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

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.

2002 ◽  
Vol 97 (6) ◽  
pp. 1302-1305 ◽  
Author(s):  
Takao Kamezaki ◽  
Kiyoyuki Yanaka ◽  
Sohji Nagase ◽  
Keishi Fujita ◽  
Noriyuki Kato ◽  
...  

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.


1991 ◽  
Vol 74 (1) ◽  
pp. 14-20 ◽  
Author(s):  
Juha Öhman ◽  
Antti Servo ◽  
Olli Heiskanen

✓ A prospective series of 265 patients with aneurysmal subarachnoid hemorrhage (SAH) of Grades I to III (Hunt and Hess classification) upon admission were evaluated as to neurological outcome and computerized tomography (CT) findings 1 to 3 years (mean 1.4 years) after the SAH and surgery. A total of 73 patients underwent acute surgery (within 72 hours after the bleed: Days 0 to 3), 86 were operated on subacutely (between Days 4 and 7), and 91 had late surgery (on Day 8 or later). Fifteen patients died before surgery was undertaken and another 20 patients died during the follow-up period. A total of 104 patients received nimodipine and the rest of the patients received either placebo (109 patients) or no medication (52 patients). A logistical regression analysis revealed the following prognostic factors for cerebral infarction, in order of importance: the amount of blood on the primary CT scan; postoperative angiographic vasospasm; the timing of the operation; and a history of hypertension. The use of nimodipine was associated with a significant reduction of cerebral infarcts visualized by CT scanning in patients who received intermediate or late surgery. In patients who underwent acute surgery no significant difference between the incidence of cerebral infarcts was observed.


2003 ◽  
Vol 99 (4) ◽  
pp. 644-652 ◽  
Author(s):  
R. Loch Macdonald ◽  
Axel Rosengart ◽  
Dezheng Huo ◽  
Theodore Karrison

Object. The goal of this study was to determine factors associated with the development of symptomatic vasospasm among patients with aneurysmal subarachnoid hemorrhage (SAH) who participated in the randomized, double-blind, placebo-controlled trials of tirilazad between 1991 and 1997. Methods. Data obtained from 3567 patients entered into trials of tirilazad were analyzed using uni- and multivariate logistic regression to determine factors that predict the development of symptomatic vasospasm. Symptomatic vasospasm was defined by clinical criteria accompanied by laboratory- and radiologically determined exclusion of other causes of neurological deterioration. Transcranial Doppler ultrasonographic and/or angiographic confirmation was not required. In these patients, the aneurysms were scheduled to be treated surgically, and no patient undergoing endovascular treatment was included. A multivariate analysis showed that factors significantly associated with vasospasm were age 40 to 59 years, history of hypertension, worse neurological grade, thicker blood clot on the cranial computerized tomography (CT) scan obtained on hospital admission, larger aneurysm size, presence of intraventricular hemorrhage (IVH), prophylactic use of induced hypertension, and not participating in the first European tirilazad study. Conclusions. Symptomatic vasospasm was associated with the amount of SAH on the CT scan, the presence of IVH, and the patient's neurological grade. The association with patient age may reflect alterations in vessel reactivity associated with age. A history of hypertension may render the brain more susceptible to symptoms from vasospasm. The explanation for the relationships with aneurysm size, use of prophylactic induced hypertension, and the particular study is unclear.


2003 ◽  
Vol 99 (2) ◽  
pp. 271-275 ◽  
Author(s):  
Jay U. Howington ◽  
Scott C. Kutz ◽  
Gregory E. Wilding ◽  
Deepak Awasthi

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; preexistent 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.


2002 ◽  
Vol 97 (5) ◽  
pp. 1036-1041 ◽  
Author(s):  
Eva H. Brilstra ◽  
Ale Algra ◽  
Gabriel J. E. Rinkel ◽  
Cornelis A. F. Tulleken ◽  
Jan van Gijn

Object. Neurosurgical clip application is the standard method used to prevent rebleeding in patients with aneurysmal subarachnoid hemorrhage (SAH). The authors assessed the magnitude of the reduction in poor outcomes that accompanies a strategy aimed at surgery. Methods. Three hundred forty-six consecutive patients with aneurysmal SAH were studied. The authors estimated the number of surgically treated patients with good outcomes who would have had poor outcomes as a consequence of rebleeding if clip application had not been performed (A). They also assessed the number of patients whose poor outcomes were exclusively caused by operative complications (B). Without an operation some of these patients would have had poor outcomes because of rebleeding (C). The authors represented the number of patients in whom poor outcome was prevented by surgery with the following formula: A − B + C. They assessed the relationships between baseline characteristics of patients and aneurysms and the likelihood that a patient underwent surgery, the risk of operative complications, and the risk of rebleeding. The absolute reduction in the risk of poor outcome found in patients who undergo surgery was 9.7%. This implies that to prevent a poor outcome in one patient, surgery had to be performed in 10. The relative risk of poor outcome following surgery compared with that after conservative treatment was estimated to be 0.81. Logistic regression analysis showed a statistically significant relationship between patient age older than 65 years and the occurrence of operative complications (odds ratio [OR] 2.49; 95% confidence interval [CI] 1.03–6.03), between age older than 65 years and the likelihood of undergoing surgery (OR 0.12; 95% CI 0.07–0.2), and between a poor clinical condition at admission and the likelihood of undergoing surgery (OR 0.26; 95% CI 0.14–0.47). The authors did not identify any predictive factors for rebleeding when the Cox proportional hazard model was used. Conclusions. The beneficial effect of a treatment strategy in which the goal is surgery is substantial. If new treatment modalities such as embolization with coils are explored, these should carefully be compared with surgery before they are generally introduced.


