The risks of blood transfusion in patients with subarachnoid hemorrhage.

To the Editor: I read with much interest the recently published recommendations of the Neurocritical Care Society’s Consensus Conference on the ‘‘Critical Care management of patients following aneurysmal subarachnoid hemorrhage (SAH)’’ [1]. These guidelines state ‘‘there was wide agreement... that data supporting restrictive transfusion in medical patients do not apply to SAH’’ and that ‘‘patients should receive packed RBC transfusion to maintain hemoglobin concentration above 8–10 g/dl (moderate quality evidence, strong recommendation).’’ I believe that the literature does not support these recommendations. The pathophysiologic consequences following allogenic red blood cell (RBC) transfusion are complex and poorly understood [2]. It is however well recognized that RBC transfusions result in immunosuppression (perhaps lifelong) with an increased risk of infection (and tumor recurrence), are proinflammatory increasing the risk of acute lung injury and multi-organ failure as well as being prothrombotic [2–6]. The effects of RBC transfusion on tissue oxygenation are complex, with clinical and experimental data demonstrating that an increase in the calculated oxygen delivery does not necessarily translate into increased oxygen uptake, even in patients with an oxygen debt [7, 8]. Dhar et al. [9] evaluated the effect of RBC transfusion on oxygen kinetics in eight anemic patients following a SAH. While transfusion resulted in a 15% rise in hemoglobin and an 18% increase in calculated oxygen delivery, the global cerebral metabolic rate of oxygen (in ml/100 g/min) remained unchanged. In addition, it is important to recognize that the mean age of transfused blood in the United States in 24 days, being considerably older in major metropolitan medical centers [10]. ‘‘Aged’’ RBC’s have been shown to paradoxically decrease tissue oxygenation and are independent predictors of hospital complications and death in medical and surgical patients [7, 11–16]. Despite the fact that 13 million units of blood are transfused annually in the US and over 60 million worldwide [17], there is scanty evidence that non-bleeding, hemodynamically stable patients actually benefit from blood transfusion. Indeed, current data suggest that in these patients blood transfusion increases the risk of infection, ARDS, and death [18]. Anemia is a common finding in patients who have suffered a SAH, with over 50% of patients having a nadir hematocrit less than 30% [19–22]. Multiple factors likely contribute to the development of an anemia following SAH, including blood loss during surgery, venesection, gastrointestinal and other sources of blood loss, decreased production of erythropoietin, and impaired erythropoiesis [22]. The nadir hemoglobin is generally related to the admission Hunt and Hess grade [21, 22]. Anemia after SAH has been reported to be associated with worse outcomes [21, 23]. The association between anemia and worse outcomes does not necessarily imply that correction of the anemia with blood transfusions will improve outcome. This is important, as data suggest that between 35 and 60% of patients suffering a SAH receive a blood transfusion during their hospitalization [21–26]. Apart from the risks noted in ICU patients, there may be additional risks of blood transfusion in patients with SAH. Nitric oxide (NO) plays a critical role in regulating vasomotor tone and NO metabolism may influence the risk and severity of vasospasm after SAH [27]. Erythrocytes carry NO for release in vessels, whereas transfused erythrocytes lack stored NO and may exacerbate vasospasm [28, 29]. P. E. Marik (&) Department of Medicine, Eastern Virginia Medical School, 825 Fairfax Ave, Suite 410, Norfolk, VA 23507, USA e-mail: marikpe@evms.edu