pancuronium has been researched along with Acute-Disease* in 15 studies
1 review(s) available for pancuronium and Acute-Disease
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[Status asthmaticus. Acute myopathy induced by cortisone and neuropathy during resuscitation].
A female patient treated by mechanical ventilation with high doses of pancuronium and methylprednisolone for status asthmaticus presented with acute total areflexic and severe amyotrophic tetraplegia; she died after multiple organ failure. Muscle biopsy confirmed the clinical diagnosis of "acute corticosteroid myopathy", precipitated by a corticosteroid "disuse hypersensitivity" after pancuronium. The electromyogram showed a critical illness polyneuropathy, secondary to multiple organ failure. Nerve biopsy was normal. The respective parts played by corticosteroids, curare-like derivatives and intensive care in the genesis of unexplained difficulty in weaning from the ventilator are discussed. Topics: Acute Disease; Aged; Fatal Outcome; Female; Humans; Methylprednisolone; Multiple Organ Failure; Muscular Diseases; Nervous System Diseases; Neural Conduction; Pancuronium; Respiration, Artificial; Resuscitation; Status Asthmaticus | 1993 |
4 trial(s) available for pancuronium and Acute-Disease
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Myopathy following mechanical ventilation for acute severe asthma: the role of muscle relaxants and corticosteroids.
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 | 1999 |
Neurophysiological monitoring of pharmacological manipulation in acute organophosphate (OP) poisoning. The effects of pralidoxime, magnesium sulphate and pancuronium.
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 | 1998 |
The effect of single-dose and continuous skeletal muscle paralysis on respiratory system compliance in paediatric intensive care patients.
To investigate the effect of single dose and continuous skeletal muscle paralysis on respiratory system compliance in 53 paediatric intensive care patients.. Prospective clinical study.. Multidisciplinary paediatric intensive care unit.. Twenty-three children ventilated for acute pulmonary pathology, and 30 ventilated for isolated intracranial pathology, who initially had normal lungs.. The 23 patients with acute pulmonary pathology received a single dose of muscle relaxant to facilitate diagnostic procedures. Fifteen patients with isolated intracranial pathology received continuous skeletal muscle paralysis for longer than 24 h, and the other 15 received no paralysis.. Respiratory system compliance deteriorated by 14% from 0.519 +/- 0.2 to 0.445 +/- 0.18 ml cmH2O-1 kg-1 (p < 0.001) following a single dose of muscle relaxant in the 23 patients with acute pulmonary pathology. In the 15 with isolated intracranial pathology who received continuous skeletal muscle paralysis there was a progressive deterioration in compliance, which reached 50% of the initial compliance by day 4 of paralysis (p < 0.001) and improved back to normal following discontinuation of paralysis. There were no changes in compliance in the 15 patients with isolated intracranial pathology who were ventilated but not paralysed. The paralysed patients required mechanical ventilation longer than the non-paralysed patients (p < 0.001), and 26% of these patients developed nosocomial pneumonia (p = 0.03), a complication that was not seen in the non-paralysed patients.. Skeletal muscle paralysis results in immediate and progressive deterioration of respiratory system compliance and increased incidence of nosocomial pneumonia. The benefits of paralysis should be balanced against the risks of deteriorating pulmonary function. Topics: Acute Disease; Adolescent; Brain Diseases; Child; Child, Preschool; Craniocerebral Trauma; Cross Infection; Humans; Infant; Lung Compliance; Lung Diseases; Neuromuscular Nondepolarizing Agents; Pancuronium; Pneumonia; Prospective Studies; Respiration, Artificial; Time Factors | 1996 |
Respiratory mechanics by least squares fitting in mechanically ventilated patients: applications during paralysis and during pressure support ventilation.
