Metabolic encephalopathy caused by nitrous oxide ('laughing gas') induced hyperammonaemia.
Marissa Ginette Danielle Vive, Galia Valentinova Anguelova, Sjoerd Duim, Herman Marcel André Hofstee
BMJ Case Reports November 25, 2019 DOI: 10.1136/bcr-2019-232163 (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 26-year-old man |
| Interventions | vitamin B12 lactulose |
| Duration | 3-month follow-up |
| Keywords | Emergency medicine Peripheral nerve disease Sedation Vitamins and supplements |
| Key findings | Nitrous oxide use can cause hyperammonaemia leading to metabolic encephalopathy, which improves with vitamin B12 and lactulose treatment. |
Abstract
A 26-year-old man presented at the emergency department with confusion and decreased consciousness after several days of vomiting. In the preceding 6 months, he had used a 2-litre tank of nitrous oxide (N2O) weekly. His metabolic encephalopathy was caused by hyperammonaemia which probably resulted from interference of N2O-induced vitamin B12 deficiency with ammonia degradation. A catabolic state might have contributed to the hyperammonaemia in this case. After treatment with vitamin B12 and lactulose, both his consciousness and hyperammonaemia improved. He reported no residual complaints after 3 months of follow-up. Since N2O is increasingly used as a recreational drug, we recommend considering hyperammonaemia as a cause of metabolic encephalopathy in cases of N2O use and altered mental status.