Evaluation of changes in circulating blood volume during acute and very acute stages of subarachnoid hemorrhage: implications for the management of hypovolemia

OBJECT: Circulating blood volume (cBV) is reported to decrease in patients who suffer a subarachnoid hemorrhage (SAH), but little is known about the correlation between changes in cBV, and patient clinical condition and time course after SAH, especially during the very acute stage. To determine appropriate management of patients with SAH, the authors measured cBV by using pulse spectrophotometry immediately after patient admission. They also evaluated whether the timing of surgery influenced changes in cBV. METHODS: Circulating blood volume was measured in a total of 73 patients who were divided into the following three groups: Group A (very acute SAH) consisted of 14 SAH cases, Group B (acute SAH) included 34 SAH cases, and Group C (controls) included 25 other neurosurgical cases. All patients in Group A underwent aneurysm clipping within 6 hours after onset of SAH, whereas all patients in Group B underwent aneurysm clipping within 72 hours after onset. Hypervolemic therapy was not performed in patients with SAH. Before surgery, cBV was significantly lower in patients in Group B than in those in Group C, but there was no significant difference in this parameter when comparing Groups A and C. Although there was a transient drop in cBV in Group B patients for at least 3 days after surgery, there was no significant change in cBV in Group A patients during the study period. None of the Group A patients suffered from symptomatic vasospasm; however, four Group B patients did experience symptomatic vasospasm. CONCLUSIONS: The authors assert that normovolemic fluid management is appropriate for patients who undergo surgery during the very acute stage of SAH, whereas a relatively hypervolemic therapy is necessary for 3 to 5 days after operation to prevent early hypovolemia in patients who undergo surgery during the acute stage of SAH.     

Platelet derived growth factor and subarachnoid haemorrage: A study on cisternal cerebrospinal fluid

Summary Platelet derived growth factor (PDGF) was identified as a powerful mitogenic growth factor which is released from activated platelets and has a marked activity as vasoconstrictor agent. In the present study we have measured cisternal cerebrospinal fluid (CSF) levels of PDGF in 72 patients operated on for intracranial aneurysm in order to verify whether it might be related to the clinical aspects of SAH with special regard to symptomatic vasospasm.CSF samples were obtained at surgery by cisternal puncture of the subarachnoid cistern the nearest to the aneurysm before aneurysm isolation and exclusion. The specimen were frozen in liquid nitrogen and stored at-80 ° C until analysis. PDGF was measured using a commercially available reagent. Values are expressed as pg/ml of CSF.In 18 cases no radiological and clinical signs of SAH were detected and the mean cisternal CSF level of PDGF was 885.0±104.5 pg/ml; 20 patients were operated on between day 1 and 3 from the last SAH episode: mean cisternal CSF level of PDGF was 1917.5±459.4 pg/ml. In 34 patients treated with delayed surgery protocol, mean cisternal CSF level of PDGF was 995.3±73.8 pg/ml. Statistical analysis showed significant differences between groups (P: 0.011). In the subgroup of patients operated on within day 3 after SAH, 6 presented vasospasm and had mean cisternal CSF PDGF level which was significantly higher (P<0.01) than in 14 patients without vasospasm. In the delayed surgical patients there was no significant difference in cisternal CSF levels of PDGF considering the occurrence of vasospasm.The results of the present study suggest that (a) after SAH there is a significant release of PDGF early after SAH and (b) higher levels of PDGF found in cisternal CSF of patients operated on within 72 hours after SAH may be predictive of symptomatic vasospasm.     

