BACKGROUND AND PURPOSE: Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) infection is associated with hypercoagulability. We sought to evaluate the demographic and clinical characteristics of cerebral venous thrombosis among patients hospitalized for coronavirus disease 2019 (COVID-19) at 6 tertiary care centers in the New York City metropolitan area.
MATERIALS AND METHODS:We conducted a retrospective multicenter cohort study of 13,500 consecutive patients with COVID-19 who were hospitalized between March 1 and May 30, 2020. RESULTS: Of 13,500 patients with COVID-19, twelve had imaging-proved cerebral venous thrombosis with an incidence of 8.8 per 10,000 during 3 months, which is considerably higher than the reported incidence of cerebral venous thrombosis in the general population of 5 per million annually. There was a male preponderance (8 men, 4 women) and an average age of 49 years (95% CI, 36-62 years; range, 17-95 years). Only 1 patient (8%) had a history of thromboembolic disease. Neurologic symptoms secondary to cerebral venous thrombosis occurred within 24 hours of the onset of the respiratory and constitutional symptoms in 58% of cases, and 75% had venous infarction, hemorrhage, or both on brain imaging. Management consisted of anticoagulation, endovascular thrombectomy, and surgical hematoma evacuation. The mortality rate was 25%.
CONCLUSIONS:Early evidence suggests a higher-than-expected frequency of cerebral venous thrombosis among patients hospitalized for COVID-19. Cerebral venous thrombosis should be included in the differential diagnosis of neurologic syndromes associated with SARS-CoV-2 infection. ABBREVIATIONS: COVID-19 ¼ coronavirus disease 2019; CVST ¼ cerebral venous sinus thrombosis; CVT ¼ cerebral venous thrombosis; SARS-CoV-2 ¼ Severe Acute Respiratory Syndrome coronavirus 2 C oronavirus disease 2019 (COVID-19) is predominantly an acute respiratory disease caused by a single-stranded RNA virus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which originated in Wuhan, China. 1 The virus possesses a spike protein that binds to angiotensin-converting enzyme receptors, expressed on respiratory epithelium, facilitating entry into the host cell. [2][3][4] Susceptibility of organ systems to this virus may depend on the extent of expression of angiotensin-converting enzyme receptors on cell surfaces. These receptors are expressed on endothelial cells, pericytes, macrophages, glial cells, and cardiac myocytes. [2][3][4] Viral entry into these cells can lead to diverse manifestations such as acute respiratory distress syndrome, acute kidney injury, transaminitis, cardiac injury, and neurologic complications. [3][4][5][6] Neurologic symptoms include headache, confusion, hypogeusia, hyposmia, myalgias, and delirium, while neurologic complications include acute ischemic stroke, encephalitis, and Guillain-Barre syndrome. 3,[6][7][8] Postmortem data have revealed cerebral edema and partial neuronal degeneration in some patients as well. 9 Early evidence suggests an inc...