Journal de toxicologie clinique
Libre accès
ISSN: 2161-0495
ISSN: 2161-0495
Michelle Miles, Bannet Munoozi, John Tran, Steven Yung
Introduction Recreational nitrous oxide use been a commonly used drug among adolescents due to its easy access and its effects have rapid onset. Few have described the relationship between thromboembolic phenomenon and nitrous oxide use in which it causes homocysteinemia due to a functional B12 deficiency resulting in a hypercoagulable state. Here we present a case of a patient with severely elevated homocysteine levels and extensive thromboembolic disease as a result of recreational nitrous oxide use. Case Presentation: A 41 year-old woman with history of twenty years of daily nitrous oxide use complicated by peripheral neuropathy and presented with chest pain and shortness of breath. The patient stated she had difficulty breathing for the past several days and felt like she could not catch her breath. On exam, patient had bilateral lower extremity tenderness and edema with bilateral toe cyanosis. CT angiogram showed bilateral submassive pulmonary emboli. Further imaging revealed bilateral above the knee DVT and extensive IVC thrombus involving the right renal vein. Laboratory data showed vitamin B12 423 pg/ml (normal: 211-911 pg/ml), folate 9.3 ng/ml (normal: 3.1-17.5 ng/ml), methylmalonic acid level elevated 3.36 µmol/L (normal: .0-.40 µmol/L) and homocysteine severely elevated 70.9 (normal 5.0-15.0 mcmol/L). She was started on therapeutic heparin and then bridged to warfarin. After two months of complete cessation from nitrous oxide and therapeutic anticoagulation, a repeat CT angiogram showed near complete resolution of pulmonary emboli and drastically lower homocysteine level. Conclusion: Nitrous oxide abuse causes a hypercoagulable state by creating a functional B12 deficiency which raises homocysteine levels resulting in thromboembolic phenomenon. Clinicians should be aware of this potentially life threatening complication of nitrous oxide use.