The effects of physical treatment on induced fever in humans.

PURPOSE: Initial treatments for fever include the amelioration of underlying causes and administration of antipyretic medications. However, patients who fail these treatments are often actively cooled, which may be counterproductive because decreasing skin temperature increases the thermoregulatory core target temperature. Cooling may also provoke metabolic and autonomic stress and thermal discomfort. SUBJECTS AND METHODS: We studied 9 subjects, each on 3 days. Fever was induced each day with 100,000 IU/kg of interleukin-2 administered intravenously (elapsed time zero). Randomly assigned treatments were 1) control (a cotton blanket), 2) cooling (forced air at 15 degrees C), or 3) self-adjust (forced-air warming adjusted to comfort). Treatments were maintained for 3 to 8 elapsed hours. RESULTS: Peak core temperatures (mean +/- SD) were 38.4 +/- 0.5 degrees C on the control day, 38.1 +/- 0.5 degrees C on the cooling day, and 38.5 +/- 0.4 degrees C on the self-adjust day. Integrated core temperatures were 6.0 +/- 1.6 degrees C x h on the control day, 5.7 +/- 2.2 degrees C x h on the cooling day, and 6.4 +/- 1.2 degrees C x h on the self-adjust day. Neither peak nor integrated core temperatures differed significantly on the 3 days. Shivering was common on the cooling day but otherwise rare. Oxygen consumption was normal on the control and self-adjust days but increased 35% to 40% during cooling (P = 0.0001). Mean arterial pressure and plasma norepinephrine and epinephrine concentrations were significantly greater during cooling (P <0.05). On a self-reported thermal comfort scale, the subjects were miserable during cooling and significantly more comfortable on the self-adjust than control day (P <0.05). CONCLUSION: We conclude that active cooling should be avoided in unsedated patients with moderate fever, because it does not reduce core temperature but does increase metabolic rate, activate the autonomic nervous system, and provoke thermal discomfort.

Perioperative collagen deposition in elderly and young men and women.

HYPOTHESIS: Women deposit more collagen after major abdominal surgery than men. DESIGN: A post hoc analysis of data obtained from 2 prospective, randomized, double-blind clinical trials. SETTING: University hospital general surgical service. PATIENTS: One hundred sixteen patients undergoing colon resection. MAIN OUTCOME MEASURES: Protein and hydroxyproline (collagen) deposition during the first 7 postoperative days in expanded polytetrafluoroethylene implants positioned subcutaneously. RESULTS: On univariate analysis, men and women deposited comparable amounts of collagen (257 +/- 120 vs 281 +/- 117 ng/mm, respectively). When potential confounding factors were entered into a generalized mixed-effects model, only the interaction between age and sex was a significant factor (P = .047). Collagen deposition decreased with age in men, being 317 +/- 133 ng/mm in men younger than 45 years, but only 238 +/- 113 ng/mm in those older than 45 years (P = .03). In contrast, collagen deposition was virtually identical in women younger than 45 years (280 +/- 133 ng/mm) and in those older than 45 years (281 +/- 110 ng/mm). Only 3 of these women were receiving hormone replacement therapy. CONCLUSIONS: Collagen deposition after surgery decreased significantly with age in men, while remaining unchanged in women. Younger men and women deposited similar amounts of collagen. Therefore, older men made less collagen after surgery than older women, perhaps explaining the consistent observation that wound dehiscence is twice as common in men than in women. Our results differ from previous studies conducted in healthy, nonsurgical volunteers, which showed that (1) young women made significantly more collagen than young men and (2) collagen deposition was reduced in postmenopausal women, but deposition returned to premenopausal values with hormone replacement therapy. Differences between our results and those reported previously likely stem from the populations studied. In particular, multiple perioperative factors decrease collagen deposition, which apparently obscures the differences observed previously in healthy, unstressed volunteers.

Postoperative hemodynamic and thermoregulatory consequences of intraoperative core hypothermia.

