Symptomatic hydrocephalus following aneurysmal subarachnoid hemorrhage

The results of a series of 500 consecutive patients who underwent aneurysmal surgery between 1969 and 1980 are reported. The incidence of significant symptomatic hydrocephalus secondary to spontaneous rupture of an intracranial aneurysm was 16.4%. Hydrocephalus was most frequent after rupture of aneurysms of the anterior communicating artery. Only one-third of the patients had more than one episode of subarachnoid hemorrhage before surgery. In 64% of the patients with preoperative hydrocephalus, there was angiographic evidence of spasm. In certain cases, the hydrocephalus must be treated before the offending aneurysm can be managed.     

Monocyte chemoattractant protein-1 predicts outcome and vasospasm following aneurysmal subarachnoid hemorrhage

OBJECT: Despite efforts to elucidate both the molecular mechanism and the clinical predictors of vasospasm after aneurysmal subarachnoid hemorrhage (ASAH), its pathogenesis remains unclear. Monocyte chemoattractant protein-1 (MCP-1) is a chemokine that has been firmly implicated in the pathophysiology of vasospasm and in neural tissue injury following focal ischemia in both animal models and human studies. The authors hypothesized that MCP-1 would be found in increased concentrations in the blood and cerebrospinal fluid (CSF) of patients with ASAH and would correlate with both outcome and the occurrence of vasospasm. METHODS: Seventy-seven patients who presented with ASAH were prospectively enrolled in this study between July 2001 and May 2002. Using an enzyme-linked immunosorbent assay, MCP-1 levels were measured in serum daily and in CSF when available. The mean serum and CSF MCP-1 concentrations were calculated for each patient throughout the entire hospital stay. Neurological outcome was evaluated at discharge or 14 days posthemorrhage using the modified Rankin Scale. Vasospasm was evaluated on angiography. RESULTS: The serum MCP-1 concentrations correlated with negative outcome such that a 10% increase in concentration predicted a 25% increase in the probability of a poor outcome, whereas the serum MCP-1 levels did not correlate with vasospasm. Concentrations of MCP-1 in the CSF, however, proved to be significantly higher in patients with angiographically demonstrated vasospasm. CONCLUSIONS: These findings suggest a role for MCP-1 in neurological injury and imply that it may act as a biomarker of poor outcome in the serum and of vasospasm in the CSF.     

Case-control study of clinical outcome after aneurysmal subarachnoid hemorrhage

The clinical and neuropathological features of 84 nonsurvivors of aneurysmal subarachnoid hemorrhage (consecutive autopsy series) were compared with those of 51 survivors (consecutive clinical series). The groups differed significantly in the type of bleeding: 58% of the nonsurvivors had massive subarachnoid hemorrhage (MSAH) compared to 10% of the survivors (P less than 0.00001); 54% of the nonsurvivors had intraventricular hemorrhage (IVH) compared to 29% of the survivors (P less than 0.008); 45% of the nonsurvivors had intracerebral hematoma (ICH) compared to 8% of the survivors (P less than 0.00001). Only 1 of the 19 patients with both MSAH and ICH survived. The incidence of cerebral infarction was similar in nonsurvivors (31%) and survivors (29%). In the absence of associated MSAH, IVH, or ICH, cerebral infarction was uncommon (11%). Documented in-hospital rebleeding was uncommon in nonsurvivors (13%) and survivors (2%). Admission neurological status did not predict outcome independent of the extent of the initial bleeding. Comparison of the two groups suggests that the type and extent of initial bleeding are the most important determinants of mortality in aneurysmal subarachnoid hemorrhage.     

Early operation and overall outcome in aneurysmal subarachnoid hemorrhage

Over a 3-year period, 251 individuals in a population of 1.46 million were known to have suffered an aneurysmal subarachnoid hemorrhage (SAH). Forty-three individuals (17%) were either found dead or were dead on arrival at a hospital or forensic department. Forty-nine patients (20%) were at no stage in their clinical course considered to be surgical candidates. Six patients (2% of the total series) were initially in good condition, but subsequently deteriorated during the acute phase and were not treated surgically. Nineteen poor-risk patients (8% of the total series) underwent emergency surgery because of a life-threatening intracerebral hematoma; 105 patients (42% of the total series or 69% of the surgically treated patients) were operated on at the acute stage, and 29 patients (11% of the total series or 19% of the surgically treated patients) underwent late surgery. Of the total series, 107 patients (42%) recovered without neurological deficits; the overall morbidity rate was 19%, and the mortality rate was 39%. Of 99 Grade I to III patients who were operated on at the acute stage, 76% recovered without neurological deficits, and 4% died. It is concluded that the overall outcome in aneurysmal SAH remains poor, mainly because of the large group of patients who are permanently devastated by their initial bleed.     

