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Review
. 2020 Jul;50(1):54-67.
doi: 10.1007/s11239-020-02134-3.

COVID-19 update: Covid-19-associated coagulopathy

Richard C Becker  1
Affiliations
Review

COVID-19 update: Covid-19-associated coagulopathy

Richard C Becker. J Thromb Thrombolysis. 2020 Jul.
No abstract available

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Shows a damaged alveolus with enlarged nuclei and cytologic atypia (a) with abundant DNA (red) and RNA (green) within tissue sections and virally infected cells with an abundance of extracellular DNA and RNA in the cytoplasm (b) co-localized with fibrin and extracellular nucleic acids (c). d is a control lung specimen. Panels e and f show focal degeneration of cardiomyocytes. A pathology hallmark of Covid-19 infection is diffuse small vessel (venule, arteriole and capillary) platelet–fibrin thrombosis and intravascular megakaryocytes in all major organs, including the heart, lungs, kidneys, liver and mesenteric fat. From [9] with permission
Fig. 2
Fig. 2
The mechanism(s) underlying a prolonged thrombophilic state following Covid-19 infection are unknown, but may be related to diffuse vascular endothelial cell infection, injury and dysfunction. Viral particles and inclusion bodies are seen within endothelial cells of the glomerular capillary loops (a and b); in panel c, inflammatory cells are observed within capillaries serving the small intestine, while panel d demonstrates apoptotic endothelial cells and mononuclear cells. The available clinical and pathological evidence, coupled with strong and mature data that supports a relationship between CFRNA, polyphosphate and factor XI activation, raises a logical scientific premise that requires investigation. From [23] with permission
Fig. 3
Fig. 3
Neutrophil extracellular traps (NETs) consist of extracellular chromatin strands (nucleic acids, DNA) wrapped around histones (nucleosomes) and inter-woven with fibrin strands. NETs are an ideal foundation or template for binding activated platelets, erythrocytes and leukocytes, activating factor XI and generating thrombin for fibrin production
Fig. 4
Fig. 4
D-dimer is a fibrin degradation product or small protein fragment present in the peripheral blood after fibrin is formed from fibrinogen (in the presence of thrombin) and subsequently degraded by plasminogen activators. Its name is derived from having D fragments of the fibrin protein joined by a covalently bound cross-link (factor XIII)
Fig. 5
Fig. 5
Virchow’s Triad represents a fundamental construct in which three components interact to establish an environment favoring or provoking thrombosis. They include abnormalities of the blood vessel wall or endothelial surface, altered blood flow and prothrombotic constituents within the circulating blood. In Covid-19-associated coagulopathy there is wide-scale endothelial cell inflammation and dysfunction, abnormal flow dynamics and activated platelets, high concentrations of von Willebrand Factor, cell free DNA, histones and viral RNA that collectively cause factor XI activation, thrombin generation and fibrin formation
See this image and copyright information in PMC

References

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