Cardiovascular and pulmonary complications of aneurysmal subarachnoid hemorrhage

Cardiopulmonary complications after aneurysmal subarachnoid hemorrhage negatively affect overall morbidity and mortality. An electronic literature search was performed for English-language articles focused on cardiopulmonary complications with subarachnoid hemorrhage published through October 2010. A total of 278 citations were identified, including 72 clinical studies. In most cases, study quality was low or very low. Cardiac injury, evidenced by an elevation in troponin levels, is reported in about one-third of patients after aneurysmal subarachnoid hemorrhage. Arrhythmias also occur in about one-third of patients after subarachnoid hemorrhage. The incidence of pulmonary complications, especially neurogenic pulmonary edema, is more difficult to establish from available literature. Cardiopulmonary complications have been linked to worsened clinical outcome, suggesting a role for cardiac monitoring and interventions

Anemia and transfusion after subarachnoid hemorrhage

Delayed cerebral ischemia after subarachnoid hemorrhage (SAH) may be affected by a number of factors, including cerebral blood flow and oxygen delivery. Anemia affects about half of patients with SAH and is associated with worse outcome. Anemia also may contribute to the development of or exacerbate delayed cerebral ischemia. This review was designed to examine the prevalence and impact of anemia in patients with SAH and to evaluate the effects of transfusion. A literature search was made to identify original research on anemia and transfusion in SAH patients. A total of 27 articles were identified that addressed the effects of red blood cell transfusion (RBCT) on brain physiology, anemia in SAH, and clinical management with RBCT or erythropoietin. Most studies provided retrospectively analyzed data of very low-quality according to the GRADE criteria. While RBCT can have beneficial effects on brain physiology, RBCT may be associated with medical complications, infection, vasospasm, and poor outcome after SAH. The effects may vary with disease severity or the presence of vasospasm, but it remains unclear whether RBCTs are a marker of disease severity or a cause of worse outcome. Erythropoietin data are limited. The literature review further suggests that the results of the Transfusion Requirements in Critical Care Trial and subsequent observational studies on RBCT in general critical care do not apply to SAH patients and that randomized trials to address the role of RBCT in SAH are required

Triggers for Aggressive Interventions in Subarachnoid Hemorrhage

Ischemia is a common cause of secondary neuronal injury after aneurysmal subarachnoid hemorrhage. An electronic literature search was conducted to identify clinical signs and laboratory data that could serve as predictors for delayed cerebral ischemia and define triggers for additional diagnostic testing or more aggressive intervention. Fifteen articles describing original research that included some discussion of triggers were identified and reviewed. Quality of evidence was considered very low to moderate for included studies. Using data from these studies and expert opinion, a variety of clinical signs and monitoring data were identified as potentially useful triggers for additional tests or aggressive treatments. These data were used to develop a sequence that might be employed in the clinical management of subarachnoid hemorrhage to determine which patients need additional attention, testing, or interventions to reduce/prevent ischemia caused by vasospasm

SAH pituitary adrenal dysfunction

Disruption of the hypothalamic-pituitary-adrenal axis may occur after aneurysmal subarachnoid hemorrhage, resulting in hypopituitarism. An electronic literature search was conducted to identify articles with English-language abstracts published between 1980 and March 2011 that addressed hypothalamic-pituitary-adrenal axis insufficiency and hormone replacement. A total of 18 observational and prospective, randomized studies were selected for this review. Limited data are available evaluating pituitary effects during the acute stage after subarachnoid hemorrhage, with inconsistent results reported. Overall, acutely after subarachnoid hemorrhage, cortisol levels may initially be supranormal, decreasing toward normal levels over time. During the months to years after subarachnoid hemorrhage, pituitary deficiency may occur in up to one in three patients. Limited data suggest modest outcome benefits with fludrocortisone and no benefit or harm from corticosteroids

Critical Care Management of Patients Following Aneurysmal Subarachnoid Hemorrhage : Recommendations from the Neurocritical Care Society's Multidisciplinary Consensus Conference

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 ofSAHto 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

Hemodynamic management of subarachnoid hemorrhage

Hemodynamic augmentation therapy is considered standard treatment to help prevent and treat vasospasm and delayed cerebral ischemia. Standard triple- H therapy combines volume expansion (hypervolemia), blood pressure augmentation (hypertension), and hemodilution. An electronic literature search was conducted of English-language papers published between 2000 and October 2010 that focused on hemodynamic augmentation therapies in patients with subarachnoid hemorrhage. Among the eligible reports identified, 11 addressed volume expansion, 10 blood pressure management, 4 inotropic therapy, and 12 hemodynamic augmentation in patients with unsecured aneurysms. While hypovolemia should be avoided, hypervolemia did not appear to confer additional benefits over normovolemic therapy, with an excess of side effects occurring in patients treated with hypervolemic targets. Overall, hypertension was associated with higher cerebral blood flow, regardless of volume status (normo- or hypervolemia), with neurological symptom reversal seen in two-thirds of treated patients. Limited data were available for evaluating inotropic agents or hemodynamic augmentation in patients with additional unsecured aneurysms. In the context of sparse data, no incremental risk of aneurysmal rupture has been reported with the induction of hemodynamic augmentation

Endocrine function following acute SAH

Disruption of the hypothalamic-pituitary-adrenal axes may occur after aneurysmal subarachnoid hemorrhage, resulting in hypopituitarism. An electronic literature search was conducted to identify articles with English-language abstracts published between 1980 and March 2011, which addressed hypothalamic-pituitary-adrenal axis insufficiency and hormone replacement. A total of 18 observational and prospective, randomized studies were selected for this review. Limited data are available, evaluating pituitary effects during the acute stage after subarachnoid hemorrhage, with inconsistent results being reported. Overall, after acute subarachnoid hemorrhage, cortisol levels may initially be supranormal, decreasing toward normal levels over time. During the months to years after subarachnoid hemorrhage, pituitary deficiency may occur in one out of three patients. Limited data suggest modest outcome benefits with fludrocortisone and no benefit or harm from corticosteroids

Summary of evidence on immediate statins therapy following aneurysmal subarachnoid hemorrhage

Statins were shown to have neuroprotective effects, with reduced vasospasm and delayed ischemic deficits in statin-treated patients after aneurysmal subarachnoid hemorrhage in two small, randomized, controlled clinical trials published in 2005. This review consolidated data from available published studies evaluating statin treatment for subarachnoid hemorrhage. A literature search was conducted to identify original research studies published through October 2010 testing immediate treatment with a statin in statin-na\uefve patients following aneurysmal SAH. Six randomized controlled clinical trials and four observational studies were identified. Despite inconsistent results among studies, a meta-analysis of randomized controlled data showed a significant reduction in delayed ischemic deficits with statins. Effect on vasospasm was more difficult to determine, due to differences in definitions used among studies. Interpretations from observational studies were limited by the use of relatively small sample sizes, historical controls, and treatment variability