To evaluate a least squares fitting technique for the purpose of measuring total respiratory compliance (Crs) and resistance (Rrs) in patients submitted to partial ventilatory support, without the need for esophageal pressure measurement.. Prospective, randomized study.. A general ICU of a University Hospital.. 11 patients in acute respiratory failure, intubated and assisted by pressure support ventilation (PSV).. Patients were ventilated at 4 different levels of pressure support. At the end of the study, they were paralyzed for diagnostic reasons and submitted to volume controlled ventilation (CMV).. A least squares fitting (LSF) method was applied to measure Crs and Rrs at different levels of pressure support as well as in CMV. Crs and Rrs calculated by the LSF method were compared to reference values which were obtained in PSV by measurement of esophageal pressure, and in CMV by the application of the constant flow, end-inspiratory occlusion method. Inspiratory activity was measured by P0.1. In CMV, Crs and Rrs measured by the LSF method are close to quasistatic compliance (-1.5 +/- 1.5 ml/cmH2O) and to the mean value of minimum and maximum end-inspiratory resistance (+0.9 +/- 2.5 cmH2O/(l/s)). Applied during PSV, the LSF method leads to gross underestimation of Rrs (-10.4 +/- 2.3 cmH2O/(l/s)) and overestimation of Crs (+35.2 +/- 33 ml/cmH2O) whenever the set pressure support level is low and the activity of the respiratory muscles is high (P0.1 was 4.6 +/- 3.1 cmH2O). However, satisfactory estimations of Crs and Rrs by the LSF method were obtained at increased pressure support levels, resulting in a mean error of -0.4 +/- 6 ml/cmH2O and -2.8 +/- 1.5 cmH2O/(l/s), respectively. This condition was coincident with a P0.1 of 1.6 +/- 0.7 cmH2O.. The LSF method allows non-invasive evaluation of respiratory mechanics during PSV, provided that a near-relaxation condition is obtained by means of an adequately increased pressure support level. The measurement of P0.1 may be helpful for titrating the pressure support in order to obtain the condition of near-relaxation. Topics: Acute Disease; Adult; Aged; Airway Resistance; Female; Humans; Least-Squares Analysis; Lung Compliance; Male; Middle Aged; Monitoring, Physiologic; Pancuronium; Positive-Pressure Respiration; Prospective Studies; Reproducibility of Results; Respiratory Insufficiency | 1995 |
10 other study(ies) available for pancuronium and Acute-Disease
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[Respiratory muscle weakness after prolonged use of hydrocortisone and pancuronium bromide].
A 30-year-old man was admitted because of status asthmaticus. He required 7 days of artificial ventilation and was treated with hydrocortisone 1.2 g.day-1 and bronchodilaters. Pancuronium bromide 0.08 mg.kg-1.hr-1 was given for 64 hours for the ease of artificial ventilation. On day 3, severely elevated airway pressure resulted in left pneumothorax and isoflurane 1% was given for the following 2 days. Respiratory muscle weakness was evident 24 hours after discontinuation of pancuronium infusion on day 5 while full 4 twitches of TOF on the adductor pollicis muscle were seen at the time. The respiratory muscle weakness continued for another 3 days and he was extubated on day 8. Serum creatine kinase concentration rose to 2178 U.l-1 on day 6 and returned to normal on day 11. Hematurea, hyperpyrexia and metabolic acidosis were never seen during the course. Acute corticosteroid myopathy was suspected to be the cause of the prolonged respiratory muscle weakness. Topics: Acute Disease; Adult; Anti-Inflammatory Agents; Drug Therapy, Combination; Humans; Hydrocortisone; Male; Muscle Weakness; Neuromuscular Nondepolarizing Agents; Pancuronium; Respiratory Muscles; Status Asthmaticus; Time Factors | 2000 |
Paralysis of ventilated newborn babies does not influence resistance of the total respiratory system.
