Magnesium infusion for vasospasm prophylaxis after subarachnoid hemorrhage

2006 ◽  
Vol 105 (5) ◽  
pp. 723-729 ◽  
Author(s):  
Martina Stippler ◽  
Elizabeth Crago ◽  
Elad I. Levy ◽  
Mary E. Kerr ◽  
Howard Yonas ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Doppler Ultrasonography ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Treated Group ◽  
Aneurysm Rupture ◽  
Current Standard ◽  
Ruptured Aneurysms ◽  
Symptomatic Vasospasm ◽  
Fisher Grade ◽  
Significant Difference

Object Despite the application of current standard therapies, vasospasm continues to result in death or major disability in patients treated for ruptured aneurysms. The authors investigated the effectiveness of continous MgSO4 infusion for vasospasm prophylaxis. Methods Seventy-six adults (mean age 54.6 years; 71% women; 92% Caucasian) were included in this comparative matched-cohort study of patients with aneurysmal subarachnoid hemorrhage on the basis of computed tomography (CT) findings. Thirty-eight patients who received continuous MgSO4 infusion were matched for age, race, sex, treatment option, Fisher grade, and Hunt and Hess grade to 38 historical control individuals who did not receive MgSO4 infusion. Twelve grams of MgSO4 in 500 ml normal saline was given intravenously daily for 12 days if the patient presented within 48 hours of aneurysm rupture. Vasospasm was diagnosed on the basis of digital substraction angiography, CT angiography, and transcranial Doppler ultrasonography, and evidence of neurological deterioration. Symptomatic vasospasm was present at a significantly lower frequency in patients who received MgSO4 infusion (18%) compared with patients who did not receive MgSO4 (42%) (p = 0.025). There was no significant difference in mortality rate at discharge (p = 0.328). A trend toward improved outcome as measured by the modifed Rankin Scale (p = 0.084), but not the Glasgow Outcome Scale (p = 1.0), was seen in the MgSO4-treated group. Conclusions Analysis of the results suggests that MgSO4 infusion may have a role in cerebral vasospasm prophylaxis if therapy is initiated within 48 hours of aneurysm rupture.

Effect of Clipping, Craniotomy, or Intravascular Coiling on Cerebral Vasospasm and Patient Outcome after Aneurysmal Subarachnoid Hemorrhage

Neurosurgery ◽  
2004 ◽  
Vol 55 (4) ◽  
pp. 779-789 ◽  
Author(s):  
Brian L. Hoh ◽  
Mehmet A. Topcuoglu ◽  
Aneesh B. Singhal ◽  
Johnny C. Pryor ◽  
James D. Rabinov ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Hospital Mortality ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Poor Grade ◽  
Poor Outcome ◽  
Symptomatic Vasospasm ◽  
Fisher Grade ◽  
Significant Difference ◽  
Good Grade ◽  
Grade 3

