Succinylcholine and neuromuscular blockade monitoring.

Abstract

We thank Rodney et al. for presenting their strategy for managing neuromuscular blockade 1. However, they do not mention succinylcholine, for which neuromuscular monitoring may also be useful, particularly in detecting patients with pseudocholinesterase abnormalities 2, 3. We report a case of prolonged apnoea with neuromuscular blockade monitoring following succinylcholine administration. A 68-year-old patient at our hospital spontaneously recovered neuromuscular function 16 min after 1 mg.kg−1 succinylcholine administration for tracheal intubation, with the train-of-four ratio (TOFr, calibrated adductor pollicis brevis acceleromyography (GE Healthcare, Helsinki, Finland)) increasing to 0.8 (Fig. 3a). Tetanic stimulation was not used to check for post-tetanic facilitation. Rocuronium 20 mg was then administered (Fig. 3b). At the end of surgery, 49 min later, the TOFr was 0.2, and 1 mg atropine + 2.5 mg neostigmine were administered (Fig. 3c). The TOFr rose to 0.65, before falling back to 0.2 (Fig. 3d), increasing to 0.35 after a second dose of 1 mg neostigmine. Recognising the possibility of rocuronium sensitivity, 200 mg sugammadex was administered, increasing the TOFr to 0.7, but without enabling the patient to maintain spontaneous breathing, even when a second dose of 200 mg sugammadex was administered 10 min later. The patient was transferred to the surgical intensive care unit and his trachea extubated uneventfully six hours later. He reported no intra-operative awareness. His pseudocholinesterase level was found to be 2,500 U.L−1 (normal range 4,500–13,950 U/L) and his dibucaine number 30.6% (40–60% = atypical heterozygote). Succinylcholine hydrolysis by butyrylcholinesterase (pseudocholinesterase) normally leads to full TOFr recovery within 10–15 min 4. In the case reported, TOFr recovered to 0.8 but without complete recovery of twitch magnitude, which does not exclude type-2 neuromuscular blockade. Rocuronium accentuated blockade, and neostigmine produced mild transitory recovery by antagonism but appeared to potentiate type-1 blockade. Although TOFr improved with 400 mg sugammadex, clinical recovery was insufficient. Low plasma pseudocholinesterase levels and a low dibucaine number subsequently confirmed abnormal cholinesterase function. Rodney et al. are right to conclude that quantitative monitoring of neuromuscular blockade and effective reversal should be mandatory. This case demonstrates that such monitoring should also be used routinely when succinylcholine is administered.