Simvastatin for the prevention of symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage: a single-institution prospective cohort study

2009 ◽  
Vol 110 (5) ◽  
pp. 968-974 ◽  
Author(s):  
Matthew J. McGirt ◽  
Giannina L. Garces Ambrossi ◽  
Judy Huang ◽  
Rafael J. Tamargo
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Mortality Rate ◽  
Hospital Mortality ◽  
Cerebral Vasospasm ◽  
Glasgow Outcome Scale ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Poor Outcome ◽  
Symptomatic Vasospasm ◽  
Scale Scores ◽  
Length Of Hospitalization

Object Vasospasm is the major cause of disability and death after aneurysmal subarachnoid hemorrhage (aSAH). Although the results of 2 randomized clinical trials demonstrated that statin decreases the incidence of symptomatic cerebral vasospasm after aSAH, retrospective studies have failed to confirm this. The authors conducted a prospective observational study to determine whether a standardized regimen of simvastatin would reduce the incidence of cerebral vasospasm and improve neurological outcomes in patients with aSAH. Methods Since 1991, all patients with aSAH admitted to the authors' institution have been prospectively followed up with standardized outcomes recording. Starting in September 2005, all patients admitted with aSAH were given enteral simvastatin (80 mg/day for 14 days) in addition to the standard care. The incidence of symptomatic cerebral vasospasm, length of hospitalization, in-hospital mortality rate, and discharge Glasgow Outcome Scale scores in these 170 patients were compared to data obtained in 170 consecutive patients who underwent treatment in our unit prior to the introduction of statin therapy. Results The 5-year study period included 340 consecutively treated patients (170 who received statins and 170 who did not). Patients who received simvastatin therapy were more frequently male (29 vs 20%) and had a smaller median aneurysm diameter (6 vs 7 mm). Baseline characteristics were otherwise similar between the cohorts. There were no differences in the incidence of symptomatic vasospasm (25.3 vs 30.5%; p = 0.277), in-hospital mortality rate (18 vs 15%; p = 0.468), length of hospitalization (21 ± 15 vs 19 ± 12 days; p = 0.281), or poor outcome at discharge (Glasgow Outcome Scale Scores 1–2: 21.7 vs 18.2%; p = 0.416) between the simvastatin and nonstatin cohorts. There were no statin-related complications. Conclusions The uniform introduction of simvastatin did not reduce the incidence of symptomatic cerebral vasospasm, death, or poor outcome in patients with aSAH. Simvastatin was well tolerated, but its benefit may be less than has been previously reported.

scholarly journals Increased levels of lipid peroxides as predictive of symptomatic vasospasm and poor outcome after aneurysmal subarachnoid hemorrhage

2002 ◽  
Vol 97 (6) ◽  
pp. 1302-1305 ◽  
Author(s):  
Takao Kamezaki ◽  
Kiyoyuki Yanaka ◽  
Sohji Nagase ◽  
Keishi Fujita ◽  
Noriyuki Kato ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Lipid Peroxides ◽  
Medical Complication ◽  
Content Type ◽  
Poor Outcome ◽  
Symptomatic Vasospasm ◽  
Delayed Cerebral Vasospasm ◽  
Fine Print

Object. Cerebral vasospasm remains a devastating medical complication of aneurysmal subarachnoid hemorrhage (SAH). Reactive oxygen species and subsequent lipid peroxidation are reported to participate in the causes of cerebral vasospasm. This clinical study was performed to investigate the relationships between levels of lipid peroxides in cerebrospinal fluid (CSF) and both delayed cerebral vasospasm and clinical outcome after SAH. Methods. Levels of phosphatidylcholine hydroperoxide (PCOOH) and cholesteryl ester hydroperoxide (CEOOH) in the CSF were measured in 20 patients with aneurysmal SAH. The patients' CSF was collected within 48 hours of hemorrhage onset and on Day 6 or 7 post-SAH. On Day 7, angiography was performed to verify the degree and extent of the vasospasm. The relationship between the patients' clinical profiles and the levels of lipid peroxides in the CSF were investigated. Both PCOOH and CEOOH were detectable in CSF, and their levels decreased within 7 days after onset of SAH. The levels of CEOOH within 48 hours after onset of hemorrhage were significantly higher in patients in whom symptomatic vasospasm later developed than in patients in whom symptomatic vasospasm did not develop (p = 0.002). Levels of PCOOH measured within 48 hours after onset of hemorrhage were significantly higher in patients with poor outcomes than in patients with good outcomes (p = 0.043). Conclusions. Increased levels of lipid peroxides measured in the CSF during the acute stage of SAH were predictive of both symptomatic vasospasm and poor outcome. Measurements of lipid peroxides in the CSF may be useful prognostically for patient outcomes as well as for predicting symptomatic vasospasm.

