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.

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.

Effect of AT877 on cerebral vasospasm after aneurysmal subarachnoid hemorrhage

1992 ◽  
Vol 76 (4) ◽  
pp. 571-577 ◽  
Author(s):  
Masato Shibuya ◽  
Yoshio Suzuki ◽  
Kenichiro Sugita ◽  
Isamu Saito ◽  
Tomio Sasaki ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Double Blind Trial ◽  
Double Blind ◽  
Content Type ◽  
Blind Trial ◽  
Symptomatic Vasospasm ◽  
Delayed Cerebral Vasospasm ◽  
Number Of Patients ◽  
Fine Print

✓ With the cooperation of 60 neurosurgical centers in Japan, a prospective randomized placebo-controlled double-blind trial of a new calcium antagonist AT877 (hexahydro-1-(5-isoquinolinesulfonyl)-1H-1,4-diazepine hydrochloride, or fasudil hydrochloride) was undertaken to determine the drug's effect on delayed cerebral vasospasm in patients with a ruptured cerebral aneurysm. A total of 276 patients, who underwent surgery within 3 days after subarachnoid hemorrhage (SAH) of Hunt and Hess Grades I to IV, were entered into the study. Nine patients were excluded because of protocol violation. The remaining 267 patients received either 30 mg AT877 or a placebo (saline) by intravenous injection over 30 minutes, three times a day for 14 days following surgery. Demographic and clinical data were well matched between the two groups. It was found that AT877 reduced angiographically demonstrable vasospasm by 38% (from 61% in the placebo group to 38% in the AT877 group, p = 0.0023), low-density regions on computerized tomography associated with vasospasm by 58% (from 38% to 16%, p = 0.0013), and symptomatic vasospasm by 30% (from 50% to 35%, p = 0.0247). Furthermore, AT877 reduced the number of patients with a poor clinical outcome associated with vasospasm (moderate disability or worse on the Glasgow Outcome Scale at 1 month after SAH) by 54% (from 26% to 12%, p = 0.0152). There were no serious adverse events reported in the AT877 group. This is the first report of a placebo-controlled double-blind trial that has demonstrated a significant reduction in angiographically revealed vasospasm by intravenous drug therapy.

Age and outcome after aneurysmal subarachnoid hemorrhage: why do older patients fare worse?

1996 ◽  
Vol 85 (3) ◽  
pp. 410-418 ◽  
Author(s):  
Giuseppe Lanzino ◽  
Neal F. Kassell ◽  
Teresa P. Germanson ◽  
Gail L. Kongable ◽  
Laura L. Truskowski ◽  
...  
Keyword(s):  
Prognostic Factors ◽  
Subarachnoid Hemorrhage ◽  
Age Groups ◽  
Age Group ◽  
Content Type ◽  
Poor Outcome ◽  
Symptomatic Vasospasm ◽  
Age Related ◽  
Increased Risk ◽  
Fine Print

✓ Advanced age is a recognized prognostic indicator of poor outcome after subarachnoid hemorrhage (SAH). The relationship of age to other prognostic factors and outcome was evaluated using data from the multicenter randomized trial of nicardipine in SAH conducted in 21 neurosurgical centers in North America. Among the 906 patients who were studied, five different age groups were considered: 40 years or less, 41 to 50, 51 to 60, 61 to 70, and more than 71 years. Twenty-three percent of the individuals enrolled were older than 60 years of age. Women outnumbered men in all age groups. Level of consciousness (p = 0.0002) and World Federation of Neurological Surgeons grade (p = 0.0001) at admission worsened with advancing age. Age was also related to the presence of a thick subarachnoid clot (p = 0.0001), intraventricular hemorrhage (p = 0.0003), and hydrocephalus (p = 0.0001) on an admission computerized tomography scan. The rebleeding rate increased from 4.5% in the youngest age group to 16.4% in patients more than 70 years of age (p = 0.002). As expected, preexisting medical conditions, such as diabetes (p = 0.028), hypertension (p = 0.0001), and pulmonary (p = 0.0084), myocardial (p = 0.0001), and cerebrovascular diseases (p = 0.0001), were positively associated with age. There were no age-related differences in the day of admission following SAH, timing of the surgery and/or location, and size (small vs. large) of the ruptured aneurysm. During the treatment period, the incidence of severe complications (that is, those complications considered life threatening by the reporting investigator) increased with advancing age, occurring in 28%, 33%, 36%, 40%, and 46% of the patients in each advancing age group, respectively (p = 0.0002). No differences were observed in the reported frequency of surgical complications. No age-related differences were found in the overall incidence of angiographic vasospasm; however, symptomatic vasospasm was more frequently reported in the older age groups (p = 0.01). Overall outcome, assessed using the Glasgow Outcome Scale at 3 months post-SAH, was poorer with advancing age (p < 0.001). Multivariate analysis of overall outcome, adjusting for the different prognostic factors, did not remove the age effect, which suggests that the aging brain has a less optimal response to the initial bleeding. Age as a risk factor is a continuum; however, there seems to be a significant increased risk of poor outcome after the age of 60 years.

