Without any positive body warming, the core temperature of patients usually decreases precipitously for 1 h, then decreases slowly for 2–3 hr, and finally becomes constant after the induction of general anesthesia (1,2). If we could predict the extent of the hypothermia in the early phase of general anesthesia, appropriate warming techniques could be used (3,4). Precipitous hypothermia during the first hour of anesthesia results largely from a core-to-peripheral redistribution of body heat such that, in the following hours, the core body temperature slowly decreases when heat loss exceeds heat production (5,6). Peripheral skin temperature (e.g., palmar skin temperature) represents the heat content of peripheral tissues (5), and body fat, especially subcutaneous adipose tissue, plays a protective role in reducing the heat loss from skin through its low thermal conductivity (7). The present study was, therefore, conducted to clarify the predictive variables of hypothermia in the early phase of general anesthesia by using the following methods: 1) the measurement of palmar skin temperature by using an infrared thermometer and 2) the measurement of total body fat (TBF) by using a skinfold technique (8,9).
This study was approved by the Sapporo Medical University Ethical Committee on Human Research, and informed consent was obtained from each patient. We studied 60 ASA physical status I or II adult patients who required general anesthesia for surgery on the lumbar vertebrae (e.g., disk herniation, spondylolisthesis) because the area of skin exposed in the prone position is large. Patients with a history of thyroid disease, dysautonomia, Raynaud’s syndrome, or malignant hyperthermia were excluded. Each patient participated on a single study day between October 1998 and March 1999. The patients’ height was 159 ± 7 cm (mean ± SD), weight 63 ± 8 kg, and age 58 ± 10 yr. Ambient temperature was maintained at 23.2°C ± 0.7°C and ambient relative humidity at 31% ± 8% during the study. The patients were premedicated with an oral administration of 50 mg pentobarbital 1 h before the operation. No other premedication was given.
Studies began at approximately 9:00 AM, and all patients fasted for 8 h before the study. In the operating room, the following variables were measured: 1) right palmar skin temperature and 2) skinfold thickness at two selected sites for the estimation of TBF. Right midpalmar skin temperature was measured four times with an infrared thermometer (FirstTemp GeniusTM; Kendall, Mansfield, MA) positioned 4–5 mm above the skin surface. Maximal and minimal values were discarded, and the remaining two were averaged and used for statistical analysis. Skinfold measurements were performed on the right side of each patient with a standard caliper (FAT-O-METERTM; Health & Education Services, Addison, IL). The skinfold measurement sites were as follows: 1) the arm-vertical skinfold in the midline of the back of the arm, half-way between the acromion and olecranon processes and 2) the scapula-oblique skinfold on a line running downward, at an angle of approximately 30° from vertical, from the inferior angle of the scapula. Each measurement was repeated until successive readings differed by not more than 1 mm. The two measurements were then averaged, and TBF ([w/w]%) was calculated by using the appropriate age and sex specific regression equation of Durnin and Womersley (9) and the Siri equation (10). During the study, all patients were covered with a single unwarmed cotton blanket (11).
An IV catheter was inserted into an antecubital vein on the left arm, and lactated Ringer’s solution, prewarmed to 37°C, was infused at approximately 5 mL · kg−1 · h−1. Anesthesia was induced by the IV administration of 4–5 mg/kg thiamylal with 0.1 mg/kg vecuronium, and the trachea was intubated. Immediately after the anesthetic induction, a rectal temperature probe was inserted to a depth of 6 cm and taped in place, and the rectal temperature, taken to represent core temperature, was monitored continuously during the operation by using a thermometer (CTM-205TM; Terumo, Tokyo, Japan). Anesthesia was maintained with 1.0% to 1.2% isoflurane in nitrous oxide (4 L/min) and oxygen (2 L/min). Ventilation was controlled at a rate and volume sufficient to maintain PETCO2 near 35 mm Hg. The anesthetic circuit we used was a semiclosed circle system with a total gas flow of 6 L/min; the inspiratory gas was neither warmed nor humidified.
Each patient was fixed in the prone position and covered with 2–3 unwarmed cotton blankets. During the operation, no warming equipment was used except for prewarmed Ringer’s solution. After approximately 3 h, general anesthesia was discontinued, and the trachea was extubated. Study measurements ceased at that point, and the patients were warmed with a forced-air warming system (Bair HuggerTM; Augustine Medical, Eden Prairie, MN) in patients in which the rectal temperature was <35.5°C.
The gradient of the hypothermia induced by general anesthesia was divided into two parts: 1) a precipitous decrease for the first hour and 2) a slow decrease for the following 2–3 h. We compared these temperature gradients with the preoperative palmar skin temperature and with the calculated TBF. All data were expressed as mean ± SD in the text and in the scatter diagrams shown in the figures. These relationships were assessed by analysis of the variance of regression coefficients. In all comparisons, values of P < 0.01 and of r > 0.60 were considered significant.
