To the Editor:—
Exaggerated sensitivity to vecuronium in a brain dead woman 1has an additional contributing factor, namely, the acute action of phenytoin. There is a difference in acute or chronic use of phenytoin. It has a weak postjunctional blocking effect that, in the acute phase, causes a partial blockade at the neuromuscular junction. 2This is not generally realized in the awake patient receiving phenytoin, but it contributes to blockade by nondepolarizing muscle relaxants should the patient require anesthesia. 3,4
This partial blockade, in time, likely about 10 days to 2 weeks, promotes increased numbers of extra-junctional nicotinic acetylcholine receptors, resulting in resistance to nondepolarizing muscle relaxants (receptor upregulation). 5The woman described in this article was in the acute phase of phenytoin administration, so that potentiation of the effect of vecuronium was due, in part, to residual vecuronium or its metabolite (pharmacokinetics), acute phase phenytoin (pharmacodynamics), steroids, and perhaps her acute central nervous system depression. She had received 1.5 mg/kg vecuronium in more than 15 hours, and recovered normal responses after more than 60 hours.
However, the likely major factor in all this is the overdose of vecuronium, because the lack of neuromuscular monitoring during its administration prevented identification of the time of complete neuromuscular blockade.
