scholarly journals Muscle weakness and wasting in pediatric critical illness

2021 ◽  
Vol 5 ◽  
pp. 13-13
Author(s):  
Chengsi Ong ◽  
Jan Hau Lee ◽  
Zudin A. Puthucheary
Keyword(s):  
Critical Illness ◽  
Muscle Weakness

scholarly journals Janus kinase inhibition prevents cancer- and myocardial infarction-mediated diaphragm muscle weakness in mice

2016 ◽  
Vol 310 (8) ◽  
pp. R707-R710 ◽  
Author(s):  
Ira J. Smith ◽  
Brandon Roberts ◽  
Adam Beharry ◽  
Guillermo L. Godinez ◽  
Donald G. Payan ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Critical Illness ◽  
Muscle Weakness ◽  
Janus Kinase ◽  
Diaphragm Muscle ◽  
Vehicle Group ◽  
Specific Force ◽  
Tumor Bearing ◽  
Sham Surgery ◽  
Diaphragm Weakness

Respiratory dysfunction is prevalent in critically ill patients and can lead to adverse clinical outcomes, including respiratory failure and increased mortality. Respiratory muscles, which normally sustain respiration through inspiratory muscle contractions, become weakened during critical illness, and recent studies suggest that respiratory muscle weakness is related to systemic inflammation. Here, we investigate the pathophysiological role of the inflammatory JAK1/3 signaling pathway in diaphragm weakness in two distinct experimental models of critical illness. In the first experiment, mice received subcutaneous injections of PBS or C26 cancer cells and were fed chow formulated with or without the JAK1/3 inhibitor R548 for 26 days. Diaphragm specific force was significantly reduced in tumor-bearing mice receiving standard chow; however, treatment with the JAK1/3 inhibitor completely prevented diaphragm weakness. Diaphragm cross-sectional area was diminished by ∼25% in tumor-bearing mice but was similar to healthy mice in tumor-bearing animals treated with R548. In the second study, mice received sham surgery or coronary artery ligation, leading to myocardial infarction (MI), and were treated with R548 or vehicle 1 h postsurgery, and once daily for 3 days. Diaphragm specific force was comparable between sham surgery/vehicle, sham surgery/R548 and MI/R548 groups, but significantly decreased in the MI/vehicle group. Markers of oxidative damage and activated caspase-3, mechanisms previously identified to reduce muscle contractility, were not elevated in diaphragm extracts. These experiments implicate JAK1/3 signaling in cancer- and MI-mediated diaphragm weakness in mice, and provide a compelling case for further investigation.

Physiotherapy in critically ill patients

2017 ◽  
Author(s):  
R Gosselink ◽  
J Roeseler
Keyword(s):  
Critical Illness ◽  
Critically Ill ◽  
Muscle Weakness ◽  
Critically Ill Patients ◽  
Joint Stiffness ◽  
Evidence Based ◽  
Strong Focus ◽  
Weaning Failure ◽  
Functional Exercise ◽  
Physical Deconditioning

Physiotherapists are involved in the management of patients with critical illness. Physiotherapy assessment of critically ill patients is less driven by medical diagnosis; instead, there is a strong focus on deficiencies at a pathophysiological and functional level. An accurate and valid assessment of respiratory conditions (retained airway secretions, atelectasis, and respiratory muscle weakness), physical deconditioning, and related problems (muscle weakness, joint stiffness, impaired functional exercise capacity, physical inactivity, and emotional function) allows the identifying of targets for physiotherapy. Evidence-based targets for physiotherapy are deconditioning, impaired airway clearance, atelectasis, (re-)intubation avoidance, and weaning failure. Early physical activity and mobility are key in the prevention, attenuation, or reversion of physical deconditioning related to critical illness. A variety of modalities for exercise training and early mobility are evidence-based and are implemented, depending on the stage of critical illness, comorbid conditions, and cooperation of the patient. The physiotherapist should be responsible for implementing mobilization plans and exercise prescription and make recommendations for their progression, jointly with medical and nursing staff.

scholarly journals Cholesterol and its association with muscle weakness in critical illness

Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Daniel A. Hofmaenner ◽  
Anna Kleyman ◽  
Mervyn Singer
Keyword(s):  
Critical Illness ◽  
Muscle Weakness

Physiotherapy in critically ill patients

2021 ◽  
pp. 373-384
Author(s):  
Rik Gosselink ◽  
Jean Roeseler
Keyword(s):  
Critical Illness ◽  
Critically Ill ◽  
Muscle Weakness ◽  
Critically Ill Patients ◽  
Joint Stiffness ◽  
Evidence Based ◽  
Strong Focus ◽  
Functional Exercise ◽  
Valid Assessment ◽  
Physical Deconditioning

