Mechanical Ventilation–induced Diaphragm Atrophy Strongly Impacts Clinical Outcomes

Diaphragm dysfunction worsens outcomes in mechanically ventilated patients, but the clinical impact of potentially preventable changes in diaphragm structure and function caused by mechanical ventilation is unknown. To determine whether diaphragm atrophy developing during mechanical ventilation lead...

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Published inAmerican journal of respiratory and critical care medicine Vol. 197; no. 2; pp. 204 - 213
Main Authors Goligher, Ewan C., Dres, Martin, Fan, Eddy, Rubenfeld, Gordon D., Scales, Damon C., Herridge, Margaret S., Vorona, Stefannie, Sklar, Michael C., Rittayamai, Nuttapol, Lanys, Ashley, Murray, Alistair, Brace, Deborah, Urrea, Cristian, Reid, W. Darlene, Tomlinson, George, Slutsky, Arthur S., Kavanagh, Brian P., Brochard, Laurent J., Ferguson, Niall D.
Format Journal Article
LanguageEnglish
Published United States American Thoracic Society 15.01.2018
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Abstract Diaphragm dysfunction worsens outcomes in mechanically ventilated patients, but the clinical impact of potentially preventable changes in diaphragm structure and function caused by mechanical ventilation is unknown. To determine whether diaphragm atrophy developing during mechanical ventilation leads to prolonged ventilation. Diaphragm thickness was measured daily by ultrasound in adults requiring invasive mechanical ventilation; inspiratory effort was assessed by thickening fraction. The primary outcome was time to liberation from ventilation. Secondary outcomes included complications (reintubation, tracheostomy, prolonged ventilation, or death). Associations were adjusted for age, severity of illness, sepsis, sedation, neuromuscular blockade, and comorbidity. Of 211 patients enrolled, 191 had two or more diaphragm thickness measurements. Thickness decreased more than 10% in 78 patients (41%) by median Day 4 (interquartile range, 3-5). Development of decreased thickness was associated with a lower daily probability of liberation from ventilation (adjusted hazard ratio, 0.69; 95% confidence interval [CI], 0.54-0.87; per 10% decrease), prolonged ICU admission (adjusted duration ratio, 1.71; 95% CI, 1.29-2.27), and a higher risk of complications (adjusted odds ratio, 3.00; 95% CI, 1.34-6.72). Development of increased thickness (n = 47; 24%) also predicted prolonged ventilation (adjusted duration ratio, 1.38; 95% CI, 1.00-1.90). Decreasing thickness was related to abnormally low inspiratory effort; increasing thickness was related to excessive effort. Patients with thickening fraction between 15% and 30% (similar to breathing at rest) during the first 3 days had the shortest duration of ventilation. Diaphragm atrophy developing during mechanical ventilation strongly impacts clinical outcomes. Targeting an inspiratory effort level similar to that of healthy subjects at rest might accelerate liberation from ventilation.
AbstractList Rationale: Diaphragm dysfunction worsens outcomes in mechanically ventilated patients, but the clinical impact of potentially preventable changes in diaphragm structure and function caused by mechanical ventilation is unknown.Objectives: To determine whether diaphragm atrophy developing during mechanical ventilation leads to prolonged ventilation.Methods: Diaphragm thickness was measured daily by ultrasound in adults requiring invasive mechanical ventilation; inspiratory effort was assessed by thickening fraction. The primary outcome was time to liberation from ventilation. Secondary outcomes included complications (reintubation, tracheostomy, prolonged ventilation, or death). Associations were adjusted for age, severity of illness, sepsis, sedation, neuromuscular blockade, and comorbidity.Measurements and Main Results: Of 211 patients enrolled, 191 had two or more diaphragm thickness measurements. Thickness decreased more than 10% in 78 patients (41%) by median Day 4 (interquartile range, 3-5). Development of decreased thickness was associated with a lower daily probability of liberation from ventilation (adjusted hazard ratio, 0.69; 95% confidence interval [CI], 0.54-0.87; per 10% decrease), prolonged ICU admission (adjusted duration ratio, 1.71; 95% CI, 1.29-2.27), and a higher risk of complications (adjusted odds ratio, 3.00; 95% CI, 1.34-6.72). Development of increased thickness (n = 47; 24%) also predicted prolonged ventilation (adjusted duration ratio, 1.38; 95% CI, 1.00-1.90). Decreasing thickness was related to abnormally low inspiratory effort; increasing thickness was related to excessive effort. Patients with thickening fraction between 15% and 30% (similar to breathing at rest) during the first 3 days had the shortest duration of ventilation.Conclusions: Diaphragm atrophy developing during mechanical ventilation strongly impacts clinical outcomes. Targeting an inspiratory effort level similar to that of healthy subjects at rest might accelerate liberation from ventilation.
