Case Presentation: A 23-year-old female with history of depression and suicidal ideation presented to the emergency department after being found unconscious at home, surrounded by bottles of bupropion and hydroxyzine. On arrival, she was obtunded, diffusely cyanotic, and had poorly palpable pulses. Vitals were remarkable for hypotension, tachycardia, tachypnea, and hypoxemia to 88% on pulse oximetry. She underwent intubation, though hypoxemia was refractory to maximal oxygen supplementation. Blood drawn appeared “dark chocolate” in color. Blood gas with co-oximetry revealed a methemoglobin level of 57%, and Toxicology was consulted. The patient received three doses of methylene blue (MB) and orogastric lavage, resulting in improved oxygenation and resolution of cyanosis and methemoglobinemia. She was monitored in the intensive care unit with frequent methemoglobin checks due to risk of recurrent methemoglobinemia from residual intestinal toxin, which would warrant escalation to exchange transfusion. Following extubation, the patient disclosed ingesting sodium nitrite shortly before EMS arrival. She continued recovery without significant hypoxemic injury.
Discussion: Acquired methemoglobinemia results from exposure to oxidant stressors that convert iron from the ferrous (Fe²⁺) to the ferric (Fe³⁺) state, effectively reducing its oxygen-binding capacity and causing a functional anemia. Common oxidants include local anesthetics, antibiotics, antineoplastics, and various nitrites and nitrates in foods, pharmaceuticals, and recreational drugs. Severe cases may progress to central nervous system depression, cardiovascular collapse, and death if not treated promptly.This case underscores the importance of maintaining a high index of suspicion for acquired methemoglobinemia in patients presenting with unexplained cyanosis and hypoxemia unresponsive to supplemental oxygen. Supportive findings include chocolate-colored blood and a saturation gap between pulse oximetry (SpO2) and arterial blood gas (SaO2) measurements. Pulse oximetry is unreliable, necessitating co-oximetry for accurate diagnosis. First-line therapy is intravenous MB at 1 mg/kg for severe methemoglobinemia (level > 30%), with repeat dosing up to a total of 7 mg/kg, and consideration of exchange transfusion if unresponsive to MB. Consequently, simultaneous Hematology and Toxicology consultation is recommended. Alternative therapies include ascorbic acid and hyperbaric oxygen, though these have been shown to have poor efficacy in the acute setting.This case also highlights the need to address regulatory measures for sodium nitrite, a substance commonly used in industrial settings, yet available without a license or prescription. Recently, it has gained popularity in pro-suicide forums and has been linked to the increasing incidence of acquired methemoglobinemia, and new barriers to access are warranted.
Conclusions: Methemoglobinemia is a life-threatening toxidrome and requires prompt recognition to prevent catastrophic hypoxemic injury. In this patient, the combination of refractory hypoxemia, cyanosis, and chocolate-colored blood led to swift confirmation of the diagnosis and administration of MB, resulting in complete recovery. Early Toxicology and Hematology consultation is essential for guiding management. Additionally, the rising prevalence of sodium nitrite–related self-harm highlights an urgent need for regulatory safeguards around this increasingly misused compound.