Symptomatic Vasospasm In Patients Research Articles

Effect of Intrathecal Urokinase Infusion on Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Vasospasm following an aneurysmal subarachnoid hemorrhage (SAH) causes serious neurological complications, despite surgical clipping of the aneurysm. Intrathecal urokinase (UK) infusion has been shown to effectively prevent symptomatic vasospasm in patients who have undergone endovascular obliteration of the ruptured aneurysms. To investigate whether intrathecal UK infusion can prevent symptomatic vasospasm in patients undergoing surgical or endovascular treatment. A total of 90 patients with severe aneurysmal SAH were enrolled and assigned to a surgical neck clipping (n= 56) or an endovascular coil embolization (n= 34) groups. After treatment, UK infusion from the lumbar drain was repeated in 32 patients in the surgical neck clipping group (group B) and all in the endovascular coil embolization group (group C) until complete resolution of the SAH was observed on computed tomography. The remaining 24 of the surgical neck clipping group, without UK infusion, were assigned to group A. Symptomatic vasospasm occurred in 7 (29.2%) patients in group A, 2 (6.3%) in group B, and none in group C (group A vs. group B [P=0.02]; group B vs. group C [P=0.14]). Excellent clinical outcomes (modified Rankin score, 0 or 1) were observed in 37.5%, 59.4%, and 76.5% of patients in group A, B, and C, respectively (group A vs. group B [P=0.11]). Clearance of SAH via intrathecal UK infusion significantly reduced symptomatic vasospasm in patients in both UK groups, resulting in better clinical outcomes.

Abstract TP532: Decreased Serum Sodium Levels Predict Symptomatic Vasospasm in Patients With Subarachnoid Hemorrhage

Background: Symptomatic vasospasm (SVS) is one of the major causes of morbidity and mortality in patients with subarachnoid hemorrhage (SAH). Hyponatremia and dehydration due to natriuresis after SAH is related to SVS and predicts it. Therefore, nowadays most institutions target to euvolemia and eunatremia in SAH patients to avoid complications. In this study, we retrospectively investigated the predictors of SVS in terms of water and sodium homeostasisunder maintaining euvolemia and eunatremia after SAH. We also analyzed the relationship between hyponatremia and the effect of treatment modality (clipping and endovascular coiling). Methods: We monitored changes in serum sodium levels, serum osmolarity, daily sodium intake, daily urine volume, and daily water balance during 14 days after SAH. Outcome was assessed using the modified Rankin scale one month after subarachnoid hemorrhage. Results: Among 105 patients, 29 (27.6%) had SVS. Patients with SVS were older than those without SVS and SVS affected outcome. Serum sodium levels were sequentially significantly decreased within normal range from one day before occurrence of SVS.Among the patients, 67 (63.8%) were treated with surgical clipping and 38 (36.2%) were treated with endovascular coiling. The group with coiling suffered significantly more severe hyponatremia and had less urine volume compared with the clipping group. Conclusions: SVS occurs more often in older patients and affects outcome. Serum sodium level decrease occurs one day before SVS. This observation may help predict SVS. A further large prospective study is necessary to resolve the detailed relationships among hyponatremia, urine volume, treatment modality and SVS in patients with SAH.

Decreased serum sodium levels predict symptomatic vasospasm in patients with subarachnoid hemorrhage

Background: Symptomatic vasospasm is a major cause of morbidity and mortality in subarachnoid hemorrhage patients. Hyponatremia and dehydration due to natriuresis after subarachnoid hemorrhage are related to symptomatic vasospasm. Therefore, most institutions are currently targeting euvolemia and eunatremia in subarachnoid hemorrhage patients to avoid complications. We retrospectively investigated the predictors of symptomatic vasospasm with respect to water and sodium homeostasis, while maintaining euvolemia and eunatremia after subarachnoid hemorrhage. Methods: We monitored changes in serum sodium levels, serum osmolarity, daily sodium intake, daily urine volume, and daily water balance for 14days after subarachnoid hemorrhage. Outcomes were assessed using the modified Rankin scale at 1month after subarachnoid hemorrhage. Results: Among 97 patients, 27 (27.8%) had symptomatic vasospasm. Patients with symptomatic vasospasm were older than those without symptomatic vasospasm; the occurrence of symptomatic vasospasm affected outcomes. Serum sodium levels were sequentially significantly decreased, but within the normal range from 1day before the occurrence of symptomatic vasospasm. Serum osmolarity of the spasm group was lower than that of the non-spasm group. Conclusions: Symptomatic vasospasm occurs more often in older patients and affects outcomes. A decrease in serum sodium levels occurs a day before symptomatic vasospasm. This observation may help predict symptomatic vasospasm.

