Faculty Opinions recommendation of Hyperoxia may be related to delayed cerebral ischemia and poor outcome after subarachnoid haemorrhage.

2016 ◽  
Author(s):  
Federico Bilotta
Keyword(s):  
Cerebral Ischemia ◽  
Subarachnoid Haemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Poor Outcome

scholarly journals Hyperoxia may be related to delayed cerebral ischemia and poor outcome after subarachnoid haemorrhage

2014 ◽  
Vol 85 (12) ◽  
pp. 1301-1307 ◽  
Author(s):  
Sang-Beom Jeon ◽  
H Alex Choi ◽  
Neeraj Badjatia ◽  
J Michael Schmidt ◽  
Hector Lantigua ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Subarachnoid Haemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Poor Outcome

scholarly journals Literature Review of Aneurysmal Subarachnoid Hemorrhage from Incidence to Treatment Options

2020 ◽  
Vol 18 (1) ◽  
pp. 70-78
Author(s):  
Ieva Buce-Satoba ◽  
Daina Rozkalne ◽  
Jevgenijs Stepanovs ◽  
Biruta Mamaja ◽  
Gaida Krumina ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cerebral Ischemia ◽  
Literature Review ◽  
Glasgow Coma Scale ◽  
Subarachnoid Haemorrhage ◽  
Cerebral Vasospasm ◽  
Treatment Options ◽  
Delayed Cerebral Ischemia ◽  
Late Complications ◽  
Aneurysmal Subarachnoid Haemorrhage

SummaryIntroductionAneurysmal subarachnoid haemorrhage (SAH) is associated with high mortality and morbidity. Rebleeding, cerebral vasospasm (VS) with delayed cerebral ischemia (DCI) are major complications after SAH associated with poor neurological outcome.Aim of the studyTo summarize the existing research data on the SAH from incidence, risk factors and clinical presentation to diagnostic, monitoring and treatment options after SAH.Materials and MethodsLiterature review was carried out to identify factors associated with SAH using specific keywords (aneurysmal subarachnoid haemorrhage, rebleeding, cerebral vasospasm, delayed cerebral ischemia) in the PUBMED database. In the time period from 2000 to 2019, 34 full articles were reviewed.ResultsAccording to the literature, the key risk factors for cerebral aneurysms and the SAH are hypertension, smoking, chronic alcohol abuse, family history of intracranial aneurysms in first-degree relatives and female sex. The key risk factor for early complication - rebleeding after SAH - is hypertension. The factors responsible for late complications - cerebral VS and DCI after SAH - are initially lower Glasgow coma scale and higher grades of Fisher scale, where grade IV and III predict cerebral VS in 31–37%. Furthermore, hyperglycaemic state, hyponatremia, hypotension and cerebral hypoperfusion, increased level of Troponin correlate with the incidence of cerebral VS and DCI. Although the golden standard to detect cerebral VS is digital subtraction angiography, CT angiography has become a routine examination. Transcranial doppler sonography is recommended and regional cerebral oximetry also seems to be promising. To avoid rebleeding for wide-necked, gigantic aneurysms or when SAH is combined with intraparenchymal hematoma, surgical clipping is preferred. For posterior circulation aneurisms, poor grade SAH and patients with age >70 years superior is endovascular treatment. To avoid late complications, the pharmacological method is used with Nimodipine.ConclusionsSAH is still associated with poor clinical outcome due to the development of early and late complications. The highest risk patients are those with low Glasgow coma scale and high grades of Fisher scale. Timely performed obliteration methods of the ruptured aneurysm are crucial and Nimodipine is the main agent to prevent cerebral VS and DCI.

