Iron Administration in the Critically III

Anemia is a common pathology in intensive care unit (ICU) patients. The pathophysiology of anemia includes altered iron metabolism with decreased erythropoiesis. Under normal conditions, there is a balance between iron transport by transferrin, making iron available for incorporation in hemoglobin, and iron storage as ferritin. In inflammatory processes, this balance is disturbed and plays a central role in the development of anemia. Typically, the inflammatory process is associated with a low concentration of serum iron, high ferritin and low transferrin. Effective erythropoiesis requires both erythropoietin (EPO) and iron. Critically ill patients have inappropriately low EPO levels, and several studies have been conducted to assess the potential benefits of exogenous EPO supplementation. EPO treatment plus iron administration reduced the number of red blood cell (RBC) transfusions needed but had no effects on outcome in terms of ICU infection rates or mortality. Iron can have adverse effects, including inhibition of phagocytosis, inhibition of intracellular killing of bacteria, and altered polymorphonuclear cell function. Iron overload has also been shown to cause increased apoptosis in patients with hemochromatosis. Further study is needed to accurately define the precise role of iron in the development of anemia in critically ill patients, and to determine the potential benefits and risks of iron supplementation.