Introduction: Nitrous oxide (N2O) recreationally used as “whippets,” is increasingly associated with thrombotic complications due to its impact on vitamin B12 metabolism and homocysteine levels. While neurologic effects are more commonly recognized, thromboembolic events like pulmonary embolism (PE) remain rare and underdiagnosed Description: A 20-year-old Chinese male college student was found unresponsive after inhaling N2O. He had reported severe shortness of breath, dizziness, and confusion. On EMS arrival, vitals revealed SpO2 50%, BP 84/54 mmHg, and HR 167 bpm. Empty N2O canisters were found at the scene. Labs showed high anion gap metabolic acidosis (bicarbonate 15 mmol/L, anion gap 29), acute kidney injury (creatinine 2.16 mg/dL), elevated troponin (241.74 ng/mL), and hyperhomocysteinemia (>50 µmol/L). CT angiography showed bilateral PE with extensive right-sided clot burden and right heart strain. Echo confirmed right ventricular enlargement and dysfunction. No DVT was found on Doppler. He was initially managed at an outside hospital with tPA (100 mg IV), heparin, fluids, and intubation, but remained in shock. After transfer, he underwent catheter-directed suction embolectomy using the Inari FlowTriever system with significant clot removal and improved perfusion. He was extubated within 24 hours, transitioned to apixaban, and started on vitamin B12 and folate. He was discharged in stable condition Discussion: N2O inactivates vitamin B12 by inhibiting methionine synthase, leading to hyper-homocysteinemia and a prothrombotic state. This case highlights an uncommon but life-threatening consequence of N2O use in a young patient without traditional PE risk factors. It underscores the need to consider N2O toxicity in similar clinical presentations and demonstrates the importance of early recognition and aggressive intervention. Vitamin supplementation may support recovery, though its role in preventing thrombosis remains unclear.
Bansal et al. (Sun,) studied this question.