To the Editor:--Mivacurium is a short-acting nondepolarizing muscle relaxant hydrolyzed by plasma cholinesterase. The in vitro rate of hydrolysis is approximately 70% of that of succinylcholine. Ostergaard et al. showed that mivacurium, in a dose as small as 0.03 mg *symbol* kg sup -1, can produce an intense and prolonged neuromuscular block in patients with atypical esterase; the resulting block could not be antagonized by neostigmine except after the administration of human plasma cholinesterase. .
Mivacurium may be the relaxant of choice in patients undergoing short surgical procedures, and it is frustrating to have unanticipated prolonged mivacurium-induced neuromuscular block after such procedures. Thus, it may be desirable to use a test dose of mivacurium to predict unusual sensitivity. Mivacurium in the general population has an ED50and ED95of approximately 0.043 and 0.075 mg *symbol* kg sup -1, respectively. A dose of 0.15 mg *symbol* kg sup -1 (twice the ED95) is recommended for tracheal intubation. Our report suggests the use of a test dose of 0.015 mg *symbol* kg sup -1 mivacurium, which is one-tenth the recommended intubating dose. In five adult female patients scheduled for minor gynecologic procedures (dilation and curettage or tubal ligation), a preoperative blood sample showed a plasma cholinesterase activity and dibucaine number (DN) within the normal range (75–85). Anesthesia was induced with 2.5 mg *symbol* kg sup -1 propofol, and neuromuscular transmission was monitored by the Datex Relaxograph. In all five patients, administration of 0.015 mg *symbol* kg sup -1 mivacurium produced 0–15% neuromuscular block within 3–4 min. No block was observed in two patients, 5% block in one patient, 10% block in one patient, and 15% block in the last patient. This was considered a normal response to the test dose, and hence, the intubating dose of 0.15 mg *symbol* kg sup -1 mivacurium was administered and was followed by complete neuromuscular block within 2–3 min. Spontaneous recovery of neuromuscular transmission up to 25–50% was noted after 10–20 min.
The neuromuscular block of the test dose in the five normal patients was compared to that achieved in a 29-yr-old woman scheduled for tubal ligation who was known to be homozygous for the atypical genes (DN 23). In this patient, after intravenous propofol administration, 0.015 mg *symbol* kg sup -1 mivacurium produced about 95–98% neuromuscular block, and the patient showed 10% recovery of neuromuscular transmission after 30 min. At that time, 0.05 mg *symbol* kg sup -1 neostigmine reversed the block. Figure 1shows the response to mivacurium in the atypical patient, as compared to one of the normal patients.
Our observations suggest that the test dose of mivacurium can predict unusual sensitivity to mivacurium in patients with atypical esterase while producing a degree and duration of block that can be reversed easily with neostigmine. In patients with normal esterase, the test dose produces only minimal or no neuromuscular block and may serve as a priming dose that enhances the onset of the subsequent intubating dose of mivacurium.
In conclusion, the use of a test dose of mivacurium of 0.015 mg *symbol* kg sup -1 (about 1 mg in the average adult) can predict the unanticipated intense and prolonged mivacurium-induced neuromuscular block in patients with atypical plasma cholinesterase.
Anis Baraka, M.D., F.R.C.A., Professor and Chairman, Department of Anesthesiology, American University of Beirut, Beirut, Lebanon.
