Paediatrics chapters

Iron deficiency anaemia in children

The commonest blood disorder of childhood: why toddlers on cow's milk become iron deficient, the order in which tests turn abnormal, how to tell it from thalassaemia trait, and how oral iron is given and its response checked.

UHS PGET syllabus: Haematologic disorders (8 MCQs), Haematologic disorders: microcytic anaemias; iron deficiency anaemia: aetiology, pathophysiology, clinical features, diagnosis and managementUpdated November 2026
In 30 seconds
  • Iron deficiency is the commonest haematological disease of childhood; the classic patient is a toddler drinking large amounts of cow's milk with little solid food, or a child losing blood (hookworm, cow's milk protein allergy, Meckel's).
  • Tests turn abnormal in order: RDW rises first, then ferritin falls, then serum iron falls and TIBC rises, then a microcytic hypochromic anaemia appears; ferritin low, TIBC high separates it from thalassaemia trait (Mentzer index 12.5 or more; below 12.5 points to trait).
  • Treat with oral elemental iron between meals; reticulocytes rise in 2-4 days, haemoglobin within weeks, and iron is continued 2-3 months after the haemoglobin normalises to refill stores.
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Overview

Iron deficiency anaemia is a microcytic, hypochromic anaemia caused by too little iron to make haemoglobin. It is the commonest haematological disease of infancy and childhood and the commonest cause of anaemia worldwide. Rapid growth, low iron intake and poor absorption all add up in young children.

Beyond anaemia, iron deficiency affects the brain: apathy, irritability, poor attention and, if it occurs in infancy, possible long-term learning problems.

Iron balance in children

  • Most body iron is in haemoglobin; it is carried in plasma by transferrin and stored as ferritin in the liver, marrow and spleen.
  • A newborn has about 0.3-0.5 g of iron; an adult about 5 g. To make up the difference a child must absorb roughly 1 mg a day, but less than 10% of dietary iron is absorbed, so the diet must supply much more (Akbar quotes about 8-15 mg daily).
  • A term baby's stores last for the first 6 months or so. Iron deficiency before 6 months in a term infant (or before birth weight doubles in a preterm infant) is unusual unless there is blood loss (Nelson).
  • Breast milk contains little iron, but it is absorbed much better than iron from cow's milk.

Causes

Nutritional (the commonest)

  • Large volumes of cow's milk (low iron, poorly absorbed, displaces solid food) and a diet low in meat and green vegetables.
  • Late or poor weaning; prolonged exclusive milk feeding.
  • Increased demand: preterm and low birth weight babies, rapid growth, cyanotic congenital heart disease, adolescence.
  • Mother anaemic, many closely spaced pregnancies.

Poor absorption

  • Coeliac disease, other malabsorption, Giardia infection, chronic diarrhoea.

Blood loss

PeriodCauses
Before or at birthFeto-maternal or twin-to-twin transfusion, placental abruption or praevia, cord bleeding
NewbornHaemorrhagic disease of the newborn
Infancy and childhoodCow's milk protein allergy (occult gut bleeding), hookworm, Meckel's diverticulum, peptic ulcer, rectal polyps, inflammatory bowel disease, epistaxis
Adolescent girlsMenstrual loss
Exam trap

In infants, cow's milk causes iron deficiency in two ways: it is poor in absorbable iron, and cow's milk protein intolerance can cause hidden intestinal blood loss.

High-yield

Always check the stool for occult blood and think of hookworm in a child from an endemic area.

Pathophysiology: the stages

Iron deficiency develops slowly:

  1. Stores empty first: ferritin falls, but haemoglobin is still normal. The RDW rises early as new red cells come out smaller.
  2. Iron-deficient red cell production: serum iron falls, TIBC rises, transferrin saturation falls. Haemoglobin synthesis suffers once saturation drops to about 10-15%.
  3. Anaemia: first normocytic, then microcytic and hypochromic as it worsens.

Iron is also part of cytochromes and enzymes such as monoamine oxidase, which explains the behavioural and muscle effects even before anaemia is marked.

Clinical features

  • Mild deficiency: often no symptoms.
  • Moderate to severe: irritability, anorexia, lethargy, easy fatigue, poor attention and school performance.
  • Pallor; the classic "milk baby" is chubby, pale and sallow.
  • Pica (eating earth, ice or other non-food items), which also raises suspicion of lead poisoning.
  • Koilonychia (spoon nails), angular stomatitis, glossitis, blue sclerae.
  • Tachycardia, systolic flow murmur.
  • Very severe anaemia (Akbar: Hb below 3 g/dL) can cause heart failure: gallop rhythm, cardiomegaly, hepatomegaly, raised neck veins, crackles.
  • Other effects: poor muscle endurance, impaired immunity.

Investigations

Blood count and film

  • Low haemoglobin, low MCV, MCH and MCHC.
  • High RDW (anisocytosis); RDW above about 14.5% fits iron deficiency (Akbar).
  • Film: small, pale red cells with a wide central pallor; anisocytosis and poikilocytes.
  • Reticulocytes normal or slightly raised; white cells normal.

Iron studies

TestIron deficiency
Serum ferritinLow (below about 12 ng/mL); the best reflection of stores
Serum ironLow
TIBC (transferrin)High
Transferrin saturationLow (usually under 20%)
Erythrocyte protoporphyrin (FEP)High
Bone marrow iron (rarely needed)Absent
Exam trap

In inflammation ferritin is normal or high, so a child with both inflammation and iron deficiency may have a misleadingly normal ferritin.

A therapeutic test of iron

In an otherwise well child with a typical history and blood picture, a course of oral iron with a documented rise in haemoglobin is the most practical confirmation of the diagnosis (Nelson), provided the child is actually re-checked.

