Redistribution Of Body Heat Research Articles

Association between preoperative toe perfusion index and maternal core temperature decrease during cesarean delivery under spinal anesthesia: a prospective cohort study

BackgroundThe main mechanism of body temperature decrease during cesarean delivery under spinal anesthesia is core-to-peripheral redistribution of body heat, attributable to vasodilation. Perfusion index (PI) obtained with a pulse oximeter helps to assess peripheral perfusion dynamics by detecting the change in peripheral vascular tone. This study aimed to examine whether preoperative toe PI could predict the decrease in core temperature induced by spinal anesthesia during cesarean delivery.MethodsParturients undergoing scheduled cesarean delivery under combined spinal-epidural anesthesia from September 2019 to March 2020 were enrolled in this single-center prospective cohort study. All parturients received 0.5% hyperbaric bupivacaine (10 mg) with fentanyl (15 μg) intrathecally. A pulse oximeter probe was placed on the left second toe for continuous PI measurement. The 3 M™ Bair Hugger™ Temperature Monitoring System placed over the right temporal region was used to record core temperature over time. We evaluated the association between the maximum core temperature decrease, which is the primary outcome, and the preoperative toe PI at operating room (OR) admission using a segmented regression model (SRM) and a generalized additive model (GAM). The maximum core temperature decrease was defined as the difference between core temperature at OR admission and minimum intraoperative core temperature.ResultsForty-eight patients were evaluated. In the SRM, the slope for the association between the maximum core temperature decrease and the preoperative toe PI changed from 0.031 to 0.124 after PI = 2.4%. Likewise, with the GAM, there was a small core temperature decrease when preoperative toe PI was greater than 2.0 to 3.0%.ConclusionsLow preoperative toe PI was associated with maternal core temperature decrease during cesarean delivery under spinal anesthesia. Preoperative toe PI is a simple, non-invasive, and effective tool for the early prediction of perioperative core temperature decrease during cesarean delivery.Trial registrationUMIN Clinical Trials Registry (registry number: UMIN000037965).

Thermographic skin temperature measurement compared with cold sensation in predicting the efficacy and distribution of epidural anesthesia

Due to the high rates of epidural failure (3–32%), novel techniques are required to objectively assess the successfulness of an epidural block. In this study we therefore investigated whether thermographic temperature measurements have a higher predictive value for a successful epidural block when compared to the cold sensation test as gold standard. Epidural anesthesia was induced in 61 patients undergoing elective abdominal, thoracic or orthopedic surgery. A thermographic picture was recorded at 5, 10 and 15 min following epidural anesthesia induction. After 15 min a cold sensation test was performed. Epidural anesthesia is associated with a decrease in skin temperature. Thermography predicts a successful epidural block with a sensitivity of 54% and a PPV of 92% and a specificity of 67% and a NPV of 17%. The cold sensation test shows a higher sensitivity and PPV than thermography (97 and 93%), but a lower specificity and NPV than thermography (25 and 50%). Thermographic temperature measurements can be used as an additional and objective method for the assessment of the effectiveness of an epidural block next to the cold sensation test, but have a low sensitivity and negative predictive value. The local decrease in temperature as observed in our study during epidural anesthesia is mainly attributed to a core-to-peripheral redistribution of body heat and vasodilation.

The effect of 30 to 60 minutes of forced-air pre-warming on maintaining intraoperative core temperatures during the first hour post-anesthesia induction in adult patients undergoing general anesthesia

The objective of this review is to identify the effectiveness of 30 to 60 minutes of forced-air pre-warming on maintaining intraoperative core temperatures in adult patients undergoing general anesthesia. The review question will focus on the effects of forced-air pre-warming on preventing redistribution hypothermia in the first hour post induction of anesthesia, which is considered the most critical due to an internal core-to-peripheral redistribution of body heat and subsequent loss of heat to the operative room surroundings.

Forced air warming devices in orthopaedics: a focused review of the literature.

