Subarachnoid hemorrhage (SAH) is an acute cerebrovascular event which can have devastating effects on the central nervous system as well as a profound impact on several other organs. SAH patients are routinely admitted to an intensive care unit and are cared for by a multidisciplinary team. A lack of high quality data has led to numerous approaches to management and limited guidance on choosing among them. Existing guidelines emphasize risk factors, prevention, natural history, and prevention of rebleeding, but provide limited discussion of the complex critical care issues involved in the care of SAH patients. The Neurocritical Care Society organized an international, multidisciplinary consensus conference on the critical care management of SAH to address this need. Experts from neurocritical care, neurosurgery, neurology, interventional neuroradiology, and neuroanesthesiology from Europe and North America were recruited based on their publications and expertise. A jury of four experienced neurointensivists was selected for their experience in clinical investigations and development of practice guidelines. Recommendations were developed based on literature review using the GRADE system, discussion integrating the literature with the collective experience of the participants and critical review by an impartial jury. Recommendations were developed using the GRADE system. Emphasis was placed on the principle that recommendations should be based not only on the quality of the data but also tradeoffs and translation into practice. Strong consideration was given to providing guidance and recommendations for all issues faced in the daily management of SAH patients, even in the absence of high quality data.

Background and Purpose-Statins may improve cerebral vasomotor reactivity through cholesterol-dependent and -independent mechanisms. A phase II randomized controlled trial was conducted to examine the hypothesis that acute pravastatin treatment could improve cerebrovascular autoregulation and reduce vasospasm-related complications after aneurysmal subarachnoid hemorrhage (SAH). Methods-A total of 80 aneurysmal SAH (aSAH) patients (18 to 84 years of age) within 72 hours from the ictus were randomized equally to receive either oral pravastatin (40 mg) or placebo daily for up to 14 days. Primary end points were the incidence, duration, and severity of cerebral vasospasm, and duration of impaired autoregulation estimated from transcranial Doppler ultrasonography. Secondary end points were the incidence of vasospasm-related delayed ischemic deficits (DIDs) and disability at discharge. Results-Prerandomization characteristics were balanced between the 2 groups. No treatment-related complication was observed. The incidences of vasospasm and severe vasospasm were reduced by 32% (Pϭ0.006) and 42% (Pϭ0.044), respectively, and the duration of severe vasospasm was shortened by 0.8 days (Pϭ0.068) in the pravastatin group. These measurements were maximal on the ipsilateral side of ruptured aneurysms. The duration of impaired autoregulation was shortened bilaterally (PՅ0.01), and the incidence of vasospasm-related DIDs and mortality were decreased by 83% (PϽ0.001) and 75% (Pϭ0.037), respectively, in the pravastatin group. Conclusion-Acute treatment with pravastatin after aSAH is safe and ameliorates cerebral vasospasm, improves cerebral autoregulation, and reduces vasospasm-related DID. Unfavorable outcome at discharge was reduced primarily because of a reduction in overall mortality. This is the first demonstration of clinical benefits with immediate statin therapy for an acute cerebrovascular disorder. (Stroke. 2005;36:1627-1632.)

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Background and Purpose-We have previously demonstrated that acute pravastatin therapy after aneurysmal subarachnoid hemorrhage ameliorates vasospasm-related delayed ischemic deficits. This study assesses the effects of pravastatin on the frequency and intensity for rescue therapy, length of inpatient stay, and long-term outcome at 6 months. Methods-Eighty aneurysmal subarachnoid hemorrhage patients (age 18 to 84 years, onset 1.8Ϯ1.3 days) were randomized to receive daily oral pravastatin (40 mg) or placebo for up to 14 days. Clinical events were recorded during the trial. Six-month outcome was assessed using the Short Form 36 and the modified Rankin Scale. Results-Although no significant difference in the outcome at discharge was found between the trial groups, multivariate analysis showed pravastatin therapy reduced unfavorable outcome by 73% (Pϭ0.041). The benefit persisted at 6 months (Pϭ0.063) and was notable in the physical (PϽ0.001) and psychosocial (PϽ0.001) aspects measured using Short Form 36. Furthermore, the acute pravastatin therapy reduced the requirement for triple-H therapy (hypertensive, hypervolemic, hemodilution; Pϭ0.045) and mortality related to vasospasm (Pϭ0.02) and sepsis (Pϭ0.001); no significant difference was found in the length of inpatient stay between the trial groups. Conclusions-This trial demonstrates that acute statin treatment reduces traditional rescue therapy for vasospasm after aneurysmal subarachnoid hemorrhage. Improvement in early outcome has proved robust at 6 months, particularly in relation to physical and psychosocial (Short Form 36) outcome.

