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Objectives: We tested the hypothesis that admission serum magnesium levels are associated with extent of hemorrhage in patients with aneurysmal subarachnoid hemorrhage., Design: Single-center prospective observational study., Setting: Tertiary hospital neurologic ICU., Patients: Patients with aneurysmal subarachnoid hemorrhage., Interventions: Clinically indicated CT scans and serum laboratory studies., Measurements and Main Results: Demographic, clinical, laboratory, and radiographic data were analyzed. Extent of initial hemorrhage was graded semi-quantitatively on admission CT scans using the modified Fisher scale (grades: 0, no radiographic hemorrhage; 1, thin [< 1 mm in depth] subarachnoid hemorrhage; 2, thin subarachnoid hemorrhage with intraventricular hemorrhage; 3, thick [≥ 1 mm] subarachnoid hemorrhage; 4, thick subarachnoid hemorrhage with intraventricular hemorrhage). We used both ordinal (modified Fisher scale) and dichotomized (thick vs thin subarachnoid hemorrhage) univariate and adjusted logistic regression models to assess associations between serum magnesium and radiographic subarachnoid hemorrhage severity. Data from 354 patients (mean age 55 ± 14 yr, 28.5% male, median admission Glasgow Coma Scale 14 [10-15]) were analyzed. Mean magnesium was lower in patients with thick versus thin subarachnoid hemorrhage (1.92 vs 1.99 mg/dL; p = 0.022). A monotonic trend across categories of modified Fisher scale was found using analysis of variance and Spearman rank correlation (p = 0.015 and p = 0.008, respectively). In adjusted ordinal and binary regression models, lower magnesium levels were associated with higher modified Fisher scale (odds ratio 0.33 per 1 mg/dL increase; 95% CI, 0.14-0.77; p = 0.011) and with thick subarachnoid hemorrhage (odds ratio 0.29 per 1 mg/dL increase; 95% CI, 0.10-0.78; p = 0.015)., Conclusions: These data support the hypothesis that magnesium influences hemorrhage severity in patients with aneurysmal subarachnoid hemorrhage, potentially through a hemostatic mechanism.

Object: Vasopressor-induced hypertension (VIH) is an established treatment for patients with aneurysmal subarachnoid hemorrhage (SAH) who develop vasospasm and delayed cerebral ischemia (DCI). However, the safety of VIH in patients with coincident, unruptured, unprotected intracranial aneurysms is uncertain., Methods: This retrospective multiinstitutional study identified 1) patients with aneurysmal SAH and 1 or more unruptured, unprotected aneurysms who required VIH therapy (VIH group), and 2) patients with aneurysmal SAH and 1 or more unruptured, unprotected aneurysms who did not require VIH therapy (non-VIH group). All patients had previously undergone surgical or endovascular treatment for the presumed ruptured aneurysm. Comparisons between the VIH and non-VIH patients were made in terms of the patient characteristics, clinical and radiographic severity of SAH, total number of aneurysms, number of ruptured/unruptured aneurysms, aneurysm location/size, number of unruptured and unprotected aneurysms during VIH, severity of vasospasm, degree of hypervolemia, and degree and duration of VIH therapy., Results: For the VIH group (n = 176), 484 aneurysms were diagnosed, 231 aneurysms were treated, and 253 unruptured aneurysms were left unprotected during 1293 total days of VIH therapy (5.12 total years of VIH therapy for unruptured, unprotected aneurysms). For the non-VIH group (n = 73), 207 aneurysms were diagnosed, 93 aneurysms were treated, and 114 unruptured aneurysms were left unprotected. For the VIH and non-VIH groups, the mean sizes of the ruptured (7.2 ± 0.3 vs 7.8 ± 0.6 mm, respectively; p = 0.27) and unruptured (3.4 ± 0.2 vs 3.2 ± 0.2 mm, respectively; p = 0.40) aneurysms did not differ. The authors observed 1 new SAH from a previously unruptured, unprotected aneurysm in each group (1 of 176 vs 1 of 73 patients; p = 0.50). Baseline patient characteristics and comorbidities were similar between groups. While the degree of hypervolemia was similar between the VIH and non-VIH patients (fluid balance over the first 10 days of therapy: 3146.2 ± 296.4 vs 2910.5 ± 450.7 ml, respectively; p = 0.67), VIH resulted in a significant increase in mean arterial pressure (mean increase over the first 10 days of therapy relative to baseline: 125.1% ± 1.0% vs 98.2% ± 1.2%, respectively; p < 0.01) and systolic blood pressure (125.6% ± 1.1% vs. 104.1% ± 5.2%, respectively; p < 0.01)., Conclusions: For small, unruptured, unprotected intracranial aneurysms in SAH patients, the frequency of aneurysm rupture during VIH therapy is rare. The authors do not recommend withholding VIH therapy from these patients.

