pancuronium and Neuromuscular-Diseases

We Japanese anesthesiologists can now use rocuronium as well as vecuronium. Although the onset of rocuronium is more rapid, the non-depolarizing neuromuscular blocking (NMB) agent has similar characteristics of duration and recovery compared to vecuronium. Reversal of NMB is therefore essential to recover patients safely. Conventional standard of reversal of NMB [train of four (TOF) >0.7] is not enough to have sufficient vital capacity and inspiratory force, resulting in pulmonary regurgitation or atelectasis. Even though the reversal of NMB cannot sufficiently be completed by anti-cholinesterase (ChE) agents such as neostigmine, it is needed to reverse the NMB because of their late spontaneous recovery. We also have to take care of patients with neuromusclar diseases such as Duchenne-type muscle dystrophy, when we use anti-ChE agents. Sugammadex is a novel and unique compound designed as an antagonist of rocuronium and possibly other steroid NMB agents. Sugammadex exerts its effect by forming very tight water-soluble complexes at a 1 : 1 ratio with steroid NMB agents (rocuronium>vecuronium>>pancuronium). PhaseIII trials in Japan as well as Europe and the US have just been finished, and it is expected to be used clinically in the near future.

Topics: Androstanols; Anesthesia Recovery Period; Cholinesterase Inhibitors; Clinical Trials, Phase III as Topic; gamma-Cyclodextrins; Humans; Neostigmine; Neuromuscular Blocking Agents; Neuromuscular Diseases; Pancuronium; Rocuronium; Sugammadex; Vecuronium Bromide

Topics: Adult; Aged; Alcuronium; Child; Drug Interactions; Drug Utilization; Female; Gallamine Triethiodide; Humans; Infant, Newborn; Kidney Diseases; Liver Diseases; Maternal-Fetal Exchange; Neuromuscular Blocking Agents; Neuromuscular Depolarizing Agents; Neuromuscular Diseases; Neuromuscular Junction; Pancuronium; Pregnancy; Pyridinium Compounds; Succinylcholine; Synaptic Transmission; Tubocurarine

Acute myopathy following mechanical ventilation for near-fatal asthma (NFA) has been described recently, and some researchers have suggested that this complication is related to the use of neuromuscular blocking agents (NMBAs) and corticosteroids (CSs).. To determine the incidence of acute myopathy in a group of patients and to examine the most important predictors of its development.. A retrospective cohort study over a 10-year period (1985 to 1995) of all asthma patients who received mechanical ventilation at two centers in Vancouver (designated center 1 and center 2).. In center 1, there were 58 patients who had 64 episodes of NFA, and in center 2, there were 28 patients who had 30 episodes. NMBAs were used in 30 of 86 admissions for acute severe asthma (35%). The mean (+/- SD) duration of muscle paralysis was 3.1+/-2.3 days. A total of 9 patients (10.4%) developed significant myopathy. The incidence of myopathy was 9 of 30 (30%) among patients who received NMBAs. In a multiple logistic regression model, the development of myopathy was only significantly associated with the duration of muscle relaxation. The odds ratio for the development of myopathy increased by 2.1 (95% confidence interval, 1.4 to 3.2) with each additional day of muscle relaxation. The dose and the type of the CS were not significantly associated with the myopathy in the multiple logistic regression analysis.. Our study showed that there is a high incidence of acute myopathy when NMBAs are used for NFA. The incidence of myopathy increases with each additional day of muscle relaxation.

Topics: Acute Disease; Adult; APACHE; Asthma; Electromyography; Female; Follow-Up Studies; Glucocorticoids; Humans; Hydrocortisone; Incidence; Male; Methylprednisolone; Middle Aged; Neuromuscular Blocking Agents; Neuromuscular Diseases; Odds Ratio; Pancuronium; Respiration, Artificial; Retrospective Studies

