Abstract
Dr Nath's timely editorial1 lists the neurologic complications of coronavirus infections. On behalf of coauthors, I highlight 5 patients with large artery stroke in the 2003 severe acute respiratory syndrome (SARS) outbreak in Singapore, arising from SARS-CoV-1 virus infection.2 Of 206 patients, 48 required intensive care and 32 died. Four of the 5 patients with stroke were critically ill and 3 died. The strokes were deemed thromboembolic. At autopsy, 1 patient had occipital lobe infarction, sterile vegetations in multiple valves, deep venous thrombosis, and pulmonary embolism; this prompted low-molecular-weight heparin (LMWH) use in subsequent critically ill patients with SARS. Nevertheless, a significant number of patients suffered venous thromboembolism, despite adequate treatment with LMWH.3 Three patients received intravenous immunoglobulin (IVIg) empirically, which might have contributed to stroke. The induction of hfgl2 prothrombinase gene by SARS-CoV-1 in experiments raised the possibility of a direct prothrombotic effect of that coronavirus.4 Only 8 patients underwent autopsy; therefore, more strokes may have gone undiagnosed. It is easy to miss stroke in critically ill patients who are heavily sedated and paralyzed. With increasing anecdotal reports ([journals.lww.com/neurotodayonline][1]), and the use of IVIg in desperately ill patients with COVID-19,5 we reiterate vigilance against strokes and thrombotic complications in critically ill coronavirus infected patients. [1]: https://journals.lww.com/neurotodayonline
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