Iron-Deficiency Anemia in a 15-Month-Old Toddler
This child has severe iron-deficiency anemia and should be started immediately on oral iron supplementation at 3 mg/kg/day of elemental iron given between meals, while concurrently investigating the underlying cause of iron loss. 1
Diagnostic Interpretation
The laboratory profile confirms iron-deficiency anemia:
Severe microcytosis (MCV 23.6 fL) combined with markedly elevated RDW (35.5%) is pathognomonic for iron deficiency, as this pattern reflects a mixed population of older normocytic cells and newer microcytic cells produced during iron-depleted erythropoiesis. 2
Transferrin saturation of 10% (well below the diagnostic threshold of 16–20%) confirms iron-deficient erythropoiesis, even when other parameters may be equivocal. 3, 2
Elevated total iron-binding capacity (476 µg/dL) reflects the body's compensatory attempt to capture any available iron, a hallmark of true iron deficiency. 3
The neutrophil proportion of 20.4% indicates relative neutropenia, which can occur in severe iron deficiency but is not the primary concern here. 4
The markedly elevated vitamin B12 level (1856 pg/mL) is incidental and does not contribute to the anemia; macrocytic anemia from B12 deficiency is uncommon in 15-month-olds and would produce elevated MCV, not microcytosis. 5, 4
Normal ALT (27 U/L) and mildly elevated AST (54 U/L) do not suggest significant liver disease that would confound ferritin interpretation. 2
BUN of 20 mg/dL is at the upper limit of normal and may reflect mild dehydration or dietary protein intake, but does not indicate renal disease contributing to anemia. 4
Immediate Treatment Protocol
Begin therapeutic iron supplementation without waiting for additional confirmatory tests:
Prescribe 3 mg/kg/day of elemental iron drops administered between meals to optimize gastrointestinal absorption and minimize interference from food. 1, 3
Recheck hemoglobin concentration in 4 weeks; an increase of ≥1 g/dL (or hematocrit ≥3%) confirms the diagnosis of iron-deficiency anemia and validates the treatment approach. 1
If hemoglobin rises appropriately, continue iron therapy for 2 additional months after normalization to replenish iron stores, then recheck hemoglobin and reassess approximately 6 months after completing treatment. 1
Investigation of Underlying Cause
Concurrent with iron therapy, identify the source of iron deficiency:
Obtain a detailed dietary history focusing on cow's milk intake; children aged 1–5 years who consume >24 oz of cow's milk daily are at high risk for iron deficiency due to occult gastrointestinal blood loss and displacement of iron-rich foods. 1
Assess whether the child was introduced to cow's milk before 12 months of age, a major risk factor for iron deficiency in this age group. 1
Evaluate whether the child received iron-fortified formula or adequate iron from complementary foods after 6 months if breastfed, as breast milk alone does not provide sufficient iron beyond this age. 1
Screen for gastrointestinal blood loss if dietary history does not fully explain the severity of anemia or if the child fails to respond to iron therapy despite documented compliance. 1
Dietary Counseling
Provide specific nutritional guidance to the family:
Limit cow's milk, goat's milk, or soy milk to no more than 24 oz per day to prevent displacement of iron-rich foods and reduce risk of occult GI bleeding. 1
Encourage consumption of iron-fortified cereals (two or more servings daily), which can meet a toddler's iron requirement at this age. 1
Recommend one daily serving of vitamin C-rich foods (fruits, vegetables, or juice) with meals to enhance iron absorption from plant-based sources. 1
Introduce plain, pureed meats as a source of highly bioavailable heme iron. 1
Monitoring for Treatment Failure
If the anemia does not respond after 4 weeks of adherent iron therapy:
Consider alternative diagnoses including β-thalassemia trait, although the markedly elevated RDW (35.5%) strongly favors iron deficiency over thalassemia, which typically shows RDW ≤14%. 3, 2
Order hemoglobin electrophoresis only if iron studies normalize but microcytosis persists, as thalassemia trait would show normal iron parameters with disproportionately low MCV. 3, 2
Evaluate for rare genetic disorders of iron metabolism (e.g., IRIDA, SLC11A2 defects) if there is failure to respond to both oral and intravenous iron, although these conditions are exceedingly uncommon in this age group. 3, 6
Screen for lead poisoning in high-risk populations, as lead toxicity can cause microcytic anemia with normal or elevated iron stores. 1, 7
Common Pitfalls to Avoid
Do not order hemoglobin electrophoresis as a first-line test; the combination of severe microcytosis, elevated RDW, and low transferrin saturation definitively establishes iron deficiency, making thalassemia screening unnecessary at this stage. 3, 2
Do not attribute the elevated vitamin B12 to a pathologic process; B12 levels can be elevated in children without clinical significance, and B12 deficiency does not cause microcytic anemia. 5, 4
Do not delay iron therapy while awaiting additional testing; presumptive treatment is appropriate when clinical and laboratory features strongly suggest iron deficiency, and therapeutic response confirms the diagnosis. 1
Do not assume dietary insufficiency alone explains the anemia without investigating cow's milk intake and potential GI blood loss, as excessive cow's milk consumption is the most common modifiable risk factor in this age group. 1
Do not discontinue iron therapy once hemoglobin normalizes; continue for 2 additional months to replenish iron stores and prevent early recurrence. 1, 3