Abstract
Acute respiratory distress syndrome (ARDS) remains a serious illness with significant morbidity and mortality, characterized by hypoxemic respiratory failure most commonly due to pneumonia, sepsis, and aspiration. Early and accurate diagnosis of ARDS depends upon clinical suspicion and chest imaging. Coronavirus disease 2019 (COVID-19) is an important novel cause of ARDS with a distinct time course, imaging and laboratory features from the time of SARS-CoV-2 infection to hypoxemic respiratory failure, which may allow diagnosis and management prior to or at earlier stages of ARDS. Treatment of ARDS remains largely supportive, and consists of incremental respiratory support (high flow nasal oxygen, non-invasive respiratory support, and invasive mechanical ventilation), and avoidance of iatrogenic complications, all of which improve clinical outcomes. COVID-19-associated ARDS is largely similar to other causes of ARDS with respect to pathology and respiratory physiology, and as such, COVID-19 patients with hypoxemic respiratory failure should typically be managed as other patients with ARDS. Non-invasive respiratory support may be beneficial in avoiding intubation in COVID-19 respiratory failure including mild ARDS, especially under conditions of resource constraints or to avoid overwhelming critical care resources. Compared to other causes of ARDS, medical therapies may improve outcomes in COVID-19-associated ARDS, such as dexamethasone and remdesivir. Future improved clinical outcomes in ARDS of all causes depends upon individual patient physiological and biological endotyping in order to improve accuracy and timeliness of diagnosis as well as optimal targeting of future therapies in the right patient at the right time in their disease.
Highlights
Acute respiratory distress syndrome (ARDS) is a serious clinical illness, defined by severe hypoxemic respiratory failure, which continues to be associated with significant morbidity, mortality, and healthcare resource utilization
ARDS is characterized by the rapid development of severe lung inflammation causing damage to alveolar epithelial cells (AEC) and pulmonary microvascular endothelial cells (EC)
Dysfunction of the alveolar-capillary endothelial barrier results in diffuse alveolar damage (DAD), which includes an initial exudative phase characterized by high-permeability, proteinaceous pulmonary interstitial and alveolar edema associated with the injury and death of EC as well as AEC desquamation, and a delayed fibroproliferative phase comprising fibrosis in intraluminal and interstitial compartments, and type II AEC proliferation (Table 1) [13,14]
Summary
Acute respiratory distress syndrome (ARDS) is a serious clinical illness, defined by severe hypoxemic respiratory failure, which continues to be associated with significant morbidity, mortality, and healthcare resource utilization. ARDS has been intensively investigated for more than 50 years, resulting in our current understanding of a clinical-physiologic syndrome of lung inflammation and injury, biologically driven by a plethora of inflammatory cells and soluble molecules (i.e., cytokines). Many patients continue to suffer more severe, prolonged ARDS and worse clinical outcomes including higher mortality. Novel causes of ARDS, like coronavirus disease 2019 (COVID-19) are contributing to significant human disease and will undoubtedly continue to do so in the future. We will highlight unique aspects of COVID-19 as an important, novel cause of ARDS
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