Role of coil embolization and arterial injection in elderly subarachnoid hemorrhage patients: preliminary report

With the recent advanced aging seen in society, the number of elderly patients with aneurismal subarachnoid hemorrhage (SAH) is increasing. We focused on current management of SAH in patients who were over 75 years old. From January 1st, 2004 to the end of June, 2007, we had treated 170 SAH patients including 39 who were over 75 years old. We divided the patients into three groups : Coiling Group, Clipping Group, and conservative treatment group (Conservative Group). We analyzed the Hunt-Kosnik grade (H-K), the rate of symptomatic vasospasm, the rate of shunting operation, the Glasgow Outcome Scale (GOS) at 30 days after the onset of SAH, bed rest periods and rate of shunt operation retrospectively. The Conservative Group included many H-K poor grade cases. Symptomatic vasospasm occurred significantly less in the Coiling Group. Rates of shunting operation did not have any significant change. GOS of the Coiling Group and Clipping Group had no significant change, due to the effectiveness of arterial injection for vasospasm. Patients in the Coiling Group started walking significantly earlier than members of other groups. Twenty-five percent of the Clipping Group needed a shunt operation but no patients of the Coiling Group needed a shunt. For elderly SAH patients, we recommend doing coil embolization or clipping and maintaining the patients' activity in daily life. Interventional treatment is necessary to improve results for elderly SAH patients.     

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.     

Risk of cerebral vasopasm after subarachnoid hemorrhage reduced by statin therapy: A multivariate analysis of an institutional experience

OBJECT: Impairment of endothelial nitric oxide synthase (eNOS), endothelium-dependent relaxation, and cerebrovascular autoregulation all occur in vasospastic cerebral arteries following subarachnoid hemorrhage (SAH). The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or statins, both improve endothelial function and increase eNOS messenger RNA, protein, and enzymatic activity threefold. Increasing experimental evidence in animal models of SAH suggests that statins may ameliorate cerebral vasospasm. The authors hypothesized that patients chronically treated with statins would have a decreased risk of symptomatic vasospasm after SAH. METHODS: The authors retrospectively reviewed the charts of 115 patients with SAH who were consecutively admitted to the Neuroscience Intensive Care Unit of Duke University between 1998 and 2001. The independent association of statin therapy to symptomatic vasospasm was assessed using multivariate logistic regression analysis. Fifteen patients (13%) admitted with SAH were receiving statin therapy for at least 1 month before admission. Forty-nine patients (43%) experienced symptomatic vasospasm a mean of 5.8 +/- 3 days after onset of SAH. Current statin therapy on admission (odds ratio [OR] 0.09, 95% confidence interval [CI] 0.01-0.77) was independently associated with an 11-fold reduction in the risk of symptomatic vasospasm. Fisher Grade 3 SAH (OR 2.82, 95% CI 1.50-5.71) and rupture of anterior cerebral or internal carotid artery aneurysm (OR 3.77, 95% CI 1.29-10.91) were independently associated with an increased risk of symptomatic vasospasm. CONCLUSIONS: In this retrospective case series, patients who received statin therapy for at least 1 month demonstrated an 11-fold decrease in the risk of developing symptomatic vasospasm after SAH.     

Effect of clot removal on cerebral vasospasm

The effect of clot removal on cerebral vasospasm was studied in 104 patients with aneurysmal subarachnoid hemorrhage (SAH). The series included patients who fulfilled all of the following criteria: operation was performed by Day 3 after the ictus; the patient's preoperative clinical grade was between Grades I and IV; there was no rebleeding; computerized tomography (CT) showed only SAH; and carotid angiograms were performed by Day 2 and repeated between Days 7 and 9. Both the degree of SAH on CT and angiographic vasospasm were graded from 0 to III. The relationship of the SAH grade in the basal frontal interhemispheric fissure (IHF) to the presence of vasospasm at the A2 segments of the anterior cerebral artery and the relationship of the SAH grade in the sylvian stems to the presence of vasospasm at the M1 segments of the middle cerebral artery were analyzed. Correlation of preoperative and postoperative SAH grades with the angiographic vasospasm grades, with the incidence of symptomatic vasospasm, and with the low-density area on CT could be found in the A2 and M1 territories. Decrease of cisternal blood measured by CT after the operation did not relate directly to the reduction of vasospasm. When the SAH was Grade II or III in the basal frontal IHF, the angiographic vasospasm grades at the A2 were significantly lower in patients with surgery via the interhemispheric approach than in those with surgery via the pterional approach. Symptomatic vasospasm occurred in two of the eight cases operated on by the interhemispheric approach compared with 11 of the 22 cases approached via the pterional route. In patients with a pterional approach, there was no significant difference in severity of vasospasm in the M1 territory between the side of approach and the opposite side. No consistent relationship could be found between the time interval from SAH to operation and the severity of vasospasm. While clot removal may ameliorate cerebral vasospasm, its effect per se does not seem to be significant.     

