Edrophonium antagonism of intense mivacurium-induced neuromuscular block in children

We have studied the time course of recovery after administration of edrophonium during intense mivacurium block in children aged 2-10 yr, using thumb acceleration in response to train-of-four (TOF) stimulation. Forty-three children receiving alfentanil, propofol, nitrous oxide, isoflurane anaesthesia and mivacurium 0.2 mg kg-1 were allocated randomly to one of three groups. Patients in group 1 (n = 15) received edrophonium 1 mg kg-1, 2 min after maximum block (intense block group). At the time of administration of edrophonium in this group, there was no response to TOF stimulation (100% block) and the post-tetanic count was 10.7 (range 0-20). Patients in group 2 received the same dose of edrophonium after 10% recovery of the first twitch (T1) in the TOF (conventional reversal). Patients in group 3 (n = 13) recovered spontaneously. All patients developed complete suppression of twitch height in response to the bolus dose of mivacurium. All recovery times were measured from the point of maximum block after mivacurium. Mean time for 25% recovery of T1 (clinical duration) was 3.8 (SD 1.1) min in the intense block group. This was significantly shorter than the conventional reversal (8.3 (2.4) min) and spontaneous recovery (9.2 (3.5) min) groups (P < 0.001). The times for 75% and 90% recovery of T1 were shorter in the intense block group (9.4 (2.8), 12.3 (4.2) min) compared with the conventional (13.1 (3.8), 17.3 (4.8) min) and spontaneous recovery (14.9 (4.5), 17.9 (5.2) min) groups (P < 0.01). Total recovery time required for 70% recovery of the TOF ratio (T4/T1) was 8.8 (2.4) min in the intense block group. This was significantly shorter than the conventional reversal (11.9 (3.2) min) (P < 0.05) and spontaneous recovery (17.1 (4.0) min) groups (P < 0.001). Conventional reversal was associated with a shorter total recovery time compared with spontaneous recovery (P < 0.01). The recovery index (time interval between T1 25% and 75%) was comparable in groups 1-3 (5.5 (2.0), 4.8 (2.1) and 5.7 (1.4) min respectively). Ten minutes after development of maximum block, the numbers of patients who recovered adequately (TOF ratio 70% or more) were, respectively, 12 (80%), 8 (53%) and 1 (8%) in groups 1-3. We conclude that edrophonium antagonized intense (no response to TOF stimulation) mivacurium-induced block in children, with significant reduction in the recovery times of T1 and TOF ratio compared with conventional reversal and spontaneous recovery.      

Effect of metoclopramide on mivacurium-induced neuromuscular block

In order to investigate the effect of metoclopramide on the duration of action of mivacurium, 45 patients were randomized into three groups. Group M10 (n = 15) and M20 (n = 15) received 10 and 20 mg of metoclopramide i.v., respectively, and group S (n = 15) received saline 2 min before induction of anesthesia with fentanyl, thiopental and mivacurium. Plasma cholinesterase activity (pCHE) was measured before induction of anesthesia and 2 min after injection of metoclopramide and saline. Neuromuscular block was monitored by a force transducer using train of four nerve stimulation. Anesthesia was maintained with isoflurane and N2O. Time to recovery of a twitch height of 90% was significantly prolonged in group M10 and M20 (44 +/- 15 and 57 +/- 10 min) as compared to group S, 32 +/- 9 min, P < 0.05). A slight but significant decrease in pCHE was observed in group M20. Because of the risk of prolonged duration of action of mivacurium, neuromuscular blockade should always be monitored whenever metoclopramide is given before injection of mivacurium.     

Prolonged mivacurium-induced neuromuscular block. Case report

A 38-year-old white male patient was admitted to the hospital for elective surgery. General anesthesia was performed with propofol, alfentanil, nitrous oxide and mivacurium as neuromuscular blocker. Seven months before he had the same surgery without anesthetic problems (he received: propofol, vecuronium bromide, fentanil, nitrous oxide). Neuromuscular monitoring was carried out because the patient was included in a study assessing the clinical effect of mivacurium in microlaryngoscopy surgery. After mivacurium administration the first signs of recovery from neuromuscular block were observed after 255 min. The tracheal tube was withdrawn after 410 min from mivacurium administration, at this time the T1 was 80% of the control values and 7 min later the T1 reached 98%.     

