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Introduction Subarachnoid hemorrhage (SAH) is a devastating form of stroke. Causes and mechanisms of in-hospital death after SAH in the modern era of neurocritical care remain incompletely understood. Methods We studied 1200 consecutive SAH patients prospectively enrolled in the Columbia University SAH Outcomes Project between July 1996 and January 2009. Analysis was performed to identify predictors of in-hospital mortality. Results In-hospital mortality was 18 % (216/1200): 3 % for Hunt-Hess grade 1 or 2, 9 % for grade 3, 24 % for grade 4, and 71 % for grade 5. The most common adjudicated primary causes of death or neurological devastation leading to withdrawal of support were direct effects of the primary hemorrhage (55 %), aneurysm rebleeding (17 %), and medical complications (15 %). Among those who died, brain death was declared in 42 %, 50 % were do-not-resuscitate at the time of cardiac death (86 % of whom had life support actively withdrawn), and 8 % died despite full support. Admission predictors of mortality were age, loss of consciousness at ictus, admission Glasgow Coma Scale score, large aneurysm size, Acute Physiology and Chronic Health Evaluation II (APACHE II) physiologic subscore, and Modified Fisher Scale score. Hospital complications that further increased the risk of dying in multivariable analysis included rebleeding, global cerebral edema, hypernatremia, clinical signs of brain stem herniation, hypotension of less than 90 mm Hg treated with pressors, pulmonary edema, myocardial ischemia, and hepatic failure. Delayed cerebral ischemia, defined as deterioration or infarction from vasospasm, did not predict mortality. Conclusion Strategies directed toward minimizing early brain injury and aneurysm rebleeding, along with prevention and treatment of medical complication, hold the best promise for further reducing mortality after SAH.

Background Intracerebral hemorrhage (ICH) causes 15 % of strokes annually in the United States. Methods Using the National Hospital Discharge Survey, we studied the disposition and mortality trends of ICH admissions from 1979 to 2008. Cases were identified using the International Classification of Disease, 9th Revision, Clinical-Modification code 431. Results There was an annualized increase in the admission rate of ICH from about an average of 24,000 cases (12.9 per 100,000 persons per year) during the first epoch to 40,600 cases (17.0 per 100,000 persons per year) during the second epoch. Thereafter, the annual admission rate after ICH remained stable with about 63,000 cases (21 per 100,000 persons per year) during the last epoch. Nonwhites experienced higher growth rates than whites, and the risk of ICH was higher across all age subgroups, in men than women, and nonwhites compared with whites. In-hospital mortality after ICH fell significantly from 45 % (95 % CI , 31–59 %) during the first epoch (1979–1983) to 34 % (95 % CI , 20–38 %) during the second epoch (1984–1988) ( p  = 0.03) but did not change significantly after that. Groups with higher in-hospital mortality were whites, women, and persons older than 65 years, black women younger than 45 years, and middle-aged black men. Average days of care for ICH hospitalizations decreased significantly. Conclusion Though the ICH admission rate increased and the in-hospital mortality decreased during the first epochs of the study, these have not significantly changed over the last two decades. ICH remains the most severe form of stroke with limited options to improve survival. More research targeting novel therapies to improve outcomes after ICH is desperately needed.

ABSTRACT BACKGROUND: Risk factors for poor quality of life (QOL) after subarachnoid hemorrhage (SAH) remain poorly described. OBJECTIVE: To identify the frequency and predictors of poor QOL 1 year after SAH. METHODS: We studied 1-year QOL in a prospectively collected cohort of 1181 consecutively admitted SAH survivors between July 1996 and May 2013. Patient clinical, radiographic, surgical, and acute clinical course information was recorded. Reduced QOL (overall, physical, and psychosocial) at 1 year was assessed with the Sickness Impact Profile and defined as 2 SD below population-based normative Sickness Impact Profile values. Logistic regression leveraging multiple imputation to handle missing data was used to evaluate reduced QOL. RESULTS: Poor overall QOL was observed in 35% of patients. Multivariable analysis revealed that nonwhite ethnicity, high school education or less, history of depression, poor clinical grade (Hunt-Hess Grade ≥3), and delayed infarction were predictors of poor overall and psychosocial QOL. Poor physical QOL was additionally associated with older age, hydrocephalus, pneumonia, and sepsis. At 1 year, patients with poor QOL had increased difficulty concentrating, cognitive dysfunction, depression, and reduced activities of daily living. More than 91% of patients with poor QOL failed to fully return to work. These patients frequently received physical rehabilitation, but few received cognitive rehabilitation or emotional-behavioral support. CONCLUSION: Reduced QOL affects as many as one-third of SAH survivors 1 year after SAH. Delayed infarction is the most important in-hospital modifiable factor that affects QOL. Increased attention to cognitive and emotional difficulties after hospital discharge may help patients achieve greater QOL.

