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BACKGROUND:In Japan, routine clinical care does not normally involve the use of a monitoring device to guide the administration of neuromuscular blocking drugs or their antagonists. Although most previous reports demonstrate that sugammadex offers more rapid and reliable antagonism from rocuronium-i

BACKGROUND: Facilitation of the spread of neuraxial anesthesia in pregnant women may be attributable in part to compression of the dural sac by the engorged epidural venous plexus. In this study, we used magnetic resonance imaging to examine pregnancy-induced changes in the lumbosacral cerebrospinal fluid (CSF) volume and dural sac surface area. METHODS: Magnetic resonance images of 18 healthy women (mean age 29 yr, mean height 158 cm, and mean weight 58 kg) were obtained to measure lumbosacral CSF volume and dural sac surface area in the nonpregnant and pregnant states (median 36 wk gestation [31-39]) and the paired images were compared. RESULTS: The mean lumbosacral CSF volume and dural sac surface area in the nonpregnant state were 39.6 +/- 5.8 mL and 11.0 +/- 0.8 cm(2), respectively. Pregnancy was associated with compression of the dural sac, resulting in a significantly reduced mean CSF volume (33.2 +/- 6.2 mL) and dural sac surface area (9.9 +/- 1.0 cm(2)) in all subjects (P < 0.001). The mean change in CSF volume and dural sac surface area was 16.7% +/- 0.8% and 10.0% +/- 0.5%, respectively. Gestational week (between 31 and 39 wk) correlated significantly with the reduction in CSF volume (rho = 0.74, P < 0.001) and dural sac surface area (rho = 0.66, P < 0.01). CONCLUSIONS: These findings indicate an association between gestational week (Weeks 31-39) and a reduction in both CSF volume and dural sac surface area. These reductions may, at least in part, explain the facilitation of the spread of intrathecal anesthesia in pregnant women.

Local angiogenic therapy with recombinant human basic fibroblast growth factor (rhbFGF) has been used to promote wound healing. To obtain useful information for the development of optimal angiogenic therapy, we chronologically evaluated the effects of a single local application of rhbFGF on angiogenesis in a rabbit ear chamber model of wound healing by observing the subcutaneous vessel bed intravitally. New vessel formation during wound healing was macroscopically and microscopically evaluated for 5 wk. Each rabbit ear chamber received a single dose of 6 microg rhbFGF (treatment B1: n = 13), 18 microg rhbFGF (treatment B2: n = 16), or physiological saline as control (n = 13). At 1 wk the newly vascularized area was significantly larger in groups B1 and B2 than in control. At 2 wk, the vascularized areas in groups B1, B2, and control were similar. At 5 wk, the percentage of rabbits with complete vascularization was significantly larger in group B1 than in control. Capillary density at 5 wk was similar among the three groups. These results suggest that locally applied rhbFGF accelerated angiogenesis during early wound healing in rabbits; however, this effect was transient and no increase in capillary density occurred at the completion of vascularization.

Reported effect-site concentrations of propofol at loss of consciousness and recovery of consciousness vary widely. Thus, no single concentration based on a population average will prove optimal for individual patients. We therefore tested the hypothesis that individual propofol effect-site concentrations at loss and return of consciousness are similar. Propofol effect-site concentrations at loss and recovery of consciousness were estimated with a target-control infusion system in 20 adults. Propofol effect-site concentrations were gradually increased until the volunteers lost consciousness (no response to verbal stimuli); unconsciousness was maintained for 15 min, and the volunteers were then awakened. This protocol was repeated three times in each volunteer. Our major outcomes were the concentration producing unconsciousness and the relationship between the estimated effect-site concentrations at loss and recovery of consciousness. The target effect-site propofol concentration was 2.0 +/- 0.9 at loss of consciousness and 1.8 +/- 0.7 at return of consciousness (P

