Sodium nitrate is used as a food preservative and color fixative. Sodium nitrate poisoning has occurred in the setting of well water contamination with nitrogenous waste runoff. Most clinically significant exposures result from improper labeling or unintentional use. We describe a case of severe methemoglobinemia associated with intentional sodium nitrate ingestion. A 23-year-old female presented to the emergency department (ED) for an intentional ingestion of sodium nitrate obtained from an online distributor. On arrival, blood pressure was 89/42 mmHg and oxygen saturation was 74% on pulse oximetry. Due to clinical decline, the patient underwent endotracheal intubation in the ED. Co-oximetry demonstrated a methemoglobin (MetHb) level of 92.7%, which is among the highest recorded MetHb levels. The patient received two doses of 1 mg/kg methylene blue and experienced dramatic clinical improvement and subsequent successful extubation. Healthy erythrocytes undergo oxidative stress from normal metabolism resulting in spontaneous formation of MetHb. Reduction of MetHb to hemoglobin occurs via the protective enzymes cytochrome-b5 reductase and nicotinamide adenine dinucleotide phosphate (NADPH) MetHb reductase. Sodium nitrate acts as an oxidizing agent causing methemoglobinemia. Treatment includes methylene blue, which acts as a cofactor for NADPH MetHb reductase. KEYWORDS Methemoglobinemia; sodium nitrate, methylene blueCONTACT Maricel Dela Cruz