Myeloneuropathy Due to Vitamin B12 Deficiency lnduced by Nitrous Oxide Anesthaesia

Abstract

Background: Nitrous oxide is an general anesthaetic agent that inactivates vitamin B12. A subclinical vitamin B12 deficiency could be symptomatic with the use of nitrouse oxide anesthaesia. Neurological, gastrointestinal and hematological disorders occur as a result of B12 deficiency. Objective: We describe a 58 year old patient introduced with subacute combined degeneration and sensorial axonal neuropathy associated with vitamin B12 deficiency 6 weeks after the thyroidectomy operation at which a nitrous oxide anesthaesia was used. Findings: The patient presented with ataxia, loss of vibration and positional sense and hypoesthesia extending towards to level C4. We found megaloblastic anemia, hyperintence T2 signals at cervical and upper thoracal region in the posteromedial part of the spinal cord in cervical spinal MRI and electrophysiological evidence of sensorial axonal neuropathy. One month after the vitamin B12 replacement therapy, the patient's clinical symptoms were improved and an MRI reevaluation of the condition three months after the initiation of the therapy showed partial regression of spinal cord lesions. Result: Vitamin B12 deficiency in duced by nitrouse oxide anesthesia should be differentially diagnosed in patients with an advancing myelopathy, neuropathy and cognitive changes during the postoperative period and vitamin B12 replacemant therapy should be initiated at early stages.