Recovery from mivacurium-induced neuromuscular blockade after neurosurgical procedures of long duration

Study Objective: To determine if recovery following prolonged (5 hours in length or greater) infusions of mivacurium is different from recovery after single bolus administration.

Design: open-labelled, controlled study.

Setting: Inpatient neurosurgical service at a university hospital.

Patients: 36 patients between the ages of 18 to 65 without significant history of renal, hepatic, cardiac, or metabolic disease undergoing neurosurgical procedures. 21 patients had craniotomies or skull base procedures of an estimated length of 5 hours or greater; 15 patients (control) underwent short neurosurgical operations (two hours or less).

Interventions: Intravenous (IV) mivacurium 0.15 mg/kg was given with stable general anesthesia with 70% nitrous oxide in oxygen, 0.2% to 0.3% end-tidal isoflurane, and continuous infusion of fentanyl. The control group was allowed to recover spontaneously after single bolus administration while neuromuscular blockade was maintained in the study group with a continuous infusion of mivacurium until 30 minutes before completion of surgery, at which time the infusion was discontinued and neuromuscular function was allowed to recover spontaneously.

Measurements and Main Results: The evoked compound electromyogram of the adductor pollicis brevis muscle was measured during stimulation of the ulnar nerve at 2 Hz for 2 seconds at 10-second intervals. Measurements included time to 50% and 90% depression of twitch (T₁ of the TOF response), time to T₁ equal to 25% (T₁25), 50% (T₁50), and 75% (T₁75) of baseline, and TOF ratio (TR) at 10%, 25%, 50%, and 75% recovery. Recovery index (RI), which is T₁75 minus T₁25, was also determined. All mivacurium infusion rates decreased during surgery. Recovery rates were significantly longer in the long infusion (LI) group than the control group. RI was also increased in the LI group compared with the single bolus control (11.3 ± 1.2 minutes vs. 7.1 ± 0.8 minutes p < 0.05).

Conclusions: Recovery following mivacurium by prolonged continuous infusion was slower than that observed after single bolus administration in this patient population. Clinically, this increased time to recovery may be insignificant.     

The nature of spontaneous recovery from mivacurium-induced neuromuscular block

The hypothesis of this study was that, in a given patient, recovery from a tracheal intubating dose of mivacurium would indicate the time course of spontaneous recovery after discontinuation of an infusion of mivacurium. Thirty-eight male patients consented to participate in the study. After induction of anesthesia and endotracheal intubation, the ulnar nerve was stimulated with train-of-four (TOF) stimuli at 12-s intervals. Patients received 0.3 mg/kg mivacurium in two evenly divided doses of 0.15 mg/kg each, separated by 30 s. Complete ablation of TOF responses occurred in most patients. Once the first twitch in the TOF (T ) had recovered to 25% of its baseline height, a mivacurium infusion was begun to maintain 95% suppression of T1. As surgery was nearing completion, the infusion was discontinued, and neuromuscular function was allowed to recover spontaneously. Data were analyzed for recovery intervals after the administration of the initial doses of mivacurium and after discontinuation of the infusion. Analysis of variance was used to determine the strength of correlation between the time from administration of the initial 0.3 mg/kg dose to 5% recovery of T1 and the times to recovery of TOF ratios of 70% and 90%. The 25%-75% recovery interval after discontinuation of the infusion ranged from 2.8 to 11.3 min. The time interval after administration of mivacurium 0.3 mg/kg to 5% recovery of T1 correlated with both the time to recovery of a TOF ratio of 70% and 90%. Recovery to a TOF of 90% after discontinuation of the infusion required approximately the same amount of time as recovery to 5% T1 after the administration of 0.3 mg/kg mivacurium. Each patient's recovery of neuromuscular function after discontinuation of a mivacurium infusion was related to his recovery after the administration of 0.3 mg/kg mivacurium. Therefore, the need for pharmacologic antagonism of block can be anticipated well before the end of an anesthetic. IMPLICATIONS: Mivacurium (0.3 mg/kg) was administered to 38 patients. As they began to recover muscle strength, a mivacurium infusion was begun and later discontinued as surgery was nearing completion. Each patient's early recovery (administration to 5% recovery of T1) after the initial dose of mivacurium correlated well with more complete recovery of muscle strength after discontinuation of an infusion. This relationship enables early prediction of recovery speed after a mivacurium infusion.     

