ABSTRACT
Objective: To further characterize the relationship between markers of inflammation and outcome in patients undergoing mechanical thrombectomy for acute stroke. Background: Inflammation and infection after ischemic stroke are known to exacerbate tissue injury and worsen clinical outcome. Thrombectomy has become standard of care in stroke, but little data exist regarding how inflammation affects outcome after thrombectomy. Design/Methods: We performed retrospective chart review of stroke patients who underwent mechanical thrombectomy at 2 tertiary academic centers between December 2018 and November 2020. The relationship between discharge mortality, admission WBC count, admission neutrophil percentage, peak WBC count, and fever (peak temperature >38°C) were analyzed using the Wilcoxon rank sum test, Student's t-test, and Fisher's exact test. Multivariable analysis was performed to test for independent predictors of discharge mortality. Analyses were performed for the entire cohort, then repeated in a cohort excluding COVIDpositive patients. Results: Of 254 patients who had thrombectomy for acute stroke, 42 (16.5%) died prior to discharge. Mortality was associated with admission WBC count (10.7 [8.9-14] vs. 8.6 [7-12], p=0.0064), admission neutrophil percentage (78% ± 11 vs. 70% ± 14, p=0.0001), peak WBC count (17 [13-22] vs. 12 [8.9-15], p<0.0001), and fever (71% vs. 29%, p<0.0001). In multivariable analysis, admission WBC count (OR 14, CI 1.5-158, p=0.024), neutrophil percentage (OR 1.04, CI 1.0-1.1, p=0.039), peak WBC count (OR 343, CI 27-5702, p<0.0001) and fever (OR 8.6, CI 3.6-23, p<0.0001) were significantly predictive of discharge mortality after controlling for age, admission NIHSS and post-thrombectomy ASPECTS score. Fifteen patients tested positive for COVID-19. In analyses excluding these patients, peak WBC count and fever remained independent predictors of discharge mortality. Conclusions: Elevated markers of inflammation during hospitalization predict discharge mortality in patients who undergo mechanical thrombectomy for acute stroke. Further study is warranted to investigate causation and identify opportunities to improve quality of care in this patient population.
ABSTRACT
BACKGROUND AND PURPOSE: Various patterns of leukoencephalopathy have been described in coronavirus disease 2019 (COVID-19). In this article, we aimed to describe the clinical and imaging features of acute disseminated leukoencephalopathy in critically ill patients with COVID-19 and the imaging evolution during a short-term follow-up. MATERIALS AND METHODS: We identified and reviewed the clinical data, laboratory results, imaging findings, and outcomes for 8 critically ill patients with COVID-19 with acute disseminated leukoencephalopathy. RESULTS: All patients demonstrated multiple areas of white matter changes in both cerebral hemispheres; 87.5% (7/8) of patients had a posterior predilection. Four patients (50%) had short-term follow-up imaging within a median of 17 days after the first MR imaging; they developed brain atrophy, and their white matter lesions evolved into necrotizing cystic cavitations. All (8/8) patients had inflammatory cytokine release syndrome as demonstrated by elevated interleukin-6, D-dimer, lactate dehydrogenase, erythrocyte sedimentation rate, C-reactive protein, and ferritin levels. Most (7/8; 87.5%) patients were on prolonged ventilator support (median, 44.5 days; interquartile range, 20.5 days). These patients had poor functional outcomes (6/8 [75%] patients were discharged with mRS 5) and high mortality (2/8, 25%). CONCLUSIONS: Critically ill patients with COVID-19 can develop acute disseminated leukoencephalopathy that evolves into cystic degeneration of white matter lesions with brain atrophy during a short period, which we dubbed virus-associated necrotizing disseminated acute leukoencephalopathy. This may be the result of COVID-19-related endothelial injury, cytokine storm, or thrombotic microangiopathy.