[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]