Many medical specialties have recognized the importance of assessing whether or not practitioners are following established guidelines for appropriate care. Such guidelines are typically evidence-based and available to most practitioners. Those insurers who pay for medical care have adopted financial incentives to encourage physicians to follow clinical guidelines.
Recognizing the numerous complications of perioperative hypothermia, the American Society of Anesthesiologists (ASA) has recently recommended that postoperative temperature become a basis for assessing physician compliance with current guidelines on the prevention of hypothermia. To quote from the current draft document: “We propose that achievement of an immediate postoperative temperature greater than 36°C is an important, beneficial and realistic goal for patients undergoing general anesthesia lasting more than 60 min.”*
At our institution, we observed a number of patients with temperatures <36°C, immediately after electroconvulsive therapy (ECT) when readings were measured with an infrared ear thermometer. Although we agree that preventing hypothermia is a desirable goal, we hypothesized that temperature changes during anesthesia for ECT as measured by infrared tympanic thermometry may not meet the ASA guidelines for postoperative temperature maintenance. Of course, ECT is typically a 10- to 20-min procedure, well below the ASA threshold of 60 min for applying this guideline. Presumably this reflects a belief that patients do not cool enough in a few minutes to merit application of the guidelines. However, we were still curious: what would happen if this guideline were applied to our population of ECT patients?
This study was approved by the IRB of the University of Florida. The IRB determined this research study was exempt from the usual requirement for informed consent. Twenty-five patients who received a total of 101 consecutive anesthetics to facilitate ECT were studied. All patients were given IV methohexital sodium, 0.5–1 mg/kg, for induction of anesthesia, followed by IV succinylcholine chloride, 0.5–1 mg/kg, to facilitate muscle relaxation and attenuate the convulsive response to application of an electroconvulsive current. The patients also received an IV dose of esmolol hydrochloride and/or labetalol hydrochloride to modify the sympathetic response anticipated with ECT. Some also received an IV dose of glycopyrrolate, when a parasympathetic response, resulting in profound bradycardia or decreased heart rates, was observed on a previous treatment. The exact doses of methohexital, succinylcholine, esmolol, labetalol, and glycopyrrolate administered were based on the clinical judgment of the anesthesiologist caring for the patient. Ventilation was achieved with 100% oxygen via a Mapleson D system using a 10 L/min fresh gas flow rate, both before and after the ECT current was applied. Manual bag and mask ventilation was discontinued when the anesthesiologist judged that the return of spontaneous ventilation was adequate. An IV solution of normal saline at room temperature was administered during the procedure, in an amount not exceeding 300 mL. The convulsive response to the ECT was monitored by an electroencephalogram. The length and intensity of current applied during ECT and the frequency of treatments were determined by the treating psychiatrist from the patient's response.
Patients wore two hospital gowns on their upper torso and their regular garments below the waist during the procedure. They were in a bed with their body covered by a light weight blanket. The ECT treatment room and postanesthesia care unit (PACU) were in immediately adjacent rooms constructed with a walk-through between them. They shared a common climate control system with the thermostat set at 20°C.
Each patient's temperature was measured using an ear thermometer (Infrared Tympanic Thermometer, Sherwood Medical, St. Louis, MO) shortly before the induction of anesthesia, and then again upon delivery of the patient to the PACU. The ear thermometer was used as is customary in our clinical practice and was not recalibrated between each measurement. Temperatures were taken by one of three nurses who were consistently assigned to the ECT suite throughout the study.
The anesthetic time was listed as the time from beginning of anesthesia induction until the patient was delivered to the PACU.
Statistical analysis was performed with SigmaStat 3.1 (Systat Software, Inc., Point Richmond, CA). Nominal data (i.e., ≥36°C or <36°C) analysis between groups was performed using χ2 testing with Yates correction. Before parametric testing for continuous data, the assumption of normality was tested using the Kolmogorov–Smirnov test with Lilliefors' correction. For normally distributed data, paired t-testing was performed with two-tailed protection. Summary data of continuous measurements are reported as mean ± sd. Nonlinear regression was used to determine the correlation coefficients. The odds ratio 95% confidence interval was calculated using Woolf's approximation. P < 0.05 was considered to be statistically significant.
The data sets for 101 observations of temperature before and after anesthesia and ECT were analyzed. The mean case duration was 15.1 ± 2.7 min with a range of 11.0–23.0 min. The mean temperature of all patients before anesthesia was 36.2°C ± 0.6°C with a range of 35.5°C–38.6°C. The mean temperature after anesthesia was 36.4°C ± 0.4°C with a range of 35.5°C–37.5°C, and markedly varied from the mean temperature before anesthesia (P < 0.001). The overall mean change in temperature was 0.2°C ± 0.4°C with a range of −1.4° to +1.0°C. With respect to individual data, the number of patients with a decrease, no change, or an increase in temperature postanesthesia when compared with preanesthesia was 30, 7, and 64, respectively. This variation in temperature did not appear to correlate (r 2 = 0.0009) to case duration. A mild, inverse correlation (r 2 = 0.4204) was noted with respect to temperature change and preanesthetic temperature for these subjects.
