Dexmedetomidine in a Child with Methylphenidate Intoxication
Pediatric Intensive Care Unit, Section of Critical Care Medicine, Children's Hospital Colorado, 13123 East 17th Ave, Mail Stop 8414, Aurora, CO, 80045, USA, .The Indian Journal of Pediatrics (Impact Factor: 0.87). 05/2012; 80(4). DOI: 10.1007/s12098-012-0757-1
Methylphenidate intoxication, due to accidental ingestion, is a common occurrence in pediatrics. Symptoms of extreme agitation are typically controlled with benzodiazepines or barbiturates. There is, however, a legitimate risk of mechanical ventilation due to respiratory depression with increasing doses of benzodiazepines. The authors describe a case of 7-y-old girl with methylphenidate toxicity where dexmedetomidine was successfully used to manage agitation and cardiovascular stimulation without respiratory compromise.
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ABSTRACT: Introduction. Although clinical use of dexmedetomidine (DEX), an alpha2-adrenergic receptor agonist, has increased, its role in patients admitted to intensive care units secondary to toxicological sequelae has not been well established. Objectives. The primary objective of this study was to describe clinical and adverse effects observed in poisoned patients receiving DEX for sedation. Methods. This was an observational case series with retrospective chart review of poisoned patients who received DEX for sedation at an academic medical center. The primary endpoint was incidence of adverse effects of DEX therapy including bradycardia, hypotension, seizures, and arrhythmias. For comparison, vital signs were collected hourly for the 5 h preceding the DEX therapy and every hour during DEX therapy until the therapy ended. Additional endpoints included therapy duration; time within target Richmond Agitation Sedation Score (RASS); and concomitant sedation, analgesia, and vasopressor requirements. Results. Twenty-two patients were included. Median initial and median DEX infusion rates were similar to the commonly used rates for sedation. Median heart rate was lower during the therapy (82 vs. 93 beats/minute, p < 0.05). Median systolic blood pressure before and during therapy was similar (111 vs. 109 mmHg, p = 0.745). Five patients experienced an adverse effect per study definitions during therapy. No additional adverse effects were noted. Median time within target RASS and duration of therapy was 6.5 and 44.5 h, respectively. Seventeen patients (77%) had concomitant use of other sedation and/or analgesia with four (23%) of these patients requiring additional agents after DEX initiation. Seven patients (32%) had concomitant vasopressor support with four (57%) of these patients requiring vasopressor support after DEX initiation. Conclusion. Common adverse effects of DEX were noted in this study. The requirement for vasopressor support during therapy warrants further investigation into the safety of DEX in poisoned patients. Larger, comparative studies need to be performed before the use of DEX can be routinely recommended in poisoned patients.Clinical Toxicology 05/2014; 52(5). DOI:10.3109/15563650.2014.913175 · 3.67 Impact Factor
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ABSTRACT: There is considerable evidence for an increase of methylphenidate (MPH) abuse; thus, physicians might be confronted more frequently with MPH intoxications. Possible symptoms of intoxications with MPH are orofacial, stereotypic movements and tics as well as tachycardia, cardiac arrhythmias, arterial hypertension, hyperthermia, hallucinations and epileptic seizures. Here we report a patient who demonstrated somnolence as an uncommon clinical feature of MPH intoxication. The patient exhibited subnormal MPH serum levels (3 μg/l), however markedly increased serum levels of ritalinic acid (821 μg/l; inactive metabolite of MPH), that finally confirmed the initially suspected MPH intoxication. Due to the short half-life of orally administered MPH (t1/2~3 h) the sole measurement of MPH serum levels might be misleading concerning the proof of MPH overdosing in some cases. Parallel measurement of MPH and ritalinic acid is recommended in cases with suspected MPH intoxication and insufficient anamnestic data.Pharmacopsychiatry 08/2014; 47(6). DOI:10.1055/s-0034-1387700 · 1.85 Impact Factor
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ABSTRACT: Overdose of amphetamine, related derivatives, and analogues (ARDA) continues to be a serious worldwide health problem. Patients frequently present to the hospital and require treatment for agitation, psychosis, and hyperadrenegic symptoms leading to pathologic sequelae and mortality. To review the pharmacologic treatment of agitation, psychosis, and the hyperadrenergic state resulting from ARDA toxicity. MEDLINE, PsycINFO, and the Cochrane Library were searched from inception to September 2014. Articles on pharmacologic treatment of ARDA-induced agitation, psychosis, and hyperadrenergic symptoms were selected. Evidence was graded using Oxford CEBM. Treatment recommendations were compared to current ACCF/AHA guidelines. The search resulted in 6082 articles with 81 eligible treatment involving 835 human subjects. There were 6 high-quality studies supporting the use of antipsychotics and benzodiazepines for control of agitation and psychosis. There were several case reports detailing the successful use of dexmedetomidine for this indication. There were 9 high-quality studies reporting the overall safety and efficacy of β-blockers for control of hypertension and tachycardia associated with ARDA. There were 3 high-quality studies of calcium channel blockers. There were 2 level I studies of α-blockers and a small number of case reports for nitric oxide-mediated vasodilators. High-quality evidence for pharmacologic treatment of overdose from ARDA is limited but can help guide management of acute agitation, psychosis, tachycardia, and hypertension. The use of butyrophenone and later-generation antipsychotics, benzodiazepines, and β-blockers is recommended based on existing evidence. Future randomized prospective trials are needed to evaluate new agents and further define treatment of these patients. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.Drug and Alcohol Dependence 02/2015; 150. DOI:10.1016/j.drugalcdep.2015.01.040 · 3.42 Impact Factor
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