THE REVERSAL OF PROFOUND MIVACURIUM-INDUCED NEUROMUSCULAR BLOCKADE

Purpose: Mivacurium is metabolized by plasma cholinesterase catalyzed ester hydrolysis. Acetylcholinesterase antagonists used in the reversa l of muscle relaxation may also inhibit plasma cholinesterase and, the refore, delay the hydrolysis of mivacurium. The clinical interaction b etween acetylcholinesterase antagonists and mivacurium induced neuromu scular blockade was studied. Method: Intraoperative muscle relaxation was maintained with a mivacurium infusion to achieve a constant intens e block (first twitch, T-1, 2-3% of control). Patients were randomly d ivided into three groups. Patients in Group I received no anticholines terase, in Group 2 neostigmine 0.07 mg . kg(-1), and in Group 3 edroph onium 1 mg . kg(-1). The times between termination of the mivacurium i nfusion (Group 1) or the administration of the anticholinesterase (Gro ups 2 and 3) to 25%, 50%, 75% and 95% TI recovery, and to 50%, 70% and 90% recover), in the ratio, T-4/T-1 (TR) were recorded. Result: In th e neostigmine Group, TI recovery to 25%, 50% and 75% (2.32 +/- 1.41, 3 .90 +/- 1.85 and 6.88 +/- 2.66 min) was accelerated compared with cont rol (2.32 +/- 1.34, 5.78 +/- 2.22, and 8.58 +/- 3.60, and), but recove ry 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 +/- 1 1.06 and 31.37 +/- 12.11 min vs 11.75 +/- 3.74, 13.78 +/- 4.39 and 17. 86 +/- 6.44 min). However all T-1 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 T-1 and 6.86 +/- 3.93, 9.05 +/- 4.51 and 1 2.24 +/- 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.