Risk factors for ischemic lesions following aneurysmal subarachnoid hemorrhage

OBJECT: The aim of this study was to test whether enoxaparin treatment (40 mg subcutaneously once daily) reduces the risk of cerebral infarction after subarachnoid hemorrhage (SAH) and to investigate predictive risk factors for permanent ischemic lesions visible on follow-up computerized tomography (CT) scans obtained 3 months after SAH. METHODS: After undergoing surgery for a ruptured aneurysm, 170 patients were randomized in a prospective, double-blind, placebo-controlled trial to test the effect of enoxaparin on the occurrence of ischemic lesions, which were demonstrated on follow-up CT scans available for 156 patients. The presence of lesions correlated highly with an impaired outcome, as assessed using both the Glasgow Outcome and modified Rankin Scales (p < 0.01). Lesions occurred in 101 (65%) of the 156 patients. In half of the patients (51 patients) no lesion was visible on the CT scan obtained on the 1st postoperative day in 51 patients. On univariate analysis, the presence of lesions at 3 months post-SAH was not associated with enoxaparin treatment but did correlate with several clinical, radiological, and prehemorrhage variables. Significant independent risk factors for lesions consisted of an impaired initial clinical condition (odds ratio [OR] 2.63, 95% confidence interval [CI] 1.03-6.73), amount of subarachnoid blood (OR 6.51, 95% CI 2.27-18.65), nocturnal occurrence of SAH (that is, between 12:01 a.m. and 8:00 a.m.; OR 4.32, 95% CI 1.28-14.52), fixed symptoms of delayed ischemia (OR 5.21, 95% CI 1.02-26.49), duration of temporary artery occlusion during surgery (OR 1.66 per minute, 95% CI 1.20-2.31), and body mass index (OR 1.13/kg/m2, 95% CI 1.01-1.28). CONCLUSIONS: The presence of ischemic lesions can be predicted by the severity of bleeding, delayed cerebral ischemia, excess weight, duration of temporary artery occlusion, and occurrence of nocturnal aneurysm rupture.     

Characterization of perioperative seizures and epilepsy following aneurysmal subarachnoid hemorrhage

OBJECT: The reported incidence, timing, and predictive factors of perioperative seizures and epilepsy after subarachnoid hemorrhage (SAH) have differed considerably because of a lack of uniform definitions and variable follow-up periods. In this study the authors evaluate the incidence, temporal course, and predictive factors of perioperative seizures and epilepsy during long-term follow up of patients with SAH who underwent surgical treatment. METHODS: Two hundred seventeen patients who survived more than 2 years after surgery for ruptured intracranial aneurysms were enrolled and retrospectively studied. Episodes were categorized into onset seizures (< or = 12 hours of initial hemorrhage), preoperative seizures, postoperative seizures, and late epilepsy, according to their timing. The mean follow-up time was 78.7 months (range 24-157 months). Forty-six patients (21.2%) had at least one seizure post-SAH. Seventeen patients (7.8%) had onset seizures, five (2.3%) had preoperative seizures, four (1.8%) had postoperative seizures, 21 (9.7%) had at least one seizure episode after the 1st week postoperatively, and late epilepsy developed in 15 (6.9%). One (3.8%) of 26 patients with perioperative seizures (onset, preoperative, or postoperative seizure) had late epilepsy at follow up. The mean latency between the operation and the onset of late epilepsy was 8.3 months (range 0.3-19 months). Younger age (< 40 years old), loss of consciousness of more than 1 hour at ictus, and Fisher Grade 3 or greater on computerized tomography scans proved to be significantly related to onset seizures. Onset seizure was also a significant predictor of persistent neurological deficits (Glasgow Outcome Scale Scores 2-4) at follow up. Factors associated with the development of late epilepsy were loss of consciousness of more than 1 hour at ictus and persistent postoperative neurological deficit. CONCLUSIONS: Although up to one fifth of patients experienced seizure(s) after SAH, more than half had seizure(s) during the perioperative period. The frequency of late epilepsy in patients with perioperative seizures (7.8%) was not significantly higher than those without such seizures (6.8%). Perioperative seizures did not recur frequently and were not a significant predictor for late epilepsy.     