Effect of Red Blood Cell Transfusion on Unfavorable Neurologic Outcome and Symptomatic Vasospasm in Patients with Cerebral Aneurysmal Rupture: Old versus Fresh Blood

Red blood cell (RBC) transfusion, especially with "old" blood, is associated with adverse clinical outcomes. We compared the effects of fresh blood versus old blood transfusion on poor neurologic outcomes and symptomatic vasospasm in patients with ruptured cerebral aneurysms. In this retrospective study, 211 patients with aneurysmal rupture were divided into 3 groups: nontransfusion (n = 136), fresh blood (RBC storage ≤ 14 days) transfusion (n = 39), and old blood (RBC storage >14 days) transfusion (n = 36). Unfavorable neurologic outcomes (modified Rankin Scale score ≥ 3) and symptomatic cerebral vasospasm were assessed. The incidence of unfavorable neurologic outcomes was significantly higher in the fresh blood and old blood transfusion groups compared with the nontransfused group (71.8% and 58.3% vs. 21.3%; P < 0.01); the incidence of symptomatic vasospasm was significantly higher in the old blood group compared with the fresh blood and nontransfusion groups (57.1% vs. 26.7% and 22.2%; P < 0.05). On binary logistic regression, old age, Hunt and Hess grade 3-4, high postoperative C-reactive protein level, RBC transfusion, delayed infarction, and hydrocephalus were independent predictors of unfavorable neurologic outcomes. Young age, Fisher grade 3-4, old RBC transfusion, and surgical clipping were independent predictors of postoperative symptomatic vasospasm. RBC transfusion itself, regardless of the duration of RBC storage, was associated with unfavorable neurologic outcomes in patients with ruptured cerebral aneurysms. Also, old blood transfusion, but not fresh blood transfusion, was associated with increased symptomatic cerebral vasospasm.

Predictors of Symptomatic Vasospasm After Subarachnoid Hemorrhage: A Single Center Study of 457 Consecutive Cases.

We set forth to identify predictors of symptomatic vasospasm in patients with subarachnoid hemorrhage (SAH). We used multivariate logistic regression analysis of the prospective, hospital based, single center register of the Department of Neurosurgery, University of Debrecen, Hungary. Evaluated patients' characteristics were: sex, age, Hunt-Hess grade on admission, location of aneurysm, thickness of blood clot on initial CT scan (Fisher grade), hypertension. Between 1987 and 2004, 567 SAH cases were registered, 457 were included in this study. Symptomatic vasospasm developed in 22.5% of the cases. In univariate analysis, Hunt-Hess grades 2 and 3 and female sex were predictive for symptomatic vasospasm. In multivariate analysis, female sex remained a significant predictor: OR: 1.8 (1.005-3.2). Women are at more danger of developing symptomatic vasospasm after subarachnoid hemorrhage.

The relationship between ruptured aneurysm location, subarachnoid hemorrhage clot thickness, and incidence of radiographic or symptomatic vasospasm in patients enrolled in a prospective randomized controlled trial

The relationship between ruptured aneurysm location, subarachnoid hemorrhage clot thickness, and incidence of radiographic or symptomatic vasospasm in patients enrolled in a prospective randomized controlled trial

Cerebral vasospasm in patients over 80 years treated by coil embolization for ruptured cerebral aneurysms.

