Nitrous oxide and vitamin B12
Editor,—The paper by Kanagasundaramet al 1 on the use of nitrous oxide to alleviate pain and anxiety during painful procedures fails to mention the effect of this gas on cobalamin metabolism. Nitrous oxide inactivates cob(I)alamin, the active derivative of vitamin B12 and essential cofactor for the transfer of the methyl group from methyltetrahydrofolate to homocysteine to form methionine. For subjects with good body stores of cobalamin this effect is unimportant, but no-one using this agent should remain unaware of the potentially devastating complications in the nervous system of using nitrous oxide in subjects who are of borderline or deficient vitamin B12 status. Onset of subacute combined degeneration affecting the brain and spinal cord is a well documented event when individuals with low body stores of cobalamin are exposed to nitrous oxide.2
There is a long list of situations which put children at special risk of cobalamin deficiency—for example, diets low in animal products, synthetic feeding of any description, small bowel malfunction, any prolonged illness with disturbance of feeding behaviour, especially if combined with increased metabolic demands—for example, systemic malignancy or chemotherapy. Children with chronic conditions often need painful procedures, and depleted cobalamin stores may not be apparent unless measurements of serum B12 are made routinely. What is more, repeated use of nitrous oxide depletes the body stores of cobalamin even in well people.
Given the scale of use which would result from routine use of nitrous oxide in children undergoing painful procedures, there should be real concern about the potential for an accident in a child with occult cobalamin deficiency. The message must be: never forget vitamin B12 when thinking of using nitrous oxide.