The current focus on maintaining normal body temperature in the operating room makes the use of patient warming devices routine—or even mandatory—in many hospitals. Forced air warming devices such as the Bair Hugger (3M Healthcare, St. Paul, Minnesota) maintain or increase core temperature in patients during the perioperative period, with benefits that include reduced surgical wound infections, maintenance of normal coagulation, and faster discharge from the post-anesthesia care unit (PACU)1-5. However, some recent literature has raised concerns regarding a possible increased risk of deep surgical site infections specifically associated with the use of the forced air warming systems in the orthopaedic operating room5-12. One concern is that a convective device could disrupt unidirectional downward laminar airflow, which may be especially critical in joint arthroplasty operating rooms. This concern is based on theoretical mechanisms, laboratory simulations, retrospective case series, and studies showing potentially pathogenic organisms growing in the hoses and filters of forced air warming devices6-12. However, multiple other studies13-15 and a Continuing Education statement by the Association of periOperative Registered Nurses (AORN)16 suggest that proper use of the forced air warming devices mitigates or eliminates this risk while maximizing the benefits of patient warming. The purpose of the present manuscript is to review the current literature on the use of patient warming devices in orthopaedic surgery, specifically in joint arthroplasty. Hypothermia (core body temperature, <36°C) is a constant risk during general anesthesia because of factors such as impaired thermoregulation, heat loss secondary to a cold operating room, redistribution of body heat from the core to the vasodilated periphery, and infusion of cool intravenous fluids. Major adverse consequences of perioperative hypothermia can include adrenergic activation, myocardial ischemia, thermal discomfort, decreased drug metabolism, coagulopathy and increased …

Ketamine and tramadol for the prevention of shivering during spinal anaesthesia.

Anaesthesia and surgery promote significant thermal disorder in the human body. Spinal anaesthesia causes lower limb vasodilation and redistribution of body heat from central to the peripheral compartments. This was a prospective, randomised, double-blind clinical study to compare the effectiveness of IV ketamine and tramadol in the prevention of shivering associated with spinal anaesthesia. We prospectively studied 150 ASA classification I and II patients between 18 and 70 years old scheduled for any elective surgery performed under spinal anaesthesia. Patients were randomly allocated to receive either prophylactic IV ketamine 0.5 mg/kg (Group K), IV tramadol 0.5 mg/kg (Group T) or normal saline as control (Group P) after intrathecal injection of 0.5% hyperbaric bupivacaine 12.5 mg (2.5 ml) and 25 mcg fentanyl. The frequency and degree of shivering, haemodynamic parameters, core body temperature and side effects of the studied drugs were recorded for the first 30 minutes. The incidence of shivering was 8% in Group K, 16% in Group T and 24% in Group P. This result was statistically significant between Groups K and P. Patients from Group K also exhibited significantly higher mean arterial blood pressure and heart rate at 5 and 15 minutes post intrathecal injection while their mean core temperature was also significantly higher. Side effects such as nausea, vomiting, hallucination, agitation and sweating were comparable between all three groups. Patients from Group K however, had significant higher incidence of behavioural changes (blunted affect or catatonic state) and nystagmus. Prophylactic use of IV ketamine 0.5 mg/kg significantly reduced the frequency and the intensity of perioperative shivering associated with spinal anaesthesia but also exhibited some side effects of the drug. Lower doses of prophylactic ketamine should be studied.

The effect of warmed inspired gases on body temperature during arthroscopic shoulder surgery under general anesthesia

BackgroundPerioperative hypothermia can develop easily during shoulder arthroscopy, because cold irrigation can directly influence core body temperature. The authors investigated whether active warming and humidification of inspired gases reduces falls in core body temperature and allows redistribution of body heat in patients undergoing arthroscopic shoulder surgery under general anesthesia.MethodsPatients scheduled for arthroscopic shoulder surgery were randomly assigned to receive either room temperature inspired gases using a conventional respiratory circuit (the control group, n = 20) or inspired gases humidified and heated using a humidified and electrically heated circuit (HHC) (the heated group, n = 20).ResultsCore temperatures were significantly lower in both groups from 30 min after anesthesia induction, but were significantly higher in the heated group than in the control group from 75 to 120 min after anesthesia induction.ConclusionsIn this study the use of a humidified and electrically heated circuit did not prevent core temperature falling during arthroscopic shoulder surgery, but it was found to decrease reductions in core temperature from 75 min after anesthesia induction.

