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Respiratory Distress Syndrome

Respiratory Medicine · NLM MeSH · updated 2026-11-04 · version 1

Citations verified against PubMedNot yet clinician-reviewed9 referencesApproximately 4 min read

A syndrome characterized by progressive life-threatening respiratory insufficiency in the absence of known lung diseases, usually following a systemic insult such as surgery or major trauma.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 3 complete abstracts (681 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

A syndrome characterized by progressive life-threatening respiratory insufficiency in the absence of known lung diseases, usually following a systemic insult such as surgery or major trauma.

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Distress Syndrome, Respiratory; Distress Syndromes, Respiratory; Respiratory Distress Syndromes; Syndrome, Respiratory Distress; Shock Lung; Lung, Shock; Respiratory Distress Syndrome, Adult; Adult Respiratory Distress Syndrome.

Where it fits in the MeSH classification

Broader topics
Lung Diseases; Respiration Disorders
Narrower topics
Respiratory Distress Syndrome, Newborn
See also
Acute Chest Syndrome

Related concepts

  • Respiratory Insufficiency
  • Lung Diseases
  • Trauma

Research landscape

PubMed indexes 44,003 records tagged with the MeSH heading “Respiratory Distress Syndrome” (counts retrieved 2026-11-04). 9,980 of them (22.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 16,094 records.

Reviews account for 7,369 records (16.7%) and meta-analyses for 734. Randomized controlled trials number 1,910 (4.3%) as a share of all records on the topic.

PubMed records by publication periodthrough 1999: 16,094 records; 2000-2009: 8,403 records; 2010-2019: 9,526 records; 2020 onward: 9,980 records16,094through 19998,4032000-20099,5262010-20199,9802020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 199916,094
2000-20098,403
2010-20199,526
2020 onward9,980
Share of records by publication typeReviews: 16.7 percent; Meta-analyses: 1.7 percent; Randomized controlled trials: 4.3 percentReviews16.7% (7,369)Meta-analyses1.7% (734)Randomized controlled trials4.3% (1,910)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 44,003 PubMed records
TypeRecordsShare
Reviews7,36916.7%
Meta-analyses7341.7%
Randomized controlled trials1,9104.3%

Method: PubMed query "Respiratory Distress Syndrome"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.

Reading the evidence in respiratory medicine

Research on airway and lung disease mixes lung-function tests, symptom diaries, imaging and hospital records, so what was measured and in whom matters as much as the result. Many conditions here, such as asthma and COPD, vary between people and over time, and exposure studies (smoking, pollution, workplace dust) show association rather than proof of cause. Nothing on this page is advice about treatment or inhalers; anyone with breathing difficulty should seek care from a qualified clinician. Check how the condition was defined, the severity of the people studied and whether outcomes were symptoms, lung function or hospital admissions.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Lung-protective ventilation strategy in acute respiratory distress syndrome: a critical reappraisal of current practice
Park KJ
2025Review article
Design not recorded in structured metadata
13cc by
PMID 41121191 · DOI · PMC12538788
Longitudinal multiomic signatures of ARDS and sepsis inflammatory phenotypes identify pathways associated with mortality
Alipanah-Lechner N, Neyton L, Sinha P, Leroux C, Bardillon K, Carrillo SA, et al.
2026Randomized controlled trial
Design not recorded in structured metadata
12cc by
PMID 41329523 · DOI · PMC12867137
Ferroptosis in sepsis induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS): a potential therapeutic strategy
Wang L, Zhang W, Feng X
2025Review article
Design not recorded in structured metadata
11cc by
PMID 41383584 · DOI · PMC12689393

Lung-protective ventilation strategy in acute respiratory distress syndrome: a critical reappraisal of current practice [1]

Review article Park KJ · · 2025 · cited 13 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Recognition of ventilator-induced lung injury has led to the development of lung-protective ventilation strategies, significantly influencing the management of acute respiratory distress syndrome (ARDS).
Closing excerpt
Further studies are needed to establish an individualized, patient-centred approach that allows more flexible and moderate settings.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (255 words)

