This lady has presented with 'pica', i.e. craving of non-food items with little or no nutritional value, followed by ingestion of these substances to satisfy the said cravings. While pica is mainly encountered in children, adults may also experience this symptom; in such cases, this is due to either pregnancy, nutritional deficiencies, or a psychiatric disorder. Note that the first of the above is excluded by the negative urine pregnancy test; in addition, the normal psychiatric evaluation makes a psychiatric disorder clinically less likely. However, a nutritional deficiency is quite plausible, given that she is a vegetarian, and also breastfeeding. Examination reveals the presence of pallor and a functional murmur. Could she be anemic? A complete blood count is a logical next step, and reveals several important findings: - Severely diminished hemoglobin levels - Low mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentration (MCHC) values - An increased red cell distribution width (RDW) - A reticulocyte count which is lower than one would expect given the degree of anemia - A slight thrombocytosis The first two findings listed above indicate that a severe, microcytic hypochromic anemia is present; this can be caused by either iron deficiency anemia (IDA), or by certain hemoglobinopathies (most importantly, thalassemia). However, the increased RDW and unusually low reticulocyte count are most suggestive of IDA; in thalassemia, the RDW is usually normal or low, and reticulocyte counts are either normal or elevated. Note that a thrombocytosis can occur in both conditions. A peripheral blood film (blood picture) and iron studies should follow; the former confirms the presence of a microcytic anemia, and additionally demonstrates anisopoikilocytosis (which favors IDA); the latter shows extremely low serum iron and ferritin levels, and low transferrin receptor saturation, and high serum transferrin levels, confirming the presence of iron deficiency. Note that bone marrow studies are not required to diagnose IDA. As mentioned earlier, the IDA in this patient is most likely secondary to poor dietary intake of iron, and the extra demands placed on her body by breastfeeding and repeat pregnancies; thus, a trial of oral iron therapy is a good initial choice. However, if the anemia continues to persist, she should receive further evaluation as to a potential source of gastrointestinal bleeding. She should also receive nutritional advice from a professional, regarding how to improve her diet. While her anemia is severe, her symptoms are relatively mild, and thus, transfusion is probably best avoided for now; there is no role for splenectomy in her management.
Iron deficiency is the most common nutritional deficiency across the globe; this gives rise to iron deficiency anemia (IDA) when levels of iron in the body are depleted to the point that erythropoiesis is impaired. The prevalence of the condition varies depending on factors such as age, gender, physiological and pathological states, and adverse environmental and economic conditions. The highest prevalence is seen in adolescent females, presumably due to the combined effects of menstrual losses, insufficient intake, and allowances for rapid growth. In addition, it is estimated that the majority of preschool children and pregnant women in developing countries are victims of IDA, as are 30% to 40% of their compatriots in developed countries. IDA is also common in the elderly, possibly because of factors such as lessening appetite, malabsorption, and the presence of numerous comorbid conditions (which may themselves result in food restrictions). As mentioned above, any condition that results in increased iron loss, increased iron demand, inadequate iron intake, or impaired iron absorption can cause IDA. Chronic blood loss, usually from gastrointestinal or genitourinary tract (by way of gastrointestinal malignancies, hookworm infestation, ulcers, or heavy menstruation) and acute blood (loss due to any cause) are notable mechanisms of excessive loss. Periods of rapid growth, pregnancy, and erythropoietin therapy increase the demand for iron, while prolonged achlorhydria (as in postgastrectomy patients), malabsorption syndromes (such as tropical sprue and celiac disease), chronic diseases, and starch and clay consumption diminish iron absorption. Mild IDA is usually asymptomatic; as the severity of anemia increases, patients gradually begin to experience symptoms. The initial symptoms and signs are those of anemia, and include pallor, fatigue, headache, dizziness, shortness of breath and palpitations. As the deficiency worsens, clinical features which are more specific to iron deficiency appear; these include glossitis, angular stomatitis, pica, koilonychia, dysphagia, esophageal webbing, and impaired cognitive function. The diagnosis of IDA requires evidence of anemia and iron deficiency. A complete blood count is the first choice in this regard, as this will help assess the severity of the anemia, and also reveal evidence of microcytic hypochromic erythropoiesis, i.e. reduced mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentration (MCHC) values. A peripheral blood film typically shows poikilocytosis and anisocytosis, in addition to hypochromic microcytic red cells. Note that severe IDA gives rise to a bizarre blood film with target cells, nucleated red blood cells and usually, increased platelets. Serum ferritin levels correlate well with body iron stores, thus exceptionally low levels (<25 ng/ mL) are suggestive of depletion; note that this occurs before red blood cell indices are affected. Unfortunately, coexisting inflammatory disease can mask this, as ferritin is an acute phase reactant and may thus be spuriously elevated. Changes in the iron-transporting protein transferrin are also useful in the diagnosis of IDA; as there is less iron to be bound, transferrin saturation decreases, while the total iron binding capacity (TIBC) increases. Serum transferrin receptor assays are a highly specific indicator for iron deficiency; due to compensatory upregulation of transferrin receptors at the cellular level, high levels are seen in these patients. Bone marrow studies allow for definitive diagnosis of IDA, and typically show absent or severely depleted iron stores. However, these are rarely performed, given their invasive nature. Oral iron therapy with ferrous sulfate or ferrous gluconate is the first-line treatment in these patients; simultaneous vitamin C supplementation will help enhance intestinal iron absorption. Patients who are on concomitant calcium supplements (e.g. pregnant women) should be advised to take iron at a different time of the day, as the former interferes with the absorption of iron by competing for the same intestinal cotransporter. Ingestion of foods containing tannins (e.g. tea), phytates (e.g. cereal) and drugs that increase gastric pH (e.g. proton pump inhibitors, H2 receptor blockers) should also be discouraged, as these substances reduce iron absorption. Note that the iron supplementation may result in adverse effects such as gastric discomfort and a disagreeable metallic taste; while the use of sustained release preparations mitigates this, these are not recommended as a first choice, since they release a lesser quantity of iron. Parenteral iron therapy is reserved for conditions such as oral iron intolerance, extremely poor patient compliance, intestinal malabsorption syndromes, and persistent intractable bleeding. Note that parenteral therapy is invasive, can be extremely painful (when administered intramuscularly), and can result in adverse effects such as anaphylactic reactions (when given intravenously). Following iron therapy, hemoglobin levels are expected to rise by 1 g/dL every two to three weeks; note that supplementation should be continued for at least 3 months following correction of anemia, so as to restore the depleted iron stores. Note also that patients with symptomatic anemia and asymptomatic patients who are at risk of hypoxia or coronary insufficiency (i.e. hemoglobin < 10 g/dL) should be offered transfusional support with packed red cells. Following the acute management, specific treatment of the underlying cause should be commenced. Patients with diet related IDA should be offered nutritional advice on how to incorporate iron rich food into their diet. Similar to other nutritional deficiencies, IDA is better prevented than treated. Preventive strategies include reducing poverty, improving access to diversified diets (especially in individuals at risk), changing feeding practices, and improving health care and sanitation.