mivacurium and Apnea

Butyrylcholinesterase deficiency prolongs the effects of the drugs it degrades; succinylcholine and mivacurium. Existing literature on butyrylcholinesterase deficiency is dominated by genetic and biochemical studies. We searched MEDLINE, Embase, Web of Science and Biosis to systematically review the causes and clinical consequences of butyrylcholinesterase deficiency. We considered outcomes clinically relevant if neuromuscular blockade, induced by succinylcholine or mivacurium, was assessed using clinical criteria or neuromuscular monitoring. We included 66 studies: 25 randomised controlled trials; 13 clinically controlled trials; 26 prospective observational studies; 1 retrospective study; and 1 qualitative study. Data heterogeneity precluded quantitative synthesis. Studies described genetic, physiological, acquired or pharmacologically induced causes of butyrylcholinesterase deficiency. The prolongation of neuromuscular blockade by butyrylcholinesterase deficiency was most pronounced with homozygosity of a genetic variant, but other more common factors included increasing age, pregnancy, severe liver disease, burn injuries and drug interactions.

Topics: Anesthesia; Apnea; Butyrylcholinesterase; Humans; Metabolism, Inborn Errors; Mivacurium; Neuromuscular Blockade; Neuromuscular Monitoring; Succinylcholine

Takotsubo cardiomyopathy is an acute syndrome characterized by cardiac failure from disturbances in the contractility of the left ventricle. It is presumably caused by sympathetic over stimulation. We describe a case of postoperatively developed Takotsubo cardiomyopathy in a 69-year-old female. The syndrome developed in connection with awareness during complete residual paralysis. The literature on this syndrome is reviewed and implications for anaesthesia described.

Topics: Aged; Anesthesia, Intravenous; Apnea; Butyrylcholinesterase; Delayed Emergence from Anesthesia; Female; Humans; Intraoperative Awareness; Isoquinolines; Laryngeal Diseases; Metabolism, Inborn Errors; Mivacurium; Myocardial Infarction; Neuromuscular Nondepolarizing Agents; Polyps; Postoperative Complications; Takotsubo Cardiomyopathy; Vocal Cords

To distinguish among potential predictors of early, easy intubation in children, including apnea, neuromuscular block at two sites, and time, after administration of 0.3 mg/kg of mivacurium.. Prospective, randomized study.. Operating rooms of Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania.. 60 ASA physical status I and II children aged 2 through 7 years, scheduled for elective surgical procedures requiring endotracheal intubation.. After premedication with midazolam, general anesthesia was induced with halothane and nitrous oxide, and patients were randomly assigned to one of four groups. Mivacurium 0.3 mg/kg was given and tracheal intubation was begun 45 seconds after its injection, or when apnea, block of the orbicularis oculi, (OO) or block of the adductor pollicis (AP) was noted. Intubation conditions were evaluated by an experienced endoscopist.. The first clinical event after administration of mivacurium 0.3 mg/kg was apnea at 43 seconds (median) (average 48 seconds, SEM 2 seconds) after injection. The difference in the time at which neuromuscular block occurred at the AP (median 75 seconds) (average 77 seconds, SEM 2 seconds) and the OO (median 63 seconds) (average 68 seconds, SEM 4 seconds) was statistically, but not clinically, significantly different. All nine intubations that were begun at least 90 seconds after administration of mivacurium resulted in good or excellent intubation conditions, as did 30 of the 51 intubations started earlier.. In children, there is no advantage to monitoring neuromuscular function at the OO rather than the AP. After administration of 0.3 mg/kg of mivacurium, a 90-second interval before the start of intubation was a better predictor of good intubation conditions during halothane anesthesia (1% inspired) than were changes in evoked neuromuscular function.