Although the difficulty of tracheal intubation in the lateral position has not been systematically evaluated, airway loss during surgery in a laterally positioned patient may have hazardous consequences. We explored whether the intubating laryngeal mask airway (ILMA) facilitates tracheal intubation in patients with normal airway anatomy, i.e., Mallampati gradeor=3 and thyromental distanceor=5 cm, positioned in the lateral position. We evaluated whether this technique can be used as a rescue when the airway is lost during the middle of surgery in laterally positioned patients with respect to success rate and intubation time. Anesthesia was induced with propofol, fentanyl, and vecuronium in 50 patients undergoing spine surgery for lumbar disk herniation (Lateral) and 50 undergoing other surgical procedures (Supine). Patients having disk surgery (Lateral) were positioned on their right or left sides before induction of general anesthesia, and intubation was performed in that position. Patients in the control group (Supine) were anesthetized in supine position, and intubation was performed in that position. Intubation was performed blindly via an ILMA in both groups. The time required for intubation and number and types of adjusting maneuvers used were recorded. Data were compared by the Mann-Whitney U test, Fisher's exact test, chi(2) test, or unpaired Student's t-test, as appropriate. Data presented as mean (SD). Demographic and airway measures were similar in the two groups, except for mouth opening, which was slightly wider in patients in the lateral position: 5.1 (0.9) versus 4.6 (0.7) cm. The time required for intubation was similar in each group ( approximately 25 s), as was intubation success (96%). We conclude that blind intubation via an ILMA offers a frequent success rate and a clinically acceptable intubation time (1 min) even in the lateral position.Blind intubation via the intubating laryngeal mask airway (ILMA) offers frequent success and a clinically acceptable intubation time even in patients in the lateral position.

UNLABELLED The onset time of neuromuscular blocking drugs is partially determined by circulatory factors, including muscle blood flow and cardiac output. We thus tested the hypothesis that a bolus of ephedrine accelerates the onset of vecuronium neuromuscular block by increasing cardiac output. A prospective, randomized study was conducted in 53 patients scheduled for elective surgery. After the induction of anesthesia, the ulnar nerve was stimulated supramaximally every 10 s, and the evoked twitch response of the adductor pollicis was recorded with accelerometry. Patients were maintained under anesthesia with continuous infusion of propofol for 10 min and then randomly assigned to ephedrine 210 microg/kg (n = 27) or an equivalent volume of saline (n = 26). The test solution was given 1 min before the administration of 0.1 mg/kg of vecuronium. Cardiac output was monitored with impedance cardiography. Ephedrine, but not saline, increased cardiac index (17%; P = 0.003). Nonetheless, the onset of 90% neuromuscular block was virtually identical in the patients given ephedrine (183 +/- 41 s) and saline (181 +/- 47 s). There was no correlation between cardiac index and onset of the blockade. We conclude that the onset of the vecuronium-induced neuromuscular block is primarily determined by factors other than cardiac output. The combination of ephedrine and vecuronium thus cannot be substituted for rapid-acting nondepolarizing muscle relaxants. IMPLICATIONS Ephedrine increased cardiac index but failed to speed onset of neuromuscular block with vecuronium. We conclude that ephedrine administration does not shorten the onset time of vecuronium.

UNLABELLED Widespread use of new airway devices, such as the laryngeal mask airway (LMA) and the cuffed oropharyngeal airway (COPA), preclude measuring core temperature in the distal esophagus. Therefore, we tested the hypothesis that core temperature measured with a thermocouple positioned on a LMA or COPA is sufficiently accurate and precise for clinical use. Temperatures were recorded from thermocouples positioned on the cuffs of LMAs or COPAs in 36 patients scheduled for prolonged orthopedic surgery or therapeutic hyperthermia for cancer. These temperatures, recorded at 15-min intervals, were compared with simultaneously obtained nasopharynx and tympanic membrane temperatures. Data were compared by linear regression and the bias calculated. Temperatures measured on the LMA correlated well with both nasopharyngeal (r(2) = 0.94) and tympanic membrane (r(2) = 0.94) temperatures. Temperatures measured on the COPA also correlated well with those on the nasopharynx (r(2) = 0.97) and tympanic membrane (r(2) = 0.96). The fraction of temperatures that differed from nasopharynx temperature by more than +/-0.5 degrees C was 8% with LMA and 11% with COPA; the fraction of temperatures that differed from tympanic temperature by more than +/-0.5 degrees C was 7% with LMA and 10% with COPA. These results suggest that body temperature measured from the cuffs of COPA or LMAs is sufficiently accurate for routine clinical use. IMPLICATIONS Temperatures measured on airway devices correlated well with independent measurements of core body temperature. Thus, body temperature measured on the cuffs of airway devices is sufficiently accurate for routine use.