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.

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.

Effect of Cilostazol on Cerebral Vasospasm and Outcome in Patients with Aneurysmal Subarachnoid Hemorrhage: A Randomized, Double-Blind, Placebo-Controlled Trial

2016 ◽  
Vol 42 (1-2) ◽  
pp. 97-105 ◽  
Author(s):  
Naoya Matsuda ◽  
Masato Naraoka ◽  
Hiroki Ohkuma ◽  
Norihito Shimamura ◽  
Katsuhiro Ito ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Control Group ◽  
Independent Factor ◽  
Double Blind ◽  
End Points ◽  
Double Blind Placebo ◽  
Poor Outcome

Background: Several clinical studies have indicated the efficacy of cilostazol, a selective inhibitor of phosphodiesterase 3, in preventing cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). They were not double-blinded trial resulting in disunited results on assessment of end points among the studies. The randomized, double-blind, placebo-controlled study was performed to assess the effectiveness of cilostazol on cerebral vasospasm. Methods: Patients with aneurysmal SAH admitted within 24 h after the ictus who met the following criteria were enrolled in this study: SAH on CT scan was diffuse thick, diffuse thin, or local thick, Hunt and Hess score was less than 4, administration of cilostazol or placebo could be started within 48 h of SAH. Patients were randomly allocated to placebo or cilostazol after repair of a ruptured saccular aneurysm by aneurysmal neck clipping or endovascular coiling, and the administration of cilostazol or placebo was continued up to 14 days after initiation of treatment. The primary end point was the occurrence of symptomatic vasospasm (sVS), and secondary end points were angiographic vasospasm (aVS) evaluated on digital subtraction angiography, vasospasm-related new cerebral infarction evaluated on CT scan or MRI, and clinical outcome at 3 months of SAH as assessed by Glasgow Outcome Scale, in which poor outcome was defined as severe disability, vegetative state, and death. All end points were evaluated with blinded assessment. Results: One hundred forty eight patients were randomly allocated to the cilostazol group (n = 74) or the control group (n = 74). The occurrence of sVS was significantly lower in the cilostazol group than in the control group (10.8 vs. 24.3%, p = 0.031), and multiple logistic analysis showed that cilostazol use was an independent factor reducing sVS (OR 0.293, 95% CI 0.099-0.568, p = 0.027). The incidence of aVS and vasospasm-related cerebral infarction were not significantly different between the groups. Poor outcome was significantly lower in the cilostazol group than in the control group (5.4 vs. 17.6%, p = 0.011), and multiple logistic analyses demonstrated that cilostazol use was an independent factor that reduced the incidence of poor outcome (OR 0.221, 95% CI 0.054-0.903, p = 0.035). Severe adverse events due to cilostazol administration did not occur during the study period. Conclusions: Cilostazol administration is effective in preventing sVS and improving outcomes without severe adverse events. A larger-scale study including more cases was necessary to confirm this efficacy of cilostazol.

STATIN USE WAS NOT ASSOCIATED WITH LESS VASOSPASM OR IMPROVED OUTCOME AFTER SUBARACHNOID HEMORRHAGE

Neurosurgery ◽  
2008 ◽  
Vol 62 (2) ◽  
pp. 422-430 ◽  
Author(s):  
Andreas H. Kramer ◽  
Matthew J. Gurka ◽  
Bart Nathan ◽  
Aaron S. Dumont ◽  
Neal F. Kassell ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Vegetative State ◽  
Treatment Protocol ◽  
Poor Outcome ◽  
Reductase Inhibitors ◽  
Symptomatic Vasospasm ◽  
Endovascular Coil Embolization ◽  
Baseline Characteristics ◽  
Statin Use