Paralysis with pancuronium bromide is used in newborn infants to facilitate ventilatory support during respiratory failure. Changes in lung mechanics have been attributed to paralysis. The aim of this study was to examine whether or not paralysis per se has an influence on the passive respiratory mechanics, resistance (Rrs) and compliance (Crs) of the respiratory system in newborn infants. In 30 infants with acute respiratory failure, Rrs was measured during paralysis with pancuronium bromide and after stopping pancuronium bromide (group A). Rrs was also measured in an additional 10 ventilated infants in a reversed fashion (group B): Rrs was measured first in nonparalysed infants and then they were paralysed, mainly for diagnostic procedures, and the Rrs measurement repeated. As Rrs is highly dependent on lung volume, several parameters, that depend directly on lung volume were recorded: inspiratory oxygen fraction (FI,O2), arterial oxygen tension/alveolar oxygen tension (a/A) ratio and volume above functional residual capacity (FRC). In group A, the Rrs was not different during (0.236+/-0.09 cmH2O x s x mL(-1)) and after (0.237+/-0.07 cmH2O x s x mL(-1)) paralysis. Also, in group B, Rrs did not change (0.207+/-0.046 versus 0.221+/-0.046 cm x s x mL(-1) without versus with pancuronium bromide). FI,O2, a/A ratio and volume above FRC remained constant during paralysis. These data demonstrate that paralysis does not influence the resistance of the total respiratory system in ventilated term and preterm infants when measured at comparable lung volumes. Topics: Acute Disease; Airway Resistance; Female; Functional Residual Capacity; Humans; Infant, Newborn; Lung Compliance; Male; Neuromuscular Nondepolarizing Agents; Oxygen; Pancuronium; Respiration, Artificial; Respiratory Insufficiency | 1999 |
Muscle weakness in mechanically ventilated patients with severe asthma.
Patients who undergo mechanical ventilation for severe asthma are at risk of developing diffuse muscle weakness because of acute myopathy. The relative importance of corticosteroids and neuromuscular paralysis in causing the myopathy is controversial, and it is uncertain whether the chemical structure of the drug used to induce paralysis influences the risk of myopathy. Using a retrospective cohort study design, we evaluated 107 consecutive episodes of mechanical ventilation for severe asthma to assess (1) the incidence of clinically significant weakness in patients treated with corticosteroids alone versus corticosteroids with neuromuscular paralysis, (2) the influence of the duration of paralysis on the incidence of muscle weakness, and (3) the relative risk of weakness in patients paralyzed with the nonsteroidal drug atracurium versus an aminosteroid paralytic agent (pancuronium, vecuronium). The use of corticosteroids and a neuromuscular blocking agent was associated with a much higher incidence of muscle weakness as compared with the use of corticosteroids alone (20 of 69 versus O of 38, p < 0.001). The 20 weak patients were paralyzed significantly longer than the 49 patients who received a neuromuscular blocking agent without subsequent weakness (3.4 +/- 2.4 versus 0.6 +/- 0.7 d, p < 0.001). Eighteen of the 20 weak patients had been paralyzed for more than 24 h. The incidence of weakness was not reduced when paralysis was achieved with atracurium as opposed to an aminosteroid neuromuscular blocking agent. In conclusion, corticosteroid-treated patients with severe asthma who undergo prolonged neuromuscular paralysis are at significant risk for the development of muscle weakness, and the risk of weakness is not reduced by use of atracurium. Topics: Acute Disease; Adolescent; Adult; Aged; Albuterol; Asthma; Atracurium; Bronchodilator Agents; Cohort Studies; Female; Glucocorticoids; Humans; Incidence; Male; Methylprednisolone; Middle Aged; Muscle Weakness; Muscular Diseases; Neuromuscular Nondepolarizing Agents; Pancuronium; Respiration, Artificial; Retrospective Studies; Risk Factors; Time Factors; Vecuronium Bromide | 1996 |
[Rhabdomyolysis in severe acute asthma].
A case is reported of a 74-year-old man who developed rhabdomyolysis during treatment for status asthmaticus. This patient had a history of asthma. He was admitted after a cardiac arrest during a severe asthma attack. Continuous muscle relaxation (4 mg.h-1 of pancuronium for 10 days; total dose 960 mg) was required to carry out mechanical ventilation. Bronchodilators and high doses of steroids (300 mg.day-1 of methylprednisolone for 10 days) were also given. After the administration of muscle relaxant had been discontinued, the patient displayed a severe, predominantly proximal, quadriplegia as well as a raised blood creatinine kinase concentration. The urine was brown coloured over a 24 h period. Rhabdomyolysis was confirmed by muscle biopsy. The patient recovered over a period of one month. This case is discussed in the light of some other similar reports in the literature. It seems that the combination of muscle relaxant with high doses of steroids is to be incriminated. Topics: Acute Disease; Aged; Creatine Kinase; Critical Care; Drug Therapy, Combination; Humans; Male; Methylprednisolone; Pancuronium; Rhabdomyolysis; Status Asthmaticus | 1993 |
Acute respiratory failure neuropathy: a variant of critical illness polyneuropathy.