2009 ◽  
Vol 110 (5) ◽  
pp. 989-995 ◽  
Author(s):  
Seppo Juvela ◽  
Jari Siironen ◽  
Jaakko Lappalainen

Object After aneurysmal subarachnoid hemorrhage (SAH), conflicting results concerning an association between the APOE genotype and impaired outcome have been reported. The authors tested prospectively whether APOE ε2 or ε4 allele–containing genotypes (ε2+ and ε4+) affect outcome after SAH. Methods Previous disease histories and clinical and radiological variables were recorded for 105 patients who were admitted within 48 hours after SAH. Fifteen patients (14%) had the ε2+ genotype and 31 (17%) had ε4+ genotypes. Factors predicting poor outcome according to the Glasgow Outcome Scale and cerebral infarction visible on CT scans obtained at 3 months after SAH were tested with multiple logistic regression analyses. Results Apolipoprotein E ε2 or ε4–containing genotypes were not associated with outcome, occurrence of cerebral infarction, or with any of their predictors, either in univariate or multivariate analysis. Poor outcome was predicted independently by the occurrence of intraventricular bleeding and intracerebral hematoma as well as by elevated levels of both plasma glucose and D-dimer, and delayed cerebral ischemia (p < 0.05 for each factor), and in univariate analysis only by clinical condition on admission and patient age. Cerebral infarction was predicted independently according to clinical condition on admission (p < 0.05), amount of subarachnoid blood (p < 0.01), duration of intraoperative parent artery clipping (p < 0.01), and body mass index (p < 0.05). In the univariate analysis only cerebral infarction was also predicted by patient age, intracerebral hematoma, and delayed cerebral ischemia. Conclusions Severity of bleeding for the most part predicts outcome after SAH; APOE polymorphisms seem to have no prognostic value for outcome after SAH. This result was in accordance with the findings from the largest ischemic stroke studies.


2000 ◽  
Vol 92 (3) ◽  
pp. 390-400 ◽  
Author(s):  
Seppo Juvela

Object. The pathogenesis of cerebral vasospasm and delayed ischemia after subarachnoid hemorrhage (SAH) seems to be complex. An important mediator of chronic vasospasm may be endothelin (ET), with its powerful and long-lasting vasoconstricting activity. In this study the author investigated the correlation between serial plasma concentrations of ET and ischemic symptoms, angiographically demonstrated evidence of vasospasm, and computerized tomography (CT) findings after aneurysmal SAH.Methods. Endothelin-1 immunoreactivity in plasma was studied in 70 patients with aneurysmal SAH and in 25 healthy volunteers by using a double-antibody sandwich-enzyme immunoassay (immunometric) technique.On the whole, mean plasma ET concentrations in patients with SAH (mean ± standard error of mean, 2.1 ± 0.1 pg/ml) did not differ from those of healthy volunteers (1.9 ± 0.2 pg/ml). Endothelin concentrations were significantly higher (p < 0.05) in patients who experienced delayed cerebral ischemia with fixed neurological deficits compared with those in other patients (post-SAH Days 0–5, 3.1 ± 0.8 pg/ml compared with 2.1 ± 0.2 pg/ml; post-SAH Days 6–14, 2.5 ± 0.4 pg/ml compared with 1.9 ± 0.2 pg/ml). Patients with angiographic evidence of severe vasospasm also had significantly (p < 0.05) elevated ET concentrations (post-SAH Days 0–5, 3.2 ± 0.8 pg/ml; post-SAH Days 6–14, 2.7 ± 0.5 pg/ml) as did those with a cerebral infarction larger than a lacuna on the follow-up CT scan (post-SAH Days 0–5, 3.1 ± 0.8 pg/ml; post-SAH Days 6–14, 2.5 ± 0.4 pg/ml) compared with other patients. Patients in whom angiography revealed diffuse moderate-to-severe vasospasm had significantly (p < 0.05) higher ET levels than other patients within 24 hours before or after angiography (2.6 ± 0.3 compared with 1.9 ± 0.2 pg/ml). In addition, patients with a history of hypertension or cigarette smoking experienced cerebral infarctions significantly more often than other patients, although angiography did not demonstrate severe or diffuse vasospasm more often in these patients than in others.Conclusions. Endothelin concentrations seem to correlate with delayed cerebral ischemia and vasospasm after SAH. The highest levels of ET are predictive of the symptoms of cerebral ischemia and vasospasm, and ET may also worsen ischemia in patients with a history of hypertension. Thus, ET may be an important causal or contributing factor to vasospasm, but its significance in the pathogenesis of vasospasm remains unknown.