Topics: Apnea; Body Temperature; Child, Preschool; Electrocardiography; Eye Movements; Female; Humans; Intubation, Intratracheal; Isoquinolines; Male; Mivacurium; Monitoring, Intraoperative; Neuromuscular Nondepolarizing Agents; Preanesthetic Medication; Prospective Studies; Synaptic Transmission

Variants of butyrylcholinesterase are frequently associated with prolonged response to suxamethonium or mivacurium. Butyrylcholinesterase (BChE) can be characterized by phenotyping and determination of genotype. Inappropriate timing of blood sampling might interfere with phenotyping methods. However, guidelines regarding delay between exposure to anaesthesia and testing are not clearly defined. In this study, the BChE activity and phenotype in an early (T1) and late (T2) phase were compared and the phenotype/genotype correlation was assessed.. Patients with a prolonged paralysis after mivacurium or suxamethonium were selected after ethical committee approval and written consent. BChE activity was based on butyrylthiocholine hydrolysis rate and phenotyping on differential inhibition of BChE activity with dibucaine and fluoride. DNA sequencing allowed genotypic characterization.. We included the results of 20 patients with prolonged neuromuscular block (NMB) induced by mivacurium or suxamethonium. In these patients, BChE activity was different at T1 and T2 (2120 [1506-2733] U L. Anaesthesia interfered with BChE activity, but not with phenotyping. Phenotyping can be performed on blood drawn during or immediately after recovery of mivacurium or suxamethonium to screen for clinically relevant variants of BChE. However, accurate diagnosis of BChE deficiency needs further confirmation by determination of genotype.

Topics: Apnea; Butyrylcholinesterase; Humans; Mivacurium; Neuromuscular Blockade; Succinylcholine

Pseudocholinesterase deficiency, sometimes called butyrylcholinesterase deficiency, is a rare disorder in which the neuromuscular blocking drugs succinylcholine and mivacurium cannot be metabolized properly in the blood plasma. This disorder can either be acquired as a result of certain comorbidities or it can be inherited genetically. Anesthesia providers must understand the pathophysiology of pseudocholinesterase deficiency and be prepared to safely and effectively manage patients who show signs and symptoms consistent with the disorder after the use of the indicated neuromuscular blocking drugs. This article summarizes the pharmacologic and physiologic data relevant to understanding the basic pathophysiology associated with pseudocholinesterase deficiency and illustrates a case study of a young woman suspected of having the disorder after a prolonged delay in emergence from general anesthesia.

Topics: Apnea; Butyrylcholinesterase; Female; Humans; Metabolism, Inborn Errors; Mivacurium; Succinylcholine

Pseudocholinesterase or butyrylcholinesterase (BChE) inactivates the relaxant drugs mivacurium and suxamethonium. A deficiency in plasma activity of this enzyme may result in prolonged muscular paralysis and subsequently the need for an extended duration of mechanical ventilation. We report the case of a 65-year-old patient who was diagnosed with butyrylcholinesterase deficiency for the first time during elective surgery. Neuromuscular monitoring constitutes a central diagnostic asset in ensuring patient safety.

Topics: Aged; Anesthesia Recovery Period; Anesthesia, General; Apnea; Butyrylcholinesterase; Humans; Intraoperative Awareness; Isoquinolines; Male; Metabolism, Inborn Errors; Mivacurium; Monitoring, Intraoperative; Neuromuscular Depolarizing Agents; Neuromuscular Nondepolarizing Agents; Preanesthetic Medication; Succinylcholine

Mutations in the butyrylcholinesterase gene can lead to a prolonged effect of the neuromuscular blocking agents, succinylcholine and mivacurium. If the anaesthesiologist is not aware of this condition, it may result in insufficient respiration after tracheal extubation. However, this can be avoided with the use of objective neuromuscular monitoring if used adequately. Three case reports of prolonged effect of succinylcholine or mivacurium were presented to illustrate the importance of neuromuscular monitoring during anaesthesia. In the first case, continuous intraoperative neuromuscular monitoring allowed a prolonged neuromuscular blockade to be discovered prior to tracheal extubation of the patient. The patient was extubated after successful reversal of the neuromuscular blockade. On the contrary, neuromuscular monitoring was not used during anaesthesia in the second patient; hence, the prolonged effect of the neuromuscular blocking agent was not discovered until after extubation. In the third patient, the lack of response to nerve stimulation was interpreted as a technical failure and the prolonged effect of succinylcholine was discovered when general anaesthesia was terminated. Both patients had insufficient respiration. They were therefore re-sedated, transferred to the intensive care unit and the tracheas were extubated after full recovery from neuromuscular blockade. We recommend the use of monitoring every time these agents are used, even with short-acting drugs like succinylcholine and mivacurium.