In a previous phase 2 placebo-controlled trial, recombinant activated factor VII (rFVIIa) reduced growth of the hematoma and improved survival and functional outcome in patients with intracerebral hemorrhage. Those findings were not reproduced in this phase 3 trial, in which rFVIIa reduced hematoma growth but did not improve clinical outcomes. In this phase 3 trial, recombinant activated factor VII (rFVIIa) reduced hematoma growth but did not improve clinical outcomes in patients with intracerebral hemorrhage. Intracerebral hemorrhage is the most devastating form of stroke. Approximately 40% of patients with intracerebral hemorrhage die within 30 days, and the majority of survivors are left with severe disability. 1 , 2 Hematoma growth occurs in up to 70% of patients who have intracerebral hemorrhage documented by computed tomographic (CT) scanning performed within 3 hours after the onset of symptoms. 3 , 4 Furthermore, hemorrhage expansion is an independent determinant of death and disability. 4 In addition to intracerebral-hemorrhage growth, other predictors of poor outcome include age, baseline volume of the hemorrhage, Glasgow Coma Scale score, intraventricular hemorrhage, and infratentorial location. 5 There is no . . .

Therapeutic hypothermia is widely recognized to have neuroprotective effects in various clinical settings, from cardiac arrest to traumatic brain injury; however, the practical application of this therapy is not without risk. Choi et al . highlight current methods and protocols of targeted temperature management, and discuss the practical considerations for hypothermia as a therapy for patients with acute brain injury. Hypothermia is widely accepted as the gold-standard method by which the body can protect the brain. Therapeutic cooling—or targeted temperature management (TTM)—is increasingly being used to prevent secondary brain injury in patients admitted to the emergency department and intensive care unit. Rapid cooling to 33 °C for 24 h is considered the standard of care for minimizing neurological injury after cardiac arrest, mild-to-moderate hypothermia (33–35 °C) can be used as an effective component of multimodal therapy for patients with elevated intracranial pressure, and advanced cooling technology can control fever in patients who have experienced trauma, haemorrhagic stroke, or other forms of severe brain injury. However, the practical application of therapeutic hypothermia is not trivial, and the treatment carries risks. Development of clinical management protocols that focus on detection and control of shivering and minimize the risk of other potential complications of TTM will be essential to maximize the benefits of this emerging therapeutic modality. This Review provides an overview of the potential neuroprotective mechanisms of hypothermia, practical considerations for the application of TTM, and disease-specific evidence for the use of this therapy in patients with acute brain injuries. Key Points Targeted temperature management (TTM) is the most powerful mechanism of neuroprotection currently available Hypothermia is proven to have clinically beneficial effects in preventing secondary brain injury in patients who have experienced cardiac arrest, and in neonates with hypoxic–ischaemic injuries Cooling is an effective mechanism to reduce intracranial pressure in patients who do not respond to standard medications Shivering is a common and potentially damaging adverse effect of TTM that needs to be controlled