Topics: Acute Disease; Adrenal Cortex Hormones; Critical Illness; Electromyography; Humans; Neuromuscular Diseases; Pancuronium; Respiratory Insufficiency | 1993 |
[A case of motor neuropathy with pyramidal sign due to prolonged administration of high dose of pancuronium bromide (Myoblock)].
We reported a case of motor neuropathy with pyramidal sign following prolonged administration of a high dose of muscle relaxant, pancuronium bromide (Myoblock). A 40-year-old male was admitted to our hospital with acute episode of pancreatitis. He was treated with artificial ventilation and Myoblock to manage delirious state, disseminated intravascular coagulation and multiple organ failure. Total dose of 823 mg (24 mg/day) of Myoblock was given intravenously over 36 days. After Myoblock was discontinued, he regained his consciousness and marked muscle weakness with atrophy was noted in both limbs, more severe in distal lower limbs, without any noticeable sensory and sphincter disturbances. Motor nerve conduction studies showed normal nerve conduction velocities with markedly decreased amplitude of compound muscle action potentials. Repetitive nerve stimulation studies revealed decrement response after tetanic stimulation, which disappeared later. Needle EMG showed active denervation potentials and marked polyphasic motor unit potentials. Muscle biopsy revealed neurogenic muscle atrophy with fragmented acetylcholine esterase-positive postsynaptic sites. Sural nerve biopsy showed slight to moderate degree of axonal degeneration of myelinated fibers. Clinical, electrophysiological, and pathological studies above indicated that the main affected sites were neuromuscular junctions including the terminal twigs of motor neurones and postsynaptic membrane, and pyramidal tracts, predominant in lower limbs. About one month after the recognition of the muscle weakness, his muscle strength improved gradually, however, spasticity with hyperreflexia and pathologic reflexes of both legs were found, and became more prominent thereafter. Intensive physiotherapy and rehabilitation led improvement to the point that he became able to ambulate with walking-aids about 7 months later, but marked spasticity persisted.(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Acute Disease; Adult; Humans; Male; Motor Neuron Disease; Pancreatitis; Pancuronium; Pyramidal Tracts; Time Factors | 1993 |
[Acute myopathy complicating prolonged curarization and corticoid therapy for status asthmaticus].
Topics: Acute Disease; Adult; Drug Therapy, Combination; Female; Humans; Hydrocortisone; Methylprednisolone; Pancuronium; Rhabdomyolysis; Status Asthmaticus; Vecuronium Bromide | 1992 |
Complete ophthalmoplegia as a complication of acute corticosteroid- and pancuronium-associated myopathy.
We report acute complete external ophthalmoplegia and severe myopathy in a patient treated with high doses of IV methylprednisolone and pancuronium. Awareness of this rare syndrome in a common clinical setting can lead to prompt recognition and avoid confusion with other causes of acute weakness and ophthalmoparesis. Topics: Acute Disease; Humans; Male; Methylprednisolone; Middle Aged; Muscular Diseases; Ophthalmoplegia; Pancuronium | 1991 |
[Use of Pavulon in artificial respiration following acute poisoning].
Topics: Acute Disease; Carbon Monoxide Poisoning; Ethylene Glycols; Humans; Pancuronium; Respiration, Artificial | 1982 |
Acute hypertension immediately after coronary artery surgery.
Hypertension immediately after coronary surgery is a problem in about one third of the patients so treated. This report discusses the possible causes of postoperative hypertension and describes several means of controlling the complication. Topics: Acute Disease; Anesthesia, Inhalation; Coronary Vessels; Humans; Hypertension; Methoxyflurane; Nitroglycerin; Nitroprusside; Nitrous Oxide; Oxygen; Pancuronium; Postoperative Complications; Promazine; Tubocurarine | 1976 |