The neuromuscular transmission failure in acute organophosphate (OP) poisoning occurs because of the irreversible inactivation of the enzyme acetylcholinesterase located in the neuromuscular junction, and is distinguished neuroelectrophysiologically by single electrical stimulus-induced repetitive responses and either a decremental or a decrement-increment response upon high-rate repetitive nerve stimulation (RNS). Understandably, the administration of pharmacological agents with actions at different sites in the neuromuscular junction would alter the neuroelectrophysiological findings in acute OP poisoning.. The effect of several pharmacological agents including pralidoxime (10 patients), magnesium sulphate (4 patients) and pancuronium (7 patients) on the neuroelectrophysiological abnormalities was studied in 21 patients with acute OP poisoning.. Pralidoxime administration produced neurophysiological amelioration in 11 out of 15 occasions. In those cases where it produced a beneficial effect, pralidoxime administration was continued and its neuroelectrophysiological effects were studied daily. The efficacy of pralidoxime administration was demonstrated by neuroelectrophysiological testing for a maximum of 6 days after poisoning. Three types of neuroelectrophysiological responses to pralidoxime were noted: (i) lack of neuroelectrophysiological improvement (two patients); (ii) initial improvement with subsequent lack of improvement (two patients); and (iii) initial improvement with subsequent normalisation of neuromuscular transmission (5 patients). Normalisation of the electrodiagnostic tests and the failure of pralidoxime to ameliorate the neuromuscular transmission abnormalities were neuroelectrophysiological indications for the discontinuation of pralidoxime treatment. The administration of magnesium sulphate (MgSO4.7H2O, 4 g intravenous) resulted in a decrease in the CMAP amplitude, loss of the repetitive response and conversion of the decrement-increment response at high-rate RNS to an incremental response. Repetitive responses and the decremental response at high-rate RNS also disappeared after the administration of pancuronium (0.5 mg intravenous) to 6 patients. However, in one case where pancuronium administration was preceded by pralidoxime, there occurred a dramatic worsening of the neuromuscular transmission defect.. While the administration of all 3 agents-- pralidoxime, magnesium sulphate and pancuronium-- resulted in the reversion of the neuroelectrophysiological defects, only pralidoxime is contended to be therapeutically useful. The therapeutic benefit due to its administration is limited by a short duration of action, and hence it is recommended that it should be administered for a longer period of time under neuroelectrophysiolgical guidance.

Topics: Acute Disease; Antidotes; Electroencephalography; Humans; Insecticides; Magnesium Sulfate; Monitoring, Physiologic; Neuromuscular Diseases; Neuromuscular Junction; Nicotinic Antagonists; Organophosphorus Compounds; Pancuronium; Pralidoxime Compounds; Synaptic Transmission; Treatment Outcome

Nine patients with organophosphorus (OP) intoxication developing neuromuscular transmission defects were given pancuronium 1, 2, or 4 mg intravenously (IV). Thirteen patient controls with hypoxic encephalopathy received similar dosages. The responses were monitored electrophysiologically using single and repetitive nerve stimulation (20 and 50 Hz). In OP patients, pancuronium did not alter the amplitude of the single CMAP, whereas its repetitive discharges were reduced. Severe neuromuscular blocks were reversed only partially by pancuronium 4 mg. In less severe blocks, 1 and 2 mg resulted in marked improvement. In the patient controls, pancuronium 4 mg induced a severe neuromuscular block but not with 1 and 2 mg. Pancuronium dosages necessary to reverse severe OP-induced neuromuscular blockade produce a neuromuscular block when AChE activity is normal. Low dosages have little effect on normal neuromuscular transmission, but improve the block to a mild degree and may be useful as part of treatment in OP intoxications.

Topics: Acetylcholinesterase; Action Potentials; Adult; Dose-Response Relationship, Drug; Electric Stimulation; Humans; Injections, Intravenous; Motor Endplate; Movement Disorders; Neuromuscular Diseases; Organophosphate Poisoning; Pancuronium; Synaptic Transmission; Time Factors

Long-term administration of pancuronium for ventilatory support of adults with ARDS may result in severe tetraparesis, with areflexia and atrophy of distal muscles. This adverse effect occurs rarely in paediatric intensive care units. We describe a case of tetraparesis after prolonged pancuronium infusion in a 9-month-old girl who experienced a severe bronchopneumonia caused by para-influenza virus, requiring endotracheal intubation and mechanical ventilation. To decrease chest wall rigidity, pancuronium was administered over 11 days, with a total dose of approximately 120 mg of pancuronium bromide. The day after discontinuation of the muscle relaxant she had a severe tetraplegia with areflexia, but normal head movements. Electromyography showed a normal neuromuscular transmission. She recovered from tetraplegia three months later. Other causes of peripheral neuropathy were eliminated. Electroencephalograms and head CT-scans were normal. The recovery pattern observed in our patient corresponded to the process of regeneration seen after axonal degeneration. It is suggested that these neuromuscular complications were caused by prolonged high-dosage pancuronium treatment, associated with corticosteroid and aminoglycoside administration.

