Secondary Logo

Journal Logo

Analgesia: The open mind: Research Reports

Some Unanswered Questions About Temperature Management

Roth, Jonathan V. MD

Author Information
doi: 10.1213/ANE.0b013e3181b763ae
  • Free
  • Take the CME Test

Much has been learned about perioperative temperature management in recent years. Most of the research has focused on the problem of hypothermia; deservingly so, because it is the most frequent and significant perioperative temperature problem and is associated with many well-known complications (discussed below).1 However, with the exception of malignant hyperthermia, relatively little attention has been directed to the appropriate management of the hyperthermic patient, in particular, the febrile patient. Section I of this article will discuss the unresolved issue of temperature management in the infected, febrile patient.

Section II will discuss the relative importance of intraoperative versus postoperative hypothermia. Because of the effective intraoperative active warming techniques now available, patients can initially become hypothermic intraoperatively but warm sufficiently, so that by the end of the surgical case, they are considered to be normothermic (i.e., ≥36.0°C). Prewarming is currently the only effective way to mitigate the initial redistribution hypothermia that occurs in all patients upon induction of general anesthesia. However, prewarming requires resource utilization, is not a standard of care, and is not universally used. Further evidence that intraoperative, and not just postoperative, hypothermia causes adverse outcomes would further demonstrate the value of prewarming and provide more impetus to use prewarming much more frequently.

Anecdotally, this author finds that the use of active warming in short duration cases varies with institutions and practitioners. The SCIP (Surgical Care Improvement Project) rules from Centers for Medicare and Medicaid Services evaluate the practitioners only for cases lasting more than 1 h.2 Also, it is difficult to demonstrate an increase in core temperature from our active warming techniques (e.g., forced air warming) until at least 30 min have elapsed.3,4 For both of these reasons, there may be less motivation to aggressively warm patients having short duration cases. Section III will provide arguments as to why aggressive warming techniques may be important in short duration cases, even in the absence of a demonstrable intraoperative increase in core temperature, and will suggest needed research.

What Is the Optimal Temperature Management Strategy for the Infected Febrile Patient?

Hyperthermia, an increase of body temperature by definition, can be febrile or nonfebrile. This discussion applies to the febrile patient (i.e., a regulated increase in temperature due to an increased thermoregulatory set point) and not to nonfebrile hyperthermia (i.e., an unregulated temperature increase when the body temperature is higher than the thermoregulatory set point).

The primary treatment of febrile hyperthermia (fever) due to an infection is the treatment of the underlying infection. While such treatment is ongoing, the question at hand is whether fever is a harmful byproduct of infection or a host-defense response. If it is harmful, we should actively, or at least permissively, cool the febrile patient. If it is the latter, we should try to maintain the patient’s temperature at the increased thermoregulatory set point. Although this question may still be unanswered,5 others believe there is overwhelming evidence that fever is a beneficial part of a coordinated defense.6,7 The lines of evidence include evolutionary, correlative, antipyretic, and hyperthermia/hypothermia studies.6 For example, infectious illnesses in animals are of longer duration and mortality rates increase if the fever is treated.6 Additionally, because the febrile response is highly regulated, it likely has an adaptive role.6 Some of the enzymes involved in immune defense have their temperature optima not at 37°C, but at a higher temperature. We may have evolved to mount our best immune defense at an increased temperature.

Second, if the patient’s temperature decreases below his or her elevated thermoregulatory set point, even if the patient’s temperature is still above 37°C, the patient will postoperatively, or intraoperatively, mount a response to increase his or her temperature back to the elevated set point similar to a nonfebrile patient who becomes hypothermic. This response has a high metabolic cost and is likely undesirable. Also, there is some risk in administering antipyretic therapy to maintain the lower temperature, and antipyretics may be ineffective.5 Unfortunately, there is no way to know if the thermoregulatory set point changes during surgery, and if so by how much and in which direction. (In those patients in whom this author chooses to maintain an increased temperature, this author makes the assumption that the thermoregulatory set point will not significantly change during the surgical procedure, and thus tries to maintain the patient’s temperature at the first measured core temperature.)

