Endovascular treatment for cerebral vasospasm following aneurysmal subarachnoid hemorrhage: predictors of outcome and retreatment

2017 ◽  
Vol 10 (4) ◽  
pp. 367-374 ◽  
Author(s):  
Jennifer D Sokolowski ◽  
Ching-Jen Chen ◽  
Dale Ding ◽  
Thomas J Buell ◽  
Daniel M Raper ◽  
...  
Keyword(s):  
Multivariate Analysis ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Initial Treatment ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Smoking Status ◽  
Functional Independence ◽  
Study Cohort ◽  
Good Outcome ◽  
Symptomatic Vasospasm

ObjectiveAlthough endovascular therapy has been widely adopted for the treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH), its effect on clinical outcomes remains incompletely understood. The aims of this retrospective cohort study are to evaluate the outcomes of endovascular intervention for post-aSAH vasospasm and identify predictors of functional independence at discharge and repeat endovascular vasospasm treatment.MethodsWe assessed the baseline and outcomes data for patients with aSAH who underwent endovascular vasospasm treatment at our institution, including intra-arterial (IA) vasodilator infusion and angioplasty. Statistical analyses were performed to determine factors associated with good outcome at discharge (modified Rankin Scale 0–2) and repeat endovascular vasospasm treatment.ResultsThe study cohort comprised 159 patients with a mean age of 52 years. Good outcome was achieved in 17% of patients at discharge (26/150 patients), with an in-hospital mortality rate of 22% (33/150 patients). In the multivariate analysis, age (OR 0.895; p=0.009) and positive smoking status (OR 0.206; p=0.040) were negative independent predictors of good outcome. Endovascular retreatment was performed in 34% (53/156 patients). In the multivariate analysis, older age (OR 0.950; p=0.004), symptomatic vasospasm (OR 0.441; p=0.046), initial treatment with angioplasty alone (OR 0.096; p=0.039), and initial treatment with combined IA vasodilator infusion and angioplasty (OR 0.342; p=0.026) were negative independent predictors of retreatment.ConclusionWe found a modest rate of functional independence at discharge in patients with aSAH who underwent endovascular vasospasm treatment. Older patients and smokers had worse functional outcomes at discharge. Initial use of angioplasty appears to decrease the need for subsequent retreatment.

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.

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.

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 Multivariate Analysis of Predictors of Cerebral Vasospasm Occurrence After Aneurysmal Subarachnoid Hemorrhage

Stroke ◽  
1999 ◽  
Vol 30 (7) ◽  
pp. 1402-1408 ◽  
Author(s):  
Claire Charpentier ◽  
Gerard Audibert ◽  
Francis Guillemin ◽  
Thierry Civit ◽  
Xavier Ducrocq ◽  
...  
Keyword(s):  
Multivariate Analysis ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage

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.

ANGIOGRAPHIC AND HEMODYNAMIC EFFECT OF HIGH CONCENTRATION OF INTRA-ARTERIAL NICARDIPINE IN CEREBRAL VASOSPASM

Neurosurgery ◽  
2008 ◽  
Vol 63 (6) ◽  
pp. 1080-1087 ◽  
Author(s):  
Italo Linfante ◽  
Raquel Delgado-Mederos ◽  
Vincenzo Andreone ◽  
Matthew Gounis ◽  
Laura Hendricks ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Subarachnoid Hemorrhage ◽  
Intracranial Pressure ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Vessel Diameter ◽  
High Concentration ◽  
Symptomatic Vasospasm ◽  
High Concentrations

Abstract OBJECTIVE Nicardipine has been used to treat cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage. Intra-arterial (IA) infusion of high concentrations of nicardipine decreases procedure time, but it may affect hemodynamic parameters. In addition, a quantitative measurement of improvement of vessel diameter on the angiograms has not been performed. METHODS We conducted a single-center, retrospective database analysis of consecutive patients with symptomatic vasospasm after aneurysmal subarachnoid hemorrhage who failed medical management and received IA nicardipine between September 2005 and June 2006. Nicardipine (1 mg/mL/min) was infused intra-arterially by microcatheter. Blood pressure, heart rate, and intracranial pressure were recorded during the infusion. The effect of IA nicardipine on the vessel's diameter was measured on angiography by two blinded investigators. RESULTS Forty-six treatment sessions were performed in 22 consecutive patients (13 women; age, 56.4 ±13 years). Fourteen patients received IA nicardipine alone, and 8 patients had additional angioplasty. The average nicardipine dose was 12 ± 10 mg (range, 2–25 mg). The mean decrease of systolic, diastolic, and mean blood pressure was 17.4 ± 18.3 mm Hg, 7.7 ± 10.4 mm Hg, and 10.9 ± 11.6 mm Hg, respectively. There was no change in intracranial pressure. Measurement of 49 vessels in the 14 patients treated with nicardipine alone showed a significant increase in arterial diameters (range, 1–74%; P < 0.0001). At the time of discharge, 11 patients (50%) were functionally independent (modified Rankin Scale score, 0–2). CONCLUSION High concentrations of IA nicardipine infusion have a reversible effect on blood pressure and heart rate. IA nicardipine results also in a significant improvement in vessel diameter in patients with vasospasm after aneurysmal subarachnoid hemorrhage.

