What are the pathophysiological phases of ARDS, and how do these manifest on imaging?
The first phase of ARDS is known as the acute or exudative phase. This begins 1 to 7 days after the initial insult and is characterized by interstitial and alveolar protein-rich (exudative) pulmonary edema with the accumulation of neutrophils, macrophages, and red blood cells. Endothelial and epithelial injury are present with denuding of the alveolar epithelium, reducing surfactant production and leading to areas of atelectasis. Prominent hyaline membranes are present.
The subacute or proliferative phase begins around 7 to 14 days after the insult. At this point, some edema has been reabsorbed and the body is now attempting to repair the alveolar-capillary unit via proliferating type II pneumocytes. The inflammatory response begins to decrease and one may begin to see infiltration of fibroblasts and collage deposition.
The chronic or fibrotic phase is seen after around day 14. The inflammatory cells present in the first two phases are no longer seen. Areas of fibrosis may be present, although not all cases of ARDS result in fulminant regions of pulmonary fibrosis.
As noted above, within the first few hours there may be no radiographic evidence of ARDS. During the acute phase, one will typically see a rapid appearance of widespread, usually symmetric, pulmonary airspace opacities which can mimic cardiogenic pulmonary edema. Uniform bilateral airspace opacity is more often seen with ARDS than with cardiogenic pulmonary edema and tends to fluctuate less from day to day on chest radiographs when due to ARDS. Air bronchograms may be seen in ARDS but are almost never seen in cardiogenic pulmonary edema. Furthermore, most patients with ARDS are intubated, so that absence of an endotracheal tube makes ARDS less likely.
During the subacute phase, the opacities begin to appear more coarse and sharply defined. In later stages, one can see varying degrees of fibrotic change ranging from none to multifocal areas of scarring. Interestingly, the scarring can occur in areas that were unaffected by the airspace process, namely the anterior or nondependent portions of lung. This is the result of ventilator-associated lung injury, related to oxygen toxicity and barotrauma, whereas the consolidated lung is more protected from this phenomenon.