Neurocritical care
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Hypovolemia is common after subarachnoid hemorrhage, and fluid imbalance negatively affects clinical outcome. Standard bedside volume measures fail to adequately assess fluid status after subarachnoid hemorrhage. ⋯ These studies highlight that fluid status is often affected and difficult to assess after subarachnoid hemorrhage. Both non-invasive and invasive monitors may be used to more accurately define volume status.
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Hyponatremia is the most common electrolyte imbalance seen in patients with aneurysmal subarachnoid hemorrhage, occurring in one-third to one-half of patients. Hyponatremia may be caused by cerebral salt wasting and by the syndrome of inappropriate secretion of antidiuretic hormone or a combination of both. Limited data are available describing hyponatremia treatment in subarachnoid hemorrhage patients. ⋯ Seven appropriate articles were identified as followed: three testing fludrocortisone, two hydrocortisone, and one each for hypertonic saline and 5% albumin. Data quality for treatment efficacy and safety were moderate for corticosteroid studies and low or very low for hypertonic saline and 5% albumin. Available data, although limited, support early treatment with corticosteroids to limit hyponatremia, with fludrocortisone causing fewer side effects.
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An electronic literature search through August 2010 was performed to obtain articles describing fever incidence, impact, and treatment in patients with subarachnoid hemorrhage. A total of 24 original research studies evaluating fever in SAH were identified, with studies evaluating fever and outcome, temperature control strategies, and shivering. Fever during acute hospitalization for subarachnoid hemorrhage was consistently linked with worsened outcome and increased mortality. Antipyretic medications, surface cooling, and intravascular cooling may all reduce temperatures in patients with subarachnoid hemorrhage; however, benefits from cooling may be offset by negative consequences from shivering.
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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. ⋯ 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.
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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. ⋯ 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.