Recognition of ventilator-induced lung injury has led to the development of lung-protective ventilation strategies, significantly influencing the management of acute respiratory distress syndrome (ARDS). By the end of the 20th century, five randomized controlled trials had compared the survival benefits of low tidal volume (VT) ventilation with those of traditional high VT ventilation. Two studies demonstrated favourable outcomes, most notably the landmark ARDS Network trial, which established the widely recommended VT of 6 mL/kg predicted body weight. However, the universal application of a fixed VT has been controversial, with poor adherence in clinical practice. The two trials used a greater contrast in VTs (6 vs. 12 mL/kg) than did the others (7-11 mL/kg) and incorporated methodological extremes, including toleration of elevated airway pressures or encouragement of unnecessary increases. In addition, disparities in underlying aetiologies and ventilatory parameters, such as unbalanced positive end-expiratory pressure and respiratory rates, may have influenced the results. There is no conclusive evidence to support the superiority of 6 mL/kg over intermediate VTs (7-10 mL/kg). Many subsequent studies have suggested that VT requirements should be individualized on the basis of lung mechanics and physiological status. The benefits of the current recommendations may be limited by factors such as the severity of hypoxemia, lung compliance, dead-space fraction, and inaccuracies in formula-based lung volume estimation. The goal of mechanical ventilation in ARDS patients is supportive rather than curative; therefore, a moderate approach is recommended in clinical practice. Further studies are needed to establish an individualized, patient-centred approach that allows more flexible and moderate settings.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41121191 · DOI · PMC12538788

Longitudinal multiomic signatures of ARDS and sepsis inflammatory phenotypes identify pathways associated with mortality [2]

Randomized controlled trial Alipanah-Lechner N, Neyton L, Sinha P, Leroux C, Bardillon K, Carrillo SA, et al. · · 2026 · cited 12 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
BACKGROUNDCritically ill patients with acute respiratory distress syndrome (ARDS) and sepsis exhibit distinct inflammatory phenotypes with divergent clinical outcomes, but the underlying molecular mechanisms remain poorly understood.
Closing excerpt
FUNDINGNIH National Heart, Lung, and Blood Institute and National Institute of General Medical Sciences.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (255 words)

BACKGROUNDCritically ill patients with acute respiratory distress syndrome (ARDS) and sepsis exhibit distinct inflammatory phenotypes with divergent clinical outcomes, but the underlying molecular mechanisms remain poorly understood. These phenotypes, derived from clinical data and protein biomarkers, were associated with metabolic differences in a pilot study.METHODSWe performed integrative multiomics analysis of blood samples from 160 patients with ARDS in the ROSE trial, randomly selecting 80 patients from each latent class analysis-defined inflammatory phenotype (hyperinflammatory and hypoinflammatory) with phenotype probability greater than 0.9. Untargeted plasma metabolomics and whole-blood transcriptomics at day 0 and day 2 were analyzed using multimodal factor analysis (MEFISTO). The primary outcome was 90-day mortality, with validation in an independent critically ill sepsis cohort (EARLI).RESULTSMultiomics integration revealed 4 molecular signatures associated with mortality: (a) enhanced innate immune activation coupled with increased glycolysis (associated with hyperinflammatory phenotype), (b) hepatic dysfunction and immune dysfunction paired with impaired fatty acid β-oxidation (associated with hyperinflammatory phenotype), (c) interferon program suppression coupled with altered mitochondrial respiration (associated with hyperinflammatory phenotype), and (d) redox impairment and cell proliferation pathways (not associated with inflammatory phenotype). These signatures persisted through day 2 of trial enrollment. Within-phenotype analysis revealed distinct mortality-associated pathways in each group. All molecular signatures were validated in the independent EARLI cohort.CONCLUSIONInflammatory phenotypes of ARDS reflect distinct underlying biological processes with both phenotype-specific and phenotype-independent pathways influencing patient outcomes, all characterized by mitochondrial dysfunction. These findings suggest potential therapeutic targets for precise treatment strategies in critical illness.FUNDINGNIH National Heart, Lung, and Blood Institute and National Institute of General Medical Sciences.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41329523 · DOI · PMC12867137

Ferroptosis in sepsis induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS): a potential therapeutic strategy [3]

Review article Wang L, Zhang W, Feng X · · 2025 · cited 11 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Sepsis induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS) remains a devastating complication of sepsis, marked by uncontrolled pulmonary inflammation, alveolar-capillary barrier disruption, and high mortality.
Closing excerpt
This review also discusses major challenges to clinical translation and highlights further directions for the treatment and prevention of sepsis induced ALI/ARDS.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (171 words)

Sepsis induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS) remains a devastating complication of sepsis, marked by uncontrolled pulmonary inflammation, alveolar-capillary barrier disruption, and high mortality. Despite advances in supportive care, no targeted medicines are currently available. Ferroptosis is an iron-dependent and non-apoptotic form of cell death characterized by the iron induced accumulation of lipid reactive oxygen species (ROS). Emerging evidence indicates that ferroptosis is involved in the progression of sepsis induced ALI/ARDS, although the mechanism of action of ferroptosis in sepsis induced ALI/ARDS is still poorly understood. This mini-review summarizes the mechanism of ferroptosis action on sepsis induced ALI/ARDS, with particular focus on immune dysregulation, endothelial/epithelial dysfunction, and oxidative stress. We highlight key molecular pathways, including glutathione peroxidase 4 (GPX4) inactivation, iron metabolism disruption, and lipid peroxidation cascades, supported by both preclinical studies and emerging clinical correlates. Furthermore, discuss the potential therapeutic approaches currently used to treat ARDS. This review also discusses major challenges to clinical translation and highlights further directions for the treatment and prevention of sepsis induced ALI/ARDS.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41383584 · DOI · PMC12689393