Clazosentan, an endothelin receptor antagonist, significantly and dose-dependently reduced angiographic vasospasm after aneurysmal subarachnoid haemorrhage (aSAH). We investigated whether clazosentan reduced vasospasm-related morbidity and all-cause mortality. In this randomised, double-blind, placebo-controlled, phase 3 study, we randomly assigned patients with aSAH secured by surgical clipping to clazosentan (5 mg/h, n=768) or placebo (n=389) for up to 14 days (27 countries, 102 sites, inpatient and outpatient settings) using an interactive web response system. The primary composite endpoint (week 6) included all-cause mortality, vasospasm-related new cerebral infarcts, delayed ischaemic neurological deficit due to vasospasm, and rescue therapy for vasospasm. The main secondary endpoint was dichotomised extended Glasgow outcome scale (GOSE; week 12). This trial is registered with ClinicalTrials.gov, number NCT00558311. In the all-treated dataset, the primary endpoint was met in 161 (21%) of 764 clazosentan-treated patients and 97 (25%) of 383 placebo-treated patients (relative risk reduction 17%, 95% CI −4 to 33; p=0·10). Poor functional outcome (GOSE score ≤4) occurred in 224 (29%) clazosentan-treated patients and 95 (25%) placebo-treated patients (−18%, −45 to 4; p=0·10). Lung complications, anaemia, and hypotension were more common with clazosentan. Mortality (week 12) was 6% in both groups. Clazosentan at 5 mg/h had no significant effect on mortality and vasospasm-related morbidity or functional outcome. Further investigation of patients undergoing endovascular coiling of ruptured aneurysms is needed to fully understand the potential usefulness of clazosentan in patients with aSAH. Actelion Pharmaceuticals.

BackgroundEndovascular treatment (EVT) is the standard of care for selected patients with acute ischemic stroke (AIS) due to large vessel occlusion (LVO).ObjectiveTo systematically review the available data on: (1) incidence, predictors, and outcomes of patients with reocclusion after successful EVT for AIS and, (2) the characteristics, complications, and outcomes of patients with reocclusion treated with repeated EVT (rEVT) within 30 days of the first procedure.MethodsPubMed was searched (between January 2012 and April 2021) to identify studies reporting reocclusion following successful EVT (Thrombolysis in Cerebral Infarction ≥2b) in patients with AIS due to LVO. Pooled incidence of reocclusion per 100 patients with successful recanalization following EVT was calculated using a random-effects model with Freeman-Tukey double arcsine transformation. Extracted incidences of reocclusion according to etiology and use of intravenous thrombolysis were pooled using random-effects meta-analytic models.ResultsA total of 840 studies was identified and seven studies qualified for the quantitative analysis, which described 91 same-vessel reocclusions occurring within the first 7 days after treatment among 2067 patients (4.9%; 95% CI 3% to 7%, I2=70.2%). Large vessel atherosclerosis was associated with an increased risk of reocclusion (OR=3.44, 95% CI 1.12 to 10.61, I2=50%). We identified 90 patients treated with rEVT for recurrent LVO, described in five studies. The rates of procedural complications, mortality, and unfavorable functional outcome at 3 months were 18.0%, 18.9%, and 60.3%, respectively.ConclusionIn cohorts of patients with AIS due to LVO, 5% of patients experienced reocclusion within 7 days after successful EVT. Repeated EVT can be a safe and effective treatment for selected patients with reocclusion.

