Dexmedetomidine Alleviates Propofol Infusion Syndrome-Induced Myocardial Injury through Inhibiting Ferroptosis Associated with Accumulation of Reactive Oxygen Species.
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To observe the effect of dexmedetomidine (Dex) on propofol infusion syndrome (PRIS)-induced myocardial injury and explore the roles of ferroptosis and accumulation of reactive oxygen species (ROS).Keywords:
Dexmedetomidine
Cardiotoxicity
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Aims & Objectives: The use of sedatives in mechanically ventilated children is common. Adult studies have demonstrated that early deep sedation significantly predicts mortality and other studies suggest detrimental effects of benzodiazepines on developing brains. Dexmedetomidine has reported neuroprotection and arousable sedation, however there is little evidence for its use in PICU. We aimed to assess the feasibility and safety of administering dexmedetomidine compared to standard sedation. Methods Pilot prospective, multicentre, randomised, controlled trial on mechanically ventilated children for greater than 24 hours. 57 patients were randomised to dexmedetomidine targeted to light sedation (SBS -1 to +1) or standard sedation based on local practice across five sites. Main feasibility outcomes were time to randomisation and proportion of SBS assessments (first 48 hours) in the light/deep sedation range. Safety outcomes were incidence of adverse events, vasopressor and device removal. Results Randomisation occurred within a median (IQR) of 6.25 hrs (2.35,9) after intubation. Patients in the dexmedetomidine sedation (n=29) mean (SD) PIM3 score was 0.032 (0.034) versus 0.035 (0.066; p=0.83) in the standard sedation (n=28). A significantly higher proportion of SBS assessments were in the light sedation range (-1 to +1) in the first 48 hours (289/385 [75.06%] vs 228/361 [63.16%]; p=0.001) with dexmedetomidine. There was no difference in vasopressor use or accidental device removal. One SAE was reported in the dexmedetomidine group. Conclusions Dexmedetomidine for sedation was feasible, appeared safe, and achieved early light sedation whilst minimising benzodiazepine exposure. The findings of this study justify further investigation of the use of dexmedetomidine for early goal directed sedation.
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We aimed to safely introduce dexmedetomidine into a nurse-led sedation service for magnetic resonance imaging in children. Secondary aims were to increase the number of children eligible for sedation and to increase the actual number of children having sedation performed by our nurse sedation team. We analysed 1768 consecutive intravenous and 219 intranasal dexmedetomidine sedation episodes in infants, children and adolescents having magnetic resonance imaging scans between March 2016 and March 2022. The overall sedation success rate was 98.4%, with a 98.9% success rate for intravenous dexmedetomidine and a 95.0% success rate for intranasal dexmedetomidine. The incidence of scan interruption during intravenous and intranasal dexmedetomidine sedation was 8.8% and 21.9%, respectively. We conclude that paediatric sedation with dexmedetomidine for magnetic resonance scanning is safe and successful.
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Dexmedetomidine
Midazolam
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Acquisition of transthoracic echocardiographic (TTEcho) images in children often requires sedation. The optimal sedative for TTEcho has not been determined. Children with congenital heart disease are repeatedly exposed to sedatives and anesthetics that may affect brain development. Dexmedetomidine, which in animals alters brain structure to a lesser degree, may offer advantages in this vulnerable population.A prospective, randomized, double-blind trial enrolled 280 children 3-24 months of age undergoing outpatient TTEcho, comparing 2.5 µg·kg intranasal dexmedetomidine to 5 mg·kg oral pentobarbital. Rescue sedation, for both groups, was intranasal dexmedetomidine 1 µg·kg. The primary outcome was adequate sedation within 30 minutes without rescue sedation, assessed by blinded personnel. Secondary outcomes included number of sonographer pauses, image quality in relation to motion artifacts, and parental satisfaction.Success rates with a single dose were not different between sedation techniques; 85% in the pentobarbital group and 84% in the dexmedetomidine group (P = .8697). Median onset of adequate sedation was marginally faster with pentobarbital (16.5 [interquartile range, 13-21] vs 18 [16-23] minutes for dexmedetomidine [P = .0095]). Time from drug administration to discharge was not different (P = .8238) at 70.5 (64-83) minutes with pentobarbital and 70 (63-82) minutes with dexmedetomidine. Ninety-five percent of sedation failures with pentobarbital and 100% of dexmedetomidine failures had successful rescue sedation with intranasal dexmedetomidine.Intranasal dexmedetomidine was comparable to oral pentobarbital sedation for TTEcho sedation in infants and did not increase the risk of clinically important adverse events. Intranasal dexmedetomidine appears to be an effective "rescue" sedative for both failed pentobarbital and dexmedetomidine sedation. Dexmedetomidine could be a safer option for repeated sedation in children, but further studies are needed to assess long-term consequence of repeated sedation in this high-risk population.