Abstract OBJECTIVE: Although several recent studies have suggested that the incidence of vasospasm after aneurysmal subarachnoid hemorrhage is lower in patients undergoing aneurysmal coiling as compared with clipping, other studies have had conflicting results. We reviewed our experience over 8 years and assessed whether clipping, craniotomy, or coiling affects patient outcomes or the risk for vasospasm. METHODS: We included 515 patients with aneurysmal subarachnoid hemorrhage, identified prospectively from November 2000 to February 2003 (243 patients) and retrospectively from November 1995 to October 2000 (272 patients), by using International Classification of Diseases, 9th Revision, codes for subarachnoid hemorrhage. We classified patients as follows: clipping (413 patients), coiling (79 patients), and craniotomy (436 patients, including all 413 patients who underwent clipping plus 23 who underwent coiling as well as craniotomy for various reasons). We studied four outcome measures: total vasospasm, symptomatic vasospasm, poor outcome (modified Rankin score 3–6), and in-hospital mortality. To assess the risk of total vasospasm and symptomatic vasospasm, we performed multivariate regression analyses adjusting for age, Fisher grade, Hunt and Hess grade, aneurysm location (anterior versus posterior circulation), and aneurysm treatment modality. To assess the risk for poor outcome and in-hospital mortality, we adjusted for all the above variables as well as for total and symptomatic vasospasm. RESULTS: In the clipping group there was 63% total vasospasm and 28% symptomatic vasospasm; in the coiling group there was 54% total vasospasm and 33% symptomatic vasospasm; and in the craniotomy group there was 64% total vasospasm and 28% symptomatic vasospasm. In the multivariate analysis, age <50 years (P = 0.0099) and Fisher Grade 3 (P < 0.00001) predicted total vasospasm, and Fisher Grade 3 (P < 0.000001) and Hunt and Hess Grade IV or V (P = 0.018) predicted symptomatic vasospasm. Predictors of poor outcome were age ≥50 years (P < 0.0001), Fisher Grade 3 (P = 0.0072), Hunt and Hess Grade IV or V (P < 0.00001), symptomatic vasospasm (P < 0.0001), and coiling (P = 0.0314 versus clipping and P = 0.045 versus craniotomy). Predictors of in-hospital mortality were age ≥ 50 years (P = 0.0030), Hunt and Hess Grade IV or V (P = 0.0001), symptomatic vasospasm (P < 0.00001), and coiling (P = 0.008 versus clipping and P = 0.0013 versus craniotomy). There was no significant difference in total vasospasm or symptomatic vasospasm when patients who underwent clipping or craniotomy were compared with patients who underwent coiling. In patients with Hunt and Hess Grade I to III (“good grade”), clipping and craniotomy were associated with better outcome and less in-hospital mortality, but there was no difference in total vasospasm or symptomatic vasospasm versus coiling. In patients with Hunt and Hess Grade IV or V (“poor grade”), there was no difference in any outcome measure among the treatment groups. CONCLUSION: In a single-center, retrospective, nonrandomized study, performance of clipping and/or craniotomy had significantly better outcome and lower mortality at discharge than coiling in good-grade patients but had no effect on total vasospasm or symptomatic vasospasm in good- or poor-grade patients.

scholarly journals APOE Genotype and Functional Outcome Following Aneurysmal Subarachnoid Hemorrhage

2008 ◽  
Vol 10 (3) ◽  
pp. 205-212 ◽  
Author(s):  
Matthew J. Gallek ◽  
Yvette P. Conley ◽  
Paula R. Sherwood ◽  
Michael B. Horowitz ◽  
Amin Kassam ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Functional Outcomes ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Apoe Genotype ◽  
Aneurysm Rupture ◽  
Apoe4 Allele ◽  
Fisher Grade ◽  
Severity Of Injury ◽  
Angiographic Data ◽  
The Central Nervous System

Apolipoprotein E (apoE), the major apolipoprotein in the central nervous system, has been shown to influence neurologic disease progression and response to neurologic injury in a gene-specific manner. Presence of the APOE4 allele is associated with poorer response to traumatic brain injury and ischemic stroke, but the association between APOE genotype and outcome following aneurysmal subarachnoid hemorrhage (SAH) remains unclear. The purpose of this project was to investigate the association between APOE genotype and outcome after SAH. We also explored the association of APOE4 genotype and cerebral vasospasm (CV) presence in a subsample of our population with available angiographic data. A sample of 206 aneurysmal SAH participants had APOE genotyping performed, Glasgow outcome scores (GOS) and modified Rankin scores (MRS) collected at 3 and 6 months after aneurysm rupture. No significant association was found between the presence of the APOE4 genotype and functional outcomes controlling for age, race, size of hemorrhage (Fisher grade), and severity of injury (Hunt & Hess grade). However when controlling for CV and the covariates listed above, individuals with the APOE4 allele had worse functional outcomes at both time points. The presence of the APOE2 allele was not associated with functional outcomes even when considering presence of CV. There was no difference in mortality associated with APOE4 presence, APOE2 presence, or presence of CV. These findings suggest APOE4 allele is associated with poor outcome after aneurysmal SAH.