Hyperglycemia, excess weight, and history of hypertension as risk factors for poor outcome and cerebral infarction after aneurysmal subarachnoid hemorrhage

2005 ◽  
Vol 102 (6) ◽  
pp. 998-1003 ◽  
Author(s):  
Seppo Juvela ◽  
Jari Siironen ◽  
Johanna Kuhmonen
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Patient Outcomes ◽  
Plasma Glucose ◽  
Clinical Condition ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Poor Outcome ◽  
History Of ◽  
Fine Print

Object. Stress-induced hyperglycemia has been shown to be associated with poor outcome after aneurysmal subarachnoid hemorrhage (SAH). The authors prospectively tested whether hyperglycemia, independent of other factors, affects patient outcomes and the occurrence of cerebral infarction after SAH. Methods. Previous diseases, health habits, medications, clinical condition, and neuroimaging variables were recorded for 175 patients with SAH who were admitted to the hospital within 48 hours after bleeding. The plasma level of glucose was measured at admission and the fasting value of glucose was measured in the morning after aneurysm occlusion. Factors found to be independently predictive of patient outcomes at 3 months after SAH onset and the appearance of cerebral infarction were tested by performing multiple logistic regression. Plasma glucose values at admission were found to be associated with patient age, body mass index (BMI), history of hypertension, clinical condition, amount of subarachnoid or intraventricular blood, shunt-dependent hydrocephalus, outcome variables, and the appearance of cerebral infarction. When considered independently of age, clinical condition, or amount of subarachnoid, intraventricular, or intracerebral blood, the plasma glucose values at admission predicted poor outcome (per millimole/liter the odds ratio [OR] was 1.24 with a 95% confidence interval [CI] of 1.02–1.51). After an adjustment was made for the amount of subarachnoid blood, the clinical condition, and the duration of temporary artery occlusion during surgery, the BMI was found to be a significant predictor (per kilogram/square meter the OR was 1.15 with a 95% CI of 1.02–1.29) for the finding of cerebral infarction on the follow-up computerized tomography scan. Hypertension (OR 3.11, 95% CI 1.11–8.73)—but not plasma glucose (OR 1.06, 95% CI 0.87–1.29)—also predicted the occurrence of infarction when tested instead of the BMI. Conclusions. Independent of the severity of bleeding, hyperglycemia at admission seems to impair outcome, and excess weight and hypertension appear to elevate the risk of cerebral infarction after SAH.

Efficacy of transluminal angioplasty for the management of symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage

2000 ◽  
Vol 92 (2) ◽  
pp. 284-290 ◽  
Author(s):  
Richard S. Polin ◽  
Volker A. Coenen ◽  
Carolyn Apperson Hansen ◽  
Peter Shin ◽  
Mustafa K. Baskaya ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Scale Score ◽  
Cerebral Vasospasm ◽  
Medical Management ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Conditional Logistic Regression ◽  
Study Drug ◽  
Transluminal Angioplasty ◽  
Content Type ◽  
Fine Print

Object. Transluminal angioplasty has become a widely used adjunct therapy to medical management of symptomatic cerebral vasospasm following subarachnoid hemorrhage (SAH). Despite anecdotal reports of universal, angiographically confirmed reversal of vasospasm and high rates of clinical improvement, no rigorous examination of the efficacy of this procedure has been conducted. In this study the authors assess the efficacy of the aforementioned procedure.Methods. Thirty-eight patients enrolled as part of the North American trial of tirilazad in aneurysmal SAH underwent transluminal angioplasty for symptomatic cerebral vasospasm. Fifty-three percent of these patients showed good recovery or moderate disability based on their 3-month Glasgow Outcome Scale score.Among the 38 patients who underwent angioplasty, the severity and type of vasospasm, use of papaverine in addition to balloon angioplasty, timing of treatment, and dose of study drug did not have an effect on the outcome. The results of their neurological examinations improved in only four of the 38 patients immediately after the procedure. A conditional logistic regression analysis was performed in which these patients were compared with individuals matched for age, sex, dose of study drug, admission neurological grade, and modified Glasgow Coma Scale score at the time of angioplasty. No effect on favorable outcomes was found for this procedure.Conclusions. Transluminal cerebral angioplasty is very effective in reversing angiographically confirmed vasospasm, and anecdotal reports of its clinical utility are numerous. However, in this report the authors conclude that its superiority to medical management for symptomatic cerebral vasospasm is questionable.

