Intra-operative rewarming with Hot Dog(®) resistive heating and forced-air heating: a trial of lower-body warming.

Resistive heating is an alternative to forced-air warming which is currently the most commonly used intra-operative warming system. We therefore tested the hypothesis that rewarming rates are similar with Hot Dog(®) (Augustine Biomedical) resistive and Bair Hugger(®) (Arizant) forced-air heating systems. We evaluated 28 patients having major maxillary tumour surgery. During the establishment of invasive monitoring, patients became hypothermic, dropping their core temperature to about 35 °C. They were then randomly assigned to rewarming with lower-body resistive (n = 14) or forced-air (n = 14) heating, with each system set to 'high'. Our primary outcome was the rewarming rate during active heating over a core temperature range from 35 to 37 °C. Morphometric characteristics were comparable in both groups. Temperature increased at twice the rate in patients assigned to forced-air warming, with an estimated mean (SE) slope of 0.49 (0.03) °C.h(-1) vs 0.24 (0.02) °C.h(-1) (p < 0.001). Resistive heating warmed at half the rate of forced air.

The influence of 2 surgical bandage systems on wound tissue oxygen tension.

HYPOTHESIS: Local wound heating improves tissue oxygen tension in postoperative patients. SETTING: University hospital. PATIENTS: Forty normothermic and well-hydrated patients recovering from elective open abdominal surgery. INTERVENTIONS: A comparison between an experimental bandage system (Warm-Up; Augustine Medical Inc, Eden Prairie, Minn) and conventional gauze covered with elastic adhesive (Medipore Dress-it; 3M, St Paul, Minn). The experimental system is heated to 38 degrees C and does not touch the wound. MAIN OUTCOME MEASURES: Subcutaneous tissue oxygen tension was measured postoperatively and on the first postoperative day. In a subgroup, we also evaluated the effects of bandage pressure per se on tissue oxygen. RESULTS: Initial postoperative tissue oxygen tensions were approximately 30 mm Hg greater with the experimental bandage, even before warming. Subcutaneous oxygen tension during heating remained significantly greater in patients with the warmed bandage than the conventional elastic bandage (116 +/- 40 vs 85 +/- 34 mm Hg, respectively) while the patients were breathing approximately 50% oxygen. The difference was smaller on the first postoperative day, but still statistically significant (82 +/- 30 vs 65 +/- 22 mm Hg, respectively). In the subgroup analysis, tissue oxygen tension increased significantly by 12 +/- 4 mm Hg when the heating bandage was substituted for a conventional bandage (P<.001). CONCLUSION: In normothermic and well-hydrated surgical patients, much benefit from the heating bandage system appears to result from pressure relief. These data suggest that relieving wound pressure markedly improves tissue perfusion and oxygenation.

Postanaesthetic considerations and complications after ambulatory anaesthesia.

Ambulatory or day-case surgery is being employed to an ever-increasing extent. Although it has many advantages, it is not suited to the needs of every patient. For example, patients who live alone, particularly the elderly, might well not be able to care for themselves adequately after such surgery and are probably at a higher risk of developing complications, including infections. Furthermore, pain treatment may be insufficient, as a consequence of which recovery can be prolonged and the resumption of normal daily activities might be delayed. Nausea, dizziness and vomiting can also prolong recovery and need to be adequately treated after ambulatory surgery. Therefore, the often cited cost effectiveness of ambulatory surgery is questionable if complications cannot be prevented or treated effectively.

Circadian changes in the sweating-to-vasoconstriction interthreshold range.