167 High Throughput Metabolite Profiling Identifies Plasma Anandamide as a Biomarker of Functional Outcome After Aneurysmal Subarachnoid Hemorrhage

Neurosurgery ◽  
2017 ◽  
Vol 64 (CN_suppl_1) ◽  
pp. 242-243
Author(s):  
Christopher J Stapleton ◽  
Hannah Irvine ◽  
Zoe Wolcott ◽  
Aman B Patel ◽  
Jonathan Rosand ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Subarachnoid Hemorrhage ◽  
Functional Outcome ◽  
High Throughput ◽  
Metabolite Profiling ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Plasma Samples ◽  
Symptomatic Vasospasm ◽  
Good Functional Outcome ◽  
Fisher Grade

Abstract INTRODUCTION The quantification of metabolites in plasma samples in patients with aneurysmal subarachnoid hemorrhage (aSAH) can highlight important alterations in critical metabolic pathways. As metabolites reflect changes associated with disease conditions, metabolite profiling (metabolomics) can identify candidate biomarkers for disease and potentially uncover pathways for intervention. METHODS We performed high throughput metabolite profiling across a broad spectrum of chemical classes (173 metabolites) on plasma samples taken from 119 patients with aSAH. Samples were drawn at 3 time points following ictus: 2–4, 7–10, and 12–14 days. Univariate and logistic regression analyses were performed to examine the relation of each metabolite with multiple outcome variables, including short- and long-term functional outcome (modified Rankin Scale, mRS). RESULTS >A good functional outcome (mRS 0–2) was found in 63.1% and 66.7% of patients at 30 and 90 days, respectively, following aSAH. Plasma concentrations of the endogenous cannabinoid anandamide during days 2–4 after aneurysmal SAH were decreased by 48.1% (P < 0.0001) and 57.6% (P <0.0001) in patients with mRS 0–2 at 30 and 90 days, respectively. A similar statistical result was noted with plasma anandamide concentrations averaged across all time periods. Logistic regression further demonstrated that anandamide remained an independent predictor of functional outcome (30 days: P = 0.04; 90 days: P = 0.03), even after adjusting for other factors that influence outcome, including age, World Federation of Neurological Surgeons grade (WFNS), Fisher grade, and symptomatic vasospasm. CONCLUSION Decreased plasma anandamide following aSAH predicts a good functional outcome at 30 and 90 days. While a role for anandamide in aneurysmal SAH has not been previously reported, elevated anandamide levels have been implicated in neuronal apoptosis and cerebral edema in the acutely injured brain. These data highlight the increasing capability of metabolomics techniques in profiling large-sized cohorts to illuminate novel markers of disease and potential metabolic regulators.

A randomized controlled trial of high-dose intravenous nicardipine in aneurysmal subarachnoid hemorrhage

1993 ◽  
Vol 78 (4) ◽  
pp. 537-547 ◽  
Author(s):  
E. Clarke Haley ◽  
Neal F. Kassell ◽  
James C. Torner ◽  
_ _
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Controlled Trial ◽  
Treated Group ◽  
High Dose ◽  
Similar Frequency ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Delayed Cerebral Vasospasm ◽  
Fine Print

✓ Because of their action as cerebral vasodilators, dihydropyridine calcium antagonists have received intense scrutiny for their potential benefit in ameliorating the devastating consequences of delayed cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). From October, 1987, to September, 1989, 41 North American neurosurgical centers in the Cooperative Aneurysm Study accrued 906 patients with recent (Days 0 to 7) aneurysmal SAH into a prospective randomized double-blind placebo-controlled trial of high-dose intravenous nicardipine to test whether treatment with this agent improved overall outcome. Eligible patients received 0.15 mg/kg/hr of either nicardipine or placebo by continuous infusion for up to 14 days following hemorrhage. The 449 patients randomly assigned to the nicardipine-treated group and the 457 patients assigned to the placebo-treated group were balanced with regard to prognostic factors for ischemic deficits from vasospasm and for overall outcome. Other medical and surgical interventions were used with similar frequency in both groups, except that antihypertensive agents were used less frequently in the nicardipine-treated patients (26% of the nicardipine-treated group vs. 43% of the placebo-treated group, p < 0.001), and more patients in the placebo-treated group had intentional hypervolemia, induced hypertension, and/or hemodilution administered therapeutically for symptomatic vasospasm (38% of the placebo-treated group vs. 25% of the nicardipine-treated group, p < 0.001). The incidence of symptomatic vasospasm during the treatment period was higher in the placebo-treated group (46%) than in the nicardipine-treated group (32%) (p < 0.001). Despite the reduction in symptomatic vasospasm in the nicardipine-treated group, overall outcome at 3 months was similar between the two groups. Fifty-five percent of nicardipine-treated patients were rated as having a good recovery according to the Glasgow Outcome Scale at follow-up review and 17% were dead, compared to 56% and 18%, respectively, in the placebo-treated group (not statistically significant). These data suggest that high-dose intravenous nicardipine treatment is associated with a reduced incidence of symptomatic vasospasm in patients with recent aneurysmal SAH, but not with an improvement in overall outcome at 3 months when compared to standard management in North America. It is postulated that, while nicardipine prevents vasospasm, hypertensive/hypervolemic therapy may be effective in reversing ischemic deficits from vasospasm once they occur.

