Dexmedetomidine for patients with croup.
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ABSTRACT:
SUBMITTER: Tsuboi N
PROVIDER: S-EPMC8426286 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BACKGROUND:Glucocorticoids are commonly used for croup in children. This is an update of a Cochrane Review published in 1999 and previously updated in 2004 and 2011. OBJECTIVES:To examine the effects of glucocorticoids for the treatment of croup in children aged 0 to 18 years. SEARCH METHODS:We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (the Cochrane Library, Issue 2, 2018), which includes the Cochrane Acute Respiratory Infections Group's Specialised Register, Ovid MEDLINE Epub Ahead of Print, In-Process & Other Non-Indexed Citations and Ovid MEDLINE (1946 to 3 April 2018), and Embase (Ovid) (1996 to 3 April 2018, week 14), and the trials registers ClinicalTrials.gov (3 April 2018) and the World Health Organization International Clinical Trials Registry Platform (ICTRP, 3 April 2018). We scanned the reference lists of relevant systematic reviews and of the included studies. SELECTION CRITERIA:We included randomised controlled trials (RCTs) that investigated children aged 0 to 18 years with croup and measured the effects of glucocorticoids, alone or in combination, compared to placebo or another pharmacologic treatment. The studies needed to report at least one of our primary or secondary outcomes: change in croup score; return visits, (re)admissions or both; length of stay; patient improvement; use of additional treatments; and adverse events. DATA COLLECTION AND ANALYSIS:One author extracted data from each study and another verified the extraction. We entered the data into Review Manager 5 for meta-analysis. Two review authors independently assessed risk of bias for each study using the Cochrane 'Risk of bias' tool and the certainty of the body of evidence for the primary outcomes using the GRADE approach. MAIN RESULTS:We added five new RCTs with 330 children. This review now includes 43 RCTs with a total of 4565 children. We assessed most (98%) studies as at high or unclear risk of bias. Compared to placebo, glucocorticoids improved symptoms of croup at two hours (standardised mean difference (SMD) -0.65, 95% confidence interval (CI) -1.13 to -0.18; 7 RCTs; 426 children; moderate-certainty evidence), and the effect lasted for at least 24 hours (SMD -0.86, 95% CI -1.40 to -0.31; 8 RCTs; 351 children; low-certainty evidence). Compared to placebo, glucocorticoids reduced the rate of return visits or (re)admissions or both (risk ratio 0.52, 95% CI 0.36 to 0.75; 10 RCTs; 1679 children; moderate-certainty evidence). Glucocorticoid treatment reduced the length of stay in hospital by about 15 hours (mean difference -14.90, 95% CI -23.58 to -6.22; 8 RCTs; 476 children). Serious adverse events were infrequent. Publication bias was not evident. Uncertainty remains with regard to the optimal type, dose, and mode of administration of glucocorticoids for reducing croup symptoms in children. AUTHORS' CONCLUSIONS:Glucocorticoids reduced symptoms of croup at two hours, shortened hospital stays, and reduced the rate of return visits to care. Our conclusions have changed, as the previous version of this review reported that glucocorticoids reduced symptoms of croup within six hours.
| S-EPMC6513469 | biostudies-literature
Project description:Croup is a clinical diagnosis, and the available evidence suggests that, except in rare cases, ancillary testing, such as radiologic imaging, is not helpful. Given the paucity of inpatient-specific evidence for croup care, we hypothesized that there would be marked variability in the use of not routinely indicated resources (NRIRs). Our primary study objective was to describe the variation and predictors of variation in the use of NRIRs. This was a retrospective cohort study that used the Pediatric Health Information System database of generally healthy inpatients with croup aged 6 months to 15 years who were admitted between January 1, 2012 and September 30, 2014. We measured variability in the use of NRIRs: chest and lateral neck radiographs, viral testing, parenteral steroids, and antibiotics. Risk-adjusted analysis was used to compare resource utilization adjusted for hospital-specific effects and average case mix. The cohort included 26 hospitals and 6236 patients with a median age of 18 months. Nine percent of patients required intensive care services, and 3% had a 30-day readmission for croup. We found marked variability in adjusted and unadjusted utilization across hospitals for all resources. In the risk-adjusted analysis, hospital-specific effects rather than patient characteristics were the main predictor of variability in the use of NRIRs. We observed an up to fivefold difference in NRIR utilization attributable to hospital-level practice variability in inpatient croup care. This study highlights a need for inpatient-specific evidence and quality-improvement interventions to reduce unnecessary utilization and to improve patient outcomes.