Thermoregulatory defenses are characterized by thresholds, the core temperatures triggering each response. Core body temperature is normally maintained within the interthreshold range, temperatures between the sweating and vasoconstriction thresholds that do not trigger autonomic defenses. This range usually spans only some 0.2 degrees C, but it remains unknown whether similar precision is maintained during the circadian core temperature cycle of about 0.8 degrees C. Accordingly, we evaluated the interthreshold range at four times of the day. We studied ten male volunteers, each at 3 a.m., 8 a.m., 3 p.m., and 8 p.m. At least 12 h elapsed between tests, and the order was randomly assigned. At each study time, volunteers were warmed peripherally until sweating was observed. Skin temperature was subsequently kept constant while core temperature was decreased by central-venous infusion of ice-cold fluid until peripheral vasoconstriction was detected. The volunteers were not permitted to sleep during threshold determinations, although sleep was not otherwise controlled. The core temperature triggering an evaporative water loss of 40 g.m-2.h-1 identified the sweating threshold. Similarly, the vasoconstriction threshold was defined by the core temperature triggering the initial decreases in plethysmographic finger tip blood flow. The interthreshold range at 3 a.m. was twice that observed at the other study times (P<0.05). Our data suggest that autonomic control of body temperature is reduced at 3 a.m., even when sleep is denied. This result contradicts the general perception that circadian variation alters the thermoregulatory target temperature, but not precision of body temperature control.

Local radiant heating increases subcutaneous oxygen tension.

BACKGROUND: We evaluated a novel bandage that incorporates a thermostatically controlled radiant heater. We first determined optimal bandage temperature, based on increases in subcutaneous oxygen tension, a measure correlating well with resistance to infection and wound strength. We then tested the hypothesis that prolonged radiant heating would increase collagen deposition in experimental thigh wounds. METHODS: The experimental bandages were positioned on the anterior thigh of 8 volunteers, and heated for 2 hours at 38 degrees C, 42 degrees C, or 46 degrees C, in a random order. Subcutaneous oxygen tension under the bandage was recorded from an electrode positioned within a subcutaneous tonometer. We studied 10 volunteers in the second protocol. For 1 week, the experimental bandage was continuously applied to one thigh, and heated to 38 degrees C using a 2-hour on/off cycle. On the alternate week, a standard gauze bandage was applied to the contralateral thigh. Treatment order was randomly assigned. Wound collagen deposition under each bandage was evaluated with subcutaneous polytetrafluoroethylene tubes, which were removed and assayed for hydroxyproline on the eighth day. Data are presented as means +/- SDs. RESULTS: Skin temperature during heating ranged from 36 degrees C to 37.5 degrees C. Oxygen tension increased approximately 50% during heating, but the increase was comparable at the three tested temperatures. Even after heating was discontinued, subcutaneous oxygen tension remained elevated for the remaining 3 study hours. Collagen deposition after 1 week of active heating was 3.4 +/- 1.0 microg/ cm. After 1 week of control treatment, collagen deposition was 3.2 +/- 1.1 microg/cm (P = not significant). CONCLUSIONS: Our data suggest that radiant heating at 38 degrees C significantly increases subcutaneous oxygen tension, and presumably resistance to infection. However, prolonged heating at this temperature does not increase wound collagen deposition.

Efficacy of intraoperative cooling methods.

BACKGROUND: Patients may require perioperative cooling for a variety of reasons including treatment of a malignant hyperthermia crisis and induction of therapeutic hypothermia for neurosurgery. The authors compared heat transfer and core cooling rates with five cooling methods. METHODS: Six healthy volunteers were anesthetized with desflurane and nitrous oxide. The cooling methods were 1) circulating water (5 degrees C, full-length mattress and cover), 2) forced air (10 degrees C, full-length cover), 3) gastric lavage (500 ml iced water every 10 min), 4) bladder lavage (300 ml iced Ringer's solution every 10 min), and 5) ice-water immersion. Each method was applied for 40 min or until the volunteers' core temperatures approached 34 degrees C. The volunteers were rewarmed to normothermia between treatments. Core cooling rates were evaluated using linear regression. RESULTS: The first volunteer developed abdominal cramping and diarrhea after gastric lavage. Consequently, the technique was not again attempted. Bladder lavage increased heat loss approximately 10 W and decreased core temperature 0.8 +/- 0.3 degrees C/h (r2 = 0.99 +/- 0.002; means +/- SD). Forced-air and circulating-water cooling comparably increased heat flux, approximately 170 W. Consequently, core cooling rates were similar during the two treatments at 1.7 +/- 0.5 degrees C/h (r2 = 0.99 +/- 0.001) and 1.6 +/- 1.1 degrees C/h (r2 = 0.98 +/- 0.02), respectively. Immersion in an ice water slurry increased heat loss approximately 600-800 W and decreased core temperature 9.7 +/- 4.4 degrees C/h (r2 = 0.98 +/- 0.01). Immersion cooling was associated with an afterdrop of approximately 2 degrees C. CONCLUSIONS: Bladder lavage provided only trivial cooling and gastric lavage provoked complications. Forced-air and circulating-water cooling transferred relatively little heat but are noninvasive and easy to implement. Forced-air or circulating-water cooling, perhaps combined with intravenous administration of refrigerated fluids, may be sufficient in some patients. When noninvasive methods prove insufficient for rapid cooling, ice-water immersion or peritoneal lavage probably should be the next lines of defense.