Efficacy and toxicity of thromboxane synthetase inhibitor for cerebral vasospasm after subarachnoid hemorrhage

The efficacy and possible side effects of thromboxane A2 (TXA2) synthetase inhibitor in the treatment of cerebral vasospasm after subarachnoid hemorrhage (SAH) were assessed for 24 patients who presented with grades I to IV of the Hunt and Hess classification. All patients underwent aneurysmal clipping within 48 hours after SAH. Postoperatively, TXA2 synthetase inhibitor, Cataclot [sodium (E)-3-[p-(1H-imidazol-1-ylmethyl)phenyl]-2-propenoate] was administered to 13 patients by continuous drip infusion at a dose of 1 microgram/kg/min for 8 to 14 days (group A). The remaining 11 patients did not receive this drug (group B). Of the 13 patients in group A, seven patients (54%) showed no symptomatic vasospasm after SAH. Four patients (31%) developed a transient deterioration of consciousness and/or motor disturbance. Three of these patients fully recovered, while one of them showed a mild neurological deficit on discharge. One patient (8%) developed permanent dysphasia and hemiparesis as a result of ischemic brain damage due to vasospasm. One patient (8%) died of the side effect. On the other hand, of the 11 patients in group B, only three (27%) showed no symptomatic vasospasm. One (9%) patient presented a transient neurological deficit but fully recovered upon discharge. Four patients (36%) showed permanent neurological deficits, although they all could lead an independent life after discharge. The three remaining patients developed a severe disturbance of consciousness caused by ischemia due to vasospasm, and two of them died within 1 month after the onset of SAH. In the group treated with Cataclot, two patients developed an epidural hematoma late during the administration of the drug. Of these two, one patient died of increased intracranial pressure that was accelerated by the complication. These results indicate that TXA2 synthetase inhibitor is effective in not only decreasing the occurrence of symptomatic vasospasm but also reducing the neurological deterioration due to vasospasm after SAH. However, this drug has a hazardous side effect in that it may promote a tendency to bleed, which caused death in one of our patients.     

Subarachnoid hemorrhage on computed tomography scanning and the development of cerebral vasospasm: the Fisher grade revisited

BACKGROUND: The Fisher grade (FG) is widely used to predict cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). We revisited the grading scale to determine its validity in the era of modern management. METHODS: We retrospectively reviewed the records of 134 patients with SAH. The amount and distribution of subarachnoid blood on admission computed tomography (CT) scan was quantified according to the FG and compared with development of symptomatic vasospasm. RESULTS: We reviewed 134 patients (median age, 54) who presented with aneurysmal SAH. Six (5%) were FG 1, 34 (25%) were FG 2, 25 (19%) were FG 3, and 69 (51%) were FG 4. Symptomatic vasospasm developed in no (0%) FG 1, 8 (24%) FG 2, 7 (28 %) FG 3, and 13 (19%) FG 4 patients (28 of 134 total patients; 21%). Development of symptomatic vasospasm was not associated with admission FG, Hunt and Hess grade, age, sex, or location of blood on presenting CT scan. Elevated transcranial Doppler blood flow velocity was associated with blood in the basal cisterns (P = .0047), lateral ventricles (P = .026), or blood in any ventricle (P = .04). Postoperative angiograms were obtained in 57 patients; moderate to severe vasospasm was observed in 5 (15%) FG 2, 6 (24%) FG 3, and 14 (20%) FG 4 patients. Twenty patients (71%) with symptomatic vasospasm had moderate or severe angiographic vasospasm. Angiographic vasospasm was associated with intraventricular blood (P = .054) but not with FG. CONCLUSIONS: Symptomatic vasospasm occurred in 21% of cases. The FG correlated with symptomatic vasospasm in only half the patients. A new predictive CT grading scale for vasospasm may be necessary.     

