Abstract

Introduction: Endovascular thrombectomy (EVT) has revolutionized the care of emergent large vessel occlusion (ELVO) stroke patients. It is, therefore, crucial to optimize its delivery to eligible candidates. Within hub-and-spoke hospital system models, some patients first present to distant spoke hospitals and require transfer to hub hospitals for EVT. We sought to understand changes in EVT eligibility during transfer. Methods: Consecutive EVT candidates presenting to 25 spokes from 2018 to 2020 with pre-transfer CTA-defined ELVO and Alberta Stroke Program Early CT Score ≥6 were identified from a prospectively maintained database. Outcomes of interest included hub EVT, reasons for EVT ineligibility, and 90-day functional independence (modified Rankin Scale, mRS ≤2). Results: Among 258 patients, the median age was 70 years (IQR 60-81) and 50% were female. Forty-four percent underwent EVT upon hub arrival, of which 87% achieved Thrombolysis in Cerebral Infarction 2b-3 reperfusion. Compared to EVT-eligible patients, ineligible patients were older (73 vs 68 years, p=0.04), had lower NIH Stroke Scale (NIHSS, 10 vs 16, p<0.0001), longer LKW-hub arrival time (8.4 vs 4.6 hours, p<0.0001), and received less IV alteplase (32% vs 45%, p=0.04). The clinical reasons cited for becoming EVT ineligible upon hub arrival included large established infarct (49%), mild symptoms (33%), recanalization (6%), distal occlusion location (5%), subocclusive lesion (3%), and goals of care (3%). Becoming EVT ineligible independently reduced the odds of 90-day functional independence (aOR=0.26, 95%CI=0.12,0.56; p=0.001), even when controlling for age, NIHSS, and LKW-hub arrival time. Conclusions: These data support that approaches to increase EVT eligibility among ELVO transfers may improve long term outcomes. Infarct growth represents the primary reason for ineligibility. Possible interventions include direct field triage to the hub when feasible, improving inter-hospital transfer times, supporting ischemic penumbra before EVT, and developing novel agents to slow infarct growth.

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