Anemia in critically ill patients.

Anemia is common in acute critically ill patients. Although blood loss, either by trauma, surgery, phlebotomies or gastrointestinal bleeding, may play a role, the anemia in these patients bears many similarities to the anemia characteristic of chronic disease. Serum iron is low with a high concentration of ferritin and low-to-normal transferrin and serum transferrin receptor levels. Several mechanisms may be involved, with inflammation playing a crucial role. Although the exact nature of the inflammatory response and the role of various cytokines need further elucidation, it is known that inflammation blunts the responsiveness of the hormone erythropoietin and induces functional iron deficiency. Iron is trapped in cells of the mononuclear phagocytic system and its release is temporarily blocked. The bone marrow is still capable of incorporating iron and of responding to treatment with recombinant human erythropoietin (rh-EPO). The duration of the anemia is related to the persistence of the inflammation. Although the effects of anemia on morbidity and mortality in the critically ill are poorly defined, a restrictive transfusion policy, in which hemoglobin concentration is maintained between 7.0 and 9.0 g/dl, proves to be at least as effective as, if not superior to, a more liberal regimen. In individual situations, such as in cardiovascular and cancer patients, higher thresholds may be appropriate. The administration of rh-EPO is an alternative to reduce the need for red blood cell transfusions and to avoid transfusion-related complications. Although its efficacy has been shown, questions regarding cost-benefit, dose regimen and clinical outcomes need to be answered before its large-scale use can be recommended.