Predominant involvement of motor fibres in patients with critical illness polyneuropathy.

Hund, Ernst; Genzwürker, Harald; Böhrer, H.; Jakob, Heinz; Thiele, Rudolf; Hacke, Werner

doi:10.1093/bja/78.3.274

Cited by 70 publications

(45 citation statements)

References 30 publications

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“…First, the presence and persistence of sepsis, systemic inflammatory response syndrome (SIRS), and multiple organ failure appear to hold a central role. Sepsis was the main suspect in the early days of the discovery of CIP, as it was a common feature in the first case reports (67,812), and the incidence of CIP reported in patients with sepsis was very high (52,333). Sepsis, multiple organ failure, and its severity were found to be associated with CIP (166,403,415,416).…”

Section: A Risk Factors For the Development Of Icuacquired Neuromuscmentioning

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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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: A Risk Factors For the Development Of Icuacquired Neuromuscmentioning

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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“…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

157

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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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“…Failure of weaning from the ventilator may be a first sign on ICU. Although the motor failure often predominates [14] distal loss of sensitivity to light touch, pain, temperature, and vibration may also be apparent [10].…”

Section: Definition and Clinical Featuresmentioning

confidence: 99%

“…Moreover, electrophysiological disturbances can be found in the early stage of the inflammatory response 2-5 days after admission to ICU before clinical evidence of neuromuscular damage evolves [27]. While the involvement of motor fibers predominates in most cases [14] also sensory abnormalities are found [28].…”

Section: Diagnostic Featuresmentioning

confidence: 99%

“…2) and appears earliest about 14 days after axonal damage. Median time to develop denervation in EMG was found to be 21 days after admission to the ICU [14] and therefore can not be used as an early detection strategy for CIP. However, spontaneous activity also can be apparent in myopathy and could be found in CIM at earlier time points [24].…”

Section: Diagnostic Featuresmentioning

confidence: 99%

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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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Predominant involvement of motor fibres in patients with critical illness polyneuropathy.

Cited by 70 publications

References 30 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

Neurological Sequelae of Sepsis: II) Neuromuscular Weakness

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