The reversal of profound mivacurium-induced neuromuscular blockade

Abstract

Purpose: Mivacurium is metabolized by plasma cholinesterase catalyzed ester hydrolysis. Acetylcholinesterase antagonists used in the reversal of muscle relaxation may also inhibit plasma cholinesterase and, therefore, delay the hydrolysis of mivacurium. The clinical interaction between acetylcholinesterase antagonists and mivacurium induced neuromuscular blockade was studied. Method: Intraoperative muscle relaxation was maintained with a mivacurium infusion to achieve a constant intense block (first twitch, T1, 2-3% of control). Patients were randomly divided into three groups. Patients in Group 1 received no anticholinesterase, in Group 2 neostigmine 0.07 mg · kg-1, and in Group 3 edrophonium 1 mg · kg-1. The times between termination of the mivacurium infusion (Group 1) or the administration of the anticholinesterase (Groups 2 and 3) to 25%, 50%, 75% and 95% T1 recovery, and to 50%, 70% and 90% recovery in the ratio, T4/T1 (TR) were recorded. Result: In the neostigmine Group, T1 recovery to 25%, 50% and 75% (2.32 ± 1.41, 3.90 ± 1.85 and 6.88 ± 2.66 min) was accelerated compared with control (3.36 ± 1.34, 5.78 ± 2.22, and 8.58 ± 3.60), but recovery to 95% (18.53 ± 9.09 vs 13.29 ± 5.24 min) was delayed. Also, TR recovery to 50%, 70%, and 90% was slower (14.47 ± 8.73, 21.25 ± 11.06 and 31.37 ± 12.11 min vs 11.75 ± 3.74, 13.78 ± 4.39 and 17.86 ± 6.44 min). However, all T1 and TR recovery times were decreased in the edrophonium group (0.88 ± 0.51, 2.00 ± 1.50, 4.97 ± 2.96, and 9.35 ± 5.24 min for T1 and 6.86 ± 3.93, 9.05 ± 4.51 and 12.24 ± 6.66 min for TR). Conclusion: Neostigmine reversal of intense mivacurium neuromuscular block should be avoided, as this may result in prolongation of the block.