Diaphragm dysfunction worsens outcomes in mechanically ventilated patients, but the clinical impact of potentially preventable changes in diaphragm structure and function caused by mechanical ventilation is unknown.RATIONALEDiaphragm dysfunction worsens outcomes in mechanically ventilated patients, but the clinical impact of potentially preventable changes in diaphragm structure and function caused by mechanical ventilation is unknown.To determine whether diaphragm atrophy developing during mechanical ventilation leads to prolonged ventilation.OBJECTIVESTo determine whether diaphragm atrophy developing during mechanical ventilation leads to prolonged ventilation.Diaphragm thickness was measured daily by ultrasound in adults requiring invasive mechanical ventilation; inspiratory effort was assessed by thickening fraction. The primary outcome was time to liberation from ventilation. Secondary outcomes included complications (reintubation, tracheostomy, prolonged ventilation, or death). Associations were adjusted for age, severity of illness, sepsis, sedation, neuromuscular blockade, and comorbidity.METHODSDiaphragm thickness was measured daily by ultrasound in adults requiring invasive mechanical ventilation; inspiratory effort was assessed by thickening fraction. The primary outcome was time to liberation from ventilation. Secondary outcomes included complications (reintubation, tracheostomy, prolonged ventilation, or death). Associations were adjusted for age, severity of illness, sepsis, sedation, neuromuscular blockade, and comorbidity.Of 211 patients enrolled, 191 had two or more diaphragm thickness measurements. Thickness decreased more than 10% in 78 patients (41%) by median Day 4 (interquartile range, 3-5). Development of decreased thickness was associated with a lower daily probability of liberation from ventilation (adjusted hazard ratio, 0.69; 95% confidence interval [CI], 0.54-0.87; per 10% decrease), prolonged ICU admission (adjusted duration ratio, 1.71; 95% CI, 1.29-2.27), and a higher risk of complications (adjusted odds ratio, 3.00; 95% CI, 1.34-6.72). Development of increased thickness (n = 47; 24%) also predicted prolonged ventilation (adjusted duration ratio, 1.38; 95% CI, 1.00-1.90). Decreasing thickness was related to abnormally low inspiratory effort; increasing thickness was related to excessive effort. Patients with thickening fraction between 15% and 30% (similar to breathing at rest) during the first 3 days had the shortest duration of ventilation.MEASUREMENTS AND MAIN RESULTSOf 211 patients enrolled, 191 had two or more diaphragm thickness measurements. Thickness decreased more than 10% in 78 patients (41%) by median Day 4 (interquartile range, 3-5). Development of decreased thickness was associated with a lower daily probability of liberation from ventilation (adjusted hazard ratio, 0.69; 95% confidence interval [CI], 0.54-0.87; per 10% decrease), prolonged ICU admission (adjusted duration ratio, 1.71; 95% CI, 1.29-2.27), and a higher risk of complications (adjusted odds ratio, 3.00; 95% CI, 1.34-6.72). Development of increased thickness (n = 47; 24%) also predicted prolonged ventilation (adjusted duration ratio, 1.38; 95% CI, 1.00-1.90). Decreasing thickness was related to abnormally low inspiratory effort; increasing thickness was related to excessive effort. Patients with thickening fraction between 15% and 30% (similar to breathing at rest) during the first 3 days had the shortest duration of ventilation.Diaphragm atrophy developing during mechanical ventilation strongly impacts clinical outcomes. Targeting an inspiratory effort level similar to that of healthy subjects at rest might accelerate liberation from ventilation.CONCLUSIONSDiaphragm atrophy developing during mechanical ventilation strongly impacts clinical outcomes. Targeting an inspiratory effort level similar to that of healthy subjects at rest might accelerate liberation from ventilation.
