A systematic review of outcomes in postoperative pain studies in paediatric and adolescent patients: towards development of a core outcome set.

Systematic reviews of postoperative pain in children have called into question the consistency of outcomes measured by clinical triallists as well as the measurement instruments used for assessment. Core outcome set methodology may be a solution to improve standardisation. This study provides an evidence-based foundation for the development of a core outcome set for paediatric postoperative pain studies. We searched ClinicalTrials.gov to identify relevant postoperative pain studies in children. The search yielded 300 registered trials. The following data were then extracted from each of the trials: phase of trial; study type; study design; sample size; all outcomes; whether the outcome was listed as primary, secondary, or tertiary; the measurement instrument for each reported outcome; the specific metric for each outcome; and the type of clinical procedure. Following screening, 134 studies were included in our study. Pain measurement was the most commonly reported outcome (n = 123), followed by total postoperative analgesic dosage (n = 83) and side-effects (n = 25). Temporal trends indicated that pain assessment and unexpected events increased in use between 2000 and 2016, whereas postoperative analgesia measurement decreased. We found a lack of standardisation among outcomes and measurement instruments in paediatric postoperative pain studies. Development of a core outcome set may improve the quality of future trials and allow for more accurate study-to-study comparisons.

Postoperative beneficial effects of esmolol in treated hypertensive patients undergoing laparoscopic cholecystectomy.

BACKGROUND: In an attempt to decrease haemodynamic instability and early postoperative complications such as nausea, vomiting, and pain, esmolol was added to the routine alfentanil infusion of patients with treated hypertension undergoing laparoscopic cholecystectomy. METHODS: Forty consecutive ASA class II patients with controlled hypertension about to undergo laparoscopic cholecystectomy were randomized into two groups: an esmolol group (Group E, n=20) was given a 1 mg kg(-1) bolus of esmolol and a placebo group (Group P, n=20) was given an identical volume of Ringer's lactate. The rate of esmolol infusion was adjusted to keep the heart rate between 65 and 75 beats min(-1) and was 5-10 microg kg(-1) min(-1) throughout the procedure. After operation, patients reported their nausea using a four-point scale. RESULTS: Esmolol had an opioid-sparing effect intraoperatively (P=0.001). Postoperative requirements for antiemetics were significantly less in the esmolol group, with no antiemetics given to eight patients. In the placebo group, however, all patients required at least one dose of antiemetic (P=0.007). The frequency of PONV did not correlate to the amounts of alfentanil, propofol, postoperative antiemetics consumed, or to female gender, non-smoking status, and history of PONV or motion sickness. Postoperative analgesic consumption in Group E was significantly lower than in Group P (P=0.012). CONCLUSIONS: Esmolol had an opioid-sparing effect in the intraoperative and immediate postoperative period in hypertensive patients undergoing laparoscopy. When combined with alfentanil, it was more effective than placebo in decreasing early PONV.

Midazolams cardiac depressant effects and their lack of reversal by flumazenil in isolated rabbit hearts.

Midazolam is known to cause a dose-dependent increase and decrease in the contractile force of the myocardium. Whether flumazenil can reverse these effects of midazolam remains unclear. In this study, we determined the cardiac effects of midazolam and the counter effect of flumazenil on midazolam-induced myocardial depression in isolated rabbit hearts. Rabbit hearts were isolated and perfused using the Langendorff technique, and left ventricle pressure and heart rate were measured by a pressure transducer in the left ventricle. One set of hearts were perfused with increasing concentrations of midazolam for 10 min, another set were perfused with concomitant midazolam and flumazenil. Concentrations of 5, 10, 20 and 50 microM midazolam decreased left ventricle pressure significantly (P < 0.01, P < 0.05, P < 0.01, P < 0.01, respectively). Heart rates decreased with concentrations of 10, 20 and 50 microM midazolam (P < 0.01, P < 0.01, P < 0.05, respectively). Flumazenil had no effect on the midazolam-induced decrease in left ventricle pressure and heart rate. Midazolam decreased the cardiac contractile force and heart rate of isolated rabbit hearts in a concentration-dependent manner. The failure of flumazenil to reverse these effects suggest that this cardiac depressant effect of midazolam is not mediated through peripheral benzodiazepine receptors.