With respect to using 36.0°C as an arbitrary cut-off value to parse data, 35 subjects were cooler than this temperature before the procedure. For these cooler patients, the mean temperature before and after anesthesia was 35.6°C ± 0.2°C and 36.1°C ± 0.3°C, respectively (P < 0.001), to yield a mean temperature increase of 0.5°C ± 0.3°C. For subjects with a preanesthetic temperature ≥36°C (n = 66), the mean temperature before and after the anesthetic was 36.5°C ± 0.4°C and 36.5°C ± 0.4°C, respectively (P = 0.540), with a mean temperature change of 0.0°C ± 0.4°C.
For all subjects, 18 patients had temperatures <36.0°C after anesthesia and ECT, a value less than the number of patients (n = 35) with preanesthetic temperatures <36.0°C (P = 0.010). Of these 18 subjects, 14 (78%) had preanesthetic temperatures <36.0°C. Generally, 14 of 35 patients (40.0%) with preanesthetic temperatures <36.0°C also had postanesthetic temperatures <36.0°C, whereas only 4 of 66 patients (6.1%) with preanesthetic temperatures ≥36.0°C had postanesthetic values <36.0°C (P < 0.001). Based on these data, the odds ratio to arrive in the PACU after anesthesia and ECT with a temperature <36.0°C was 10.3 (95% confidence intervals: 7.7–13.8) if the preanesthetic temperature was also <36.0°C compared with a preanesthetic temperature ≥36.0°C.
Figure 1 shows the preanesthetic (x-axis) and postanesthetic (y-axis) temperatures. The preanesthetic temperatures have been moved slightly left or right when two data points had identical values so that all points are visible. The figure is divided into four quadrants: A (preanesthetic ≥36°C, postanesthetic <36°C), B (preanesthetic ≥36°C, postanesthetic ≥36°C), C (preanesthetic <36°C, postanesthetic ≥36°C), D (preanesthetic <36°C, postanesthetic <36°C). Of these, the only quadrant that reflects patient cooling is quadrant A with four subjects. The preanesthetic temperatures of these four subjects were 36.1, 36.2, 36.2, and 36.3. These subjects were thus at the threshold of hypothermia just prior to the ECT, and their postanesthetic temperature indicated cooling to just below the hypothermic threshold.
If we apply the ASA performance guideline for hypothermia to this population (ignoring the short duration of these cases), we would identify 18% of our patients as not meeting the standard. Even if the standard were only to apply to patients not hypothermic prior to the procedure, 4% of our patients would have failed the standard.
Examination of Figure 1 shows that there is a large amount of variability in the data. For example, the temperature before the procedure only poorly predicts the temperature after the procedure, even though the procedure only lasted 11–23 min. For the 30% of patients who had a decrease in temperature from before anesthesia to delivery to the PACU, one etiology for this temperature decrease could have been measurement technique error. A number of studies have documented that infrared tympanic thermometers are not reliable.1,2 Our data suggest that reliance on an inaccurate device measurement, as is routinely done in clinical practice, could yield indications that performance guidelines were not being met, largely based on spurious data.
An alternative explanation for the decrease in temperature is the ventilation system that was used, namely the Mapleson D system. In this system, fresh gas flow is delivered directly from wall oxygen. There is no humidification system, nor warming system for gases in the circuit. In 64% of the 100 anesthetics, the patients' temperatures increased from before anesthesia to delivery to the PACU. Although we cannot be certain as to the etiology of the temperature increase, the fasciculations that would occur in some patients with succinylcholine administration or the muscle contractions during motor seizures that would occur in others when the ECT shock is administered may have produced sufficient metabolic heat that led to an increase in body temperature. This is consistent with the report of Ozinsky, who documented an increase in body temperature both after administration of succinylcholine and after administration of electroconvulsive shock in 50 patients. He postulated that heat production during muscle contraction was responsible for the increase in temperature.3 Cosgrove, however, reported a decrease in temperature in 10 patients who received ECT for depression. He postulated that this response may have been the result of interference with one of the temperature regulating centers in the hypothalamus.4 He does not mention the anesthesia circuit used in his patients, and so it is not possible to determine whether this may have also contributed to his findings.
We did not calibrate our aural measurements against oral measurement instruments because, if these temperature threshold criteria are to be used as a basis for making financial (reimbursement) decisions, we wanted to follow the usual clinical practice at our institution. Thus, our data provide an important cautionary tale. If the ASA adopts the proposed temperature guidelines, institutions will need to very carefully consider how they are measuring temperature in the postoperative period. There will be financial consequences for failing to accurately measure temperature. Perhaps that is entirely appropriate. If preventing hypothermia is a meritorious clinical goal, then institutions that have not made an adequate investment in temperature measurement cannot assess whether they are meeting this minimal standard for their patients. Also, this begs the question whether the arbitrary selection of a postanesthetic temperature of 36°C to determine whether any case met the standard is appropriate. If these patients' temperatures were below 36°C before the anesthetic was administered, what proof is there that the patients would benefit if the temperature were increased to above 36°C during the course of the anesthetic?