Neuromuscular complications in patients given pavulon/sr (pancuronium bromide) during artificial ventilation

Coul, A. A. W. Op De; Lambregts, P.C.L.A.; Koeman, J.; Puyenbroek, M.J.E. van; Laak, H.J. ter; Gabreëls-Festen, A.A.W.M.

doi:10.1016/0303-8467(85)90060-5

Cited by 206 publications

(71 citation statements)

References 5 publications

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“…Tendon reflexes are generally attenuated. Facial and extraocular muscles are generally spared but may occasionally be involved (100,382,529,643). As in CIP, weaning failure is reported as a dominant symptom (382,383).…”

Section: History Time Course and Clinical Features Of Icu-relatmentioning

confidence: 99%

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The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

300

329

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Critical illness polyneuropathies (CIP) and myopathies (CIM) are common complications of critical illness. Several weakness syndromes are summarized under the term intensive care unit-acquired weakness (ICUAW). We propose a classification of different ICUAW forms (CIM, CIP, sepsis-induced, steroid-denervation myopathy) and pathophysiological mechanisms from clinical and animal model data. Triggers include sepsis, mechanical ventilation, muscle unloading, steroid treatment, or denervation. Some ICUAW forms require stringent diagnostic features; CIM is marked by membrane hypoexcitability, severe atrophy, preferential myosin loss, ultrastructural alterations, and inadequate autophagy activation while myopathies in pure sepsis do not reproduce marked myosin loss. Reduced membrane excitability results from depolarization and ion channel dysfunction. Mitochondrial dysfunction contributes to energy-dependent processes. Ubiquitin proteasome and calpain activation trigger muscle proteolysis and atrophy while protein synthesis is impaired. Myosin loss is more pronounced than actin loss in CIM. Protein quality control is altered by inadequate autophagy. Ca 2ϩ dysregulation is present through altered Ca 2ϩ homeostasis. We highlight clinical hallmarks, trigger factors, and potential mechanisms from human studies and animal models that allow separation of risk factors that may trigger distinct mechanisms contributing to weakness. During critical illness, altered inflammatory (cytokines) and metabolic pathways deteriorate muscle function. ICUAW prevention/treatment is limited, e.g., tight glycemic control, delaying nutrition, and early mobilization. Future challenges include identification of primary/secondary events during the time course of critical illness, the interplay between membrane excitability, bioenergetic failure and differential proteolysis, and finding new therapeutic targets by help of tailored animal models.

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Section: History Time Course and Clinical Features Of Icu-relatmentioning

confidence: 99%

“…In the 1980s, it was first reported that following prolonged use of neuromuscular blocking agents, some patients developed persistent weakness (529). Subsequent studies identified the mechanism underlying weakness as prolonged neuromuscular blockade (37,386,538,596,624,625).…”

Section: Neuromuscular Transmission In Critical Illnessmentioning

confidence: 99%

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

300

329

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“…Although CIN has been reported to be more frequent than CIM in several studies [3], in a study with 88 patients, the incidence ratio of CIM was reported to be three times more than CIN (42% vs. 13%). The results of this study showed that among patients who underwent EMG in ICU population, acute myopathy is three times as common as acute axonal polyneuropathy, and the outcomes from acute myopathy and acute axonal polyneuropathy may be similar [4].…”

Section: Critical Illness Neuropathy (Cin)mentioning

confidence: 79%

Neuromuscular Disorders in Critically-Ill Patients – Approaches to Electrophysiologic Changes in Critical Illness Neuropathy and Myopathy

Eslamian¹,

Rahbar²

2012

Advances in Clinical Neurophysiology

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“…Muscle atrophy and weakness leading to difficulty in weaning from the ventilator, develop frequently in patients with critical illness (sepsis and multiple organ dysfunction), complicating a variety of primary diseases (Roelofs et al 1983;Bolton et al 1984;Op de Coul et al 1985;Zochodne et al 1985Zochodne et al , 1987Williams et al 1986;Bolton 1987 ;'Lycklama ~t Nyeholt and Troost 1987). Electrophysiological studies have shown spontaneous muscle activity and reduced amplitudes of compound muscle action potentials, and also of sensory nerve action potentials.…”

Section: Introductionmentioning

confidence: 99%

“…Electrophysiological studies have shown spontaneous muscle activity and reduced amplitudes of compound muscle action potentials, and also of sensory nerve action potentials. Conduction velocities of motor and sensory nerves, distal latencies and F-wave latencies are usually normal (Op de Coul et al 1985;Bolton et al 1986;Bolton 1987;Lycklama ~ Nyeholt and Troost 1987;Zochodne et al 1987). Pathological examination may show a mild to moderate degree of axonal degeneration of peripheral nerves, and atrophy and necrosis of muscle fibres (Bolton et al 1984;Zochodne et al 1985Zochodne et al , 1987.…”

Section: Introductionmentioning

confidence: 99%

Histological investigations of muscle atrophy and end plates in two critically ill patients with generalized weakness

Wokke

Jennekens

Oord

et al. 1988

Journal of the Neurological Sciences

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SUMMARYWe describe pathological alterations at the light microscopical and ultrastructural level of motor end plates and muscle fibres in 2 critically ill patients with generalized muscular atrophy and weakness. Axonal degeneration of intramuscular nerve fibres was not conspicuous. The sural nerve in one patient showed only minor abnormalities. There was a marked atrophy of type 1 and especially type 2 muscle fibres. Nodal and ultraterminal nerve sprouts were seen in both biopsies. Motor end plates showed features of regeneration. They were enlarged in one patient. This patient was treated for a prolonged period with vecuronium bromide. Pharmacological denervation may explain the presence of fibrillation potentials, and, partially, of the histological abnormalities. Another factor which must be considered is inhibition of neuromuscular transmission by antibiotics. In addition to disuse atrophy and a minor degree of axonal neuropathy, the production of muscle proteolytic factors may be involved in the rapidly occurring massive loss of muscle fibre size in critically ill patients.

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Neuromuscular complications in patients given pavulon/sr (pancuronium bromide) during artificial ventilation

Cited by 206 publications

References 5 publications

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Neuromuscular Disorders in Critically-Ill Patients – Approaches to Electrophysiologic Changes in Critical Illness Neuropathy and Myopathy

Histological investigations of muscle atrophy and end plates in two critically ill patients with generalized weakness

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