Acute Respiratory Distress Syndrome and Corticosteroids: Reconciling Conflicting Evidence

Acute respiratory distress syndrome (ARDS) is a life-threatening form of acute inflammatory lung injury in which loss of alveolar-capillary membrane integrity produces protein-rich pulmonary edema, refractory hypoxemia, and reduced lung compliance, typically within 6-72 hours of a precipitating insult. The 2012 Berlin criteria defined ARDS by acute onset within one week of a known insult, bilateral opacities not fully explained by effusion, atelectasis, or cardiac failure, and a PaO₂/FiO₂ ratio of 300 mmHg or less with a minimum PEEP of 5 cmH₂O. The 2023 global definition expands this framework by accepting SpO₂/FiO₂ of 315 or less when SpO₂ is 97% or below, including patients supported with high-flow nasal oxygen at 30 L/min or more, permitting thoracic ultrasonography as an alternative imaging modality, and waiving the PEEP requirement in resource-limited settings. These revisions are particularly relevant to practice in low- and middle-income countries, where arterial blood gas analysis and mechanical ventilation may be unavailable. Management remains anchored in lung-protective ventilation, conservative fluid strategy, and prone positioning. Glucocorticoids remain the most contested pharmacological intervention: evidence from dexamethasone trials in ARDS and in COVID-19 suggests benefit in selected populations, yet questions persist regarding optimal agent, dose, timing relative to symptom onset, duration, the influence of ARDS subphenotypes, and the risk of secondary infection and neuromuscular weakness. This narrative review summarizes the pathophysiology, evolving diagnostic criteria, imaging findings, and current evidence on corticosteroid therapy, and considers how hyperinflammatory and hypoinflammatory subphenotypes may guide future trial design and individualized treatment.