STUDY OBJECTIVE: To evaluate the postoperative hemodynamic and thermoregulatory consequences of intraoperative core hypothermia. DESIGN: Prospective, randomized clinical trial. SETTING: Operating room and postanesthesia care unit of a university hospital. PATIENTS: 74 healthy, ASA status I, II, and III patients (average age 58 yrs) undergoing elective colon surgery. INTERVENTIONS: Patients were randomly assigned to be kept normothermic or approximately 2.5 degrees C hypothermic during surgery. Anesthesia was maintained with isoflurane, nitrous oxide, and fentanyl. Postoperatively, surgical pain was treated with patient-controlled analgesia (PCA) opioid. MEASUREMENTS AND MAIN RESULTS: An observer blinded to group assignment and core temperatures evaluated shivering, thermal comfort, surgical pain, heart rates (HRs), and blood pressures (BPs) during the first six postoperative hours. Morphometric characteristics, oxygen saturation, fluid balance, PCA-administered opioid, and visual analog pain scores were comparable in the two groups. Hypothermic patients felt uncomfortably cold during recovery, and their postoperative core temperatures remained significantly less than in the normothermic patients for more than four hours. Peripheral vasoconstriction and shivering were common in the hypothermic patients but rare in those kept normothermic. HRs and BPs were comparable in the two groups. CONCLUSIONS: These data confirm that the effects of intraoperative hypothermia on postoperative HR and BP are modest in relatively young, generally healthy patients. In contrast, intraoperative hypothermia caused substantial postoperative thermal discomfort, and full recovery from hypothermia required many hours. Delayed return to care normothermia apparently resulted largely from postoperative thermoregulatory impairment.

Lipoma of the cerebellopontine angle. Case reports and literature review.

Two patients with cerebellopontine angle (CPA) lipoma were studied. They were submitted to surgical treatment. Available literature was reviewed and 29 cases with same lesion were identified which had been treated by surgery. Clinical manifestations, possibility of diagnostic methods, surgical indications and treatment strategies are discussed. Attention is called to the peculiarities of CPA lipomas and the doubtful validity of attempting complete excision in all cases.

The effect of skin surface warming on pre-operative anxiety in neurosurgery patients.

Skin surface warming of patients not only improves thermal comfort, but has been shown to reduce anxiety in a pre-hospital setting. We tested the hypothesis that pre-operative warming can reduce pre-operative anxiety as effectively as a conventional dose of intravenous midazolam in patients undergoing neurosurgery. We randomly allocated 80 patients to four groups in the pre-operative holding area. Treatment was applied for 30-45 min with (1) passive insulation and placebo; (2) passive insulation and intravenous midazolam (30 microg.kg-1); (3) warming with forced-air and placebo; and (4) warming with forced-air and intravenous midazolam (30 microg.kg-1). Thermal comfort levels (VAS 0-100 mm) and anxiety levels (VAS 0-100 mm, Spielberger State-Trait Anxiety Inventory) were assessed twice: before the designated treatment was started and before induction of anaesthesia. In the midazolam and the midazolam/warming groups, anxiety VAS and Spielberger state anxiety scores decreased by -19 (95% CI: -29 to -9, p<0.01) and -10 (95% CI: -14 to -6, p<0.01), respectively. In the warming and the combined groups, thermal VAS increased by +26 (95% CI: 17-34, p<0.01). Pre-operative warming did not reduce anxiety VAS (p=0.11) or Spielberger state anxiety (p=0.19). The results of our study indicate that pre-operative warming can be recommended solely to improve thermal comfort, not to replace anxiolytic premedication regimens.

Ultrasound quantification of anterior soft tissue thickness fails to predict difficult laryngoscopy in obese patients.