Extracorporeal membrane oxygenation (ECMO) is increasingly used to treat severe cases of acute respiratory or cardiac failure. Hemorrhagic complications represent one of the most common complications during ECMO, and can be life threatening. The purpose of this study was to elucidate pathophysiological mechanisms of ECMO-associated hemorrhagic complications and their impact on standard and viscoelastic coagulation tests. The study cohort included 27 patients treated with VV-ECMO or VA-ECMO. Hemostasis was evaluated using standard coagulation tests and viscoelastic parameters investigated with rotational thromboelastometry. Anticoagulation and hemorrhagic complications were analyzed for up to seven days depending on ECMO duration. Hemorrhagic complications developed in 16 (59%) patients. There were 102 discrete hemorrhagic episodes among 116 24-hour-intervals, of which 27% were considered to be clinically significant. The highest number of ECMO-associated hemorrhages occurred on the 2nd and 3rd day of treatment. Respiratory tract bleeding was the most common hemorrhagic complication, occurring in 62% of the 24-hour intervals. All 24-hours-intervals were divided into two groups: \"with bleeding\" and \"without bleeding\". The probability of hemorrhage was significantly associated with abnormalities of four parameters: increased international normalized ratio (INR, sensitivity 71%, specificity 94%), increased prothrombin time (PT, sensitivity 90%, specificity 72%), decreased intrinsic pathway maximal clot firmness (MCFin, sensitivity 76%, specificity 89%), and increased extrinsic pathway clot formation time (CFTex, sensitivity 77%, specificity 87%). In conclusions, early ECMO-associated hemorrhagic complications are related to one traditional and two novel viscoelastic coagulation abnormalities: PT/INR elevation, reduced maximum clot firmness due to intrinsic pathway dysfunction (MCFin), and prolonged clot formation time due to extrinsic pathway dysfunction (CFTex). When managing hemostasis during ECMO, derangements in PT/INR, MCFin and CFTex should be focused on.

Background Vasospasm is a devastating sequelae of ruptured arteriovenous malformations (AVMs) in adults. Comorbidities and presenting factors have been suggested as risks, but only in cross-sectional studies. The objective of this study was to characterize risk factors associated with vasospasm and mortality in ruptured AVM. Methods Adult patients from the TriNetX Research Network were included, based on the ICD-10 codes, over a period of 20 years. Cox proportional hazard models assessed the hazards of vasospasm (I67.84) and mortality separately, adjusting for age, sex, comorbidities, substance use history, presenting factors (e.g., hypernatremia, hypokalemia), criteria of the National Inpatient Sample-Subarachnoid Hemorrhage Severity Score, and location of hemorrhage. Outcomes were assessed in the first 30 days following rupture. Results Among 10,375 patients with ruptured AVMs, 523 (5.3%) died and 297 (3.0%) experienced vasospasm in the first 30 days. After matching for age and sex, vasospasm was associated with increased mortality at three months (11.1% vs. 4.8%, p  = 0.003), six months (12.6% vs. 5.1%, p  = 0.001), and one year (13.5% vs. 6.9%, p  = 0.005). Female sex was protective against vasospasm within 30 days (HR = 0.714, p  = 0.007) while the greatest risk factors present on admission included subarachnoid hemorrhage (6.086, p  < 0.001), hydrocephalus (3.783, p  < 0.001), and leukocytosis (2.0677, p  < 0.001). The greatest risk factors for 30-day mortality were coma (HR = 3.700, p  < 0.001), hydrocephalus (2.698, p  < 0.001), and chronic kidney disease (1.596, p  = 0.003). Conclusions In this retrospective cohort study of 10,375 adult patients with ruptured AVMs, vasospasm occurred in approximately 3%. Risk factors for vasospasm included subarachnoid hemorrhage, male sex, hydrocephalus, and leukocytosis. The presence of vasospasm was associated with a more than twofold increase in mortality at both 30 days and one year.

In this randomized trial, treatment of patients with intracerebral hemorrhage with recombinant activated factor VII (rFVIIa) within four hours after the onset of bleeding reduced the growth of the hematoma and the rates of disability and mortality (90-day mortality was 18 percent with rFVIIa and 29 percent with placebo). Serious thromboembolic adverse events were more common among patients treated with rFVIIa than among those who received placebo. Despite the higher rates of some complications, early treatment with rFVIIa improved functional outcomes and survival among patients with intracerebral hemorrhage. Intracerebral hemorrhage is one of the most disabling forms of stroke. More than one third of patients with this disorder die within one month after the onset of symptoms, and only 20 percent regain functional independence. 1 There is currently no effective treatment for intracerebral hemorrhage. 2 The volume of the hematoma is a critical determinant of mortality and functional outcome after intracerebral hemorrhage, 3 , 4 and early hematoma growth is an important cause of neurologic deterioration. 5 – 8 An increase in volume of more than 33 percent is detectable on repeated computed tomography (CT) in 38 percent of patients initially scanned within three . . .