Unintentional Perioperative Hypothermia

Anthony G. Doufas

CASE SUMMARY

A 65-year-old, 67-kg woman with a history of hypertension undergoes a vaginal hysterectomy for a uterine myoma. Her preoperative hemoglobin and blood pressure are 11 g per dL and 160/87 mmHg, respectively. An epidural catheter is placed for postoperative pain management. After induction of general anesthesia, the patient is placed in a dorsal lithotomy position. Her core body temperature (Tc) (esophageal) is 36.5°C before surgical incision. Thermal management includes intravenous fluid warming and application of traditional blankets on the upper body. One hour after incision, Tc is 35.5°C and, despite adequate analgesia and hypnosis, heart rate and blood pressure gradually increase. The surgeon recognizes technical difficulties in completing the operation vaginally and proceeds with the abdominal hysterectomy. Upper body forced-air warming is started, and 8 mL of 0.25% bupivacaine is administered through the epidural catheter. Thirty minutes later, blood pressure is 100/66 mmHg and Tc is 34.9°C. After a 3½-hour procedure, during which the patient received 4 L crystalloids and 4 units of blood, she arrives in the recovery area with her trachea intubated, with a Tc of 35.3°C and hemoglobin of 9 g per dL. Blood pressure is 170/90 mmHg, and heart rate is 110 beats per minute with 6 to 10 multiform, ventricular extrasystoles per minute. Full body forced-air warming is applied, and 10 mg of labetalol, IV bolus is administered while an epidural analgesic infusion is initiated for pain relief. The patient’s trachea is extubated 1 hour later when her oral temperature is 36°C, and she is discharged to the ward after an overall recovery time of 2½ hours.

What Baseline Knowledge Is Relevant?

Tc is among the most tightly controlled physiologic parameters in humans. Although normal circadian and other physiology-driven variations in Tc exist, at any given time robust thermoregulatory control does not allow more than a few tenths of a degree deviation from the expected set point. In awake humans, any type of thermal insult is readily counteracted by specific physiologic responses, the intensities of which are proportional to the need for adequate temperature control. During anesthesia and surgery, inhibition of the normal thermoregulatory defenses is the major cause for a typical decrease by 1°C to 3°C in the Tc of the unwarmed patient. Therefore, albeit a widely accepted definition of perioperative mild hypothermia is lacking, an unvoiced consensus defines it as a Tc between 34°C and 36°C.

What Is the Underlying Physiology of Intraoperative Hypothermia?

▪ TEMPERATURE MONITORING

The core thermal compartment is comprised of highly perfused tissues, with a temperature that is uniform and
high compared with the rest of the body. The temperature in this compartment can be evaluated in the pulmonary artery, distal esophagus, tympanic membrane, or nasopharynx. Even during rapid thermal perturbations (e.g., cardiopulmonary bypass), these temperature monitoring sites remain reliable, although the rectal site also provides a reliable estimation of Tc during regional anesthesia.¹

Thermistors and thermocouples are the most common electrical techniques of temperature measurement used in anesthesia. Thermistor probes function through temperature-induced changes in the resistance of various semiconductor materials, whereas thermocouples exploit the development of temperature-dependent voltage at the junction of two dissimilar metals.²

▪ EVOLUTION OF HYPOTHERMIA

The administration of anesthesia is almost invariably associated with a decrease in Tc of 1°C to 3°C, depending on the type and dose of the anesthetic, amount of surgical exposure, and ambient temperature. Intraoperative hypothermia follows a characteristic pattern that consists of three distinct phases: Redistribution, linear decrease, and Tc plateau (see Fig. 45.1).³,⁴

Redistribution

In awake humans, the core thermal compartment consists of well perfused tissues of the trunk and head that are maintained at a 2°C to 4°C higher temperature than the rest of the body. This normal core-to-peripheral tissue temperature gradient is maintained by tonic thermoregulatory vasoconstriction of arteriovenous shunts in the fingers and toes.⁵