Rebleeding drives poor outcome in aneurysmal subarachnoid hemorrhage independent of delayed cerebral ischemia: a propensity-score matched cohort study

2020 ◽  
Vol 133 (2) ◽  
pp. 360-368
Author(s):  
Victor M. Lu ◽  
Christopher S. Graffeo ◽  
Avital Perry ◽  
Lucas P. Carlstrom ◽  
Leonardo Rangel-Castilla ◽  
...  
Keyword(s):  
Cohort Study ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Propensity Score ◽  
Functional Outcome ◽  
Treatment Modality ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Poor Functional Outcome ◽  
Poor Outcome

OBJECTIVEDelayed cerebral ischemia (DCI) and aneurysm rebleeding contribute to morbidity and mortality in aneurysmal subarachnoid hemorrhage (aSAH); however, the relationship between their impacts on overall functional outcome is incompletely understood.METHODSThe authors conducted a cohort study of all aSAH during the study period from 2001 to 2016. Primary end points were overall functional outcome and ischemic aSAH sequelae, defined as delayed cerebral ischemia (DCI), DCI with infarction, symptomatic vasospasm (SV), and global cerebral edema (GCE). Outcomes were compared between the rebleed and nonrebleed cohorts overall and after propensity-score matching (PSM) for risk factors and treatment modality. Univariate and multivariate ordered logistic regression analyses for functional outcomes were performed in the PSM cohort to identify predictors of poor outcome.RESULTSFour hundred fifty-five aSAH cases admitted within 24 hours of aneurysm rupture were included, of which 411 (90%) experienced initial aneurysm ruptures only, while 44 (10%) had clinically confirmed rebleeding. In the overall cohort, rebleeding was associated with significantly worse functional outcome, longer intensive care unit length of stay (LOS), and GCE (all p < 0.01); treatment modality, overall LOS, DCI, DCI with infarction, and SV were nonsignificant. In the PSM analysis of 43 matched rebleed and 43 matched nonrebleed cases, only poor functional outcome and GCE remained significantly associated with rebleeding (p < 0.01 and p = 0.02, respectively). Multivariate regression identified that both rebleeding (HR 21.5, p < 0.01) and DCI (HR 10.1, p = 0.01) independently predicted poor functional outcome.CONCLUSIONSRebleeding and DCI after aSAH are highly morbid and potentially deadly events after aSAH, which appear to have independent negative impacts on overall functional outcome. Early rebleeding did not significantly affect the risk of delayed ischemic complications.

scholarly journals Hyperoxemia during the hyperacute phase of aneurysmal subarachnoid hemorrhage is associated with delayed cerebral ischemia and poor outcome: a retrospective observational study

2019 ◽  
pp. 1-8 ◽  
Author(s):  
Shinya Fukuda ◽  
Yasutaka Koga ◽  
Motoki Fujita ◽  
Eiichi Suehiro ◽  
Kotaro Kaneda ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Favorable Outcome ◽  
Regression Analyses ◽  
Poor Outcome ◽  
Poor Outcome Group ◽  
Outcome Group

OBJECTIVEThe harmful effects of hyperoxemia have been reported in critically ill patients with various disorders, including those with brain injuries. However, the effect of hyperoxemia on aneurysmal subarachnoid hemorrhage (aSAH) patients is unclear. In this study the authors aimed to determine whether hyperoxemia during the hyperacute or acute phase in patients with aSAH is associated with delayed cerebral ischemia (DCI) and poor neurological outcome.METHODSIn this single-center retrospective study, data from patients with aSAH treated between January 2011 and June 2017 were reviewed. The patients were classified into groups according to whether they experienced DCI (DCI group and non-DCI group) and whether they had a poor outcome at discharge (poor outcome group and favorable outcome group). The background characteristics and time-weighted average (TWA) PaO2 during the first 24 hours after arrival at the treatment facility (TWA24h-PaO2) and between the first 24 hours after arrival and day 6 (TWA6d-PaO2), the hyperacute and acute phases, respectively, were compared between the groups. Factors related to DCI and poor outcome were evaluated with logistic regression analyses.RESULTSOf 197 patients with aSAH, 42 patients experienced DCI and 82 patients had a poor outcome at discharge. TWA24h-PaO2 was significantly higher in the DCI group than in the non-DCI group (186 [141–213] vs 161 [138–192] mm Hg, p = 0.029) and in the poor outcome group than in the favorable outcome group (176 [154–205] vs 156 [136–188] mm Hg, p = 0.004). TWA6d-PaO2 did not differ significantly between the groups. Logistic regression analyses revealed that higher TWA24h-PaO2 was an independent risk factor for DCI (OR 1.09, 95% CI 1.01–1.17, p = 0.037) and poor outcome (OR 1.17, 95% CI 1.06–1.29, p = 0.002).CONCLUSIONSHyperoxemia during the first 24 hours was associated with DCI and a poor outcome in patients with aSAH. Excessive oxygen therapy might have an adverse effect in the hyperacute phase of aSAH.