Maternal and Newborn Outcomes Related to Unplanned Hypothermia in Scheduled Low-Risk Cesarean Delivery Births

Neuraxial (spinal or epidural) anesthesia is the most common form of pain management during labor and birth and the method of choice for cesarean births because it allows mothers to be awake for the birth of their infant. A side effect of neuraxial anesthesia is vasodilatation, core-to-peripheral redistribution of body heat, and loss of cold perception, placing the patient at risk for developing hypothermia. Perioperative hypothermia increases the patient risk of developing morbid myocardial outcomes, coagulopathy, and increased incidence of surgical wound infection. In addition, hypothermia in the cesarean delivery patient places the newborn at risk for hypothermia. In a retrospective review of low-risk scheduled cesarean deliveries, N = 143, covering a 6-month period, 21% of mothers and 36.5% of newborns experienced hypothermia. Newborns also experienced hypoglycemia and respiratory instability.

Ephedrine and hypothermia- old drug, new use?

In this month's Korean Journal of Anesthesiologists, Cho et al. [1] evaluate the effect of ephedrine on intraoperative hypothermia in patients undergoing spine surgery. This study demonstrates that core temperature reduction during general anesthesia decreases less in patients given ephedrine than in untreated controls. These authors suggest that ephedrine is effective in maintaining core temperature through thermogenic effect as well as the inhibition of redistribution through peripheral vasoconstriction. Intraoperative hypothermia is common, and is associated with adverse outcomes including coagulopathy and increased allogenic transfusion requirement [2] , wound infection [3], and morbid cardiac complications [4]. Core hypothermia during the first hour after induction of general anesthesia results largely from an internal core-to-peripheral redistribution of body heat [5]. Ephedrine acts at α and β receptors because it has two mechanism of action. Ephedrine releases noradrenaline from adrenergic nerve terminals and can also directly stimulate adrenergic receptors. Noradrenaline induces peripheral vasoconstriction which reduces heat loss and is involved in non-shivering thermogenesis. Ephedrine has a positive inotropic effect due to its β adrenergic stimulating effect. This mixed action makes the effect of ephedrine on hypothermia more complicated. This is important because Shitara et al. [6] have demonstrated that dobutamine infusion aggravates intraoperative hypothermia after induction of anesthesia. The mechanism, apparently, is an increase in cardiac output which in turn augments convective transfer of heat from core to peripheral tissues. The α-adrenergic stimulation of ephedrine is significantly stronger than its β adrenergic effect. This current study suggests that hypothermic effect of β adrenergic stimulation might almost be offset by its α constricting effect. At this point, we should consider the use of a pure α-adrenergic agonist, phenylephrine. Ikeda et al. [7] have demonstrated that phenylephrine reduces the magnitude of anesthetic-induced core-to-peripheral redistribution of body heat. Precapillary vasoconstriction induced by phenylephrine administration counter, to some extent, the vasodilating effects of general anesthetics. In contrast to this study of ephedrine, core temperature decreases after induction of anesthesia even during phenylephrine infusion. This means that phenylephrine does not prevent the core-to-peripheral redistribution associated with arteriovenous shunt dilation, but reduces the effect of anesthetic-induced precapillary dilation. A possible problem with the use of this technique for intraoperative hypothermia is that continuous infusion of ephedrine is not suitable for hypertensive patients. Rapid tolerance to pressor effects makes it difficult to choose inotropics for hypotensive patients [8]. Although it is not clear ephedrine will be drug of choice for intraoperative hypothermia of patients undergoing spinal surgery, ephedrine may have a place as a new drug for intraoperative hypothermia.

