Background
Coronavirus Disease 2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), most frequently presents with respiratory symptoms such as fever, dyspnea, shortness of breath, cough, or myalgias. There is now a growing body of evidence that demonstrates that severe SARS-CoV-2 infections can develop clinically significant coagulopathy, inflammation, and cardiomyopathy, which have been implicated in COVID-19 associated cerebrovascular accidents (CVAs).
Case Report
We report an uncommon presentation of a 32-year-old man who sustained a large vessel cerebellar stroke associated with a severe COVID-19 infection. He presented with a headache, worse than his usual migraine, dizziness, rotary nystagmus, and dysmetria on exam but had no respiratory symptoms initially. He was not a candidate for thrombolytic therapy or endovascular therapy and was managed with clopidogrel, aspirin, and atorvastatin. During hospital admission he developed COVID-19 related hypoxia and pneumonia, but ultimately he was discharged to home rehabilitation.
Why Should an Emergency Physician Be Aware of This?
We present this case to increase awareness among emergency physicians of the growing number of reports of neurological and vascular complications such as ischemic CVAs in otherwise healthy individuals who are diagnosed with SARS-CoV-2 infection. A brief review of the current literature will help elucidate possible mechanisms, risk factors, and current treatments for CVA associated with SARS-CoV-2.
Patients evaluated in our EDOU for chest pain with an initial indeterminate TnI did not develop subsequent MI. However, these patients had an increased rate of revascularization and inpatient admission compared with controls. While our experience suggests that patients with an indeterminate TnI may be safely evaluated in an observation setting, EDOUs which treat only low-risk chest pain patients may wish to recommend inpatient admission for this patient group.
nucleocapsid (N) proteins of the SARS-CoV-2 virus are of particular interest as easily measurable potential indirect markers of both previous infection and resistance to reinfection. Previous studies in hospitalized patients have found that anti-N IgG levels decline over time. We undertook this study to characterize the kinetics of anti-N IgG in a longitudinal cohort of health care workers in an acute hospital setting.Methods: All HCWs who were either employed or part of the medical staff at six acute-care hospitals in Phoenix, AZ in June 2019 were invited to participate in a longterm study of the impact of the COVID-19 pandemic on HCWs. A cohort of 1358 HCWs provided informed consent, filled out a questionnaire regarding their health care role and potential COVID-19 symptoms, and had blood drawn between June 15 th and August 15 th, 2020 (Draw 1). The questionnaire and blood draws were repeated in October 2020 (Draw 2), January 2021 (Draw 3), and April 2021. SARS-CoV-2 anti-N IgG was measured using the Abbott Architect platform, using a signal to cutoff ratio (S/Co) greater than 1.4 as a positive result. A participant's first positive result was treated as Time 0. Anti-N IgG S/Co values at each time point were summarized as mean, median, and inter-quartile range, and differences over time were tested using the Friedman's test.Results: 290 participants (21.4%) had at least one positive IgG, with a median S/ Co of 4.96, IQR 2.37-6.67. The Month 3 median S/Co was 2.32, IQR 1.34-4.22, Month 6 median was 0.96, IQR 0.51-2.05, and Month 9 median was 0.60, IQR 0.26-1.29 (See Figure). Freidman's test for differences was significant at p<0.0001 at all time points. No participant was hospitalized for their acute COVID-19 illness. 68/244 participants (27.4%) were seronegative at 3 months, 81/126 (64.3%) at six months, and 65/84 (77.4%) at nine months.Conclusion: In a cohort of health care workers with mild to moderate COVID-19, anti-N IgG levels steadily decreased over 9 months from the initial positive IgG. The high rates of conversion to seronegative over a relatively short time frame illustrate why antibody-based testing must be interpreted cautiously when used as a definitive marker of prior COVID infection.
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