Diaphragm dysfunction worsens outcomes in mechanically ventilated patients, but the clinical impact of potentially preventable changes in diaphragm structure and function caused by mechanical ventilation is unknown. To determine whether diaphragm atrophy developing during mechanical ventilation leads to prolonged ventilation. Diaphragm thickness was measured daily by ultrasound in adults requiring invasive mechanical ventilation; inspiratory effort was assessed by thickening fraction. The primary outcome was time to liberation from ventilation. Secondary outcomes included complications (reintubation, tracheostomy, prolonged ventilation, or death). Associations were adjusted for age, severity of illness, sepsis, sedation, neuromuscular blockade, and comorbidity. Of 211 patients enrolled, 191 had two or more diaphragm thickness measurements. Thickness decreased more than 10% in 78 patients (41%) by median Day 4 (interquartile range, 3-5). Development of decreased thickness was associated with a lower daily probability of liberation from ventilation (adjusted hazard ratio, 0.69; 95% confidence interval [CI], 0.54-0.87; per 10% decrease), prolonged ICU admission (adjusted duration ratio, 1.71; 95% CI, 1.29-2.27), and a higher risk of complications (adjusted odds ratio, 3.00; 95% CI, 1.34-6.72). Development of increased thickness (n = 47; 24%) also predicted prolonged ventilation (adjusted duration ratio, 1.38; 95% CI, 1.00-1.90). Decreasing thickness was related to abnormally low inspiratory effort; increasing thickness was related to excessive effort. Patients with thickening fraction between 15% and 30% (similar to breathing at rest) during the first 3 days had the shortest duration of ventilation. Diaphragm atrophy developing during mechanical ventilation strongly impacts clinical outcomes. Targeting an inspiratory effort level similar to that of healthy subjects at rest might accelerate liberation from ventilation.
Author Dres, Martin
Brace, Deborah
Murray, Alistair
Reid, W. Darlene
Goligher, Ewan C.
Ferguson, Niall D.
Kavanagh, Brian P.
Slutsky, Arthur S.
Brochard, Laurent J.
Tomlinson, George
Scales, Damon C.
Lanys, Ashley
Urrea, Cristian
Rittayamai, Nuttapol
Vorona, Stefannie
Fan, Eddy
Rubenfeld, Gordon D.
Sklar, Michael C.
Herridge, Margaret S.
Author_xml – sequence: 1
  givenname: Ewan C.
  surname: Goligher
  fullname: Goligher, Ewan C.
  organization: Interdepartmental Division of Critical Care Medicine, Department of Physiology, Department of Medicine, Division of Respirology, Department of Medicine, University Health Network and Mount Sinai Hospital, Toronto, Canada
– sequence: 2
  givenname: Martin
  surname: Dres
  fullname: Dres, Martin
  organization: Keenan Centre for Biomedical Research, Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, Canada, Respiratory and Critical Care Department, Groupe Hospitalier Pitié Salpêtrière Charles Foix, Assistance Publique Hôpitaux de Paris, Paris, France
– sequence: 3
  givenname: Eddy
  surname: Fan
  fullname: Fan, Eddy
  organization: Interdepartmental Division of Critical Care Medicine, Department of Medicine, Institute for Health Policy, Management, and Evaluation, Division of Respirology, Department of Medicine, University Health Network and Mount Sinai Hospital, Toronto, Canada
– sequence: 4
  givenname: Gordon D.
  surname: Rubenfeld
  fullname: Rubenfeld, Gordon D.
  organization: Interdepartmental Division of Critical Care Medicine, Department of Medicine, Institute for Health Policy, Management, and Evaluation, Department of Critical Care Medicine, Sunnybrook Health Science Centre, Toronto, Canada
– sequence: 5
  givenname: Damon C.
  surname: Scales
  fullname: Scales, Damon C.
  organization: Interdepartmental Division of Critical Care Medicine, Department of Medicine, Institute for Health Policy, Management, and Evaluation, Department of Critical Care Medicine, Sunnybrook Health Science Centre, Toronto, Canada
– sequence: 6
  givenname: Margaret S.
  surname: Herridge
  fullname: Herridge, Margaret S.