Temperature and surgical wound heat loss during orthopedic surgery: computer simulations and measurements

Temperature and surgical wound heat loss during orthopedic surgery: computer simulations and measurements

Phenylephrine Attenuates Intra-Operative Hypothermia during Spinal Anaesthesia

Inadvertent hypothermia is common during spinal anaesthesia. This study was based on the hypothesis that phenylephrine might attenuate core hypothermia by inhibiting core-to-peripheral redistribution of body heat during spinal anaesthesia. In this prospective randomized study, 20 patients who underwent elective orthopaedic surgery under spinal anaesthesia were randomly assigned to receive either normal saline (control group) or continuously-infused phenylephrine 0.5 microg/kg per min (phenylephrine group). Core temperature, heart rate (HR) and mean arterial pressure (MAP) were monitored. Mean +/- SE core temperature at the end of surgery was significantly higher in the phenylephrine-treated group compared with the control group (35.9 +/- 0.1 degrees C versus 35.0 +/- 0.1 degrees C, respectively), although there was no significant difference in baseline core temperature (both groups 36.3 +/- 0.1 degrees C). Mean HR and MAP were not significantly different between the two groups. In conclusion, continuously-infused phenylephrine attenuated core hypothermia during spinal anaesthesia without any haemodynamic complications.

Temperature monitoring and perioperative thermoregulation.

Most clinically available thermometers accurately report the temperature of whatever tissue is being measured. The difficulty is that no reliably core-temperature-measuring sites are completely noninvasive and easy to use-especially in patients not undergoing general anesthesia. Nonetheless, temperature can be reliably measured in most patients. Body temperature should be measured in patients undergoing general anesthesia exceeding 30 min in duration and in patients undergoing major operations during neuraxial anesthesia. Core body temperature is normally tightly regulated. All general anesthetics produce a profound dose-dependent reduction in the core temperature, triggering cold defenses, including arteriovenous shunt vasoconstriction and shivering. Anesthetic-induced impairment of normal thermoregulatory control, with the resulting core-to-peripheral redistribution of body heat, is the primary cause of hypothermia in most patients. Neuraxial anesthesia also impairs thermoregulatory control, although to a lesser extent than does general anesthesia. Prolonged epidural analgesia is associated with hyperthermia whose cause remains unknown.

Effects of Low Dose Propofol on Core and Peripheral Temperatures during Spinal Anesthesia

Background: Core hypothermia during the first hour after induction of anesthesia results primarily from a redistribution of body heat. Propofol in low doses provides reliable sedation and is associated with fast recovery. However, propofol-induced peripheral vasodilation is likely to facilitate core-to-peripheral heat redistribution. This study was designed to evaluate the effects of low dose propofol on core and peripheral temperatures during spinal anesthesia. Methods: Fifty patients of ASA status I or II, aged 20 to 60, undergoing lower extremity surgery under spinal anesthesia were studied. Spinal anesthesia was administered to all patients, who were assigned sedation as follows: 1) control (n = 25), 2) propofol (n = 25); propofol infusion rates were, 8 mg/kg/h for the first 3 min, 4 mg/kg/h for the next 10 min, and 2 mg/kg/h for the next 15 min. Temperatures were recorded after beginning surgery at 5-min intervals for 30 min. Results: Core temperature was significantly decreased after 15, 20, 30 min of surgery in the propofol group, and this result was statistically different between the two groups. Forearm skin temperature decreased in the control group and increased in the propofol group, without significance. Fingertip skin temperature did not changed significantly in the control group, but increased significantly after 15 min in the propofol group and continued to increasing to 30 min. Forearm minus finger skin temperature gradients were not changed significantly in control group, but decreased between 5 and 30 min in the propofol group, which was statistically significant. Conclusions: Low dose propofol may induce a degree of hypothermia during spinal anesthesia. Close monitoring is needed to prevent core hypothermia, if sedation is induced using propofol during spinal anesthesia.