Chronic carbamazepine therapy does not influence mivacurium-induced neuromuscular block

Patients receiving anticonvulsant drugs chronically are relatively resistant to some non-depolarizing neuromuscular blocking drugs. We investigated the influence of chronic carbamazepine therapy on neuromuscular block induced by mivacurium in 20 otherwise healthy individuals undergoing neurosurgical operations, 10 of whom were receiving chronic treatment with carbamazepine and the other 10 served as controls. The median duration of carbamazepine therapy was 22 weeks (range 4-182 weeks). After premedication with oral diazepam, anaesthesia was induced with fentanyl and thiopentone and maintained with 0.5% isoflurane and nitrous oxide in oxygen. The ulnar nerve was stimulated and the evoked electromyogram recorded using a Datex NMT monitor. Mivacurium 0.15 mg kg-1 (2 x ED95) was given as a bolus i.v. Based on the response to the first of four stimuli, lag time, onset- time, times to recovery to 10%, 25%, 50% and 75% of baseline responses and recovery index (RI 25-75%) did not differ between the two groups. We conclude that mivacurium-induced neuromuscular block was not influenced by preceding chronic carbamazepine therapy.      

Dose-response relationships for edrophonium antagonism of mivacurium-induced neuromuscular block during N2O-enflurane-alfentanil anaesthesia

The purpose of this study was to determine the dose-response relationships for edrophonium antagonism of mivacuriuminduced neuromuscular block. Seventy-five ASA I or II adults were given mivacurium 0.15 mg · kg^{? 1} followed by an infusion (7 μg · kg^{? 1} · min^{? 1}) during alfentanil-propofol-N₂O-enflurane anaesthesia. Train-of-four stimulation (TOF) was applied to the ulnar nerve every 20 sec and the response of the adductor pollicis was recorded (Relaxograph NMT-100. Datex, Helsinki, Finland). Mivacurium infusion was modified at five-minute intervals in order to keep the height of the first twitch in TOF (T₁) at 5% of its control value. At the end of surgery, edrophonium (0.0. 0.125, 0.25, 0.5. or 1.0 mg · kg^{? 1}) combined with glycopyrrolate (0.0, 0.0012, 0.0025, 0.005, or 0.01 mg · kg^{? 1}) were administered by random allocation. Edrophonium doses of 0.25, 0.5 and 1.0 mg · kg^{? 1} were different from placebo with regard to time to attain a TOF ratio (fourth twitch in TOF/ T,) = 0.7 (13.8 ± 4.5, 11.1 ± 3.5, 11.4 ± 3.0 vs 19.7 ± 4.7 min P < 0.05). Doses of 0.5 and 1.0 mg · kg^{? 1} permitted faster recovery time of T₁ from 10 to 95% (T_{10– 95}) than did placebo (7.5 ± 3.8,8.9 ± 3.5 vs 14.5 ± 5.0 min P < 0.05). Edrophonium 0.5 mg · kg^{? 1} was different from placebo with regard to recovery time of T₁ from 25 to 75% (T_{25– 75}) (3.3 ± 2.0 vs 6.7 ± 2.0 min P < 0.05). Only edrophonium 0.5 mg · kg^{? 1} provided faster recovery than placebo with regard to all three indices. It is concluded that edrophonium 0.5 + glycopyrrolate 0.005 mg · kg^{? 1} allow the fastest recovery from a mivacurium-induced block during enflurane-N₂O anaesthesia.     

Edrophonium and human plasma cholinesterase combination for antagonism of mivacurium-induced neuromuscular block

