title: Critical Illness Myopathy (CIM) and Ventilator-Induced Diaphragm Muscle Dysfunction (VIDD): Acquired Myopathies Affecting Contractile Proteins.
abstract: Critical care and intensive care units (ICUs) have undergone dramatic changes and improvements in recent years, and critical care is today one of the fastest growing hospital disciplines. Significant improvements in treatments, removal of inefficient and harmful interventions, and introduction of advanced technological support systems have improved survival among critically ill ICU patients. However, the improved survival is associated with an increased number of patients with complications related to modern critical care. Severe muscle wasting and impaired muscle function are frequently observed in immobilized and mechanically ventilated ICU patients. Approximately 30% of mechanically ventilated and immobilized ICU patients for durations of five days and longer develop generalized muscle paralysis of all limb and trunk muscles. These patients typically have intact sensory and cognitive functions, a condition known as critical illness myopathy (CIM). Mechanical ventilation is a lifesaving treatment in critically ill ICU patients; however, the being on a ventilator creates dependence, and the weaning process occupies as much as 40% of the total time of mechanical ventilation. Furthermore, 20% to 30% of patients require prolonged intensive care due to ventilator-induced diaphragm dysfunction (VIDD), resulting in poorer outcomes, and greatly increased costs to health care providers. Our understanding of the mechanisms underlying both CIM and VIDD has increased significantly in the past decade and intervention strategies are presently being evaluated in different experimental models. This short review is restricted CIM and VIDD pathophysiology rather than giving a comprehensive review of all acquired muscle wasting conditions associated with modern critical care. © 2017 American Physiological Society. Compr Physiol 7:105-112, 2017.
authors.affiliation: Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.|Department of Clinical Neuroscience, Clinical Neurophysiology, Karolinska Institutet, Stockholm, Sweden.|Department of Biobehavioral Health, the Pennsylvania State University, University Park, Pennsylvania, USA.
authors.forename: Lars
authors.initials: L
authors.lastname: Larsson
authors.affiliation: Institute of Medical Biotechnology, Department of Chemical and Biological Engineering, Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Germany.
authors.forename: Oliver
authors.initials: O
authors.lastname: Friedrich
mesh_terms: D000818:Animals; D003285:Contractile Proteins / Q000502:physiology; D016638:Critical Illness; D003964:Diaphragm / Q000503:physiopathology*; D006801:Humans; D009135:Muscular Diseases / Q000209:etiology*; D012121:Respiration, Artificial / Q000009:adverse effects*
chemical_list: D003285:Contractile Proteins