Introduction: Vasospasm is a major cause of morbidity after subarachnoid hemorrhage (SAH), and current screening techniques (angiography, transcranial Doppler [TCD], and clinical examination) have serious limitations. Brain oximetry is a promising noninvasive tool to detect reduced brain oxygenation from vasospasm., Methods: Consecutive SAH patients at high risk for vasospasm were monitored with the INVOS (Somanetics, IL, USA) 5100C cerebral oximeter. We prospectively collected oximeter readings (rO2) with concurrent values for vital signs, intracerebral pressure (ICP), arterial blood gas measurement, and hemoglobin (HGB). Data were prospectively collected every 12 h and at clinical events (angiography, transfusion, etc.). We prospectively recorded clinical history, clinical events, radiology results, and outcomes., Results: Six patients were measured 123 times. rO2 values were correlated with the contralateral side, HGB, blood pressure, and PaO2, but not with ICP or perfusion pressure. There were no measured effects of angiography or transfusion. Patterns relating rO2 readings to clinical, angiographic, or TCD evidence of vasospasm were unclear, and there were no associations with the outcome (cerebral infarction, NIH Stroke Scale, or modified Rankin Scale)., Conclusion: INVOS rO2 readings are associated with other factors that relate to cerebral oxygen delivery but seem to be of limited use as a screening tool for vasospasm or cerebral infarction after SAH.

Background: Cerebral infarction after aneurysmal subarachnoid haemorrhage (SAH) is presumed to be due to cerebral vasospasm, defined as arterial lumen narrowing from days 3 to 14., Methods: We reviewed the computed tomography scans of 103 patients with aneurysmal SAH for radiographic cerebral infarction and controlled for other predictors of outcome. A blinded neuroradiologist reviewed the angiograms. Cerebral infarction from vasospasm was judged to be unlikely if it was visible on computed tomography within 2 calendar days of SAH or if angiography showed no vasospasm in a referable vessel, or both., Results: Cerebral infarction occurred in 29 (28%) of 103 patients with SAH. 18 patients had cerebral infarction that was unlikely to be due to vasospasm because it was visible on computed tomography by day 2 (6 (33%)) or because angiography showed no vasospasm in a referable artery (7 (39%)), or both (5 (28%)). In a multivariate model, cerebral infarction was significantly related to World Federation of Neurologic Surgeons grade (odds ratio (OR) 1.5/grade, 95% confidence interval (CI) 1.1 to 2.01, p = 0.006) and SAH-Physiologic Derangement Score (PDS) >2 (OR 3.7, 95% CI 1.4 to 9.8, p = 0.01) on admission. Global cerebral oedema (OR 4.3, 95% CI 1.5 to 12.5, p = 0.007) predicted cerebral infarction. Patients with cerebral infarction detectable by day 2 had a higher SAH-PDS than patients with later cerebral infarction (p = 0.025)., Conclusions: Many cerebral infarctions after SAH are unlikely to be caused by vasospasm because they occur too soon after SAH or because angiography shows no vasospasm in a referable artery, or both. Physiological derangement and cerebral oedema may be worthwhile targets for intervention to decrease the occurrence and clinical impact of cerebral infarction after SAH.

