Iron Deficiency Anaemia in Children

Iron deficiency anaemia (IDA) is the commonest nutritional deficiency and the single most frequent cause of anaemia in children worldwide, with the highest prevalence between 6 months and 2 years. It is a microcytic, hypochromic anaemia caused by depletion of body iron stores, and it remains a perennial NEET PG favourite because of its crisp cut-offs, smear morphology, and the National Iron Plus Initiative (NIPI).

Definition & age-specific cut-offs

Anaemia in children is defined by haemoglobin (Hb) below the WHO age-specific lower limit. Because foetal and neonatal Hb is physiologically high and then declines (physiological nadir at 6–8 weeks in term, earlier and lower in preterm), the cut-off is age-dependent — a single number cannot be applied across all paediatric ages.

Age group	Hb cut-off for anaemia (g/dL)
6 months – 59 months	< 11.0
5 – 11 years	< 11.5
12 – 14 years	< 12.0
Non-pregnant girls ≥ 15 yr	< 12.0
Pregnant adolescent	< 11.0

High-yield: WHO Hb cut-off for the 6–59 month child is < 11 g/dL — the most commonly tested single value in paediatric anaemia.

WHO severity grading of anaemia in the under-5 child: mild 10–10.9, moderate 7–9.9, severe < 7 g/dL. (Adolescent/adult cut-offs differ slightly but the under-5 grading is the exam-tested one.)

Where IDA sits in classification

IDA is a microcytic hypochromic anaemia (low MCV, low MCH, low MCHC). The classic microcytic differentials are remembered by the mnemonic "TICS": Thalassaemia, Iron deficiency, Chronic disease (anaemia of inflammation), Sideroblastic anaemia (and lead poisoning).

Iron physiology & why infants are vulnerable

A term newborn is born with ~75 mg/kg of iron, two-thirds of which is in circulating haemoglobin. Iron endowment at birth depends on maternal iron status and, critically, on the timing of cord clamping — delayed cord clamping transfers an extra 30–50 mg of iron and reduces infantile IDA.

Key physiological facts:

• Breast milk iron is low (~0.3 mg/L) but highly bioavailable (~50% absorbed) because of lactoferrin; exclusive breastfeeding suffices only up to ~6 months, after which stores deplete and complementary feeding must supply iron.
• Cow's milk is the villain: low iron content, poorly bioavailable, and it causes occult gastrointestinal blood loss (microscopic enteropathy) plus displaces iron-rich solids. Early/excessive cow's-milk feeding (especially > 500–700 mL/day under 1 year) is a classic IDA cause.
• Dietary iron exists as haem iron (meat, ~25% absorbed) and non-haem iron (cereals/vegetables, ~5% absorbed; absorption enhanced by vitamin C/ascorbate and reduced by phytates, tannins/tea, and calcium).
• Absorption occurs in the duodenum and proximal jejunum via DMT-1 after ferric→ferrous reduction; hepcidin is the master negative regulator (raised in inflammation → functional iron sequestration).

Etiology — stage of life matters

Decreased supply / stores

• Prematurity, low birth weight, twins (low endowment).
• Inadequate complementary feeding; prolonged exclusive milk diet ("milk anaemia" of toddlers).

Increased demand

• Rapid growth in infancy and the adolescent growth spurt.
• Adolescent girls — menstrual blood loss added to growth demand.

Blood loss

• Hookworm (Ancylostoma duodenale, Necator americanus) — the leading cause of chronic GI blood loss in Indian school children.
• Cow's-milk–induced occult bleed, Meckel's diverticulum, polyps, peptic disease, recurrent epistaxis.

Malabsorption

• Coeliac disease (IDA refractory to oral iron is a classic clue), chronic diarrhoea, post-gastric surgery, H. pylori.

High-yield: In a school-age Indian child with IDA, always think hookworm; in a 1–2-year-old toddler, think excess cow's milk and poor complementary feeding.

Clinical features

IDA develops insidiously; symptoms appear only when anaemia is moderate-to-severe.

• General: pallor (best seen in conjunctiva, palms, nail beds, tongue), fatigue, irritability, poor feeding, growth faltering.
• Pica — craving for non-food items (mud = geophagia, ice = pagophagia). Pagophagia is fairly specific for IDA.
• Epithelial / koilonychia (spoon-shaped nails), angular stomatitis, glossitis, brittle hair.
• Cardiac: in severe anaemia — tachycardia, flow murmur, high-output failure.
• Neurodevelopmental: the most important long-term concern — impaired cognition, attention and psychomotor development, which may be irreversible if deficiency occurs in the critical first 2 years.
• Breath-holding spells are commoner in iron-deficient infants and improve with iron therapy.
• Reduced immunity and an association with febrile seizures.