Morbid obesity is associated with difficult laryngoscopy and intubation. In the general population, bedside indices for predicting difficult intubation (i.e. Mallampati classification, thyromental distance, sternomental distance, mouth-opening and Wilson risk score) have poor-to-moderate sensitivity (20-62%) and moderate-to-fair specificity (82-97%). In the obese population, although the risk of difficult intubation after a positive Mallampati test is 34%, it is still not sufficient to be used as a single predictive test. An abundance of pretracheal soft tissue anterior to the vocal cords, as quantified by ultrasound, was a better predictor of difficult laryngoscopy than body mass index (BMI) in Israeli patients. Obesity is a growing problem in the United States: therefore we sought to confirm this finding in the obese population in the United States. We used ultrasound to quantify the neck soft tissue, from the skin to the anterior aspect of the trachea at the vocal cords, in 64 obese patients (BMI > 35). We assessed thyromental distance, mouth-opening, jaw movement, limited neck mobility, modified Mallampati score, abnormal upper teeth, neck circumference, confirmed obstructive sleep apnoea, BMI, age, race and gender as predictors. Twenty patients were classified as difficult laryngoscopy; they were older (47 +/- 9 vs 42 +/- 1 years; P = 0.048; mean +/- SD) and had less soft pretracheal tissue (20.4 +/- 3.0 vs 22.3 +/- 3.8 mm; P = 0.049) than did easy laryngoscopy patients. Multivariate regression indicated that none of the factors was an independent predictor of difficult laryngoscopy. We conclude that the thickness of pretracheal soft tissue at the level of the vocal cords is not a good predictor of difficult laryngoscopy in obese patients in the United States.

Magnesium sulphate only slightly reduces the shivering threshold in humans.

BACKGROUND: Hypothermia may be an effective treatment for stroke or acute myocardial infarction; however, it provokes vigorous shivering, which causes potentially dangerous haemodynamic responses and prevents further hypothermia. Magnesium is an attractive anti-shivering agent because it is used for treatment of postoperative shivering and provides protection against ischaemic injury in animal models. We tested the hypothesis that magnesium reduces the threshold (triggering core temperature) and gain of shivering without substantial sedation or muscle weakness. METHODS: We studied nine healthy male volunteers (18-40 yr) on two randomly assigned treatment days: (1) control and (2) magnesium (80 mg kg(-1) followed by infusion at 2 g h(-1)). Lactated Ringer's solution (4 degrees C) was infused via a central venous catheter over a period of approximately 2 h to decrease tympanic membrane temperature by approximately 1.5 degrees C h(-1). A significant and persistent increase in oxygen consumption identified the threshold. The gain of shivering was determined by the slope of oxygen consumption vs core temperature regression. Sedation was evaluated using a verbal rating score (VRS) from 0 to 10 and bispectral index (BIS) of the EEG. Peripheral muscle strength was evaluated using dynamometry and spirometry. Data were analysed using repeated measures anova; P<0.05 was statistically significant. RESULTS: Magnesium reduced the shivering threshold (36.3 [SD 0.4] degrees C vs 36.6 [0.3] degrees C, P = 0.040). It did not affect the gain of shivering (control, 437 [289] ml min(-1) degrees C(-1); magnesium, 573 [370] ml min(-1) degrees C(-1); P=0.344). The magnesium bolus did not produce significant sedation or appreciably reduce muscle strength. CONCLUSIONS: Magnesium significantly reduced the shivering threshold. However, in view of the modest absolute reduction, this finding is considered to be clinically unimportant for induction of therapeutic hypothermia.

Thermoregulation and hyperthermia.