Object. The effect on clinical outcomes of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage (SAH) in patients over 80 years who underwent coil embolization was evaluated. Methods. Forty-four cases were reviewed and divided into two groups according to patient age: Group A, 79 years or younger, and Group B, 80 or older. Patient characteristics, prevalence of symptomatic vasospasm, modified Rankin Scale (mRS) scores at discharge and frequency of symptomatic vasospasm in patients with mRS scores of 3–6 were analyzed. Results. Thirty-two (73%) of the 44 cases were categorized as Group A and 12 (27%) as Group B. Group B had a significantly higher prevalence of symptomatic vasospasm compared to Group A (P = 0.0040). mRS scores at discharge were significantly higher in Group B than in Group A (P = 0.0494). Among cases with mRS scores of 3–6, there was a significantly higher frequency of symptomatic vasospasm in Group B than in Group A (P = 0.0223). Conclusions. In our cohort of aneurysmal SAH patients treated by coil embolization, patients over 80 years of age were more likely to suffer symptomatic vasospasm, which significantly correlated with worse clinical outcomes, than those 79 years and under.

The relationship between ruptured aneurysm location, subarachnoid hemorrhage clot thickness, and incidence of radiographic or symptomatic vasospasm in patients enrolled in a prospective randomized controlled trial

Cerebral vasospasm following subarachnoid hemorrhage (SAH) causes significant morbidity in a delayed fashion. The authors recently published a new scale that grades the maximum thickness of SAH on axial CT and is predictive of vasospasm incidence. In this study, the authors further investigate whether different aneurysm locations result in different SAH clot burdens and whether any concurrent differences in ruptured aneurysm location and maximum SAH clot burden affect vasospasm incidence. Two hundred fifty patients who were part of a prospective randomized controlled trial were reviewed. Most outcome and demographic variables were included as part of the prospective randomized controlled trial. Additional variables were also collected at a later time, including vasospasm data and maximum clot thickness. Aneurysms were categorized into 1 of 6 groups: intradural internal carotid artery aneurysms, vertebral artery (VA) aneurysms (including the posterior inferior cerebellar artery), basilar trunk or basilar apex aneurysms, middle cerebral artery aneurysms, pericallosal aneurysms, and anterior communicating artery aneurysms. Twenty-nine patients with nonaneurysmal SAH were excluded. Patients with pericallosal aneurysms had the least average maximum clot burden (5.3 mm), compared with 6.4 mm for the group overall, but had the highest rate of symptomatic vasospasm (56% vs 22% overall, OR 4.9, RR 2.7, p = 0.026). Symptomatic vasospasm occurrence was tallied in patients with clinical deterioration attributable to delayed cerebral ischemia. There were no significant differences in maximum clot thickness between aneurysm sites. Middle cerebral artery aneurysms resulted in the thickest mean maximum clot (7.1 mm) but rates of symptomatic and radiographic vasospasm in this group were statistically no different compared with the overall group. Vertebral artery aneurysms had the worst 1-year modified Rankin scale (mRS) scores (3.0 vs 1.9 overall, respectively; p = 0.0249). A 1-year mRS score of 0-2 (good outcome) was found in 72% of patients overall, but in only 50% of those with pericallosal and VA aneurysms, and in 56% of those with basilar artery aneurysms (p = 0.0044). Patients with stroke from vasospasm had higher mean clot thickness (9.71 vs 6.15 mm, p = 0.004). The location of a ruptured aneurysm minimally affects the maximum thickness of the SAH clot but is predictive of symptomatic vasospasm or clinical deterioration from delayed cerebral ischemia in pericallosal aneurysms. The worst 1-year mRS outcomes in this cohort of patients were noted in those with posterior circulation aneurysms or pericallosal artery aneurysms. Patients experiencing stroke had higher mean clot burden.