Core Temperature and Skin-Surface Temperature Gradients of Ketamine and Propofol for Anesthetic Induction in Children

Background: Hypothermia after induction of anesthesia results initially from core-to-peripheral redistribution of body heat. Both central inhibition of tonic thermoregulatory vasoconstriction in arteriovenous shunts and anesthetic induced vasodilation contribute to core-to-peripheral redistribution of heat. Ketamine increases peripheral arteriolar resistance uniquely; in contrast, propofol causes profound venodilatation that other anesthetics do not. The aim of the present study is to evaluate core temperature and skin-surface temperature gradients in use of ketamine for anesthetic induction compared with propofol in children. Methods: Forty pediatric patients of ASA status I or II, undergoing elective surgery for strabismus or inguinal hernia were studied. The patients were allocated randomly to one of two groups: (i) GROUP P (n = 20): Anesthesia was induced with propofol and maintained with sevoflurane in combination with 60% nitrous oxide in oxygen. (ii) GROUP K (n = 20): Anesthesia was induced with ketamine and maintained with sevoflurane in combination with 60% nitrous oxide in oxygen. Core temperature, forearm skin temperature, fingertip skin temperature and Forearm minus fingertip, skin-temperature gradients were recorded before induction of anesthesia, 3 min after administering ketamine or propofol (just before endotracheal intubation), 5 min, and at 5-min intervals after induction of anesthesia. Results: After induction of anesthesia, core temperature in the two groups was decreased but results did not differ significantly between two groups. Forearm skin temperature was increased significantly after 20 min of anesthesia in propofol group and 15 min of anesthesia in ketamine group, but results did not differ significantly between two groups. Finger tip skin temperature was increased significantly after 3 min of anesthesia in the propofol group and 10 min of anesthesia in the ketamine group. Finger tip skin temperature of 5 min of anesthesia in propofol group increased significantly greater than in ketamine group. Forearm minus finger skin surface temperature gradients was decreased statistically significantly at 3 min of anesthesia in the propofol group and 10 min of anesthesia in the ketamine group, gradients of 5 min of anesthesia was presented statistically significant between two groups. Conclusions: For pediatric patients, after induction of anesthesia with ketamine arteriovenous shunt vasomoter status was well maintained. And maintaining vasoconstriction during induction of anesthesia reduced the magnitude of redistribution hypothermia.

Propofol in low doses causes redistribution of body heat in male volunteers

Propofol in low doses causes redistribution of body heat in male volunteers

Propofol in low doses causes redistribution of body heat in male volunteers.

Cardiovascular and mental stress in dental patients with phobias about dentistry may be reduced by propofol sedation. We tested the hypothesis that even low doses of propofol may have effects on body temperatures in male volunteers. Six healthy male volunteers were given propofol over 28 min with the following infusion rates: 8 mg kg(-1) h(-1) for the first 3 min, 4 mg kg(-1) h(-1) for the next 10 min, and 2 mg kg(-1) h(-1) for the final 15 min. Body temperatures were measured at five locations: tympanic membrane, forehead, forearm, dorsum of the hand and fingertip. Thermoregulatory vasoconstriction was evaluated using the forearm minus fingertip temperature gradient. Tympanic membrane and forehead temperatures began to decrease at 10 and 20 min, respectively, after the start of the propofol infusion, and reached a minimum at 30 min (tympanic -0.5 +/- 0.2 degrees C) and 40 min (forehead -0.6 +/- 0.2 degrees C), respectively. Peripheral skin temperatures showed an increase between 10 and 30 min in the forearm and fingertip and between 20 and 30 min in the dorsum of the hand. After 30 min, a decrease in peripheral skin temperatures was observed. The forearm minus fingertip temperature gradient changed from negative to positive after 40 min, and increased continuously thereafter (baseline -0.3 +/- 0.4 degrees C, 90 min: 6.5 +/- 1.6 degrees C). A low dose of propofol impairs tonic thermoregulatory vasoconstriction and induces heat redistribution from the core to the periphery.