Maintaining a patient at an elevated temperature increases the metabolic rate. It is estimated that for every 1°C increase in temperature, the metabolic rate increases by up to 13%. This is probably offset to some extent by the decreased metabolic rate during anesthesia. However, this increased metabolic rate may be insignificant compared with the alternative scenario. There can be a short-term increase in metabolic rate of up to 600% in the postoperative shivering patient.8 A doubling can be maintained for longer durations.9 Ciofolo et al.10 reported a more modest 80% mean increase, but 30% of their patients had significantly larger increases (200%). Maintaining normothermia has been demonstrated to reduce the postoperative metabolic rate increase that would otherwise result if the patient became hypothermic.11 With regard to causing thermal damage, increases in core temperature up to 41°C have never been shown to be harmful per se.12 In contrast, therapeutic hyperthermia with temperatures >42°C have been associated with tissue damage, such as fat necrosis.

One has to determine whether or not the benefits of remaining febrile outweigh any harm caused by the febrile state. There are specific instances in which a febrile state can be harmful. In any case where there is a possibility of neurologic injury (e.g., carotid endarterectomy, virtually all of neurosurgery and cardiac surgery, and any case in which there is a potential for a cardiac arrest), neurologic injury may be greater in the presence of an increased temperature.13 In pediatric patients, one has to be concerned about febrile seizures.14 In pregnant patients, one should be concerned about the effect of hyperthermia on the fetus. Temperatures >39°C during the first 10 wk of pregnancy when organogenesis takes place may be associated with a sixfold increased risk of neural tube defect.15 Also, although infections increase the chance of preterm labor, this may be due to the underlying disease causing cytokine release from the amniotic cells rather than the fever per se.16 Lastly, because heart rate increases as temperature increases, in patients in whom tachycardia may be harmful (e.g., ischemic heart disease, valvular heart disease, obstructive cardiomyopathy), decreasing the temperature can assist in treating the tachycardia. However, this may pose a dilemma if compensatory thermoregulatory mechanisms provoke tachycardia or other cardiac complications. In some cases, attempts to decrease a patient’s temperature may be overcome by the patient’s thermal regulatory system.17 Such a futile attempt would only wastefully increase catabolism and oxygen consumption while activating the sympathetic nervous system, a potential cause of morbid cardiac events.18,19

There are few data that address how one should manage the temperature of a febrile patient undergoing surgery.20 At least one textbook advocates treating the increased temperature of a febrile patient, but provides no justification for doing so, and acknowledges that it may worsen the situation.17 It is possible that the correct decision may be pathogen-specific.5 Although these are strong arguments to maintain a febrile patient at his or her elevated temperature (with exceptions), outcome studies are needed to affirm or refute this suggestion. An answer to this question would help us optimize care to our septic patients who are some of our sickest, and who have a significant mortality rate. Until there are outcome studies that answer this question, the individual practitioner should consider the above arguments in managing the temperature of a febrile patient.

Lastly, because there is currently no generally accepted demonstrable benefit to hyperthermia in nonfebrile patients, it would seem that nontherapeutic nonfebrile hyperthermia should generally be treated.

How Much Does Intraoperative Hypothermia Contribute to Morbid Cardiac Events and Other Complications?

Hypothermia-induced complications include morbid myocardial outcomes, surgical wound infection, coagulopathy, increased allogenic transfusions, negative nitrogen balance, delayed wound healing, delayed postanesthetic recovery, prolonged hospitalization, shivering, and patient discomfort.1 The SCIP rules evaluate practitioners by either the last intraoperative or the first postanesthesia care unit (PACU) temperature and do not take into consideration what the temperature otherwise was intraoperatively.2 Studies typically use the final intraoperative core temperature measurement to designate whether a patient was hypothermic (i.e., <36.0°C).21–23 Because there is an initial core temperature decrease (typically 0.5°C-1.5°C) after the induction of anesthesia as a result of heat redistribution from the core to the normally cooler periphery,24,25 undoubtedly there were some patients who were considered normothermic based on their final intraoperative temperature measurement, but who were actually hypothermic during part of the surgery. Patients in the end-of-case hypothermic groups tended to have significantly lower temperatures than patients in the end-of-case normothermic groups in the early postoperative period and took longer to normalize their temperature.21,23 Thus, end-of-case hypothermia also appears to be a marker for a greater degree and duration of postoperative hypothermia. There has been limited research that separates and compares these end-of-case normothermic patients into groups who either were or were not hypothermic intraoperatively.

