• Pedro Kurtz, J Michael Schmidt, Jan Claassen, Emmanuel Carrera, Luis Fernandez, Raimund Helbok, Mary Presciutti, R Morgan Stuart, E Sander Connolly, Neeraj Badjatia, Stephan A Mayer, and Kiwon Lee.
• Division of Critical Care Neurology, Department of Neurology, Columbia University, Milstein Hospital 8 Center, New York, NY 10032, USA. pkurtz@neuro.columbia.edu
• Neurocrit Care. 2010 Aug 1;13(1):10-6.

BackgroundAnemia is frequently encountered in critically ill patients and adversely affects cerebral oxygen delivery and brain tissue oxygen (PbtO2). The objective of this study is to assess whether there is an association between anemia and metabolic distress or brain tissue hypoxia in patients with subarachnoid hemorrhage.MethodsRetrospective study was conducted in a neurological intensive care unit in a university hospital. Patients with subarachnoid hemorrhage that underwent multimodality monitoring with intracranial pressure, PbtO2 and microdialysis were analyzed. The relationships between hemoglobin (Hb) concentrations and brain tissue hypoxia (PbtO2 < or = 15 mmHg) and metabolic distress (lactate/pyruvate ratio > or =40) were analyzed with general linear models of logistic function for dichotomized outcomes utilizing generalized estimating equations.ResultsA total of 359 matched neuromonitoring hours and Hb measurements were analyzed from 34 consecutive patients. The median hemoglobin was 9.7 g/dl (interquartile range 8.8-10.5). After adjusting for significant covariates, reduced hemoglobin concentration was associated with a progressively increased risk of brain tissue hypoxia (adjusted OR 1.7 [1.1-2.4]; P = 0.01 for every unit decrease). Also after adjusting for significant covariates, hemoglobin concentrations below 9 g/dl and between 9.1 and 10 g/dl were associated with an increased risk of metabolic distress as compared to concentrations between 10.1 and 11 g/dl (adjusted OR 3.7 [1.5-9.4]; P = 0.004 for Hb < or = 9 g/dl and adjusted OR 1.9 [1.1-3.3]; P = 0.03 for Hb 9.1-10 g/dl).ConclusionsAnemia is associated with a progressively increased risk of cerebral metabolic distress and brain tissue hypoxia after subarachnoid hemorrhage.

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