Iron Deficiency Anaemia in Children
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Direct answer
Iron deficiency is the commonest cause of anaemia in childhood, peaking between six months and three years — when fetal stores run out and diets are milk-heavy and iron-poor — and again in adolescence with rapid growth and menstrual losses. It produces a microcytic hypochromic anaemia with low serum iron and ferritin and a high total iron-binding capacity, and a Mentzer index (MCV divided by red cell count) above 13 separates it from thalassaemia trait. Treatment is oral elemental iron at 3-6 mg per kilogram per day, continued about three months after haemoglobin normalises to refill stores.
What you must remember
- Causes: weaning diets dominated by cow's milk (iron-poor, and a cause of occult gastrointestinal loss), prematurity and low birth weight, perinatal blood loss, hookworm infestation, malabsorption and chronic blood loss.
- Clinical picture: pallor of palms and mucosae, irritability, anorexia, fatigue and poor concentration, pica (including pagophagia — ice craving), and long-standing koilonychia and glossitis.
- Laboratory signature: low haemoglobin with low MCV and MCH, raised RDW, hypochromic microcytes on smear, low ferritin (the best store marker), low serum iron, and raised TIBC with saturation below about 16 per cent.
- Mentzer index: MCV divided by erythrocyte count — above 13 favours iron deficiency, below 13 favours thalassaemia trait, the fastest bedside discriminator between the microcytic anaemias.
- Treatment rules: oral elemental iron 3-6 mg/kg/day between meals with a vitamin C source, avoided with milk, tea and antacids; parenteral iron only for intolerance or malabsorption, transfusion only for severe decompensation.
- Response markers: reticulocytes rise within the first week — the earliest response; failure to respond means poor adherence, wrong diagnosis or ongoing loss.
- Duration: continue about three months beyond haemoglobin normalisation, alongside treatment of the cause and iron-rich weaning advice.
Common confusion
Iron deficiency against thalassaemia trait is the examination evergreen: both are microcytic, but thalassaemia trait runs in families, shows normal or high iron studies, no response to iron, target cells and a Mentzer index below 13. Anaemia of chronic disease is the third player — ferritin normal or high as an acute-phase protein with low TIBC, the mirror image. Beware interpreting ferritin during infection or inflammation, when it rises and can mask empty stores; a paired CRP helps.
Exam-focused takeaway
NEET-PG asks this in three formats. Vignette: a milk-fed toddler with pallor, pica and a microcytic hypochromic picture — the investigation of choice is iron studies with ferritin, and the Mentzer index settles any thalassaemia debate. Management: the dose (3-6 mg/kg/day elemental), the timing (empty stomach with vitamin C), the earliest response marker (reticulocytes within a week) and the duration (three months after haemoglobin normalises). One-liners: commonest cause of childhood anaemia, the meaning of a high TIBC, koilonychia, pagophagia and hookworm as the Indian cause of chronic loss.
Frequently asked questions
Why is iron deficiency commonest at six months to three years?
Fetal stores are exhausted by around six months, breast milk is iron-poor, and weaning diets are often milk-dominated — high demand meeting low supply.
What is the Mentzer index?
Mean corpuscular volume divided by red blood cell count: above 13 favours iron deficiency, below 13 favours thalassaemia trait.
Which single test best reflects iron stores?
Serum ferritin — low values confirm empty stores, interpreted alongside CRP because inflammation falsely raises it.
How is oral iron given and for how long?
Elemental iron 3-6 mg/kg/day, ideally on an empty stomach with vitamin C, continued for about three months after haemoglobin normalises.
What is the earliest sign of response?
Reticulocytosis within the first week; its absence should prompt a search for non-adherence, ongoing loss or an alternative diagnosis.