Abstract
COVID-19 infection causes substantial changes in blood coagulation. Understanding this process helps management of the patient with least injury through therapeutic misadventurism. At the heart of the disease process, there is widespread endothelial and pulmonary alveolar epithelial cell damage related to the entry and proliferation of the virus and subsequent cellular response to virus invasion. The virus directly triggers fibrinolytic system which positively increase cellular viral load, cytokine generation, exudation in the alveoli, and both intravascular and extravascular blood coagulation and fibrinolysis. The major coagulation catastrophe comes from immunocoagulation and contribution by specific and non-specific cells (lymphocytes, monocytes, and neutrophils) augmenting the process. Hypoxia also contributes and plays an independent role. Platelet activation, complement activation, and vasculitis or vasculitis-mimics take part in the process. Some of these mechanisms are well established and some are yet to be worked out. COVID-19 infection unequivocally points out the great role of cellular activation and cytokines play in coagulation process; indicates classical anticoagulants, antiplatelets, statins, complement inhibitors, and steroids in managing this infection. The author concentrates on the pathobiology of blood coagulation with perspectives on how to manage each of these steps.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