Cocaine use as a predictor of outcome in aneurysmal subarachnoid hemorrhage

OBJECT: The goal of this study was to analyze the relationship between cocaine use and outcomes of aneurysmal subarachnoid hemorrhage (SAH). METHODS: A retrospective review was performed of the medical records of patients with intracranial aneurysms treated at a single institution between January 1996 and December 2001. Only patients who presented with SAH were included in the study. The covariates chosen for the statistical analysis included the following: patient age, sex, and race; systolic and mean arterial blood pressure measurements on hospital admission; Hunt and Hess and Fisher grades; pre-existent major systemic disease; and history of alcohol, tobacco, or cocaine use. The Glasgow Outcome Scale (GOS) was used to standardize outcome and was dichotomized such that a score between 1 and 3 was considered a poor outcome and a score of 4 or 5 was considered a favorable outcome. The records of 151 patients were reviewed and 108 of these presented with aneurysmal SAH. Of these 108 patients, 36 (33.3%) had used cocaine within 24 hours before presentation. A Hunt and Hess grade of IV or V was assigned to 20 (55.6%) of 36 patients who used cocaine, compared with eight (11.1%) of 72 patients who did not; this difference was found to be statistically significant (p < 0.0001). Twenty-eight patients (77.8%) in the cocaine user group and 20 patients (27.8%) in the non-cocaine user group experienced clinically significant, angiographically confirmed vasospasm during their hospital course (p < 0.0001). Cocaine use was associated with a 2.8-fold greater risk of developing vasospasm (95% confidence interval [CI] 1.86-4.22). A GOS score of 1, 2, or 3 was assigned to 33 patients (91.7%) in the cocaine user group and to 20 patients (27.8%) in the non-cocaine user group (p < 0.0001). Cocaine use was associated with a 3.3-fold greater risk of poor outcome (95% CI 2.24-4.85). This association was found to be independent of Hunt and Hess grade as well as of vasospasm. CONCLUSIONS: Cocaine adversely affects both the presentation of and outcome in patients with aneurysmal SAH who are undergoing treatment for this disease. The vasoactive properties of the drug appear to aggravate the already tenuous situation of SAH and increase both the occurrence and influence of cerebral vasospasm. Statistical analysis demonstrates that cocaine directly affects both presentation and outcome in a significant manner. It is the authors' interpretation of the results of this retrospective review that cocaine use negatively affects outcome to such an extent that it should be considered equal to the presence of a major systemic illness when determining Hunt and Hess grade.     

Relationship between leukocytosis and ischemic complications following aneurysmal subarachnoid hemorrhage

The prognostic significance of admission leukocytosis with respect to ischemic complications of subarachnoid hemorrhage was retrospectively investigated in a series of patients with recently ruptured intracranial aneurysms. The present study concerned 47 consecutive cases admitted within 72 hours following the last hemorrhage, in the years 1982-1984. There was no difference in the admission WBC counts between patients who subsequently deteriorated due to ischemic complications and those who did not. However, the cell count rose significantly at the time of the clinical manifestations of ischemia, possibly as a result of structural damage of brain tissue and/or increased sympathetic and adrenocortical activity. The possible contribution of leukocytes to the pathogenesis of ischemic damage following subarachnoid hemorrhage--perhaps through the release of leukotrienes--will require further investigation.     

Poor-grade aneurysmal subarachnoid hemorrhage: relationship of cerebral metabolism to outcome

OBJECT: The majority of patients with poor-grade subarachnoid hemorrhage (SAH), that is, World Federation of Neurosurgical Societies (WFNS) Grades IV and V, have high morbidity and mortality rates. The objective of this study was to investigate cerebral metabolism in patients with low- compared with high-grade SAH by using bedside microdialysis and to evaluate whether microdialysis parameters are of prognostic value for outcome in SAH. METHODS: A prospective investigation was conducted in 149 patients with SAH (mean age 50.9 +/- 12.9 years); these patients were studied for 162 +/- 84 hours (mean +/- standard deviation). Lesions were classified as low-grade SAH (WFNS Grades I-III, 89 patients) and high-grade SAH (WFNS Grade IV or V, 60 patients). After approval by the local ethics committee and consent from the patient or next of kin, a microdialysis catheter was inserted into the vascular territory of the aneurysm after clip placement. The microdialysates were analyzed hourly for extracellular glucose, lactate, lactate/pyruvate (L/P) ratio, glutamate, and glycerol. The 6- and 12-month outcomes according to the Glasgow Outcome Scale and functional disability according to the modified Rankin Scale were assessed. In patients with high-grade SAH, cerebral metabolism was severely deranged compared with those who suffered low-grade SAH, with high levels (p < 0.05) of lactate, a high L/P ratio, high levels of glycerol, and, although not significant, of glutamate. Univariate analysis revealed a relationship among hyperglycemia on admission, Fisher grade, and 12-month outcome (p < 0.005). In a multivariate regression analysis performed in 131 patients, the authors identified four independent predictors of poor outcome at 12 months, in the following order of significance: WFNS grade, patient age, L/P ratio, and glutamate (p < 0.03). CONCLUSIONS: Microdialysis parameters reflected the severity of SAH. The L/P ratio was the best metabolic independent prognostic marker of 12-month outcome. A better understanding of the causes of deranged cerebral metabolism may allow the discovery of therapeutic options to improve the prognosis, especially in patients with high-grade SAH, in the future.     

