Acute respiratory distress syndrome (ARDS) can result from a variety of clinical conditions, causing lung injury either directly through local inflammation or indirectly because of systemic inflammatory mediators ARDS is associated with high morbidity and mortality.

Its pathophysiology is complex, involving the activation and dysregulation of multiple overlapping pathways related to injury, inflammation, and coagulation, both in the lung and systemically.

Sepsis is the most common cause of ARDS, with pulmonary sepsis (e.g., pneumonia) being the predominant etiology.

Non-pulmonary sepsis and non-infectious causes, such as pancreatitis, aspiration of gastric contents, and severe traumatic injuries accompanied by shock and multiple transfusions, also contribute significantly to ARDS cases.

Despite decades of experimental research into ARDS biology, these insights have rarely translated into effective therapies.

This lack of progress is often attributed to the substantial heterogeneity caused by the nonspecific clinical definition of ARDS.

Identifying subphenotypes of ARDS-more homogeneous groups within the broader ARDS population-has emerged as a promising approach to unravel the syndrome’s clinical and biological complexity, which many believe is a critical barrier to discovering effective treatments.

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