Topics: Accelerometry; Aged; Antidotes; Apnea; Appendicitis; Butyrylcholinesterase; Cholecystectomy, Laparoscopic; DNA Mutational Analysis; Female; Femoral Neck Fractures; Genotype; Humans; Hypnotics and Sedatives; Isoquinolines; Laparoscopy; Metabolism, Inborn Errors; Middle Aged; Mivacurium; Neostigmine; Neuromuscular Blockade; Neuromuscular Depolarizing Agents; Neuromuscular Monitoring; Neuromuscular Nondepolarizing Agents; Respiration, Artificial; Respiratory Paralysis; Succinylcholine; Time Factors; Young Adult

Butyrylcholinesterase deficiency is characterized by prolonged apnea after the use of muscle relaxants (suxamethonium or mivacurium) in patients who have mutations in the BCHE gene. Here, we report a case of prolonged neuromuscular block after administration of suxamethonium leading to the discovery of a novel BCHE variant (c.695T>A, p.Val204Asp). Inhibition studies, kinetic analysis and molecular dynamics were undertaken to understand how this mutation disrupts the catalytic triad and determines a "silent" phenotype. Low activity of patient plasma butyrylcholinesterase with butyrylthiocholine (BTC) and benzoylcholine, and values of dibucaine and fluoride numbers fit with heterozygous atypical silent genotype. Electrophoretic analysis of plasma BChE of the proband and his mother showed that patient has a reduced amount of tetrameric enzyme in plasma and that minor fast-moving BChE components: monomer, dimer, and monomer-albumin conjugate are missing. Kinetic analysis showed that the p.Val204Asp/p.Asp70Gly-p.Ala539Thr BChE displays a pure Michaelian behavior with BTC as the substrate. Both catalytic parameters Km = 265 µM for BTC, two times higher than that of the atypical enzyme, and a low Vmax are consistent with the absence of activity against suxamethonium. Molecular dynamic (MD) simulations showed that the overall effect of the mutation p.Val204Asp is disruption of hydrogen bonding between Gln223 and Glu441, leading Ser198 and His438 to move away from each other with subsequent disruption of the catalytic triad functionality regardless of the type of substrate. MD also showed that the enzyme volume is increased, suggesting a pre-denaturation state. This fits with the reduced concentration of p.Ala204Asp/p.Asp70Gly-p.Ala539Thr tetrameric enzyme in the plasma and non-detectable fast moving-bands on electrophoresis gels.

Topics: Alleles; Apnea; Base Sequence; Biocatalysis; Butyrylcholinesterase; DNA Mutational Analysis; Family Health; Female; Humans; Infant, Newborn; Isoquinolines; Kinetics; Male; Mivacurium; Molecular Dynamics Simulation; Mutation, Missense; Neuromuscular Depolarizing Agents; Pedigree; Succinylcholine

Topics: Apnea; Butyrylcholinesterase; Cholinesterases; Documentation; Drug Hypersensitivity; Follow-Up Studies; Humans; Isoquinolines; Medical Records; Metabolism, Inborn Errors; Mivacurium; Neuromuscular Depolarizing Agents; Neuromuscular Nondepolarizing Agents; Succinylcholine

After receiving mivacurium, a short-acting neuromuscular blocking agent used for intubation before surgery, a patient experienced prolonged paralysis and prolonged apnea that required ventilator support. Although this complication is rare, all critical care nurses should be aware of it so they can be competent in managing and providing holistic and comprehensive nursing care to the patient and the patient's family. Although this complication has been documented in the anesthesia literature, it has received little mention in critical care nursing journals.

Topics: Amputation, Surgical; Apnea; Butyrylcholinesterase; Female; Humans; Isoquinolines; Middle Aged; Mivacurium; Neuromuscular Blocking Agents; Paralysis

Mivacurium is a short-acting neuromuscular blocking drug, ideal for short surgical procedures. The brief duration of action depends on rapid hydrolysis by plasma cholinesterase. An inherited or acquired deficiency of plasma cholinesterase can prolong the effect of mivacurium. We present an unusual case of unanticipated postoperative apnea following mivacurium administration, as a result of acquired plasma cholinesterase deficiency, in a patient with previous uneventful exposure to both mivacurium and suxamethonium (succinylcholine).

