B52-02 Recreational Nitrous Oxide to Catastrophic VTE: A Case of Surgical and Mechanical Rescue

Introduction Recreational nitrous oxide use has risen significantly, often via inhalation from “whippets.” This case describes a previously healthy individual who developed extensive venous thromboembolism likely related to chronic nitrous oxide abuse, resulting in life-threatening complications requiring sternotomy, surgical thrombectomy, and mechanical circulatory support. Case Presentation A 30-year-old male with a history of inhaled nitrous oxide, cocaine, and cannabis use disorders, anxiety, and ADHD presented with two days of dyspnea and multiple syncopal episodes. On arrival, he was tachycardic (113 bpm), tachypneic, and normotensive. Laboratory testing revealed elevated D-dimer (9.5 µg/mL) and troponin in the 60s ng/L. Point-of-care ultrasound showed severe right ventricular (RV) dilation and dysfunction, confirmed by transthoracic echocardiogram. CT pulmonary angiography revealed a saddle pulmonary embolism (PE) with right heart strain (Fig. 1A) and an incidental pulmonary nodule. Anticoagulation with intravenous heparin was initiated. Interventional Radiology took him for attempted catheter-directed thrombectomy, but the procedure was aborted due to severely elevated pulmonary artery (PA) pressures (69/31 mmHg, mean ≈ 47 mmHg). Cardiothoracic surgery performed emergent sternotomy with surgical thrombectomy (Fig.1B). Intraoperatively, he developed cardiovascular collapse requiring cardiopulmonary bypass and Impella RP placement. He was transferred to a tertiary center for evaluation for venoarterial extracorporeal membrane oxygenation (VA-ECMO). Over the following days, he underwent repeat interventional radiology-guided thrombectomy and catheter-directed tissue plasminogen activator (tPA), resulting in improved RV function. ECMO was not required, and he was successfully weaned from mechanical ventilation. Discussion Our institution’s endovascular capability is limited to aspiration embolectomy rather than catheter-directed thrombolysis. Although recent series on aspiration therapies show favorable safety profiles and improvements in RV/left ventricular (LV) ratios in intermediate-risk PE, these studies involved patients with substantially lower PA pressures than seen here. In the FLARE trial of mechanical aspiration, baseline mean PA pressure (mPAP) was ∼30 mmHg, and the pulmonary hypertension subgroup averaged ∼35 mmHg. Post-procedure mPAP decreased only modestly, and patients in shock were excluded. Thus, the safety and hemodynamic effectiveness of aspiration at markedly elevated PA pressures remain uncertain. When PA pressures are extreme or procedural risk is high, early surgical thrombectomy is appropriate to avoid RV decompensation. This case also highlights the role of multidisciplinary Pulmonary Embolism Response Teams (PERT) when evidence is limited. Rising nitrous oxide use should prompt suspicion for venous thromboembolism in otherwise healthy young individuals. Conclusion Massive PE with severe pulmonary hypertension warrants early multidisciplinary discussion, given limited evidence for endovascular therapy and potential need for surgery.