The physiology of anemia and the threshold for blood transfusion

Le résumé fourni par la source

As unicellular and multicellular organisms progressed to more complex forms, the process of diffusion became an ineffective means of delivering oxygen to the tissues due to the constraints of time and distance. Since oxygen is poorly soluble in water, the process of evolution has resulted in hemoglobin, a compound capable of binding oxygen thereby increasing its solubility in the fluid milieu. In humans and other mammalian species, erythropoiesis is regulated to match the natural loss of red blood cells as they age and are removed from the system in addition to any abnormal losses that occur due to hemorrhage or hemolysis. The process of erythropoiesis is regulated by erythropoietin, a glycoprotein hormone produced by the peritubular cells of the renal cortex and the liver. Although generally regulated at a specific level, blood loss, nutritional deficiencies, increased RBC destruction, and chronic illnesses may result in anemia. Although there are compensatory mechanisms to compensate for the decreased hemoglobin concentration, at some point oxygen delivery to the tissues fails mandating the administration of allogeneic blood products to compensate for anemia. Recent work has attempted to identify the specific hemoglobin value at which this occurs. However, given significant interpatient variability and associated co-morbid conditions, there is significant variation in this hemoglobin value or the accepted “transfusion trigger”. The following chapter reviews the etiologies of anemia, discusses the homeostatic mechanisms which compensate for anemia, investigates the literature regarding the appropriate hemoglobin value to use as a “transfusion trigger”, and briefly reviews some of the adverse effects associated with allogeneic transfusions.

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