Endothelial dysfunction triggers acute respiratory distress syndrome in patients with sepsis: a narrative review

Acute respiratory distress syndrome (ARDS) is a severe organ failure occurring mainly in critically ill patients as a result of different types of insults such as sepsis, trauma or aspiration. Sepsis is the main cause of ARDS, and it contributes to a high mortality and resources consumption both in hospital setting and in the community. ARDS develops mainly an acute respiratory failure with severe and often refractory hypoxemia. ARDS also has long term implications and sequelae. Endothelial damage plays an important role in the pathogenesis of ARDS. Understanding the mechanisms of ARDS presents opportunities for novel diagnostic and therapeutic targets. Biochemical signals can be used in concert to identify and classify patients into ARDS phenotypes allowing earlier effective treatment with personalised therapies. This is a narrative review where we aimed to flesh out the pathogenetic mechanisms and heterogeneity of ARDS. We examine the links between endothelium damage and its contribution to organ failure. We have also investigated future strategies for treatment with a special emphasis in endothelial damage.

Automated summary

Acute respiratory distress syndrome (ARDS) is a severe organ failure mainly occurring in critically ill patients due to various insults such as sepsis, trauma, or aspiration. Sepsis is the leading cause of ARDS, resulting in high mortality and resource consumption. ARDS is characterized by acute respiratory failure with severe and often refractory hypoxemia. Endothelial damage plays a crucial role in the development of ARDS. Understanding the mechanisms of ARDS provides opportunities for novel diagnostic and therapeutic approaches. Biochemical signals can be utilized to identify and classify patients into ARDS phenotypes, enabling earlier personalized treatment.