Seizure Prophylaxis in Bupropion Toxicity: Is Phenobarbital the Better First-Line Choice?

Document Type

Conference Proceeding

Publication Date

2-26-2025

Publication Title

J Med Toxicol

Keywords

activated carbon, amfebutamone, benzodiazepine, benzodiazepine derivative, lorazepam, phenobarbital, radafaxine, adult, anticonvulsant activity, clinical article, conference abstract, female, first-line treatment, heart arrest, heart rate, high risk patient, human, hyperglycemia, hypotension, intensive care unit, intubation, loading drug dose, male, medical record review, observational study, poison center, prophylaxis, QTc interval, restlessness, retrospective study, seizure, single drug dose, tachycardia

Abstract

Background: Bupropion is a known cause of druginduced seizures. Previous studies have evaluated the utility of certain clinical findings, such as tachycardia, QRS and QTc durations, hyperglycemia, reported dose, and psychomotor agitation. However, limited data exists on the utility of pharmacologic seizure prophylaxis in high-risk patients. An ideal therapeutic agent would exhibit rapid onset, with sustained anticonvulsant activity and minimal sedative effects. There has not been a head-to-head comparison of phenobarbital vs. benzodiazepines in the setting of symptomatic bupropion ingestions. Methods: This single poison center retrospective observational chart review analyzing symptomatic, single substance bupropion ingestions >900mg during a six-month period (May 4 - November 4, 2024) in patients who received prophylactic benzodiazepines or phenobarbital. Patients with preceding seizures, cardiac arrest, or intubation were excluded. The following case details were compiled and enumerated: presenting (or earliest available documented) heart rate, development of seizure activity, admission to an intensive care unit (ICU), and hypotension (SBP<90 mmHg). Statistics were performed using an unpaired, one-tailed t-test. Results: Twenty-three patients met inclusion criteria, five of whom received phenobarbital and 18 who received benzodiazepines. The most common confirmed formulation of bupropion ingested were the 150/300 mg XL formulations (PB vs. BZD group) (n = 3/5 vs.10/18, respectively). Although the poison center recommendation was 10 mg/kg phenobarbital loading dose, there was no consistency in the dosing of phenobarbital. The most common benzodiazepine administered was lorazepam (n = 12/18). One patient from either group received single dose activated charcoal, with the benzodiazepineadministered patient subsequently being admitted to the ICU. Seizures (PB vs. BZD group) (n = 0/5 vs. 3/18, p = 0.04), hypotension (n = 0/5 vs. 3/18, p = 0.04), intubation (n = 0/5 vs. 2/18, p = NS) and ICU admissions (n = 0/5 vs.11/18, p < 0.0001), only occurred amongst patients in the benzodiazepine group. No significant difference existed between the mean presenting heart rate (p = NS), or intubation rates. Conclusions: Data on the efficacy of phenobarbital versus benzodiazepines for seizure prophylaxis in symptomatic bupropion toxicity is limited. Our single center retrospective review demonstrates a statistically significant difference in the number of patients with seizure activity following use of phenobarbital vs. benzodiazepines as a first-line therapy. This review is limited by its sample size, retrospective nature, at times unclear documentation of patient course, and lack of confirmatory testing of both bupropion and its hydroxybupropion metabolite. In light of these preliminary findings, phenobarbital warrants further consideration as a potential first-line agent in symptomatic bupropion overdoses.

Volume

21

Issue

2

First Page

197

Last Page

198

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