Evidence map›Paper›PMID 35274164›Full record

ReviewIntensive care medicine experimental2022

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

Lieuwe D J Bos, John G Laffey, Lorraine B Ware, Nanon F L Heijnen, Pratik Sinha, Brijesh Patel, Matthieu Jabaudon, Julie A Bastarache, Daniel F McAuley, Charlotte Summers and 2 more

Abstract readReview
In one paragraph

Review in Intensive care medicine experimental, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Molecular Phenotyping of Sepsis and Differential Response to Fluid Resuscitation.American journal of respiratory and critical care medicine · 2025
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  7. Moving from Critical Illness Syndromes toward Biologic Molecular Endotypes: Making Progress.American journal of respiratory and critical care medicine · 2025
    Article
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  11. Article
  12. Article
  13. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Lieuwe D J BosIntensive Care, Amsterdam UMC, Location AMC, 1105AZ, Amsterdam, The Netherlands. l.d.bos@amsterdamumc.nl.ORCID http://orcid.org/0000-0003-2911-4549
John G LaffeyAnaesthesia and Intensive Care Medicine, Galway University Hospitals, National University of Ireland Galway, Galway, Ireland.
Lorraine B WareDivision of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Nanon F L HeijnenDepartment of Intensive Care Medicine, Maastricht University Medical Center+, Maastricht, The Netherlands.
Pratik SinhaDepartment of Anesthesiology, School of Medicine, Washington University, St. Louis, USA.
Brijesh PatelDivision of Anaesthetics, Pain Medicine, and Intensive Care, Department of Surgery and Cancer, Imperial College, London, UK.
Matthieu JabaudonDepartment of Perioperative Medicine, CHU Clermont-Ferrand, Clermont-Ferrand, France.
Julie A BastaracheDivision of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Daniel F McAuleyWellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, Northern Ireland, UK.
Charlotte SummersDepartment of Medicine, School of Clinical Medicine, University of Cambridge, Cambridge, UK.
Carolyn S CalfeeDivision of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California, San Francisco, San Francisco, CA, USA.
Manu Shankar-HariSchool of Immunology and Microbial Sciences, King's College London, London, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

ARDSBiomarkerDefinitionDiagnosisPathophysiologyPhenotype

Identifiers

PMID35274164
PMCPMC8913033

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.