Neurologic degeneration associated with nitrous oxide anesthesia in patients with vitamin B12 deficiency
T. S. Flippo and W. D. Holder Jr
Department of General Surgery, Carolinas Medical Center, Charlotte.
Vitamin B12 (cyanocobalamin) is an integral component of two biochemical
reactions in man: the conversion of L-methylmalonyl coenzyme A into
succinyl coenzyme A and the formation of methionine by methylation of
homocysteine. The transmethylation reaction is essential to DNA synthesis
and to the maintenance of the myelin sheath by the methylation of myelin
basic protein. Active vitamin B12 contains cobalt in its reduced form
(Co+). Nitrous oxide produces irreversible oxidation to the Co++ and Co
forms that renders vitamin B12 inactive. Five cases (four from the
literature and one new case) are presented in which patients unsuspected of
having vitamin B12 deficiency developed subacute combined degeneration of
the spinal cord following nitrous oxide anesthesia. Patients with vitamin
B12 deficiency are exceedingly sensitive to neurologic deterioration
following nitrous oxide anesthesia. If unrecognized, the neurologic
deterioration becomes irreversible and may result in death.