Despite minor daily and monthly cyclical variations, body temperature remains relatively constant. Core temperature is maintained by thermoregulatory responses such as sweating, vasoconstriction and shivering, which are largely controlled by the hypothalamus. Within the hierarchy of neural structures regulating autonomic thermoregulatory responses, the preoptic area of the anterior hypothalamus plays a dominant role. In contrast, the posterior hypothalamus mediates behavioral defenses. Neurons in both regions sense core temperature and integrate central and peripheral thermal information. The setpoint temperature is then determined by relative synaptic inputs to warm-sensitive, cold-sensitive, and temperature-insensitive neurons. Fever is a regulated elevation in the preoptic setpoint temperature. Endogenous pyrogens and other fever mediators inhibit preoptic warm-sensitive neurons that normally facilitate heat loss and suppress heat production. This elevates the setpoint temperature for all thermoregulatory responses and activates cold-defenses such as vasoconstriction (which decreases heat loss) and shivering (which increases metabolic heat production). When pyrogen concentrations decrease, the setpoint temperature returns towards normal, triggering active vasodilation and sweating, which increases heat loss from the skin surface. The increasing phase of fever is often associated with shivering, which can markedly increase heart rate and cardiac output. Defervescence (and passive hyperthermia) is also often accompanied by tachycardia resulting from active precapillary vasodilation. Thus, cardiovascular complications are common throughout the febrile course and constitute the major clinical consequence of fever.

Perioperative fever.

Unlike normal thermoregulatory control, which is largely neuronally mediated, fever is activated by circulating pyrogens. Pyrogens are triggered by either infectious or non-infectious etiologies, all of which may be present in patients undergoing ambulatory surgery. Fever is a regulated elevation in the setpoint temperature for all thermoregulatory responses (warm and cold defenses). To increase core temperature according to the newly elevated setpoint, cold defenses such as vasoconstriction and shivering are activated. In contrast, anesthesia widens the interthreshold range, thus resulting in hypothermia. As a result, general anesthesia impairs the febrile response to pyrogenic stimulation. However, the precise nature of the interaction between fever and anesthesia has yet to be determined. Postoperative fever continues to be a major problem. Wound infections are responsible for many such fevers, although numerous other etiologies contribute. Initial diagnosis should thus focus on determining the etiology of fever. Once that is established, treatment can focus on the specific cause.

Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. Study of Wound Infection and Temperature Group.

BACKGROUND: Mild perioperative hypothermia, which is common during major surgery, may promote surgical-wound infection by triggering thermoregulatory vasoconstriction, which decreases subcutaneous oxygen tension. Reduced levels of oxygen in tissue impair oxidative killing by neutrophils and decrease the strength of the healing wound by reducing the deposition of collagen. Hypothermia also directly impairs immune function. We tested the hypothesis that hypothermia both increases susceptibility to surgical-wound infection and lengthens hospitalization. METHODS: Two hundred patients undergoing colorectal surgery were randomly assigned to routine intraoperative thermal care (the hypothermia group) or additional warming (the normothermia group). The patient's anesthetic care was standardized, and they were all given cefamandole and metronidazole. In a double-blind protocol, their wounds were evaluated daily until discharge from the hospital and in the clinic after two weeks; wounds containing culture-positive pus were considered infected. The patients' surgeons remained unaware of the patients' group assignments. RESULTS: The mean (+/- SD) final intraoperative core temperature was 34.7 +/- 0.6 degrees C in the hypothermia group and 36.6 +/- 0.5 degrees C in the normothermia group (P < 0.001) Surgical-wound infections were found in 18 of 96 patients assigned to hypothermia (19 percent) but in only 6 of 104 patients assigned to normothermia (6 percent, P = 0.009). The sutures were removed one day later in the patients assigned to hypothermia than in those assigned to normothermia (P = 0.002), and the duration of hospitalization was prolonged by 2.6 days (approximately 20 percent) in hypothermia group (P = 0.01). CONCLUSIONS: Hypothermia itself may delay healing and predispose patients to wound infections. Maintaining normothermia intraoperatively is likely to decrease the incidence of infectious complications in patients undergoing colorectal resection and to shorten their hospitalizations.

Morphometric influences on intraoperative core temperature changes.

