Tissue oedema is not associated with skeletal muscle weakness in septic patients

Ginz, H. F.; Bandschapp, Oliver; Urwyler, Albert; Girard, TD; Iaizzo, Paul A.

doi:10.1111/j.1399-6576.2010.02257.x

Cited by 4 publications

(7 citation statements)

References 4 publications

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“…Other studies seemed to exclude a role for edema to induce muscle weakness in septic patients. In a clinical study assessing muscle force and edema in 18 septic ICU patients, tissue edema was not associated with skeletal muscle weakness (245). More support to question the direct involvement of tissue edema in the pathophysiological mechanism of ICUAW came from a rat CLP study where EDL muscle microcirculation was observed with intravital microscopy 6 -48 h after sepsis induction (549).…”

Section: A Microcirculation-induced Denervationmentioning

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 Microcirculation-induced Denervationmentioning

confidence: 99%

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

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

300

329

View full text Add to dashboard Cite

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“…In previous work, we determined that oedema is not associated with skeletal muscle weakness in septic patients [2]. In this study we found out that interelectrode resistance does not change with oedema.…”

Section: Introductionmentioning

confidence: 73%

“…The double pulse was used because it is part of our protocol for muscle force assessment [2,9]. For each measurement session, low, medium and high levels of pulse current ( Table 2) were applied based on stimulator amplitude settings.…”

Section: Tissue Stimulation and Resistance Measuring Apparatusmentioning

confidence: 99%

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Inter-electrode tissue resistance is not affected by tissue oedema when electrically stimulating the lower limb of sepsis patients

Durfee

Young

Ginz

2014

Journal of Medical Engineering & Technology

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ICU patients typically are given large amounts of fluid and often develop oedema. The purpose of this study was to evaluate whether the oedema would change inter-electrode resistance and, thus, require a different approach to using non-invasive electrical stimulation of nerves to assess muscle force. Inter-electrode tissue resistance in the lower leg was measured by applying a 300 µs constant current pulse and measuring the current through and voltage across the stimulating electrodes. The protocol was administered to nine ICU patients with oedema, eight surgical patients without oedema and eight healthy controls. No significant difference in inter-electrode resistance was found between the three groups. For all groups, resistance decreased as stimulation current increased. In conclusion, inter-electrode resistance in ICU patients with severe oedema is the same as the resistance in regular surgical patients and healthy controls. This means that non-invasive nerve stimulation devices do not need to be designed to accommodate different resistances when used with oedema patients; however, surface stimulation does require higher current levels with oedema patients because of the increased distance between the skin surface and the targeted nerve or muscle.

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“…To create an objective measure of skeletal muscle force that does not rely on patient participation, our group has created nonvoluntary nerve‐stimulated isometric muscle force assessment systems (MFAS) for the hand, neck, and lower limb. The current version of the device is intended for bedside use and has undergone pilot testing in critically ill patients …”

mentioning

confidence: 99%