High-yield: Neurodevelopmental impairment from infantile IDA may be permanent even after correction of the anaemia — hence aggressive prevention in the under-2 age group.

Laboratory diagnosis & investigation of choice

The diagnostic sequence mirrors the pathophysiological depletion of iron:

Stage 1 – storage iron depletion → low serum ferritin (earliest change) → Stage 2 – iron-deficient erythropoiesis → low serum iron, raised TIBC, low transferrin saturation, raised free erythrocyte protoporphyrin, raised soluble transferrin receptor → Stage 3 – frank IDA → low Hb, low MCV/MCH, microcytic hypochromic smear.

Peripheral smear

Microcytic, hypochromic red cells with anisocytosis and poikilocytosis, pencil/cigar cells (elliptocytes), target cells, and occasional teardrop cells. Platelet count is often mildly raised (reactive thrombocytosis).

Iron studies

Parameter	IDA	Anaemia of chronic disease	Thalassaemia trait
Serum ferritin	Low (< 12–15 ng/mL)	Normal/High	Normal/High
Serum iron	Low	Low	Normal/High
TIBC	High	Low/Normal	Normal
Transferrin saturation	Low (< 16%)	Low	Normal/High
MCV	Low	Normal/Low	Very low (disproportionate)
RDW	High	Normal	Normal
Mentzer index (MCV/RBC)	> 13	—	< 13

High-yield: Serum ferritin is the single best (earliest, most specific) indicator of iron stores. Ferritin < 12 ng/mL (under 5 years) or < 15 ng/mL (older) confirms depletion. Caveat: ferritin is an acute-phase reactant — a "normal" ferritin during infection/inflammation does not exclude IDA.

Distinguishing IDA from thalassaemia trait is a perennial MCQ. Both are microcytic, but thalassaemia trait has a normal/high RBC count, very low MCV out of proportion to anaemia, normal RDW, and Mentzer index < 13; IDA has a low RBC count, high RDW, and Mentzer index > 13. Confirmatory test for beta-thalassaemia trait is HbA2 > 3.5% on HPLC (do iron studies first, as iron deficiency can falsely lower HbA2).

Bone marrow with Prussian blue (Perls') stain showing absent stainable iron is the gold standard but rarely needed clinically.

Stepwise diagnostic approach

Microcytic hypochromic anaemia → check serum ferritin → if low → IDA → search for cause (diet history, stool for ova/hookworm, coeliac serology if refractory) → start iron and confirm response with reticulocytosis.

Management — iron is the drug of choice

Oral iron (first line)

• Drug of choice: oral ferrous sulphate (also ferrous fumarate/gluconate). Therapeutic dose is 3–6 mg/kg/day of elemental iron, usually divided but increasingly given as a single daily/alternate-day dose (better absorption, fewer side-effects, lower hepcidin rebound).
• Give between meals / empty stomach with vitamin C (citrus); avoid milk, tea, antacids.
• Duration: continue for 2–3 months after Hb normalises to replenish stores — total roughly 3 months of therapy.
• Side-effects: black stools (harmless, counsel parents), nausea, constipation, metallic taste, teeth staining (liquid preps).

High-yield: Elemental iron content — ferrous sulphate ~20%, ferrous fumarate ~33%, ferrous gluconate ~12%. Always prescribe in terms of elemental iron.

Response to therapy (very testable timeline)

1. Subjective well-being / improved appetite — within a few days.
2. Reticulocytosis — peaks at 5–7 days (earliest objective marker).
3. Rise in Hb — ~1 g/dL per 2–3 weeks (expect ≥ 1–2 g/dL in 4 weeks); failure to rise by ≥ 1 g/dL in ~4 weeks = inadequate response.
4. Replenishment of stores — over 2–3 months.

High-yield: A reticulocyte response at day 5–10 is the earliest confirmation of correct diagnosis and adherence.

Causes of failure of oral iron ("the 5 wrongs")

Wrong diagnosis (thalassaemia/ACD), wrong dose, poor compliance, ongoing blood loss (hookworm, Meckel's), or malabsorption (coeliac, H. pylori).

Parenteral / transfusion

• Parenteral iron (iron sucrose, ferric carboxymaltose) — reserved for intolerance, malabsorption, non-compliance, or chronic loss exceeding oral intake. Calculate dose; older iron-dextran carried anaphylaxis risk.
• Packed-cell transfusion — only for symptomatic severe anaemia (Hb < 4 g/dL, or < 5 with infection/failure); give slowly with diuretic to avoid fluid overload in chronic anaemia.

Treating the cause

Deworm (single-dose albendazole 400 mg; 200 mg if 12–24 months) for suspected hookworm, treat coeliac/H. pylori, restrict cow's milk to < 500 mL/day in toddlers, and optimise complementary feeding.