Intraoperative core hypothermia develops in three characteristic phases: 1) core-to-peripheral redistribution of body heat that is most prominent during the first hour after induction of anesthesia; 2) subsequent slow linear decrease in core temperature resulting largely from heat loss exceeding metabolic heat production; and 3) core temperature plateau resulting when thermoregulatory vasoconstriction decreases cutaneous heat loss and constrains metabolic heat to the core thermal compartment. Accordingly, we tested the hypotheses that: 1) core cooling does not depend on body fat (BF) or the ratio of weight-to-surface area (Wt/SA) during the initial redistribution phase; 2) the core cooling phase; 2) the core cooling rate is a function of the Wt/SA ratio during the second phase; and 3) the rate of core cooling during the plateau phase (after vasoconstriction) will be determined by the percentage of BF. In 40 patients undergoing elective colon surgery, the amount of redistribution hypothermia was inversely proportional to the percentage of BF (delta TC = 0.034.BF-2.2, r2 = 0.63) and the Wt/SA ratio (delta TC = 0.052.Wt/SA-3.35, r2 = 0.66). The core cooled linearly during the second phase, and the cooling rate was inversely proportional to the Wt/SA ratio (rate = 0.035.(Wt/SA)-2.2, r2 = 0.29). Thermoregulatory vasoconstriction was effective in virtually all patients independent of their morphology, and produced a four-fold reduction in the core cooling rate. These results indicate that patient morphometric characteristics substantially influence intraoperative core temperature changes, and that the effect depends on the hypothermia phase.

Relative contribution of skin and core temperatures to vasoconstriction and shivering thresholds during isoflurane anesthesia.

BACKGROUND: Thermoregulatory control is based on both skin and core temperatures. Skin temperature contributes approximately 20% to control of vasoconstriction and shivering in unanesthetized humans. However, this value has been used to arithmetically compensate for the cutaneous contribution to thermoregulatory control during anesthesia--although there was little basis for assuming that the relation was unchanged by anesthesia. It even remains unknown whether the relation between skin and core temperatures remains linear during anesthesia. We therefore tested the hypothesis that mean skin temperature contributes approximately 20% to control of vasoconstriction and shivering, and that the contribution is linear during general anesthesia. METHODS: Eight healthy male volunteers each participated on 3 separate days. On each day, they were anesthetized with 0.6 minimum alveolar concentrations of isoflurane. They then were assigned in random order to a mean skin temperature of 29, 31.5, or 34 degrees C. Their cores were subsequently cooled by central-venous administration of fluid at approximately 3 degrees C until vasoconstriction and shivering were detected. The relation between skin and core temperatures at the threshold for each response in each volunteer was determined by linear regression. The proportionality constant was then determined from the slope of this regression. These values were compared with those reported previously in similar but unanesthetized subjects. RESULTS: There was a linear relation between mean skin and core temperatures at the vasoconstriction and shivering thresholds in each volunteer: r2 = 0.98+/-0.02 for vasoconstriction, and 0.96+/-0.04 for shivering. The cutaneous contribution to thermoregulatory control, however, differed among the volunteers and was not necessarily the same for vasoconstriction and shivering in individual subjects. Overall, skin temperature contributed 21+/-8% to vasoconstriction, and 18+/-10% to shivering. These values did not differ significantly from those identified previously in unanesthetized volunteers: 20+/-6% and 19+/-8%, respectively. CONCLUSIONS: The results in anesthetized volunteers were virtually identical to those reported previously in unanesthetized subjects. In both cases, the cutaneous contribution to control of vasoconstriction and shivering was linear and near 20%. These data indicate that a proportionality constant of approximately 20% can be used to compensate for experimentally induced skin-temperature manipulations in anesthetized as well as unanesthetized subjects.

Paralysis only slightly reduces the febrile response to interleukin-2 during isoflurane anesthesia.