Postanesthetic vasoconstriction slows peripheral-to-core transfer of cutaneous heat, thereby isolating the core thermal compartment.

UNLABELLED: Forced-air warming during anesthesia increases core temperature comparably with and without thermoregulatory vasoconstriction. In contrast, postoperative forced-air warming may be no more effective than passive insulation. Nonthermoregulatory anesthesia-induced vasodilation may thus influence heat transfer. We compared postanesthetic core rewarming rates in volunteers given cotton blankets or forced air. Additionally, we compared increases in peripheral and core heat contents in the postanesthetic period with data previously acquired during anesthesia to determine how much vasomotion alters intercompartmental heat transfer. Six men were anesthetized and cooled passively until their core temperatures reached 34 degrees C. Anesthesia was then discontinued, and shivering was prevented by giving meperidine. On one day, the volunteers were covered with warmed blankets for 2 h; on the other, volunteers were warmed with forced air. Peripheral tissue heat contents were determined from intramuscular and skin thermocouples. Predicted changes in core temperature were calculated assuming that increases in body heat content were evenly distributed. Predicted changes were thus those that would be expected if vasomotor activity did not impair peripheral-to-core transfer of applied heat. These results were compared with those obtained previously in a similar study of anesthetized volunteers. Body heat content increased 159 +/- 35 kcal (mean +/- SD) more during forced-air than during blanket warming (P < 0.001). Both peripheral and core temperatures increased significantly faster during active warming: 3.3 +/- 0.7 degrees C and 1.1 +/- 0.4 degrees C, respectively. Nonetheless, predicted core temperature increase during forced-air warming exceeded the actual temperature increase by 0.8 +/- 0.3 degree C (P < 0.001). Vasoconstriction thus isolated core tissues from heat applied to the periphery, with the result that core heat content increased 32 +/- 12 kcal less than expected after 2 h of forced-air warming (P < 0.001). In contrast, predicted and actual core temperatures differed only slightly in the anesthetized volunteers previously studied. In contrast to four previous studies, our results indicate that forced-air warming increases core temperature faster than warm blankets. Postanesthetic vasoconstriction nonetheless impeded peripheral-to-core heat transfer, with the result that core temperatures in the two groups differed less than might be expected based on systemic heat balance estimates. IMPLICATIONS: Comparing intercompartmental heat flow in our previous and current studies suggests that anesthetic-induced vasodilation influences intercompartmental heat transfer and distribution of body heat more than thermoregulatory shunt vasomotion.

Lack of nonshivering thermogenesis in infants anesthetized with fentanyl and propofol.

