Suicidal attempts through intentional medication ingestion commonly occur in adolescents. Of which, bupropion harbors increased risk of medical complications and higher morbidity risks. In setting of acute toxic ingestion, multiple confounding factors - poison metabolism rate, amount of medications taken, and interactions between multiple medications ingested - must be considered in electroencephalogram (EEG) interpretation and clinical prognostication. Although loss of brainstem reflexes, anoxic myoclonus, and evolving electrographic burst suppression pattern may be highly for poor prognosis, premature prognostication should be avoided to allow for complete metabolism and elimination of ingested medications.

We present a case of a 15-year-old adolescent girl who was hospitalized for acute encephalopathy and first lifetime generalized tonic clonic seizures after intentionally ingesting her mother’s antidepressant medications including extended release bupropion and sertraline.  Despite holding sedation and multiple evaluations, she demonstrated lack of brainstem reflexes. Continuous video monitoring EEG showed activity consistent with metabolic encephalopathy. However,  the background EEG activity gradually evolved to a burst suppression pattern, and multiple myoclonic jerks in bilateral upper extremities were also observed. Despite these findings, 35 hours after initial ingestion, she exhibited rapid clinical improvement, demonstrating sluggish reactive pupils, positive corneal reflexes, and eventual purposeful movement. At time of discharge, she exhibited a non-focal neurological examination with mild anterograde amnesia.

Electrographic burst suppression in the setting of a comatose examination is usually portends poor prognosis. In our patient, she not only ingested a large quantity of extended release bupropion, but she also ingested an unknown amount of sertraline which may have contributed to delayed metabolism. it is thus essential to recognize possible etiologies and confounding elements that could contribute to this type of presentation.  Ultimately, a comprehensive understanding of the different etiologies and clinical symptoms of metabolic encephalopathies will empower physicians to provide improved patient care and appropriate prognostication.