To the Editor, Global warming, considered one of the greatest health threats of the 21st century, is linked to greenhouse gas emissions. The major greenhouse gases-carbon dioxide (CO 2), methane, nitrous oxide, and chlorofluorocarbonshave been well studied and regulated. The contributions from the healthcare industry, however, have been largely ignored or excused under the guise of medical necessity. 1 Nevertheless, a considerable portion of hospital waste is generated in the operating room, and anesthesiologists are in an ideal position to take a leadership role to minimize the hospital-related negative environmental impact. Volatile anesthetic drugs are halogenated fluorocarbons and potent greenhouse gases, as measured by their global warming potential (GWP), which is a relative measure of how much heat a given gas traps in the atmosphere compared with a similar mass of CO 2. Because most volatile agents remain in the atmosphere for one to 15 years, 2 the GWP is often expressed over a 20-year time horizon (GWP 20). This value represents the amount of heat trapped by the gas over a 20-year period, compared with a similar mass of CO 2. For example, the GWP 20 values for desflurane, isoflurane, and sevoflurane are 6810, 1800, and 440, respectively. 2 The carbon dioxide equivalent (CDE 20) is the product of the GWP 20 and the quantity of the gas. Colloquially referred to as the ''carbon footprint,''

BACKGROUND: Dexmedetomidine is a highly selective α2-adrenergic agonist, which is increasingly used in pediatric anesthesia and intensive care. Potential adverse effects that have not been rigorously evaluated in children include its effects on blood glucose and serum potassium concentrations, which are relevant due to the associations of derangements of both parameters with undesired outcomes. We investigated the effects of 3 different doses of dexmedetomidine on these outcomes in a randomized controlled trial in children undergoing elective surgery. METHODS: Sixty-four American Society of Anesthesiologists I–II children were randomized to receive either dexmedetomidine 0.25 µg/kg, dexmedetomidine 0.5 µg/kg, dexmedetomidine 0.75 µg/kg, or 0 µg/kg (control), as a bolus administered over 60 seconds after induction of anesthesia. Changes in plasma glucose and serum potassium concentrations were measured in venous blood sampled before and at 15 and 30 minutes after study drug administration. Data were plotted within and between groups and analyzed using a constrained longitudinal data approach. RESULTS: Forty-nine children completed the study. Mean glucose levels at 15 and 30 minutes were elevated with estimated changes from baseline of 0.37 mmol/L (95% CI, 0.29–0.45 mmol/L) and 0.05 mmol/L (95% CI, 0.00–0.10 mmol/L), respectively. At 15 minutes, there was a linear dose–response relationship (1.07 mmol/L/μg/kg [95% CI, 0.57–1.58 mmol/L/μg/kg]), but there was no appreciable effect of dexmedetomidine at 30 minutes (0.15 mmol/L/μg/kg [95% CI, −0.40 to 0.70 mmol/L/μg/kg]). Potassium levels were depressed relative to baseline, with a mean difference at 15 minutes of −0.20 mEq/L (95% CI, −0.28 to −0.12 mEq/L) and at 30 minutes of −0.12 mEq/L (95% CI, −0.15 to −0.08 mEq/L), but there was no appreciable effect of dexmedetomidine at either time. CONCLUSIONS: Small elevations in glucose and decreases in potassium were observed after induction of anesthesia in children. The elevation in glucose at 15 minutes depended on the dose of dexmedetomidine administered. These preliminary data warrant further investigation.

