Translational research in ARDS patients: new biological phenotypes

The acute respiratory distress syndrome (ARDS) represents a critical pulmonary disease entity which is pathophysiologically characterized by pulmonary endothelial injury and alveolar epithelial barrier disruption. In clinical practice intensive care givers use the Berlin definition of ARDS, established in 2012 in order to classify patients into three categories of severity on the basis of the PaO2/FiO2 ratio and other ventilatory parameters [1]. Depending on the degree of disease severity (from “mild” to “severe”) several supportive therapeutic interventions are considered, ranging from protective ventilation to extracorporeal membrane oxygenation (ECMO) [2]. Currently, the Berlin definition does not directly register the underlying pathophysiological mechanisms in ARDS like endothelial barrier dysfunction or altered endothelial cell behavior in the course of the disease [1, 3]. Regarding the development of pathophysiologically driven therapy options an integration of biomarkers for ARDS (like circulating endothelial cells, CECs) into the current clinical classification systems might be necessary.