Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Iron-deficiency anaemia and dietary causes
Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Severe symptomatic anaemia
Syncope, marked breathlessness, chest pain, heart failure, reduced consciousness, shock, ongoing major bleeding or profound pallor with tachycardia requires urgent paediatric assessment rather than routine outpatient iron treatment.
Action: Use ABCDE, obtain urgent senior paediatric and haematology input, take blood for FBC, reticulocytes, film, group and save and cause-directed tests, and discuss carefully prescribed red-cell transfusion when cardiovascular compromise or critical anaemia is present.
Overview
Recognise iron deficiency across infancy, childhood and adolescence, confirm it without mistaking inflammation or thalassaemia for deficiency, treat with a calculated elemental-iron regimen, and correct the nutritional or pathological cause while protecting growth and development.
Start with age, gestation and birth weight; feeding from birth; timing and variety of complementary foods; milk volume; meat, fish, pulses and fortified cereals; tea; restricted or selective eating; medicines and supplements; and food access. Ask about pica, fatigue, breathlessness, headaches, dizziness, restless legs, infections, concentration, development, growth and school function. In adolescents ask privately and sensitively about menstruation, dietary restriction and pregnancy possibility where relevant.
Examine colour in good light, pulse, respiratory effort, cardiac signs, oral mucosa and nails, then measure weight and height on appropriate centile charts. Look for jaundice, lymphadenopathy, hepatosplenomegaly, bruising, bleeding and signs of chronic gastrointestinal disease. A well child with mild diet-related deficiency can usually be managed in the community; cardiovascular symptoms, profound anaemia or diagnostic red flags need same-day paediatric discussion.
Practice
Two practice questions
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Question 1 of 2
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Paediatrics and child healthOriginal SBA
Microcytic anaemia first-line confirmation
A 20-month-old who drinks large volumes of cow's milk is pale and tired. FBC shows a microcytic anaemia. Which investigation pair is most useful first to support iron deficiency and interpret ferritin safely?
Sources and review status3 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
The first diagnostic step is FBC, MCV, MCH, RDW, ferritin and CRP or another inflammatory marker. Low haemoglobin with low MCV/MCH and low ferritin is typical. Ferritin is an acute-phase reactant, so inflammatory context matters. Serum iron fluctuates and is not a stand-alone diagnostic test. Film, reticulocytes and selected B12, folate, haemolysis, renal, liver and thyroid tests clarify atypical patterns. Haemoglobin analysis follows when microcytosis is disproportionate or stores are adequate.
Treat the child and the cause together. Prescribe a named formulation by elemental-iron dose, check the caregiver can measure it, and explain that dark stool, nausea, abdominal discomfort, constipation and tooth staining can occur. Absorption is greatest away from food, milk, calcium and antacids, but tolerability and adherence matter; a smaller dose with food may be preferable to abandonment. Brush teeth after liquid iron or use a straw where developmentally safe.
Dietary correction is specific, not simply 'eat better': offer iron-fortified cereals, meat or fish where eaten, beans, lentils, tofu, eggs and green vegetables in varied meals; pair plant sources with vitamin-C-rich food and avoid excessive milk displacing meals. A dietitian is valuable for vegan diets, feeding difficulty, neurodevelopmental needs, allergy restriction, faltering growth or food insecurity. Address heavy periods, coeliac disease, gastrointestinal loss or inflammation rather than relying on repeated supplements.
Review adherence, dose and response at 2 to 4 weeks. A rising reticulocyte count and haemoglobin supports the working diagnosis, while recovery of ferritin documents store replacement. If response is absent, confirm that the prescribed elemental dose was actually dispensed and taken, then revisit blood loss, malabsorption, inflammation and alternative diagnoses. Intravenous iron is specialist treatment when oral therapy is ineffective, unsafe or not absorbed; transfusion is reserved for clinical compromise, not a number alone.
Key points
The common childhood pattern is tiredness, pallor, poor appetite, irritability, reduced concentration or pica with a microcytic, hypochromic blood count.
First-line investigation is FBC with red-cell indices, ferritin and an inflammatory marker; interpret haemoglobin and MCV against age-specific laboratory ranges.
A low ferritin is strong evidence of depleted stores, but normal or raised ferritin does not exclude deficiency during infection, inflammation or liver disease.
Check the blood film and reticulocyte count when anaemia is marked, the pattern is atypical, another cytopenia exists or haemolysis and marrow disease remain possible.
First-line treatment for confirmed uncomplicated deficiency is oral elemental iron, calculated from the elemental rather than salt content, alongside cause-directed dietary change.