This preliminary study showed that EPO seemed to reduce delayed cerebral ischemia following aSAH via decreasing severity of vasospasm and shortening impaired autoregulation.

Background and Purpose-The goal of this study was to examine the effects of hypertonic saline on cerebral blood flow (CBF) in poor-grade patients with subarachnoid hemorrhage. Methods-We administered 23.5% hypertonic saline (2 mL/kg IV) 1 time to 10 patients, 2 times to 7 patients, and 3 times to 1 patient. All patients had transcranial Doppler (TCD), intracranial pressure (ICP) monitoring, and analysis of serum sodium and osmolality; 6 had xenon CT (XeCT). Data were used to characterize the changes in CBF, cerebral vascular resistance (CVR), ICP, cerebral perfusion pressure (CPP), and potential rheological mechanisms of action. .7, and 27.1 minutes, respectively. In the second treatment episode, all these parameters had the same response except estimated CVR, which did not reach statistical significance. XeCT confirmed the increase in CBF (22.9%, Pϭ0.02) without regional differences. A fall in CBF after hypertonic saline was identified in only a single region of interest in a patient in whom baseline flow was low but not infarcted. Serum sodium rose by 11.4 and 8.8 mmol/L, and osmolality rose by 26.7 and 16.3 mosm/L in the first and second treatment episodes, respectively. Hemoglobin decreased by 0.7 and 0.6 g/L and hematocrit decreased by 1.9% and 2.4% in the first and second treatment episodes, respectively. Conclusions-We found that 23.5% hypertonic saline increases CBF in poor-grade patients with subarachnoid hemorrhage. These effects are associated with improved indexes of blood rheology. Potential therapeutic benefits are discussed. Results-In

Background and Purpose— Delayed cerebral ischemia and infarction due to reduced CBF remains the leading cause of poor outcome after aneurysmal subarachnoid hemorrhage. Hypertonic saline (HS) is associated with an increase in CBF. This study explores whether CBF enhancement with HS in patients with poor-grade subarachnoid hemorrhage is associated with improved cerebral tissue oxygenation. Methods— Continuous monitoring of arterial blood pressure, intracranial pressure, cerebral perfusion pressure, brain tissue oxygen, carbon dioxide, pH, and middle cerebral artery flow velocity was performed in 44 patients. Patients were given an infusion (2 mL/kg) of 23.5% HS. In 16 patients, xenon CT scanning was also performed. CBF in a region surrounding the tissue oxygen sensor was calculated. Data are mean±SD. Results— Thirty minutes postinfusion, a significant increase in arterial blood pressure, cerebral perfusion pressure, flow velocity, brain tissue pH, and brain tissue oxygen was seen together with a decrease in intracranial pressure ( P <0.05). Intracranial pressure remained reduced for >300 minutes and flow velocity elevated for >240 minutes. A significant increase in brain tissue oxygen persisted for 240 minutes. Average baseline regional CBF was 33.9±13.5 mL/100 g/min, rising by 20.3%±37.4% ( P <0.05) after HS. Patients with favorable outcome responded better to HS in terms of increased CBF, brain tissue oxygen, and pH and reduced intracranial pressure compared with those with an unfavorable outcome. A sustained increase in brain tissue oxygen (beyond 210 minutes) was associated with favorable outcome ( P <0.023). Conclusion— HS augments CBF in patients with poor-grade subarachnoid hemorrhage and significantly improves cerebral oxygenation for 4 hours postinfusion. Favorable outcome is associated with an improvement in brain tissue oxygen beyond 210 minutes.