Serious adverse outcomes from perioperative hypothermia are well documented. Consequently, intraoperative warming has become routine. We thus evaluated the efficacy of a novel, nondisposable carbon-fiber resistive-heating system. Twenty-four patients undergoing open abdominal surgery lasting approximately 4 h were randomly assigned to warming with 1) a full-length circulating water mattress set at 42 degrees C, 2) a lower-body forced-air cover with the blower set on high, or 3) a three-extremity carbon-fiber resistive-heating blanket set to 42 degrees C. Patients were anesthetized with a combination of continuous epidural and general anesthesia. All fluids were warmed to 37 degrees C, and ambient temperature was kept near 22 degrees C. Core (tympanic membrane) temperature changes among the groups were compared by using factorial analysis of variance and Scheffé F tests; results are presented as means +/- SD. Potential confounding factors did not differ significantly among the groups. In the first 2 h of surgery, core temperature decreased by 1.9 degrees C +/- 0.5 degrees C in the circulating-water group, 1.0 degrees C +/- 0.6 degrees C in the forced-air group, and 0.8 degrees C +/- 0.2 degrees C in the resistive-heating group. At the end of surgery, the decreases were 2.0 degrees C +/- 0.8 degrees C in the circulating-water group, 0.6 degrees C +/- 1.0 degrees C in the forced-air group, and 0.5 degrees C +/- 0.4 degrees C in the resistive-heating group. Core temperature decreases were significantly greater in the circulating-water group at all times after 150 elapsed minutes; however, temperature changes in the forced-air and resistive-heating groups never differed significantly. Even during major abdominal surgery, resistive heating maintains core temperature as effectively as forced air.Efficacy was similar for forced-air and resistive heating, and both maintained intraoperative core temperature far better than circulating-water mattresses. We thus conclude that even during major abdominal surgery, resistive heating maintains core temperature as effectively as forced air.

Shivering has been proposed as an etiology of postoperative hypoxemia. The difficulty with this theory is that hypoxemia inhibits shivering in unanesthetized cats, rats, and humans. However, anesthesia inhibits many protective reflexes, including the ventilatory response to hypoxemia. We therefore tested the hypothesis that arterial hypoxemia fails to inhibit shivering in lightly anesthetized rabbits. Rabbits were intubated and instrumented during exposure to surgical concentrations of anesthesia, and anesthesia was then maintained with 0.2 minimum alveolar anesthetic concentration isoflurane. The core was cooled at a rate of 2-3 degrees C/h by perfusing water at 10 degrees C through a colonic thermode. Core temperatures were recorded from the distal esophagus. Sustained, vigorous shivering was considered physiologically significant. The core temperature that triggering significant shivering identified the thermoregulatory threshold for this response. Arterial blood was sampled for gas analysis at the shivering threshold in each rabbit. Hypoxemia linearly reduced the shivering threshold from 36.7 degrees C at 130 mm Hg to 35.4 degrees C at 50 mm Hg (threshold = PaO2.0.019 + 34.3; r2 = 0.49). We failed to confirm our hypothesis: instead, even mild hypoxemia reduced the shivering threshold1 C. A 1 C decrease in the shivering threshold is likely to prevent or stop most postoperative shivering because it exceeds the reduction produced by many effective anti-shivering drugs. These data do not support the theory that shivering causes postoperative hypoxemia.Shivering has been proposed as an etiology of postoperative hypoxemia. Our data, in contrast, show that mild hypoxemia inhibits shivering. Shivering is thus unlikely to be a cause of postoperative hypoxemia.

