Polyneuropathies in critically ill patients: A prospective evaluation

Berek, Klaus; Margreiter, Josef; Willeit, Johann; Berek, A.; Schmutzhard, Erich; Mutz, N.

doi:10.1007/bf02044106

Cited by 170 publications

(70 citation statements)

References 19 publications

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“…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%

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

Appleton

Kinsella

Quasim

2014

Journal of the Intensive Care Society

151

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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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Section: Quality Of Included Studiesmentioning

confidence: 99%

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

Appleton

Kinsella

Quasim

2014

Journal of the Intensive Care Society

151

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“…However, these changes can be seen later in the course of the disease than ENG changes occur. Thus, ENG is superior in the diagnosis of CIP to clinical neurological examination [31] or nerve biopsies, maybe because ENG can also detect functional nerve failure e.g. impairment of axonal transport and transmembrane potential [30].…”

Section: Diagnostic Featuresmentioning

confidence: 99%

Neurological Sequelae of Sepsis: II) Neuromuscular Weakness

Axer¹

2011

TOCCMJ

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Abstract:Critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) have been established as separate entities of muscular weakness in critically ill patients, although both may be associated to each other in some respects. Both are associated to systemic inflammatory response syndrome, sepsis, and severe sepsis. Major signs of nerve and muscle disturbances in critically ill patients are muscle weakness and problems of weaning from the ventilator. Electroneurographic measurements help to detect CIP early in the course of the disease, while muscle biopsy seems to date the diagnostic tool of choice to detect CIM. Sepsis therapy is the major target to prevent the development of CIP and CIM. However, no specific therapy of CIP and CIM has been established in the past. Therefore, management of patients with CIP and CIM is mainly supportive. Neuromuscular weakness cause elongated times of ventilation, elongated hospital stay, elongated times of rehabilitation, and increased mortality. This review provides an overview of clinical and diagnostic features of CIP and CIM, and summarizes current pathophysiological and therapeutic concepts.

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“…In septic patients, CIP and critical illness myopathy (CIM) often coexist [2,3], and the incidence in patients with sepsis or septic shock varies between 70% and 80% [1]. Taken together, the results of the clinical study performed by Dr. Mohammadi and colleagues, and our in vitro study on the interaction of endotoxin with voltage-gated sodium channels suggest that endotoxin might be a crucial factor in the development of neuromuscular sequelae of sepsis already at a very early stage after onset of sepsis.…”

Section: Commentmentioning

confidence: 99%

“…Endotoxin reduced sodium channel availability at depolarized membrane potentials during acute application of high concentrations (C50 ng/ml) and after prolonged exposure (1 h) to a clinically relevant concentration (300 pg/ml). After 24 h of in vitro incubation with 300 pg/ml endotoxin, the reduction of sodium channel availability was irreversible and independent from the membrane potential.In septic patients, CIP and critical illness myopathy (CIM) often coexist [2,3], and the incidence in patients with sepsis or septic shock varies between 70% and 80% [1]. Taken together, the results of the clinical study performed by Dr. Mohammadi and colleagues, and our in vitro study on the interaction of endotoxin with voltage-gated sodium channels suggest that endotoxin might be a crucial factor in the development of neuromuscular sequelae of sepsis already at a very early stage after onset of sepsis.…”

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confidence: 99%

The role of endotoxin in critical illness myopathy and polyneuropathy

et al. 2009

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CommentSirs: We read the article by Dr. Mohammadi and colleagues dealing with parameters that correlate with the severity of early stage critical illness polyneuropathy (CIP) with great interest [5]. The authors performed nerve conduction studies and electromyography in 20 consecutive patients with severe sepsis or septic shock from day 1 to day 14 after onset of sepsis. The essential finding was a reduction in the amplitude in the compound action potential of the median and/or peroneal nerve which was reduced in 75% of patients already at day 1, and in 88% of patients at day 7. Remarkably, the reduction in the amplitude of the compound motor action potential correlated with the serum concentrations of endotoxin and interleukin-2-receptors. We have recently shown a direct interaction of endotoxin with heterologously expressed voltage-gated skeletal muscle sodium channels in vitro [4]. Endotoxin reduced sodium channel availability at depolarized membrane potentials during acute application of high concentrations (C50 ng/ml) and after prolonged exposure (1 h) to a clinically relevant concentration (300 pg/ml). After 24 h of in vitro incubation with 300 pg/ml endotoxin, the reduction of sodium channel availability was irreversible and independent from the membrane potential.In septic patients, CIP and critical illness myopathy (CIM) often coexist [2,3], and the incidence in patients with sepsis or septic shock varies between 70% and 80% [1]. Taken together, the results of the clinical study performed by Dr. Mohammadi and colleagues, and our in vitro study on the interaction of endotoxin with voltage-gated sodium channels suggest that endotoxin might be a crucial factor in the development of neuromuscular sequelae of sepsis already at a very early stage after onset of sepsis. This highlights the need for development of anti-endotoxin strategies to prevent CIM and CIP.

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Polyneuropathies in critically ill patients: A prospective evaluation

Abstract: In our patient population the frequency of the development of polyneuropathy was high (81.8%). Electrophysiologic investigation is superior to clinical neurologic examination in the detection of polyneuropathies.

Cited by 170 publications

References 19 publications

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

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

Neurological Sequelae of Sepsis: II) Neuromuscular Weakness

The role of endotoxin in critical illness myopathy and polyneuropathy

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