Objective: Higher-goal hemoglobin (hgb) and more packed red blood cell transfusions lead to worse outcomes in general critical care patients. There are few data on hgb, transfusion, and outcomes after aneurysmal subarachnoid hemorrhage (SAH)., Methods: We reviewed the daily hgb levels of 103 patients with aneurysmal SAH. Cerebral infarction was diagnosed by computed tomographic scan. We corrected for Hunt and Hess grade, age, and angiographic vasospasm in multivariate models., Results: Of 103 patients, the mean age was 55.3 +/- 14.5 years, 63% were women, and 29% were Hunt and Hess Grades 4 and 5; hgb values steadily declined from 12.6 +/- 1.7 g/dl the day of SAH to 10.4 +/- 1.2 g/dl by Day 14. Patients who died had lower hgb than survivors on Days 0, 1, 2, 4, 6, 10, 11, and 12 (P < or = 0.05). Higher mean hgb was associated with reduced odds of poor outcome (odds ratio, 0.57 per g/dl; 95% confidence interval [CI], 0.38-0.87; P = 0.008) after correcting for Hunt and Hess grade, age, and vasospasm; results for hgb on Days 0 and 1 were similar. Higher Day 0 (odds ratio, 0.7 per g/dl; 95% CI, 0.5-0.99; P = 0.05) and mean hgb (odds ratio, 0.57 per g/dl; 95% CI, 0.38-0.87; P = 0.009) predicted a lower risk of cerebral infarction independent of vasospasm. There were no associations between hgb and other prognostic variables., Conclusion: We found that SAH patients with higher initial and mean hgb values had improved outcomes. Higher hgb in SAH patients may be beneficial. The efficacy and safety of blood transfusions to increase hgb in patients with SAH may warrant further study.

Background: Aneurysm rebleeding has historically been an important cause of mortality after subarachnoid hemorrhage (SAH)., Objective: To describe the frequency and impact of rebleeding in the modern era of aneurysm care, which emphasizes early surgical or endovascular treatment., Design: Inception cohort., Setting: Tertiary care medical center., Patients: A total of 574 patients enrolled in the Columbia University SAH Outcomes Project between August 1996 and June 2002. Early aneurysm repair was performed whenever feasible., Main Outcome Measures: Rebleeding was defined by prespecified clinical and radiographic criteria, excluding prehospital, intraprocedural, and postrepair events. Functional outcome was assessed at 3 months with the modified Rankin Scale. Multiple logistic regression was used to identify predictors of rebleeding, poor functional outcome, and mortality., Results: Rebleeding occurred in 40 (6.9%) of the 574 patients; most cases (73%) occurred within 3 days of ictus. Hunt-Hess grade on admission (odds ratio [OR], 1.92 per grade; 95% confidence interval [CI], 1.33-2.75; P<.001) and maximal aneurysm diameter (OR, 1.07/mm; 95% CI, 1.01-1.13; P = .005) were independent predictors of rebleeding. After controlling for Hunt-Hess grade and aneurysm size, rebleeding was associated with a markedly reduced chance of survival with functional independence (modified Rankin Scale score,

Objective: Hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), which exhibit beneficial cerebrovascular effects by modulating inflammation and nitric oxide production, have not been evaluated in acute aneurysmal subarachnoid hemorrhage (SAH) patients. The effect of prior statin use on 14-day functional outcome and on prevention of vasospasm-induced delayed cerebral ischemia (DCI) or stroke during hospitalization was analyzed., Methods: We conducted a 1:2 matched (age, admission Hunt and Hess grade, vascular disease/risk history) cohort study of 20 SAH patients on statins and 40 SAH controls. The primary outcome was functional outcome at 14 days (Modified Lawton Physical Self-Maintenance Scale and Barthel Index scale scores). Secondary outcomes were 14-day mortality, Modified Rankin Scale score, DCI, DCI supported by angiography/transcranial Doppler [TCD], cerebral infarctions of any type, and TCD highest mean velocity elevation., Results: Statin users demonstrated a significant protective effect on 14-day Barthel Index scale and Modified Lawton Physical Self-Maintenance Scale scores (77 +/- 10 versus 39 +/- 8, P = 0.003; 12 +/- 7 versus 19 +/- 9, P = 0.03, respectively). Moreover, statin users demonstrated a significantly lower incidence of DCI and DCI supported by angiography/TCD (10% versus 43%, P = 0.02; 5% versus 35%, P = 0.01, respectively), cerebral infarctions of any type (25% versus 63%, P = 0.01), and baseline-to-final TCD highest mean velocity change of 50 cm/s or greater (18% versus 51%, P = 0.03)., Conclusion: SAH statin users demonstrated significant improvement in 14-day functional outcome, a significantly lower incidence of DCI and cerebral infarctions of any type, as well as prevention of TCD highest mean velocity elevation. However, we did not find a significant statin impact on mortality or global outcome (Modified Rankin Scale) in this small sample. This study provides clinical evidence for the potential therapeutic benefit of statins after acute SAH.