Early Inhibition of Natriuresis Suppresses Symptomatic Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage

Background: Hyponatremia is a common complication occurring in one third of patients after subarachnoid hemorrhage (SAH). One mechanism that likely mediates the development of hyponatremia in SAH is cerebral salt wasting syndrome (CSWS), which induces natriuresis and reduces total blood volume, resulting in a risk of symptomatic vasospasm (SVS). The mineral corticoid fludrocortisone acetate enhances sodium reabsorption in the renal distal tubules and may help prevent post-SAH hyponatremia. However, management with fludrocortisone acetate is ineffective if hyponatremia is advanced, because CSWS and subsequent SVS develop rapidly. Therefore, an additional earlier marker is required to predict the development of hyponatremia for the initiation of immediate treatment in select patients. However, no conclusive evidence exists showing that hyponatremia influences the risk of SVS, and no standard treatment protocol exists for treating hyponatremia in patients with SAH. This study was undertaken to evaluate whether selective early treatment of hyponatremia prevents SVS in patients with increased urinary sodium excretion in the early phase following SAH. Methods: A total of 103 patients with aneurysmal SAH were managed for a postoperative electrolyte disorder after aneurysmal clipping or coil embolization. Between 2004 and 2007 (period 1), 54 patients started treatment to correct the electrolyte disorder after hyponatremia had occurred. Between 2007 and 2011 (period 2), 49 patients were prospectively subjected to sodium replacement treatment according to their daily sodium balance, and inhibition of natriuresis with fludrocortisone acetate was initiated just after an increase in urinary sodium excretion >300 mEq/day. The occurrence of hyponatremia, SVS, and outcomes were compared between the two periods. Results: Hyponatremia was observed in 14 patients (26%) in period 1 and 7 patients (14%) in period 2. The incidence of fludrocortisone acetate administration was significantly higher, and initiation of electrolyte correction was significantly earlier, in period 2 patients. We observed a significant difference in the frequency of SVS, which occurred in 10 patients (18.5%) in period 1 and 3 patients (6.1%) in period 2. Both urinary sodium excretion and urine volume at day 7 were significantly different between the two periods. However, no significant difference was observed in overall outcome between the two periods. Conclusions: Early inhibition of natriuresis with fludrocortisone acetate before the occurrence of hyponatremia prevented SVS after aneurysmal SAH. Increased urinary sodium excretion in the early phase of SAH is a good indicator for the initiation of electrolyte correction with fludrocortisone acetate.

The Postoperative C-reactive Protein Level can be a Useful Prognostic Factor for Poor Outcome and Symptomatic Vasospasm in Patients With Aneurysmal Subarachnoid Hemorrhage

Ninety-three patients undergoing surgical or endovascular operation secondary to aneurysmal subarachnoid hemorrhage (SAH) were retrospectively analyzed to determine the influence of the different time points of C-reactive protein (CRP) measurement on the prediction of vasospasm and clinical outcome. Laboratory data such as the CRP level and the white blood cell count, preoperative demographic and clinical data, intraoperative and postoperative data, and complications such as intracerebral hemorrhage, hydrocephalus, vasospasm, and surgical decompression were collected at hospital discharge or symptomatic vasospasm and used as predictable factors for poor outcome (Modified Rankin Scale score 4 to 6). Twenty-three and 28 patients showed poor outcome and symptomatic vasospasm after SAH, respectively. Both preoperative and postoperative CRP levels were significantly higher in patients with a poor outcome compared with patients with a good outcome (P<0.05). The area under the receiver operating characteristic curve of CRP measured on postoperative day 1 or 2 (CRP POD1-2) for predicting a poor clinical outcome was 0.870, and its cutoff point of 4 mg/dL had a sensitivity of 0.826 and a specificity of 0.843. A high CRP level after aneurysm treatment was associated with severe neurological deterioration on admission, cerebral infarction, intracerebral hemorrhage, and surgical decompression (P<0.05). CRP POD1-2, and not the preoperative CRP, was an independent factor in predicting symptomatic vasospasm (P<0.05). In patients with symptomatic vasospasm, an increase in the postoperative CRP was associated with the time profile of developing symptomatic vasospasm. Postoperative CRP, especially CRP POD1-2, can be a useful prognostic factor for both poor outcome and symptomatic vasospasm in patients with aneurysmal SAH.

