precision and accuracy of intraoperative temperature monitoring. Anesth Analg 1983; 62:211-4
Glosten B, Sessler DI, Faure EAM, Stoen R, Thisted RA, Karl L: Central temperature changes are not perceived during epidural anesthesia. Anesthesiology 1992; 77:10-6
Ikeda T, Sessler DI, Marder D, Xiong J: The influence of thermoregulatory vasomotion and ambient temperature variation on the accuracy of core-temperature estimates by cutaneous liquid-crystal thermometers. Anesthesiology 1997; 86:603-12
Iaizzo PA, Kehler CH, Zink RS, Belani KG, Sessler DI: Thermal response in acute porcine malignant hyperthermia. Anesth Analg 1996; 82:803-9
Ash CJ, Cook JR, McMurry TA, Auner CR: The use of rectal temperature to monitor heat stroke. Mo Med 1992; 89:283-8
Sessler DI: Perioperative hypothermia. N Engl J Med 1997; 336:1730-7
Roe CF: Effect of bowel exposure on body temperature during surgical operations. Am J Surg 1971; 122:13-5
Illievich UM, Zornow MH, Choi KT, Strnat MAP, Scheeller MS: Effects of hypothermia or anesthetics on hippocampal glutamate and glycine concentrations after repeated transient global cerebral ischemia. Anesthesiology 1994; 80:177-86
Todd MM, Warner DS: A comfortable hypothesis reevaluated: Cerebral metabolic depression and brain protection during ischemia (editorial). Anesthesiology 1992; 76:161-4
Keykhah MM, Hagerdal M, Welsh FA, Barrer MA, Sisco F, Harp JR: Effect of high vs. low arterial blood oxygen content on cerebral energy metabolite levels during hypoxia with normothermia and hypothermia in the rat. Anesthesiology 1980; 52:492-5
Iaizzo PA, Kehler CH, Carr RJ, Sessler DI, Belani KG: Prior hypothermia attenuates malignant hyperthermia in susceptible swine. Anesth Analg 1996; 82:782-9
Nelson TE: Porcine malignant hyperthermia: Critical temperatures for in vivo and in vitro responses. Anesthesiology 1990; 73:449-54
Heier T, Caldwell JE, Sessler DI, Miller RD: Mild intraoperative hypothermia increases duration of action and spontaneous recovery of vecuronium blockade during nitrous oxide-isoflurane anesthesia in humans. Anesthesiology 1991; 74:815-9
Leslie K, Sessler DI, Bjorksten AR, Moayeri A: Mild hypothermia alters propofol pharmacokinetics and increases the duration of action of atracurium. Anesth Analg 1995; 80:1007-14
Heier T, Caldwell JE, Sharma ML, Gruenke LD, Miller RD: Mild intraoperative hypothermia does not change the pharmacodynamics (concentration-effect relationship) of vecuronium in humans. Anesth Analg 1994; 78:973-7
Carli F, Emery PW, Freemantle CAJ: Effect of peroperative normothermia on postoperative protein metabolism in elderly patients undergoing hip arthroplasty. Br J Anaesth 1989; 63:276-82
Valeri CR, Khabbaz K, Khuri SF, Marquardt C, Ragno G, Feinhold H, Gray AD, Axford T: Effect of skin temperature on platelet function in patients undergoing extracorporeal bypass. J Thorac Cardiovasc Surg 1992; 104:108-16
Reed L, Johnston TD, Hudson JD, Fischer RP: The disparity between hypothermic coagulopathy and clotting studies. J Trauma 1992; 33:465-70
Staab DB, Sorensen VJ, Fath JJ, Raman SBK, Horst HM, Obeid, F N: Coagulation defects resulting from ambient temperature-induced hypothermia. J Trauma 1994; 36:634-8
Just B, Delva E, Camus Y, Lienhart A: Oxygen uptake during recovery following naloxone. Anesthesiology 1992; 76:60-4
Kurz A, Sessler DI, Narzt E, Bekar A, Lenhardt R, Huemer G: Postoperative hemodynamic and thermoregulatory consequences of intraoperative core hypothermia. J Clin Anesth 1995; 7:359-66
Sessler DI, Rubinstein EH, Moayeri A: Physiological responses to mild perianesthetic hypothermia in humans. Anesthesiology 1991; 75:594-610
Lenhardt R, Marker E, Goll V, Tschernich H, Kurz A, Sessler DI, Narzt E, Lackner F: Mild intraoperative hypothermia prolongs postoperative recovery. Anesthesiology 1997; 87:1318-23
Schmied H, Kurz A, Sessler DI, Kozek S, Reiter A: Mild intraoperative hypothermia increases blood loss and allogeneic transfusion requirements during total hip arthroplasty. Lancet 1996; 347:289-92
Frank SM, Fleisher LA, Breslow MJ, Higgins MS, Olson KF, Kelly S, Beattie C: Perioperative maintenance of normothermia reduces the incidence of morbid cardiac events: A randomized clinical trial. JAMA 1997; 277:1127-34
Kurz A, Sessler DI, Lenhardt RA: Study of wound infections and temperature group: Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. N Engl J Med 1996; 334:1209-15