BACKGROUND: Fever sometimes occurs during anesthesia. However, it is rare considering how often pyrogenic causes are likely to be present and how common fever is after surgery. This low incidence results in part from dose-dependent inhibition of fever by volatile anesthetics. Paralysis, however, may contribute by preventing shivering and the associated increase in metabolic heat production. Therefore the authors tested the hypothesis that paralysis during anesthesia decreases the febrile response to pyrogen administration. METHODS: Seven volunteers each participated on two study days. They were given 30 IU/g intravenous interleukin-2, followed 90 min later by an additional 70 IU/g dose. Anesthesia was induced 30 min after the second dose and maintained for 6 h with 0.6 minimum alveolar concentration isoflurane. The volunteers were randomly assigned to (1) paralysis with vecuronium or (2) no muscle relaxants. Body heat content and distribution were determined from measured tissue and skin temperatures. Data are presented as mean +/- SD; P < 0.05 was considered significant. RESULTS: There was no clinically important difference in peak core (tympanic membrane) temperatures on the unparalyzed (37.6+/-0.9 degrees C) and paralyzed (37.2+/-0.6 degrees C) days. Core heat content increased 1.2+/-0.7 kcal/kg over the last 5 h of anesthesia on the unparalyzed day, but only by 0.9+/-0.4 kcal/kg when the volunteers were paralyzed. Peripheral tissue heat content increased 0.1+/-1.1 kcal/kg on the unparalyzed day but decreased 1.1+/-0.7 kcal/kg when the volunteers were paralyzed. Consequently, body heat content increased 1.3+/-1.3 kcal/kg on the unparalyzed day but decreased significantly by 0.2+/-0.8 kcal/kg when the volunteers were paralyzed. CONCLUSIONS: Paralysis prevented shivering from increasing the metabolic rate. Consequently, body heat content decreased during paralysis, whereas otherwise it increased. Thermoregulatory vasoconstriction was nonetheless able to maintain similar peak and integrated core temperatures on each study day. Administration of muscle relaxants thus is not the primary explanation for the relative paucity of intraoperative fever.

Bispectral EEG index during nitrous oxide administration.

BACKGROUND: Nitrous oxide (N2O) is a commonly used sedative for painful diagnostic procedures and dental work. The authors sought to characterize the effects of N2O on quantitative electroencephalographic (EEG) variables including the bispectral index (BIS), a quantitative parameter developed to correlate with the level of sedation induced by a variety of agents. METHODS: Healthy young adult volunteers (n = 13) were given a randomized sequence of N2O/O2 combinations via face mask. Five concentrations of N2O (10, 20, 30, 40, and 50% atm) were administered for 15 min (20 min for the first step). EEG was recorded from bilateral frontal poles continuously. At the end of each exposure, level of sedation was assessed using primarily the Observer Assessment of Alertness/Sedation (OAA/S) scale. RESULTS: One subject withdrew from the study because of emesis at 50% N2O. N2O (50%) increased theta, beta, 40-50 Hz, and 70-110 Hz band powers. BIS and spectral edge frequency during 50% N2O/O2 did not differ significantly from baseline values. Abrupt decreases from higher to lower concentrations frequently evoked a profound, transient slowing of activity. No significant change in OAA/S was detected during the study. CONCLUSIONS: Although the spectral content of the EEG changed during N2O administration, reflecting some pharmacologic effect, the subjects remained cooperative and responsive throughout, and therefore N2O can only be considered a weak sedative at the tested concentrations. Despite changes in the lower and higher frequency ranges of EEG activity, the BIS did not change, which is consistent with its design objective as a specific measure of hypnosis.

Opioids inhibit febrile responses in humans, whereas epidural analgesia does not: an explanation for hyperthermia during epidural analgesia.