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

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.     

Effects of intravascular volume expansion on cerebral blood flow in patients with ruptured cerebral aneurysms

To clarify the effect of intravascular volume expansion on cerebral blood flow (CBF) in patients after subarachnoid hemorrhage (SAH), we performed 55 pairs of regional CBF measurements using the xenon-133 inhalation method before and after volume expansion in 35 patients with ruptured cerebral aneurysms. CBF was calculated as the hemispheric mean value of the initial slope index. To accomplish volume expansion, we transfused 500 ml of 5% human serum albumin in half an hour. After volume expansion with albumin, the hemoglobin value decreased significantly (P less than 0.005). Volume expansion did not change the mean arterial blood pressure. During the first 2 weeks after SAH, CBF decreased significantly after volume expansion (P less than 0.005). During the 3rd week after SAH and subsequently to the 4th week after SAH, volume expansion produced no change in CBF. In patients with symptomatic vasospasm, CBF decreased significantly after volume expansion (P less than 0.005). In patients without symptomatic vasospasm, volume expansion produced no change in CBF. The results of this study suggest that increasing the intravascular volume above normal by volume expansion does not increase CBF or reverse symptomatic vasospasm.     

Effect of early operation on cerebral vasospasm

The effect of early operation on cerebral vasospasm was studied in 150 patients with aneurysmal subarachnoid hemorrhages who fulfilled all of the following criteria: admission by day 2 after subarachnoid hemorrhage, no rebleeding, clinical grades I to IV on admission, subarachnoid hemorrhage alone on computed tomography scan, not operated on between days 4 and 20, and availability of bilateral carotid angiograms done by day 2 and redone between days 7 and 9. The patients were divided into two groups: those operated on by day 3 (group 1: 116 patients) and those operated on after day 20 or not operated on (group 2: 34 patients). Severity of both subarachnoid hemorrhage on computed tomography scan and angiographic vasospasm were graded into 0-IV. Angiographic vasospasm was observed in 95% of group 1 and in 88% of group 2 patients. A significant difference could not be found between groups 1 and 2 in the angiographic vasospasm grades. The incidence of symptomatic vasospasm in group 1 was 18%, which was significantly lower than the 44% in group 2. In group 1 patients with subarachnoid hemorrhage grades II to III, the incidences of symptomatic vasospasm and low density area on computed tomography scan were 13% and 10%, respectively. Both of these rates were significantly lower than those in group 2, which were 50% and 36%, respectively. However, in patients with subarachnoid hemorrhage grade IV, no differences could be found between groups 1 and 2. There was a close correlation between the angiographic vasospasm grades and the incidence of symptomatic vasospasm in group 1. However, in group 1, no correlation could be observed between the site of ruptured aneurysms or the timing of operations and vasospasm. Although there is still a limit to the effect of early operation on cerebral vasospasm in patients with subarachnoid hemorrhage grade IV, symptomatic vasospasm after subarachnoid hemorrhage may be ameliorated by early operation in patients with subarachnoid hemorrhage grades II to III.     