Leukocytosis as an independent risk factor for cerebral vasospasm following aneurysmal subarachnoid hemorrhage

2003 ◽  
Vol 98 (6) ◽  
pp. 1222-1226 ◽  
Author(s):  
Matthew J. McGirt ◽  
John C. Mavropoulos ◽  
Laura Y. McGirt ◽  
Michael J. Alexander ◽  
Allan H. Friedman ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Leukocyte Count ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Fisher Grade ◽  
Increased Risk ◽  
Grade 3 ◽  
Fine Print

Object. The identification of patients at an increased risk for cerebral vasospasm after subarachnoid hemorrhage (SAH) may allow for more aggressive treatment and improved patient outcomes. Note, however, that blood clot size on admission remains the only factor consistently demonstrated to increase the risk of cerebral vasospasm after SAH. The goal of this study was to assess whether clinical, radiographic, or serological variables could be used to identify patients at an increased risk for cerebral vasospasm. Methods. A retrospective review was conducted in all patients with aneurysmal or spontaneous nonaneurysmal SAH who were admitted to the authors' institution between 1995 and 2001. Underlying vascular diseases (hypertension or chronic diabetes mellitus), Hunt and Hess and Fisher grades, patient age, aneurysm location, craniotomy compared with endovascular aneurysm stabilization, medications on admission, postoperative steroid agent use, and the occurrence of fever, hydrocephalus, or leukocytosis were assessed as predictors of vasospasm. Two hundred twenty-four patients were treated for SAH during the review period. One hundred one patients (45%) developed symptomatic vasospasm. Peak vasospasm occurred 5.8 ± 3 days after SAH. There were four independent predictors of vasospasm: Fisher Grade 3 SAH (odds ratio [OR] 7.5, 95% confidence interval [CI] 3.5–15.8), peak serum leukocyte count (OR 1.09, 95% CI 1.02–1.16), rupture of a posterior cerebral artery (PCA) aneurysm (OR 0.05, 95% CI 0.01–0.41), and spontaneous nonaneurysmal SAH (OR 0.14, 95% CI 0.04–0.45). A serum leukocyte count greater than 15 × 109/L was independently associated with a 3.3-fold increase in the likelihood of developing vasospasm (OR 3.33, 95% CI 1.74–6.38). Conclusions. During this 7-year period, spontaneous nonaneurysmal SAH and ruptured PCA aneurysms decreased the odds of developing vasospasm sevenfold and 20-fold, respectively. The presence of Fisher Grade 3 SAH on admission or a peak leukocyte count greater than 15 × 109/L increased the odds of vasospasm sevenfold and threefold, respectively. Monitoring of the serum leukocyte count may allow for early diagnosis and treatment of vasospasm.

scholarly journals Sphingosine 1-phosphate levels in cerebrospinal fluid after subarachnoid hemorrhage

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Anika Männer ◽  
Dominique Thomas ◽  
Marlies Wagner ◽  
Jürgen Konczalla ◽  
Helmuth Steinmetz ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Neurological Outcome ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
High Sensitivity ◽  
Control Subjects ◽  
Symptomatic Vasospasm ◽  
Significant Difference ◽  
Hemorrhage Volume