BACKGROUND: Sweating, vasoconstriction, and shivering have been observed during general anesthesia. Among these, vasoconstriction is especially important because-once triggered-it minimizes further hypothermia. Surprisingly, the core-temperature plateau associated with vasoconstriction appears to preserve core temperature better in infants and children than adults. This observation suggests that vasoconstriction in anesthetized infants may be accompanied by hypermetabolism. Consistent with this theory, unanesthetized infants rely on nonshivering thermogenesis to double heat production when vasoconstriction alone is insufficient. Accordingly, the authors tested the hypothesis that intraoperative core hypothermia triggers nonshivering thermogenesis in infants. METHODS: With Ethics Committee approval and written parental consent, the authors studied six infants undergoing abdominal surgery. All were aged 1 day to 9 months and weighed 2.4-9 kg. Anesthesia was maintained with propofol and fentanyl. The infants were mechanically ventilated and allowed to cool passively until core (distal esophageal) temperatures reached 34-34.5 degrees C. Oxygen consumption-the authors' index of metabolic rate-was recorded throughout cooling. Because nonshivering thermogenesis triples circulating norepinephrine concentrations, arterial blood was analyzed for plasma catecholamines at approximately 0.5 degree C intervals. Thermoregulatory vasoconstriction was evaluated using forearm-fingertip, skin-surface gradients, with gradients exceeding 4 degrees C, indicating intense vasoconstriction. The patients were subsequently rapidly rewarmed to 37 degrees C. Regression analysis was used to correlate changes in oxygen consumption and plasma catecholamine concentrations with core temperature. RESULTS: All patients were vasoconstricted by the time core temperature reached 36 degrees C. Further reduction in core temperature to 34-34.5 degrees C did not increase oxygen consumption. Instead, oxygen consumption decreased linearly. Hypothermia also failed to increase plasma catecholamine concentrations. CONCLUSIONS: Even at core temperatures approximately 2 degrees C below the vasoconstriction threshold, there was no evidence of nonshivering thermogenesis. This finding is surprising because all other major thermoregulatory responses have been detected during anesthesia. Infants and children thus appear similar to adults in being unable to increase metabolic rate in response to mild intraoperative hypothermia.

Isoflurane produces marked and nonlinear decreases in the vasoconstriction and shivering thresholds.

In summary, we present a new model for evaluating thermoregulatory effects of drug administration, pregnancy, illness, etc. Specifically, we experimentally manipulated both skin and core temperatures, and subsequently compensated for the changes in skin temperature using the relationships between skin and core contributions to thermoregulatory control. We thus were able to report our results for warm- and cold-responses in terms of calculated core-temperature thresholds at a single designated skin temperature. Advantages of this model include its being nearly noninvasive and requiring relatively little core temperature manipulation. Using this technique, we have shown that the shape and magnitude of thermoregulatory impairment produced by various anesthetic drugs differs. Propofol linearly increases the sweating threshold and linearly decreases the vasoconstriction and shivering threshold. In contrast, volatile anesthetics produce a nonlinear reduction in the major cold-response thresholds, reducing the vasoconstriction and shivering thresholds disproportionately at higher anesthetic concentrations. Midazolam not only produces a different magnitude of thermoregulatory impairment, but also a novel pattern of threshold changes. Anesthetic-induced thermoregulatory impairment thus depends both on anesthetic type and dose.

Thermoregulatory vasoconstriction does not impede core warming during cutaneous heating.

Recent studies evaluating perioperative cutaneous-to-core heat transfer indicate that: Thermoregulatory vasoconstriction prevents further core cooling in anesthetized subjects during mild cooling. Thermoregulatory vasoconstriction only slightly decreases core cooling rates in anesthetized subjects during vigorous cooling. Thermoregulatory vasoconstriction does not impair vigorous core rewarming during anesthesia. Vigorous postanesthetic cutaneous warming increases core temperature much faster than passive insulation. Under conditions of mild thermal stress, thermoregulatory vasoconstriction is thus able to protect core temperature by reducing cutaneous heat transfer and functionally isolating the peripheral and core thermal compartment. Consequently, anesthetic-induced alterations in vasomotor tone is one of the major factors influencing core temperature in patients who are not actively cooled or warmed. In contrast, thermoregulatory tone is insufficient to prevent core temperature perturbations in patients undergoing vigorous cutaneous cooling or warming.

Isoflurane produces marked and nonlinear decreases in the vasoconstriction and shivering thresholds.

