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Introduction: Re-bleeding can have significant adverse consequences, but has not been well described in isolated nontraumatic convexity subarachnoid hemorrhage (cSAH), and therefore we sought to report the clinical spectrum of re-bleed in this population. Methods: With IRB approval, we retrospectively reviewed consecutive nontraumatic cSAH admitted to our institution from August 1, 2006 to June 1, 2016. cSAH was defined as radiographic hemorrhage isolated to the convexities, without cisternal component. Trauma was excluded. Data was abstracted on demographics, medical history, neuroimaging, etiology, and clinical presentation. Good clinical outcome was defined as modified rankin score of 0-2 at 3 months. Results: Among 93 cSAH patients, re-bleed occurred in 9 (10%) patients. The mean age of patients with re-bleed was 55.6 years (range, 24-68) and 8 (89%) were women. The majority 6 (67%) were Hispanic. Most patients 8 (89%) presented with severe headache. The etiology of cSAH was reversible cerebral vasoconstriction syndrome (RCVS) in 6 (67%), amyloid angiopathy in 1 (11%), cerebral venous thrombosis (CVT) in 1 (11%), and post-procedural related in 1 (11%). Initial re-bleeding was new remote subarachnoid hemorrhage in 1 (11%) and new intracerebral hemorrhage in 8 (89%). Clinical symptoms of initial re-bleeding included isolated worsening headache in 2 (22%), focal neurological deficits in 4 (44%), and no clinical change in 3 (33%). Time from initial neuroimaging documenting cSAH to CT documenting re-bleed was 40 hours (range, 5 - 74), and re-bleed occurred within 60 hrs in most patients (89%). Two patients had subsequent re-bleeding (due to CVT and RCVS) documented at 1.9 and 11.8 hours after the initial re-bleed CT. Good clinical outcome was seen in 7 (78%) . Conclusion: Re-bleeding was seen in 10% of cSAH patients and in the majority of patients occurred early, within 2.5 days. Clinicians should be aware of this potential complication of cSAH.

Introduction: Although alterations in fibrinogen and fibrinogen degradation products are well-established after intravenous tissue plasminogen activator (IVtPA) in acute stroke, IVtPA is not recognized to cause markedly abnormal international normalized ratio (INR). Methods: With IRB approval, we prospectively screened 99 consecutive acute stroke patients who received IVtPA admitted from November 1, 2015 to July 1, 2016. Laboratory tests including INR, activated partial thromboplastin time (aPTT), fibrinogen, and d-Dimer were drawn at intervals of 6, 12, 24, and 48 hours. Data was collected on patient demographics, last known normal (LKN), IVtpA dose and timing, and National Institutes of Health Stroke Scale (NIHSS). Post-IVtPA coagulopathy was defined as INR ≥ 1.5. Reference range for fibrinogen was 190 - 395 mg/dL. Results: Among 44 patients prospectively enrolled, the mean age was 66.5 years (range, 32 to 91). Mean time from LKN to IVtPA administration was 2.6 hours (range 0.07 to 10.8). Initial pre-IVTPA mean NIHSS was 14 (range, 3 to 26) and 24 hour mean NIHSS was 7.4, (range 0 to 30). Mean pre-IVtPA INR was 1.05 (range, 0.9 to 1.4). Mean peak post-IVtPA INR was 1.28 (range 1.01 to 3.08). Mean deviation of actual to ideal IVtPA dose was 1.02 mg (range, 22.9 to 14.4). Post IVtPA coagulopathy occurred in 6 patients (14%), with peak INR noted at a mean of 13 hours after IVtPA administration (range, 5.6 to 18.6). Five patients of the six (83%) with post IVtPA coagulopathy had low fibrinogen, and mean fibrinogen nadir was 97 mg/dL (range, 37 to 242). Post-IVtPA coagulopathy was not significantly associated with initial NIHSS, 24 hour NIHSS, LKN to IVtPA time, or deviation of actual IVtPA dose from ideal dose. Conclusion: Post-IVtpA coagulopathy occurs in 14% of patients when studied prospectively and is associated with hypofibrinogenemia, but does not appear to correlate with severity of stroke or IVtPA dosing/timing.

