Critical illness myopathy (CIM), a complication of critical illness and mechanical ventilation in the ICU, is associated with increased ICU and hospital length of stay, morbidity and mortality. Peripheral skeletal muscle atrophy and impaired contractility occurs rapidly in the ICU, and recovery post critical illness resolution is heterogeneous, with some patients recovering skeletal muscle mass and function while others experience sustained muscle weakness months and years post-hospital discharge. Respiratory muscle weakness, most notably the diaphragm, also occurs in the critically ill ventilated patient. It delays extubation and contributes to prolonged ICU admission.
Post-ICU discharge persistent weakness may lead to loss of physical functional independence for the patient, having negative consequences on families and caregivers, and increasing health care costs. Although risk factors are well defined for CIM and the development of CIM is assumed to be multifactorial, the precise underlying etiology remains elusive.
This series of studies is intended to advance our understanding of 1) the pathophysiology underpinning peripheral skeletal muscle wasting and impaired contractility both in the acute stages of critical illness in the ICU, and sustained dysfunction months following ICU discharge, 2) mechanism of diaphragmatic muscle injury and/or weakness and 3) therapies that prevent and/or treat existing muscle atrophy and/or weakness in the critically ill patient and survivor.
We are seeking original research manuscripts addressing mechanisms of CIM and diaphragmatic weakness in the ICU in animal models, translational research or research in physiology of muscle function in the ICU patient or critical illness survivor. Development of novel models of CIM, both short and long term, to enable study of pathogenesis and treatment modalities, are also welcome. Studies focused in culture systems, provided they delineate/address precise cellular mechanism of therapies shown to impact muscle loss or recovery in the ICU or post discharge, are of interest. Intervention studies aimed at improving muscle function, observational studies examining changes in muscle structure, and review manuscripts summarizing our current understanding of the mechanisms of the phenomenon, identifying biggest gaps in knowledge for future research/highlighting future potential therapies will also be considered.
Critical illness myopathy (CIM), a complication of critical illness and mechanical ventilation in the ICU, is associated with increased ICU and hospital length of stay, morbidity and mortality. Peripheral skeletal muscle atrophy and impaired contractility occurs rapidly in the ICU, and recovery post critical illness resolution is heterogeneous, with some patients recovering skeletal muscle mass and function while others experience sustained muscle weakness months and years post-hospital discharge. Respiratory muscle weakness, most notably the diaphragm, also occurs in the critically ill ventilated patient. It delays extubation and contributes to prolonged ICU admission.
Post-ICU discharge persistent weakness may lead to loss of physical functional independence for the patient, having negative consequences on families and caregivers, and increasing health care costs. Although risk factors are well defined for CIM and the development of CIM is assumed to be multifactorial, the precise underlying etiology remains elusive.
This series of studies is intended to advance our understanding of 1) the pathophysiology underpinning peripheral skeletal muscle wasting and impaired contractility both in the acute stages of critical illness in the ICU, and sustained dysfunction months following ICU discharge, 2) mechanism of diaphragmatic muscle injury and/or weakness and 3) therapies that prevent and/or treat existing muscle atrophy and/or weakness in the critically ill patient and survivor.
We are seeking original research manuscripts addressing mechanisms of CIM and diaphragmatic weakness in the ICU in animal models, translational research or research in physiology of muscle function in the ICU patient or critical illness survivor. Development of novel models of CIM, both short and long term, to enable study of pathogenesis and treatment modalities, are also welcome. Studies focused in culture systems, provided they delineate/address precise cellular mechanism of therapies shown to impact muscle loss or recovery in the ICU or post discharge, are of interest. Intervention studies aimed at improving muscle function, observational studies examining changes in muscle structure, and review manuscripts summarizing our current understanding of the mechanisms of the phenomenon, identifying biggest gaps in knowledge for future research/highlighting future potential therapies will also be considered.