SEVERE NEUROLOGIC DEFICIT AFTER NITROUS-OXIDE ANESTHESIA

THE interaction of nitrous oxide and vitamin B-12 is well known from experimental studies in animals and anecdotal clinical reports.(1-4) Nitrous oxide oxidizes cobalamin in vitamin B-12 and disrupts several pathways involved in one-carbon chemistry. The result is an irreversible inactivation of the enzyme methionine synthase, which requires vitamin B-12 in the +1 oxidation state to act as its coenzyme. The clinical syndrome associated with oxidation of vitamin B-12 develops after prolonged exposure to nitrous oxide and consists of megaloblastic erythropoiesis and subacute combined degeneration of the spinal cord.(2-4) We present the case of a patient who developed a severe neurologic deficit 6 weeks after anesthesia with nitrous oxide.