Metoprolol treatment of dual cocaine and bupropion cardiovascular and central nervous system toxicity

Richards, John R.; Gould, Jessica B; Laurin, Erik G.; Albertson, Timothy E

doi:10.15441/ceem.17.247

Cited by 3 publications

(5 citation statements)

References 12 publications

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“…In fact, with seizures seen in just over a quarter of all cases (21 of overall N = 80) and only one additional case picked up by application of the composite endpoint, there was no need to add multifaceted composite endpoints to capture instances of significant bupropion toxicity. The low rate of death is consistent with that previously reported in the literature [13].…”

Section: Discussionsupporting

confidence: 92%

“…The overall rate of co-ingestant presence was just over 1 in 3 cases in the overall group, but as compared with the younger age group, teenage cases were more than three times as likely to have co-ingestants. Bupropion has toxicity synergism with certain co-ingestants such as cocaine (not known to be encountered in this study), so clinicians should consider the possibility of multiple-drug exposure when refractory complications are seen after bupropion use [13]. However, more likely, the higher rates of seizures in the older population likely represent a difference in intent (unintentional vs. intentional ingestion) and the inherent difference in dose consumed.…”

Section: Discussionmentioning

confidence: 94%

“…The first aim was to evaluate a large group of pediatric bupropion cases in order to characterize patient presentations and assess for predictors (with associated relative risks) involving the main toxicity manifestation of seizure. The second study aim was to assess for differences in bupropion ingestion characteristics (including toxicity) in younger children (aged up to 12 years) versus adolescents (aged [13][14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

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Pediatric Bupropion Ingestions in Adolescents vs. Younger Children—a Tale of Two Populations

et al. 2019

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Background Bupropion is a unique class of antidepressant. In overdose, it is associated with tachycardia, altered mental status, and a dose-dependent risk of seizures, which can be delayed. Despite being a common medication, there is a paucity of data comparing toxicity in younger versus older children with bupropion exposures. The primary purpose of this study is to examine bupropion toxicity in pediatric patients and assess for toxicity differences between younger and older (teenaged) groups. Methods This single-center, observational cohort study reviewed pediatric patients presenting to a toxicology service between 2011 and 2018. The primary outcome measures evaluated were the presence of any seizure, delayed seizure (defined as occurring at least 6 hours after hospital arrival), and a composite endpoint of seizure, hypotension, or need for endotracheal intubation. Patients were subdivided into two groups-those 12 years and under, compared with those 13-17 years.Results A total of 80 unique pediatric cases were identified. Overall, the median (IQR) age was 14 (2.4-16) years. Patients under 13 years accounted for 31 (39%) of cases, whereas the remaining 49 cases were adolescents. Compared with the adolescents, the younger patients were less likely to be female (41.9% vs. 71.4%; p = 0.009) and more likely to have an unintentional ingestion (100% vs. 10.2%; p < 0.001). The younger group was more likely to present to health care earlier after the ingestion (median 61 (IQR 39-103) min vs. 139 (67-399) min; p = 0.002). The older group was more likely to be tachycardic (73.5% vs. 19.4%; p < 0.001), have sustained tachycardia (71.4% vs. 29% p < 0.001), and more likely to have altered mental status on arrival (38.8% vs. 6.5%; p < 0.001). Seizures were also much more likely in the older group (40.8% vs. 3.2%; p < 0.001). Adolescents were much more likely than younger children to reach the pre-defined composite endpoint (42.9% vs. 6.5%; p < 0.001), but this was largely driven by the seizures. Conclusion Bupropion ingestions are relatively common among pediatric patients. However, adolescents are much more likely to present with more severe toxicity. Seizures are uncommon among younger children with exploratory ingestions.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

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Pediatric Bupropion Ingestions in Adolescents vs. Younger Children—a Tale of Two Populations

et al. 2019

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“…For other sympathomimetic agents, after a thorough and critical assessment of a given patient and symptoms, the use of a non-selective alpha and beta-adrenergic antagonist such as labetalol has been proposed [ 148 , 149 ]. It is also interesting to note the successful treatment of combined sympathomimetic intoxications with labetalol [ 151 , 152 ].…”

Section: Management/treatment Strategiesmentioning

confidence: 99%

The clinical toxicology of caffeine: A review and case study

Willson¹

2018

Toxicology Reports

183

138

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Caffeine is a widely recognized psychostimulant compound with a long history of consumption by humans. While it has received a significant amount of attention there is still much to be learned with respect to its toxicology in humans, especially in cases of overdose. A review of the history of consumption and the clinical toxicology of caffeine including clinical features, pharmacokinetics, toxicokinetics, a thorough examination of mechanism of action and management/treatment strategies are undertaken. While higher (i.e., several grams) quantities of caffeine are known to cause toxicity and potentially lethality, cases of mainly younger individuals who have experienced severe side effects and death despite consuming doses not otherwise known to cause such harm is troubling and deserves further study. An attempted case reconstruction is performed in an effort to shed light on this issue with a focus on the pharmacokinetics and pharmacodynamics of caffeine.

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“…Due to the assumption that all sympathomimetic agents are similar (i.e., the original hypothesis was based upon cocaine intoxication), this led to the practice of avoiding the use of beta-adrenergic receptor antagonists in cases of overdose with sympathomimetic agents [123,124]. However, some clinicians have discovered that this view is unwarranted [[122], [123], [124], [125], [126], [127], [128], [129], [130], [131]], demonstrating clear benefit with the use of beta-adrenergic receptor antagonists in cases of sympathomimetic agent intoxications (including ephedrine and pseudoephedrine), while even proponents of the unopposed alpha effect hypothesis have acknowledged that sympathomimetic agents may have divergent toxicological effects, allowing for deviation from the hypothesized contraindication [132].…”

Section: Incorrect Attributions Of Causality and Treatment Errorsmentioning

confidence: 99%

Sympathomimetic amine compounds and hepatotoxicity: Not all are alike—Key distinctions noted in a short review

Willson¹

2019

Toxicology Reports

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Sympathomimetic amine compounds are often pooled together and incorrectly assumed to be interchangeable with respect to potential adverse effects. A brief and specific review of sympathomimetic compounds and one instance (i.e., hepatotoxicity) where these compounds have been improperly grouped together is covered. A review of the proposed mechanisms through which known hepatotoxic sympathomimetic agents (e.g., 3,4-methylenedioxymethamphetamine or MDMA, methamphetamine and amphetamine) cause liver injury, along with a corresponding review of in vitro data, interventional data, animal model studies and observational data allow for a comparison/contrast of different agents and reveals a lack of potential toxicity for some agents (e.g., pseudoephedrine, phenylephrine, ephedrine, 1,3-dimethylamylamine, phentermine) in this broad category. Data show that compounds within the broad group of sympathomimetics display divergent pharmacological and toxicological profiles and can be clearly distinguished with respect to liver injury. These data serve as a reminder to clinicians and others, that even small structural differences between molecules can lead to drastically different pharmacological/toxicological profiles and that one should not assume that all sympathomimetic agents are hepatotoxic. Such assumptions could lead to diagnostic errors and incorrect or insufficient treatment.

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Metoprolol treatment of dual cocaine and bupropion cardiovascular and central nervous system toxicity

Cited by 3 publications

References 12 publications

Pediatric Bupropion Ingestions in Adolescents vs. Younger Children—a Tale of Two Populations

Pediatric Bupropion Ingestions in Adolescents vs. Younger Children—a Tale of Two Populations

The clinical toxicology of caffeine: A review and case study

Sympathomimetic amine compounds and hepatotoxicity: Not all are alike—Key distinctions noted in a short review

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