Some of the hypothermia-induced complications (such as intraoperative coagulopathy) must result from intraoperative hypothermia. Melling et al.26 found that patients who were prewarmed for 30 min had lower surgical infection rates. The intraoperative and early postoperative period seems to be the critical time period during which surgical infections become established.22,27 Hence, maintaining normothermia during this critical time would be expected to reduce the surgical infection rate. However, there is evidence to suggest that some morbid cardiac complications may be a consequence, at least in part, not of intraoperative but of postoperative hypothermia. There are studies that report no differences in the rates of intraoperative morbid cardiac events between end-of-case normothermic versus end-of-case hypothermic patients; the differences occurred in the postoperative period.21,28 Activation of the sympathetic nervous system because of postoperative hypothermia is one plausible mechanism of myocardial ischemia. Frank et al.19 found that hypothermic patients had a greater degree of vasoconstriction, higher plasma norepinephrine concentrations, and higher arterial blood pressures in the early postoperative period. It was suggested that there might be an intraoperative protective effect of the anesthetic that diminishes postoperatively. Logically, it should follow that if postoperative hypothermia can be avoided or reduced, the rates of complications might also be reduced.

Thus, it would seem that hypothermia should be avoided both intraoperatively and postoperatively. Our ability to prevent the initial temperature decrease due to redistribution has previously been very limited. There is mounting evidence that effective prewarming significantly attenuates the initial decrease in core temperature.29–33 Prewarming in combination with intraoperative active warming has the potential to largely eliminate (or at least greatly reduce) the problems of intraoperative and postoperative hypothermia. Further research that compares the outcomes between 1) patients who never become hypothermic at any time, and 2) those who were hypothermic intraoperatively but were normothermic at the end of the case, would shed more light on the relative contributions of intraoperative versus postoperative hypothermia to the complications attributed to hypothermia, because the magnitude and duration of postoperative hypothermia would be minimized in both of these groups. This comparison would help further determine the true value of prewarming. At this time, even though prewarming is likely to decrease surgical infection rates, blood loss, and transfusion requirement,20,26,34 and in many cases increase the likelihood of normothermia at the end of the case, imminent universal implementation of prewarming is not likely because it will not fit into the current clinical routine of many hospitals and it requires additional resource utilization. Until such time, intraoperative active warming will likely remain as the primary tactic for combating hypothermia in many patients.

Lastly, although there are good reasons to be aggressive in addressing the problem of hypothermia, there are reasons why we should be wary about overwarming nonfebrile patients. First, an increase in body temperature is known to increase heart rate and oxygen utilization, factors that predispose to myocardial ischemia in the patient at risk. Second, just as a greater degree of cerebral cell death occurs from ischemia in the presence of hyperthermia compared with normothermia, there is also evidence to suggest that there will be more myocardial damage if myocardial ischemia occurs in the presence of hyperthermia as compared with normothermia.35,36

Should We Use Active Warming in the Short Duration Case, Particularly in the Absence of Prewarming?

At this time, a new thermal management standard is emerging that will only apply to surgical cases lasting longer than 1 h.37 In addition, studies report that one cannot demonstrate any increase in core temperature from forced air warming until after a significant period of time, typically 30 or more minutes.3,4 As a result, some may conclude that there are no benefits of active warming in short duration cases. This, in combination with an absence of a regulatory imperative for aggressive temperature management in short duration cases, may result in underutilization of active warming in short duration cases. Anecdotally, this author finds that the use of active warming (and prewarming) in short duration cases varies with institutions and practitioners.

When using forced air warming, the peripheral temperature has to increase before core temperature can increase.4 An increase in peripheral temperature contributes to the increase in core temperature in at least 2 ways. First, metabolic heat that is generated in the core normally dissipates along thermal gradients to the periphery, then the skin, and ultimately to the cooler environment. If the core-to-periphery gradient is decreased by increasing peripheral temperature, the rate of heat transfer from the core to periphery is expected to decrease. As a result, more of the heat produced in the core would remain in the core resulting in an increase (or a lesser decrease) in core temperature. Second, if the peripheral temperature increases above that of core temperature, there will be a direct transfer of heat to the core from the periphery, thus increasing the core temperature.