Neuropeptide Y in the primate model of subarachnoid hemorrhage

1992 ◽  
Vol 77 (3) ◽  
pp. 417-423 ◽  
Author(s):  
Ryszard M. Pluta ◽  
Anna Deka-Starosta ◽  
Alois Zauner ◽  
Jay K. Morgan ◽  
Karin M. Muraszko ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Neuropeptide Y ◽  
Cerebral Vasospasm ◽  
Primate Model ◽  
Content Type ◽  
Peripheral Plasma ◽  
Delayed Cerebral Vasospasm ◽  
Arterial Plasma ◽  
Fine Print

✓ The cause of cerebral vasospasm after subarachnoid hemorrhage (SAH) remains unknown. Recently, an association between the potent vasoconstricting peptide, neuropeptide Y, and delayed cerebral vasospasm after SAH has been postulated. This was based on the findings of increased neuropeptide Y levels in the cerebrospinal fluid (CSF) and plasma after SAH in animals and humans. For this study, the primate model of SAH was used to assess the possible role of neuropeptide Y in delayed vasospasm after SAH. Fifteen cynomolgus monkeys underwent placement of a clot of either whole blood or red blood cells in the subarachnoid space around the middle cerebral artery (MCA). Sequential arteriography for assessment of MCA diameter and sampling of blood and CSF for neuropeptide Y were performed: before SAH (Day 0); 7 days after SAH, when signs of delayed cerebral vasospasm peak in this model and in humans; 12 days after SAH; and 28 days after SAH. Subarachnoid hemorrhage did not evoke changes in CSF or plasma levels of neuropeptide Y. Nine monkeys had arteriographic evidence of vasospasm on Day 7, but no change in neuropeptide Y levels occurred in plasma or CSF. In addition, neuropeptide Y levels did not change, even after resolution of vasospasm on Day 12 or Day 28. Neuropeptide Y levels were substantially higher in CSF than in arterial plasma (p < 0.003 at each interval). No correlation was found between neuropeptide Y levels in CSF and in plasma. These results do not confirm a relationship between neuropeptide Y levels in the CSF or peripheral plasma and delayed cerebral vasospasm in SAH.

Natriuretic peptide system and endothelin in aneurysmal subarachnoid hemorrhage

1997 ◽  
Vol 87 (2) ◽  
pp. 275-280 ◽  
Author(s):  
Eelco F. M. Wijdicks ◽  
Wouter I. Schievink ◽  
John C. Burnett
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Natriuretic Peptide ◽  
Cerebral Vasospasm ◽  
Fluid Balance ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Peptide System ◽  
Natriuretic Peptide System ◽  
Fine Print

✓ The natriuretic peptide system consists of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). The system is implicated in the control of body fluid homeostasis, causes natriuresis and diuresis (ANP and BNP), and regulates vascular tone (CNP). A reciprocal relationship between ANP and endothelin (ET) has been suggested, and earlier studies have documented a possible role of ET in cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The authors studied plasma ANP, BNP, CNP, and ET for 6 consecutive days in 13 patients with SAH by using radioimmunoassay. The median admission values for ANP were 31.5 pg/ml (range 16.8–323 pg/ml [normal 15 ± 7 pg/ml]); for BNP, 45.3 pg/ml (range 2.2–80.2 pg/ml [normal 12 ± 9 pg/ml]); for CNP, 7.7 pg/ml (range < 2–20 pg/ml [normal 5.2 ± 3 pg/ml]); and for ET, 11 pg/ml (range 6.5–25.1 pg/ml [normal 7.2 ± 4 pg/ml]). Additional increases (defined as > 100% increase on two consecutive measurements) were noted in ANP (11 patients), BNP (10 patients), and CNP (three patients), and resulted in a negative fluid balance in 10 of the 13 patients. The CNP increased in three of four patients with cerebral vasospasm and in one of nine patients without cerebral vasospasm (Fisher's exact test, p = 0.2). No major fluctuations in plasma ET were noted. In seven patients, the plasma ET level did not increase beyond 10 pg/ml during the days of measurement. In six patients, only an occasional sample showed an increase to a maximum of 25 pg/ml. Changes in BNP, ANP, and CNP were independent of each other. The authors conclude that both plasma ANP and BNP increase after SAH and often result in a negative fluid balance. Plasma ANP and BNP seem differentially regulated in the presence of SAH but not by the level of the plasma ET. The possible role of CNP as a regulatory response to cerebral vasospasm needs further exploration.