Intra-Arterial Nimodipine Infusion for Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage

This study evaluated the efficacy of intra-arterial nimodipine infusion for symptomatic vasospasm in patients with aneurysmal subarachnoid hemorrhage (aSAH). Clinical data collected from 42 consecutive patients with symptomatic vasospasm after aSAH were retrospectively reviewed. Forty-two patients underwent 101 sessions of intra-arterial nimodipine infusion. Angiographic response, immediate clinical response, and clinical outcome were evaluated at discharge and six months later. Angiographic improvement was achieved in 82.2% of patients. The immediate clinical improvement rate was 68.3%, while the deterioration rate was 5.0%. A favorable clinical outcome was achieved in 76.2% at discharge and 84.6% six months. Vasospasm-related infarction occurred in 21.4%. There was no drug-related complication. The nimodipine group showed satisfactory outcomes. Nimodipine can be recommended as an effective and safe intra-arterial agent for the treatment of symptomatic vasospasm after aSAH.

Metaanalysis of Tirilazad Mesylate in Patients with Aneurysmal Subarachnoid Hemorrhage

Tirilazad is a non-glucocorticoid, 21-aminosteriod that inhibits lipid peroxidation. It had neuroprotective effects in experimental ischemic stroke and reduced angiographic vasospasm after experimental subarachnoid hemorrhage (SAH). Five randomized clinical trials of tirilazad were conducted in patients with SAH. We performed a meta-analysis of these trials to assess the effect of tirilazad on unfavorable outcome, symptomatic vasospasm, and cerebral infarction after SAH. Data from 3,797 patients were analyzed and modeled using random effect and Mantel-Haenszel meta-analyses and multivariable logistic regression to determine the effect of tirilazad on clinical outcome, symptomatic vasospasm, and cerebral infarction. Clinical outcome was assessed 3 months after SAH using the Glasgow outcome scale, and symptomatic vasospasm was defined by clinical criteria with laboratory and radiological exclusion of other causes of neurological deterioration. The five trials were randomized, double-blind, and placebo-controlled. Tirilazad did not significantly decrease unfavorable clinical outcome on the GOS (odds ratio [OR] 1.04, 95% confidence interval [CI] 0.89-1.20) or cerebral infarction (OR 1.04, 95% CI 0.89-1.22). There was a significant reduction in symptomatic vasospasm in patients treated with tirilazad (OR 0.80, 95% CI 0.69-0.93). There was no heterogeneity across the five trials. Tirilazad had no effect on clinical outcome but did decrease symptomatic vasospasm in five trials of aneurysmal SAH. The dissociation between clinical outcome and symptomatic vasospasm deserves further investigation.

Endothelial Nitric Oxide Synthase Gene Single-Nucleotide Polymorphism Predicts Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Vasospasm is a major cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage (aSAH). Studies have shown a link between single-nucleotide polymorphisms (SNPs) in the endothelial nitric oxide synthase (eNOS) gene and the incidence of coronary spasm and aneurysms. Alterations in the eNOS T-786 SNP may lead to an increased risk of post-aSAH cerebral vasospasm. In this prospective clinical study, 77 aSAH patients provided genetic material and were followed for the occurrence of vasospasm. In multivariate logistic regression analysis, genotype was the only factor predictive of vasospasm. The odds ratio (OR) for symptomatic vasospasm in patients with one T allele was 3.3 (95% confidence interval (CI): 1.1 to 10.0, P=0.034) and 10.9 for TT. Patients with angiographic spasm were 3.6 times more likely to have a T allele (95% CI: 1.3 to 9.6, P=0.013; for TT: OR 12.6). Patients with severe vasospasm requiring endovascular therapy were more likely to have a T allele (OR 3.5, 95% CI: 1.3 to 9.5, P=0.016; for TT: OR 12.0). Patients with the T allele of the eNOS gene are more likely to have severe vasospasm. Presence of this genotype may allow the identification of individuals at high risk for post-aSAH vasospasm and lead to early treatment and improved outcome.

