Prolonged Reversible Quadriparesis in Mechanically Ventilated Patients Who Received Long-term Infusions of Vecuronium

doi:10.1378/chest.100.3.877

Chest

Volume 100, Issue 3, September 1991, Pages 877-878

https://doi.org/10.1378/chest.100.3.877 Get rights and content

The use of neuromuscular blocking agents, particularly pancuronium, in patients receiving mechanical ventilation has been reported to cause prolonged paralysis and atrophy. We describe two mechanically ventilated patients with asthma who developed prolonged muscular weakness and atrophy after receiving the shorter-acting agent vecuronium. These cases illustrate the potential of any neuromuscular blocking agent to cause these complications, especially in patients who are immobile, have decreased renal or liver function, or receive concomitant myotoxic agents.

Section snippets

CASE 1

A 20-year-old female patient who presented in status asthmaticus required intubation and mechanical ventilation. She was treated with metaproterenol, aminophylline, and methylprednisolone. A lobar pneumonia was treated empirically with erythromycin and tobramycin. Eight days after hospital admission sputum stain was positive for Legionella, and the tobramycin therapy was discontinued.

Because of high peak ventilatory pressure and agitation, a vecuronium drip at 4 to 6 mg/h was started on the day

DISCUSSION

The muscle weakness and disuse atrophy experienced by our patients were similar to the findings reported in patients who received pancuronium.1, 2, 3 Op de Cool et al¹ observed that 12 of 60 patients treated with pancuronium infusions for longer than 6 days (for a total dose of 54 to 1,340 mg) had development of neuromuscular complications, including muscle atrophy, muscle paresis, and cranial nerve paresis. Complete recovery occurred in seven patients over 2 weeks to 5 months, and two patients

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Citation Excerpt :
As authors have hypothesized that ventilator-induced diaphragmatic dysfunction can develop due to a mismatch between energy substrate and energy expenditure, a similar mechanism may be at work with hyperglycemia. Some early muscle biopsies in CINMA noted myopathy with large vacuoles, thought to be glycogen [5,11]. The value of tight glucose control in critically ill patients was reported in 2001, in a randomized controlled trial of more than 1500 surgical ICU patients on mechanical ventilation [115].
Weakness is common in critically ill patients, associated with prolonged mechanical ventilation and increased mortality. Corticosteroids and neuromuscular blockade (NMB) administration have been implicated as etiologies of acquired weakness in the intensive care unit. Medical literature since the 1970s is replete with case reports and small case series of patients with weakness after receiving high-dose corticosteroids, prolonged NMB, or both. Several risk factors for weakness appear in the early literature, including large doses of steroids, the dose and duration of NMB, hyperglycemia, and the duration of mechanical ventilation. With improved quality of data, however, the association between weakness and steroids or NMB wanes. This may reflect changes in clinical practice, such as a reduction in steroid dosing, use of cisatracurium besylate instead of aminosteroid NMBs, improved glycemic control, or trends in minimizing mechanical ventilatory support. Thus, based on the most recent and high-quality literature, neither corticosteroids in commonly used doses nor NMB is associated with increased duration of mechanical ventilation, the greatest morbidity of weakness. Minimizing ventilator support as soon as the patient's condition allows may be associated with a reduction in weakness-related morbidity.
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Mechanisms of Neurologic Failure in Critical Illness
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Of the three studies that adjusted for other risk factors in a multivariable model, only one found neuromuscular blockers to be independently associated with CINMA [185]. The use of nondepolarizing drugs such as vecuronium or pancuronium, especially in the presence of renal insufficiency, can lead to an accumulation of active drug and metabolites with significant prolongation of muscle paralysis independently of the development of CINMA [188–191]; differentiation CINMA and residual muscle relaxant effects can be made using electroneuromyographic repetitive stimulation, with demonstration of a decremental response amplitude in the presence of drug-induced paralysis. Several groups have suggested that neuromuscular blockers and corticosteroids exert synergistic effects in causing critical illness myopathy [192–194], but robust evidence to support this hypothesis is lacking.
Critical illness frequently is associated with neurologic failure that may involve the central and peripheral nervous systems. Central nervous system failure is associated with a spectrum of neurobehavioral changes including delirium, coma, and long-term cognitive dysfunction. Peripheral neurologic failure, or critical illness neuromuscular abnormalities, is suggested by diffuse arreflexic weakness and protracted respiratory insufficiency, and may also persist long after the acute hospitalization. While the burden of neurological disease complicating critical illness is considerable, preventive or therapeutic options are limited. This article provides an overview of research evaluating the relationship between critical illness and neurologic function, with a special emphasis on underlying mechanisms.
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This chapter reviews the clinical, electrophysiologic, and histopathologic manifestations of toxic myopathies that occur in humans. The evaluation of patients with suspected toxic myopathies should begin with a thorough general medical and focused neuromuscular assessment, followed by supportive laboratory and electrodiagnostic investigations. The identification of systemic manifestations—such as cardiomyopathy or skin rash—may help identify some toxic myopathies. Electrodiagnostic testing plays an important role in the evaluation of myopathies by confirming a clinically suspected process affecting muscles, determining the severity and distribution of a disease, and quantifying the degree of abnormality in some instances. However, electrodiagnostic studies also have limitations. Routinely performed studies are less sensitive in identifying myopathies, especially mild cases or those presenting early in the course, than in identifying neurogenic processes. In addition, electromyography (EMG) is limited in ability to determine the etiology of a myopathy because most electrophysiologic abnormalities occur in a wide variety of muscle diseases and are not unique to toxic myopathies.
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1999, Annales de Readaptation et de Medecine Physique
Les complications neuromusculaires de réanimation constituent une entité nouvelle.
Nous décrivons les caractéristiques de ces entités à la lumière des données de la littérature.
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La prise en charge rééducative doit être débutée précocement afin d'éviter l'incurie orthopédique, les séquelles neurologiques, et de permettre une réinsertion sociale.
Abstract
Neuromuscular complications acquired during the stage in the intensive care unit form a new entity.
In light of this account, we describe the features of these neuromuscular complications.
Three neuromuscular deficits are described: the so-called critical illness polyneuropathy, the neuromyopathic changes associated with corticosteroids and/or neuromuscular blocking agents, and the catabolic myopathy.
Physical therapy must be started rapidly to avoid orthopedic negligence, neurologic after-effects, and to promote social rehabilitation.

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Chest

Prolonged Reversible Quadriparesis in Mechanically Ventilated Patients Who Received Long-term Infusions of Vecuronium

Section snippets

CASE 1

DISCUSSION

J Allergy Clin Immunol

Br J Anaesth

J Neurol Sci

Neuromuscular complications in patients given Pavulon (pancuronium bromide) during artificial ventilation.

Clin Neurol Neurosurg

Disuse atrophy in a ventilated patient with status asthmaticus receiving neuromuscular blockade.

Crit Care Med