Abstract Background and purpose Sphingosin-1-phosphate (S1P) plays a crucial role as a signaling molecule in the immune system and the vasculature. Previous studies suggested a role as a vasoconstrictor of cerebral arteries via the S1P3-Receptor. Cerebral vasospasm (VS) following aneurysmal subarachnoid hemorrhage (SAH) is a major cause of disability and poor neurological outcome. Early detection of vasospasm could facilitate the prevention of cerebral ischemia in SAH patients. The aim of this prospective case-control study was to characterize the dynamics of S1P in the cerebrospinal fluid (CSF) of patients with SAH in relation to hemorrhage volume, the occurrence of VS, and neurological outcome. Methods S1P levels in CSF of 18 control subjects and 18 SAH patients with placement of an external ventricular drainage (EVD) were determined by high sensitivity mass spectrometry from day 1 through 14 after SAH onset. Hemorrhage volume, development of asymptomatic vasospasm (aVS) and symptomatic vasospasm (sVS), and neurological outcome were correlated to day 1 S1P levels. Results The intrathecal S1P levels of SAH patients were higher than those of the control subjects, and correlated with hemorrhage volume. There was no significant difference in S1P levels between patients with aVS and those with sVS. S1P levels significantly correlated with neurological outcome on a sliding modified Rankin scale. Conclusion S1P levels were highest directly after placement of the EVD and correlated strongly with hemorrhage volume, which may be caused by the intrathecal clot and subsequent lysis of red blood cells, an important source of S1P. We did not detect a second peak of S1P release over the course of the intensive care period.

scholarly journals Twenty-four–hour emergency intervention versus early intervention in aneurysmal subarachnoid hemorrhage

2018 ◽  
Vol 128 (5) ◽  
pp. 1297-1303 ◽  
Author(s):  
Joseph R. Linzey ◽  
Craig Williamson ◽  
Venkatakrishna Rajajee ◽  
Kyle Sheehan ◽  
B. Gregory Thompson ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Aneurysm Rupture ◽  
Ruptured Aneurysms ◽  
Academic Center ◽  
Diagnostic Angiography ◽  
Rebleeding Rate ◽  
Independent Review ◽  
Critical Care Management ◽  
Aneurysm Repair

OBJECTIVERecent observational data suggest that ultra-early treatment of ruptured aneurysms prevents rebleeding, thus improving clinical outcomes. However, advances in critical care management of patients with ruptured aneurysms may reduce the rate of rebleeding in comparison with earlier trials, such as the International Cooperative Study on the Timing of Aneurysm Surgery. The objective of the present study was to determine if an ultra-early aneurysm repair protocol will or will not significantly reduce the number of incidents of rebleeding following aneurysmal subarachnoid hemorrhage (SAH).METHODSA retrospective analysis of data from a prospectively collected cohort of patients with SAH was performed. Rebleeding was diagnosed as new or expanded hemorrhage on CT, which was determined by independent review conducted by multiple physicians. Preventability of rebleeding by ultra-early aneurysm clipping or coiling was also independently reviewed. Standard statistics were used to determine statistically significant differences between the demographic characteristics of those with rebleeding compared with those without.RESULTSOf 317 patients with aneurysmal SAH, 24 (7.6%, 95% CI 4.7–10.5) experienced rebleeding at any time point following initial aneurysm rupture. Only 1/24 (4.2%, 95% CI −3.8 to 12.2) incidents of rebleeding could have been prevented by a 24-hour ultra-early aneurysm repair protocol. The other 23 incidents could not have been prevented for the following reasons: rebleeding prior to admission to the authors’ institution (14/23, 60.9%); initial diagnostic angiography negative for aneurysm (4/23, 17.4%); postoperative rebleeding (2/23, 8.7%); patient unable to undergo operation due to medical instability (2/23, 8.7%); intraoperative rebleeding (1/23, 4.3%).CONCLUSIONSAt a single tertiary academic center, the overall rebleeding rate was 7.6% (95% CI 4.7–10.5) for those presenting with ruptured aneurysms. Implementation of a 24-hour ultra-early aneurysm repair protocol would only result in, at most, a 0.3% (95% CI −0.3 to 0.9) reduction in the incidence of rebleeding.