Thus, even in the absence of a demonstrable intraoperative increase in core temperature, a warmer periphery resulting from active warming may allow a patient to normalize his or her temperature more quickly. This may translate into a quicker PACU recovery and may reduce or eliminate the duration of uncomfortable shivering. There are conflicting data with regard to duration of PACU stay in different populations. In children recovering from peripheral surgery, hypothermia had no influence.38 In adults having longer duration surgery, hypothermia prolonged postanesthetic recovery.33,39 In addition, a warmer skin temperature may attenuate the adrenergic and metabolic responses to hypothermia, which are potential causes of myocardial ischemia.40 It logically follows that a shorter degree and duration of postoperative hypothermia has the potential to decrease cardiac complications. Further research is required to support or refute the hypothesis that active warming in short cases, even with no demonstrable increase in intraoperative core temperature, decreases cardiac complications associated with hypothermia. To the extent that postoperative hypothermia contributes to other complications (e.g., surgical infection), additional benefits may accrue. Although active intraoperative warming is likely to be beneficial in short cases, there may not be enough time for intraoperative active warming to be fully effective. It seems likely that the most effective strategy for short duration cases would need to include prewarming.

The patients at risk who are most likely to benefit from more aggressive prophylaxis and treatment of hypothermia include the elderly and those with comorbid conditions. Because of SCIP, there is incentive to practice aggressive temperature management in patients undergoing colon surgery in order to reduce surgical infections. Although we should endeavor to treat all patients the same, when resources are limited, a need to prioritize exists. If an institution has limited ability to use prewarming, one can justify giving priority to these aforementioned classes of patients.

Harper et al.41 argue that despite knowledge and guidelines, implementation of warming strategies remains patchy both in the United States and the United Kingdom. It is hoped that this communication will have a positive impact with regard to interest, knowledge, and compliance for optimal perioperative temperature management.


