Anesthesia and analgesia
-
Anesthesia and analgesia · May 1999
Distress during the induction of anesthesia and postoperative behavioral outcomes.
We determined whether children who are extremely anxious during the induction of anesthesia are more at risk of developing postoperative negative behavioral changes compared with children who appear calm during the induction process. Children (n = 91) aged 1-7 yr scheduled for general anesthesia and elective outpatient surgery were recruited. Using validated measures of preoperative anxiety and postoperative behaviors, children were evaluated during the induction of general anesthesia and on Postoperative Days 1, 2, 3, 7, and 14. Using a multivariate logistic regression model, in which the dependent variable was the presence or absence of postoperative negative behavioral changes and the independent variables included several potential predictors, we demonstrated that anxiety of the child, time after surgery, and type of surgical procedure were predictors for postoperative maladaptive behavior. The frequency of negative postoperative behavioral changes decreased with time after surgery, and the frequency of negative postoperative behavioral changes increased when the child exhibited increased anxiety during the induction of anesthesia. Finally, we found a significant correlation (r) of 0.42 (P = 0.004) between the anxiety of the child during induction and the excitement score on arrival to the postanesthesia care unit. We conclude that children who are anxious during the induction of anesthesia have an increased likelihood of developing postoperative negative behavioral changes. We recommend that anesthesiologists advise parents of children who are anxious during the induction of anesthesia of the increased likelihood that their children will develop postoperative negative behavioral changes such as nightmares, separation anxiety, and aggression toward authority. ⋯ Anesthesiologists who care for children who are anxious during the induction of anesthesia should inform parents that these children have an increased likelihood of developing postoperative negative behavioral changes.
-
Anesthesia and analgesia · May 1999
Comparative StudyComparison between the European and North American protocols for diagnosis of malignant hyperthermia susceptibility in humans.
We compared the diagnostic outcome of in vitro contracture tests for diagnosis of malignant hyperthermia susceptibility performed according to the European Malignant Hyperthermia Group protocol and the North American Malignant Hyperthermia Group protocol. The aim of the study was to compare the two major diagnostic tests of malignant hyperthermia susceptibility to have basic data for a common worldwide protocol. We evaluated 156 patients and 17 control individuals. The accordance in diagnostic outcome was 87%. The diverging outcomes between the two protocols were found in a group of patients reacting in few muscle strips and close to the cutoff limits. A 100% accordance in diagnostic outcome was found in individuals with contractures in at least five of six tested muscle strips. In both protocols, contractures close to the cutoff limits in a few muscle strips in scientific studies should be considered as unknown results. ⋯ We compared the two major protocols for investigating malignant hyperthermia susceptibility. There was 87% accordance in diagnostic outcome. The diverging outcomes were seen in individuals with less reproducible test results near the cutoff limits. In scientific studies, such results should be considered as unknown.
-
Anesthesia and analgesia · May 1999
S(+)-ketamine, but not R(-)-ketamine, reduces postischemic adherence of neutrophils in the coronary system of isolated guinea pig hearts.
Polymorphonuclear neutrophils (PMN) play a crucial role in the initiation of reperfusion injury. In a previous study, we found that ketamine reduced the postischemic adherence of PMN to the intact coronary system of isolated guinea pig hearts. Because ketamine is a racemic mixture (1:1) of two optical enantiomers, we looked for possible differences in action between the stereoisomers. Seventy-six guinea pig hearts were perfused in the "Langendorff" mode under conditions of constant flow (5 mL/min) using modified Krebs-Henseleit buffer. After 15 min of global warm ischemia, freshly isolated human PMN (10(6)) were infused as a bolus into the coronary system during the second minute of reperfusion. PMN adhesion was expressed as the numeric difference between PMN recovered in the effluent and those applied. Series A hearts received 5 microM S(+), 5 microM R(-), or 10 microM racemic ketamine starting 20 min before ischemia and during reperfusion. In Series B hearts, 10 microM nitro-L-arginine, an inhibitor of NO synthase, was added to the perfusate. In Series C, PMN were preincubated for 15 min with 5 microM S(+)- or R(-)-ketamine. Coronary vascular leak was assessed by measuring the rate of formation of transudate on the epicardial surface. Ischemia/reperfusion without anesthetics increased coronary PMN adherence from 25.5% +/-2.3% (basal) to 35.3%+/-1.5% of the number applied. S(+)-ketamine reduced postischemic adherence in each series (A, 25.5%+/-5.1%; B, 22.5%+/-1.7%; C, 25.3%+/-7.7%), as did racemate (A, 26.4%+/-3.7%). Although 5 microM R(-)-ketamine had no effect on adhesion (A, 30.5%+/-6.7%; B, 34.3%+/-5.1%; C, 34.3%+/-4.3%), it significantly increased vascular leak in the presence of NOLAG. These findings indicate stereoselective differences in biological action between the two ketamine isomers: S(+)-ketamine inhibited PMN adherence, R(-)-ketamine worsened coronary vascular leak in reperfused isolated hearts. ⋯ In this study, we demonstrated stereoselective differences in the biologic action of the two ketamine isomers in an animal model of myocardial ischemia. Polymorphonuclear neutrophil adherence to the coronary vasculature after ischemia was inhibited by S(+)-ketamine, whereas R(-)-ketamine increased coronary vascular fluid leak.
-
Anesthesia and analgesia · May 1999
Treatment of intraoperative refractory hypotension with terlipressin in patients chronically treated with an antagonist of the renin-angiotensin system.
The goal of the present study was to determine whether terlipressin, an agonist of the vasopressin system, could counteract perioperative hypotension refractory to common vasopressor therapy and to analyze its circulatory effects. We enrolled 51 consecutive vascular surgical patients chronically treated with angiotensin-converting enzyme inhibitors or antagonists of the receptor of angiotensin II, who received a standardized opioid-propofol anesthetic. Of these 51 patients, 32 had at least one episode of hypotension, which responded to epinephrine or phenylephrine. In 10 other patients, systolic arterial pressure (SAP) did not remain above 100 mm Hg for 1 min, despite three bolus doses of ephedrine or phenylephrine. In these patients, we injected a bolus of 1 mg of terlipressin, repeated twice if necessary. Hemodynamic and echocardiographic variables were recorded every 30 s over 6 min. In eight patients, arterial pressure was restored with one injection of terlipressin; in two other patients, three injections were necessary. One minute after the last injection of terlipressin, the SAP increased from 88+/-3 to 100+/-4 mm Hg and reached 117+/-5 mm Hg (P = 0.001) 3 min after the injection and remained stable around this value. This increase in SAP was associated with significant changes in left ventricular end-diastolic area (17.9+/-2 vs 20.2+/-2.2 cm2; P = 0.003), end-systolic area (8.1+/-1.3 vs 9.6+/-1.5 cm2; P = 0.004), end-systolic wall stress (45+/-8 vs 66+/-12; P = 0.001), and heart rate (60+/-4 vs 55+/-3 bpm; P = 0.001). Fractional area change and velocity of fiber shortening did not change significantly. No additional injection of vasopressor was required during the perioperative period. No change in ST segment was observed after the injection. ⋯ Terlipressin is effective to rapidly correct refractory hypotension in patients chronically treated with antagonists of the renin-angiotensin system without impairing left ventricular function.