Rainer Lenhardt

Mild Intraoperative Hypothermia Prolongs Postanesthetic Recovery

Background: Intraoperative hypothermia is common and persists for several hours after surgery. Hypothermia may prolong immediate recovery by augmenting anesthetic potency, delaying drug metabolism, producing hemodynamic instability, or depressing cognitive function. Accordingly, the authors tested the hypothesis that intraoperative hypothermia prolongs postoperative recovery. Methods: Patients undergoing elective major abdominal surgery (n = 150) were anesthetized with isoflurane, nitrous oxide, and fentanyl. They were randomly assigned to routine thermal management (hypothermia) or extra warming (normothermia). Postoperative surgical pain was treated with patient‐controlled analgesia. Fitness for discharge from the post‐anesthesia care unit was evaluated at 20‐min intervals by investigators blinded to group assignment and postoperative core temperatures. Scoring was based on a modification of a previously published system that included activity, ventilation, consciousness, and hemodynamic responses. Patients were considered fit for discharge when they sustained a score of 80% (13 points) for at least two consecutive measurement periods. Results: Morphometric characteristics and anesthetic management were similar in each group. Final intraoperative core temperatures differed by [nearly =] 2 [degree sign] Celsius: 34.8 +/‐ 0.6 versus 36.7 +/‐ 0.6 [degree sign] Celsius (mean +/‐ SD, P < 0.001). Postoperative pain scores and postoperative use of patient‐controlled opioid were similar. Hypothermic patients required [nearly =] 40 min longer (94 +/‐ 65 vs. 53 +/‐ 36 min) to reach fitness for discharge, even when return to normothermia was not a criterion (P < 0.001). Duration of recovery in the two groups differed by [nearly =] 90 min when a core temperature > 36 [degree sign] Celsius was also required (P < 0.001). Conclusion: Maintaining core normothermia decreases the duration of postanesthetic recovery and may, therefore, reduce costs of care.

Bispectral EEG Index during Nitrous Oxide Administration

Background Nitrous oxide (N2 O) is a commonly used sedative for painful diagnostic procedures and dental work. The authors sought to characterize the effects of N2 O 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 N2 O/O2 combinations via face mask. Five concentrations of N2 O (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% N (2) O. N2 O (50%) increased theta, beta, 40 - 50 Hz, and 70 - 110 Hz band powers. BIS and spectral edge frequency during 50% N2 O/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 N (2) O administration, reflecting some pharmacologic effect, the subjects remained cooperative and responsive throughout, and therefore N2 O 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.

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 degrees C range. This in vivo temperature dependence was matched in vitro. Impaired neutrophil oxidative killing may contribute to the observed hypothermia-induced reduction in resistance to infection. (Anesth Analg 1996;82:810-6)

Thermoregulatory thresholds during epidural and spinal anesthesia.

BackgroundThere 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. MethodsSix male volunteers participated on three consecutive study days: epidural or spinal anesthesia were randomly assigned on the 1st and 3rd days (± 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°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 (± 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 (± T10 level). As in the volunteers, the shivering threshold was defined as the tympanic membrane temperature triggering a sustained increase in oxygen consumption. ResultsThe thresholds and ranges were similar during epidural and spinal anesthesia in the volunteers. However, the sweating-to-vasoconstriction (interthreshold) 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. ConclusionsComparable 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 interthreshold and sweating-to-shivering ranges.

Ondansetron is no More Effective than Supplemental Intraoperative Oxygen for Prevention of Postoperative Nausea and Vomiting