Elevated cerebrospinal fluid and serum YKL-40 levels are not associated with symptomatic vasospasm in patients with aneurysmal subarachnoid haemorrhage

YKL-40 is a newly discovered matrix protein that is thought to be released during the acute stages of inflammation. It has recently been speculated that YKL-40 may serve as a specific serological marker of neutrophil function at the site of tissue inflammation. Our aim was to determine whether the levels of YKL-40 in both the cerebrospinal fluid and sera of 22 patients with aneurysmal subarachnoid haemorrhage were associated with either vasospasm or outcome. The levels were also compared with those of 16 control patients with hydrocephalus. We found that patients with aneurysmal subarachnoid haemorrhage had significantly higher YKL-40 levels in both cerebrospinal fluid and serum than controls. However, elevated YKL-40 levels were not associated with symptomatic vasospasm or 6-month outcome. We show that elevated YKL-40 levels are not correlated with the severity of subarachnoid haemorrhage and cannot be used as a serological marker of inflammation in patients with an aneurysm rupture.

CSF hypocretin-1/orexin-A concentrations in patients with subarachnoid hemorrhage (SAH)

The aim of this study was to examine the role of the hypothalamic hypocretin/orexin system in complications of delayed ischemic neuronal deficit (DIND) resulting from symptomatic vasospasm in patients with aneurysmal subarachnoid hemorrhage (SAH). CSF hypocretin-1/orexin-A levels were measured in 15 SAH patients. DIND complications occurred in seven patients with symptomatic vasospasm. Hypocretin-1/orexin-A levels were low in SAH patients during the 10 days following the SAH event. CSF hypocretin-1/orexin-A levels were lower in patients with DIND complications than in those who did not develop DIND. A significant transient decline in CSF hypocretin-1/orexin-A levels was also observed at the onset of DIND in all patients with symptomatic vasospasm. The reduced hypocretin/orexin production observed in SAH patients may reflect reduced brain function due to the decrease in cerebral blood flow. These results, taken together with recent experimental findings in rats that indicate hypocretin receptor 1 (orexin 1 receptor) mRNA and protein are elevated following middle cerebral artery occlusion, suggest that a reduction in hypocretin/orexin production in SAH and DIND patients is associated with alterations in brain hypocretin/orexin signaling in response to ischemia.

Prevention of Symptomatic Vasospasm After Aneurysmal Subarachnoid Hemorrhage by Intraoperative Cisternal Fibrinolysis Using Tissue-Type Plasminogen Activator Combined With Continuous Cisternal Drainage

The efficacy of intraoperative cisternal irrigation using tissue-type plasminogen activator (tPA) combined with continuous cisternal drainage was assessed for the prevention of symptomatic vasospasm in patients with aneurysmal subarachnoid hemorrhage (SAH). Seventy consecutive patients underwent direct surgery for aneurysm clipping within 48 hours of SAH and had computed tomography (CT) findings classified as Fisher group III or IV with densities of more than 65 Hounsfield units (HU). Fibrinolysis of the cisternal clots was performed during surgery using 1.6 mg tPA in 55 cases or 3.2 mg tPA in 15 cases. If postoperative CT within 24 hours of surgery showed areas with density more than 65 HU, additional tPA (0.8 mg/day) was administered into the cisternal catheter until the high density areas disappeared. The cisternal drainage catheters were left in place until day 14. Additional tPA injection was necessary in four of the 55 patients receiving 1.6 mg tPA. Symptomatic vasospasm occurred in three patients (4.3%) and two patients had low density areas on CT. Permanent deficit (hemiparesis) due to cerebral vasospasm remained in only one patient. Intraoperative cisternal irrigation with tPA combined with cisternal drainage is safe and effective for the prevention of symptomatic vasospasm following SAH.

Symptomatic vasospasm diagnosis after subarachnoid hemorrhage: evaluation of transcranial Doppler ultrasound and cerebral angiography as related to compromised vascular distribution.