BACKGROUND: Desflurane decreases the vasoconstriction and shivering thresholds disproportionately at high anesthetic concentrations. This result contrasts with the authors' previous report that isoflurane decreases the vasoconstriction threshold linearly. It is surprising that the basic shape of the concentration-response curve should differ with these two otherwise similar anesthetics. Therefore, the hypothesis that isoflurane produces a nonlinear reduction in the vasoconstriction threshold was tested. Because the effect of isoflurane on shivering remains unknown, the extent to which isoflurane reduces the shivering threshold also was determined. METHODS: Eight men volunteered to be studied on four randomly ordered days: (1) a target end-tidal isoflurane concentration of 0.55%, (2) a target concentration of 0.7%, (3) control (no anesthesia) and a target end-tidal concentration of 0.85%, and (4) a target end-tidal concentration of 1.0%. Volunteers were surface-cooled until peripheral vasoconstriction and shivering were observed. We arithmetically compensated for changes in skin temperature using the established linear cutaneous contributions to control for each response. From the calculated thresholds (core temperatures triggering responses at a designated skin temperature of 34 degrees C), the concentration-response relation was determined. RESULTS: Isoflurane administration produced a dose-dependent reduction in the vasoconstriction and shivering thresholds, decreasing each approximately 4.6 degrees C at an end-tidal concentration of 1%. Residual analysis indicated that the vasoconstriction and shivering thresholds were decreased in a nonlinear fashion during isoflurane administration. The vasoconstriction-to-shivering range was 1.5 +/- 0.8 degree C without isoflurane, and did not change significantly during isoflurane administration. CONCLUSIONS: The vasoconstriction-to-shivering range remained unchanged by isoflurane administration. In this regard, the effects of isoflurane are similar to those of desflurane, propofol, and alfentanil. The current data differ from the authors' previous report, in that the dose-dependence for vasoconstriction was nonlinear, with isoflurane reducing the threshold disproportionately at higher anesthetic concentrations. Differing dose-dependence in the two studies may result either because the current study's volunteers were not exposed to surgical stimulation and were given less isoflurane, or because of design limitations in the previous protocol.

Rapid core-to-peripheral tissue heat transfer during cutaneous cooling.

Perioperative thermal manipulations are usually directed at the skin surface because methods of directly warming the core are invasive or ineffective. However, inadequate heat flow between peripheral and core compartments will decrease the rate at which core temperature changes. We therefore determined whether core hypothermia is delayed after initiation of surface cooling. Six volunteers were anesthetized with propofol and midazolam, and maintained under three layers of passive insulation for 2.5-4 h. Subsequently, the skin surface was cooled using forced air, 1000 L/min, at 10 degrees C. Isoflurane was added as necessary to maintain arteriovenous shunt vasodilation. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Average arm and leg (peripheral) tissue temperatures were determined from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. Overall body heat content decreased approximately 234 kcal during 2.5 h of active cooling. Core temperature, which was nearly constant before active cooling, decreased approximately 1.3 degrees C/h. There was no delay between initiation of active cooling and the decrease in core temperature. Furthermore, peripheral (arm and leg) and core (trunk and head) tissue heat contents decreased at virtually the same rates: approximately 50 kcal/h and approximately 47 kcal/h, respectively. These data indicate that there is little restriction of heat flow between peripheral and core tissues in vasodilated, anesthetized subjects.

Effective pain relief with continuous intrapleural bupivacaine after thoracotomy in infants and children.

The effect of continuous intrapleural bupivacaine on pain relief after lateral thoracotomy was studied in nine infants (< or = 15 kg body weight) and 11 children (> 15 kg body weight). An intrapleural catheter was inserted under direct vision during surgery. After extubation, the patients were transferred to the ICU where vital signs and pain scores were monitored. An intrapleural infusion of bupivacaine 0.25% with adrenaline was given at a loading dose of 0.625 mg.kg-1 body weight followed by a continuous infusion with a starting rate of 1.25 mg.kg-1.h-1. Haemodynamic and respiratory parameters did not differ significantly from control values throughout the study period in either group. The mean infusion rate could be reduced stepwise in both groups to 0.75 +/- 0.32 mg.kg-1.h-1 and 0.73 +/- 0.38 mg.kg-1.h-1 respectively. The pain score indicated a rapid onset of analgesia in both groups and remained low during the study period. The degree of analgesia amongst other factors was position dependent. The lack of any recognizable side effects or complications related to this method has been most encouraging. Only one child required a supplementary dose of an opioid. We conclude that continuous intrapleural access has proved to be a safe and suitable route for pain relief in infants and children following thoracotomy.

Thermoregulatory vasoconstriction and perianesthetic heat transfer.