Elderly patients become more hypothermic during surgery, shiver less postoperatively, and take longer to rewarm than younger patients. Similarly, the vasoconstriction threshold (triggering core temperature) is reduced approximately 1 degree C in elderly patients during nitrous oxide/isoflurane anesthesia. Accordingly, we tested the hypothesis that the vasoconstriction threshold in the elderly is also reduced approximately 1 degree C during nitrous oxide and sevoflurane anesthesia. Eleven young patients aged 30-50 yr and 14 elderly patients aged 60-80 yr were anesthetized with nitrous oxide (50%) and sevoflurane (1%). Mean skin temperature was calculated from four sites. Fingertip blood flow was estimated using forearm minus fingertip skin-temperature gradients, with a gradient of 0 degree C identifying onset of vasoconstriction. The distal esophageal temperature triggering onset of vasoconstriction identified the threshold for this thermoregulatory defense. The data from five patients who did not vasoconstrict at minimum core temperatures of 33-34 degrees C were eliminated, leaving 10 patients in each group. The vasoconstriction threshold was significantly less in the elderly (35.0 +/- 0.8 degrees C) than in younger patients (35.8 +/- 0.3 degrees C), despite similar mean skin temperatures (mean +/- SD, P0.01, Student's t-test). Age dependence of thermoregulatory vasoconstriction during nitrous oxide/sevoflurane anesthesia is similar to that previously observed during nitrous oxide/isoflurane anesthesia.

The core temperature triggering thermoregulatory arteriovenous shunt constriction is designated the threshold for vasoconstriction. High thresholds are generally desirable because vasoconstriction helps prevent further core hypothermia by decreasing cutaneous heat loss and constraining metabolic heat to the core thermal compartment. Previous studies suggest that nitrous oxide (N2O) may inhibit thermoregulatory vasoconstriction less than comparable doses of volatile anesthetics. To confirm this impression, we tested the hypothesis that 0.5 minimum alveolar anesthetic concentration (MAC) N2O combined with 0.5 MAC sevoflurane or isoflurane would reduce the vasoconstriction threshold less than 1.0 MAC sevoflurane or isoflurane. With institutional review board approval, we studied 40 patients, aged 20-60 yr, undergoing open abdominal surgery. No premedication was given. Ten patients each were anesthetized with: 1) N2O (50%) and 0.5 MAC sevoflurane (1%); 2) sevoflurane alone (2%); 3) N2O (60%) and 0.5 MAC isoflurane (0.6%); and, 4) isoflurane alone (1.2%). A forearm minus fingertip, skin temperature gradientor = 0 degree C was considered significant vasoconstriction; the esophageal temperature triggering vasoconstriction identified the threshold. Morphometric characteristics were comparable in each group. The threshold for vasoconstriction was 35.8 +/- 0.3 degrees C in the patients given 50% N2O combined with 0.5 MAC sevoflurane, which was significantly greater than that in those given 1.0 MAC sevoflurane: 35.1 +/- 0.4 degrees C. Similarly, the threshold for vasoconstriction was 35.9 +/- 0.3 degrees C in the patients given 60% N2O combined with 0.5 MAC isoflurane, which was significantly greater than that in those given 1.0 MAC isoflurane: 35.0 +/- 0.5 degrees C. We thus conclude that N2O impairs thermoregulation less than sevoflurane or isoflurane.

We tested the hypothesis that once thermoregulatory vasoconstriction is triggered at a given core temperature during isoflurane anesthesia, redilation starts at a substantially higher core temperature. To avoid direct perception of cutaneous cooling and warming, we used epidural anesthesia and limited our thermal manipulations to the blocked area. Seven volunteers were anesthetized with isoflurane/epidural anesthesia (approximately T9 dermatomal level). Core hypothermia was induced by surface cooling restricted to the legs. Cooling was continued until fingertip blood flow suddenly decreased (vasoconstriction threshold). The core was then rewarmed by heating the legs until fingertip flow suddenly increased toward initial values (redilation threshold). The difference between the two thresholds defined the direction-dependent hysteresis. Vasoconstriction occurred at 35.2 +/- 0.6 degrees C and vasodilation at 36.2 +/- 0.5 degrees C (P < 0.01, paired t-test); consequently, the hysteresis was 1.0 +/- 0.6 degrees C. The observed hysteresis suggests that thermoregulatory responses during combined isoflurane/epidural anesthesia are not determined simply by instantaneous thermal input to central controllers, but may also depend on the direction of core temperature change.