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*Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Medical Institutions; and
Medical Student, University of Maryland, Baltimore, Maryland
Address correspondence and reprint requests to Steven M. Frank, MD, Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Hospital, Carnegie 442, 600 N. Wolfe St., Baltimore, MD 21287. Address e-mail to sfrank{at}welchlink.welch.jhu.edu
| Abstract |
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Implications: The results of this survey of practicing anesthesiologists indicate that body temperature is often not monitored in patients receiving regional anesthesia. It is therefore likely that significant hypothermia goes undetected and untreated in these patients.
| Introduction |
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Intraoperative temperature monitoring became popular in the early 1960s when malignant hyperthermia (MH) was described as a rare but often fatal risk of GA (6). Although hyperthermia may occur late in the clinical course of MH, the high mortality rate prompted the routine measurement of body temperature during GA. Because RA is not associated with MH, temperature monitoring was not thought to be important in patients receiving RA. Other reasons for not monitoring temperature during RA may be the unfounded belief that RA does not alter body temperature, or the lack of a convenient site for placement of a temperature probe, because the usual monitoring sites (nasopharynx, esophagus, and oropharynx) are not well tolerated in awake or sedated patients.
Over the past decade, several studies indicate that RA significantly impairs thermoregulation and predisposes patients to hypothermia in the typically cold operating room environment (7). In fact, there is good evidence that the risk of hypothermia is equivalent during epidural and general anesthesia, especially when the block level is relatively high (T4-6) (7). Without temperature monitoring, hypothermia during RA will be neither recognized, prevented, nor treated. Even when conscious, patients receiving RA are often asymptomatic from hypothermia because autonomic (8) and behavioral (9) thermoregulatory responses are impaired. Patients are thus unable to report the sensation of cold during core hypothermia.
To determine practice patterns for body temperature monitoring and to test the hypothesis that body temperature is often ignored during RA, we surveyed practicing members of the ASA.
| Methods |
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The questions used for the survey were as follows:
| Results |
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| Discussion |
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The following sites for core temperature monitoring are listed in order from most to least accurate for correlation with true core (blood) temperature (10,11): pulmonary artery, tympanic membrane, esophagus, nasopharynx, oropharynx, urinary bladder, rectum, axilla, skin. Accessible sites that are tolerated during RA are the tympanic membrane, urinary bladder, rectum, axilla, and skin-surface. Urinary bladder and rectal temperatures are considered intermediate sites rather than core sites because when core temperature changes, temperatures in the bladder and rectum lag behind because of isolation from the central core. These sites should thus overestimate core temperature during shorter surgical procedures. Another potential limitation of rectal and bladder sites during RA is that vasodilation redistributes heat toward the lower body, which may artificially increase the temperatures measured at these sites. Axillary temperature monitoring requires correct probe placement over the axillary artery and even then is likely to underestimate core temperature (11).
The most commonly used single monitoring technique during RA is liquid crystal thermometry on the forehead skin-surface. These devices are manufactured with a built-in offset, because skin temperature is 23°C lower than core during steady-state conditions, but the actual difference depends on vasomotor tone and ambient temperature (12). It is likely that, during RA, the core-to-skin gradient is increased because of compensatory vasoconstriction above the level of the block (7); thus, liquid crystal thermometers placed above the block level may significantly underestimate core temperature during RA. This hypothesis, however, has not yet been tested. Thus, there are three potential reasons why skin temperature estimates of core temperature may be inaccurate (12). The internal redistribution of body heat is accompanied by an increased mean skin temperature from systemic vasodilation. Skin blood flow can be altered significantly by thermoregulatory vasoconstriction during the perioperative period. Finally, changes in ambient temperature may contribute to altered skin temperature.
The forehead skin is a common site for measuring cutaneous temperature. Reasons for selecting this site go beyond convenience and accessibility (12). There is little variability among individuals because forehead subcutaneous tissue insulation is minimal. Compared with some other areas, the forehead skin has fewer thermoregulatory arteriovenous shunts that could dramatically alter skin temperature without comparable central temperature changes. A study comparing liquid-crystal monitors with forehead thermistors under clinical conditions simulating intraoperative hypothermia found that the two types of monitors were comparable in both rapidity and linearity of responses, but not in accuracy (13). Changes in liquid crystal thermometry have been shown to accurately reflect core temperature trends in adults only during the very immediate postoperative period, but not 15, 30, 45, and 60 min postoperatively (14). When large changes in body temperature are induced (e.g., cardiopulmonary bypass), liquid crystal skin surface thermometry provides a reasonably accurate assessment of core temperature (15).