The deleterious effects of methamphetamine use on initial presentation and clinical outcomes in aneurysmal subarachnoid hemorrhage

2012 ◽  
Vol 117 (4) ◽  
pp. 781-786 ◽  
Author(s):  
Noah C. Beadell ◽  
Eric M. Thompson ◽  
Johnny B. Delashaw ◽  
Justin S. Cetas
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Glasgow Outcome Scale ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Multivariate Logistic Regression Analysis ◽  
Hospital Length ◽  
Hospital Length Of Stay ◽  
Strong Trend ◽  
Fisher Grade ◽  
Significant Difference

Object The objective of this study was to retrospectively look at methamphetamine (MA) use in patients with aneurysmal subarachnoid hemorrhage (SAH) to determine if MA use affects clinical presentation and outcomes after aneurysmal SAH. Methods A retrospective review of patients admitted to the Oregon Health & Science University neurosurgical service with aneurysmal SAH during the past 6 years was undertaken. Variables analyzed included MA use, age, sex, cigarette use, Hunt and Hess grade, Fisher grade, admission blood pressure, aneurysm characteristics, occurrence of vasospasm, hospital length of stay (LOS), cerebral infarction, aneurysm treatment, and Glasgow Outcome Scale (GOS) score. Data differences between MA users and nonusers were statistically analyzed using multivariate logistic regression analysis. A separate comparison with randomly selected age-matched nonuser controls was also performed. Results Twenty-eight (7%) of 374 patients with aneurysmal SAH were identified as MA users. Methamphetamine users were younger than nonusers (45.2 vs 55.9 years, respectively; p <0.001). Despite a younger age, MA users had significantly higher Hunt and Hess grades than nonusers (3.0 vs 2.5, respectively; p <0.020) and age-matched controls (3.0 vs 2.0, respectively; p <0.001). Earliest available mean arterial pressure was significantly higher in MA users (122.1 vs 109.7, respectively; p = 0.005) than all nonusers but not age-matched controls. Methamphetamine users had significantly higher vasospasm rates than nonusers (92.9% vs 71.1%, respectively; p = 0.008) but similar rates as age-matched controls (92.9% vs 89.3%, respectively; p = 0.500). Glasgow Outcome Scale score did not differ significantly between users and nonusers (3 vs 4, respectively; p = 0.170), but users had significantly lower GOS scores than age-matched controls (3 vs 5, respectively; p <0.001). There was no statistically significant difference in the LOS between users and nonusers (18 days vs 16 days, respectively; p = 0.431) or users and age-matched controls (18 days vs 14 days, respectively; p = 0.250). In the multivariate analysis, MA use (OR 3.777, p = 0.018), age (p <0.001), Fisher grade (p = 0.011), Hunt and Hess grade (p <0.001), and cerebral infarction (p <0.001) were predictors of poor GOS score. The only predictor of vasospasm was age (p <0.001), although a strong predictive trend in MA use (p = 0.149) was found. Predictors of a hospital LOS >15 days included age (p = 0.002), Fisher grade (p = 0.002), Hunt and Hess grade (p <0.001), and cerebral infarction (p <0.001). Predictors of cerebral infarction include male sex (p = 0.022) and Hunt and Hess grade (p = 0.006), with vasospasm demonstrating a strong trend (p = 0.056). Conclusions A history of MA use may predict poorer outcomes in patients who present with aneurysmal SAH. Methamphetamine users have significantly worse presentations and outcomes when compared with age-matched controls.

Cigarette smoking—induced increase in the risk of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage

1997 ◽  
Vol 87 (3) ◽  
pp. 381-384 ◽  
Author(s):  
Todd M. Lasner ◽  
Robert J. Weil ◽  
Howard A. Riina ◽  
Joseph T. King ◽  
Eric L. Zager ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Alcohol Abuse ◽  
Cigarette Smoking ◽  
Cerebral Vasospasm ◽  
Odds Ratio ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
World Federation ◽  
Symptomatic Vasospasm ◽  
Fisher Grade ◽  
Grade 3