Background: Dexmedetomidine is a useful anesthetic adjunct, increasingly popular during pediatric surgery and procedural sedation. Its half-life of 2-3 hours might prolong recovery and discharge times when compared with an un-supplemented propofol anesthetic. This may create an additional burden in a busy post-anesthetic care unit (PACU).Aim: To investigate whether intraoperative adjuvant dexmedetomidine delays PACU discharge in patients undergoing propofol anesthesia for day surgery or procedural investigations with minimal anticipated post-procedural pain. Methods:We conducted a retrospective review of outpatient procedures performed during a six-month period including pediatric patients, ASA physical status I-III, who underwent intravenous anesthesia with propofol and remifentanil for magnetic resonance imaging (MRI), strabismus repair, upper gastrointestinal endoscopy, or combined upper/lower gastrointestinal endoscopy. Patients receiving a sedative premedication, long-acting opioids, or volatile anesthetics for maintenance of anesthesia, were excluded. Duration of PACU stay was compared for patients who did or did not receive intraoperative dexmedetomidine in the four procedure groups.Results: Charts were reviewed for 359 patients; 130 (36%) received dexmedetomidine. Median differences in duration of PACU stay for dexmedetomidine versus nondexmedetomidine cases were: 5 minutes (95%CI 0 to 10, p=0.037) for MRI; 5 minutes (95%CI −3 to 15, p=0.258) for strabismus surgery; 7 minutes (95%CI 3 to 10, p<0.001) for upper endoscopy; and 5 minutes (95%CI 1 to 12, p=0.021) for combined upper/ lower endoscopy. Linear regression (F=61.1, adjusted R 2 =0.40) indicated a significant relationship between dexmedetomidine dose (estimate 14.6 minutes per μg/kg, 95%CI 8.2 to 21.1, p<0.001) and duration of PACU stay. Conclusion:We found evidence for a small association of intraoperative dexmedetomidine with duration of recovery from propofol anesthesia for a set of common outpatient procedures, with a potential dose relationship equivalent to approximately 15 minutes delay per μg/kg dexmedetomidine administered. Future research into the benefits of dexmedetomidine in pediatric anesthesia should further evaluate this relationship.

BACKGROUND: Dexmedetomidine is a highly selective α2-adrenergic agonist, which is increasingly used in pediatric anesthesia and intensive care. Potential adverse effects that have not been rigorously evaluated in children include its effects on myocardial repolarization, which is important given that the drug is listed as a possible risk factor for torsades de pointes. We investigated the effect of 3 different doses of dexmedetomidine on myocardial repolarization and transmural dispersion in children undergoing elective surgery with total IV anesthesia. METHODS: Sixty-four American Society of Anesthesiologists I–II children 3–10 years of age were randomized to receive dexmedetomidine 0.25 µg/kg, 0.5 µg/kg, 0.75 µg/kg, or 0 µg/kg (control), as a bolus administered over 60 seconds, after induction of anesthesia. Pre- and postintervention 12-lead electrocardiograms were recorded. The interval between the peak and the end of the electrocardiogram T wave (Tp-e; transmural dispersion) and heart rate–corrected QT intervals (myocardial repolarization) were measured by a pediatric electrophysiologist blinded to group allocation. Data were analyzed using an analysis of covariance regression model. The study was powered to detect a 25-millisecond difference in Tp-e. RESULTS: Forty-eight children completed the study, with data analyzed from 12 participants per group. There were no instances of dysrhythmias. Tp-e values were unaffected by dexmedetomidine administration at any of the studied doses (F = 0.09; P = .96). Mean (99% CI) within-group differences were all <2 milliseconds (−5 to 8). Postintervention, corrected QT interval increased in the control group, but decreased in some dexmedetomidine groups (F = 7.23; P < .001), specifically the dexmedetomidine 0.5 and 0.75 µg/kg doses. Within groups, the mean (99% CI) differences between pre- and postintervention corrected QT interval were 12.4 milliseconds (−5.8 to 30.6) in the control group, −9.0 milliseconds (−24.9 to 6.9) for dexmedetomidine 0.25 µg/kg, −18.6 milliseconds (−33.7 to −3.5) for dexmedetomidine 0.5 µg/kg, and −14.1 milliseconds (−27.4 to −0.8) for dexmedetomidine 0.75 µg/kg. CONCLUSIONS: Of the bolus doses of dexmedetomidine studied, none had an effect on Tp-e and the dexmedetomidine 0.5 and 0.75 µg/kg doses shortened corrected QT intervals when measured at 1 minute after dexmedetomidine bolus injection during total IV anesthesia. There is no evidence for an increased risk of torsades de pointes in this context.