Postpartum Patients Have Slightly Prolonged Neuromuscular Block After Mivacurium

Postpartum patients have decreased plasma cholinesterase activity, which may slow the metabolism of mivacurium.We compared the duration of a mivacurium neuromuscular block in 11 women undergoing postpartum tubal ligation 36-99 h after delivery with that in 11 control women undergoing gynecological surgery. Anesthesia was induced with propofol and fentanyl and maintained with propofol and nitrous oxide. Neuromuscular block was monitored by electromyography, and the ulnar nerve was stimulated transcutaneously using a train-of-four pattern. Patients received a bolus dose of mivacurium 0.15 mg/kg. The median (range) duration of neuromuscular block until 25% recovery of the first twitch response was longer in the postpartum group, 19.4 (15.6-25.2) min, compared with the control group, 16.3 (11.0-23.4) min (P = 0.04). The median (range) plasma cholinesterase activity was decreased in the postpartum group, 4.0 (0.1-5.5) kU/L, compared with the control group, 7.1 (6.2-10.0) kU/L (P < 0.001). The duration of neuromuscular block was inversely correlated with cholinesterase activity (Kendall rank correlation tau = -0.43, P = 0.005). The slight prolongation of neuromuscular block should not be significant clinically. Implications: Postpartum patients have decreased amounts of the plasma cholinesterase enzyme. This would slow the metabolism of the muscle relaxant mivacurium. However, the duration of muscle paralysis is only prolonged by approximately 3 min, which would not normally cause any significant problems.

[1]  A. Benzer,et al.  Extended Duration of Action of Rocuronium in Postpartum Patients , 1997, Anesthesia and analgesia.

[2]  L. Skovgaard,et al.  Good Clinical Research Practice (GCRP) in pharmacodynamic studies of neuromuscular blocking agents , 1996, Acta anaesthesiologica Scandinavica.

[3]  J. Viby-Mogensen Mvacurium block in patients with abnormal plasma chohnesterase , 1995 .

[4]  O. Meretoja,et al.  Interaction Between Mivacurium and Succinylcholine , 1995, Anesthesia and Analgesia.

[5]  R. Mirakhur,et al.  The Influence of the Duration of Control Stimulation on the Onset and Recovery of Neuromuscular Block , 1995, Anesthesia and analgesia.

[6]  D. Morgan,et al.  Lean Body Mass as a Predictor of Drug Dosage , 1994, Clinical pharmacokinetics.

[7]  L. Skovgaard,et al.  Influence of plasma cholinesterase activity on recovery from mivacurium‐induced neuromuscular blockade in phenotypically normal patients , 1992 .

[8]  S. Basta Clinical pharmacology of mivacurium chloride: a review. , 1992, Journal of clinical anesthesia.

[9]  P. Mair,et al.  Comparison of Vecuronium‐ and Atracurium‐Induced Neuromuscular Blockade in Postpartum and Nonpregnant Patients , 1991, Anesthesia and analgesia.

[10]  T. H. Joyce,et al.  The effect of H2-receptor antagonist premedication on the duration of vecuronium-induced neuromuscular blockade in postpartum patients. , 1989 .

[11]  T. H. Joyce,et al.  Vecuronium and prolonged neuromuscular blockade in postpartum patients. , 1987, Anesthesiology.

[12]  B. Gutsche,et al.  Succinylcholine Pharmacodynamics in Peripartum Patients , 1985, Anesthesiology.

[13]  R. Evans,et al.  Plasma cholinesterase changes during pregnancy , 1980, Anaesthesia.

[14]  M. Whittaker Plasma cholinesterase variants and the anaesthetist , 1980, Anaesthesia.

[15]  J. Liddell,et al.  Value of butyrylthiocholine assay for identification of cholinesterase variants. , 1970, Journal of medical genetics.

[16]  H. Harris,et al.  Differential Inhibition of Human Serum Cholinesterase with Fluoride: Recognition of Two New Phenotypes , 1961, Nature.