Background and Purpose:
We aimed to investigate the acute stroke presentations during the coronavirus disease 2019 (COVID-19) pandemic.
Methods:
The data were obtained from a health system with 19 emergency departments in northeast Ohio in the United States. Baseline period from January 1 to March 8, 2020, was compared with the COVID period from March 9, to April 2, 2020. The variables included were total daily stroke alerts across the hospital emergency departments, thrombolysis, time to presentation, stroke severity, time from door-to-imaging, time from door-to-needle in thrombolysis, and time from door-to-puncture in thrombectomy. The 2 time periods were compared using nonparametric statistics and Poisson regression.
Results:
Nine hundred two stroke alerts during the period across the emergency departments were analyzed. Total daily stroke alerts decreased from median, 10 (interquartile range, 8–13) during baseline period to median, 8 (interquartile range, 4–10,
P
=0.001) during COVID period. Time to presentation, stroke severity, and time to treatment were unchanged. COVID period was associated with decrease in stroke alerts with rate ratio of 0.70 (95% CI, 0.60–0.28). Thrombolysis also decreased with rate ratio, 0.52 (95% CI, 0.28–0.97) but thrombectomy remained unchanged rate ratio, 0.93 (95% CI, 0.52–1.62)
Conclusions:
We observed a significant decrease in acute stroke presentations by ≈30% across emergency departments at the time of surge of COVID-19 cases. This observation could be attributed to true decline in stroke incidence or patients not seeking medical attention for emergencies during the pandemic.
Compared with the traditional ambulance model, telemedicine-enabled ambulance-based thrombolysis resulted in significantly decreased time to imaging and treatment.
Intensive lowering of SBP <140 mm Hg in acute ICH, particularly allowing SBP <120 mm Hg, is associated with increased remote cerebral ischemic lesions and acute neurologic deterioration.
Atrial fibrillation (AF) is an important risk factor for ischemic stroke resulting in a fivefold increased stroke risk and a twofold increased mortality. Our understanding of stroke mechanisms in AF has evolved since the concept of atrial cardiopathy was introduced as an underlying pathological change, with both AF and thromboembolism being common manifestations and outcomes. Despite the strong association with stroke, there is no evidence that screening for AF in asymptomatic patients improves clinical outcomes; however, there is strong evidence that patients with embolic stroke of undetermined source may require long-term monitoring to detect silent or paroxysmal AF. Stroke prevention in patients at risk, assessed by the CHA2DS2-VASc score, was traditionally achieved with warfarin; however, direct oral anticoagulants have solidified their role as safe and effective alternatives. Additionally, left atrial appendage exclusion has emerged as a viable option in patients intolerant of anticoagulation. When patients with AF have an acute stroke, the timing of initiation or resumption of anticoagulation for secondary stroke prevention has to be balanced against the risk of hemorrhagic conversion. Multiple randomized clinical trials are currently underway to determine the best timing for administration of anticoagulants following acute ischemic stroke.
Bloodstream infection is the leading cause of mortality in left ventricular assist device. Bloodstream infection is a risk factor for intracranial hemorrhage. We report three left ventricular assist device recipients who presented with bloodstream infection and developed subarachnoid hemorrhage. Case 1, a 37-year-old male with non-ischemic cardiomyopathy with HeartMate II, presented with confusion and found to have serratia bloodstream infection and left frontal lobe subarachnoid hemorrhage. Cerebral angiogram showed a right M3/M4 branch infectious intracranial aneurysm. He was treated with coil embolization and underwent device exchange. Case 2, a 41-year-old male with non-ischemic cardiomyopathy with HeartMate II presented with confusion and found to have methicillin-resistant staphylococcus aureus bloodstream infection and bilateral frontal convexity subarachnoid hemorrhage. Cerebral angiogram showed left M3 and left A3 infectious intracranial aneurysms, which were treated with antibiotics alone. Case 3, a 58-year-old female with ischemic cardiomyopathy with HeartMate II presented with fever, found to have candida albicans bloodstream infection and a parieto-occipital enhancing lesion concerning for cerebral abscess. Repeat computed tomography brain a week later showed a new right frontal subarachnoid hemorrhage. Cerebral angiogram showed a M4/M5 junction infectious intracranial aneurysm; patient was not a surgical candidate and was transitioned to hospice. This case series emphasizes that left ventricular assist device–associated subarachnoid hemorrhage may be caused by infectious intracranial aneurysms when acute bloodstream infections are present.
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