Acute Respiratory Distress Syndrome

Acute Respiratory Distress Syndrome (ARDS) 

● Symptoms and Causes  

Figure 4: Systemic versus alveolar inflammation in the development of acute respiratory distress syndrome

Systemic and alveolar inflammation are not necessarily correlated in patients with acute respiratory distress syndrome (ARDS). The panels show differences between systemic hypoinflammatory (A, C) and hyperinflammatory (B, D) inflammation, and the differences between alveolar hypoinflammatory (A, B) and hyperinflammatory (C, D) inflammation. Although these panels illustrate the extreme situations of systemic without alveolar inflammation and alveolar without systemic inflammation, the severity of systemic and alveolar inflammation exists on a spectrum that probably varies considerably from patient to patient, contributing to heterogeneity. (A) The normal alveolus, without inflammation or injury. (B) The changes observed in the hyperinflammatory subphenotype, which is characterised by systemic inflammation, endothelial dysfunction, and coagulation. Without alveolar inflammation, the injury caused by inflammation is driven from the systemic compartment towards the alveolar compartment (yellow arrow), resulting in increased permeability and alveolar oedema. (C) The changes in patients with alveolar hyperinflammation without a systemic hyperinflammatory subphenotype. Alveolar epithelial cells, alveolar macrophages, and neutrophils have a central role in proinflammatory cytokine production. Epithelial cells and macrophages are essential in production of proinflammatory molecules. Neutrophils produce various injurious molecules that damage type 1 and type 2 pneumocytes resulting in increased levels of pneumocyte injury markers. Without systemic inflammation, the injury caused by inflammation in this scenario is driven from the alveolar towards the systemic compartment (yellow arrow), also resulting in increased permeability and alveolar oedema. (D) The combined presence of systemic and alveolar hyperinflammation. Under these circumstances, inflammation induces lung injury, increased permeability, and alveolar oedema.

DOI: 10.1016/S0140-6736(22)01485-4