ARDS Phenotypes

The establishment of clear definitions of ARDS has led to significant advances in the standardization of populations in research studies; however, a number of studies have shown significant heterogeneity within the population of patients meeting consensus criteria for ARDS [13, 63]. Heterogeneity has been described on the basis of

Fig. 2.1 Acute respiratory distress syndrome phenotypes related to sepsis, cancer, trauma, and transfusion. HLA human leukocyte antigen, ICAM-1 intercellular adhesion molecule 1, NET neutrophil extracellular traps, SP-D surfactant protein D, TRALItransfusion-related acute lung injury, vWF von Willebrand factor, WBC white blood cell predisposing insult, such as sepsis, cancer, transfusion, and trauma, or by mechanism of injury, such as direct or indirect pulmonary injury [7]. One recent example corroborating the distinction in ARDS phenotypes relates to the presence or absence of diffuse alveolar damage (DAD) on postmortem analysis. Lorente et al. [31] showed that non-survivors of ARDS have different clinical characteristics depending on the underlying histology. Patients with ARDS and DAD at postmortem had a different clinical phenotype than patients with ARDS and other histologic findings without DAD. These findings support the concept that the presence of DAD defines a specific subphenotype within patients with the clinical diagnosis of ARDS. How to detect this or other phenotypes at bedside remains unclear. Figure 2.1 provides an overview of the most common ARDS phenotypes, including expected biomarker levels, likely risk factors, and association with specific injuries.