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth [4]
    Roberts D, Brown J, Medley N, Dalziel SR · Cochrane Database Syst Rev · 2017 · cited 552 times (Europe PMC)
  • Research article Prone Position for Acute Respiratory Distress Syndrome. A Systematic Review and Meta-Analysis [5]
    Munshi L, Del Sorbo L, Adhikari NKJ, Hodgson CL, Wunsch H, Meade MO, et al. · Ann Am Thorac Soc · 2017 · cited 388 times (Europe PMC)
  • Research article Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth [6]
    McGoldrick E, Stewart F, Parker R, Dalziel SR · Cochrane Database Syst Rev · 2020 · cited 357 times (Europe PMC)
  • Research article Conservative fluid management or deresuscitation for patients with sepsis or acute respiratory distress syndrome following the resuscitation phase of critical illness: a systematic review and meta-analysis [7]
    Silversides JA, Major E, Ferguson AJ, Mann EE, McAuley DF, Marshall JC, et al. · Intensive Care Med · 2017 · cited 282 times (Europe PMC)
  • Research article Venovenous extracorporeal membrane oxygenation for acute respiratory distress syndrome: a systematic review and meta-analysis [8]
    Munshi L, Walkey A, Goligher E, Pham T, Uleryk EM, Fan E · Lancet Respir Med · 2019 · cited 272 times (Europe PMC)
  • Research article ECMO for severe ARDS: systematic review and individual patient data meta-analysis [9]
    Combes A, Peek GJ, Hajage D, Hardy P, Abrams D, Schmidt M, et al. · Intensive Care Med · 2020 · cited 269 times (Europe PMC)

References

  1. Park KJ. Lung-protective ventilation strategy in acute respiratory distress syndrome: a critical reappraisal of current practice. . 2025. PMID 41121191 · DOI · PMC12538788
  2. Alipanah-Lechner N, Neyton L, Sinha P, Leroux C, Bardillon K, Carrillo SA, et al.. Longitudinal multiomic signatures of ARDS and sepsis inflammatory phenotypes identify pathways associated with mortality. . 2026. PMID 41329523 · DOI · PMC12867137
  3. Wang L, Zhang W, Feng X. Ferroptosis in sepsis induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS): a potential therapeutic strategy. . 2025. PMID 41383584 · DOI · PMC12689393
  4. Roberts D, Brown J, Medley N, Dalziel SR. Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev. 2017. PMID 28321847 · DOI · PMC6464568
  5. Munshi L, Del Sorbo L, Adhikari NKJ, Hodgson CL, Wunsch H, Meade MO, et al.. Prone Position for Acute Respiratory Distress Syndrome. A Systematic Review and Meta-Analysis. Ann Am Thorac Soc. 2017. PMID 29068269 · DOI
  6. McGoldrick E, Stewart F, Parker R, Dalziel SR. Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev. 2020. PMID 33368142 · DOI · PMC8094626
  7. Silversides JA, Major E, Ferguson AJ, Mann EE, McAuley DF, Marshall JC, et al.. Conservative fluid management or deresuscitation for patients with sepsis or acute respiratory distress syndrome following the resuscitation phase of critical illness: a systematic review and meta-analysis. Intensive Care Med. 2017. PMID 27734109 · DOI
  8. Munshi L, Walkey A, Goligher E, Pham T, Uleryk EM, Fan E. Venovenous extracorporeal membrane oxygenation for acute respiratory distress syndrome: a systematic review and meta-analysis. Lancet Respir Med. 2019. PMID 30642776 · DOI
  9. Combes A, Peek GJ, Hajage D, Hardy P, Abrams D, Schmidt M, et al.. ECMO for severe ARDS: systematic review and individual patient data meta-analysis. Intensive Care Med. 2020. PMID 33021684 · DOI · PMC7537368

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-11-04.

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At a glance

44,003
PubMed records on this heading
23%
published since 2020
7,369
review articles
1,910
randomized trials
9
verified references below

Counts come from PubMed on 2026-11-04; they show how much has been written, not how strong the evidence is.

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