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Depression
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Intravenous pentobarbital has been used in the past to sedate pediatric patients in preparation for MRI; however, the drug has unpredictable sedation time. Dexmedetomidine, because of its short half-life, is gaining popularity for pediatric MRI sedation in settings where the use of propofol is restricted for nonanesthesiologists. The objective was to compare induction time, recovery time, total sedation time, sedation failure rate, and adverse outcomes of patients sedated with pentobarbital and dexmedetomidine in preparation for pediatric MRI.We reviewed a sedation database that contains clinical data for all children undergoing MRI studies while sedated with pentobarbital or dexmedetomidine between May 15, 2008, and October 30, 2010.During the study period, 281 sedations were induced in preparation for MRI (160 with pentobarbital, and 121 with dexmedetomidine). The 2 groups were comparable with regard to age, weight, gender, and American Society of Anesthesiologists status. The dexmedetomidine group had a significantly shorter recovery time (39 ± 21 vs 49 ± 27 minutes [P = .002]) and total sedation time (107 ± 28 vs 157 ± 44 minutes [P = .0001]). Induction time was similar between the groups. The adverse event rate for the study population was 3%.Dexmedetomidine and pentobarbital can both be used successfully for MRI sedation in children. However, dexmedetomidine had a significantly shorter recovery time and total sedation time in our population.
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Summary Objectives: To examine the effects of dexmedetomidine sedation on EEG background and epileptiform activity in children, comparing it to natural sleep. Aim: To provide quantitative and qualitative descriptions of the effect of dexmedetomidine sedation on the EEG of children. Background: Children with intractable epilepsy admitted for surgery undergo 5 days of continuous EEG monitoring as well as nuclear medicine imaging studies with dexmedetomidine for sedation. Continuous EEG monitoring of each child during both natural sleep and dexmedetomidine‐induced sedation provides a unique opportunity to evaluate the effects of dexmedetomidine on the EEG of children. Materials/methods: Sixteen children undergoing dexmedetomidine sedation for nuclear medicine studies and simultaneous continuous EEG monitoring were studied. EEG segments during sedation were compared to samples of naturally occurring stage II sleep from the same child. Standard visual EEG analysis, quantification of delta, theta, alpha, beta, and total RMS power, number and location of spike foci, and frequency of spike activity were compared. Results: The EEG during dexmedetomidine sedation resembled stage II sleep. During sedation, statistically significant increases in power of 16% for theta ( P = 0.01), 21% for alpha ( P = 0.03), and 40% for beta ( P < 0.01) were observed, but not for delta ( P = 0.63) or total EEG power ( P = 0.61). Spike frequency increased by 47% during sedation but no new spike foci or seizures were observed. Conclusion: Dexmedetomidine sedation elicited an EEG pattern similar to that of Stage II sleep with modest increases in theta, alpha, and beta activity. Dexmedetomidine does not hinder interpretation of the EEG, suggesting that it may be a uniquely useful agent for EEG sedation in children.
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Alpha (finance)
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Objective To observe the sedative effect of dexmedetomidine on the patients with Cerebral Lesions in ICU.Methods Dexmedetomidine is given by continuous infusion following a load dose to provide satifactory sedation in 50 patients with Cerebral Lesions.Maintain Ramsay score 2 ～ 5 points.Results The sedation efficiency was(86.6 ± 7.3) %.The average infusion rate of midazolam during the sedative period was (0.52 +0.13) μg/(kg·h),while the signs of life remained stable.Conclusion Dexmedetomidine can provide satisfactory sedation and unique advantage for ICU patients.
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Midazolam
Continuous Infusion
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Dexmedetomidine has the favorable properties of sedation, sympatholysis, analgesia, and a low risk of apnea. These properties suggest that dexmedetomidine may be useful in procedural sedation. In view of this, we conducted a pilot trial to determine the feasibility of using dexmedetomidine as a sole agent for providing sedation during awake diagnostic flexible bronchoscopy. Patients presenting for awake diagnostic flexible bronchoscopy consented to participate in a trial of dexmedetomidine sedation for the procedure. In addition to local anesthetic topicalization of the airways, dexmedetomidine was infused at 0.5 μg/kg over 10 minutes followed by an infusion of 0.2 to 0.7 μg/kg/h titrating to a Ramsay Sedation Scale score of 3. Hemodynamic parameters (heart rate, blood pressure), oxygenation status (pulse oximetry), adverse events, use of rescue sedation, and patient and proceduralist satisfaction were recorded during the trial. Five of 9 recruited patients required rescue sedation to allow the procedure to proceed. Dexmedetomidine as a sole agent at an infusion of 0.5 μg/kg over 10 minutes followed by an infusion of 0.2 to 0.7 μg/kg/h is unable to provide adequate sedation for awake diagnostic flexible bronchoscopy without the need for rescue sedation in a large proportion of patients.
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