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Nitrous oxide-induced myeloneuropathy in a Thai adolescent: a case report
S Puetpaiboon1,2, M Meepolprapai3, P Saengpanit4
1Division of Ambulatory Pediatrics (Adolescent Medicine), Department of Pediatrics, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Abstract:
Nitrous oxide, an inhalational anaesthetic, is popular with adolescents worldwide as an accessible recreational drug which induces a euphoric effect. However, chronic abuse leads to serious complications such as myeloneuropathy and bone marrow suppression by inactivation of vitamin B12. A 17-year-old girl presented with nitrous oxide-induced myeloneuropathy. She reported chronic nitrous oxide inhalation for 10 months and was admitted to the emergency department on account of repeated falls for 2 weeks. She also had ascending paraesthesia in both legs and urinary incontinence. Neurological examination demonstrated bilateral lower extremity weakness [motor power: proximal muscles 4/5, plantar flexion and extensor hallucis longus (EHL) 3/5], decreased sensation, proprioception and vibration of the lower extremities. Deep tendon reflexes were absent in the ankles and knees. Laboratory results demonstrated mild anaemia [Hb 11.2 g/dL (12.0-16.0), haematocrit 35.4% (36-50), MCV 89.4 fl (78-102)] with significant hypersegmented neutrophils in a peripheral blood smear. Serum vitamin B12 was 340 pg/mL (197-771), but serum homocysteine was increased at 65.8 µmol/L (5-15). A nerve conduction study was prolonged, and F-waves were absent from the bilateral perineal and tibial nerves, indicating diffuse demyelinating motor polyneuropathy. Magnetic resonance imaging of the whole spine demonstrated faint T2 hypersignal intensity and an inverted V-shape appearance at the posterior column of the upper thoracic cord (around T2-T6), a pathognomonic sign of vitamin B12 deficiency or subacute combined degeneration of the nitrous oxide-induced myeloneuropathy. A 7-day course of 1000 µg cyanocobalamin was given intramuscularly, followed by weekly doses for 4 weeks. Supplements of daily oral vitamin B1, B6 and B12 (65 µg vitamin B12) were administered, along with rehabilitation. At the 6-months outpatient follow-up, there were a few residual neurological abnormalities: weakness of the left EHL (grade 4/5) and an absent deep tendon reflex in the left ankle. This case emphasises the significant health consequences of chronic abuse of nitrous oxide, myeloneuropathy and megaloblastic anaemia, by inactivation of vitamin B12. The myelopathy is noticeably improved by cyanocobalamin.Abbreviations: EHL: extensor hallucis longus; MRI: magnetic resonance imaging; NCS: nerve conduction study.
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