| S-EPMC5369680 | biostudies-literature
Project description:OBJECTIVE:To determine the effectiveness of glucocorticoid treatment in children with croup. DESIGN:Meta-analysis of randomised controlled trials that examine the effectiveness of glucocorticoid treatment in children with croup. MAIN OUTCOME MEASURES:Score on scale measuring severity of croup, use of cointerventions (adrenaline (epinephrine), antibiotics, or supplemental glucocorticoids), length of stay in accident and emergency or in hospital, and rate of hospitalisation. RESULTS:Twenty four studies met the inclusion criteria. Glucocorticoid treatment was associated with an improvement in the croup severity score at 6 hours with an effect size of -1.0 (95% confidence interval -1.5 to -0.6) and at 12 hours -1.0 (-1.6 to -0.4); at 24 hours this improvement was no longer significant (-1.0, -2.0 to 0.1). There was a decrease in the number of adrenaline treatments needed in children treated with glucocorticoids: a decrease of 9% (95% confidence interval 2% to 16%) among those treated with budesonide and of 12% (4% to 20%) among those treated with dexamethasone. There was also a decrease in the length of time spent in accident and emergency (-11 hours, 95% confidence interval -18 to 4 hours), and for inpatients hospital stay was reduced by 16 hours (-31 to 1 hour). Publication bias seems to play a part in these results. CONCLUSIONS:Dexamethasone and budesonide are effective in relieving the symptoms of croup as early as 6 hours after treatment. Fewer cointerventions are used and the length of time spent in hospital is decreased in patients treated with glucocorticoids.
| S-EPMC28209 | biostudies-literature
Project description:IntroductionForeign body (FB) aspiration is one of the causes of respiratory distress in infants is an extremely dangerous and potentially life-threatening event. The diagnosis of FB aspiration is difficult because the signs and symptoms vary according to the degree of airway blockage or location of the FB.Patient concernsAn 11-month-old female infant visited a hospital because of a sudden onset cough. She was relatively healthy without fever, rhinorrhea cyanosis, or poor feeding. On physical examination, auscultation revealed inspiratory stridor without wheezing and crackles.DiagnosisCroup was suspected when considering the history, physical examination, and imaging. However, she did not respond to a 4-day course of treatment for croup. Flexible laryngoscopic examination was performed, and we identified a thin, flat, and sharp FB embedded in the subglottic region.InterventionsEmergency surgery was performed to remove the FB. Short-term intravenous corticosteroids and antibiotics were used to prevent laryngeal swelling and aspiration pneumonia.OutcomesOne week after the procedure, the laryngeal mucosa had completely healed.ConclusionFB aspiration should be considered in an infant with an impression of croup. In particular, if there is no response to medical or conservative treatment for croup, further evaluation is needed.
| S-EPMC8284713 | biostudies-literature
Project description:Dexmedetomidine (DEX) is a fairly new alfa2-agonist which has been increasingly used in recent years for analgosedation, mostly because it offers a unique ability of providing both moderate level of sedation and analgesia without respiratory depression. Despite of many papers published, there are still only a few concerning the PK of the drug given as long-term infusion in ICU patients. The aim of this work was to characterize the population pharmacokinetics of dexmedetomidine and to investigate the potential benefits of individualization of drug dosing based on patient characteristics in the heterogeneous group of medical and surgical patients staying in intensive care unit. This study was performed in the group of 17 males and 10 females patients with a median age of 59.5 years and median body weight of 75 kg. Blood samples for dexmedetomidine assay were collected from arterial catheter, during and after discontinuation of a standard infusion, that ranged from 24 to 102 h. The following covariates were examined to influence dexmedetomidine PK: age, sex, body weight, patients' health status described by Sequential Organ Failure Assessment Score (SOFA), inotropes usage, and infusion duration. The dexmedetomidine PK was best described by a two-compartment model. The typical values of PK parameters were estimated as 27 L for the volume of the central compartment, 87.6 L for the volume of the peripheral compartment, 38.5 L/h (9.2 mL/min/kg for a 70 kg patient) for systemic clearance and 46.4 L/h for the distribution clearance. Those values are consistent with literature findings. We were unable to show any significant relationship between collected covariates and dexmedetomidine PK. This study does not provide sufficient evidence to support the individualization of dexmedetomidine dosing based on age, sex, body weight, SOFA, and infusion duration.
