Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2020 Nov 1:260:118431.
doi: 10.1016/j.lfs.2020.118431. Epub 2020 Sep 15.

SARS-CoV-2 and coagulation disorders in different organs

Affiliations
Review

SARS-CoV-2 and coagulation disorders in different organs

Sathishkumar Vinayagam et al. Life Sci. .

Abstract

Coronavirus disease 2019 (COVID-19) is a prominent pandemic disease that emerged in China and hurriedly stretched worldwide. There are many reports on COVID-19 associated with the amplified incidence of thrombotic events. In this review, we focused on COVID-19 coupled with the coagulopathy contributes to severe outcome inclusive of comorbidities such as venous thromboembolism, stroke, diabetes, lung, heart attack, AKI, and liver injury. Initially, the COVID-19 patient associated coagulation disorders show an elevated level of the D-dimer, fibrinogen, and less lymphocyte count such as lymphopenia. COVID-19 associated with the Kawasaki disease has acute vasculitis in childhood which further affects the vessels found all over the body. COVID-19 linked with the thrombotic microangiopathy triggers the multiple vasculitis along with the arterioles thrombosis, medium, large venous and arterial vessels mediates the disseminated intravascular coagulation (DIC). SARS-Co-V-2 patients have reduced primary platelet production, increased destruction of the platelet, decreased circulating platelet leads to the condition of increased thrombocytopenia which contributes to the coagulation disorder. Endothelial dysfunction plays an important role in the coagulation disorders via increased generation of the thrombin and stops fibrinolysis further leads to hypercoagulopathy. Along with that endothelial dysfunction activates the complement system pathways and contributes to the acute and chronic inflammation via cytokine storm with the production of the cytokines and chemokines, coagulation in different organs such as lung, brain, liver, heart, kidney and further leads to multi-organ failure.

Keywords: COVID-19; Coagulation; Complement system; Disseminated intravascular coagulation; Hypercoagulability; Inflammation; SARS-CoV-2; Thromboembolism.

PubMed Disclaimer

Conflict of interest statement

The authors declare that there is no conflict of interest.

Figures

Unlabelled Image
Graphical abstract
Fig. 1
Fig. 1
A pictorial representation of COVID-19 patients associated with thrombocytopenia with its mechanism. It is through 3 main mechanisms such as via reducing the platelet, augmenting the platelet reduction, and attenuates the circulating platelets and how it leads to the condition of thrombocytopenia upon SARS-CoV-2 infection.
Fig. 2
Fig. 2
Schematic representation of the activation of the complement system by SARS-CoV-2 leads to the blood clot in different organs. SARS-CoV-2 binds with the receptor ACE-2 and mediates tissue injury via AT1R. On the other hand, SARS-CoV2 binds with the receptor ACE-2 and activates the complement system such as lectin and classical. The end substance of the classical is C3a and C3b. C3a, which is involved in the inflammation and activation of the platelet. The C3b is involved in the formation of the C5a and C5b. This C5a activates the platelet and mediates inflammation. This C5b forms the membrane attack complex (MAC), this MAC activates the microvascular complement deposition, coagulation, and inflammation. The coagulation is activated by the thrombomodulin. On the other hand, C5R mediates the platelet activation, aggregations, and discharge of the procoagulant microparticles (PMP), and formation of the blood clots. This further causes the blood clot in the different organs.
Fig. 3
Fig. 3
Schematic representation of the blood clot in different organs and their outcome. A blood clot in the lungs is due to the condition of occlusion and formation of the micro thrombosis, acute pulmonary embolism, alveolar damage, mild pleurisy, inflammation, increased level of the LDL, D-dimer, and C-reactive protein and thrombocytopenia; a Blood clot in the kidney leads to the condition of the acute kidney injury through the activation of the complement, cytokine storm, hypercoagulability, microangiopathy, a clot in the catheter tube; a blood clot in pregnancy has hyperfibrinogenemia, thrombosis, and coagulopathy with elevated D-dimer level. Brain clot in the brain is due to the elevated D-dimer level, LVOs, anosmia, loss of smell, increased LDH, APL, and ferritin; bowel abnormalities due to the ischemia with the patchy necrosis; a blood clot in the skin and toe due to the hypercoagulopathy, skin lesions leads to the condition of the COVID19 toes; a blood clot in liver and heart leads to a heart attack.

References

    1. Lu R., Zhao X., Li J., Niu P., Yang B., Wu H., Wang W., Song H., Huang B., Zhu N. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet. 2020;395:565–574. - PMC - PubMed
    1. Cascella M., Rajnik M., Cuomo A., Dulebohn S.C., Di Napoli R. StatPearls Publishing; 2020. Features, Evaluation and Treatment Coronavirus (COVID-19), StatPearls [Internet] - PubMed
    1. WHO report . 2020. Coronavirus Disease (COVID-19) Pandemic.
    1. Giovanetti M., Benvenuto D., Angeletti S., Ciccozzi M. The first two cases of 2019-nCoV in Italy: where they come from? J. Med. Virol. 2020;92(5):518–521. doi: 10.1002/jmv.25699. - DOI - PMC - PubMed
    1. Paraskevis D., Kostaki E.G., Magiorkinis G., Panayiotakopoulos G., Sourvinos G., Tsiodras S. Full-genome evolutionary analysis of the novel corona virus (2019-nCoV) rejects the hypothesis of emergence as a result of a recent recombination event. Infect. Genet. Evol. 2020;79:104212. - PMC - PubMed

MeSH terms