[10],
A dysfunctional procoagulant state with ultimate activation of the coagulation cascade, an acceleration of the already established vasculopathy, and vascular thrombosis are keys in the cases mentioned above, explicitly numbers 1 and 2. Those patients developed strokes secondary to a large vessel disease with complete occlusion of the corresponding internal carotid artery.
About the SARS-COV-2 induced coagulopathy, the inflammatory process has been associated with an increased level of D-Dimer and fibrin degradation products. These two parameters’ value was higher in severe CVOID-19 cases than their milder counterparts [17]. This has subsequently led to the prolongation of P.T. and APTT and a DIC picture with increased mortality [1]. The incidence of thrombotic complications in patients with severe SARS-COV-2 infection, especially those who required critical care admission, was high, which indicates the underlying coagulation derangement correlated with the viral burden and severity. [7,13] Panigada et al. described thrombo-elastography findings in a patient with COVID-19 admitted to the intensive care unit revealed a dramatic increase in D Dimer, fibrinogen, and von Willebrand factor. Factor VIII was decreased along with antithrombin [12]