Differential diagnosis of microcytic anaemia

TestIron deficiencyBeta-thalassaemia traitAnaemia of inflammation
Serum ferritinLowNormal to highNormal to high
Serum ironLowNormalLow
TIBCHighNormalLow or normal
RDWHighNormalNormal or high
RBC countLowHigh for the HbLow
HbA2NormalRaisedNormal
FEPHighNormal or slightly highHigh
  • Lead poisoning also causes microcytosis with basophilic stippling, and often coexists with iron deficiency.
  • In anaemia of chronic inflammation, hepcidin blocks iron release and absorption, so iron is present but locked away.

Mentzer index

Divide the MCV (fL) by the red cell count (millions per microlitre). In thalassaemia trait the marrow makes many small cells, so the red cell count is high and the index is below about 12.5; in iron deficiency it is usually higher.

Worked example: Mentzer index

Child A: MCV 62 fL, RBC 5.6 million/µL
62 ÷ 5.6 = 11.1 → below 12.5, suggests thalassaemia trait
Child B: MCV 62 fL, RBC 4.0 million/µL
62 ÷ 4.0 = 15.5 → above 12.5, suggests iron deficiency

Memory hook

Thalassaemia trait = "Too many, Too small": high red cell count, so a low Mentzer index.

Management

Oral iron (first line)

  • Give elemental iron by mouth, 3-6 mg/kg/day (Akbar), ideally between meals for better absorption.
  • Treat the cause: cut cow's milk down to a sensible amount, introduce iron-rich weaning foods (meat, eggs, green vegetables), deworm, treat malabsorption or a bleeding lesion.
  • Continue iron for 2-3 months after the haemoglobin has normalised to refill the stores.

Expected response

Time after starting ironWhat happens
12-48 hoursChild feels better: less irritable, better appetite
2-4 daysReticulocytes rise (peak about 5-7 days)
4-30 daysHaemoglobin rises (roughly 0.1-0.4 g/dL a day)
1-3 monthsIron stores refilled
High-yield

The earliest objective sign of response is a rise in reticulocytes within a few days; the earliest clinical change is an improvement in mood and appetite.

Failure to respond

If haemoglobin has not risen after about 2 weeks, re-assess for:

  • Poor compliance (the commonest reason) or wrong dose.
  • Continuing blood loss.
  • Infection or inflammation.
  • Malabsorption (coeliac disease).
  • Wrong diagnosis: thalassaemia trait, lead poisoning, anaemia of inflammation.

Parenteral iron

Used only occasionally: malabsorption, diarrhoea, or poor compliance with oral iron.

Blood transfusion

Reserved for very severe anaemia with heart failure or another emergency. Akbar advises small volumes of packed cells (2-3 mL/kg) given very slowly, repeated after 12-24 hours if needed, because rapid transfusion can worsen failure.

Exam trap

A child with a haemoglobin of 5 g/dL who is well compensated does not need transfusion; oral iron works quickly. Decide on the cardiovascular state, not the number.

High-yield

Poor compliance is the commonest reason oral iron appears to fail.

Prevention

  • Encourage breastfeeding.
  • Breastfed babies need an iron source from about 4-6 months: Akbar suggests supplemental iron from 4 months; Nelson from 6 months, with iron-rich solid foods at 6 months.
  • Formula-fed infants should have iron-fortified formula for the first year.
  • Avoid plain cow's milk before 1 year and limit it in toddlers.
  • Preterm and low birth weight babies need iron supplements.
  • Menstruating girls need an iron-rich diet.
Exam focus

Expect: a pale toddler on mostly cow's milk; the commonest anaemia in children; the earliest test to change (RDW) and the best test of stores (ferritin); iron profile (low ferritin, low iron, high TIBC, low saturation) versus thalassaemia trait (normal ferritin, raised HbA2, high RBC count, Mentzer below 12.5) and anaemia of inflammation (low TIBC); koilonychia and pica; oral elemental iron 3-6 mg/kg/day between meals; reticulocytes as the first measurable response; continuing iron 2-3 months after correction; causes of non-response; and occult blood loss such as hookworm or cow's milk protein allergy.

Quick revision

  • Commonest childhood anaemia; peak in toddlers and teenage girls.
  • Cow's milk: low absorbable iron plus occult gut bleeding.
  • Order of change: ferritin and RDW, then iron and TIBC, then microcytic anaemia.
  • Ferritin low, TIBC high, saturation low, RDW high.
  • Thalassaemia trait: normal ferritin, high RBC count, raised HbA2, Mentzer below 12.5.
  • Oral iron 3-6 mg/kg/day elemental, between meals.
  • Reticulocytes up in 2-4 days; Hb within weeks; continue 2-3 months after normal.
  • No response in 2 weeks: compliance, bleeding, infection, malabsorption, wrong diagnosis.
  • Transfuse only for failure, slowly in small volumes.

Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).

FAQ

What is the first laboratory sign of iron deficiency?

A rising red cell distribution width and falling ferritin appear before the haemoglobin drops; the microcytic anaemia comes last.

How do I tell iron deficiency from thalassaemia trait on a blood count?

Thalassaemia trait has a relatively high red cell count, a normal RDW and a Mentzer index below about 12.5, while iron deficiency has a high RDW, low ferritin and a higher index. Haemoglobin A2 is raised in beta-thalassaemia trait.

How long should iron be given?

Until the haemoglobin is normal and then for another 2-3 months, so that the body's iron stores are refilled.

When is a blood transfusion needed in iron deficiency?

Only when the anaemia is causing heart failure or another emergency; most children, even with quite low haemoglobin, recover well on oral iron.