Supplemental oxygen maintained during and for 2 h after colon resection halves the incidence of nausea and vomiting. Whether supplemental oxygen restricted to the intraoperative period is sufficient remains unknown. Similarly, the relative efficacy of supplemental oxygen and ondansetron is unknown. We tested the hypothesis that intraoperative supplemental oxygen reduces the incidence of postoperative nausea and vomiting. Patients (n = 240) undergoing gynecological laparoscopy were given a standardized isoflurane anesthetic. After induction, they were randomly assigned to the following three groups: routine oxygen administration with 30% oxygen, balance nitrogen (30% Oxygen group), supplemental oxygen administration with 80% oxygen, balance nitrogen (80% Oxygen group), and Ondansetron 8 mg (immediately after induction), combined with 30% oxygen, balance nitrogen (Ondansetron group). The overall incidence of nausea and/or vomiting during the initial 24 postoperative h was 44% in the patients assigned to 30% oxygen and 30% in the Ondansetron group, but only 22% in those given 80% oxygen. The incidence was thus halved by supplemental oxygen and was significantly less than with 30% oxygen. There were, however, no significant differences between the 30% oxygen and ondansetron groups, or between the ondansetron and 80% oxygen groups. We conclude that supplemental oxygen effectively prevents postoperative nausea and vomiting after gynecological laparoscopic surgery; furthermore, ondansetron is no more effective than supplemental oxygen. IMPLICATIONS Supplemental oxygen reduces the risk of postoperative nausea and vomiting (PONV) as well or better than 8 mg of ondansetron. Because oxygen is inexpensive and essentially risk-free, supplemental oxygen is a preferable method of reducing PONV.

Dexmedetomidine and Meperidine Additively Reduce the Shivering Threshold in Humans

Background and Purpose— Hypothermia might prove to be therapeutically beneficial in stroke victims; however, even mild hypothermia provokes vigorous shivering. Meperidine and dexmedetomidine each linearly reduce the shivering threshold (triggering core temperature) with minimal sedation. We tested the hypothesis that meperidine and dexmedetomidine synergistically reduce the shivering threshold without producing substantial sedation or respiratory depression. Methods— We studied 10 healthy male volunteers (18 to 40 years) on 4 days: (1) control (no drug); (2) meperidine (target plasma level 0.3 &mgr;g/mL); (3) dexmedetomidine (target plasma level 0.4 ng/mL); and (4) meperidine plus dexmedetomidine (target plasma levels of 0.3 &mgr;g/mL and 0.4 ng/mL, respectively). Lactated Ringer’s solution (≈4°C) was infused through a central venous catheter to decrease tympanic membrane temperature by ≈2.5°C/h; mean skin temperature was maintained at 31°C. An increase in oxygen consumption >25% of baseline identified the shivering threshold. Sedation was evaluated by using the Observer’s Assessment of Sedation/Alertness scale. Two-way repeated-measures ANOVA was used to identify interactions between drugs. Data are presented as mean±SD;P <0.05 was statistically significant. Results— The shivering thresholds on the study days were as follows: control, 36.7±0.3°C; dexmedetomidine, 36.0±0.5°C (P <0.001 from control); meperidine, 35.5±0.6°C (P <0.001); and meperidine plus dexmedetomidine, 34.7±0.6°C (P <0.001). Although meperidine and dexmedetomidine each reduced the shivering threshold, their interaction was not synergistic but additive (P =0.19). There was trivial sedation with either drug alone or in combination. Respiratory rate and end-tidal Pco2 were well preserved on all days. Conclusions— Dexmedetomidine and meperidine additively reduce the shivering threshold; in the small doses tested, the combination produced only mild sedation and no respiratory toxicity.

Effects of a circulating-water garment and forced-air warming on body heat content and core temperature.

Background: Forced-air warming is sometimes unable to maintain perioperative normothermia. Therefore, the authors compared heat transfer, regional heat distribution, and core rewarming of forced-air warming with a novel circulating-water garment. Methods: Nine volunteers were each evaluated on two randomly ordered study days. They were anesthetized and cooled to a core temperature near 34°C. The volunteers were subsequently warmed for 2.5 h with either a circulating-water garment or a forced-air cover. 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 18 intramuscular needle thermocouples, 15 skin thermal flux transducers, and “deep” hand and foot thermometers. Results: Heat production (approximately 60 kcal/h) and loss (approximately 45 kcal/h) were similar with each treatment before warming. The increases in heat transfer across anterior portions of the skin surface were similar with each warming system (approximately 65 kcal/h). Forced-air warming had no effect on posterior heat transfer, whereas circulating-water transferred 21 ± 9 kcal/h through the posterior skin surface after a half hour of warming. Over 2.5 h, circulating water thus increased body heat content 56% more than forced air. Core temperatures thus increased faster than with circulating water than forced air, especially during the first hour, with the result that core temperature was 1.1° ± 0.7°C greater after 2.5 h (P < 0.001). Peripheral tissue heat content increased twice as much as core heat content with each device, but the core-to-peripheral tissue temperature gradient remained positive throughout the study. Conclusions: The circulating-water system transferred more heat than forced air, with the difference resulting largely from posterior heating. Circulating water rewarmed patients 0.4°C/h faster than forced air. A substantial peripheral-to-core tissue temperature gradient with each device indicated that peripheral tissues insulated the core, thus slowing heat transfer.

