SARS-CoV-2-Associated Guillain-Barre Syndrome is Common but Under- recognised and Under- reported.

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Post-SARS-CoV-2 vaccination venous sinus thrombosis: a literature review of 308 cases.

There is accumulating evidence that SARS-CoV-2 vaccinations can be complicated by venous sinus thrombosis (VST). This review aimed at summarising and discussing previous and recent advances regarding the diagnosis, pathogenesis, treatment, and outcome of post-SARS-CoV-2 vaccination VST. At least 308 patients with post-SARS-CoV-2 vaccination VST have been reported as per the end of July 2021. Ages among these 308 patients ranged between 22 and 81 years, 69 were male and 197 were female. Post-SARS-CoV-2 vaccination VST most commonly occurred with the ChAdOx1-S vaccine followed by the BNT126b2 vaccine. In the vast majority of cases, VST occurred after the first dose. Only in six patients did VST occur after the second dose. Latency between vaccination and onset of VST ranged between 0 and 24 days. Regarding treatment, most patients received heparin followed by oral anticoagulants. Seven patients received IVIGs and six patients received steroids because of concomitant vaccine-induced immune thrombotic thrombocytopenia. Complete recovery was reported in 5 patients. Partial recovery was reported in 9 patients. Eight patients were alive or discharged. Sixty-two patients died. The outcome was not specified in the remainder. In conclusion, SARS-CoV-2 vaccinations can be complicated by VST. There is female preponderance and the outcome is frequently poor.

Sinus venous thrombosis as a complication of COVID-19-associated hypercoagulability.

Sinus venous thrombosis (SVT) is an increasingly recognised complication of not only SARS-CoV-2 infections, but also of SARS-CoV-2 vaccinations. SVT is attributed to hypercoagulability, a common complication of COVID-19, disregarding the severity of the infection. Hypercoagulability in COVID-19 is explained by direct activation of platelets, enhancing coagulation, by direct infection and indirect activation of endothelial cells by SARS-CoV-2, shifting endothelial cells from an anti-thrombotic to a pro-thrombotic state, by direct activation of complement pathways, promoting thrombin generation, or by immune thrombocytopenia, which also generates a thrombogenic state. Since SVT may occur even in anticoagulated COVID-19 patients and may have an unfavourable outcome, all efforts must be made to prevent this complication or to treat it accurately.