We have compared the reversal characteristics of mivacurium after administration of an edrophonium-plasma cholinesterase (PCHE) combination with that produced by each antagonist alone. Forty ASA I adults were given mivacurium 0.15 mg kg-1 during fentanyl-thiopentone- nitrous oxide-isoflurane anaesthesia. TOF stimulation was applied to the ulnar nerve every 12 s, and the force of contraction of the adductor pollicis muscle was recorded. When spontaneous recovery of first twitch height (T1) reached 10% of its initial control value, patients were allocated randomly to one of four groups (n = 10 in each). Neuromuscular function in patients in group 1 (control group) was allowed to recover spontaneously. Patients in groups 2-4, respectively, received edrophonium 1 mg kg-1 (group ED), exogenous PCHE equivalent to activity present in 25 ml kg-1 of human plasma (group PCHE) or edrophonium 1 mg kg-1 with exogenous human PCHE equivalent to the activity present in 25 ml kg-1 of human plasma (combination group). The time to attain a TOF ratio of 0.75 in the combination group was 4.6 (SD 0.9) min. This was shorter (P < 0.01) than that observed in patients in the control (16.8 (3.3) min), ED (8.9 (3.6) min) and PCHE (9.3 (1.6) min) groups. There was no difference in recovery indices between groups ED and PCHE. We have demonstrated that the edrophonium- PCHE combination significantly accelerated recovery of mivacurium- induced block compared with that observed with the use of individual antagonists.      

Comparison of neostigmine-induced recovery with spontaneous recovery from mivacurium-induced neuromuscular block

In 24 ASA I–II adults anaesthetized with thiopentone,fentanyl and nitrous oxide in oxygen, we studied neuromusculartransmission with isometric adductor pollicis monitoring. Patientsreceived mivacurium 0.2 mg kg^–1 followed by an infusionlasting at least 60 min and adjusted to maintain twitch heightat 1–5%. After termination of the mivacurium infusion,when twitch height spontaneously regained 25% of its controlvalue, the patients were allocated to two groups of 12 patientseach. In group NEO patients received neostigmine 40 µgkg^–1 and atropine 15 µg kg^–1 and in groupSPO neuromuscular transmission was allowed to recover spontaneously.Twitch height was measured every 10 s and train-of-four (TOF)(2Hz) every 3 min. After 15 min, residual force after tetanicstimulation (50 and 100 Hz, 5-s duration (RF50_HZ, RF100_Hz),1 min apart) were recorded sequentially. At 15 min, mean TOFratio was greater in group NEO (0.94 (SEM 0.01)) than in groupSPO (0.87 (0.02)) (P < 0.01). All patients in group NEO recoveredto a TOF ratio greater than 0.7 after 6 min compared with 15min in group SPO (P < 0.005). A TOF ratio greater than 0.9was observed in all patients in group NEO compared with onlysix in group SPO (P < 0.025). Nevertheless, RF50_HZ and RF100_HZdid not differ significantly (0.92 (0.01) (group NEO), 0.91(0.01) (group SPO) and 0.83 (0.02) (group NEO), 0.78 (0.03)(group SPO), respectively). We conclude that although therewas a high degree of spontaneous recovery, administration ofneostigmine-atropine accelerated the rate of recovery of neuromusculartransmission after mivacurium and greatly increased the numberof patients satisfying the criteria for complete recovery ofneuromuscular transmission (TOF ratio < 0.9) within 15 min.     

The reversal of profound mivacurium-induced neuromuscular blockade

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, and), 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.     

Onset and duration of mivacurium-induced neuromuscular block in patients with Duchenne muscular dystrophy

Background. To determine the response to mivacurium, we prospectivelystudied onset time and complete spontaneous recovery from mivacurium-inducedneuromuscular block in patients with Duchenne muscular dystrophy(DMD). Methods. Twelve boys with DMD, age 5–14 yr, seven of themwheelchair-bound, ASA II–III, and 12 age- and sex-matchedcontrols (ASA I) were enrolled in the study. Anaesthesia wasinduced with fentanyl 2–3 µg kg^–1 and propofol3–4 mg kg^–1 titrated to effect, and maintained bycontinuous i.v. infusion of propofol 8–12 mg kg^–1and remifentanil as required. The lungs were ventilated withoxygen in air. Neuromuscular transmission was assessed by acceleromyographyusing train-of-four (TOF) stimulation every 15 s. After baselinereadings, a single dose of mivacurium 0.2 mg kg^–1 wasgiven. The following variables were recorded: (i) lag time;(ii) onset time; (iii) peak effect; (iv) recovery of first twitchfrom the TOF response to 10, 25 and 90% (T₁₀, T₂₅, T₉₀) relativeto baseline; (v) recovery index (time between 25 and 75% recoveryof first twitch); and (vi) recovery time (time between 25% recoveryof first twitch and recovery of TOF ratio to 90%). For comparisonbetween the groups the Mann–Whitney U-test was applied. Results. There were no differences between the groups in lagtime, onset time and peak effect. However, all recorded recoveryindices were significantly (P<0.05) prolonged in the DMDgroup. The median (range) for time points T₁₀, T₂₅ and T₉₀ inthe DMD and control group was 12.0 (8–16) vs 8.4 (5–15)min, 14.1 (9–20) vs 10.5 (7–17) min and 26.9 (15–40)vs 15.9 (12–23) min, respectively. The recovery indexand recovery time were similarly prolonged in the DMD group. Conclusions. These results support the assumption that mivacurium-inducedneuromuscular block is prolonged in patients with DMD. This study was presented at the Annual Meeting of the AmericanSociety of Anaesthesiologists, Las Vegas, October 2004. These authors contributed equally to this work.     

