Effect of transcutaneous electrical muscle stimulation on muscle volume in patients with septic shock*

Poulsen, J.C. Navarro; Møller, Kirsten; Jensen, C. E.; Weisdorf, Sigge; Kehlet, Henrik; Perner, Anders

doi:10.1097/ccm.0b013e318205c7bc

Cited by 122 publications

(195 citation statements)

References 50 publications

Supporting

Mentioning

169

Contrasting

Unclassified

Order By: Relevance

“…Preliminary results in small samples of critically ill patients were promising and found that EMS preserved muscle mass (237,272,474), reduced muscle catabolism (73), and exerted shortterm systemic microcirculatory effects (238). In another eight patients with septic shock however, 7 days of EMS did not preserve muscle volume (555). Several randomized studies examining the effects of EMS on muscle function in the ICU recently emerged.…”

Section: Electrical Muscle Stimulationmentioning

confidence: 97%

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

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.

show abstract

Section: Electrical Muscle Stimulationmentioning

confidence: 97%

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

show abstract

“…Muscle strength and muscle protein synthesis were improved more on Physical Disabilities -Therapeutic Implicationsthe stimulated side limb, although the muscle cross-sectional area and muscle mass decreased in both limbs [125,126]. A previous RCT using NMES indicated increased muscle strength and decreased mechanical ventilator duration and the incidence of ICUAW decreased from 39.3 to 12.5% in the NMES intervention group [127].…”

Section: Neuromuscular Electrical Stimulationmentioning

confidence: 99%

Skeletal Muscle Dysfunction in Critical Illness

Iida¹,

Sakuma²

2017

Physical Disabilities - Therapeutic Implications

View full text Add to dashboard Cite

Despite improvements in critical illness survival rates with recent developments in medical care, many patients still have long-term physical disabilities following stays in the intensive care unit (ICU). Critical illness-induced muscle weakness, so-called ICU-acquired weakness (ICU-AW), is a common occurrence in approximately 50% of critically ill patients in the ICU requiring mechanical ventilation for >7 days. ICU-AW contributes to increases in duration of mechanical ventilation and lengths of ICU and hospital stays and may persist among survivors for several years after discharge. Risk factors for ICU-AW include systemic inflammatory responses, severe sepsis, muscle inactivity, hyperglycemia, and use of neuromuscular blockers. Thus, the development of muscle wasting is suggested to be associated with pathophysiological alterations leading to an imbalance between muscle proteolysis and proteosynthesis through several cellular signaling networks. This chapter presents a review of the literature regarding critical illness-induced muscle wasting and describes potential treatment of excessive muscle catabolism.

show abstract

“…J. Poulsen и соавт. [32] в 2011 г. в исследовании со схожим дизайном показали, что у 8 пациентов с септическим шоком 7-дневный курс ЭСМ не оказывает влияния на количество мышечной ткани. У пациентов произошла атрофия мышц как на стороне стимуляции, так и на противоположной.…”

Section: клинические данные использования эсм в оритunclassified