Physiotherapists are involved in the management of patients with critical illness. Physiotherapy assessment of critically ill patients is less driven by medical diagnosis; instead, there is a strong focus on deficiencies at a pathophysiological and functional level. An accurate and valid assessment of respiratory conditions (retained airway secretions, atelectasis, and respiratory muscle weakness), physical deconditioning, and related problems (muscle weakness, joint stiffness, impaired functional exercise capacity, physical inactivity, and emotional function) allows the identifying of targets for physiotherapy. Evidence-based targets for physiotherapy are deconditioning, impaired airway clearance, atelectasis, (re-)intubation avoidance, and weaning failure. Early physical activity and mobility are key in the prevention, attenuation, or reversion of physical deconditioning related to critical illness. A variety of modalities for exercise training and early mobility are evidence-based and are implemented, depending on the stage of critical illness, comorbid conditions, and cooperation of the patient. The physiotherapist should be responsible for implementing mobilization plans and exercise prescription and make recommendations for their progression, jointly with medical and nursing staff.

scholarly journals Altered cholesterol homeostasis in critical illness-induced muscle weakness: effect of exogenous 3-hydroxybutyrate

Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Chloë Goossens ◽  
Ruben Weckx ◽  
Sarah Derde ◽  
Sarah Vander Perre ◽  
Inge Derese ◽  
...  
Keyword(s):  
Critical Illness ◽  
Critically Ill ◽  
Muscle Weakness ◽  
Serum Cholesterol ◽  
Critically Ill Patients ◽  
Muscle Force ◽  
Plasma Cholesterol ◽  
Cholesterol Homeostasis ◽  
Protective Mechanism ◽  
The Impact

Abstract Background Muscle weakness is a complication of critical illness which hampers recovery. In critically ill mice, supplementation with the ketone body 3-hydroxybutyrate has been shown to improve muscle force and to normalize illness-induced hypocholesterolemia. We hypothesized that altered cholesterol homeostasis is involved in development of critical illness-induced muscle weakness and that this pathway can be affected by 3-hydroxybutyrate. Methods In both human critically ill patients and septic mice, the association between circulating cholesterol concentrations and muscle weakness was assessed. In septic mice, the impact of 3-hydroxybutyrate supplementation on cholesterol homeostasis was evaluated with use of tracer technology and through analysis of markers of cholesterol metabolism and downstream pathways. Results Serum cholesterol concentrations were lower in weak than in non-weak critically ill patients, and in multivariable analysis adjusting for baseline risk factors, serum cholesterol was inversely correlated with weakness. In septic mice, plasma cholesterol correlated positively with muscle force. In septic mice, exogenous 3-hydroxybutyrate increased plasma cholesterol and altered cholesterol homeostasis, by normalization of plasma mevalonate and elevation of muscular, but not hepatic, expression of cholesterol synthesis genes. In septic mice, tracer technology revealed that 3-hydroxybutyrate was preferentially taken up by muscle and metabolized into cholesterol precursor mevalonate, rather than TCA metabolites. The 3-hydroxybutyrate protection against weakness was not related to ubiquinone or downstream myofiber mitochondrial function, whereas cholesterol content in myofibers was increased. Conclusions These findings point to a role for low cholesterol in critical illness-induced muscle weakness and to a protective mechanism-of-action for 3-hydroxybutyrate supplementation.

Long-Term Implications of ICU-Acquired Muscle Weakness

2014 ◽  
Author(s):  
Nicola Latronico ◽  
Simone Piva ◽  
Victoria McCredie
Keyword(s):  
Critical Illness ◽  
Muscle Weakness ◽  
Critical Illness Polyneuropathy ◽  
Foot Drop ◽  
Sensory Loss ◽  
Post Discharge ◽  
Effective Measure ◽  
Increased Risk ◽  
Evidenced Based

Intensive care unit-acquired weakness (ICUAW) is a significant and common complication with major implications for survivors of critical illness. ICUAW is a clinical diagnosis made in the presence of generalized muscle weakness that occurs in the setting of critical illness when other causes of muscle weakness have been excluded. Critical illness polyneuropathy and myopathy are the most common causes of ICUAW. Short-term implications of ICUAW include alveolar hypoventilation and an increased risk of pulmonary aspiration, atelectasis, and pneumonia—factors which may contribute to acute respiratory failure and ICU re-admission. In the long term, ICUAW has been associated with physical disturbances, including unsteady gait, sensory loss, foot drop, and, in more severe cases, persistent quadriparesis and ventilator dependency. ICUAW appears to heavily influence the failure of ICU patients to return to baseline health status post-discharge. There is a paucity of evidenced-based therapeutic strategies to reduce the incidence of ICUAW; however, early rehabilitative therapy might represent an effective measure in improving functional status.

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