General anesthesia inhibits tonic thermoregulatory vasoconstriction by both a central and a peripheral vasodilating effect. Vasodilation promotes the redistribution of heat from the core compartment to the peripheral tissues of the body, resulting in a relatively hypothermic core (Fig. 45.1, A→B). Up to 80% of the typical decrease of 1.5°C in Tc during the first hour of anesthesia is attributed to heat redistribution.⁴

Linear Phase

The redistribution phase of hypothermia is followed by a slow, linear decrease in Tc that represents a net heat loss to the environment (Fig. 45.1, B→C) through the skin or the operating field.³ Total cutaneous heat loss can be considered as a linear function of the skin-to-ambient temperature difference and is mediated through four different mechanisms: Radiation, conduction, convection, and evaporation. Radiation is the most important of those mechanisms and, when combined with convection, is responsible for 70% to 90% of the total heat loss in the intraoperative patient.²,⁶

FIGURE 45.1 Schematic presentation of the three phases of intraoperative hypothermia, based on data from Matsukawa et al.⁴ and Kurz et al.³ The human body, as shown in the inset, is denoted by a 5-limb star with a dense black core representing the high-heat central thermal compartment and a low-heat surrounding gray area indicating the peripheral tissues. A: The typical preoperative patient is vasoconstricted with a large core-to-peripheral tissue temperature gradient and a clear distinction between the two thermal compartments. B: After anesthesia-induced peripheral vasodilation, heat driven by the temperature gradient flows toward the periphery of the body. Therefore, core temperature decreases, and the two body compartments become more homogeneous (redistribution hypothermia, A→B). C: Radiation- and convection-mediated losses have the higher impact on systemic heat balance during the linear phase in the core temperature decrease (B→C). At this point, hypothermia activates thermoregulatory vasoconstriction in an effort to constrain heat in the body core and restore the normal core-to-periphery temperature gradient. D: During thermal plateau (C→D), core temperature becomes stable or even increases slightly. However, the total heat content of the body continues to decline, largely at the expense of the peripheral thermal compartment. (Data from: Matsukawa T, Sessler DI, Sessler AM, et al. Heat flow and distribution during induction of general anesthesia. Anesthesiology. 1995;82:662 and Kurz A, Sessler DI, Christensen R, et al. Heat balance and distribution during the core-temperature plateau in anesthetized humans. Anesthesiology. 1995;83:491.)

Radiation is the transfer of heat between two surfaces through photons and depends on the temperature difference between the two bodies, as well as their ability to absorb and emit heat (emissivity). Human skin has a high emissivity, meaning that it absorbs and emits heat very efficiently. Conduction, on the other hand, is responsible for the direct transfer of heat between two adjacent
surfaces through the kinetic energy of molecules being transferred to adjacent molecules. The constant flow of air surrounding the patient in the operating room facilitates conduction and results in the convection current, which carries heat away from the body.²,⁷

Core Temperature Plateau

The last phase of a typical intraoperative hypothermia curve is a Tc plateau and usually develops after 2 to 4 hours of anesthesia and surgery (Fig. 45.1, C→D). The plateau is sometimes passively, and sometimes actively, maintained. A passive Tc plateau results when metabolic heat production equals heat loss without activating thermoregulatory defenses.⁸ It usually occurs during small operations in well insulated patients. As hypothermia progresses, the body tends to lose heat less rapidly; simultaneously, although at a much slower rate, anesthetic- and hypothermia-induced reductions in heat production occur. The evolution of these dynamic events eventually produces a Tc plateau, when heat loss decreases to the point that equals heat production.

The amount and effectiveness of insulation are important in determining the Tc at which a thermal steady state is attained. During this phase, active cutaneous warming can substantially decrease heat loss and maintain a passive plateau, even during large operations in a cold environment.

