4/25/2024 0 Comments Cute abella nn model set 108![]() ![]() Weakness appears to be triggered by critical illness and the ICU course regardless of the underlying primary condition ( 382, 453, 528). These conditions are the primary cause of muscle weakness and paralysis during and following critical illness ( 402). This condition can either affect the peripheral nerves (critical illness polyneuropathy, CIP), skeletal muscle (critical illness myopathy, CIM) or both (critical illness polyneuromyopathy, CIPNM) ( 6, 402, 404, 747). The loss of flesh and strength is very striking.” This description of the symptoms in a condition of acute critical illness, in acute broncho-pneumonic phthisis, by Sir William Osler in his classical textbook on “principles and practice of medicine” ( 531) is one of the first analytical observations linking an aberrant systemic inflammatory response to a failure of the peripheral nervous system, i.e., muscle wasting and weakness. There may be repeated chills the temperature is high, the pulse rapid, and the respirations are increased. Haemorrhage initiates the attack in a few cases. “In adults the disease may attack persons in good health, but who are overworked or ‘run down’ from any cause. 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. ICUAW prevention/treatment is limited, e.g., tight glycemic control, delaying nutrition, and early mobilization. During critical illness, altered inflammatory (cytokines) and metabolic pathways deteriorate muscle function. 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. Ca 2+ dysregulation is present through altered Ca 2+ homeostasis. Protein quality control is altered by inadequate autophagy. Myosin loss is more pronounced than actin loss in CIM. Ubiquitin proteasome and calpain activation trigger muscle proteolysis and atrophy while protein synthesis is impaired. Mitochondrial dysfunction contributes to energy-dependent processes. Reduced membrane excitability results from depolarization and ion channel dysfunction. 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. Triggers include sepsis, mechanical ventilation, muscle unloading, steroid treatment, or denervation. We propose a classification of different ICUAW forms (CIM, CIP, sepsis-induced, steroid-denervation myopathy) and pathophysiological mechanisms from clinical and animal model data. ![]() Several weakness syndromes are summarized under the term intensive care unit-acquired weakness (ICUAW). Critical illness polyneuropathies (CIP) and myopathies (CIM) are common complications of critical illness. ![]()
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