Topics: Aged; Apnea; Butyrylcholinesterase; Humans; Isoquinolines; Male; Malnutrition; Mivacurium; Neuromuscular Blockade; Neuromuscular Nondepolarizing Agents; Postoperative Complications

Human butyrylcholinesterase is the enzyme responsible of mivacurium and succinylcholine metabolism, which may be significantly impaired when mutation Asp70Gly is found in patients. We describe a simple PCR method for the detection of this variant. Thirteen out of sixteen patients tested after prolonged apnea were positive for the presence of this mutation (50.0% homozygotes and 31.3% heterozygotes), suggesting that this test contributes to the explanation of some clinical events and to their prevention in relatives of these patients.

Topics: Apnea; Butyrylcholinesterase; Female; Genetic Testing; Genetic Variation; Heterozygote; Homozygote; Humans; Isoquinolines; Male; Mivacurium; Pharmacogenetics; Point Mutation; Polymerase Chain Reaction; Polymorphism, Restriction Fragment Length; Succinylcholine

Succinylcholine and mivacurium are degraded more slowly in patients with a qualitatively or quantitatively reduced plasma cholinesterase and are therefore known for inducing a prolonged postoperative apnea. Perioperative laboratory screening even including plasma cholinesterase activity testing will not prevent this due to a possible aberration only in the qualitative cholinesterase activity. This is illustrated by introducing two cases reports of prolonged apnea after administration of mivacurium or succinylcholine. The pathophysiology of plasma cholinesterase is reviewed including genetically determined variants and the degradation pathways of mivacurium and succinylcholine. Only extensive laboratory chemical tests are sufficient to prevent this possible complication. Due to the rare incidence there is no evidence for recommending these laboratory investigations in all patients. Once prolonged apnea occurs following the administration of mivacurium or succinylcholine the best choice is ongoing ventilation combined with a sufficient sedation.

Topics: Apnea; Cholinesterases; Humans; Isoquinolines; Male; Middle Aged; Mivacurium; Neuromuscular Depolarizing Agents; Neuromuscular Nondepolarizing Agents; Postoperative Complications; Succinylcholine

We present a case of unanticipated postoperative apnoea in a patient with associated medical illness to illustrate the diagnostic difficulty that can arise in the detection and subsequent management of mivacurium apnoea. A high index of suspicion is essential in the presence of concomitant medical conditions that may cause prolonged apnoea. To our knowledge, no report exists documenting the unanticipated occurrence of mivacurium apnoea in a patient with previously undiagnosed pseudocholinesterase deficiency and concomitant medical illness who has previously undergone 'balanced' general anaesthesia.

Topics: Anesthesia, General; Apnea; Butyrylcholinesterase; Female; Humans; Isoquinolines; Middle Aged; Mivacurium; Neuromuscular Nondepolarizing Agents

A fit 36-year-old parturient received a general anaesthetic for manual removal of a retained placenta. She underwent rapid sequence induction of anaesthesia with suxamethonium, shortly followed by 10 mg of mivacurium. One hour later she had failed to establish adequate ventilation despite administration of drugs to reverse neuromuscular blockade. A provisional diagnosis of suxamethonium-related apnoea was made and her lungs were ventilated overnight on the Intensive Care Unit. Plasma cholinesterase levels at the time were reduced to one-third of normal, with normal dibucaine and fluoride numbers. One month later her levels were back within the reference range.

Topics: Adult; Apnea; Cholinesterases; Female; Humans; Isoquinolines; Mivacurium; Neuromuscular Depolarizing Agents; Neuromuscular Nondepolarizing Agents; Postpartum Period; Pregnancy; Succinylcholine

Topics: Apnea; Humans; Isoquinolines; Mivacurium; Neuromuscular Depolarizing Agents

Topics: Anesthesia, General; Apnea; Child; Cholinesterases; Female; Humans; Isoquinolines; Mivacurium; Neuromuscular Nondepolarizing Agents

Topics: Adult; Apnea; Female; Humans; Isoquinolines; Mivacurium; Neostigmine; Nerve Block; Neuromuscular Junction; Neuromuscular Nondepolarizing Agents; Time Factors

Topics: Anesthesiology; Apnea; Butyrylcholinesterase; Drug Synergism; Humans; Isoquinolines; Mivacurium; Physostigmine

Topics: Apnea; Humans; Isoquinolines; Mivacurium; Physostigmine