Subacute Combined Degeneration Provoked by Nitrous Oxide Anethesia Patients with Cobalamin Deficiency

Abstract

Vitamin B₁₂ deficiency leads to neuropathological changes in humans, principally subacute combined degeneration (SCD) of the spinal cord and polyneuropathy. Less commonly it causes encephalopathy leading to degeneration and optic neuropathy. Myelopathy may develop after nitrous oxide anesthesia in asymptomatic patients or those with borderline vitamin B₁₂ deficiency or overlooked cases. It can result from chronic recreational use of N₂O or industrial exposure. This presentation will focus on myelopathy and SCD.

Abstracted from Ahn and Brown 2005

Updates

2009

Chaugny et al.

Nitrous oxide is widely used in anesthesia. It is usually safe but may be associated with severe side effects when it is used repeatedly or on a prolonged time. Here, we report a case of drug-induced subacute combined spinal cord degeneration related to cobalamin deficiency.

Case Report

A 20-year-old man with sickle-cell disease (SS) who was followed for severe recurrent vaso-occlusive crisis with repeated hospital admissions presented with ascending motor and sensitive neurological deficits that were later associated with bladder dysfunction. He was first considered to develop Guillain-Barre syndrome. However, persisting neurological signs despite adequate treatment lately led to diagnose subacute combined medullar degeneration due to abnormal cobalamin (vitamin B12) metabolism induced by repeated use of nitrous oxide during painful episodes of sickle-cell disease. Inhaled nitric oxide is widely used in the treatment of vaso-occlusive crisis. Clinicians should be aware of possible severe neurologic side effects.

Reference

Chaugny C, Simon J, Collin-masson H, et al. Vitamin B12 deficiency due to nitrous oxide use: unrecognized cause of combined spinal cord degeneration. Rev Med Interne. 2014;35(5):328–32.

2015

Pugliese et al.

Recreational Use of Nitrous Oxide

A case of subacute combined degeneration (SCD) of the spinal cord manifesting as severe ataxia and urinary retention in a patient with a history of heavy nitrous oxide abuse and self-supplementation with cyanocobalamin is reported.

Case Report

A 27-year-old woman was treated in the emergency department for complaints of abdominal pain and inability to urinate for about 12 h. The patient also complained of worsening lower-extremity weakness for 10 days and a “pins and needles” sensation in the lower extremities for approximately 1 year. She reported nitrous oxide abuse over 3 years (an average of 100–200 “whippit” cartridges daily on 3 or 4 days per week), as well as long-term self-medication with oral and i.m. cyanocobalamin for the purpose of preventing nitrous oxide-induced neurologic symptoms. Results of magnetic resonance imaging (MRI) were highly suggestive of SCD, which is typically seen in primary vitamin B12 deficiency but has been reported in the context of chronic nitrous oxide exposure. Treatment was initiated with cyanocobalamin 1000 μg i.m. daily, to be continued for 5 days and followed by a four-week regimen of 1000 μg i.m. weekly. The patient was discharged after 3 days, despite continued symptoms, with instructions to obtain ongoing care but was lost to follow-up.

Reference

Pugliese RS, Slagle EJ, Oettinger GR, Neuburger KJ, Ambrose TM. Subacute combined degeneration of the spinal cord in a patient abusing nitrous oxide and self-medicating with cyanocobalamin. Am J Health Syst Pharm. 2015;72(11):952–7.