TY - JOUR
T1 - Acute respiratory distress syndrome
T2 - causes, pathophysiology, and phenotypes
AU - Bos, Lieuwe D. J.
AU - Ware, Lorraine B.
N1 - Funding Information: LDB is supported by the Amsterdam UMC fellowship, Health Holland, and by the Dutch Lung Foundation (Longfonds) through the Dirkje Postma Award. We thank Diana Lim (Molecular Medicine Programme, University of Utah, Salt Lake City, Utah) for her assistance with illustrations. Publisher Copyright: © 2022 Elsevier Ltd
PY - 2022/10/1
Y1 - 2022/10/1
N2 - Acute respiratory distress syndrome (ARDS) is a common clinical syndrome of acute respiratory failure as a result of diffuse lung inflammation and oedema. ARDS can be precipitated by a variety of causes. The pathophysiology of ARDS is complex and involves the activation and dysregulation of multiple overlapping and interacting pathways of injury, inflammation, and coagulation, both in the lung and systemically. Mechanical ventilation can contribute to a cycle of lung injury and inflammation. Resolution of inflammation is a coordinated process that requires downregulation of proinflammatory pathways and upregulation of anti-inflammatory pathways. The heterogeneity of the clinical syndrome, along with its biology, physiology, and radiology, has increasingly been recognised and incorporated into identification of phenotypes. A precision-medicine approach that improves the identification of more homogeneous ARDS phenotypes should lead to an improved understanding of its pathophysiological mechanisms and how they differ from patient to patient.
AB - Acute respiratory distress syndrome (ARDS) is a common clinical syndrome of acute respiratory failure as a result of diffuse lung inflammation and oedema. ARDS can be precipitated by a variety of causes. The pathophysiology of ARDS is complex and involves the activation and dysregulation of multiple overlapping and interacting pathways of injury, inflammation, and coagulation, both in the lung and systemically. Mechanical ventilation can contribute to a cycle of lung injury and inflammation. Resolution of inflammation is a coordinated process that requires downregulation of proinflammatory pathways and upregulation of anti-inflammatory pathways. The heterogeneity of the clinical syndrome, along with its biology, physiology, and radiology, has increasingly been recognised and incorporated into identification of phenotypes. A precision-medicine approach that improves the identification of more homogeneous ARDS phenotypes should lead to an improved understanding of its pathophysiological mechanisms and how they differ from patient to patient.
UR - http://www.scopus.com/inward/record.url?scp=85138998896&partnerID=8YFLogxK
U2 - https://doi.org/10.1016/S0140-6736(22)01485-4
DO - https://doi.org/10.1016/S0140-6736(22)01485-4
M3 - Review article
C2 - 36070787
SN - 0140-6736
VL - 400
SP - 1145
EP - 1156
JO - Lancet
JF - Lancet
IS - 10358
ER -