Abstract OBJECTIVE The development of delayed ischemia caused by cerebral vasospasm remains a common cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage. Preliminary studies suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) may decrease the risk of vasospasm, but additional study is required. METHODS Beginning in May 2006, our treatment protocol for patients presenting with subarachnoid hemorrhage was altered to routinely include the use of 80 mg of simvastatin per day for 14 days. Before this time, only patients with other indications for statins were treated. The charts of 203 consecutive patients over a period of 27 months were retrospectively reviewed, and 150 patients were included in the analysis, of whom 71 patients received statins. These patients were compared with 79 untreated patients to determine whether or not the use of statins was associated with a reduction in the occurrence of vasospasm, delayed infarction, or poor outcome (death, vegetative state, or severe disability). RESULTS Patients who were treated with statins and those who were not had similar baseline characteristics, although more patients in the former group were managed with endovascular coil embolization. There were no statistically significant differences in the proportion of patients developing at least moderate radiographic vasospasm (41% with statins versus 42% without, P = 0.91), symptomatic vasospasm (32% with statins versus 25% without, P = 0.34), delayed infarction (23% with statins versus 28% without, P = 0.46), or poor outcome (39% with statins versus 35% without, P = 0.61). After adjustment for differences in baseline characteristics, including the method of aneurysm treatment, statins were still not significantly protective. CONCLUSION The addition of statins to standard care was not associated with any reduction in the development of vasospasm or improvement in outcomes after aneurysmal subarachnoid hemorrhage. If there is a benefit to statin use, it may be smaller than suggested by previous studies. However, further randomized controlled trials are awaited.

Persistent perioperative hyperglycemia as an independent predictor of poor outcome after aneurysmal subarachnoid hemorrhage

2007 ◽  
Vol 107 (6) ◽  
pp. 1080-1085 ◽  
Author(s):  
Matthew J. McGirt ◽  
Graeme F. Woodworth ◽  
Mohammed Ali ◽  
Khoi D. Than ◽  
Rafael J. Tamargo ◽  
...  
Keyword(s):  
Multivariate Analysis ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Univariate Analysis ◽  
Serum Glucose ◽  
Glucose Levels ◽  
Poor Outcome ◽  
Persistent Hyperglycemia

Object The authors of previous studies have shown that admission hyperglycemia or perioperative hyperglycemic events may predispose a patient to poor outcome after aneurysmal subarachnoid hemorrhage (SAH). The results of experimental evidence have suggested that hyperglycemia may exacerbate ischemic central nervous system injury. It remains to be clarified whether a single hyperglycemic event or persistent hyperglycemia is predictive of poor outcome after aneurysmal SAH. Methods Ninety-seven patients undergoing treatment for aneurysmal SAH were observed, and all perioperative variables were entered into a database of prospectively recorded data. Daily serum glucose values were retrospectively added. Patients were examined at hospital discharge (14–21 days after SAH onset), and Glasgow Outcome Scale (GOS) scores were prospectively documented. The GOS score at last follow-up was retrospectively determined. Serum glucose greater than 200 mg/dl for 2 or more consecutive days was defined as persistent hyperglycemia. Outcome was categorized as “poor” (dependent function [GOS Score 1–3]) or “good” (independent function [GOS Score 4 or 5]) at discharge. The independent association of 2-week and final follow-up outcome (GOS score) with the daily serum glucose levels was assessed using a multivariate analysis. Results In the univariate analysis, increasing age, increasing Hunt and Hess grade, hypertension, ventriculomegaly on admission computed tomography scan, Caucasian race, and higher mean daily glucose levels were associated with poor (dependent) 2-week outcome after aneurysmal SAH. In the multivariate analysis, older age, the occurrence of symptomatic cerebral vasospasm, increasing admission Hunt and Hess grade, and persistent hyperglycemia were independent predictors of poor (dependent) outcome 2 weeks after aneurysmal SAH. Admission Hunt and Hess grade and persistent hyperglycemia were independent predictors of poor outcome at last follow-up examination a mean 10 ± 3 months after aneurysmal SAH. Isolated hyperglycemic events did not predict poor outcome. Patients with persistent hyperglycemia were 10-fold more likely to have a poor (dependent) 2-week outcome and sevenfold more likely to have a poor outcome a mean 10 months after aneurysmal SAH independent of admission Hunt and Hess grade, occurrence of cerebral vasospasm, or all comorbidities. Conclusions Patients with persistent hyperglycemia were seven times more likely to have a poor outcome at a mean of 10 months after aneurysmal SAH. Isolated hyperglycemic events were not predictive of poor outcome. Serum glucose levels in the acute setting of aneurysmal SAH may help predict outcomes months after surgery.

