Association of Recent Use of Non-Vitamin K Antagonist Oral Anticoagulants With Intracranial Hemorrhage Among Patients With Acute Ischemic Stroke Treated With Alteplase.

Importance: Current guidelines recommend against use of intravenous alteplase in patients with acute ischemic stroke who are taking non-vitamin K antagonist oral anticoagulants (NOACs). Objective: To evaluate the safety and functional outcomes of intravenous alteplase among patients who were taking NOACs prior to stroke and compare outcomes with patients who were not taking long-term anticoagulants. Design, Setting, and Participants: A retrospective cohort study of 163 038 patients with acute ischemic stroke either taking NOACs or not taking anticoagulants prior to stroke and treated with intravenous alteplase within 4.5 hours of symptom onset at 1752 US hospitals participating in the Get With The Guidelines-Stroke program between April 2015 and March 2020, with complementary data from the Addressing Real-world Anticoagulant Management Issues in Stroke registry. Exposures: Prestroke treatment with NOACs within 7 days prior to alteplase treatment. Main Outcomes and Measures: The primary outcome was symptomatic intracranial hemorrhage occurring within 36 hours after intravenous alteplase administration. There were 4 secondary safety outcomes, including inpatient mortality, and 7 secondary functional outcomes assessed at hospital discharge, including the proportion of patients discharged home. Results: Of 163 038 patients treated with intravenous alteplase (median age, 70 [IQR, 59 to 81] years; 49.1% women), 2207 (1.4%) were taking NOACs and 160 831 (98.6%) were not taking anticoagulants prior to their stroke. Patients taking NOACs were older (median age, 75 [IQR, 64 to 82] years vs 70 [IQR, 58 to 81] years for those not taking anticoagulants), had a higher prevalence of cardiovascular comorbidities, and experienced more severe strokes (median National Institutes of Health Stroke Scale score, 10 [IQR, 5 to 17] vs 7 [IQR, 4 to 14]) (all standardized differences >10). The unadjusted rate of symptomatic intracranial hemorrhage was 3.7% (95% CI, 2.9% to 4.5%) for patients taking NOACs vs 3.2% (95% CI, 3.1% to 3.3%) for patients not taking anticoagulants. After adjusting for baseline clinical factors, the risk of symptomatic intracranial hemorrhage was not significantly different between groups (adjusted odds ratio [OR], 0.88 [95% CI, 0.70 to 1.10]; adjusted risk difference [RD], -0.51% [95% CI, -1.36% to 0.34%]). There were no significant differences in the secondary safety outcomes, including inpatient mortality (6.3% for patients taking NOACs vs 4.9% for patients not taking anticoagulants; adjusted OR, 0.84 [95% CI, 0.69 to 1.01]; adjusted RD, -1.20% [95% CI, -2.39% to -0%]). Of the secondary functional outcomes, 4 of 7 showed significant differences in favor of the NOAC group after adjustment, including the proportion of patients discharged home (45.9% vs 53.6% for patients not taking anticoagulants; adjusted OR, 1.17 [95% CI, 1.06 to 1.29]; adjusted RD, 3.84% [95% CI, 1.46% to 6.22%]). Conclusions and Relevance: Among patients with acute ischemic stroke treated with intravenous alteplase, use of NOACs within the preceding 7 days, compared with no use of anticoagulants, was not associated with a significantly increased risk of intracranial hemorrhage.

Structured handoff checklists improve clinical measures in patients discharged from the neurointensive care unit.

While up to 80% of medical errors may result from poor communication at clinical transitions of care, there has been relatively little study of the effect of standardized communication tools on clinical quality measures. We prospectively examined the effect of a standardized handoff checklist on clinical outcomes for patients dismissed from the neurointensive care unit. We found that the checklist resulted in significant reductions in patients transferred with inaccurate medication reconciliation and unnecessary urinary catheters. Participating physicians were surveyed and generally viewed the handoff checklist favorably. Standardized communication tools such as checklists may play a useful role in reducing medical errors related to communication between patient care teams.