Unmasked residual neuromuscular block after administration of vecuronium for days

IMPLICATIONS: Significant neuromuscular block may be present in patients who have received vecuronium for days.     

Blood flow and mivacurium-induced neuromuscular block at the orbicularis oculi and adductor pollicis muscles

We have studied the pattern of blood flow and pharmacodynamic profile of mivacurium-induced block at the adductor pollicis and orbicularis oculi muscles. We studied 30 adult patients anaesthetized with fentanyl, thiopentone, nitrous oxide-isoflurane, and mivacurium 0.2 mg kg-1. Neuromuscular transmission was monitored with accelerometry (TOF Guard, Biometer, Denmark). Blood flow was measured at the two muscles with the use of a laser Doppler flowmeter (Laserflo BPM2, Vasamedics, USA). All patients developed 100% neuromuscular block at the adductor pollicis muscle. Mean maximum neuromuscular block at the orbicularis oculi was 96.4 (SD 3.5)% (ns). Onset time, time required for 25% and 75% recovery of the first twitch in the train-of-four (T1), and a train- of-four ratio (T4/T1) of 90% at the orbicularis oculi were respectively, mean 130.4 (SD 28.5) s, 9.1 (3.2) min, 16.2 (3.9) min and 20.2 (4.3) min and were significantly shorter than the corresponding values at the adductor pollicis: 202.7 (37.2) s, 12.9 (3.9) min, 21.1 (5.1) min and 30.8 (7.4) min. For a given T1, there was significantly less train-of-four fade (T4/T1) at the orbicularis oculi than at the adductor pollicis muscle during recovery. Blood flow was comparable at the two muscles before induction of anaesthesia. Thiopentone significantly increased thenar muscle blood flow from 2.9 (1.5) to 12.3 (6.8) ml 100 g-1 min-1, with a further increase to 22.7 (8.0) ml 100 g- 1 min-1 after isoflurane (P < 0.001). Blood flow at the orbicularis oculi was not altered by thiopentone or isoflurane and was consistently lower than that at the adductor pollicis muscle. We conclude that the different pharmacodynamic profiles of mivacurium-induced block at the orbicularis oculi and adductor pollicis muscles were not related primarily to a difference in blood flows.      

Recovery of neuromuscular function after atracurium and pancuronium maintenance of pancuronium block

The study was undertaken to determine whether a neuromuscular blockade induced with pancuronium but maintained with atracurium was associated with a shorter time to complete recovery after administration of neostigmine than if the blockade was maintained with pancuronium alone. Anaesthesia consisted of thiopentone, N₂O/O₂/enflurane and fentanyl, and the neuromuscular blockade, induced by pancuronium 0.1 mg · kg^?1 was monitored by the force of contraction of adductor pollicis during major abdominal surgery lasting 2–5 hr. In 24 patients — Group 1 — atracurium 0.07 mg · kg^?1 was repeated when the first twitch of the train-of-four (TOF) returned to 25% of control (T₁/ TC 25). In 28 patients — Group 2 — pancuronium 0.015 mg · kg^?1 was given at similar recovery of T₁/ TC. At the end of surgery, neostigmine 0.07 mg · kg^?1 and glycopyrrolate 0.015 mg · kg^?1 were given to reverse the residual neuromuscular blockade which was indicated by a T₁/TC of less than 25% in all patients. The time from injection of the reversal drugs to a TOF ratio of 70% was similar in both groups (Group 1, 11.6 ± 7.6 min; Group 2, 10.1 ± 6 min; P = NS), but the recovery index was smaller in Group 2 (Group 1, 4 ± 2.6 min; Group 2, 2.61 ± 1.2 min; P < 0.05). Furthermore, there was no difference between groups in the duration of action of each redose. The study showed that when compared with pancuronium, equipotent doses of atracurium were not associated with (a) a shorter time to complete recovery from a neuromuscular blockade induced with pancuronium or (b) a shorter duration of action.     

