An 81-year-old patient had prolonged competitive neuromuscular blockade with train-of-four ratios of 0.1 and 0.5, respectively, after two successive anaesthesia procedures (enflurane-N2O/O2; vecuronium-succinylcholine-sequence) for transurethral prostate resection. Although antagonism with neostigmine was promptly successful after the first, 65-min period of anaesthesia (1.5 mg vecuronium for
... [Show full abstract] precurarization, 100 mg succinylcholine for intubation, 3 mg vecuronium), repetitive and chronologically staggered administration of neostigmine after the second, 30-min period of anaesthesia (1 mg vecuronium for precurarization, 100 mg succinylcholine for intubation) had hardly any effect, so that the patient had to be ventilated mechanically for a total of 4.5 h. Laboratory analysis revealed homozygous, atypical, plasma cholinesterase (790 U/l; dibucaine number 23; genotype E
a
1E
a
1). This retrospectively confirmed a succinylcholine-induced phase II block in both instances, as had already been suspected following the second anaesthetic procedure. The degree of block transformation, and thus the available time, are decisive in explaining the diverse effects of antagonism here. It must be assumed that a complete phase II block developed after the first succinylcholine exposure owing to the longer duration of anaesthesia; the purely competitive component (train-of-four ratio 0.1) was easily antagonized by neostigmine. At the time of the attempted antagonism after the second, shorter period of anaesthesia, however, block transformation was still incomplete (train-of-four ratio 0.5). The administration of neostigmine therefore rather intensified the depolarization segment of the mixed block, so that repeated attempts at antagonism then inhibited any further block transformation.