✓ Vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is correlated with the thickness of blood within the basal cisterns on the initial computerized tomography (CT) scan. To identify additional risk factors for symptomatic vasospasm, the authors performed a prospective analysis of 75 consecutively admitted patients who were treated for aneurysmal SAH. Five patients who died before treatment or were comatose postoperatively were excluded from the study. Of the remaining 70 patients, demographic (age, gender, and race) and clinical (hypertension, diabetes, coronary artery disease, smoking, alcohol abuse, illicit drug use, sentinel headache, Fisher grade, Hunt and Hess grade, World Federation of Neurological Surgeons grade, and ruptured aneurysm location) parameters were evaluated using multivariate logistic regression to determine factors independently associated with cerebral vasospasm. All patients were treated with hypervolemic therapy and administration of nimodipine as prophylaxis for vasospasm. Cerebral vasospasm was suspected in cases that exhibited (by elevation of transcranial Doppler velocities) neurological deterioration 3 to 14 days after SAH with no other explanation and was confirmed either by clinical improvement in response to induced hypertension or by cerebral angiography. The mean age of the patients was 50 years. Sixty-three percent of the patients were women, 74% were white, 64% were cigarette smokers, and 46% were hypertensive. Ten percent of the patients suffered from alcohol abuse, 19% from sentinel bleed, and 49% had a Fisher Grade 3 SAH. Twenty-nine percent of the patients developed symptomatic vasospasm. Multivariate analysis demonstrated that cigarette smoking (p = 0.033; odds ratio 4.7, 95% confidence interval [CI] 2.4–8.9) and Fisher Grade 3, that is, thick subarachnoid clot (p = 0.008; odds ratio 5.1, 95% CI 2–13.1), were independent predictors of symptomatic vasospasm. The authors make the novel observation that cigarette smoking increases the risk of symptomatic vasospasm after aneurysmal SAH, independent of Fisher grade.

Effects of cilostazol on cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a multicenter prospective, randomized, open-label blinded end point trial

2013 ◽  
Vol 118 (1) ◽  
pp. 121-130 ◽  
Author(s):  
Nobuo Senbokuya ◽  
Hiroyuki Kinouchi ◽  
Kazuya Kanemaru ◽  
Yasuhiro Ohashi ◽  
Akira Fukamachi ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Control Group ◽  
Fisher Exact Test ◽  
Exact Test ◽  
Symptomatic Vasospasm ◽  
Angiographic Vasospasm ◽  
Significant Difference ◽  
Length Of Hospitalization

Object Cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is a major cause of subsequent morbidity and mortality. Cilostazol, a selective inhibitor of phosphodiesterase 3, may attenuate cerebral vasospasm because of its antiplatelet and vasodilatory effects. A multicenter prospective randomized trial was conducted to investigate the effect of cilostazol on cerebral vasospasm. Methods Patients admitted with SAH caused by a ruptured anterior circulation aneurysm who were in Hunt and Kosnik Grades I to IV and were treated by clipping within 72 hours of SAH onset were enrolled at 7 neurosurgical sites in Japan. These patients were assigned to one of 2 groups: the usual therapy group (control group) or the add-on 100 mg cilostazol twice daily group (cilostazol group). The group assignments were done by a computer-generated randomization sequence. The primary study end point was the onset of symptomatic vasospasm. Secondary end points were the onset of angiographic vasospasm and new cerebral infarctions related to cerebral vasospasm, clinical outcome as assessed by the modified Rankin scale, and length of hospitalization. All end points were assessed for the intention-to-treat population. Results Between November 2009 and December 2010, 114 patients with SAH were treated by clipping within 72 hours from the onset of SAH and were screened. Five patients were excluded because no consent was given. Thus, 109 patients were randomly assigned to the cilostazol group (n = 54) or the control group (n = 55). Symptomatic vasospasm occurred in 13% (n = 7) of the cilostazol group and in 40% (n = 22) of the control group (p = 0.0021, Fisher exact test). The incidence of angiographic vasospasm was significantly lower in the cilostazol group than in the control group (50% vs 77%; p = 0.0055, Fisher exact test). Multiple logistic analyses demonstrated that nonuse of cilostazol is an independent factor for symptomatic and angiographic vasospasm. The incidence of new cerebral infarctions was also significantly lower in the cilostazol group than in the control group (11% vs 29%; p = 0.0304, Fisher exact test). Clinical outcomes at 1, 3, and 6 months after SAH in the cilostazol group were better than those in the control group, although a significant difference was not shown. There was also no significant difference in the length of hospitalization between the groups. No severe adverse event occurred during the study period. Conclusions Oral administration of cilostazol is effective in preventing cerebral vasospasm with a low risk of severe adverse events. Clinical trial registration no. UMIN000004347, University Hospital Medical Information Network Clinical Trials Registry.

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