BACKGROUND: Epidural analgesia is frequently associated with hyperthermia during labor and in the postoperative period. The conventional assumption is that hyperthermia is caused by the technique, although no convincing mechanism has been proposed. However, pain in the "control" patients is inevitably treated with opioids, which themselves attenuate fever. Fever associated with infection or tissue injury may then be suppressed by opioids in the "control" patients while being expressed normally in patients given epidural analgesia. The authors therefore tested the hypothesis that fever in humans is manifested normally during epidural analgesia, but is suppressed by low-dose intravenous opioid. METHODS: The authors studied eight volunteers, each on four study days. Fever was induced each day by 150 IU/g intravenous interleukin 2. Volunteers were randomly assigned to: (1) a control day when no opioid or epidural analgesia was given; (2) epidural analgesia using ropivacaine alone; (3) epidural analgesia using ropivacaine in combination with 2 microg/ml fentanyl; or (4) intravenous fentanyl at a target plasma concentration of 2.5 ng/ml. RESULTS: Fentanyl halved the febrile response to pyrogen, decreasing integrated core temperature from 7.0 +/- 3.2 degrees C. h on the control day, to 3.8 +/- 3.0 degrees C. h on the intravenous fentanyl day. In contrast, epidural ropivacaine and epidural ropivacaine-fentanyl did not inhibit fever. The fraction of core-temperature measurements that exceeded 38 degrees C was halved by intravenous fentanyl, and the fraction exceeding 38.5 degrees C was reduced more than fivefold. CONCLUSIONS: These data support the authors' proposed mechanism for hyperthermia during epidural analgesia. Fever during epidural analgesia should thus not be considered a complication of the anesthetic technique per se.

Mild intraoperative hypothermia reduces production of reactive oxygen intermediates by polymorphonuclear leukocytes.

Mild hypothermia directly impairs numerous immune functions in vitro. However, the in vivo effects of mild hypothermia on neutrophil phagocytosis and oxidative killing remain unknown. We tested the hypothesis that mild intraoperative hypothermia decreases neutrophil phagocytic capacity and generation of reactive oxygen intermediates (a measure of oxidative killing). Additionally, we evaluated the effects of in vitro temperature manipulations on each function. Thermal management was randomly assigned in 10 surgical patients, causing intraoperative core temperatures to range from 33 to 37 degrees C. Production of reactive oxygen intermediates and neutrophil phagocytosis were evaluated using flow cytometry at ambient temperature. Phagocytic capacity was assessed by uptake of fluorescein isothiocyanate-labeled Escherichia coli. Reactive oxygen production was estimated by the intracellular conversion of dihydrorhodamine 123 to rhodamine 123. Blood samples were obtained preoperatively, 1 h after surgery started, and 2 h postoperatively. Blood was also obtained from 10 matched control subjects and tested at 32, 37, and 40 degrees C. Neutrophil oxidative and phagocytic capacities were significantly reduced intraoperatively, compared with preoperative and postoperative values. Intraoperative production of reactive oxygen species was linearly related to core temperature. In contrast, there was no correlation between core temperature and phagocytic activity. In vitro production of reactive oxygen intermediates increased sixfold from 32 to 40 degrees C. In vitro phagocytic capacity increased fourfold in this temperature range. Production of oxidative intermediates was most closely related to intraoperative core temperature, decreasing nearly fourfold over a 4 degree C range. This in vitro temperature dependence was matched in vitro. Impaired neutrophil oxidative killing may contribute to the observed hypothermia-induced reduction in resistance to infection.

Thermoregulatory thresholds during epidural and spinal anesthesia.