Introduction: Intravenous tissue plasminogen activator (IVtPA) is a proven treatment in acute ischemic stroke but relies on weight-based dosing in a time sensitive manner. Errors in body weight estimation are common and may result in over or under-dosing of IVtPA. Methods: With IRB approval, we prospectively screened 99 consecutive patients who received IVtPA for suspected acute ischemic stroke from November 1, 2015 to July 1, 2016 as part of a prospective IVtPA study. Patients were included in this analysis who had complete data. Data was collected on patient demographics, National Institutes of Health Stroke Scale (NIHSS), body weight, and times of last known normal (LKN) and IVtPA administration. A significant error in IVtPA dosing was defined as a >10% difference in actual versus calculated IVtPA dose. Results: Among 42 patients prospectively enrolled, the mean age was 65.8 years (range, 32 to 89) and 30 (79%) of patients were transfers from outside Emergency Rooms. Mean time from LKN to IVtPA administration was 2.4 hours (range. 0.7 to 4.8). Initial pre-IVtPA mean NIHSS was 14 (range, 3 to 26). The mean % error in IVtPA dose was +1.9% (range, -29% to + 21%). Ten patients (24%) had a significant error in IVtPA dosing of > 10% of the dose, and 8 (80%) were over-doses. Patients with significant IVtPA dosing error did not differ in terms of age (65.8 vs 65.8, p 0.99), sex (female 55.6% vs 38.9%, p 0.45), race (white 70% vs 47%, p 0.28), height (164.8 vs 171.0 cm, p 0.1), or time from LKN to IVtPA (2.8 vs 2.3, p 0.15). Patients with significant IVtPA dosing errors had significantly lower baseline weight (70.3 vs 90.0 kilograms, p 0.029) and higher NIHSS (18.7 vs 12.6, p 0.018). Conclusion: Dosing errors of > 10% of the calculated IVtPA dose occur in nearly one-quarter of acute stroke patients treated in the community, and patients with lower weight and higher NIHSS were at higher risk of dosing errors.

Background and Purpose— Decreased diffusion (DD) consistent with acute ischemia may be detected on MRI after acute intracerebral hemorrhage (ICH), but its risk factors and impact on functional outcomes are not well-defined. We tested the hypotheses that DD after ICH is related to acute blood pressure (BP) reduction and lower hemoglobin and presages worse functional outcomes. Methods— Patients who underwent MRI were prospectively evaluated for DD by certified neuroradiologists blinded to outcomes. Hemoglobin and BP data were obtained via electronic queries. Outcomes were obtained at 14 days and 3 months with the modified Rankin Scale, a functional scale scored from 0 (no symptoms) to 6 (dead). We used logistic regression for dependence or death (modified Rankin Scale score 4–6). Results— DD distinct from the hematoma was found on MRI in 39 of 95 patients (41%). DD was associated with greater BP reductions from baseline and a higher risk of dependence or death at 3 months (odds ratio, 4.8; 95% confidence interval, 1.7–13.9; P =0.004) after correction for ICH score (1.8 per point; 95% confidence interval, 1.2–3.1; P =0.01). Lower hemoglobin was associated with worse ICH score, larger hematoma volume, and worse outcomes, but not DD. Conclusions— DD is common after ICH, associated with greater acute BP reductions, and associated with disability and death at 3 months in multivariate analysis. The potential benefits of acute BP reduction to reduce hematoma growth may be limited by DD. The prevention and treatment of cerebral ischemia manifested as DD are potential methods to improve outcomes.

Background and Purpose— There are few data on the effectiveness and side effects of antiepileptic drug therapy after intracerebral hemorrhage. We tested the hypothesis that antiepileptic drug use is associated with more complications and worse outcome after intracerebral hemorrhage. Methods— We prospectively enrolled 98 patients with intracerebral hemorrhage and recorded antiepileptic drug use as either prophylactic or therapeutic along with clinical characteristics. Antiepileptic drug administration and free phenytoin serum levels were retrieved from the electronic medical records. Patients with depressed mental status underwent continuous electroencephalographic monitoring. Outcomes were measured with the National Institutes of Health Stroke Scale and modified Rankin Scale at 14 days or discharge and the modified Rankin Scale at 28 days and 3 months. We constructed logistic regression models for poor outcome at 3 months with a forward conditional model. Results— Seven (7%) patients had a clinical seizure, 5 on the day of intracerebral hemorrhage. Phenytoin was associated with more fever ( P =0.03), worse National Institutes of Health Stroke Scale at 14 days (23 [9 to 42] versus 11 [4 to 23], P =0.003), and worse modified Rankin Scale at 14 days, 28 days, and 3 months. In a forward conditional logistic regression model, phenytoin prophylaxis was associated with an increased risk of poor outcome (OR, 9.8; 1.4 to 68.6; P =0.02), entering after admission National Institutes of Health Stroke Scale and age. Excluding patients with a seizure did not change the results. Levetiracetam was not associated with demographics, seizures, complications, or outcomes. Conclusions— Phenytoin was associated with more fever and worse outcomes after intracerebral hemorrhage.