Heat transfer between the core and its environment in normothermic and slightly hypothermic situations is determined largely by the influence of vasomotion on convection. Tonic vasoconstriction, the normal barrier to heat loss from the core, is impaired upon induction of anesthesia. The resulting dilation of the arteriovenous shunts leads to redistribution of heat from the core to the periphery, diminishing the temperature gradient between the two compartments. With reemergence of thermoregulatory vasoconstriction at core temperatures near 34 degrees C, the core and the periphery are again separated, with metabolic heat being largely constrained to the core. Under normal conditions of mild thermal stress, thermoregulatory vasoconstriction is thus able to protect core temperature by reducing cutaneous heat transfer and functionally isolating the peripheral and core thermal compartments. Consequently, anesthetic-induced alterations in vasomotor tone is one of the major factors influencing core temperature in patients who are not actively cooled or warmed. In contrast, thermoregulatory tone is insufficient to prevent core temperature perturbations in patients undergoing vigorous cutaneous cooling or warming.

Hemodynamic and analgesic effects of clonidine added repetitively to continuous epidural and spinal blocks.

Clonidine in spinal and epidural blocks prolongs anesthesia, but can cause hypotension and bradycardia. The aim of our study was to compare hemodynamic and analgesic effects of spinal versus epidural clonidine alone and after repetitive dosing. In a prospective, randomized, double-blind study, we evaluated 40 patients scheduled for lower extremity orthopedic surgery under continuous spinal or epidural anesthesia with bupivacaine 0.5% (initial dose 5 mg and 50 mg, respectively). In either spinal or epidural technique one-half of patients received clonidine (150 micrograms) in addition to bupivacaine. Repeat doses of the same anesthetic mixture were allowed in cases of subsequent pain. Mean arterial pressure (MAP) and heart rate were recorded for 6 h after each injection. Duration of clinically useful anesthesia was defined as the time from drug administration to first sensation of pain. Intrathecal, but not epidural, clonidine decreased MAP significantly compared with bupivacaine alone. MAP after intrathecal clonidine with bupivacaine was lower than epidural clonidine with bupivacaine 5 and 6 h after injection. Repetitive administration caused no further decrease in MAP. Onset time required to surgical anesthesia (sensory block of T11) did not differ among the four groups. Duration of spinal and epidural anesthesia was increased more than two fold by clonidine. In summary, the addition of clonidine prolongs analgesia by either route. These results may be explained by clonidine's sites of action in hemodynamic control and the density of bupivacaine-induced block.

The threshold for thermoregulatory vasoconstriction during nitrous oxide/isoflurane anesthesia is lower in elderly than in young patients.

BACKGROUND: Thermoregulatory vasoconstriction minimizes further core hypothermia during anesthesia. Elderly patients become more hypothermic during surgery than do younger patients, and take longer to rewarm postoperatively. These data indicate that perianesthetic thermoregulatory responses may be especially impaired in the elderly. Accordingly, the authors tested the hypothesis that the thermoregulatory threshold for vasoconstriction during nitrous oxide/isoflurane anesthesia is reduced more in elderly than in young patients. METHODS: The authors studied 12 young patients aged 30-50 yr and 12 elderly patients aged 60-80 yr. All were undergoing major orthopedic or open abdominal surgery. Anesthesia was induced with thiopental and fentanyl, and maintained only with nitrous oxide (70%) and isoflurane (0.6-0.8%). Core temperature was measured in the distal esophagus. Fingertip vasoconstriction was evaluated using forearm minus fingertip, skin-temperature gradients. A gradient of 4 degrees C identified significant vasoconstriction, and the core temperature triggering vasoconstriction identified the thermoregulatory threshold. RESULTS: The vasoconstriction threshold was significantly less in the elderly patients (33.9 +/- 0.6 degree C) than in the younger ones (35.1 +/- 0.3 degrees C) (P < 0.01). The gender distribution, weight, and height of the elderly and young patients did not differ significantly. The end-tidal isoflurane concentration at the time of vasoconstriction did not differ significantly in the two groups. CONCLUSIONS: These data indicate that thermoregulatory responses in the elderly are initiated at temperatures approximately 1.2 degrees C less than that in younger patients. Thus, it is likely that elderly surgical patients become more hypothermic than do younger patients, at least in part, because they fail to trigger protective thermoregulatory responses.