Abstract Introduction Pulmonary embolism (PE) is uncommon in young adults without typical risk factors. Recreational nitrous oxide (N2O) use is an under-recognized cause of venous thromboembolism (VTE) through functional vitamin B12 deficiency and hyperhomocysteinemia, leading to a prothrombotic state 1,2. Case Description A 20-year-old African American male without past medical history presented with one week of worsening shortness of breath, right-sided pleuritic chest pain, and intermittent hemoptysis. He reported daily N2O inhalation for two months, in addition to tobacco, alcohol, and occasional marijuana use, which he stopped one to two weeks prior to presentation. Two weeks earlier, he had donated plasma with localized left-arm bruising. He denied recent trauma, surgery, or immobility. On arrival, he was hemodynamically stable but tachycardic. Labs showed low-normal vitamin B12 (223 pg/ mL), elevated BNP (1,511 pg/mL), and mildly elevated troponin. Urine toxicology was positive only for cannabinoids. Chest X-ray was normal. CT pulmonary angiography revealed large bilateral pulmonary emboli in main, lobar, and segmental arteries with right ventricular enlargement (RV/LV ratio 1.5) and wedge-shaped pulmonary infarcts. Lower-extremity Doppler demonstrated non-occlusive thrombus in the left distal femoral and popliteal veins. Hypercoaguable evaluation revealed borderline DRVVT ratio 1.2 without anticardiolipin or B-2 glycoprotein antibodies, negative JAK2 testing, and otherwise unremarkable thrombophilia panel. He received intravenous heparin and underwent bilateral Inari aspiration thrombectomy, yielding a large clot burden with post-procedure improvement in pulmonary artery pressures. Echocardiography post thrombectomy showed preserved left ventricular function and no evidence of right-ventricular pressure overload. He was transitioned to oral anticoagulation and discharged with hematology follow-up. Discussion/Novelty PE in young adults without traditional risk factors should prompt evaluation for acquired prothrombotic states. N2O abuse impairs methionine synthase, causing hyperhomocysteinemia and endothelial dysfunction 1,2. In this patient, low-normal B12, recent heavy N2O use, and minor venous trauma from plasma donation likely contributed to thrombus formation. Early recognition and cessation of N2O are critical, as timely anticoagulation and thrombectomy can prevent recurrence and long-term complications. This case highlights the importance of inquiring about inhalant use in unexplained VTE and reinforces the emerging link between recreational N2O use and serious thrombotic events in young adults. References: 1. Sun W., et al. Pulmonary embolism and deep vein thrombosis caused by nitrous oxide abuse. World J Clin Cases. 2019;7:4057-4062. 2. Gernez E, et al. Nitrous Oxide Abuse: Clinical Outcomes, Pharmacology and Toxicity. Toxics. 2023;11(10):962. This abstract is funded by: None
Daoud et al. (Fri,) studied this question.