| S-EPMC5845053 | biostudies-literature
Project description:Background and objectivesAlthough the pharmacokinetics of dexmedetomidine in healthy volunteers have been studied, there are limited data about the pharmacokinetics of long-term administration of dexmedetomidine in critically ill patients.MethodsThis population pharmacokinetic analysis was performed to quantify the pharmacokinetics of dexmedetomidine in critically ill patients following infusions up to 14 days in duration. The data consisted of three phase III studies (527 patients with sparse blood sampling, for a total of 2,144 samples). Covariates were included in a full random-effects covariate model and the most important covariate relationships were tested separately. The linearity of dexmedetomidine clearance was evaluated by observing steady-state plasma concentrations acquired at various infusion rates.ResultsThe data were adequately described with a one-compartment model. The clearance of dexmedetomidine was 39 (95 % CI 37-41) L/h and volume of distribution 104 (95 % CI 93-115) L. Both clearance and volume of distribution were highly variable between patients (coefficients of variation of 62 and 57 %, respectively), which highlights the importance of dose titration by response. Covariate analysis showed a strong correlation between body weight and clearance of dexmedetomidine. The clearance of dexmedetomidine was constant in the dose range 0.2-1.4 μg/kg/h.ConclusionsThe pharmacokinetics of dexmedetomidine are dose-proportional in prolonged infusions when dosing rates of 0.2-1.4 μg/kg/h, recommended by the Dexdor(®) summary of product characteristics, are used.
| S-EPMC3717151 | biostudies-literature
Project description:This study retrospectively investigated the effect of dexmedetomidine on outcomes of patients undergoing coronary artery bypass graft (CABG) surgery.Retrospective investigation.Patients from a single tertiary medical center.A total of 724 patients undergoing CABG surgery met the inclusion criteria and were categorized into 2 groups: 345 in the dexmedetomidine group (DEX) and 379 in the nondexmedetomidine group (Non-DEX).Perioperative dexmedetomidine was used as an intravenous infusion (0.24 to 0.6 µg/kg/hour) initiated after cardiopulmonary bypass and continued for less than 24 hours postoperatively in the intensive care unit.Major outcome measures of this study were in-hospital, 30-day and 1-year all-cause mortality, delirium and major adverse cardiocerebral events. Perioperative dexmedetomidine infusion was associated with significant reductions in in-hospital, 30-day, and 1-year mortalities, compared with the patients who did not received dexmedetomidine. In-hospital, 30-day, and 1-year mortalities were 1.5% and 4.0% (adjusted odds ratio [OR], 0.332; 95% CI, 0.155 to 0.708; p = 0.0044), 2.0% and 4.5% (adjusted OR, 0.487; 95% CI, 0.253 to 0.985; p = 0.0305), and 3.2% and 6.9% (adjusted OR 0.421; 95% CI, 0.247 to 0.718, p = 0.0015), respectively. Perioperative dexmedetomidine infusion was associated with a reduced risk of delirium from 7.9% to 4.6% (adjusted OR, 0.431; 95% CI, 0.265-0.701; p = 0.0007).Dexmedetomidine infusion during CABG surgery was more likely to achieve improved in-hospital, 30-day, and 1-year survival rates, and a significantly lower incidence of delirium.
| S-EPMC4402998 | biostudies-literature
Project description:Perioperative hemodynamic fluctuations are seen more often in hypertensive patients than in normotensive patients. The purpose of our study was to investigate the perioperative hemodynamic effects of dexmedetomidine and midazolam used for premedication in hypertensive patients relative to each other and in comparison to normotensive patients.One-hundred-forty female, normotensive or hypertensive patients undergoing myomectomies or hysterectomies. They were randomly enrolled into the subgroups: Group ND (normotensive-dexmedetomidine); Group HD (hypertensive-dexmedetomine); Group NM (normotensive-midazolam); Group HM (hypertensive- midazolam). Dexmedetomidine was administered at a concentration of 0.5 ?g.kg(-1), and midazolam was administered at a concentration of 0.025 ?g.kg(-1) via intravenous (IV) infusion before the induction of anaesthesia. Haemodynamic parameters were recorded at several times (T(beginning), T(preop5 min), T(preop 10 min), T(induction), T(intubation), T(intubation 5 min), T(initial surgery), T(surgery 15 min), T(surgery 30 min), T(extubation), T(extubation 5 min)). Propofol amount for induction, time between induction and initial surgery, demand of antihypertensive therapy, rescue atropine were recorded. Quantitative clinical and demographic characteristics were compared using One Way ANOVA. The values were compared using One-way Analysis of Variance. Additionally periodic variations were examined by One way Repeated Measures Analysis of Variance for groups separately.SBP was significantly different between normotensive and hypertensive groups at the following time points: T(preop 5 min), T(preop 10 min), T(induction), T(intubation), T(intubation 5 min) and T(initial surgery). MBP was significantly different in the hypertensive groups at T(induction), T(intubation), T(intubation 5 min), T(initial surgery), T(surgery 15 min), T(surgery 30 min), T(extubation) and T(extubation 5 min). The perioperative requirements for antihypertensive drugs were significantly higher in Group HM.In the hypertensive patients, dexmedetomidine premedication provides better hemodynamic stability compared with midazolam, and because it decreases the antihypertensive requirements, its use might be beneficial.Clinicaltrials.gov identifier: NCT02058485.