367 Functional Outcome in Patients with Refractory Cerebral Vasospasm Treated with Repeat Instant Endovascular Interventions

Neurosurgery ◽  
2017 ◽  
Vol 64 (CN_suppl_1) ◽  
pp. 285-286
Author(s):  
Lukas Andereggen ◽  
Juergen Beck ◽  
Werner Z’Graggen ◽  
Gerhard Schroth ◽  
Robert H Andres ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Functional Outcome ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Rescue Therapy ◽  
Inclusion Criteria ◽  
Significant Independent Predictor ◽  
Good Outcome ◽  
Endovascular Interventions

Abstract INTRODUCTION For patients suffering from cerebral vasospasm refractory to medical and hemodynamic therapies, endovascular interventions often remain the last resort. Data from studies in large cohorts on the efficacy and safety of multiple immediate endovascular interventions are sparse. Our aim was to assess the functional outcome of multiple repeated instant endovascular interventions in patients with cerebral vasospasm refractory to medical, hemodynamic, and initial endovascular interventions. METHODS A single-center retrospective study of prospectively collected data on patients suffering from cerebral vasospasm refractory to therapies requiring at least 3 endovascular interventions during the course of treatment following aneurysmal subarachnoid hemorrhage. The primary endpoint was functional outcome at last follow-up (mRS <3). The secondary endpoint was angiographic response to endovascular therapies and appearance of cerebral infarctions. RESULTS >Over a 4-year period, 365 patients with aneurysmal subarachnoid hemorrhage were treated at our institution. Thirty-one (8.5%) met the inclusion criteria. In 52 (14%) patients, <3 endovascular interventions were performed as rescue therapy for refractory cerebral vasospasm. At last follow-up, a good outcome was noted in 18 (58%) patients with 3 or more interventions compared to 31 (61%) of those with 1 or 2 interventions (P = 0.82). The initial Hunt and Hess score <3 was a significant independent predictor of good outcome (OR 4.7, 95% CI, 1.2 18.5; P = 0.03), whereas infarcts in eloquent brain areas were significantly associated with a poor outcome (mRS 3 6; OR 13.5, 95% CI, 2.3 81.2; P = 0.004). CONCLUSION Repeated instant endovascular intervention is an aggressive but feasible last resort treatment strategy with a favorable outcome in two-thirds of patients with refractory cerebral vasospasm and in whom endovascular treatment has already been initiated.

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.

Cerebral vasospasm and delayed cerebral infarctions in 225 patients with non-aneurysmal subarachnoid hemorrhage: the underestimated risk of Fisher 3 blood distribution

2016 ◽  
Vol 8 (12) ◽  
pp. 1247-1252 ◽  
Author(s):  
Juergen Konczalla ◽  
Sepide Kashefiolasl ◽  
Nina Brawanski ◽  
Stephanie Lescher ◽  
Christian Senft ◽  
...  
Keyword(s):  
Multivariate Analysis ◽  
Subarachnoid Hemorrhage ◽  
Elderly Patients ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Patient Characteristics ◽  
Unfavorable Outcome ◽  
Bleeding Pattern ◽  
Excellent Outcome ◽  
Increased Risk

ObjectiveRecent data have shown increasing numbers of non-aneurysmal subarachnoid hemorrhage (NASAH). However, data are limited and often only small series have been published. Our objective was to analyze the rate of cerebral vasospasm (CVS), delayed cerebral infarction (DCI), and their influence on the clinical outcome, especially in patients with diffuse Fisher 3 bleeding pattern NASAH (Fi3).MethodsBetween 1999 and 2014, 225 patients had NASAH. CVS, DCI, and outcome (according to the modified Rankin Scale at 6 months) were analyzed retrospectively. Patients were stratified according to the bleeding type. After univariate analysis a multivariate analysis was performed and NASAH Fi3 was also compared with aneurysmal SAH Fi3.ResultsPatient characteristics and the outcome of perimesencephalic (PM) and non-PM (NPM) SAH were similar. Excluding Fi3, PM and NPM without Fi3 had similar patient characteristics, clinical course, and outcome. In particular, the Fi3 subgroup had a significantly increased risk of CVS, DCI, unfavorable outcome, hydrocephalus, and death. Early hydrocephalus was associated with Fi3 and intraventricular hemorrhage. The multivariate regression model showed the variables elderly patients, Fi3, and early hydrocephalus as independent and significant predictors for an unfavorable outcome. A further comparison of NASAH Fi3 with aneurysmal SAH Fi3 showed similar characteristics, CVS rate, and mortality.ConclusionsPatients with NASAH without a Fi3 bleeding pattern had a similar excellent outcome to patients with PM-SAH. Patients with Fi3 had a high risk for early hydrocephalus, CVS, DCI, and an unfavorable outcome, similar to patients with aneurysmal SAH. After multivariate analysis, early hydrocephalus, elderly patients, and Fi3 were identified as negative prognostic factors. Therefore, patients with Fi3 are at risk and need careful clinical observation.

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.

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