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🫁 Corticosteroids in ARDS: perhaps the question is no longer “yes or no” For decades, corticosteroids in ARDS have moved between enthusiasm and rejection. This new narrative review by Daoud, Villar and Annane in Intensive Care Medicine argues that the debate itself may need to change. ARDS is not a single biological disease, and corticosteroids are unlikely to have a uniform treatment effect. The physiological rationale is compelling. Glucocorticoid receptor activation influences both genomic and non-genomic pathways, suppressing NF-κB and MAPK signalling while promoting anti-inflammatory mediators. In ARDS, this intersects directly with endothelial injury, cytokine activation and fibroproliferation. But critically, these processes change with time. And timing may be one of the keys. Early dexamethasone in moderate-to-severe ARDS has shown benefit, while initiation of methylprednisolone more than 14 days after ARDS onset may be harmful. The review therefore proposes considering corticosteroids predominantly during the early inflammatory phase, generally within the first 7 days, rather than treating “ARDS” irrespective of disease stage. But perhaps the most interesting message is etiology. The evidence is strongest in COVID-19 ARDS and severe community-acquired pneumonia. In septic shock associated with ARDS, hydrocortisone is supported primarily by the septic shock evidence. Conversely, routine corticosteroids cannot currently be recommended for influenza-associated ARDS, while evidence for aspiration, trauma, pancreatitis, TRALI and other non-septic forms remains weak and largely extrapolated from heterogeneous ARDS populations. Then comes an even more interesting layer: inflammatory phenotype. Approximately 30% of ARDS patients may exhibit a hyperinflammatory phenotype characterized by higher IL-6, IL-8, sTNFR-1, PAI-1 and angiopoietin-2 concentrations, greater vasopressor requirements, metabolic acidosis and worse outcomes. Secondary analyses suggest these patients may derive greater benefit from corticosteroids than hypoinflammatory patients. But we are not ready to use this clinically. No biomarker or phenotype classifier has yet been prospectively validated to select corticosteroid therapy, and patients may transition between inflammatory phenotypes during their ICU course. Phenotype-guided corticosteroids therefore remain hypothesis-generating, not standard care. Reference 📚 Daoud T, 2026. Corticosteroids in ARDS: old controversies, new insights, and future directions. Intensive Care Medicine. doi.org/10.1007/s00134-026-0…