A CASE OF FATAL NEURO-CARDIO TOXICITY WITH BUPROPION OVERDOSAGE

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SESSION TITLE: Tuesday Fellows Case Report Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: Bupropion is an atypical antidepressant used to treat severe depression, anxiety, bipolar disorders and smoking cessation. It has structural similarities to amphetamines. Consumption of large quantities of bupropion has shown to cause a wide variety of manifestations including cardiac, neurological and behavioral issues. In our case, the patient overdosed on bupropion along with depakote leading to major cardiac manifestations including refractory hypotension, bradycardia and conduction abnormalities resulting in recurrent cardiac arrests and then death. CASE PRESENTATION: This is a 28 year old male with history of severe depression who was brought to the hospital after consumption of 30 300mg bupropion extended release pills as a part of a suicidal attempt. Unfortunately within minutes of presentation, he had a dramatic and quick neurological and cardiac deterioration that ranged from initially being oriented to completely lethargic and then status epilepticus and cardiac arrest (PEA) requiring Endo-Tracheal intubation. Although depakote consumption was reported, the EKG and cardiac manifestations were consistent with buproprion toxicity. Initial electrocardiogram(EKG) showed normal QRS, QTc intervals which then rapidly progressed to show prolongation of both intervals. Despite the toxicologist recommendations of continuing the bicarbonate drip and lipid emulsion, his medical condition continued to deteriorate and expired within eight hours of presentation. DISCUSSION: Bupropion over dosage has been reported to manifest with symptoms from development of altered mental status to status epilepticus and larger doses have reported to have refractory cardiogenic shock with significant conduction abnormalities. Unfortunately, hemodialysis is not an option and no antidote has been available for treatment. Toxicologists have described two techniques that have been used to combat buproprion toxicity. 1. Serum alkalization with sodium bicarbonate infusion has been used traditionally in the overdose of tricyclic antidepressants and has been used in bupropion overdose, as all of them are known to cause QTc prolongation. Although the mechanism is unclear, it is postulated that an increase in the sodium concentration, change in pH, or a combination of these physiological alterations may be responsible. 2. Intra-venous lipid emulsion therapy with initial bolus dose followed by a continuous infusion has been described in bupropion overdoses. The mechanism is described as a ‘lipid sink’ with the trapping of bupropion which is lipophilic and hence limiting levels of the drug. The duration from ingestion to presentation and the large dose are major reasons why our patient did not respond to aggressive therapy. CONCLUSIONS: We have to emphasize that due to the fatal neuro-cardio toxicity that bupropion overdosage may cause, we need to do more studies to help understanding and preventing this fatality. Reference #1: Florian Morazin, Agnès Lumbroso, Patrick Harry, Marcel Blaise, Alain Turcant, Philippe Montravers & Rémy Gauzit (2007) Cardiogenic shock and status epilepticus after massive bupropion overdose, Clinical Toxicology, 45:7, 794-797, DOI: 10.1080/15563650701665076 Reference #2: Bupropion-Associated QRS Prolongation Unresponsive to Sodium Bicarbonate Therapy Wills, Brandon K DO, MS; Zell-Kanter, Michele PharmD; Aks, Steven E DO American Journal of Therapeutics: March-April 2009 - Volume 16 - Issue 2 - p 193-196 https://doi.org/10.1097/MJT.0b013e3180a5bd83 DISCLOSURES: No relevant relationships by Moayyad Alziadat, source=Web Response No relevant relationships by Mohd Hazem Azzam, source=Web Response No relevant relationships by Anish Samuel, source=Web Response No relevant relationships by Rishitha Yelisetti, source=Web Response