Abstract

To the Editor:—Preoperative anemia is a common condition among surgical patients, and it is an independent risk factor for blood transfusion in major surgery with moderate to high blood loss. Consequently, the first step to be taken in the setting of elective surgery will be the preoperative identification and evaluation of anemia early enough to implement the appropriate treatment. In this regard, we read with interest the report by Theusinger et al. 1 about the use of intravenous iron sucrose for the treatment of iron deficiency anemia in orthopedic surgical patients. They found a mean maximum increase in hemoglobin (1.0 0.6 g/dl) 2 weeks after the start of intravenous iron treatment, indicating that administration of intravenous iron 2–3 weeks before surgery may be optimal. We would like to comment regarding the patients’ inclusion criteria, the dosage and administration schedule of iron sucrose, and the comparison of their data with those of the study by Cuenca et al. 2 in patients sustaining a pertrochanteric hip fracture. First, although Theusinger et al. 1 clearly defined anemia according to World Health Organization criteria as hemoglobin level 12 g/dl for women and hemoglobin 13 g/dl for men, their definition of iron deficiency was complex and somehow arbitrary. According to other authors, iron deficiency anemia is defined by anemia with mean corpuscular volume 80 fl, ferritin level 15–30 g/l, and transferrin saturation 15%. 1 On the other hand, in the event of inflammation (C-reactive protein 5 mg/l), iron deficiency may be defined as transferrin saturation 20% and ferritin 50 –100 g/l. 3 Therefore, the cutoff values used in this paper (ferritin 100 mg/l or 100 –300 g/l with transferrin saturation 20%) are compatible not only with iron deficiency anemia but also with anemia of chronic disease, with or without true iron deficiency. 3,4 Thus, it is conceivable that a mixed anemic patient population was included in this study. This may be important, because the endogenous erythropoietin response to low hemoglobin is more substantial in iron deficiency anemia than in anemia of chronic disease, and erythropoietin increases the mobilization and incorporation of iron into the erythron. 3 Inflammatory mediators involved in anemia of chronic disease also impair duodenal iron absorption and iron mobilization from body stores. 4

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