Evaluation of the calcium-antagonist nimodipine for the prevention of vasospasm after aneurysmal subarachnoid haemorrhage

Summary 70 consecutive patients admitted within four days after the first aneurysmal subarachnoid haemorrhage (SAH) were evaluated by daily transcranial Doppler ultrasound (TCD) measurement of the blood flow velocities (BFVs) of both middle cerebral arteries (MCAs) and by daily recordings of their clinical grade (Hunt and Hess). Patients with no or only little subarachnoid blood in the first CT after admission were classified as low-risk for the development of symptomatic vasospasm (VSP), and patients with big subarachnoid clots or thick layers of subarachnoid blood were graded as high-risk patients for symptomatic VSP. The first series of 33 patients received no nimodipine whereas the second series of 37 patients were treated with nimodipine 2 mg/h intravenously, starting within 24 hours after the SAH in the majority of patients. 7–14 days postoperatively, the intravenous dose was changed to oral nimodipine 60 mg/q4h for one week and then discontinued. A mean BFV curve of the side with the higher flow velocities correlated with the mean clinical status (Hunt and Hess) was calculated by computer analysis for the patients treated without nimodipine and for those receiving nimodipine in each risk group. The mean BFV curves of the same risk groups were compared in order to evaluate the effect of nimodipine for the prevention of vasospasm following SAH. The delayed neurological deficits (DIND) and the functional outcome six months after the SAH were recorded in each group and compared.Nimodipine given within four days after the SAH did not prevent vasospasm evaluated by TCD, but it significantly reduced the severity of the vasoconstriction, especially in high-risk patients. It reduced significantly the incidence of DIND in high-risk patients and improved their functional outcome. Although nimodipine may have a reduced efficacy in preventing vasospasm after early operation of high-risk patients, it probably protects the brain by increasing its tolerance to focal ischaemia.     

Risk Factors Associated with Cerebral Vasospasm following Aneurysmal Subarachnoid Hemorrhage

We studied the risk factors associated with cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). The subjects were 370 patients with ruptured aneurysms who fulfilled all of the following criteria: admission by day 2 after onset, operation performed by day 3 by the same surgeon (T.I.), Hunt-Hess grade I–IV, availability of bilateral carotid angiograms acquired by day 2 and repeated between days 7 and 9. The demographic, clinical, radiographic, surgical, laboratory, and electrocardiographic data were analyzed for angiographic vasospasm (AV), symptomatic vasospasm (SV), and cerebral infarction on computed tomography (CT) scan. Both CT-evident SAH and AV were graded as 0–IV. Among the 370 patients, AV grade III–IV, SV, and cerebral infarction occurred in 26%, 24%, and 20%, respectively. Univariate analysis showed that Hunt-Hess grade III–IV, SAH grade III–IV, intracerebral or/and intraventricular hemorrhage, rebleeding, cigarette smoking, hypertension, alcohol intake, leukocytosis, hyperglycemia, and electrocardiographic QTc prolongation, left ventricular hypertrophy (LVH), and ST depression were significantly related to at least one of AV grade III–IV, SV, or cerebral infarction. Multivariate analysis showed that SAH grade III–IV was the most important risk factor for vasospasm followed by LVH on electrocardiogram, cigarette smoking, and hypertension. AV grade III– IV, SV, and cerebral infarction occurred in 57%, 54%, and 39% of the 46 smokers with LVH, and in 43%, 49%, and 35% of the 68 patients who had both LVH and hypertension, respectively. CT-evident SAH, LVH, cigarette smoking, and hypertension are associated with vasospasm. In smokers or hypertensive patients, premorbid LVH appears to predict much more severe vasospasm.     

The role of endothelin-1 in the origin of cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage.

Plasma and cerebrospinal fluid (CSF) endothelin (ET)-1-like immunoactivity in 27 patients with aneurysmal subarachnoid hemorrhage (SAH) was measured serially by radioimmunoassay for 2 weeks after SAH onset. Mean ET-1-like immunoactivity levels in plasma of patients with SAH were highly elevated during the whole study period, while the levels in CSF of the same patients were not. Plasma ET-1-like immunoactivity levels in patients with SAH classified as Fisher computerized tomography (CT) Group 3 were higher than those in patients with SAH classified as Fisher CT Groups 1 and 2. There were no significant differences in plasma ET-1-like immunoactivity levels between the patient groups stratified by Hunt and Kosnik grade. In this series, plasma ET-1-like immunoactivity levels in the 12 patients with vasospasm were higher than those in the 15 patients without vasospasm during the 1st week; CSF ET-1-like immunoactivity levels in patients with vasospasm were in the normal range on Days 0 to 3 after SAH onset, then became elevated on Days 5 to 7 and remained high until the end of the 2nd week. In contrast, CSF ET-1-like immunoactivity levels in patients without vasospasm were within the normal range during the entire period of study. The time course of the occurrence of vasospasm and that of the increase in CSF ET-1-like immunoactivity coincided precisely. The possible role of endogenous ET-1 in the pathogenesis of vasospasm due to SAH is discussed.     

