The effect of prolonged storage of transfused RBC on tissues, specific organs, and globally on critically ill patients has never been investigated in vivo, primarily because of difficulties in accurately measuring tissue oxygenation. As a result, the shelf life for RBC was established using the proportion of cells that survive at least 24 h and median survival times, rather than an evaluation of RBC ability to deliver O 2. Based on this standard, most regulatory agencies have approved a shelf life of 42 days for RBC. However, there are well-defined biochemical and corpuscular changes to RBC during storage, collectively referred to as “the storage lesion” ( 1–3). These changes include a depletion of adenosine triphosphate and 2,3-DPG, membrane vesiculation ( 4–6), lipid peroxidation of cell membranes ( 7), and loss of deformability ( 8,9).
1 During RBC storage, changes to the storage medium occur, including a progressive decrease in pH, an increase in plasma potassium, release of free hemoglobin from lysed RBC ( 10), and the generation of cytokines and other bioreactive substances ( 11–15). The clinical consequences of transfusing modified corpuscle and storage by-products are unknown ( 16–19). If prolonged storage truly does render RBC ineffective, then critically ill patients and patients undergoing cardiac surgical procedures may well experience negative clinical consequences from prolonged RBC storage. Despite these concerns, regional and hospital blood banks have developed inventory management strategies based upon minimizing blood wastage because of outdating of products because the benefits of fresh blood remain theoretical.
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