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 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 centered dot BF - 2.2, r2 = 0.63) and the Wt/SA ratio (Delta TC = 0.052 centered dot 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 centered dot (Wt/SA) - 2.2, r2 = 0.29). Thermoregulatory vasoconstriction was effective in virtually all patients independent of their morphology, and produced a fourfold 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. (Anesth Analg 1995;80:562-7)

The New Perilaryngeal Airway (CobraPLA™) Is as Efficient as the Laryngeal Mask Airway (LMA™), But Provides Better Airway Sealing Pressures

The Laryngeal Mask Airway (LMA) is a frequently used efficient airway device, yet it sometimes seals poorly, thus reducing the efficacy of positive-pressure ventilation. The Perilaryngeal Airway (CobraPLA) is a novel airway device with a larger pharyngeal cuff (when inflated). We tested the hypothesis that the CobraPLA was superior to the LMA with regard to insertion time and airway sealing pressure and comparable to the LMA in airway adequacy and recovery characteristics. After midazolam and fentanyl administration, 81 ASA physical status I–II outpatients having elective surgery were randomized to receive an LMA or CobraPLA. Anesthesia was induced with propofol (2.5 mg/kg IV), and the airway was inserted. We measured 1) insertion time; 2) adequacy of the airway (no leak at 15-cm-H2O peak pressure or tidal volume of 5 mL/kg); 3) airway sealing pressure; 4) number of repositioning attempts; and 5) sealing quality (no leak at tidal volume of 8 mL/kg). At the end of surgery, gastric insufflation, postoperative sore throat, dysphonia, and dysphagia were evaluated. Data were compared with unpaired Student’s t-tests, χ2 tests, or Fisher’s exact tests; P < 0.05 was significant. Patient characteristics, insertion times, airway adequacy, number of repositioning attempts, and recovery were similar in each group. Airway sealing pressure was significantly greater with CobraPLA (23 ± 6 cm H2O) than LMA (18 ± 5 cm H2O, P < 0.001). The CobraPLA has insertion characteristics similar to the LMA but better airway sealing capabilities.

Nitrous oxide and risk of surgical wound infection: A randomised trial

BACKGROUND Nitrous oxide inactivates vitamin B12 and methionine synthase, thereby impairing DNA formation and, consequently, new cell formation. The gas also inhibits methionine production, which can reduce scar formation and depresses chemotactic migration by monocytes. Therefore, we assessed whether nitrous oxide increases the incidence of surgical wound infection. METHODS We recruited 418 patients aged 18-80 years, scheduled for colon resection that was expected to last more than 2 h, at three hospitals in Austria and Hungary. Patients were randomly assigned 65% intraoperative nitrous oxide (n=208) or nitrogen (n=206), with remifentanil and isoflurane. The primary outcome was the incidence of clinical postoperative wound infection, analysed by intention to treat. FINDINGS 206 patients in the nitrous oxide group and 202 in the nitrogen group were included in the final analysis. Duration of surgery was longer in the nitrogen group (3.4 h [1.5]) than in the nitrous oxide group (3.0 h [SD 1.3]) and arterial pressure (84 mm Hg [10] vs 81 mm Hg [9]), bispectral index values (53 [9] vs 44 [8]), and end-tidal isoflurane concentration (0.64% [0.14] vs 0.56% [0.13]) were greater in patients given nitrogen than in those given nitrous oxide. Infection rate was 15% (31/206) in patients given nitrous oxide and 20% (40/202) in those given nitrogen (p=0.205). Additionally, the ASEPSIS wound healing score, wound collagen deposition, number of patients admitted to critical care unit, time to first food ingestion, duration of hospital stay, and mortality did not differ between treatment groups. INTERPRETATION Nitrous oxide does not increase the incidence of surgical wound infection.