Sessler et al. (9) have described the effects of RA on thermoregulatory control in human volunteers. As with GA (16), RA causes an initial redistribution of heat in the first 3060 min, when heat is transferred from the core to the peripheral thermal compartment (17), and core temperature decreases by approximately 1°C. In addition to redistribution, there is a reduction in the thresholds for both vasoconstriction and shivering because of an increased apparent temperature, which fools the hypothalamus by sending warm signals from the lower body (18). This results in an expanded interthreshold range over which core temperature can vary and no efferent thermoregulatory responses are triggered (8,19). Even the ability to sense hypothermia is impaired during RA because the relatively warm input from the lower body overrides the sensation of core hypothermia.
There is evidence that the incidence of inadvertent hypothermia is just as great in patients receiving RA as in those receiving GA (7). Some data suggest that low regional blocks decrease the risk of hypothermia (19,20). Other studies demonstrate mixed results, with either GA (21) or RA (22,23) presenting the greatest risk of hypothermia. Risk factors for hypothermia also include cold operating rooms (20), open body cavities, significant fluid and blood administration, lean body habitus (24), and extremes of age (very young and very old) (7).
Perioperative hypothermia has been associated with adverse clinical outcomes. In high-risk patients, mild hypothermia (35.035.5°C) is associated with increased myocardial ischemia (1) and cardiac morbidity (2) in the early postoperative period. This effect seems to be adrenergically mediated based on increased norepinephrine, increased vasomotor tone, and hypertension in mildly hypothermic patients (25,26). Hypothermia-induced postoperative shivering increases total body oxygen consumption and increases patient discomfort (27). Postoperative wound infection occurs more often in patients who develop intraoperative hypothermia due to impaired oxidative killing by macrophages and lower tissue oxygen concentrations in the presence of hypothermia-induced vasoconstriction (3). Both platelet function and coagulation factors are impaired by hypothermia, thus increasing the potential for bleeding during surgery (28). Furthermore, hypothermia-related coagulopathy most likely goes undetected in the clinical setting because routine coagulation testing (prothrombin and partial thromboplastin time) is performed at a standardized temperature of 37°C (29). Because hypothermia-related adverse outcomes can occur regardless of anesthetic technique (RA versus GA), it is evident from the results in the current study that there is room for improvement in the level of care that is delivered to patients receiving RA.
There are recognized limitations to our study. It is possible that, with a larger number of survey respondents, we may have seen different results. The sample was, however, relatively well balanced between academic and private practice physicians. The surveyed physicians also covered a wide demographic area in the United States.
In summary, despite the potential for and the consequences of hypothermia, body temperature is often ignored during RA. When body temperature is monitored during RA, the methods for monitoring are often less than optimal.
| Acknowledgments |
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The authors acknowledge assistance from Susan Kelly for data collection and from Neeraj Gupta for data analysis and manuscript preparation.
| References |
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This article has been cited by other articles:
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T. Kiya, M. Yamakage, T. Hayase, J.-I. Satoh, and A. Namiki The Usefulness of an Earphone-Type Infrared Tympanic Thermometer for Intraoperative Core Temperature Monitoring Anesth. Analg., December 1, 2007; 105(6): 1688 - 1692. [Abstract] [Full Text] [PDF] |
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S. M. Frank Hypothermia After Vascular Surgery: Complications, Prevention, and Treatment Seminars in Cardiothoracic and Vascular Anesthesia, November 1, 2000; 4(4): 244 - 255. [Abstract] [PDF] |
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C. F. Arkilic, O. Akca, A. Taguchi, D. I. Sessler, and A. Kurz Temperature Monitoring and Management During Neuraxial Anesthesia: An Observational Study Anesth. Analg., September 1, 2000; 91(3): 662 - 666. [Abstract] [Full Text] [PDF] |
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D. I. Sessler Temperature Monitoring and Management During Neuraxial Anesthesia Anesth. Analg., February 1, 1999; 88(2): 243 - 243. [Full Text] [PDF] |
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