2016 ◽  
Vol 42 (1-2) ◽  
pp. 97-105 ◽  
Author(s):  
Naoya Matsuda ◽  
Masato Naraoka ◽  
Hiroki Ohkuma ◽  
Norihito Shimamura ◽  
Katsuhiro Ito ◽  
...  

Background: Several clinical studies have indicated the efficacy of cilostazol, a selective inhibitor of phosphodiesterase 3, in preventing cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). They were not double-blinded trial resulting in disunited results on assessment of end points among the studies. The randomized, double-blind, placebo-controlled study was performed to assess the effectiveness of cilostazol on cerebral vasospasm. Methods: Patients with aneurysmal SAH admitted within 24 h after the ictus who met the following criteria were enrolled in this study: SAH on CT scan was diffuse thick, diffuse thin, or local thick, Hunt and Hess score was less than 4, administration of cilostazol or placebo could be started within 48 h of SAH. Patients were randomly allocated to placebo or cilostazol after repair of a ruptured saccular aneurysm by aneurysmal neck clipping or endovascular coiling, and the administration of cilostazol or placebo was continued up to 14 days after initiation of treatment. The primary end point was the occurrence of symptomatic vasospasm (sVS), and secondary end points were angiographic vasospasm (aVS) evaluated on digital subtraction angiography, vasospasm-related new cerebral infarction evaluated on CT scan or MRI, and clinical outcome at 3 months of SAH as assessed by Glasgow Outcome Scale, in which poor outcome was defined as severe disability, vegetative state, and death. All end points were evaluated with blinded assessment. Results: One hundred forty eight patients were randomly allocated to the cilostazol group (n = 74) or the control group (n = 74). The occurrence of sVS was significantly lower in the cilostazol group than in the control group (10.8 vs. 24.3%, p = 0.031), and multiple logistic analysis showed that cilostazol use was an independent factor reducing sVS (OR 0.293, 95% CI 0.099-0.568, p = 0.027). The incidence of aVS and vasospasm-related cerebral infarction were not significantly different between the groups. Poor outcome was significantly lower in the cilostazol group than in the control group (5.4 vs. 17.6%, p = 0.011), and multiple logistic analyses demonstrated that cilostazol use was an independent factor that reduced the incidence of poor outcome (OR 0.221, 95% CI 0.054-0.903, p = 0.035). Severe adverse events due to cilostazol administration did not occur during the study period. Conclusions: Cilostazol administration is effective in preventing sVS and improving outcomes without severe adverse events. A larger-scale study including more cases was necessary to confirm this efficacy of cilostazol.


1993 ◽  
Vol 79 (6) ◽  
pp. 885-891 ◽  
Author(s):  
Giuseppe Lanzino ◽  
Neal F. Kassell ◽  
Teresa Germanson ◽  
Laura Truskowski ◽  
Wayne Alves

✓ Plasma glucose levels were studied in 616 patients admitted within 72 hours after subarachnoid hemorrhage (SAH). Glucose levels measured at admission showed a statistically significant association with Glasgow Coma Scale scores, Botterell grade, deposition of blood on computerized tomography (CT) scans, and level of consciousness at admission. Elevated glucose levels at admission predicted poor outcome. A good recovery, as assessed by the Glasgow Outcome Scale at 3 months, occurred in 70.2% of patients with normal glucose levels (≤ 120 mg/dl) and in 53.7% of patients with hyperglycemia (> 120 mg/dl) (p = 0.002). The death rates for these two groups were 6.7% and 19.9%, respectively (p = 0.001). The association was still maintained after adjusting for age (> or ≤ 50 years) and thickness of clot on CT scans (thin or thick) in the subset of patients who were alert/drowsy at admission. Increased mean glucose levels between Days 3 and 7 also predicted a worse outcome; good recovery was observed in 132 (73.7%) of 179 patients who had normal mean glucose levels (≤ 120 mg/dl) and 160 (49.7%) of 322 who had elevated mean glucose levels (> 120 mg/dl) (p < 0.0001). Death occurred in 6.7% and 20.8% of the two groups, respectively (p < 0.0001). It is concluded that admission plasma glucose levels can serve as an objective prognostic indicator after SAH. Elevated glucose levels during the 1st week after SAH also predict a poor outcome. However, a causal link between hyperglycemia and outcome after delayed cerebral ischemia, although suggested by experimental data, cannot be established on the basis of this study.


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