Diagnosis and Prevalence of Iron Deficiency in the Critically Ill

Abstract

Iron is the most prevalent oligo-nutriment and plays a key role in oxygen transport and energy production. Iron deficiency could lead to anemia but also to fatigue or muscular weakness. Iron metabolism is a closed circuit, finely tuned by the peptidic hormone hepcidin to avoid overload as well as deficiency. Inflammation and iron deficiency have opposite effect on hepcidin synthesis (with respectively an induction and repression of synthesis). The inflammation-induced synthesis of hepcidin explains the low serum levels of iron usually observed in the critically ill . The main biological markers of iron deficiency are ferritin (a value of less than 100 μg/l being indicative of true iron deficiency) and transferring saturation (a value of more than 20 % exclude iron deficiency). Unfortunately, inflammation is very frequent in critically ill patients, and these markers are often not usable. Other markers are available, which allow the diagnosis of iron-restricted erythropoiesis, in the context of “functional iron deficiency.” These markers are the percentage of hypochromic red cells (functional iron deficiency for value >10 %), reticulocyte hemoglobin content (diagnosis for value >29 pg), erythrocyte zinc protoporphyrin (reference ranges vary according to the different assays), and the soluble transferrin receptor (reference ranges vary according to the different assays). Unfortunately, they (except the last one) are not usable in case of blood transfusion. Hepcidin dosage has been proposed as a diagnosis tool and seems promising. This will be an important step, since the prevalence of iron deficiency is important in the critically ill patients, ranging from 15 % to 40 %, and possibly higher rate at ICU discharge.