key: cord-0852459-h86kidhs
authors: Páramo, José A.
title: Pulmonary Embolism, Pulmonary Microvascular Thrombosis, or Both in COVID-19?
date: 2020-07-22
journal: Clin Appl Thromb Hemost
DOI: 10.1177/1076029620933953
sha: 4d3716906fb718d92579cdfb8a59306a1a0be462
doc_id: 852459
cord_uid: h86kidhs

nan

lar damage with focal fibrin clusters mixed with mononuclear inflammatory cells as the primary mechanism of respiratory distress associated with COVID-19 and, therefore, disseminated fibrin deposits occur in the pulmonary microcirculation as a consequence of the ongoing inflammatory stimuli leading to acute lung injury and respiratory damage. 5, 6 Indeed, it has been suggested the acronym MicroCLOTS (microvascular COVID-19 lung vessels obstructive thromboinflammatory syndrome) as the pathophysiological mechanism for the acute respiratory distress syndrome caused by this coronavirus. 7 In line with this pathophysiological approach, a recent study indicates direct viral infection of endothelial cells and diffuse endothelial inflammation in lungs in patients who developed progressive respiratory failure. 8 The fact that no systematic objective screening for VTE (CT pulmonary angiogram and/ or ultrasonography) has been applied in many circumstances and the low number of deep vein thrombosis associated with pulmonary embolism in COVID-19 patients suggest that they have intrapulmonary acute microvascular thrombosis rather than embolism. 1, 2, 9 We, therefore, propose to include the term primary pulmonary thrombi which develop directly in the lungs without traveling from DVT to refer to the most common thrombotic manifestations in patients with COVID-19 infection, which may have therapeutic implications.

José A. Páramo designed and wrote the manuscript. Our institution does not require ethical approval for reporting individual cases or case series.

José A. Páramo https://orcid.org/0000-0003-1497-6242

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