Recovery of neuromuscular transmission following desensitization block.

Depolarization and desensitization neuromuscular blockade was induced with suxamethonium. Rate of recovery of neuromuscular transmission did not vary with the nature of the blockade.     

Monitoring of neuromuscular block after administration of vecuronium in patients with diabetes mellitus

Background. We studied the supramaximal current for ulnar nervestimulation during electromyographic monitoring of onset andrecovery of neuromuscular block using a neuromuscular transmissionmodule (M-NMT Module, Datex-Ohmeda) in patients with Type 2diabetes undergoing anaesthesia with nitrous oxide, oxygen,isoflurane and fentanyl. Methods. Thirty-six diabetic patients were randomly assignedto a post-tetanic count (PTC) group (n=17) or train-of-four(TOF) group (n=19). In addition, 30 non-diabetic patients weredivided into control PTC (n=15) and TOF groups (n=15). Results. In the diabetic patients (diabetes PTC and diabetesTOF groups), the mean supramaximal stimulating current was significantlyhigher than in the non-diabetic patients (control PTC and TOFgroups) (50.5 (SD 14.1) vs 33.4 (6.1) mA, P<0.01). Onsetof neuromuscular block (time to disappearance of T1) after vecuronium0.1 mg kg^–1 in the diabetic patients did not differ significantlyfrom that in the non-diabetic patients (276 (77) vs 244 (44)s, P=0.055). Time to return of PTC1 did not differ significantlybetween the diabetes and control PTC groups (21.0 (12.1) vs15.7 (5.0) min, P=0.126). Times to return of T1 and T4 in thediabetes TOF group were significantly longer than in the controlTOF group (T1: 37.5 (15.2) vs 25.7 (7.6) min, P=0.01; T4: 61.4(23.7) vs 43.5 (11.4) min, P=0.01). During recovery, PTC andT4/T1 in the diabetes PTC and TOF groups were similar to thosein the control PTC and TOF groups, respectively. T1/T0 in thediabetes TOF group was significantly less than in the controlTOF group, 80–120 min after vecuronium (P<0.05). Conclusions. In diabetic patients, supramaximal current is higherthan in non-diabetic patients. After vecuronium, onset of neuromuscularblock and recovery of PTC or T4/T1 are not altered, but timeto return of T1 or T4, and recovery of T1/T0 are delayed indiabetic patients. Br J Anaesth 2003; 90: 480–6     

The costs of intense neuromuscular block for anesthesia during endolaryngeal procedures due to waiting time.

The goal of this double-blinded, prospective study was to compare the costs incurred by waiting time of intense neuromuscular block while posttetanic count (PTC) was maintained at 0-2 during jet ventilation. Fifty patients were randomized into five groups to receive atracurium (ATR), mivacurium (MIV), rocuronium (ROC), vecuronium (VEC), and succinylcholine (SUCC). PTC < or =2 was maintained until completion of laryngomicroscopy by administering additional doses of relaxants or by adjusting the speed of the infusion of SUCC. We compared waiting time, i.e., onset time and recovery time, and costs of intense neuromuscular block. The expenses due to waiting time were calculated based on the average costs in the otorhinolaryngological operating room in Tampere University Hospital: FIM 40 (approximately $8) per minute in 1997. MIV and SUCC differ favorably from ATR, ROC, and VEC when waiting time and costs are concerned. The recovery times with MIV and SUCC were considerably shorter than those with ATR, ROC, and VEC (P < 0.001 in all pairwise comparisons). Using the muscle relaxant with the longest waiting time instead of that with the shortest waiting time (difference 21.8 min) cost more than FIM 800 (approximately $160) extra per patient. IMPLICATIONS: In this randomized, double-blinded, prospective study, we evaluated the costs of intense neuromuscular block due to waiting time. Succinylcholine and mivacurium are the most economical muscle relaxants to use when intense neuromuscular block is mandatory. Using intermediate-acting muscle relaxants results in unduly prolonged recovery time and extra costs.