| S-EPMC4279802 | biostudies-literature
Project description:In critically ill patients with neurologic disease, pupil examination abnormalities can signify evolving intracranial pathology. Analgesic and sedative medications (analgosedatives) target pupillary pathways, but it remains unknown how analgosedatives alter pupil findings in the clinical care setting. We assessed dexmedetomidine and other analgosedative associations with pupil reactivity and size in a heterogeneous cohort of critically ill patients with acute intracranial pathology.DesignRetrospective cohort study.SettingTwo neurologic ICUs between 2016 and 2018.PatientsCritically ill adult patients with pupil measurements within 60 minutes of analgosedative administration. Patients with a history of intrinsic retinal pathology, extracranial injury, inaccessible brain imaging, or no Glasgow Coma Scale (GCS) data were excluded.InterventionsNone.Measurements and main resultsWe used mixed-effects linear regression accounting for intrapatient correlations and adjusting for sex, age, GCS score, radiographic mass effect, medication confounders, and ambient light. We tested the association between an initiation or increased IV infusion of dexmedetomidine and pupil reactivity (Neurologic Pupil Index [NPi]) and resting pupil size (mm) obtained using NeurOptics NPi-200 (NeurOptics, Irvine, CA) pupillometer. Of our 221 patients with 9,897 pupil observations (median age, 60 [interquartile range, 50-68]; 59% male), 37 patients (166 pupil observations) were exposed to dexmedetomidine. Dexmedetomidine was associated with higher average NPi (β = 0.18 per 1 unit increase in rank-normalized NPi ± 0.04; p < 0.001) and smaller pupil size (β = -0.25 ± 0.05; p < 0.001). Exploratory analyses revealed that acetaminophen was associated with higher average NPi (β = 0.04 ± 0.02; p = 0.02) and that most IV infusion analgosedatives including propofol, fentanyl, and midazolam were associated with smaller pupil size.ConclusionsDexmedetomidine is associated with higher pupil reactivity (high NPi) and smaller pupil size in a cohort of critically ill patients with neurologic injury. Familiarity with expected pupil changes following analgosedative administration is important for accurate interpretation of pupil examination findings, facilitating optimal management of patients with acute intracranial pathology.
| S-EPMC9243241 | biostudies-literature
Project description:Only limited information exists on the pharmacokinetics of prolonged (> 24 hours) and high-dose dexmedetomidine infusions in critically ill patients. The aim of this study was to characterize the pharmacokinetics of long dexmedetomidine infusions and to assess the dose linearity of high doses. Additionally, we wanted to quantify for the first time in humans the concentrations of H-3, a practically inactive metabolite of dexmedetomidine.Thirteen intensive care patients with mean age of 57 years and Simplified Acute Physiology Score (SAPS) II score of 45 were included in the study. Dexmedetomidine infusion was commenced by using a constant infusion rate for the first 12 hours. After the first 12 hours, the infusion rate of dexmedetomidine was titrated between 0.1 and 2.5 ?g/kg/h by using predefined dose levels to maintain sedation in the range of 0 to -3 on the Richmond Agitation-Sedation Scale. Dexmedetomidine was continued as long as required to a maximum of 14 days. Plasma dexmedetomidine and H-3 metabolite concentrations were measured, and pharmacokinetic variables were calculated with standard noncompartmental methods. Safety and tolerability were assessed by adverse events, cardiovascular signs, and laboratory tests.The following geometric mean values (coefficient of variation) were calculated: length of infusion, 92 hours (117%); dexmedetomidine clearance, 39.7 L/h (41%); elimination half-life, 3.7 hours (38%); and volume of distribution during the elimination phase, 223 L (35%). Altogether, 116 steady-state concentrations were found in 12 subjects. The geometric mean value for clearance at steady state was 53.1 L/h (55%). A statistically significant linear relation (r2 = 0.95; P < 0.001) was found between the areas under the dexmedetomidine plasma concentration-time curves and cumulative doses of dexmedetomidine. The elimination half-life of H-3 was 9.1 hours (37%). The ratio of AUC0-? of H-3 metabolite to that of dexmedetomidine was 1.47 (105%), ranging from 0.29 to 4.4. The ratio was not statistically significantly related to the total dose of dexmedetomidine or the duration of the infusion.The results suggest linear pharmacokinetics of dexmedetomidine up to the dose of 2.5 ?g/kg/h. Despite the high dose and prolonged infusions, safety findings were as expected for dexmedetomidine and the patient population.ClinicalTrials.gov: NCT00747721.
| S-EPMC3334808 | biostudies-literature