Fatal pulmonary thromboembolism associated with excessive nitrous oxide consumption over several weeks
Stefanie Plenzig, Friederike Pijahn, Alexander Müller, Stefan W. Toennes, Silvana Petzel-Witt
International Journal of Legal Medicine August 12, 2026 DOI: 10.1007/s00414-026-03958-z (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Case study Case report Peer reviewed |
|---|---|
| Sample size | 1 |
| Population | A man in his early twenties who died after excessive nitrous oxide use |
| Intervention | Nitrous oxide |
| Duration | Approximately two months of excessive nitrous oxide use |
| Key findings | The authors propose that repeated excessive nitrous oxide consumption can cause functional vitamin B12 deficiency and related biochemical disturbances, and that this may have contributed to a fatal pulmonary embolism in a young man through suspected hyperhomocysteinemia and a coagulation disorder. They argue that this possibility should be considered in fatal thromboembolic events in young individuals, though toxicology can demonstrate recent nitrous oxide exposure but not the underlying biochemical pathology. |
Abstract
Abstract A man in his early twenties had been hospitalized due to acute nitrous oxide intoxication, during which a vitamin B12 deficiency and anaemia were also diagnosed. Two weeks later he was found dead in his apartment. Twenty empty nitrous oxide cartridges were found next to the body, and according to his mother, he had been using nitrous oxide excessively for approximately two months. The autopsy revealed a fatal pulmonary embolism secondary to deep vein thrombosis, and toxicological analysis detected nitrous oxide in low concentrations in the blood. Regarding the pulmonary embolism, a coagulation disorder attributable to suspected hyperhomocysteinemia in the setting of vitamin B12 deficiency could be considered a contributory factor – this deficiency, in turn, may possibly be related to excessive nitrous oxide consumption over several weeks. Obesity and nicotine abuse were present as additional risk factors for thromboembolic events. Reapeted excessive nitrous oxide consumption can induce profound metabolic disturbances, including functional vitamin B12 deficiency and associated biochemical derangements. In cases of fatal thromboembolic events in young individuals, this possibility should be taken into account. Toxicological analysis may demonstrate recent nitrous oxide exposure and support the hypothesis, but it cannot establish the underlying biochemical pathology.