Nefopam and tramadol for the prevention of shivering during neuraxial anesthesia

Background and Objectives: In patients undergoing neuraxial anesthesia, heat loss and core-to-peripheral redistribution of body heat causes the core temperature to decrease. The shivering threshold is therefore reached soon, and more shivering is required to prevent further hypothermia. Because shivering has deleterious metabolic and cardiovascular effects, it should ideally be prevented by pharmacologic or other means. We evaluated the usefulness of intravenous (IV) nefopam and tramadol in preventing and reducing the severity of shivering in patients undergoing neuraxial anesthesia for orthopedic surgery.Methods: Ninety patients, scheduled for neuraxial anesthesia (epidural or subarachnoid) for lower limb orthopedic surgery, were prospectively enrolled. Patients were randomly assigned to 1 of 3 groups. Immediately before neuraxial anesthesia, 30 patients received 0.15 mg/kg−1 IV nefopam in 10 mL saline, 30 patients received 0.5 mg/kg−1 IV tramadol in 10 mL saline, and a control group of 30 patients received 10 mL IV saline. Neuraxial anesthesia was induced at the L3-L4 or L4-L5 interspaces with 1 mg/kg−1 mepivacaine for epidural anesthesia and 0.2 mg/kg−1 for subarachnoid anesthesia. An investigator blinded to the antishivering drug injected recorded the frequency and degree of shivering.Results: The overall frequency and the intensity of shivering was significantly lower in patients treated with nefopam than in those treated with tramadol or placebo (P < .05 and P < .01) and in patients treated with tramadol than in those treated with placebo (P < .05).Conclusions: As a pharmacologic means of preventing shivering in patients undergoing neuraxial anesthesia, nefopam may hold the greatest promise. Reg Anesth Pain Med 2002;27:380-384.

Induction of Anesthesia with Ketamine Reduces the Magnitude of Redistribution Hypothermia

Hypothermia after induction of general anesthesia results largely from core-to-peripheral redistribution of body heat. Both central inhibition of tonic thermoregulatory vasoconstriction in arteriovenous shunts and anesthetic-induced arteriolar and venous dilation contribute to this redistribution. Ketamine, unique among anesthetics, increases peripheral arteriolar resistance; in contrast, propofol causes profound venodilation that other anesthetics do not. We therefore tested the hypothesis that induction of anesthesia with ketamine causes less core hypothermia than induction with propofol. Twenty patients undergoing elective surgery were randomly assigned to anesthetic induction with either 1.5 mg/kg ketamine (n = 10) or 2.5 mg/kg propofol (n = 10). Anesthesia in both groups was subsequently maintained with sevoflurane and 60% nitrous oxide in oxygen. Forearm minus finger, skin-temperature gradients <0 degrees C were considered indicative of significant arteriovenous shunt vasodilation. Ketamine did not cause vasodilation just after induction, whereas propofol rapidly induced vasodilation. Core temperatures in the patients given ketamine remained significantly greater than those in the patients induced with propofol. These data suggest that maintaining vasoconstriction during induction of anesthesia reduces the magnitude of redistribution hypothermia. Core hypothermia during the first hour of anesthesia was less after induction of anesthesia with ketamine than propofol. Maintaining arteriovenous shunt vasoconstriction during induction of anesthesia reduces the magnitude of redistribution hypothermia.

Core cooling by central venous infusion of ice-cold (4 degrees C and 20 degrees C) fluid: isolation of core and peripheral thermal compartments.

