Is acute respiratory distress syndrome a preventable disease?

Sixty years after its initial description, the epidemiology and pathophysiology of acute respiratory distress syndrome (ARDS) have evolved substantially. This narrative review examines whether ARDS is a preventable disease, evaluating the evidence for successful prevention of iatrogenic phenotypes and the challenges that remain for noniatrogenic causes.

We reviewed the published literature on ARDS prevention, including evidence from clinical trials, population-based epidemiologic studies, implementation research, and biological subphenotyping studies, synthesized through the framework of the multiple hit hypothesis.

For iatrogenic phenotypes, ARDS prevention has substantially succeeded. Transfusion-related acute lung injury has declined dramatically following male-predominant plasma policies. Lung-protective ventilation initiated in emergency departments and operating rooms has reduced both ARDS incidence and mortality. Bundled care approaches combining restrictive fluid and transfusion strategies, aspiration precautions, and early antimicrobials have further reduced iatrogenic lung injury. What remains under the ARDS label is an increasingly heterogeneous collection of conditions driven by upstream host–pathogen interactions and biological phenotype. Pharmacologic prevention trials in unselected populations have been consistently disappointing, likely because biologically distinct subphenotypes respond differently to treatment. Additionally, the population-attributable fraction of death from ARDS is modest, suggesting that even successful prevention may not translate into proportional mortality reduction.

Extending prevention beyond iatrogenic causes will require precision approaches: phenotype-targeted pharmacotherapy, individualized mechanical ventilation, and systematic implementation of evidence-based practices across the care continuum.