Hypomagnesemia after aneurysmal subarachnoid hemorrhage

OBJECTIVE: Hypomagnesemia frequently occurs in hospitalized patients, and it is associated with poor outcome. We assessed the frequency and time distribution of hypomagnesemia after aneurysmal subarachnoid hemorrhage (SAH) and its relationship to the severity of SAH, delayed cerebral ischemia (DCI), and outcome after 3 months. METHODS: Serum magnesium was measured in 107 consecutive patients admitted within 48 hours after SAH. Hypomagnesemia (serum magnesium <0.70 mmol/L) at admission was related to clinical and initial computed tomographic characteristics by means of the Mann-Whitney U test. Hypomagnesemia at admission and during the DCI onset period (Days 2-12) was related to the occurrence of DCI and hypomagnesemia at admission, and hypomagnesemia that occurred any time during the first 3 weeks after SAH was related to outcome. RESULTS: Hypomagnesemia at admission was found in 41 patients (38%) and was associated with more cisternal (P = 0.006) and ventricular (P = 0.005) blood, a longer duration of unconsciousness (P = 0.007), and a worse World Federation of Neurosurgical Societies scale score at admission (P = 0.001). The crude hazard ratio for DCI with hypomagnesemia at admission was 2.4 (95% confidence interval, 1.0-5.6), and after multivariate adjustment it was 1.9 (95% confidence interval, 0.7-4.7). The hazard ratio of hypomagnesemia from Days 2 to 12 for patients with DCI was 3.2 (range, 1.1-8.9) after multivariate adjustment. The crude odds ratio for poor outcome (Glasgow Outcome Scale score, 1-3) with hypomagnesemia at admission was 2.5 (range, 1.1-5.5). Hypomagnesemia at admission did not contribute to the prediction of outcome in the multivariate model. CONCLUSION: Hypomagnesemia is frequently present after SAH and is associated with severity of SAH. Hypomagnesemia occurring between Days 2 and 12 after SAH predicts DCI.     

Poor-grade aneurysmal subarachnoid hemorrhage: outcome after treatment with urgent surgery

OBJECTIVE: We sought to determine whether the rebleeding rate in poor-grade patients justified a period of supportive observation before selective treatment and whether unselected ultraearly surgery would lead to acceptable results. METHODS: A prospectively audited, nonselected series of 177 consecutive poor-grade (i.e., World Federation of Neurological Surgeons Grades IV and V) patients with aneurysmal subarachnoid hemorrhage managed during a 9-year period was analyzed. A management policy of aggressive ultraearly surgery (not selected by age or by grade) was followed. Coiling was not available. Outcomes were assessed at 3 months. RESULTS: Despite the aggressive management policy, surgery could be performed in only 132 poor-grade patients (75%). Twenty percent of all patients were 70 years of age or older (15% of the surgical cases). All surgery was performed within 12 hours of subarachnoid hemorrhage (majority <6 h). Preoperative rebleeding occurred within the first 12 hours (>85% within 6 h) in 20% of the patients, which is four times the rate found in good-grade patients managed according to the same policy. Outcome assessment performed at 3 months in the 132 poor-grade surgical patients revealed that 40% were independent, 15% were dependent, and 45% had died. There was no significant difference in outcomes for young and old (70+ yr) poor-grade surgical patients (P > 0.05). CONCLUSION: The high ultraearly rebleeding rate indicates a need to urgently secure the ruptured aneurysm by performing surgery or coiling, and this indication is more pronounced for poor-grade patients than for good-grade patients. The outcome results of ultraearly surgery indicate that a nonselective policy does not lead to a large number of dependent survivors, even among elderly poor-grade patients.