Prevention & national programmes

Programme / strategy	Key facts
Anaemia Mukt Bharat (AMB)	Umbrella 6×6×6 strategy (6 interventions × 6 beneficiary groups × 6 institutional mechanisms); target life-cycle reduction of anaemia.
National Iron Plus Initiative (NIPI)	Life-cycle approach: biweekly IFA syrup (1 mL = 20 mg elemental iron) for 6–60 months; WIFS for school children and adolescents; deworming.
WIFS (Weekly Iron & Folic Acid Supplementation)	School children 6–10 yr: weekly IFA 45 mg iron + 400 µg folic acid (pink tablet); adolescents 10–19 yr: weekly 100 mg iron + 500 µg folic acid (blue tablet); biannual albendazole.
Prophylaxis under NIPI	6–60 months: ~1 mL IFA syrup biweekly; pregnant/lactating women: 1 IFA tablet (60 mg iron) daily + deworming.

High-yield: WIFS = weekly IFA + biannual albendazole; school children get 45 mg iron, adolescents 100 mg iron. Frequently asked colour-coding: pink tablet (children) vs blue tablet (adolescents).

Other preventive levers: delayed cord clamping, exclusive breastfeeding to 6 months with timely iron-rich complementary feeding, iron-fortified cereals, and restricting cow's milk in infancy.

Complications

• Irreversible neurocognitive and behavioural deficits (poor school performance) if deficiency in the first 2 years.
• Growth retardation, impaired immunity, increased infection susceptibility.
• High-output cardiac failure in severe anaemia.
• Increased lead absorption (DMT-1 upregulation) — IDA and plumbism coexist.
• Breath-holding spells, pica complications (lead ingestion, parasitic load from geophagia).

Key differentials

• Beta-thalassaemia trait/minor — microcytosis out of proportion, normal RDW, raised HbA2 (see table). Iron not indicated; iron overload risk.
• Anaemia of chronic disease/inflammation — high ferritin, low TIBC, hepcidin-mediated; treat underlying disease.
• Sideroblastic anaemia / lead poisoning — basophilic stippling, ring sideroblasts, dimorphic smear; raised serum iron and ferritin.
• Anaemia of prematurity — normocytic, low erythropoietin.
• Vitamin B12 / folate deficiency — macrocytic (a dimorphic picture if combined with iron deficiency, giving a normal-looking MCV with high RDW).

Recently asked / exam angle

• Hb cut-off < 11 g/dL for the 6–59-month child (WHO) — repeatedly asked.
• Earliest lab marker of iron deficiency = low serum ferritin; earliest therapeutic response = reticulocytosis at day 5–7.
• Mentzer index (MCV/RBC) > 13 → IDA, < 13 → thalassaemia trait — a classic discriminator MCQ.
• WIFS doses and tablet colours under NIPI/AMB — favourite community-medicine-flavoured paediatrics question.
• Cow's milk as a cause (occult GI bleed + low bioavailability) in toddlers; hookworm in school children.
• Elemental iron content of salts and the 3–6 mg/kg/day therapeutic dose.
• Duration of therapy = continue ~3 months after Hb normalises to refill stores.
• Pica/pagophagia, koilonychia, and reactive thrombocytosis as bedside/lab clues.
• Mentzer vs RDW vs HbA2 sequencing: iron studies before HPLC because deficiency lowers HbA2.

Rapid revision

1. IDA = microcytic, hypochromic; commonest nutritional anaemia, peak at 6 months–2 years.
2. WHO Hb cut-offs: < 11 (6–59 mo), < 11.5 (5–11 yr), < 12 (12–14 yr).
3. Under-5 severity: mild 10–10.9, moderate 7–9.9, severe < 7 g/dL.
4. Serum ferritin = earliest, most specific marker of stores; falsely raised in inflammation.
5. Iron studies in IDA: low ferritin, low iron, high TIBC, transferrin saturation < 16%, high RDW.
6. Smear: pencil cells, anisopoikilocytosis, target cells, reactive thrombocytosis.
7. Mentzer index > 13 → IDA; < 13 → thalassaemia trait (confirm with HbA2 > 3.5%).
8. DOC = oral ferrous sulphate, 3–6 mg/kg/day elemental iron, with vitamin C, away from milk/tea.
9. Reticulocytosis at day 5–7; Hb rises ~1 g/dL/2–3 weeks; continue iron 3 months after Hb normalises.
10. Toddler IDA → think excess cow's milk; school child IDA → think hookworm (albendazole 400 mg).
11. WIFS: school children weekly 45 mg iron + 400 µg folate (pink); adolescents weekly 100 mg iron + 500 µg folate (blue) + biannual deworming.
12. Infantile IDA can cause irreversible neurodevelopmental deficit — prevention is paramount.