Rectal temperature was 37.1°C ± 0.4°C at the beginning of the study. The temperature gradients of the redistribution hypothermia (the precipitous decrease in rectal temperature for the first hour) and of the unbalanced heat loss-production hypothermia (the slow decrease in rectal temperature for the following 2–3 h) were 0.50°C ± 0.27°C and 0.39°C ± 0.29°C, respectively. Ten percent (6 of 60) of the patients had a rectal temperature of <35.5°C at the end of the study and needed warming with a forced-air warming system.
The palmar skin temperature measured by using an infrared thermometer was 30.2°C ± 2.6°C (25.6–35.4°C). The preoperative palmar skin temperature had a significant linear relationship with the precipitous decrease in rectal temperature over the first hour (y = 2.70–0.07 ×x, r = 0.69, P < 0.0001) (Fig. 1). There was, however, no relationship between the palmar skin temperature and the gradient of the slow decrease in temperature for the following 2–3 h (r = 0.067, P = 0.61).
The TBF calculated by measuring two representative skin folds was 24.2% ± 6.4% (12.5%–43.2%). The relationship between TBF (x) and the gradient of the slow decrease for the following 2–3 h (y) is shown in Figure 2. TBF had a significant linear relationship with the subsequent slow decrease in rectal temperature (y = 1.08–0.03 ×x, r = 0.63, P < 0.0001). There was, however, no relationship between TBF and the gradient of the precipitous decrease in temperature over the first hour (r = 0.25, P = 0.054).
One of the major findings of our study is that, in patients who received general anesthesia in a prone position, the palmar skin temperature had a significant linear relationship with the gradient of precipitous decrease in rectal temperature over the first hour. The body can be divided into two components: 1) the core, consisting of the trunk and head, and 2) the periphery, comprising the arms and legs. There is normally a 3–4°C tissue temperature gradient between these two components. This gradient is maintained by thermoregulatory vasoconstriction, which provides a thermal barrier between core and peripheral tissues (12). As shown in some studies (13–15), most general anesthetics, including isoflurane (16,17), are direct vasodilators, and all impair central thermoregulatory control, thus inhibiting normal tonic thermoregulatory vasoconstriction. Anesthetic-induced vasodilation allows redistribution of heat from the core thermal compartment to peripheral tissues (5). This process markedly decreases core temperature, although mean body temperature and body heat content remain unchanged (1,18). Therefore, the mean body temperature of the peripheral component has a major effect on the redistribution hypothermia and preoperative palmar skin temperature, easily measured by using an infrared thermometer, and could be a predictive variable of the extent of the hypothermia.
Isoflurane-induced vasodilation only slightly increases cutaneous heat loss (1), suggesting that increased heat loss is not the major cause of hypothermia immediately after the induction of anesthesia. This suggestion is supported by the fact that there was no relationship between TBF, which plays a protective role in reducing heat loss, and the gradient of the precipitous decrease in temperature over the first hour in our study.
We also found that the TBF, measured by a skinfold technique, had a significant linear relationship with the subsequent slow decrease in rectal temperature for the following two to three hours and that there was no relationship between the palmar skin temperature and the gradient of the temperature decrease. Redistribution of body heat between peripheral and core components seems to be completed within one hour after the induction of general anesthesia (1,18), and it is therefore convincing that there was no relationship between the representative peripheral temperature we used, palmar skin temperature, and the slow decrease in core temperature during the second and third hours of general anesthesia. The induction of general anesthesia decreases metabolic heat production by approximately 20% (18) and increases cutaneous heat loss by approximately 7% (1). The rather small imbalance between heat production and heat loss could explain the slow decrease in core temperature in the second and third hours after the induction of general anesthesia (1,18). The possibility that this imbalance is the cause of the slow decrease in the core temperature is supported by the fact that TBF had a linear relationship with the temperature decrease. Body fat, especially subcutaneous adipose tissue, plays a protective role in reducing heat loss from the skin surface through its low thermal conductivity (7). Anderson and Martin (7) reported that the thermal conductivity of the adipose tissue layer varies from 0.50 to 0.97 × 10−3 kcal/(cm · s−1 · °C−1), being significantly lower (by approximately 20%) in obese volunteers [6.66 ± 0.45 × 10−4 kcal/(cm · s−1 · °C−1)] than in lean volunteers [8.22 ± 0.93 × 10−4 kcal/(cm · s−1 · °C−1)]. Therefore, we could predict the extent of the decrease in core temperature during the two to three hours after the induction of general anesthesia by measuring TBF; in other words, by measuring the thickness of a representative skinfold. The increase in cutaneous heat loss (7%) (1) is rather small compared with the decrease in heat production (20%) (18), and Kurz et al. (19) demonstrated that body fat had only a small influence on core pooling rates during the second phase of the hypothermia curve. TBF had, however, a significant linear relationship with the temperature decrease in the second and third hours after the anesthetic induction in our study. This result could be caused, in part, by the large area of skin exposed in the prone position.
In conclusion, the extent of hypothermia can be predicted in the early phase of general anesthesia by simple measurements (palmar skin temperature and skinfold thickness).
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