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Subarachnoid hemorrhage from a ruptured intracranial saccular aneurysm is associated with a high rate of morbidity and mortality. Most complications occur two to three weeks after the initial hemorrhage. The key to minimizing morbidity and mortality is early and aggressive intensive-care management. The Cleveland Clinic Neurosurgical Intensive Care Unit approach is reviewed.

The circulatory changes in the cortex around a cerebral arteriovenous malformation (AVM) were studied in 18 patients. The AVMs had rapid circulation times with early draining veins on angiography. Local cortical blood flow (ICoBF) was measured with cortically applied thermister/Peltier stack arrays. The AVMs had a more pronounced effect on ICoBF at a 2- to 4-cm distance from the AVM margin than in the adjacent cortex. Mean preexcision ICoBF was 62.9 ± 6.7 (SE) ml/100 g/minute (i.e., similar to normal controls) near the AVM margin and 43.0 ± 4.2 ml/100 g/minute far (i.e., >2 cm) from the AVM. CO2 reactivity (COR) before excision was 1.1 ± 0.3 ml/100 g/minute/torr of CO2 (i.e., similar to normal controls) at near sites and 0.6 ± 0.3 ml/100 g/minute/torr of CO2 at far sites. The mean postexcision near ICoBF remained stable at 55.8 ± 5.1 ml/100 g/minute at near sites, but the far ICoBF significantly increased (P < 0.05) to 57.2 ± 6.8 ml/100 g/minute. The cortical feeding artery pressure was substantially below the normal cortical artery pressure in 50% of the cases studied. Pressure in these arteries normalized after occlusion and AVM excision, resulting in a rapid increase in cortical artery perfusion pressure. Draining red vein pressure, which was elevated before AVM excision, also dropped after excision, contributing to the increase in perfusion pressure. Two patients who developed the normal perfusion pressure breakthrough syndrome (PBS) after operation had low ICoBF and disturbed COR before AVM excision and marked increase of ICoBF after excision. Factors that contribute to the development of PBS include: (a) low ICoBF around an AVM; (b) impaired COR; (c) low cortical artery pressure before AVM excision; (d) normalization in cortical artery pressure after AVM removal; and (e) substantial increase in ICoBF after AVM removal. Maintenance of a low systemic arterial blood pressure during the early postoperative period is essential in reducing the risk of severe cerebral edema.

2100 Background: Anaplastic oligodendroglial tumors include both anaplastic oligodendroglioma (AO), and anaplastic oligoastrocytoma (AOA), histological categories of WHO grade 3 gliomas. There is limited data on specific prognostic factors for patients with these tumors. Methods: After obtaining IRB approval, the Cleveland Clinic Brain Tumor and Neuro-Oncology Center’s database was used to identify patients with histologically confirmed AO and AOA at the time of diagnosis. Multivariable analysis was conducted with use of a Cox proportional hazards model and a stepwise selection algorithm that used p

2076 Background: Low-grade gliomas account for 10-20% of all primary brain tumors. There is limited data on specific prognostic factors for patients with low-grade gliomas. Methods: After obtaining IRB approval, the Cleveland Clinic Brain Tumor and Neuro-Oncology Center’s database was used to identify patients with histologically confirmed grade 2 glioma at the time of diagnosis. Multivariable analysis was conducted with use of a Cox proportional hazards model and a stepwise selection algorithm that used p

e13567 Background: Albumin levels are widely used to estimate patients’ nutritional status. Low perioperative albumin levels are associated with worse outcomes. Moreover, Prognostic Nutritional Index (PNI), which is calculated from serum albumin levels and peripheral blood lymphocyte count as follows: PNI = (Albumin x 10) + (0.005 x ALC), has been used to predict both short and long term outcomes in patients with wide variety of tumors. The primary objective of this study was to characterize perioperative albumin levels and PNI in newly diagnosed GBM patients. Secondary objectives included associations between albumin levels and PNI on progression free survival (PFS) and overall survival (OS). Methods: We retrospectively reviewed 568 newly diagnosed GBM patients who underwent surgery followed by standard of care chemoradiation. We analyzed the association between albumin and PNI on age, sex, MGMT methylation status, and extent of surgical resection on PFS and OS using a multivariate Cox proportional hazard model. Results: Of the 568 patients collected, 355 (62.5%) were males, 158 (27.8%) had gross total resection of the tumor, and 197(42.5%) were MGMT methylated. Both albumin and PNI were associated with OS but not PFS. The hazard ratio (HR) for OS among the top 2 quartiles of both albumin level and PNI were significantly higher than the bottom two quartiles. The median albumin level was 4.0 and the median PNI was 40. The point for significant high hazard ratio (HR) was around median value for both Albumin and PNI based on restricted cubic spine Cox regression models. The Kaplan-Meir (KM) estimated median OS was 15.2 months for albumin > 4, and 7.6 for albumin ≤4. The KM estimated median OS was 14.6 months for PNI > 40, and 5.7 for PNI≤40 (P logrank < 0.001 for both). While controlling for other factors that may also be associated with early death including age, gender, surgery type and MGMT status, HR = 1.9 (95% CI = 1.4- = 2.6) for Albumin < 4, and HR = 2.1 (95% CI = 1.5- 3.0) for PNI < 40 compared to their counterpart. Conclusions: Glioblastoma patients with perioperative albumin > 4 had a median OS of 15.2 months and 7.6 months for albumin ≤4, and a median OS of 14.6 months for PNI > 40 and 5.7 months for PNI≤40 (P logrank < 0.001 for both).

Fifteen patients who had undergone neurovascular surgery for arteriovenous malformations or cerebrovascular aneurysms and had intracranial pressure (ICP) monitors were studied. The patients had been treated initially with sodium nitroprusside to maintain their arterial BP in a prescribed range, but, because of excessive nitroprusside dose requirements, they were considered either to have refractory BP or to be at risk for thiocyanate toxicity. Intravenous labetalol therapy was started either by frequent bolus pulse therapy every 1 to 2 h or by continuous infusion therapy. The degree of desired arterial BP control and the effects on ICP and cerebral perfusion pressure (CPP) were assessed and compared with the results during nitroprusside therapy. The degree of arterial BP control with labetalol was assessed to be good; 11 patients were weaned off nitroprusside and the remaining four patients had a substantial reduction in their nitroprusside requirements, needing an average of only 1.5 micrograms/kg.min of nitroprusside to control their BP compared with average requirements of 10 micrograms/kg.min of nitroprusside before labetalol therapy. Labetalol therapy improved CPP in six patients and ICP in five patients, with no significant change in cerebral pressure in the remainder. Overall, the CPP in the 15 patients improved from 63 +/- 15 (SD) mm Hg with nitroprusside to 65 +/- 10 mm Hg with labetalol therapy and the ICP decreased from 11.3 +/- 6.1 mm Hg with nitroprusside to 8.6 +/- 3.1 mm Hg with labetalol therapy (p less than .05 by Wilcoxon matched pairs).(ABSTRACT TRUNCATED AT 250 WORDS)