Recognizing the signs and symptoms of aneurysmal subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) is a devastating neurologic condition with a high mortality and long term neurological morbidity in 50% of survivors. In addition, SAH commonly affects young patients causing substantial loss of productive life years and resulting in significant long term healthcare costs. Early recognition of the signs and symptoms of SAH is absolutely critical to earlier intervention, and delays in diagnosis can have devastating consequences. To avoid such delays in SAH diagnosis, the medical provider should recognize its signs and symptoms. Neuroimgaging, cerebrospinal fluid examination and angiography (invasive or non-invasive) facilitate early diagnosis of SAH. The purpose of this review is not to provide an exhaustive critique of the available literature, rather, it is to provide an overview that will better enable a provider to recognize and initiate the workup of patients with SAH.

Long-term natural history of incidentally discovered cavernous malformations in a single-center cohort.

OBJECT: The aim of this study was to determine the prospective hemorrhage rate in a group of retrospectively identified patients in whom symptoms had an unclear relationship to an intracerebral cavernous malformation (ICM) or the malformation itself was an incidental finding. METHODS: Patients with incidentally discovered ICMs diagnosed between 1989 and 1999 were identified from a previously published cohort. Those with ICMs having an unclear relationship with existing symptoms were also eligible for analysis. Updated clinical and radiographic data pertaining to symptomatic intracerebral hemorrhage related to the ICM or new seizures were obtained through medical chart review and mail survey. In select patients, phone calls were made and death certificates were obtained when possible. The prospective hemorrhage rate was calculated as the number of prospective hemorrhages divided by the number of patient-years of follow-up. RESULTS: There were 1311 patient-years of follow-up among the 107 patients (49.5% male; mean age at diagnosis 52 years) eligible for this study. Forty-four patients died in the follow-up period, and the cause of death could be determined in 34 (77%). Two patients had a prospective hemorrhage, which was definitively related to the ICM in only one. Thus, the definitive prospective bleed rate was 0.08% per patient-year. No new seizures developed in any of the patients during the follow-up period. CONCLUSIONS: The risk of prospective hemorrhage in patients presenting asymptomatically with ICM is very low. This information can be useful in managing such patients and may be most applicable to those with a single ICM.

The acutely comatose patient: clinical approach and diagnosis.

A patient's acute and persistent unresponsiveness in the emergency department often triggers a neurology consultation. Given the many potential causes of unresponsiveness, the initial objective of the neurologist should be a comprehensive history and physical examination, which should allow localization of the lesion, if possible, and an initial narrowing of the differential diagnosis. In addition, neuroimaging review and laboratory evaluation have come to play an increasingly important role in identification of the potential causes of unresponsiveness. However, in some instances, the computed tomography or the magnetic resonance imaging scans are normal and sorting out the cause and depth of unresponsiveness requires clinical skill. The neurologist is adept at correctly moving through a differential diagnosis and this has a profound effect on management. Once appropriate treatment has been initiated, the outcome can be assessed. Recovery from coma can be prolonged, but is less likely if early involvement of the brainstem is apparent.

Subtherapeutic international normalized ratio in warfarin-treated patients increases the risk for symptomatic intracerebral hemorrhage after intravenous thrombolysis.

BACKGROUND AND PURPOSE: There is uncertainty whether warfarin-treated patients (despite international normalized ratio < 1.7) have increased risks of symptomatic intracerebral hemorrhage after intravenous thrombolysis. METHODS: Vascular risk factors, stroke subtype, and outcome measures were compared between warfarin- and nonwarfarin-treated patients undergoing acute thrombolysis within 3 hours of symptom onset. RESULTS: From 212 patients (mean age, 74 ± 14 years; 50% men) studied, 14 (6.5%) had prior warfarin use. After adjusting for age, baseline National Institutes of Health Stroke Scale, and stroke subtype, warfarin-treated patients had significantly increased risks of developing symptomatic intracerebral hemorrhage (adjusted OR, 14.7; 95% CI, 1.3 to 54.3). A trend for poorer stroke recovery and increased mortality was observed in warfarin-treated patients on univariate, but not on multivariable, analyses. CONCLUSIONS: Warfarin-treated patients with stroke have increased risks of symptomatic intracerebral hemorrhage after thrombolytic treatment. These data raise safety concerns of thrombolytic treatment in warfarin-treated patients with subtherapeutic international normalized ratio.