Transfusion
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While transfusion of red blood cells (RBCs) is effective at preventing morbidity and mortality in anemic patients, studies have indicated that some RBC components have functional defects ("RBC storage lesions") that may actually cause adverse events when transfused. For example, in some studies patients transfused with RBCs stored more than 14 days have had statistically worse outcomes than those receiving "fresher" RBC units. Recipient-specific factors may also contribute to the occurrence of these adverse events. ⋯ Under certain circumstances, these variables are "aligned" such that NO concentrations are markedly reduced, leading to vasoconstriction, decreased local blood flow, and insufficient O(2) delivery to end organs. Under these circumstances, the likelihood of morbidity and mortality escalates. If the key tenets of the INOBA hypothesis are confirmed, it may lead to improved transfusion methods including altered RBC storage and/or processing conditions, novel transfusion recipient screening methods, and improved RBC-recipient matching.
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The specific negative clinical manifestations associated with the transfusion of stored red blood cells (RBCs) and the corresponding mechanisms responsible for such phenomena remain poorly defined. Our recent studies document that leukoreduced older RBC units potentiate transfusion-related toxicity in trauma patients. ⋯ The central mechanisms proposed to mediate this microcirculatory alteration include: 1) the loss of RBC-dependent control of nitric oxide-mediated homeostasis concerning vasodilation and 2) immune cell and complement activation. In this review, we outline the background for our hypothesis and detail our current investigations toward the understanding of this pathophysiology.