• Neurocritical care · Feb 2010

    Factors associated with the development of anemia after subarachnoid hemorrhage.

    • Tomoko R Sampson, Rajat Dhar, and Michael N Diringer.
    • Department of Neurology, Washington University School of Medicine, 660 S. Euclid Ave, Campus Box 8111, Saint Louis, MO 63110, USA.
    • Neurocrit Care. 2010 Feb 1;12(1):4-9.

    IntroductionAnemia is common after subarachnoid hemorrhage (SAH) and may exacerbate the reduction in oxygen delivery that underlies delayed cerebral ischemia. Fall in hemoglobin may relate to blood loss as well as inflammatory suppression of erythropoiesis. Identifying factors associated with anemia may facilitate targeted interventions, such as the use of erythropoiesis-stimulating agents, which could minimize the burden of anemia and reduce red blood cell (RBC) transfusion requirements.MethodsWe analyzed a cohort of patients with spontaneous SAH admitted over a 3-year period who survived at least 4 days. All patients had daily hematocrit values drawn while in the ICU. Multivariate regression was performed to determine baseline and early post-admission variables associated with development of anemia (defined as hematocrit < 30%).ResultsAnemia developed in 47% of 243 patients with SAH after a mean of 3.5 days (median 2 days). Admission variables independently associated with anemia were female gender (OR 3.7, 95% CI 1.8-7.6), baseline hematocrit < 36% (OR 3.9, 1.5-10.1 compared to 36-45%), history of hypertension (OR 2.1, 1.05-4.2), and poor clinical grade (OR 5.9, 2.3-15.0). Surgical aneurysm treatment (OR 13.5, 6.0-30.3) and greater admission SIRS score (OR 5.7, 1.7-19.2 if 3-4 criteria for systemic inflammatory response syndrome were met on day of admission compared to none) were also associated with fall in hematocrit.ConclusionsIt may be possible to predict those most likely to develop anemia using simple baseline clinical variables. Anemia was strongly related to surgery, likely through greater blood loss, and greater systemic inflammatory response on admission, possibly explained by cytokine-mediated inhibition of RBC production.

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