Administration of hypertonic (3%) sodium chloride/acetate in hyponatremic patients with symptomatic vasospasm following subarachnoid hemorrhage.

A retrospective study was carried out to evaluate the effect of hypertonic (3%) saline chloride/acetate on various hemodynamic parameters in mildly hyponatremic patients with symptomatic vasospasm following aneurysmal subarachnoid hemorrhage (SAH). We identified 29 hyponatremic (serum sodium < 135 mEq/L) patients who received hypertonic (3%) sodium chloride/acetate as a continuous infusion. Administration of hypertonic (3%) sodium chloride/acetate resulted in higher central venous pressures and positive fluid balance, with a concomitant increase in serum sodium and chloride concentrations without metabolic acidosis. There were no changes in mean cerebral blood flow velocities after infusion of hypertonic (3%) sodium chloride/acetate. We found no reports of congestive heart failure, pulmonary edema, metabolic acidosis, coagulopathy, intracranial hemorrhages, or central pontine myelinolysis in any of these patients. We conclude that hypertonic (3%) sodium chloride/acetate can be administered to patients with mild hyponatremia in the setting of symptomatic vasospasm following SAH without untoward effects. Sample size and limitations of a retrospective analysis preclude conclusions about safety and efficacy of hypertonic (3%) sodium chloride/acetate administration in this patient population. However, our results support justification for a prospective, randomized, double-blind trial of hypertonic (3%) sodium chloride/acetate versus normal saline in patients with symptomatic vasospasm following SAH.     

Effect of arachnoid plasty using fibrin glue membrane after clipping of ruptured aneurysm on the occurrence of complications and outcome in the elderly patients

Summary Background. In elderly patients with aneurysmal subarachnoid hemorrhage (SAH), complications including vasosopasm, subdural effusion, and late hydrocephalus, are liable to occur even after aneurysmal surgery. We examined prospectively the efficacy of arachnoid plasty using fibrin glue membrane during surgery of ruptured aneurysms in the elderly patients for preventing complications. The effects on the modified Rankin scale (mRS) and the Glasgow outcome scale (GOS) 3 months after SAH were noted. Methods. Total of 31 patients aged more than 70 years selected from a consecutive series of patients with aneurysmal SAH, were divided into two groups alternately, a group with arachnoid plasty (n = 16) and a control group without arachnoid plasty (n = 15). Statistical analyses were performed to assess relationships among various clinical and neuroradiological variables, especially between arachnoid plasty and occurrence of symptomatic vasospasm, subdural effusion, late hydrocephalus, or outcome such as mRS and GOS 3 months after onset. Findings. Statistical analyses revealed that arachnoid plasty were associated with late hydrocephalus and subdural effusion negatively, but with better mRS at 3 months after SAH. A tendency to be associated with less frequent symptomatic vasospasm was also noted. Conclusion. Arachnoid plasty using fibrin glue is suggested to be effective in preventing complications associated with SAH and aneurysmal surgery. A better outcome in the elderly patients can be achieved.     

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

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.     