Apolipoprotein E genotype and outcome after aneurysmal subarachnoid hemorrhage

2009 ◽  
Vol 110 (5) ◽  
pp. 989-995 ◽  
Author(s):  
Seppo Juvela ◽  
Jari Siironen ◽  
Jaakko Lappalainen
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Apolipoprotein E ◽  
Clinical Condition ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Univariate Analysis ◽  
Delayed Cerebral Ischemia ◽  
Intracerebral Hematoma ◽  
Poor Outcome

Object After aneurysmal subarachnoid hemorrhage (SAH), conflicting results concerning an association between the APOE genotype and impaired outcome have been reported. The authors tested prospectively whether APOE ε2 or ε4 allele–containing genotypes (ε2+ and ε4+) affect outcome after SAH. Methods Previous disease histories and clinical and radiological variables were recorded for 105 patients who were admitted within 48 hours after SAH. Fifteen patients (14%) had the ε2+ genotype and 31 (17%) had ε4+ genotypes. Factors predicting poor outcome according to the Glasgow Outcome Scale and cerebral infarction visible on CT scans obtained at 3 months after SAH were tested with multiple logistic regression analyses. Results Apolipoprotein E ε2 or ε4–containing genotypes were not associated with outcome, occurrence of cerebral infarction, or with any of their predictors, either in univariate or multivariate analysis. Poor outcome was predicted independently by the occurrence of intraventricular bleeding and intracerebral hematoma as well as by elevated levels of both plasma glucose and D-dimer, and delayed cerebral ischemia (p < 0.05 for each factor), and in univariate analysis only by clinical condition on admission and patient age. Cerebral infarction was predicted independently according to clinical condition on admission (p < 0.05), amount of subarachnoid blood (p < 0.01), duration of intraoperative parent artery clipping (p < 0.01), and body mass index (p < 0.05). In the univariate analysis only cerebral infarction was also predicted by patient age, intracerebral hematoma, and delayed cerebral ischemia. Conclusions Severity of bleeding for the most part predicts outcome after SAH; APOE polymorphisms seem to have no prognostic value for outcome after SAH. This result was in accordance with the findings from the largest ischemic stroke studies.

scholarly journals Effect of pharmaceutical treatment on vasospasm, delayed cerebral ischemia, and clinical outcome in patients with aneurysmal subarachnoid hemorrhage: A systematic review and meta-analysis

2011 ◽  
Vol 31 (6) ◽  
pp. 1443-1451 ◽  
Author(s):  
Nima Etminan ◽  
Mervyn DI Vergouwen ◽  
Don Ilodigwe ◽  
R Loch Macdonald
Keyword(s):  
Systematic Review ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Clinical Outcome ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Meta Analysis ◽  
Delayed Cerebral Ischemia ◽  
Double Blind ◽  
Poor Outcome ◽  
Methodological Problems

As it is often assumed that delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) is caused by vasospasm, clinical trials often focus on prevention of vasospasm with the aim to improve clinical outcome. However, the role of vasospasm in the pathogenesis of DCI and clinical outcome is possibly smaller than previously assumed. We performed a systematic review and meta-analysis on all randomized, double-blind, placebo-controlled trials that studied the effect of pharmaceutical preventive strategies on vasospasm, DCI, and clinical outcome in SAH patients to further investigate the relationship between vasospasm and clinical outcome. Effect sizes were expressed in pooled risk ratio (RR) estimates with corresponding 95% confidence intervals (CI). A total of 14 studies randomizing 4,235 patients were included. Despite a reduction of vasospasm (RR 0.80 (95% CI 0.70 to 0.92)), no statistically significant effect on poor outcome was observed (RR 0.93 (95% CI 0.85 to 1.03)). The variety of DCI definitions did not justify pooling the DCI data. We conclude that pharmaceutical treatments have significantly decreased the incidence of vasospasm, but not of poor clinical outcome. This dissociation between vasospasm and clinical outcome could result from methodological problems, sample size, insensitivity of clinical outcome measures, or from mechanisms other than vasospasm that also contribute to poor outcome.

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