A practical UK paediatric treatment range is elemental iron 3 to 6 mg/kg/day in 2 to 3 divided doses, maximum 200 mg/day, adjusted to the preparation and local formulary.
Expect reticulocyte response within about a week and a measurable haemoglobin rise over 2 to 4 weeks; absence of response is a diagnostic checkpoint, not a reason to escalate blindly.
Continue treatment after haemoglobin normalises long enough to replenish stores, commonly about three further months, then confirm recovery according to local paediatric guidance.
Aetiology
01
Insufficient dietary iron
Common contributors are delayed iron-rich complementary foods, excessive cow's milk intake, restrictive eating, low dietary variety, food insecurity and poorly planned vegetarian or vegan diets.
02
Increased requirement
Rapid growth in infancy and adolescence, prematurity and low birth weight increase iron need; menstruation adds recurrent loss after menarche.
03
Blood loss
Heavy menstrual bleeding, occult gastrointestinal bleeding, inflammatory bowel disease, parasitic infection after relevant travel and repeated phlebotomy can progressively deplete stores.
04
Impaired absorption
Coeliac disease, inflammatory gut disease, previous gastrointestinal surgery and acid suppression can reduce uptake despite apparently adequate oral intake.
Pathophysiology
1
Store depletion
Ferritin falls as hepatic and reticuloendothelial iron reserves are consumed before haemoglobin necessarily becomes abnormal, creating iron deficiency without anaemia.
2
Restricted haem synthesis
Insufficient iron limits haemoglobin production; successive red cells become smaller and contain less haemoglobin, producing microcytosis and hypochromia.
3
Reduced oxygen delivery
Falling haemoglobin lowers oxygen-carrying capacity, prompting tachycardia and increased cardiac output and causing fatigue, exertional breathlessness and reduced exercise tolerance.
4
Tissue iron effects
Iron-dependent enzymes also support cognition, motor development, immunity and epithelial integrity, so deficiency can affect function before or beyond the measured anaemia.
Clinical features and red flags
Early iron depletion
Ferritin may be low before haemoglobin falls; concentration, appetite or pica can therefore precede overt anaemia.
Typical blood-count pattern
Low age-adjusted haemoglobin, MCV and MCH with raised red-cell distribution width supports evolving iron deficiency.
Toddler dietary pattern
Large milk volumes, grazing and few iron-rich complementary foods commonly cause deficiency during rapid growth.
Adolescent pattern
Heavy periods, rapid growth, endurance sport, restrictive eating or a poorly balanced plant-based diet can combine.
Atypical anaemia
Macrocytosis, pancytopenia, organomegaly, jaundice or a non-microcytic severe anaemia demands a broader urgent assessment.
Red flags requiring action
Tachycardia at rest, gallop rhythm, syncope, breathlessness, chest pain, heart failure or haemodynamic compromise suggests anaemia severe enough for same-day hospital assessment.
Weight loss, persistent diarrhoea, blood in stool, abdominal pain or poor linear growth suggests gastrointestinal loss, coeliac disease or inflammatory bowel disease rather than diet alone.
Heavy menstrual bleeding, epistaxis, easy bruising or bleeding after procedures requires assessment of haemostatic as well as iron status.
Investigations
01First-line FBC and age-specific red-cell indicesFirst stepFirst line
Why
Confirm anaemia, identify microcytosis and detect another affected blood-cell lineage.
Interpretation and limitations
Low haemoglobin, MCV and MCH with widening RDW is typical; preserved red-cell count despite marked microcytosis favours thalassaemia trait.
02First-line ferritin with CRPFirst line
Why
Assess iron stores while identifying inflammation that can falsely elevate ferritin.
Interpretation and limitations
Low ferritin confirms depleted stores; a normal result during inflammation cannot reliably exclude iron-restricted erythropoiesis.
03Reticulocyte count and peripheral blood film
Why
Assess marrow response and identify haemolysis, blasts, abnormal morphology or mixed deficiency.
Interpretation and limitations
Reticulocytosis after treatment supports response; blasts, fragments, spherocytes or additional abnormal lineages require urgent specialist interpretation.
04Haemoglobin analysis after iron assessment
Why
Detect beta thalassaemia or another haemoglobin variant when microcytosis is unexplained.
Interpretation and limitations
Raised HbA2 supports beta thalassaemia trait, but iron deficiency can alter fractions and alpha thalassaemia may require DNA testing.
Differential diagnosis
01
Thalassaemia trait
Disproportionate microcytosis with a relatively preserved red-cell count, relevant ancestry and normal iron stores supports a haemoglobinopathy; iron is ineffective unless deficiency coexists.
