Towards a biological definition of ARDS: are treatable traits the solution?

The pathophysiology of acute respiratory distress syndrome (ARDS) includes the accumulation of protein-rich pulmonary edema in the air spaces and interstitial areas of the lung, variable degrees of epithelial injury, variable degrees of endothelial barrier disruption, transmigration of leukocytes, a...

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Published inIntensive care medicine experimental Vol. 10; no. 1; pp. 8 - 14
Main Authors Bos, Lieuwe D. J., Laffey, John G., Ware, Lorraine B., Heijnen, Nanon F. L., Sinha, Pratik, Patel, Brijesh, Jabaudon, Matthieu, Bastarache, Julie A., McAuley, Daniel F., Summers, Charlotte, Calfee, Carolyn S., Shankar-Hari, Manu
Format Journal Article
LanguageEnglish
Published Cham Springer International Publishing 11.03.2022
Springer Nature B.V
SpringerOpen
Subjects
ARDS
Biomarker
Biomarkers
Critical Care Medicine
Definition
Diagnosis
Edema
Genotype & phenotype
Intensive
Intensive care
Medical diagnosis
Medicine
Medicine & Public Health
Pathophysiology
Phenotype
Respiratory distress syndrome
Reviews
Definition
Biomarker
Phenotype
Diagnosis
Pathophysiology
ARDS
Online AccessGet full text
ISSN2197-425X
2197-425X
DOI10.1186/s40635-022-00435-w