Background and Purpose— The purpose of this study was to investigate time delays, adherence to guidelines, and their impact on outcomes in patients with warfarin-associated intracerebral hemorrhage transferred from community emergency departments to a comprehensive stroke center. Methods— We collected demographic, clinical, transfer time, treatment, and outcome data for patients transferred to our institution with warfarin-associated intracerebral hemorrhage from community emergency departments. Results— Among 928 patients with intracerebral hemorrhage, 56 (6%) with warfarin-associated intracerebral hemorrhage (median international normalized ratio, 2.55) were transferred to the comprehensive stroke center. Twenty patients received no acute reversal therapy before transfer, only 4 of whom had international normalized ratios ≤1.4 in the community emergency department. Median time of emergency department stay was 3.66 hours and median time to initiation of acute reversal therapy was 4.48 hours. Those who received ≥3 U of fresh–frozen plasma or recombinant activated Factor VIIa (11 patients) before transfer had lower repeat international normalized ratios and better discharge dispositions than those treated less aggressively. Conclusions— Treatment of warfarin-associated intracerebral hemorrhage in community emergency departments is often suboptimal and does not adhere to published guidelines. Treating coagulopathy aggressively before interhospital transfer may improve outcomes and warrants further investigation.

Background: The International Cooperative Study on the Timing of Aneurysm Surgery suggested that delayed cerebral vasospasm is a significant contributor to mortality (at 6 months) after subarachnoid hemorrhage (SAH). However, the Cincinnati population based study did not find cerebral vasospasm to be a significant contributor to short-term mortality. Methods: We reviewed 350 consecutive non-traumatic SAH patients who were hospitalized at our institution from August 1, 2006 to June 30, 2010. Data were collected on demographics, Hunt and Hess grade, presence of cerebral infarct, symptomatic vasospasm, and in-hospital mortality. Symptomatic vasospasm was defined as cerebral vasospasm that required intra-arterial therapy (pharmacologic vasodilators or angioplasty). Cerebral infarct was defined as any new radiographic infarct seen on CT or MRI (of any cause). Results: Among 350 patients with non-traumatic SAH, the mean age was 56.7 years (range, 21.5 to 89.1) and 68% were aneurysmal. The overall in-hospital mortality rate was 20.2% (71 patients). The causes of in-hospital mortality were withdrawal of support in 53 (75%), brain death in 14 (20%), and cardiopulmonary death in 4 (8%). The mean time to death was 8.1 (range 0 to 31) days, with 36% of deaths occurring within the first 2 days of hospitalization. Among patients with symptomatic cerebral vasospasm or cerebral infarct , 19% (26/139) died. In univariate and multivariate analyses, symptomatic cerebral vasospasm and cerebral infarct were not associated with in-hospital mortality. When the analysis was restricted to patients with aneurysmal SAH, cerebral vasospasm and cerebral infarct were still not predictive of in-hospital mortality. In multivariable analysis, the variables most associated with in-hospital mortality were Hunt and Hess score (HH) (p Conclusions: In-hospital mortality after SAH is associated with initial severity of hemorrhage, rebleeding, and age. Symptomatic cerebral vasospasm and cerebral infarct were not significant contributors of overall in-hospital mortality, and approximately one-third of in-hospital mortality after SAH occurs within the first 2 days of hospitalization. By design, studies that exclude patients with severe SAH tend to over-estimate the contribution of cerebral vasospasm on short-term mortality.

Background and Purpose— Antiplatelet medication use and reduced platelet activity may be associated with mortality after intracerebral hemorrhage (ICH). We tested the hypothesis that reduced platelet activity is associated with early ICH clot growth and worse outcomes. Methods— We prospectively identified patients with spontaneous ICH, measured platelet activity (VerifyNow-ASA, Accumetrics) on admission, and recorded antiplatelet medication use. ICH volume was calculated using computerized volumetric analysis. Data were analyzed with nonparametric statistics and repeated measures ANOVA as appropriate. Patients were prospectively followed for functional outcomes. Data are presented as mean±SD or median [Q1 to Q3]. Results— Reduced platelet activity (≤550 aspirin reaction units [ARU]) was associated with increased ICH volume growth ( P P =0.001), but without impact on outcomes. Reduced platelet activity was associated with worse modified Rankin Scores at 3 months ( P =0.02). Conclusions— Reduced platelet activity was associated with early ICH volume growth and worse functional outcome. Because platelet activity can be increased with platelet transfusion, increasing platelet activity is a potential method to reduce ICH volume growth and improve functional outcomes.