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Management of delayed cerebral ischemia after subarachnoid hemorrhage
For patients who survive the initial bleeding event of a ruptured brain aneurysm, delayed cerebral ischemia (DCI) is one of the most important causes of mortality and poor neurological outcome. New insights in the last decade have led to an important paradigm shift in the understanding of DCI pathogenesis. Large-vessel cerebral vasospasm has been challenged as the sole causal mechanism; new hypotheses now focus on the early brain injury, microcirculatory dysfunction, impaired autoregulation, and spreading depolarization. Prevention of DCI primarily relies on nimodipine administration and optimization of blood volume and cardiac performance. Neurological monitoring is essential for early DCI detection and intervention. Serial clinical examination combined with intermittent transcranial Doppler ultrasonography and CT angiography (with or without perfusion) is the most commonly used monitoring paradigm, and usually suffices in good grade patients. By contrast, poor grade patients (WFNS grades 4 and 5) require more advanced monitoring because stupor and coma reduce sensitivity to the effects of ischemia. Greater reliance on CT perfusion imaging, continuous electroencephalography, and invasive brain multimodality monitoring are potential strategies to improve situational awareness as it relates to detecting DCI. Pharmacologically-induced hypertension combined with volume is the established first-line therapy for DCI; a good clinical response with reversal of the presenting deficit occurs in 70 % of patients. Medically refractory DCI, defined as failure to respond adequately to these measures, should trigger step-wise escalation of rescue therapy. Level 1 rescue therapy consists of cardiac output optimization, hemoglobin optimization, and endovascular intervention, including angioplasty and intra-arterial vasodilator infusion. In highly refractory cases, level 2 rescue therapies are also considered, none of which have been validated. This review provides an overview of current state-of-the-art care for DCI management.
Journal Article
Subarachnoid hemorrhage: who dies, and why?
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.
Journal Article
The Epidemiology of Intracerebral Hemorrhage in the United States from 1979 to 2008
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.
Journal Article
Predictors of Poor Quality of Life 1 Year After Subarachnoid Hemorrhage
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.
Journal Article
Clazosentan, an endothelin receptor antagonist, in patients with aneurysmal subarachnoid haemorrhage undergoing surgical clipping: a randomised, double-blind, placebo-controlled phase 3 trial (CONSCIOUS-2)
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.
Journal Article
Clinical and pathophysiologic aspects of ECMO-associated hemorrhagic complications
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.
Journal Article
Efficacy and Safety of Recombinant Activated Factor VII for Acute Intracerebral Hemorrhage
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 . . .
Journal Article