A 22 year old female with a history of depression presented to the emergency room after a drug overdose that followed an altercation with her boyfriend. En route to the hospital, she had one generalized tonic-clonic seizure which lasted for about 30 seconds and was followed by a short post-ictal phase. On arrival to ER, she was awake and oriented. She complained of nausea and fatigue. She denied any previous history of seizures. Apart from smoking marijuana 2 days prior, she denied intake of alcohol or any other drugs. At the time of presentation, she was tachycardic, but her vitals were otherwise stable and the rest of her physical examination was normal. Her serum chemistries included: sodium 147, potassium 2.9, chloride 108, and bicarbonate 13; her anion gap was 26, and the delta/delta ratio was 1.27. Serum acetone was negative. Serum osmolality was 293, and calculated serum osmolality was 302; osmolar gap was 9. Her lactate level and other electrolytes were normal. A urine drug screen was positive for amphetamines. Management was supportive – and on the next day, her anion gap acidosis had resolved. At that time, the patient reported ingestion of 15-20 100 mg tablets of bupropion. The Naranjo adverse drug reaction probability scale indicated a probable relationship (score of 5) between bupropion and high anion gap metabolic acidosis in this case
Discussion:
Bupropion is a drug used as an atypical antidepressant as well as for smoking cessation. It affects a number of neurotransmitter systems. It is known to cause seizures as it decreases the seizure threshold. Bupropion has a chemical structure similar to amphetamines; hence the urine drug screen was falsely positive for amphetamine.
We attribute the anion gap metabolic acidosis to bupropion overdose given absence of any other possible cause from the whole clinical scenario.
Metabolic acidosis has previously been reported with bupropion overdose in the setting of profound hypotension. It is not the case in our patient who developed high anion gap metabolic acidosis due to bupropion overdose without any hypotension at the time of her presentation or hospital stay. Use of the Naranjo adverse drug reaction probability scale in our case indicated a probable relationship between bupropion and high anion gap metabolic acidosis in this case (score of 5). The timeline of starting and discontinuing the drug was consistent with the appearance of the adverse reaction; however, re-administration of the drug was not attempted. No placebo was given and no drug level was available. The exact mechanism by which bupropion can cause high anion gap metabolic acidosis is unclear, but this drug is a monocyclic aminoketone – a structure known to cause metabolic acidosis.
Conclusions: Bupropion overdose should be considered as a cause of high anion gap metabolic acidosis in the appropriate clinical setting. Recognition of drug-induced electrolyte abnormalities is crucial so that supportive care can be provided and additional unnecessary testing avoided.