Acute respiratory distress syndrome

Berlin Definition and Etiologies

ARDS meets the Berlin definition, stratified by Horowitz index; echocardiography assists exclusion of cardiogenic edema; direct (pneumonia, aspiration, trauma, burns) and indirect (sepsis, pancreatitis, polytrauma, transfusions) etiologies occur.

Pathophysiology and Ventilation

Diffuse alveolar damage shows exudative (hyaline membranes), proliferative, and fibrotic phases with reduced compliance; lung-protective ventilation (≈6 mL/kg) and minimizing driving pressure are central to reduce mortality.

Adjuncts, Prognosis, Phenotypes

Evidence for steroids, inhaled vasodilators, and ECMO is mixed; severe ARDS mortality reaches 40–50%; outcomes relate to driving pressure, SOFA, Charlson comorbidity, frailty; hyperinflammatory versus hypoinflammatory phenotypes may influence therapeutic response.

The continuing education session “Acute respiratory distress syndrome,” organized by Klinik Barmelweid and delivered by Priv.-Doz. Dr. med Daniel Hofmänner, covers definition, pathophysiology, diagnostics, therapy, and prognosis. It reviews the Berlin definition with Horovitz (PaO2/FiO2)–based stratification into mild, moderate, and severe ARDS, bilateral pulmonary infiltrates, and exclusion of cardiogenic edema, often supported by echocardiography. Direct and indirect etiologies are outlined, including pneumonia/aspiration, lung contusion, burns and trauma on the direct side, and sepsis, pancreatitis, polytrauma, transfusion-related and other immunologic phenomena on the indirect side. The pathobiology centers on diffuse alveolar damage with hyaline membranes, an exudative and proliferative phase characterized by surfactant loss, shunt hypoxemia and reduced compliance, and possible progression to a fibrotic phase. Therapeutic principles emphasize restrictive fluid management and lung-protective ventilation with low tidal volumes (around 6 mL/kg), careful PEEP management, and attention to driving pressure, while prolonged neuromuscular blockade is cautioned against. Inhaled pulmonary vasodilators can transiently improve oxygenation without proven outcome benefit, systemic corticosteroids remain controversial outside COVID-19 due to superinfection risk, and extracorporeal support is reserved for the most severe cases with careful selection given complications and variable evidence. Prognostication addresses high mortality in severe ARDS (approximately 40–50%) and associations with higher driving pressures, advanced age, comorbidity burden (e.g., Charlson Comorbidity Index), organ dysfunction (SOFA), and clinical frailty. The session also discusses emerging ARDS phenotyping (e.g., hyperinflammatory vs. hypoinflammatory profiles) and neutral overall results of statin therapy with potential signals in subgroups.