Topics: Bronchopneumonia; Female; Humans; Infant; Infant, Newborn; Infant, Premature; Neuromuscular Diseases; Neuromuscular Nondepolarizing Agents; Pancuronium; Quadriplegia; Respiration, Artificial; Respiratory Distress Syndrome, Newborn

During six consecutive months, seven patients admitted to our ICU (15 beds, general ICU, approximately 300 intubated patients per year) for acute respiratory failure requiring intubation and mechanical ventilation presented with a peculiar neuromuscular disorder. After the occurrence of this cluster group of patients, we detected two more similar but isolated cases in the following 18 months, ie, altogether 9 patients in 2 years of observation, or 1.55 percent of all intubated patients in our ICU. Sedation was achieved using midazolam, curarization was effected with the neuromuscular non-depolarizing agent pancuronium bromide (PB), and corticosteroids were administered to eight patients. Shortly after discontinuation of sedation and curarization, we observed a persistent tetraparetic syndrome and/or peroneal palsy with a concomitant increase of serum creatine kinase (CK). None of the patients was septic or had the multisystem organ failure. A strong association between CK increase and PB administration was found, whereas no patient suffered severe liver or kidney failure. The duration of the neurologic deficit ranged from 4 to 52 weeks, with only partial recovery for some patients; the duration of dysfunction was apparently related to the total dose of corticosteroids received. Two patients had difficulty being weaned from the respirator and required tracheostomy. Electrophysiologic studies showed signs of axonal neuropathy and myopathic changes, ie, motor units of brief duration, small amplitude, overly abundant for the voluntary effort being exerted. Muscle biopsies showed significant myopathic alterations, with foci of muscle necrosis in most patients and minimal lymphocytic inflammation in one patient. The neurologic complication described differs from the polyneuropathy in critically ill patients. Furthermore, PB or corticosteroids or both appear to be the causal agents. The duration of the neuromuscular dysfunction may be related to concomitant steroid therapy. The CK enzyme seems to be a marker of the disorder. This disorder is associated with myopathic alterations and axonal degeneration in some patients. Pancuronium bromide should be used with caution, particularly when associated with steroids therapy, and it may cause difficulty in weaning patients from the respirator.

Topics: Adult; Aged; Cluster Analysis; Creatine Kinase; Electromyography; Female; Humans; Intensive Care Units; Male; Middle Aged; Muscles; Neural Conduction; Neuromuscular Diseases; Pancuronium; Paresis; Respiration, Artificial

Topics: Critical Illness; Electromyography; Humans; Neuromuscular Diseases; Neuromuscular Junction; Pancuronium

Topics: Acute Disease; Adrenal Cortex Hormones; Critical Illness; Electromyography; Humans; Neuromuscular Diseases; Pancuronium; Respiratory Insufficiency

Neuromuscular blockade induced by pancuronium was monitored on the trapezius and abductor digiti minimi muscles in three patients with upper motor neurone lesions: one patient was hemiparetic and two were tetraparetic. A greater sensitivity to pancuronium was always observed on the trapezius muscle. It is suggested that the assessment of curarisation is more reliable on proximal than on distal muscles if the patient's sensitivity to relaxants is expected to be generally low.

Topics: Adult; Child; Female; Fingers; Hemiplegia; Humans; Male; Monitoring, Physiologic; Motor Neurons; Muscle Contraction; Neuromuscular Diseases; Neuromuscular Junction; Pancuronium; Quadriplegia; Shoulder; Synaptic Transmission

This paper reports on 12 patients in a 3-year period (from 1st July 1980 to 1st July 1983) who were treated with artificial ventilation and with the muscle relaxant pancuronium bromide (Pavulon), over a period of 6 days or longer. After discontinuation of this drug these patients developed severe tetraparesis with areflexia, sometimes combined with disturbances of the extraocular and facial muscles and diffuse muscular atrophy, without sensory disturbances. Seven patients recovered completely after 2-5 months, two made an incomplete recovery and three died due to the primary disease. It is suggested that these neuromuscular complications were caused by prolonged high-dosage Pavulon treatment in combination with renal and hepatic disturbances and/or the use of aminoglucosides.

Topics: Adult; Aged; Electromyography; Humans; Middle Aged; Muscles; Muscular Atrophy; Nerve Fibers, Myelinated; Neuromuscular Diseases; Pancuronium; Respiration, Artificial

Anesthesiologists are now active in the diagnosis of unusual neurologic and neuromuscular disorders. Their skill derives both from a firm understanding of basic sciences and a facility with invasive procedures. Five representative cases are presented to illustrate the scope of diagnostic neuroanesthesiology and the endeavors of the neuroanesthesiologist outside the operating theater.

Topics: Adult; Aged; Anesthesiology; Cerebral Palsy; Consultants; Electromyography; Female; Humans; Male; Medicine; Middle Aged; Muscle Contraction; Muscle Spasticity; Myasthenia Gravis; Nervous System Diseases; Neurology; Neuromuscular Diseases; Pancuronium; Peripheral Nervous System Diseases; Specialization

Topics: Adult; Aged; Anesthesia, General; Electric Stimulation; Female; Humans; Male; Middle Aged; Monitoring, Physiologic; Motor Neurons; Neuromuscular Diseases; Pancuronium

Topics: Anesthesia, Intravenous; Child; Child, Preschool; Female; Humans; Male; Muscular Atrophy; Neuromuscular Diseases; Pancuronium; Postoperative Care; Preoperative Care; Succinylcholine