Paradoxical aggravation of vasospasm with papaverine infusion following aneurysmal subarachnoid hemorrhage

1996 ◽  
Vol 84 (4) ◽  
pp. 690-695 ◽  
Author(s):  
Brent L. Clyde ◽  
Andrew D. Firlik ◽  
Anthony M. Kaufmann ◽  
MichaelP. Spearman ◽  
Howard Yonas
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Artery ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Artery Aneurysm ◽  
Anterior Communicating Artery ◽  
Left Middle Cerebral Artery ◽  
Xenon Ct ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Fine Print

✓ Reports of intraarterial papaverine infusion as treatment for cerebral vasospasm are few and documented complications are uncommon. The authors report the case of a patient with paradoxical aggravation of cerebral arterial narrowing during selective intraarterial papaverine infusion intended to treat vasospasm following aneurysmal subarachnoid hemorrhage (SAH). A 48-year-old man presented to the authors' service with symptomatic vasospasm 10 days after experiencing an SAH. The ruptured anterior communicating artery aneurysm was surgically obliterated the following day, and thereafter maximum hypervolemic and hypertensive therapies were used. However, the patient remained lethargic, and a stable xenon—computerized tomography (CT) cerebral blood flow (CBF) study revealed CBF to be 15 cc/100 g/minute in the left anterior cerebral artery (ACA) and 25 cc/100 g/minute in the right ACA territories. Cerebral arteriography demonstrated diffuse severe left ACA and mild left middle cerebral artery (MCA) vasospasm. In response intraarterial papaverine was infused into the internal carotid artery just proximal to the ophthalmic artery. During the infusion the patient became aphasic and exhibited right hemiplegia. Arteriography performed immediately after the intraarterial papaverine infusion revealed diffuse exacerbation of vasospasm in the distal ACA and MCA territories. A repeat xenon—CT CBF study showed that CBF in the left ACA and the MCA had drastically decreased (2 cc/100 g/minute and 10 cc/100 g/minute, respectively). Despite aggressive management, infarction ultimately developed. This is the first clinical case to illustrate a paradoxical effect of intraarterial papaverine treatment for vasospasm following aneurysmal SAH. The possible mechanisms of this paradoxical response and potential therapeutic reactions are reviewed.

Incidence of cerebral vasospasm after endovascular treatment of acutely ruptured aneurysms: report on 69 cases

1997 ◽  
Vol 87 (6) ◽  
pp. 830-835 ◽  
Author(s):  
Yuichi Murayama ◽  
Tim Malisch ◽  
Guido Guglielmi ◽  
Michel E. Mawad ◽  
Fernando Viñuela ◽  
...  
Keyword(s):  
Endovascular Treatment ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Surgical Removal ◽  
Content Type ◽  
Ruptured Aneurysms ◽  
Symptomatic Vasospasm ◽  
Hypervolemic Hemodilution ◽  
Detachable Coils ◽  
Fine Print

✓ Cerebral vasospasm is the most common cause of morbidity and mortality in patients admitted to the hospital after suffering aneurysmal subarachnoid hemorrhage (SAH). The early surgical removal of subarachnoid clots and irrigation of the basal cisterns have been reported to reduce the incidence of vasospasm. In contrast to surgery, the endovascular treatment of aneurysms does not allow removal of subarachnoid clots. In this study the authors measured the incidence of symptomatic vasospasm after early endovascular treatment of acutely ruptured aneurysms with Guglielmi detachable coils (GDCs). Sixty-nine patients classified as Hunt and Hess Grades I to III underwent occlusion of intracranial aneurysms via GDCs within 72 hours of rupture. The amount of blood on the initial computerized tomography (CT) scan was classified by means of Fisher's scale. Symptomatic vasospasm was defined as the onset of neurological deterioration verified with angiographic or transcranial Doppler studies. Hypertensive, hypervolemic, hemodilution therapy, with or without intracranial angioplasty, was used to treat vasospasm after GDC placement. Symptomatic vasospasm occurred in 16 (23%) of 69 patients. The clinical grade at admission and the amount of blood on the initial CT were both associated with the incidence of subsequent vasospasm. At 6-month clinical follow-up examination, 12 of these 16 patients experienced a good recovery, two were moderately disabled, and two patients had died of vasospasm. In conclusion, the 23% incidence of symptomatic vasospasm in this series compares favorably with that found in conventional surgical series of patients with acute aneurysmal SAH. These results indicate that endovascular therapy does not have an unfavorable impact on cerebral vasospasm.

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