Sheena Khan1, Alexandria Soto1, Elisabeth B Marsh2. 1. Department of Neurology, Johns Hopkins School of Medicine, 600 North Wolfe St. Phipps 446C, Baltimore, MD, 21287, USA. 2. Department of Neurology, Johns Hopkins School of Medicine, 600 North Wolfe St. Phipps 446C, Baltimore, MD, 21287, USA. ebmarsh@jhmi.edu.
Abstract
BACKGROUND AND PURPOSE: Stroke patients are currently monitored for neurological deterioration for 24 h following treatment with intravenous tissue plasminogen activator (IV tPA) or mechanical thrombectomy. This requires low nursing ratios and an intensive-care-like setting. As the half-life of IV tPA is short, many patients may not require such prolonged intensive monitoring and could be downgraded much earlier. We evaluate the frequency of neurological deterioration in the 0-12 and 12-24 h post-treatment windows. METHODS: Patients presenting with acute ischemic stroke treated with IV tPA and/or thrombectomy at our institution from 2016-2018 were prospectively followed per protocol for 24 h post-therapy (examinations every 15 min for 2 h, every 30 min for 6 h, and hourly thereafter). Neurological deteriorations were recorded along with interventions and complications. Frequency of deterioration within the 0-12 and 12-24 h post-treatment windows was determined, along with factors associated with decline at each time point. RESULTS: A total of 172 patients were treated (IV:135, IA:65, both:30). Thirty-six (21%) experienced a documented neurologic deterioration [8 due to intracerebral hemorrhage (4.7%)]. Five patients deteriorated in the 12-24 h window; all but one had experienced earlier examination changes. Elevated NIHSS was associated with a higher likelihood of deterioration overall. Early fluctuation was associated with decline after 12 h. CONCLUSIONS: New onset of neurologic deterioration is rare 12-24 h after treatment of acute stroke. Stable patients with low NIHSS scores and no ICU needs may not require intensive monitoring greater than 12 h post-treatment.
BACKGROUND AND PURPOSE:Strokepatients are currently monitored for neurological deterioration for 24 h following treatment with intravenous tissue plasminogen activator (IV tPA) or mechanical thrombectomy. This requires low nursing ratios and an intensive-care-like setting. As the half-life of IV tPA is short, many patients may not require such prolonged intensive monitoring and could be downgraded much earlier. We evaluate the frequency of neurological deterioration in the 0-12 and 12-24 h post-treatment windows. METHODS:Patients presenting with acute ischemic stroke treated with IV tPA and/or thrombectomy at our institution from 2016-2018 were prospectively followed per protocol for 24 h post-therapy (examinations every 15 min for 2 h, every 30 min for 6 h, and hourly thereafter). Neurological deteriorations were recorded along with interventions and complications. Frequency of deterioration within the 0-12 and 12-24 h post-treatment windows was determined, along with factors associated with decline at each time point. RESULTS: A total of 172 patients were treated (IV:135, IA:65, both:30). Thirty-six (21%) experienced a documented neurologic deterioration [8 due to intracerebral hemorrhage (4.7%)]. Five patients deteriorated in the 12-24 h window; all but one had experienced earlier examination changes. Elevated NIHSS was associated with a higher likelihood of deterioration overall. Early fluctuation was associated with decline after 12 h. CONCLUSIONS: New onset of neurologic deterioration is rare 12-24 h after treatment of acute stroke. Stable patients with low NIHSS scores and no ICU needs may not require intensive monitoring greater than 12 h post-treatment.