Incidence and onset of critical illness polyneuropathy in patients with septic shock

Tepper, Martin; Rakic, S.; Haas, J.A.; Woittiez, Arend Jan

doi:10.1016/s0300-2977(00)00019-x

Cited by 88 publications

(57 citation statements)

References 15 publications

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“…Within a few days of onset of critical illness, nerve conductions reveal reduced sensory and motor amplitudes (361,698,699). One likely contributor to early reduction in nerve conduction amplitudes is ion channelopathy (515).…”

Section: Clinical Diagnostic Tools and Potential Contributing Mechmentioning

confidence: 99%

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

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

279

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: Clinical Diagnostic Tools and Potential Contributing Mechmentioning

confidence: 99%

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

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

279

329

View full text Add to dashboard Cite

show abstract

“…Eleven out of the 29 (38%) 25,28,29,32,[36][37][38][39][40][41][42] observational studies were graded of low quality, 17 out of 29 (59%) 12,[14][15][16]20,24,26,27,30,[43][44][45][46][47][48][49][50] as medium and one (3%) 51 as high quality. There were four RCTs included; two studies were deemed of low risk, 22,23 one unclear risk 8 and one with high risk 31 of bias.…”

Section: Quality Of Included Studiesmentioning

confidence: 99%

“…This currently makes drawing firm conclusions regarding ICUAW difficult and may partly explain some of the inconsistent findings across the studies, such as an incidence varying from 9% 25 to 86%. 26 With the increasing recognition that the ICU care we deliver needs to ensure the optimal functional outcome of patients, further study and a better understanding of ICUAW are important next steps. There have been a significant number of studies published 8,15,16,23,24,[27][28][29][30][31][32] since the previous systematic review supporting updating the estimate of the incidence of ICUAW.…”

Section: Introductionmentioning

confidence: 99%

The incidence of intensive care unit-acquired weakness syndromes: A systematic review

Appleton

Kinsella

Quasim

2014

Journal of the Intensive Care Society

134

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We conducted a literature review of the intensive care unit-acquired weakness syndromes (critical illness polyneuropathy, critical illness myopathy and critical illness neuromyopathy) with the primary objective of determining their incidence as a combined group. Studies were identified through MEDLINE, Embase, Cochrane Database and article reference list searches and were included if they evaluated the incidence of one or more of these conditions in an adult intensive care unit population. The incidence of an intensive care unit-acquired weakness syndrome in the included studies was 40% (1080/2686 patients, 95% confidence interval 38-42%). The intensive care unit populations included were heterogeneous though largely included patients receiving mechanical ventilation for seven or more days. Additional prespecified outcomes identified that the incidence of intensive care unit-acquired weakness varied with the diagnostic technique used, being lower with clinical (413/1276, 32%, 95% CI 30-35%) compared to electrophysiological techniques (749/1591, 47%, 95% CI 45-50%). Approximately a quarter of patients were not able to comply with clinical evaluation and this may be responsible for potential underreporting of this condition.

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“…To determine whether neuropathy that develops during critical illness (14)(15)(16) can be rapidly reversible, we prospectively followed patients during the acute phase of critical illness and early recovery. This was an extension of a previous study in which we followed patients during the development of neuromuscular dysfunction early in the course of critical illness (14).…”

Section: Patients With Rapidly Reversible Neuropathymentioning

confidence: 99%

Inactivation of sodium channels underlies reversible neuropathy during critical illness in rats

Novak¹,

Nardelli²,

Cope³

et al. 2009

J. Clin. Invest.

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Neuropathy and myopathy can cause weakness during critical illness. To determine whether reduced excitability of peripheral nerves, rather than degeneration, is the mechanism underlying acute neuropathy in critically ill patients, we prospectively followed patients during the acute phase of critical illness and early recovery and assessed nerve conduction. During the period of early recovery from critical illness, patients recovered from neuropathy within days. This rapidly reversible neuropathy has not to our knowledge been previously described in critically ill patients and may be a novel type of neuropathy. In vivo intracellular recordings from dorsal root axons in septic rats revealed reduced action potential amplitude, demonstrating that reduced excitability of nerve was the mechanism underlying neuropathy. When action potentials were triggered by hyperpolarizing pulses, their amplitudes largely recovered, indicating that inactivation of sodium channels was an important contributor to reduced excitability. There was no depolarization of axon resting potential in septic rats, which ruled out a contribution of resting potential to the increased inactivation of sodium channels. Our data suggest that a hyperpolarized shift in the voltage dependence of sodium channel inactivation causes increased sodium inactivation and reduced excitability. Acquired sodium channelopathy may be the mechanism underlying acute neuropathy in critically ill patients.

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Incidence and onset of critical illness polyneuropathy in patients with septic shock

Cited by 88 publications

References 15 publications

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

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

The incidence of intensive care unit-acquired weakness syndromes: A systematic review

Inactivation of sodium channels underlies reversible neuropathy during critical illness in rats

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