To evaluate the reliability of transcranial Doppler ultrasound in detecting symptomatic vasospasm in patients after aneurysmal subarachnoid hemorrhage and monitoring response after hypertensive and endovascular treatments. Retrospective chart review. Neurosciences critical care unit in a tertiary-care university hospital. All patients admitted to a neurosciences critical care unit with the diagnosis of subarachnoid hemorrhage between January 1990 and June 1997. None We reviewed transcranial Doppler ultrasound data of 199 patients; 55 had symptomatic vasospasm. Clinical symptoms and corresponding vascular distributions were identified, as was angiographic vasospasm (n = 35). The sensitivity and specificity of transcranial Doppler ultrasound for anterior circulation vessels were calculated by using a mean cerebral blood flow velocity criterion of >120 cm/sec. Clinical diagnosis of symptomatic vasospasm was used as the standard to determine sensitivity and specificity of transcranial Doppler ultrasound and cerebral angiography. The sensitivity of transcranial Doppler ultrasound for anterior circulation in patients with symptomatic vasospasm was 73% with a specificity of 80%. The sensitivity of cerebral angiography was 80%. For individual vessels, the sensitivity and specificity of transcranial Doppler ultrasound were middle cerebral artery, 64% and 78%; anterior cerebral artery, 45% and 84%; and internal carotid artery, 80% and 77%, respectively. The mean times for symptomatic and transcranial Doppler ultrasound signs of vasospasm presentation were 6.4 +/- 2 and 6.1 +/- 3 days, respectively. In patients without symptomatic vasospasm, the mean time for mean cerebral blood flow velocities >120 cm/sec was 7.0 +/- 3 days (p <.05). Symptomatic vasospasm also was associated with thickness of clot on head computed tomography scan and rapidly increasing mean cerebral blood flow velocities. Transcranial Doppler ultrasound signs of vasospasm improved after endovascular treatment in 30 patients. The reliability of transcranial Doppler ultrasound was better at detecting high mean cerebral blood flow velocities in patients with symptomatic vasospasm related to middle cerebral and internal carotid artery distributions than for anterior cerebral artery distribution. Transcranial Doppler ultrasound was as sensitive as cerebral angiography at detecting symptomatic vasospasm. High mean cerebral blood flow velocities can be apparent before the presence of symptomatic vasospasm. Daily transcranial Doppler ultrasound monitoring could provide early identification of patients with aneurysmal subarachnoid hemorrhage who are at high risk for symptomatic vasospasm and may be helpful at following success of endovascular treatment.

Prognostic Value and Determinants of Ultraearly Angiographic Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Prognostic Value and Determinants of Ultraearly Angiographic Vasospasm after Aneurysmal Subarachnoid Hemorrhage

A randomized trial of two doses of nicardipine in aneurysmal subarachnoid hemorrhage

High-dose intravenous nicardipine has been shown to reduce the incidence of angiographic and symptomatic vasospasm in patients with aneurysmal subarachnoid hemorrhage (SAH), but treatment may be complicated by side effects, including hypotension or pulmonary edema/azotemia. From August, 1989, to January, 1991, 365 patients at 21 neurosurgical centers were entered into a randomized double-blind trial comparing high-dose (0.15 mg/kg/hr) nicardipine with a 50% lower dose (0.075 mg/kg/hr) administered by continuous intravenous infusion for up to 14 days following SAH. Patients in all neurological grades were eligible for the study. During the study period, 184 patients were randomly assigned to receive high-dose nicardipine and 181 to receive the low dose. There were no significant differences in patient age, admission neurological condition, or amount and distribution of blood clot on initial computerized tomography scan. Patients in the high-dose group received a significantly smaller proportion of the planned dose than those in the low-dose group (80% +/- 0.2% vs. 86% +/- 0.2%, p < 0.05), largely because of premature treatment termination after adverse medical events. The incidence of symptomatic vasospasm was 31% in both groups, and the overall 3-month outcomes were nearly identical. These data suggest that, from a clinical standpoint, the results of high-dose and low-dose nicardipine treatment are virtually equivalent, but administration of low-dose nicardipine is attended by fewer side effects.