In sufficiently hypothermic patients, the Tc plateau is actively maintained by intense thermoregulatory vasoconstriction. In a typical anesthetic, vasoconstriction is triggered when the patient has a Tc between 34°C and 35°C, and is generally limited to arteriovenous shunts in the fingers and toes. Therefore, in contrast to its modest effect on cutaneous heat loss⁹ and systemic heat balance, thermoregulatory vasoconstriction effectively maintains Tc by altering the distribution of heat within the body.³ By doing so, it confines metabolic heat in the body core and assists to reestablish the normal core-to-periphery temperature gradient of 3°C to 4°C. Importantly, an actively maintained Tc does not represent a thermal steady state. With vasoconstriction, total body heat content and mean body temperature continue to decline, largely as a result of losses from the peripheral compartment.¹⁰

Pediatric Patients

In contrast to adults, infants and children have small extremities compared to their heads and torsos. The small peripheral body compartment also has a diminished capacity to absorb heat. As a result, infants and small children tend to redistribute less heat to the periphery after the induction of anesthesia.¹¹ On the other hand, because of their higher surface area-to-weight ratio compared to adults, they tend to lose more heat during the linear phase of hypothermia.¹² Interestingly, in infants, a large fraction (larger than expected based on the surface area) of that heat is lost directly from the core body compartment through the thin skull and scalp.

Neuraxial Anesthesia

Spinal and epidural anesthesia produce peripheral vasodilation, and thereby promote redistribution hypothermia. Although the mass of the legs is much larger than that of the arms, the former contribute to redistribution hypothermia as much as the latter. Consequently, because redistribution during neuraxial anesthesia is typically restricted to the legs, the Tc will decrease about half as much as during general anesthesia.⁴,¹³ Nevertheless, peripheral sympathetic and motor nerve blocks impair the activation of vasoconstriction and shivering at the thermal plateau, although their activation in unblocked areas of the body is insufficient to prevent further hypothermia. Temperature monitoring during regional anesthesia is not as common as during a general anesthetic;¹⁴ consequently, the rapid progression of heat loss, especially during large operations, together with the fact that patients do not typically feel cold in that setting,¹⁵ can result in severe hypothermia.¹

Patients who receive a combination of general and neuraxial anesthesia are at an even greater risk of developing severe hypothermia because the thermoregulatory effects of these two modalities are superimposed.¹⁶

What Are the Potential Consequences of Perioperative Hypothermia?

Several complications of perioperative hypothermia have been demonstrated in prospective, randomized trials (see Table 45.1).¹⁷,¹⁸ Furthermore, safe and inexpensive methods of preventing hypothermia are available. As a result, the maintenance of intraoperative normothermia is now standard practice.

▪ CARDIOVASCULAR MORBIDITY

Shivering

Shivering is a significant complication of hypothermia. However, the notion that postoperative shivering may promote myocardial ischemia through increased oxygen consumption has not been proven. Shivering in elderly patients, a group at the highest risk for cardiac complications, is especially rare and associated with only a 38% greater oxygen consumption compared to nonshivering patients.¹⁹ As a result, shivering does not appear to be an important cause of postoperative hypoxemia in those patients. Nevertheless, several studies indicate that perioperative myocardial ischemia is not directly related to shivering but rather to the hemodynamic stress produced by the cold-induced sympathoadrenal activation.¹⁹,²⁰,²¹,²²

