Anemia is common in critically ill patients. As a consequence packed red blood cell (PRBC) transfusions are frequent in the critically ill. Over the past two decades a growing body of literature has emerged, linking PRBC transfusion to infections, immunosuppression, organ dysfunction, and a higher mortality rate. However, despite growing evidence that risk of PRBC transfusion outweighs its benefit, significant numbers of critically ill patients still receive PRBC transfusion during their intensive care unit (ICU) stay. In this paper, we summarize the current literature concerning the impact of anemia on outcomes in critically ill patients and the potential complications of PRBC transfusions. 1. Introduction Anemia is a commonly encountered clinical problem in the critically ill [1]. Ninety-five percent of critically ill patients who stay in the intensive care unit (ICU) for 72 hours or greater suffer from anemia and approximately 40% of them receive packed red blood cell (PRBC) transfusions [2, 3]. In 2001, nearly 14 million units of packed red blood cells were transfused, but the physiologic basis for transfusion in the critically ill is not without controversy [4]. In the last two decades transfusion practices have become more restrictive likely in response to prospective research. 2. Mechanisms/Etiologies of Anemia in Critically Ill Patients The etiology of anemia in critical illness is multifactorial and complex. Repeated phlebotomies, gastrointestinal blood loss, and other surgical procedures contribute significantly to the development of anemia [5, 6]. Other factors involved in pathogenesis include coagulopathies, pathogen-associated hemolysis, hypoadrenalism, and nutritional deficiencies [7, 8]. A number of studies have identified potentially correctible nutritional deficienncies in critically ill patients, including deficiencies of iron, B12, and folate. These deficiencies can lead to ineffective erythropoiesis with resultant anemia [9, 10]. Decreased erythropoietin production and/or impaired bone marrow response to erythropoietin may also play an important role in the development of anemia [11]. These effects are mediated by a variety of inflammatory cytokines such as Interleukin-1 (IL-1) and tumor necrosis factor- (TNF- ), which inhibit erythropoietin (EPO) production. Furthermore IL-1, IL-6, and TNF- suppress erythropoiesis by direct inhibitory effects on bone marrow [12]. The hyperadrenergic state following severe injury may also induce bone marrow dysfunction and failure of erythropoiesis. This effect may be mediated by IL-6 and interferon-
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