Intensive care unit-acquired weakness (ICUAW) and muscle wasting in critically ill patients with severe sepsis and septic shock

Joerg C Schefold, Jeffrey Bierbrauer, Steffen Weber-Carstens, Joerg C Schefold, Jeffrey Bierbrauer, Steffen Weber-Carstens

Abstract

Sepsis presents a major health care problem and remains one of the leading causes of death within the intensive care unit (ICU). Therapeutic approaches against severe sepsis and septic shock focus on early identification. Adequate source control, administration of antibiotics, preload optimization by fluid resuscitation and further hemodynamic stabilisation using vasopressors whenever appropriate are considered pivotal within the early-golden-hours of sepsis. However, organ dysfunction develops frequently in and represents a significant comorbidity of sepsis. A considerable amount of patients with sepsis will show signs of severe muscle wasting and/or ICU-acquired weakness (ICUAW), which describes a frequently observed complication in critically ill patients and refers to clinically weak ICU patients in whom there is no plausible aetiology other than critical illness. Some authors consider ICUAW as neuromuscular organ failure, caused by dysfunction of the motor unit, which consists of peripheral nerve, neuromuscular junction and skeletal muscle fibre. Electrophysiologic and/or biopsy studies facilitate further subclassification of ICUAW as critical illness myopathy, critical illness polyneuropathy or critical illness myoneuropathy, their combination. ICUAW may protract weaning from mechanical ventilation and impede rehabilitation measures, resulting in increased morbidity and mortality. This review provides an insight on the available literature on sepsis-mediated muscle wasting, ICUAW and their potential pathomechanisms.

Figures

Fig. 1
Fig. 1
Risk factors involved in muscle wasting and ICUAW. Both complications may overlap in septic patients, yet they present two distinct entities that should not be used synonymously. Whereas ICUAW is most likely accompanied by muscle wasting, muscle wasting is not necessarily associated with ICUAW
Fig. 2
Fig. 2
Suggested beneficial effects of electrical muscle stimulation (EMS) with regard to muscle hypertrophy, atrophy, aerobic capacity, membrane excitability and membrane translocation of GLUT4. EMS may preserve membrane excitability. Membrane translocation of GLUT4 is regulated by IGF-1, AMPK, PGC-1α and its downstream targets, which may all be affected by EMS. Atrophy gene expression (MuRF-1, atrogin-1) increases upon desphosphorylation of FoxO3 trancription factors, which is inhibited by downstream insulin signalling. EMS electrical muscle stimulation, IGF-1 insulin growth factor-1, GLUT4 glucose transporter 4, IRS-1 insulin receptor substrate 1, AMPK AMP-activated protein kinase, PI3K phopshoinositide 3-kinase, PPAR peroxisome proliferator-activated receptor, PGC-1α PPAR-γ coactivator 1α, pAKT phosphorylated Akt protein kinase B, mTOR mammalian target of rapamycin, FoxO3 forkhead box O3, MuRF muscle-specific ring finger protein
Fig. 3
Fig. 3
Muscle histologies (vastus lateralis muscle) from an ICU patient with critical illness myopathy (subclassification of ICUAW) and an ICU patient without this complication, referred to as ICU control. ATPase/Toludine blue staining differentiates type I, IIa and IIb muscle fibres as indicated

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Source: PubMed

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