TABLE 45.1 Major Clinical Consequences of Mild Perioperative Hypothermia^a

Consequence	Author	n	ΔT_core (°C)	Normothermic Group	Hypothermic Group	p
Myocardial ischemia	Frank et al.^b	300	1.3	1.4%	6.3%	<0.05
Postoperative ventricular tachycardia	Frank et al.^b	300	1.3	2.4%	7.9%	<0.05
Surgical site infection	Kurz et al.^c	200	1.9	6%	19%	<0.01
Duration of hospitalization	Kurz et al.^c	200	1.9	12.1 ± 4.4 d	14.7± 6.5 d	<0.01
Transfusion requirement	Schmied et al.^d	60	1.6	1 unit	8 units	<0.05
Surgical blood loss	Schmied et al.^d	60	1.6	1.7 ± 0.3 L	2.2 ± 0.5 L	<0.001
Surgical blood loss	Winkler et al.^e	150	0.4	488 mL	618 mL	<0.005
Surgical blood loss	Widman et al.^f	46	0.5	516 ± 272 mL	702 ± 344 mL	<0.05
Surgical blood loss	Johansson et al.^g	50	0.8	665 ± 292 mL	698 ± 314 mL	NS
Duration of postanesthetic recovery	Lenhardt et al.^h	150	1.9	53 ± 36 min	94 ± 65 min	<0.001
Postoperative thermal discomfort	Kurz et al.ⁱ	74	2.6	50 ± 10 mm VAS	18 ±9 mm VAS	<0.001
^a Only prospective, randomized human trials are included; subjective responses were evaluated by observers blinded to treatment group and core temperature. ^bFrank SM, Fleisher LA, Breslow MJ, et al. Perioperative maintenance of normothermia reduces the incidence of morbid cardiac events. A randomized clinical trial. JAMA. 1997;14:1127. ^cKurz A, Sessler DI, Lenhardt R. Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. Study of Wound Infection and Temperature Group. N Engl J Med. 1996;19:1209. ^dSchmied H, Kurz A, Sessler DI, et al. Mild hypothermia increases blood loss and transfusion requirements during total hip arthroplasty. Lancet. 1996;347(8997):289. ^eWinkler M, Akca O, Birkenberg B, et al. Aggressive warming reduces blood loss during hip arthroplasty. Anesth Analg. 2000;4:978. ^fWidman J, Hammarqvist F, Sellden E. Amino acid infusion induces thermogenesis and reduces blood loss during hip arthroplasty under spinal anesthesia. Anesth Analg. 2002;6:1757. ^gJohansson T, Lisander B, Ivarsson I. Mild hypothermia does not increase blood loss during total hip arthroplasty. Acta Anaesthesiol Scand. 1999:10:1005. ^hLenhardt R, Marker E, Goll V, et al. Mild intraoperative hypothermia prolongs postanesthetic recovery. Anesthesiology. 1997;6:1318. ⁱKurz A, Sessler DI, Narzt E, et al. Postoperative hemodynamic and thermoregulatory consequences of intraoperative core hypothermia. J Clin Anesth. 1995;5:359.
N, total number of subjects; P, percent of subjects who developed consequence; ΔT_rmcore, difference in core temperature between the treatment groups. Different outcomes of the same study are presented in separate rows; NS, nonsignificant; VAS is a 100-mm long visual analog scale (0 mm = intense cold, 100 mm = intense heat).

Myocardial Ischemia

A prospective, randomized study by Frank et al.²⁰ demonstrated that high risk, vascular surgery patients assigned to a Tc only 1.3°C lower than the control group were three times as likely to experience perioperative cardiac events, such as ischemia and ventricular tachycardia. Core hypothermia was an independent predictor of cardiac events, indicating a 55% reduction in risk when normothermia was maintained. In another study, intraoperative hypothermia and increased plasma norepinephrine proliferated ischemic events postoperatively in patients receiving general or spinal anesthesia for hip arthroplasty or peripheral vascular surgery.²³

The mechanism by which mild hypothermia triggers myocardial ischemia is not yet fully elucidated. In awake healthy volunteers, as little as a 1°C decrease in Tc was associated with intense sympathoadrenal activation and increased cardiac work.²⁴ These changes did not evoke coronary vasoconstriction and actually increased myocardial tissue perfusion to match oxygen demand.²² However, even in the absence of vasoconstriction, increased myocardial metabolic requirements in the presence of flow-limiting coronary lesions may predispose the heart to ischemia. Cold-induced hypertension in the elderly and an associated threefold increase in plasma norepinephrine concentration²⁵ are likely to augment cardiac irritability and facilitate the development of ventricular arrhythmias. Furthermore, the impaired sensitivity of arterial baroreflex function, which may even outlast core hypothermia by 1 hour,²⁶ can also contribute to a poor cardiac outcome. The fact that the great majority of adverse myocardial events occur in the postoperative period may support a protective role of anesthetics against the sympathoadrenal responses to hypothermia.

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