  organization: Interdepartmental Division of Critical Care Medicine, Department of Medicine, Division of Respirology, Department of Medicine, University Health Network and Mount Sinai Hospital, Toronto, Canada, Toronto General Research Institute, Toronto, Canada; and
– sequence: 7
  givenname: Stefannie
  surname: Vorona
  fullname: Vorona, Stefannie
  organization: Division of Respirology, Department of Medicine, University Health Network and Mount Sinai Hospital, Toronto, Canada
– sequence: 8
  givenname: Michael C.
  surname: Sklar
  fullname: Sklar, Michael C.
  organization: Department of Anesthesia, and, Keenan Centre for Biomedical Research, Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, Canada
– sequence: 9
  givenname: Nuttapol
  surname: Rittayamai
  fullname: Rittayamai, Nuttapol
  organization: Keenan Centre for Biomedical Research, Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, Canada
– sequence: 10
  givenname: Ashley
  surname: Lanys
  fullname: Lanys, Ashley
  organization: Keenan Centre for Biomedical Research, Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, Canada
– sequence: 11
  givenname: Alistair
  surname: Murray
  fullname: Murray, Alistair
  organization: Division of Respirology, Department of Medicine, University Health Network and Mount Sinai Hospital, Toronto, Canada
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  givenname: Deborah
  surname: Brace
  fullname: Brace, Deborah
  organization: Division of Respirology, Department of Medicine, University Health Network and Mount Sinai Hospital, Toronto, Canada
– sequence: 13
  givenname: Cristian
  surname: Urrea
  fullname: Urrea, Cristian
  organization: Division of Respirology, Department of Medicine, University Health Network and Mount Sinai Hospital, Toronto, Canada
– sequence: 14
  givenname: W. Darlene
  surname: Reid
  fullname: Reid, W. Darlene
  organization: Department of Physical Therapy, University of Toronto, Toronto, Canada
– sequence: 15
  givenname: George
  surname: Tomlinson
  fullname: Tomlinson, George
  organization: Division of Respirology, Department of Medicine, University Health Network and Mount Sinai Hospital, Toronto, Canada
– sequence: 16
  givenname: Arthur S.
  surname: Slutsky
  fullname: Slutsky, Arthur S.
  organization: Interdepartmental Division of Critical Care Medicine, Department of Medicine, Keenan Centre for Biomedical Research, Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, Canada
– sequence: 17
  givenname: Brian P.
  surname: Kavanagh
  fullname: Kavanagh, Brian P.
  organization: Interdepartmental Division of Critical Care Medicine, Department of Physiology, Department of Anesthesia, and, Department of Critical Care Medicine, Hospital for Sick Children, Toronto, Canada
– sequence: 18
  givenname: Laurent J.
  surname: Brochard
  fullname: Brochard, Laurent J.
  organization: Interdepartmental Division of Critical Care Medicine, Department of Medicine, Keenan Centre for Biomedical Research, Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, Canada
– sequence: 19
  givenname: Niall D.
  surname: Ferguson
  fullname: Ferguson, Niall D.
  organization: Interdepartmental Division of Critical Care Medicine, Department of Physiology, Department of Medicine, Institute for Health Policy, Management, and Evaluation, Division of Respirology, Department of Medicine, University Health Network and Mount Sinai Hospital, Toronto, Canada
BackLink https://www.ncbi.nlm.nih.gov/pubmed/28930478$$D View this record in MEDLINE/PubMed
https://hal.science/hal-03985853$$DView record in HAL
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Keywords artificial respiration
diaphragm
acute respiratory failure
weaning
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Snippet Diaphragm dysfunction worsens outcomes in mechanically ventilated patients, but the clinical impact of potentially preventable changes in diaphragm structure...
Rationale: Diaphragm dysfunction worsens outcomes in mechanically ventilated patients, but the clinical impact of potentially preventable changes in diaphragm...
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StartPage 204
SubjectTerms Clinical outcomes
Diaphragm (Anatomy)
Intensive care
Intubation
Life Sciences
Muscular system
Ostomy
Respiration
Respiratory system
Respiratory therapy
Sepsis
Ultrasonic imaging
Ventilators
Title Mechanical Ventilation–induced Diaphragm Atrophy Strongly Impacts Clinical Outcomes
URI https://www.ncbi.nlm.nih.gov/pubmed/28930478
https://www.proquest.com/docview/1991893518
https://www.proquest.com/docview/1941356700
https://hal.science/hal-03985853
Volume 197
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