1. Sessler DI. Temperature monitoring and perioperative thermoregulation. Anesthesiology 2008;109:318–38
2. Surgical Care Improvement Project, Centers for Medicare & Medicaid Services, U.S. Department of Health and Human Services. SCIP-Inf-7. Available at: Specification Manual for National Hospital Quality Measures Accessed June 15, 2009
3. Negishi C, Hasegawa K, Mukai S, Nakagawa F, Ozaki M, Sessler DI. Resistive heating and forced-air warming are comparably effective. Anesth Analg 2003;96:1683–7
4. Kimberger O, Held C, Stadelmann K, Mayer N, Hunkeler C, Sessler DI, Kurz A. Resistive polymer versus forced-air warming: comparable heat transfer and core rewarming rates in volunteers. Anesth Analg 2008;107:1621–6
5. Mackowiak PA. Concepts of fever. Arch Intern Med 1998;158:1870–81
6. Kluger MJ, Kozak W, Conn CA, Leon LR, Soszynski D. The adaptive value of fever. Infect Dis Clin North Am 1996;10:1–20
7. Mackowiak PA. Fever: blessing or curse? A unifying hypothesis. Ann Intern Med 1994;120:1037–40
8. Giesbrecht GG, Sessler DI, Mekjavic IB, Schroeder M, Bristow GW. Treatment of immersion hypothermia by direct body-to-body contact. J Appl Physiol 1994;76:2373–9
9. Horvath SM, Spurr GB, Hutt BK, Hamilton LH. Metabolic cost of shivering. J Appl Physiol 1956;8:595–602
10. Ciofolo MJ, Clergue F, Devilliers C, Ben-Ammar M, Viars P. Changes in ventilation, oxygen uptake, and carbon dioxide output during recovery from isoflurane anesthesia. Anesthesiology 1989;70:737–41
11. Just B, Delva E, Camus Y, Lienhart A. Oxygen uptake during recovery following naloxone relationship with intraopeartive heat loss. Anesthesiology 1992;76:60–4
12. Mackowiak PA, Boulant JA. Fever’s glass ceiling. Clin Infect Dis 1996;22:525–36
13. Patel P. Brain protection: the clinical reality. In: IARS 2006 Review Course Lectures. 2006:77–83
14. Mackowiak PA. Physiologic rationale for suppression of fever. Clin Infect Dis 2000;31:S185–S189
15. Milunsky A. Genetic disorders and the fetus: diagnosis, prevention and treatment. 3rd ed. Baltimore: Johns Hopkins University Press, 1992:1
16. Cunningham FG, Leveno KL, Bloom SL, Hauth JC, Gilstrap LC, Wenstrom KD. Parturition. In: Cunningham FG, Leveno KJ, Bloom SL, Hauth JC, Gilstrap L III, Wenstrom KD, eds. Williams obstetrics 22nd ed. New York: McGraw-Hill Companies, Inc., 2005:177–9
17. Sessler DI. Temperature monitoring. In: Miller RD, ed. Miller’s anesthesia. 6 th ed. Philadelphia: Elsevier Churchill Livingston, 2005:1590
18. Lenhardt R, Negishi C, Sessler DI, Vuong K, Bastanmehr H, Kim J, Bjorksten AR. The effects of physical treatment on induced fever in humans. Am J Med 1999;106:550–5
19. Frank SM, Higgins MS, Breslow MJ, Fleisher LA, Gorman RB, Sitzmann JV, Raff H, Beattie C. The catecholamine, cortisol, and hemodynamic responses to mild perioperative hypothermia. A randomized clinical trial. Anesthesiology 1995;82:83–93
20. Sheffield CW, Sessler DI, Hunt TK. Mild hypothermia during isoflurane anesthesia decreases resistance to E. coli dermal infection in guinea pigs. Acta Anaesthesiol Scand 1994;38:201–5
21. 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
22. 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
23. Schmied H, Kurz A, Sessler DI, Kozek S, Reiter A. Mild intraoperative hypothermia increases blood loss and allogenic transfusion requirements during total hip arthroplasty. Lancet 1996;347:289–92
24. Matsukawa T, Sessler DI, Christensen R, Ozaki M, Schroeder M. Heat flow and distribution during epidural anesthesia. Anesthesiology 1995;83:961–7
25. 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
26. Melling AC, Ali B, Scott EM, Leaper DJ. Effects of preoperative warming on the incidence of wound infection after clean surgery: a randomized controlled trial. Lancet 2001;358:876–80
27. Miles AA, Miles EM, Burke J. The value and duration of defense reactions of the skin to the primary lodgement of bacteria. Br J Exp Pathol 1957;38:79–96
28. Slotman GJ, Jed EH, Burchard KW. Adverse effects of hypothermia in postoperative patients. Am J Surg 1985;149:495–501
29. Sessler DI, Schroeder M, Merrifield B, Matsukawa T, Cheng C. Optimal duration and temperature of prewarming. Anesthesiology 1995;82:674–81
30. Andrzejowski J, Hoyle J, Eapen G, Turnbull D. Effect of prewarming on post-induction core temperature and the incidence of inadvertent perioperative hypothermia in patients undergoing general anesthesia. Br J Anaesth 2008;101:627–31
31. Kim JY, Shinn H, Oh YJ, Hong YW, Kwak HJ, Kwak YL. The effect of skin surface warming during anesthesia preparation on preventing redistribution hypothermia in the early postoperative period of off-pump coronary artery bypass surgery. Eur J Cardiothorac Surg 2006;29:343–7
32. Horn EP, Schroeder F, Gottschalk A, Sessler DI, Hiltmeyer N, Standl T, Schulte am Esch J. Active warming during cesarean delivery. Anesth Analg 2002;94:409–14
33. Bock M, Muller J, Bach A, Bohrer H, Martin E, Motsch J. Effects of preinduction and intraoperative warming during laparotomy. Br J Anaesth 1998;80:159–63
34. Rajagopalan S, Mascha E, Na J, Sessler DI. The effects of mild perioperative hypothermia on blood loss and transfusion requirement. Anesthesiology 2008;108:71–7
35. Chien GL, Wolff RA, Davis RF, Van Winkle DM. Normothermic range temperature affects myocardial infarct size. Cardiovasc Res 1994;28:1014–7
36. Duncker DJ, Klassen CL, Ishibashi Y, Herrlinger SH, Pavek TJ, Bache RJ. Effect of temperature on myocardial infarction in swine. Am J Physiol 1996;270:H1189–H1199
37. Hannenberg AA, Sessler DI. Improving perioperative temperature management. Anesth Analg 2008;107:1454–7
38. Bissonnette B, Sessler DI. Mild hypothermia does not impair postanesthetic recovery in infants and children. Anesth Analg 1993;76:168–72
39. Lenhardt R, Marker E, Goll V, Tschernich H, Kurz A, Sessler DI, Narzt E, Lackner F. Mild intraoperative hypothermia prolongs postanesthetic recovery. Anesthesiology 1997;87:1318–23
40. Cheng C, Matsukawa T, Sessler DI, Ozaki O, Kurz A, Merrifield B, Lin H, Olofsson P. Increasing mean skin temperature linearly reduces the core-temperature thresholds for vasoconstriction and shivering in humans. Anesthesiology 1995;82:1160–8
41. Harper CM, Andrzejowski, Alexander R. NICE and warm. Br J Anaesth 2008;101:293–5
© 2009 International Anesthesia Research Society