Canadian journal of anaesthesia = Journal canadien d'anesthésie
-
Randomized Controlled Trial Clinical Trial
Preemptive opioid analgesia does not influence pain after abdominal hysterectomy.
Opioid administration before surgical stimulus may reduce or prevent subsequent pain. We studied the effect of timing of opioid administration on the pain-related behaviour after abdominal hysterectomy. Eighty-five patients scheduled for abdominal hysterectomy were blindly randomized to receive fentanyl 10 micrograms.kg-1 before induction of anaesthesia (FA), after peritoneal incision (FB) or after removal of the uterus (FC), or sufentanil 1 micrograms.kg-1 before induction of anaesthesia (SA) or after peritoneal incision (SB) respectively. ⋯ The times from skin closure to the first analgesic request did not differ among the five groups. The VAS scores using the two-way ANOVA with repeated measurements differed among the five groups (F = 4.046, df = 4, 213, P < 0.005). The VAS scores with one-way ANOVA differed among the five groups 30 min postoperatively (F = 4.542, df = 4, 58, P < 0.003), being higher in the FA (6.5 +/- 1.8) and SA (5.9 +/- 2.1) groups than in the FC (3.2 +/- 2.5) group, and at 120 min postoperatively (F = 3.217, df = 4, 18, P < 0.05), being higher in the FA than in the FB group (6.1 +/- 1.5 and 2.6 +/- 1.9 respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
-
Randomized Controlled Trial Clinical Trial
Quantifying the effect of enflurane on atracurium infusion requirements.
The present study was designed to evaluate the interaction between atracurium and enflurane in 40 adult surgical patients using closed-loop feedback control of infusions of atracurium. Anaesthesia was induced with thiopentone and fentanyl and intubation was facilitated with atracurium 0.5 mg.kg-1 lean body mass. During the first 90 min, anaesthesia was maintained with nitrous oxide in oxygen (2:1) and fentanyl. ⋯ Patient characteristics and controller performance, i.e., the ability of the controller to maintain the neuromuscular blockade constant at the setpoint, did not differ among groups. In Group II ISS decreased from 0.33 +/- 0.12 to 0.26 +/- 0.08 mg.kg-1.hr-1 (P < 0.01), in Group III from 0.32 +/- to 0.12 to 0.24 +/- 0.08 mg.kg-1.hr-1 (P < 0.001) and in Group IV from 0.29 +/- 0.09 to 0.21 +/- 0.09 mg.kg-1.hr-1 (P < 0.001). In the control group atracurium requirements remained unchanged throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)
-
Randomized Controlled Trial Clinical Trial
Midazolam coinduction does not delay discharge after very brief propofol anaesthesia.
Previous reports have demonstrated synergism of midazolam and propofol for induction of anaesthesia in humans. We tested the hypothesis that in the presence of alfentanil, the combination of midazolam with propofol for a very brief operative procedure would not affect the recovery phase. During pre-oxygenation, 64 outpatients scheduled for dilatation and curettage received placebo, or low-dose midazolam (0.03 mg.kg-1), or high-dose midazolam (0.06 mg.kg-1) iv, in a randomized double-blind manner. ⋯ Midazolam delayed time to eye-opening (P = 0.02) but not time to discharge-readiness. This study had an 80% power to detect a 39 min difference in time to discharge-readiness. We conclude that midazolam propofol co-induction in the presence of alfentanil delays eye-opening, but does not delay discharge after anaesthesia.
-
Randomized Controlled Trial Clinical Trial
Enhancement of pressor response to intravenous phenylephrine following oral clonidine medication in awake and anaesthetized patients.
Clonidine, an alpha 2-adrenergic agonist, augments the pressor response to intravenous ephedrine. If this effect is partly due to clonidine-induced potentiation of alpha 1-adrenoceptor-mediated vasoconstriction, it is also assumed that clonidine would enhance the pressor effect of phenylephrine as an alpha 1-adrenergic agonist. The authors studied haemodynamic responses to intravenous phenylephrine in 80 patients who received either preanaesthetic medication with clonidine approximately 5 micrograms.kg-1 po (clonidine group, n = 40), or no medication (control group, n = 40). ⋯ Oral clonidine preanaesthetic medication, 5 micrograms.kg-1, augments the pressor responses to phenylephrine 2 micrograms.kg-1 iv in awake and anaesthetized patients. These results suggest that the enhancement of the pressor responses to phenylephrine following oral clonidine may be due to clonidine-induced potentiation of alpha 1-adrenoceptor-mediated vasoconstriction. This implies that restoration of blood pressure can be achieved effectively by phenylephrine in hypotensive patients with clonidine premedication.