Effect of stress-induced hyperglycemia after non-traumatic non-aneurysmal subarachnoid hemorrhage on clinical complications and functional outcomes

2021 ◽  
Author(s):  
Zeyu Zhang ◽  
Yue Zhao ◽  
Yibo Liu ◽  
Xiaoyu Wang ◽  
Houshi Xu ◽  
...  
Keyword(s):  
Risk Factors ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Functional Outcomes ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Complication Rates ◽  
Poor Outcome ◽  
Clinical Complications ◽  
Symptomatic Vasospasm ◽  
Poor Outcomes

Abstract Background Despite having an overall benign course, non-traumatic non-aneurysmal subarachnoid hemorrhage (naSAH) is still accompanied by a risk of clinical complications and poor outcomes. Risk factors and mechanisms of complications and poor outcomes after naSAH remain unknown. Our aim was to explore the effect of stress-induced hyperglycemia (SIH) on complication rates and functional outcomes in naSAH patients. Methods We retrospectively reviewed patients with naSAH admitted to our institution between 2013 and 2018. SIH was identified according to previous criterion. Symptomatic vasospasm, delayed cerebral infarction, and hydrocephalus were identified as main complications. Outcomes were reviewed using a modified Rankin Scale (mRS) at discharge, 3 months, and 12 months. A statistical analysis of clinical, radiological, and laboratory risk factors of complications and outcomes was conducted. Results 244 naSAH patients were incorporated in the cohort with 74 (30.3%) SIH. After adjusting for age, gender, hypertension, Hunt and Hess (HH) grade, modified Fisher Scale (mFS), intraventricular hemorrhage (IVH), and subarachnoid blood distribution, SIH was significantly associated with symptomatic vasospasm (P < 0.001, 12.176 [4.904–30.231]), delayed cerebral infarction (P < 0.001, 12.434 [3.850-40.161]), hydrocephalus (P = 0.008, 5.771 [1.570-21.222]), and poor outcome at 12 months (P = 0.006, 5.506 [1.632–18.581]), whereas the correlation between SIH and poor outcome at discharge (P = 0.064, 2.409 [0.951-6.100]) or 3 months (P = 0.110, 2.029 [0.852–4.833]) was not significant. Incorporation of SIH increased the area under curve (AUC) of ROC in the combined model for predicting symptomatic vasospasm (P = 0.002), delayed cerebral infarction (P = 0.024), hydrocephalus (P = 0.037), and 12-month poor outcome (P = 0.087). Conclusions SIH is a significant and independent risk factor for symptomatic vasospasm, delayed cerebral infarction, hydrocephalus, and long-term poor outcome in naSAH patients. Identifying SIH early after naSAH is important for decision-making and treatment planning.

Does Intracisternal Thrombolysis Prevent Vasospasm after Aneurysmal Subarachnoid Hemorrhage? A Meta-analysis

Neurosurgery ◽  
2004 ◽  
Vol 54 (2) ◽  
pp. 326-335 ◽  
Author(s):  
Sepideh Amin-Hanjani ◽  
Christopher S. Ogilvy ◽  
Fred G. Barker
Keyword(s):  
Subarachnoid Hemorrhage ◽  
High Risk ◽  
Confidence Interval ◽  
Glasgow Outcome Scale ◽  
Treatment Effects ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Meta Analysis ◽  
Neurological Deficits ◽  
Controlled Trials ◽  
Scale Scores

Abstract OBJECTIVE Despite existing strategies for the treatment of vasospasm after aneurysmal subarachnoid hemorrhage, vasospasm remains a persistent contributor to death and disability. The intracisternal application of thrombolytic agents to dissolve subarachnoid clot has been advocated. The goal of this analysis was to assess the currently available evidence regarding the effectiveness of this treatment. METHODS We conducted a systematic review of the published literature; all controlled trials were included. The outcomes of interest were delayed ischemic neurological deficits, poor Glasgow Outcome Scale scores, and death. A formal meta-analysis was performed with a random-effects model. RESULTS The search revealed nine trials or trial subgroups (only one of which was randomized), with a total enrollment of 652 patients. Pooled results demonstrated beneficial effects of treatment, with absolute risk reductions of 14.4% (95% confidence interval, 6.5–22.5%; P &lt; 0.001) for delayed ischemic neurological deficits, 9.5% (95% confidence interval, 4.2–14.8%; P &lt; 0.01) for poor Glasgow Outcome Scale scores, and 4.5% (95% confidence interval, 1.5–7.5%; P &lt; 0.05) for death. Regression analysis revealed that treatment effects did not significantly differ among the studies on the basis of the type of thrombolytic agent used (tissue plasminogen activator versus urokinase) or the method of administration (intraoperative versus postoperative) (P &gt; 0.10). Studies that enrolled only patients at high risk for vasospasm seemed to demonstrate greater treatment effects. CONCLUSION The meta-analysis suggests a clinically relevant and statistically significant beneficial effect of intracisternal thrombolysis. However, the results of the analysis are limited by the predominance of nonrandomized studies. Further randomized, blinded, placebo-controlled trials of high-risk patients would be justified.

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