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      Dysfunction of respiratory muscles in critically ill patients on the intensive care unit

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          Abstract

          Muscular weakness and muscle wasting may often be observed in critically ill patients on intensive care units (ICUs) and may present as failure to wean from mechanical ventilation. Importantly, mounting data demonstrate that mechanical ventilation itself may induce progressive dysfunction of the main respiratory muscle, i.e. the diaphragm. The respective condition was termed ‘ventilator‐induced diaphragmatic dysfunction’ (VIDD) and should be distinguished from peripheral muscular weakness as observed in ‘ICU‐acquired weakness (ICU‐AW)’.

          Interestingly, VIDD and ICU‐AW may often be observed in critically ill patients with, e.g. severe sepsis or septic shock, and recent data demonstrate that the pathophysiology of these conditions may overlap. VIDD may mainly be characterized on a histopathological level as disuse muscular atrophy, and data demonstrate increased proteolysis and decreased protein synthesis as important underlying pathomechanisms. However, atrophy alone does not explain the observed loss of muscular force. When, e.g. isolated muscle strips are examined and force is normalized for cross‐sectional fibre area, the loss is disproportionally larger than would be expected by atrophy alone. Nevertheless, although the exact molecular pathways for the induction of proteolytic systems remain incompletely understood, data now suggest that VIDD may also be triggered by mechanisms including decreased diaphragmatic blood flow or increased oxidative stress. Here we provide a concise review on the available literature on respiratory muscle weakness and VIDD in the critically ill. Potential underlying pathomechanisms will be discussed before the background of current diagnostic options. Furthermore, we will elucidate and speculate on potential novel future therapeutic avenues.

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          Most cited references99

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          Rapidly progressive diaphragmatic weakness and injury during mechanical ventilation in humans.

          Diaphragmatic function is a major determinant of the ability to successfully wean patients from mechanical ventilation (MV). Paradoxically, MV itself results in a rapid loss of diaphragmatic strength in animals. However, very little is known about the time course or mechanistic basis for such a phenomenon in humans. To determine in a prospective fashion the time course for development of diaphragmatic weakness during MV; and the relationship between MV duration and diaphragmatic injury or atrophy, and the status of candidate cellular pathways implicated in these phenomena. Airway occlusion pressure (TwPtr) generated by the diaphragm during phrenic nerve stimulation was measured in short-term (0.5 h; n = 6) and long-term (>5 d; n = 6) MV groups. Diaphragmatic biopsies obtained during thoracic surgery (MV for 2-3 h; n = 10) and from brain-dead organ donors (MV for 24-249 h; n = 15) were analyzed for ultrastructural injury, atrophy, and expression of proteolysis-related proteins (ubiquitin, nuclear factor-κB, and calpains). TwPtr decreased progressively during MV, with a mean reduction of 32 ± 6% after 6 days. Longer periods of MV were associated with significantly greater ultrastructural fiber injury (26.2 ± 4.8 vs. 4.7 ± 0.6% area), decreased cross-sectional area of muscle fibers (1,904 ± 220 vs. 3,100 ± 329 μm²), an increase of ubiquitinated proteins (+19%), higher expression of p65 nuclear factor-κB (+77%), and greater levels of the calcium-activated proteases calpain-1, -2, and -3 (+104%, +432%, and +266%, respectively) in the diaphragm. Diaphragmatic weakness, injury, and atrophy occur rapidly in critically ill patients during MV, and are significantly correlated with the duration of ventilator support.
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            Diaphragmatic motion studied by m-mode ultrasonography: methods, reproducibility, and normal values.

            Although diaphragmatic motion is readily studied by ultrasonography, the procedure remains poorly codified. The aim of this prospective study was to determine the reference values for diaphragmatic motion as recorded by M-mode ultrasonography. Two hundred ten healthy adult subjects (150 men, 60 women) were investigated. Both sides of the posterior diaphragm were identified, and M-mode was used to display the movement of the anatomical structures. Examinations were performed during quiet breathing, voluntary sniffing, and deep breathing. Diaphragmatic excursions were measured from the M-mode sonographic images. In addition, the reproducibility (inter- and intra-observer) was assessed. Right and left diaphragmatic motions were successfully assessed during quiet breathing in all subjects. During voluntary sniffing, the measurement was always possible on the right side, and in 208 of 210 volunteers, on the left side. During deep breathing, an obscuration of the diaphragm by the descending lung was noted in subjects with marked diaphragmatic excursion. Consequently, right diaphragmatic excursion could be measured in 195 of 210 subjects, and left diaphragmatic excursion in only 45 subjects. Finally, normal values of both diaphragmatic excursions were determined. Since the excursions were larger in men than in women, the gender should be taken into account. The lower limit values were close to 0.9 cm for women and 1 cm for men during quiet breathing, 1.6 cm for women and 1.8 cm for men during voluntary sniffing, and 3.7 cm for women and 4.7 cm for men during deep breathing. We demonstrated that M-mode ultrasonography is a reproducible method for assessing hemidiaphragmatic movement.
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              Evolution of Diaphragm Thickness during Mechanical Ventilation. Impact of Inspiratory Effort.

              Diaphragm atrophy and dysfunction have been reported in humans during mechanical ventilation, but the prevalence, causes, and functional impact of changes in diaphragm thickness during routine mechanical ventilation for critically ill patients are unknown.
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                Author and article information

                Contributors
                joerg.schefold@insel.ch
                Journal
                J Cachexia Sarcopenia Muscle
                J Cachexia Sarcopenia Muscle
                10.1007/13539.2190-6009
                JCSM
                Journal of Cachexia, Sarcopenia and Muscle
                John Wiley and Sons Inc. (Hoboken )
                2190-5991
                2190-6009
                09 March 2016
                September 2016
                : 7
                : 4 ( doiID: 10.1002/jcsm.v7.4 )
                : 403-412
                Affiliations
                [ 1 ] Department of Intensive Care Medicine, InselspitalUniversity Hospital of Bern BernSwitzerland
                [ 2 ] Department of Clinical Cardiology, InselspitalUniversity Hospital of Bern BernSwitzerland
                [ 3 ] Department of Cardiology and Center for Innovative Clinical TrialsUniversity of Göttingen GöttingenGermany
                [ 4 ] Center for Stroke Research BerlinCharite Universitätsmedizin Berlin BerlinGermany
                [ 5 ] Department of Neurosurgery and Dept. of Neurology, InselspitalUniversity Hospital of Bern BernSwitzerland
                Author notes
                [*] [* ]Correspondence to: Joerg C. Schefold, Department of Intensive Care Medicine, Inselspital, University Hospital of Bern, Freiburgstrasse 18, CH 3010 Bern, Switzerland: Email: joerg.schefold@ 123456insel.ch
                Article
                JCSM12108 JCSM-D-15-00096
                10.1002/jcsm.12108
                4788634
                27030815
                a532e61f-c945-4b11-82a0-1bcc586813b5
                © 2016 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society of Sarcopenia, Cachexia and Wasting Disorders

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 19 June 2015
                : 18 December 2015
                : 27 January 2016
                Page count
                Figures: 2, Tables: 0, Pages: 10, Words: 7341
                Categories
                Review
                Review
                Custom metadata
                2.0
                jcsm12108
                jcsm12108-hdr-0001
                September 2016
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.4 mode:remove_FC converted:06.09.2016

                Orthopedics
                vidd,diaphragm,weakness,cachexia,sepsis,mechanical ventilation,icu‐acquired weakness,weaning failure

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