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Abstract The pathophysiology of acute respiratory distress syndrome (ARDS) includes the accumulation of protein-rich pulmonary edema in the air spaces and interstitial areas of the lung, variable degrees of epithelial injury, variable degrees of endothelial barrier disruption, transmigration of leukocytes, alongside impaired fluid and ion clearance. These pathophysiological features are different between patients contributing to substantial biological heterogeneity. In this context, it is perhaps unsurprising that a wide range of pharmacological interventions targeting these pathophysiological processes have failed to improve patient outcomes. In this manuscript, our goal is to provide a narrative summary of the potential methods to capture the underlying biological heterogeneity of ARDS and discuss how this information could inform future ARDS redefinitions. We discuss what biological tests are available to identify patients with any of the following predominant biological patterns: (1) epithelial and/or endothelial injury, (2) protein rich pulmonary edema and (3) systemic or within lung inflammatory responses.
AbstractList The pathophysiology of acute respiratory distress syndrome (ARDS) includes the accumulation of protein-rich pulmonary edema in the air spaces and interstitial areas of the lung, variable degrees of epithelial injury, variable degrees of endothelial barrier disruption, transmigration of leukocytes, alongside impaired fluid and ion clearance. These pathophysiological features are different between patients contributing to substantial biological heterogeneity. In this context, it is perhaps unsurprising that a wide range of pharmacological interventions targeting these pathophysiological processes have failed to improve patient outcomes. In this manuscript, our goal is to provide a narrative summary of the potential methods to capture the underlying biological heterogeneity of ARDS and discuss how this information could inform future ARDS redefinitions. We discuss what biological tests are available to identify patients with any of the following predominant biological patterns: (1) epithelial and/or endothelial injury, (2) protein rich pulmonary edema and (3) systemic or within lung inflammatory responses.
Abstract The pathophysiology of acute respiratory distress syndrome (ARDS) includes the accumulation of protein-rich pulmonary edema in the air spaces and interstitial areas of the lung, variable degrees of epithelial injury, variable degrees of endothelial barrier disruption, transmigration of leukocytes, alongside impaired fluid and ion clearance. These pathophysiological features are different between patients contributing to substantial biological heterogeneity. In this context, it is perhaps unsurprising that a wide range of pharmacological interventions targeting these pathophysiological processes have failed to improve patient outcomes. In this manuscript, our goal is to provide a narrative summary of the potential methods to capture the underlying biological heterogeneity of ARDS and discuss how this information could inform future ARDS redefinitions. We discuss what biological tests are available to identify patients with any of the following predominant biological patterns: (1) epithelial and/or endothelial injury, (2) protein rich pulmonary edema and (3) systemic or within lung inflammatory responses.
The pathophysiology of acute respiratory distress syndrome (ARDS) includes the accumulation of protein-rich pulmonary edema in the air spaces and interstitial areas of the lung, variable degrees of epithelial injury, variable degrees of endothelial barrier disruption, transmigration of leukocytes, alongside impaired fluid and ion clearance. These pathophysiological features are different between patients contributing to substantial biological heterogeneity. In this context, it is perhaps unsurprising that a wide range of pharmacological interventions targeting these pathophysiological processes have failed to improve patient outcomes. In this manuscript, our goal is to provide a narrative summary of the potential methods to capture the underlying biological heterogeneity of ARDS and discuss how this information could inform future ARDS redefinitions. We discuss what biological tests are available to identify patients with any of the following predominant biological patterns: (1) epithelial and/or endothelial injury, (2) protein rich pulmonary edema and (3) systemic or within lung inflammatory responses.The pathophysiology of acute respiratory distress syndrome (ARDS) includes the accumulation of protein-rich pulmonary edema in the air spaces and interstitial areas of the lung, variable degrees of epithelial injury, variable degrees of endothelial barrier disruption, transmigration of leukocytes, alongside impaired fluid and ion clearance. These pathophysiological features are different between patients contributing to substantial biological heterogeneity. In this context, it is perhaps unsurprising that a wide range of pharmacological interventions targeting these pathophysiological processes have failed to improve patient outcomes. In this manuscript, our goal is to provide a narrative summary of the potential methods to capture the underlying biological heterogeneity of ARDS and discuss how this information could inform future ARDS redefinitions. We discuss what biological tests are available to identify patients with any of the following predominant biological patterns: (1) epithelial and/or endothelial injury, (2) protein rich pulmonary edema and (3) systemic or within lung inflammatory responses.
ArticleNumber 8
Author Patel, Brijesh
Heijnen, Nanon F. L.
Ware, Lorraine B.
Calfee, Carolyn S.
Laffey, John G.
Bastarache, Julie A.
Bos, Lieuwe D. J.
McAuley, Daniel F.
Shankar-Hari, Manu
Summers, Charlotte
Jabaudon, Matthieu
Sinha, Pratik
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  organization: Intensive Care, Amsterdam UMC, Location AMC
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  givenname: John G.
  surname: Laffey
  fullname: Laffey, John G.
  organization: Anaesthesia and Intensive Care Medicine, Galway University Hospitals, National University of Ireland Galway
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  givenname: Lorraine B.
  surname: Ware
  fullname: Ware, Lorraine B.
  organization: Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center
– sequence: 4
  givenname: Nanon F. L.
  surname: Heijnen
  fullname: Heijnen, Nanon F. L.
  organization: Department of Intensive Care Medicine, Maastricht University Medical Center+
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  givenname: Pratik
  surname: Sinha
  fullname: Sinha, Pratik
  organization: Department of Anesthesiology, School of Medicine, Washington University
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  givenname: Brijesh
  surname: Patel
  fullname: Patel, Brijesh
  organization: Division of Anaesthetics, Pain Medicine, and Intensive Care, Department of Surgery and Cancer, Imperial College
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  givenname: Matthieu
  surname: Jabaudon
  fullname: Jabaudon, Matthieu
  organization: Department of Perioperative Medicine, CHU Clermont-Ferrand, GReD, Université Clermont Auvergne, CNRS, INSERM
– sequence: 8
  givenname: Julie A.
  surname: Bastarache
  fullname: Bastarache, Julie A.
  organization: Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center
– sequence: 9
  givenname: Daniel F.
  surname: McAuley
  fullname: McAuley, Daniel F.
  organization: Wellcome-Wolfson Institute for Experimental Medicine, Queen’s University Belfast
– sequence: 10
  givenname: Charlotte
  surname: Summers
  fullname: Summers, Charlotte
  organization: Department of Medicine, School of Clinical Medicine, University of Cambridge
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  givenname: Carolyn S.
  surname: Calfee
  fullname: Calfee, Carolyn S.
  organization: Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California, San Francisco
– sequence: 12
  givenname: Manu
  surname: Shankar-Hari
  fullname: Shankar-Hari, Manu
  organization: School of Immunology and Microbial Sciences, King’s College London, Centre for Inflammation Research, The University of Edinburgh
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35274164$$D View this record in MEDLINE/PubMed
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Issue 1
Keywords Definition
Biomarker
Phenotype
Diagnosis
Pathophysiology
ARDS
Language English
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Snippet The pathophysiology of acute respiratory distress syndrome (ARDS) includes the accumulation of protein-rich pulmonary edema in the air spaces and interstitial...
Abstract The pathophysiology of acute respiratory distress syndrome (ARDS) includes the accumulation of protein-rich pulmonary edema in the air spaces and...
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SubjectTerms ARDS
Biomarker
Biomarkers
Critical Care Medicine
Definition
Diagnosis
Edema
Genotype & phenotype
Intensive
Intensive care
Medical diagnosis
Medicine
Medicine & Public Health
Pathophysiology
Phenotype
Respiratory distress syndrome
Reviews
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Title Towards a biological definition of ARDS: are treatable traits the solution?
URI https://link.springer.com/article/10.1186/s40635-022-00435-w
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Volume 10
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