Background: Table salt and baking soda ingestions are described in the literature independently. Reports include gastrointestinal side effects, metabolic derangements, and rarely fatality. We report a unique clinical scenario of a patient presenting after coingestion of sodium chloride and sodium bicarbonate resulting in fatality. Case Report: A 57-year-old female with an acute tramadol overdose presented to the Emergency Department after ingesting large quantities of table salt and baking soda dissolved in water to induce emesis. On arrival she had stable vital signs, normal mentation, and a benign physical exam. The patient’s mental status deteriorated and she experienced a tonic-clonic generalized seizure, which resolved spontaneously. At that time her serum sodium was noted to be 168 mEq/L and her bicarbonate was 43 mmol/L. Seizure activity resumed shortly after and she was intubated, intravenous lorazepam, phenobarbital, and propofol were administered without cessation of seizure activity. Her serum sodium at that time was determined to be >175 mEq/L and bicarbonate was >48 mmol/L. No dilutions were performed. She received 3 hours of hemodialysis and demonstrated a transient decline in her serum sodium concentration, however no further hemodialysis was performed. The primary team opted for slow correction of serum sodium. The patient developed cerebral edema and diabetes insipidus. A repeat CTA was performed 48 hours after ingestion and revealed progression of cerebral edema with tonsillar herniation and lack of significant blood flow in the intracranial vessels. The patient was declared brain dead on hospital day 4, care was withdrawn and the patient expired. Case Discussion: This patient developed cerebral edema with intracerebral hemorrhage resulting in brain death secondary to hypernatremia after ingestion of sodium chloride and sodium bicarbonate. Review of the literature suggests that acute hypernatremia should be treated with aggressive correction of electrolytes. Therapeutic options include hemodialysis and aggressive free water administration. Conclusions: Optimal therapy for acute hypernatremia from exogenous sodium ingestion requires rapid correction. It seems the most practical approach would involve aggressive free water administration with serial electrolyte assessment