BACKGROUND: There are significant physiologic differences between spinal and epidural anesthesia. Consequently, these two types of regional anesthesia may influence thermoregulatory processing differently. Accordingly, in volunteers and in patients, we tested the null hypothesis that the core-temperature thresholds triggering thermoregulatory sweating, vasoconstriction, and shivering are similar during epidural and spinal anesthesia. METHODS: Six male volunteers participated on three consecutive study days: epidural or spinal anesthesia were randomly assigned on the 1st and 3rd days (approximately T10 level); no anesthesia was given on the 2nd day. On each day, the volunteers were initially warmed until they started to sweat, and subsequently cooled by central venous infusion of cold fluid until they shivered. Mean skin temperature was kept constant near 36 degrees C throughout each study. The tympanic membrane temperatures triggering a sweating rate of 40 g.m-2.h-1, a finger flow less than 0.1 ml/min, and a marked and sustained increase in oxygen consumption (approximately 30%) were considered the thermoregulatory thresholds for sweating, vasoconstriction, and shivering, respectively. Twenty-one patients were randomly assigned to receive epidural (n = 10) or spinal (n = 11) anesthesia for knee and calf surgery (approximately T10 level). As in the volunteers, the shivering threshold was defined as the tympanic membrane temperature triggering a sustained increase in oxygen consumption. RESULTS: The thresholds and ranges were similar during epidural and spinal anesthesia in the volunteers. However, the sweating-to-vasoconstriction (inter-threshold) range, the vasoconstriction-to-shivering range, and the sweating-to-shivering range all were significantly increased by regional anesthesia. The shivering thresholds in patients assigned to epidural and spinal anesthesia were virtually identical. CONCLUSIONS: Comparable sweating, vasoconstriction, and shivering thresholds during epidural and spinal anesthesia suggest that thermoregulatory processing is similar during each type of regional anesthesia. However, thermoregulatory control was impaired during regional anesthesia, as indicated by the significantly enlarged inter-threshold and sweating-to-shivering ranges.

Efficacy of two methods for reducing postbypass afterdrop.

BACKGROUND: Afterdrop, defined as the precipitous reduction in core temperature after cardiopulmonary bypass, results from redistribution of body heat to inadequately warmed peripheral tissues. The authors tested two methods of ameliorating afterdrop: (1) forced-air warming of peripheral tissues and (2) nitroprusside-induced vasodilation. METHODS: Patients were cooled during cardiopulmonary bypass to approximately 32 degrees C and subsequently rewarmed to a nasopharyngeal temperature near 37 degrees C and a rectal temperature near 36 degrees C. Patients in the forced-air protocol (n = 20) were assigned randomly to forced-air warming or passive insulation on the legs. Active heating started with rewarming while undergoing bypass and was continued for the remainder of surgery. Patients in the nitroprusside protocol (n = 30) were assigned randomly to either a control group or sodium nitroprusside administration. Pump flow during rewarming was maintained at 2.5 l x m(-2) x min(-1) in the control patients and at 3.0 l x m(-2) x min(-1) in those assigned to sodium nitroprusside. Sodium nitroprusside was titrated to maintain a mean arterial pressure near 60 mm Hg. In all cases, a nasopharyngeal probe evaluated core (trunk and head) temperature and heat content. Peripheral compartment (arm and leg) temperature and heat content were estimated using fourth-order regressions and integration over volume from 18 intramuscular needle thermocouples, nine skin temperatures, and "deep" hand and foot temperature. RESULTS: In patients warmed with forced air, peripheral tissue temperature was higher at the end of warming and remained higher until the end of surgery. The core temperature afterdrop was reduced from 1.2+/-0.2 degrees C to 0.5+/-0.2 degrees C by forced-air warming. The duration of afterdrop also was reduced, from 50+/-11 to 27+/-14 min. In the nitroprusside group, a rectal temperature of 36 degrees C was reached after 30+/-7 min of rewarming. This was only slightly faster than the 40+/-13 min necessary in the control group. The afterdrop was 0.8+/-0.3 degrees C with nitroprusside and lasted 34+/-10 min which was similar to the 1.1+/-0.3 degrees C afterdrop that lasted 44+/-13 min in the control group. CONCLUSIONS: Cutaneous warming reduced the core temperature afterdrop by 60%. However, heat-balance data indicate that this reduction resulted primarily because forced-air heating prevented the typical decrease in body heat content after discontinuation of bypass, rather than by reducing redistribution. Nitroprusside administration slightly increased peripheral tissue temperature and heat content at the end of rewarming. However, the core-to-peripheral temperature gradient was low in both groups. Consequently, there was little redistribution in either case.