Central venous infusion of cold fluid may be a useful method of inducing therapeutic hypothermia. The aim of this study was to quantify systemic heat balance and regional distribution of body heat during and after central infusion of cold fluid. The authors studied nine volunteers, each on two separate days. Anesthesia was maintained with use of isoflurane, and on each day 40 ml/kg saline was infused centrally over 30 min. On one day, the fluid was 20 degrees C and on the other it was 4 degrees C. By use of a tympanic membrane probe core (trunk and head) temperature and heat content were evaluated. Peripheral compartment (arm and leg) temperature and heat content were estimated with use of fourth-order regressions and integration over volume from 18 intramuscular thermocouples, nine skin temperatures, and "deep" hand and foot temperature. Oxygen consumption and cutaneous heat flux estimated systemic heat balance. After 30-min infusion of 4 degrees C or 20 degrees C fluid, core temperature decreased 2.5 +/- 0.4 degrees C and 1.4 +/- 0.2 degrees C, respectively. This reduction in core temperature was 0.8 degrees C and 0.4 degrees C more than would be expected if the change in body heat content were distributed in proportion to body mass. Reduced core temperature resulted from three factors: (1) 10-20% because cutaneous heat loss exceeded metabolic heat production; (2) 50-55% from the systemic effects of the cold fluid per se; and (3) approximately 30% because the reduction in core heat content remained partially constrained to core tissues. The postinfusion period was associated with a rapid and spontaneous recovery of core temperature. This increase in core temperature was not associated with a peripheral-to-core redistribution of body heat because core temperature remained warmer than peripheral tissues even at the end of the infusion. Instead, it resulted from constraint of metabolic heat to the core thermal compartment. Central venous infusion of cold fluid decreases core temperature more than would be expected were the reduction in body heat content proportionately distributed. It thus appears to be an effective method of rapidly inducing therapeutic hypothermia. When the infusion is complete, there is a spontaneous partial recovery in core temperature that facilitates rewarming to normothermia.

Peri-operative hypothermia in the high-risk surgical patient

Peri-operative hypothermia is common in high-risk surgical patients. Anaesthesia impairs central thermoregulation, allowing redistribution of body heat. Cool ambient temperatures and high-volume fluid administration accelerate loss of heat to the environment. Randomized, controlled trials have proven that mild hypothermia increases the incidence of wound infection and prolongs hospitalization, increases the incidence of morbid cardiac events and ventricular tachycardia and impairs coagulation. Other complications include enhanced anaesthetic drug effects, prolonged recovery room stays, shivering and impaired immune function. There is compelling animal evidence for cerebral protection by mild hypothermia. However, evidence for protection in surgical patients is not yet available. The most effective means of preventing peri-operative hypothermia is active pre-warming. High ambient temperatures, warmed intravenous fluids and active cutaneous warming are useful intraoperatively, while active cutaneous warming and intravenous pethidine abolish post-operative shivering. Proper thermal management may reduce complications and improve the outcome in high-risk surgical patients.

Intraoperative Phenylephrine Infusion Decreases the Magnitude of Redistribution Hypothermia

Core hypothermia during the first hour after induction of general anesthesia results largely from an internal core-to-peripheral redistribution of body heat. This redistribution results from both central inhibition of tonic thermoregulatory vasoconstriction in the arteriovenous shunt and anesthetic-induced vasodilation. We therefore tested the hypothesis that acute administration of phenylephrine, a pure alpha-adrenergic agonist, reduces the magnitude of anesthetic-induced core-to-peripheral redistribution of body heat. Patients undergoing minor oral surgery were randomly assigned to an infusion of 0.5 [micro sign]g [middle dot] kg-1 [middle dot] min-1 phenylephrine IV or no treatment (control). The phenylephrine infusion was started immediately before anesthesia was induced with 2.5 mg/kg propofol IV. Subsequently, anesthesia was maintained with sevoflurane and 60% nitrous oxide in oxygen. Calf minus toe, skin-temperature gradients <0[degree sign]C were considered indicative of significant arteriovenous shunt vasodilation. Ambient temperature and end-tidal concentrations of maintenance sevoflurane were comparable in each group. Although there were no significant differences in skin-temperature gradients, core temperatures in the untreated patients decreased significantly more (1.2 +/- 0.4[degree sign]C) than in those given phenylephrine (0.5 +/- 0.2[degree sign]C, P < 0.001). These data suggest that maintaining precapillary vasoconstriction of blood vessels, not in the arteriovenous shunt reduces the magnitude of redistribution hypothermia. Implications: Core hypothermia immediately after induction of general anesthesia results largely from core-to-peripheral redistribution of body heat. Core temperature reduction during the first hour of anesthesia decreased less in patients given phenylephrine than in untreated controls. These data suggest that maintaining precapillary vasoconstriction possibly reduces the magnitude of redistribution hypothermia. (Anesth Analg 1999;89:462-5)