Reduction in iron ingestion, gastric acid secretion, and contact of food with absorptive mucosa are the main mechanisms involved in iron deficiency after bariatric surgery and can cause a reduction of 40.3 % in iron absorption in the first 6 months after surgery [27]. In order to prevent anemia and promote a better iron absorption, multivitamin supplements are regularly prescribed for patients [10]. However, most of commercial multivitamin complexes contain less iron than they actually need. Current recommendations for iron intake in postbariatric patients are of 40–65 mg/day of elemental iron and might be a little higher for women in reproductive age due to menstrual bleeding [28]. This level of elemental iron is present in only a few supplements for prenatal use. A double-blind randomized clinical trial showed that oral administration of 320 mg of iron sulfate twice a day prevented iron deficiency [29]. Whenever oral iron supplements are not enough for preventing deficiency, patients should be prescribed parenteral (intravenous, mainly) administration [11].

When studying iron profile, it’s important to remember that it can be changed by many factors other than iron absorption. Other micronutrient deficiencies, such as vitamin B12, folic acid, and albumin can influence changes in transferrin level, as it is a hepatic protein associated to malnutrition [30]. Inflammatory status identified by high protein C levels can also affect iron profile by increasing ferritin levels [31]. Dehydration, smoking, pregnancy, increased blood capacitance, crystalloid boluses, and even laboratory errors are often able to cause changes in hemoglobin levels.

Surgical technique should be accurate to minimize blood loss and time in the operating room. Intraoperative blood loss is not well estimated by weighting sponges or measuring contents of suction machines. It can be indirectly estimated by hemoglobin levels on the second postoperative day, which are clinically more relevant as well [32]. Resection of excessive skin and fat may lead to a decrease of 2 g/dL in anchor abdominoplasty [24] or 3 g/dL in circumferential abdominoplasty [33]. Maintenance saline solution does not result in hemodilution [34]. When given in bolus, saline is able to reduce hemoglobin level for 8 h with total recovery after that.

At the end of the surgery, the organism starts to recover from surgical trauma. Erythropoietin-stimulated bone marrow can increase its cell production capacity severalfold causing a medullar erythroid hyperplasia which is noticeable after 3–5 days [35]. Hemoglobin levels increased significantly at seven postoperative days, correcting one-third of the hemoglobin deficit due to an increase in erythopoiesis. However, after a rapid recovery in hemoglobin levels during the first week, there were no significant increases in the fourth and eighth weeks. At the end of the study, the hemoglobin levels remained significantly lower than preoperative levels [24].

The postoperative recovery from anemia is not well understood yet. Most of the studies about it regard hip arthroplasty in elderly patients [36–38]. They found an incomplete recovery of hemoglobin levels, reduced serum iron and transferrin levels, and increased ferritin levels in an eight-week follow-up. Those findings are also present in chronic disease anemia profile and have an inflammatory pathophysiology. The key phenomenon in this kind of anemia is the inability of iron stored in the reticuloendothelial system to be released to bone marrow for erythropoiesis [39, 40]. Cytokines such as interleukin-6 (IL-6) and C-reactive protein are involved in postoperative acute-phase inflammation and are increased after surgery [37]. IL-6, one of the most important mediators of this process, is responsible for an increase in hepcidin levels. Hepcidin is a liver hormone that reduces iron absorption by duodenal mucosa and release of iron from reticuloendothelial system promoting low serum iron levels [41, 42]. It is clear, then, that inflammatory response to surgical trauma limits erythopoiesis in postbariatric patients as well [24, 37].

However, as iron is essential to erythropoiesis, reduced levels of iron may also be responsible for postoperative anemia [36]. If patients have previous low storage of iron expressed by low ferritin levels preoperatively or develop iron deficiency with low ferritin 6 weeks after surgery, they are prone not to recover hemoglobin levels as they cannot sustain an intensified erythropoiesis as needed to compensate intraoperative blood loss [24, 36]. Because of the tendency for iron deficiency, postbariatric patients have low ferritin levels preoperatively (ferritin levels <30 ng/mL) [28]. What is the minimum preoperative ferritin level necessary to maintain adequate erythropoiesis after postbariatric abdominoplasty without depleting iron reserves? A theoretical calculation revealed that preoperative ferritin should be around 56 ng/mL to enable correction of the average deficit of 2.18 g/dL hemoglobin found in postbariatric abdominoplasty without depleting iron reserves [24].

This study suggests that intravenous supplementation with iron during the preoperative or perioperative period may be indicated for candidates of postbariatric abdominoplasty, to avoid postoperative depletion of iron reserves and to accelerate postoperative recovery of hemoglobin levels. Randomized and controlled prospective trials are under way to test this proposal (ISAPA trial, NCT01857011). In postbariatric patients with preoperative low ferritin levels, intravenous iron supplementation perioperatively might be a good strategy as it has been demonstrated for orthopedic patients [43]. Thus, ideal conditions would be provided for these patients for postoperative recovery of hemoglobin levels without depleting iron reserves, and next plastic surgeries would safely be kept on schedule.