Intravenous magnesium sulfate after aneurysmal subarachnoid hemorrhage: a prospective randomized pilot study

We performed a randomized, double-blind, pilot study on magnesium sulfate (MgSO4) infusion for aneurysmal subarachnoid hemorrhage (SAH).Sixty patients with SAH were randomly allocated to receive either MgSO4 80 mmol/day or saline infusion for 14 days. Patients also received intravenous nimodipine. Episodes of vasospasm were treated with hypertensive and hypervolemic therapy. Neurologic status was assessed 6 months after hemorrhage using the Barthel index and Glasgow Outcome Scale. Incidences of cardiac and pulmonary complications were also recorded.Patient characteristics, severity of SAH, and surgical treatment did not differ between groups. The incidence of symptomatic vasospasm decreased from 43% in the saline group to 23% in patients receiving MgSO4 infusion, but it did not reach statistical significance, P=0.06. For patients who had transcranial Doppler-detected vasospasm, defined as mean flow velocity >120 cm/s and a Lindegaard index >3, the duration was shorter in the magnesium group compared with controls (P<0.01). There was, however, no difference between groups in functional recovery or Glasgow Outcome Scale score. The incidence of adverse events such as brain swelling, hydrocephalus, and nosocomial infection was also similar in patients receiving MgSO4 or saline.In this small pilot study, MgSO4 infusion for aneurysmal SAH is feasible. On the basis of the preliminary data, a larger study recruiting approximately 800 patients is required to test for a possible neuroprotective effect of magnesium after SAH.     

Balloon angioplasty immediately after surgical clipping for symptomatik vasospasm on admission. Report of four cases

In spite of recent advancements in the management of ruptured aneurysm, there are still controversies as to how to threat the patients in serious conditions, one of these concerning whether to operate patients admitted with symptomatic vasospasm (vasospasm on admission) and when. While early surgery may protect patient from further rupturing, it may also increase risk of worsening by inducing much more vasospasm. Four cases of severe vasospasm associated with aneurysmal subarachnoid hemorrhage (SAH) were reported. All of these cases showed symptomatic and angiographical vasospasm on their admission 3–11 days after initial attack of SAH. All cases had a preoperative clinical grading using Hunt & Kosnik of IV, and were treated by early surgery with clipping followed by percutaneous balloon angioplasty (PTA) immediately after clipping. Two cases returned to their previous occupations, while one case remained bed ridden and one died in spite of therapy. Early surgery in this series actually prevented further rupturing, but it is not clear whether PTA immediately after clipping may prevent further deterioration by progression of vasospasm. For selected cases especially those with reversible ischemia, this combined treatment may offer more favorable results than late surgery with conservative medical care. Further investigation is necessary to support the validity of this therapy.     

Effectiveness of combining continuous cerebrospinal drainage and intermittent intrathecal urokinase injection therapy in preventing symptomatic vasospasm following aneurysmal subarachnoid haemorrhage

The effect of cisternal drainage and intrathecal urokinase (UK) injections in preventing symptomatic vasospasm after aneurysmal subarachnoid haemorrhage was retrospectively studied in 69 patients with uniform backgrounds with regard to subarachnoid haemorrhage (SAH; WFNS grade I to IV, Fisher's group 3, undergoing surgery or coil embolization within 72 h of the onset). With regard to the selection of patients, 34 patients belonging to the control group (no UK injection group) underwent the treatment during the 3-year period from 2001 to 2003, while 35 patients belonging to the UK group underwent the treatment during the 3-year period from 2004 to 2006. The incidence of symptomatic vasospasm was 5/35 with the UK group, but 12/34 with a control group. The UK injection significantly reduced the incidence of symptomatic vasospasm (p = 0.042, Pearson chi-square test), resulting in an improvement shown by the Glasgow Outcome Scale (GOS; p = 0.030, Mann-Whitney U test; Table V). The distribution on the angiographic grading scales for cerebral vasospasm significantly shifted in a positive direction for the UK group (mild 0, moderate 5, severe 0) in comparison with the control group (mild 0, moderate 4, severe 8; p = 0.014, Mann-Whitney U test). This study suggests that combining continuous cerebrospinal drainage and intermittent intrathecal UK injection therapy is a relatively simple and effective method for symptomatic vasospasm prophylaxis in patients with aneurysmal SAH.