Case Presentation: A 67-year-old male with a history of hypertension, coronary artery disease status post-stent placement in 2017, Parkinson’s disease, and prostate cancer status post-open prostatectomy in 2004, presented after being found unresponsive in a hotel room. A bottle labeled “Super Rush,” a nitrite-containing substance, was found nearby. Emergency Medical Services (EMS) reported initial bradycardia, hypotension with systolic blood pressure in the 50s, and administration of 16 mcg of push-dose epinephrine en route to the Emergency Department (ED). In the ED, his initial vital signs were temperature 96.6°F, heart rate 75 bpm, respiratory rate 24 breaths per minute, blood pressure 95/54 mmHg, and oxygen saturation 91% on room air. He was placed on high-flow nasal cannula (HFNC) oxygen at 100%/60L, resulting in improved mentation and alertness. He admitted to ingesting “Super Rush,” a product containing isobutyl nitrite. Subsequently, the patient experienced worsening oxygen saturation, obtundation, and hypotension (BP 67/50 mmHg). He was intubated for airway protection and started on norepinephrine at 5 mcg/min. Sedation was achieved using propofol and fentanyl. Laboratory results revealed a methemoglobin level of 37.5% and acute kidney injury with creatinine 1.9 mg/dL (baseline 1.0 mg/dL). Methylene blue 150 mg was administered, reducing methemoglobin to 21.1%. The patient was admitted to the medical intensive care unit for toxic encephalopathy and hemodynamic instability secondary to methemoglobinemia.
Discussion: This case illustrates a severe presentation of methemoglobinemia induced by the ingestion of isobutyl nitrite, a compound found in products marketed as “poppers.” These substances, commonly used recreationally, act as potent oxidizing agents, converting hemoglobin’s iron from the ferrous (Fe²⁺) to the ferric (Fe³⁺) state. This change impairs oxygen delivery to tissues, leading to hypoxia and cyanosis despite adequate oxygen levels in the blood. Symptoms of methemoglobinemia range from mild cyanosis to life-threatening complications such as altered mental status, profound hypoxia, and hemodynamic instability. Diagnosis is confirmed using co-oximetry, which measures methemoglobin levels directly. In this patient, a methemoglobin level of 37.5% exceeded the threshold for severe toxicity, warranting immediate intervention. Management involves discontinuation of the offending agent and administration of methylene blue, the first-line antidote. Methylene blue facilitates the reduction of methemoglobin to functional hemoglobin via the NADPH-methemoglobin reductase pathway, rapidly reversing hypoxia. In severe cases, adjunctive therapies such as exchange transfusion or hyperbaric oxygen may be considered if methylene blue fails, though they were not required in this case. Nitrite-containing products, widely available online and in stores, pose a public health risk due to their accessibility and euphoric effects. Greater public and clinical awareness is crucial for early recognition and treatment of methemoglobinemia.
Conclusions: This case highlights the life-threatening effects of nitrite ingestion, demonstrated by severe methemoglobinemia and toxic encephalopathy. Prompt diagnosis using clinical suspicion and co-oximetry, along with rapid methylene blue administration, is vital to reverse toxicity and prevent death. It underscores the need for regulation and education to curb misuse of nitrite-containing products.