Author: Yeh, Calvin H.; de Wit, Kerstin; Levy, Jerrold H.; Weitz, Jeffrey I.; Vaezzadeh, Nima; Liaw, Patricia C.; Fox-Robichaud, Alison; Soliman, Karim; Kim, Paul Y.
Title: Hypercoagulability and coronavirus disease 2019–associated hypoxemic respiratory failure: Mechanisms and emerging management paradigms Cord-id: hii4smax Document date: 2020_9_3
ID: hii4smax
Snippet: The SARS-CoV-2 viral infection causes COVID-19 pneumonia. Acute lung injury in COVID-19 is likely a result of a syndrome of hyperinflammation-driven coagulopathy occurring through immunothrombosis. This COVID-19 associated coagulopathy (CAC) is potentially the source of macrovascular complications of arterial and venous thromboembolism. Microvascular thrombosis as a result of CAC may be a defining feature increasing multiple organ failure and worsening acute lung injury. CAC may therefore be an
Document: The SARS-CoV-2 viral infection causes COVID-19 pneumonia. Acute lung injury in COVID-19 is likely a result of a syndrome of hyperinflammation-driven coagulopathy occurring through immunothrombosis. This COVID-19 associated coagulopathy (CAC) is potentially the source of macrovascular complications of arterial and venous thromboembolism. Microvascular thrombosis as a result of CAC may be a defining feature increasing multiple organ failure and worsening acute lung injury. CAC may therefore be an emerging target for COVID-19 therapies. This current opinion report addresses the mechanisms by which CAC may develop, discusses how CAC may worsen lung injury, and treatment strategies under investigation. LEVEL OF EVIDENCE: Non-systematic review. Level IV/V.
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