02
Anaemia of inflammation
Chronic infection, inflammatory disease or renal disease can lower serum iron while ferritin remains normal or raised because hepcidin restricts iron availability.
03
Haemolysis or blood disorder
Jaundice, splenomegaly, reticulocytosis, abnormal film or family history suggests haemolysis, membrane disease or another inherited red-cell disorder.
04
Marrow disease
Additional cytopenias, blasts, organomegaly, bone pain, recurrent infection or systemic illness requires urgent exclusion of leukaemia, aplasia or marrow infiltration.
Management
01Stable typical deficiencyConfirm, replace and correct intakeFirst stepThe child is clinically stable with compatible indices and depleted ferritin.+
1Calculate and prescribe elemental iron from the chosen formulation and the child's current weight.
2Give tailored food and milk advice and address menstruation or another identified source of loss.
3Review tolerance, adherence, reticulocyte or haemoglobin response and safety within 2 to 4 weeks.
4Continue after haemoglobin recovery to replenish stores and confirm sustained correction.
02Inflammatory or unclear patternResolve diagnostic uncertaintyFerritin is not low, inflammation is present or microcytosis is disproportionate.+
1Interpret ferritin with CRP, film, reticulocytes and the entire blood count.
2
Complications
01
Developmental impact
Sustained deficiency during rapid brain development is associated with impaired attention, learning, motor development and behaviour, particularly when recognition is delayed.
02
Growth and participation
Poor appetite, fatigue and reduced exercise tolerance can impair weight gain, school attendance, sport and wider social participation.
03
Cardiovascular decompensation
Severe or rapidly developing anaemia can cause high-output cardiac failure, syncope and haemodynamic instability, especially with ongoing bleeding.
04
Iron toxicity
Incorrect dosing or accidental ingestion can cause life-threatening poisoning; liquid and tablets must be stored securely away from children.
Monitoring and follow-up
Record baseline weight, height, dietary pattern, functional symptoms, haemoglobin, indices, ferritin and inflammatory context.
Check that the prescription states elemental iron and that caregivers demonstrate the correct measured volume.
Review adverse effects and actual doses taken rather than recording adherence as a simple yes or no.
Repeat FBC or an early reticulocyte assessment according to severity, usually assessing haemoglobin response within 2 to 4 weeks.
Continue follow-up until haemoglobin and stores recover and the dietary or bleeding cause has been addressed.
Track growth, appetite, development, school attendance and pica, not laboratory values alone.
Reconsider coeliac disease, inflammation, ongoing loss, haemoglobinopathy and marrow disease when recovery is incomplete.
Special situations
Ferritin needs context
Inflammation can conceal deficiency by raising ferritin, so pair it with CRP and the clinical pattern.
Dose the element
Different iron salts contain different elemental amounts; prescribing only a salt volume invites underdosing or toxicity.
Microcytosis is not synonymous with deficiency
Thalassaemia trait can produce strikingly small cells with little anaemia and no benefit from iron.
Recovery has two phases
Haemoglobin corrects before stores, so stopping immediately at a normal FBC promotes recurrence.
Diet reveals system factors
Food insecurity, sensory feeding difficulty and caregiver misunderstanding may be the treatable cause and need non-judgemental support.
Common pitfalls
01
Using serum iron alone to diagnose deficiency.
02
Giving iron indefinitely for microcytosis without checking ferritin or haemoglobinopathy.
03
Writing a liquid dose without confirming its elemental-iron concentration.
04
Assuming all childhood deficiency is dietary and missing heavy periods or gastrointestinal loss.
05
Stopping replacement as soon as haemoglobin enters the reference range.
06
Ignoring milk displacement, feeding difficulty, food access and growth.
07
Escalating to intravenous iron before verifying dose, adherence and diagnosis.
Do not prescribe iron for isolated microcytosis until deficiency is demonstrated; thalassaemia trait is common and unnecessary iron can be harmful.
Cow's milk should not be the main drink before 12 months; from around 6 months introduce varied iron-containing complementary foods in an age-appropriate texture.
Hepatosplenomegaly, lymphadenopathy, bone pain, recurrent fever, bruising or more than one cytopenia raises concern for malignancy, haemolysis or marrow failure.
A very young infant, prematurity, faltering growth, restricted diet, food insecurity, developmental regression or pica needs nutritional, developmental and safeguarding context assessed explicitly.
Failure of haemoglobin to rise despite a verified dose and adherence should prompt review of diagnosis, ongoing loss, malabsorption, inflammation, formulation and administration.
05Cause-directed coeliac and gastrointestinal testing
Why
Identify malabsorption or occult loss when diet does not explain deficiency or response is poor.
Interpretation and limitations
Use total IgA with IgA tissue-transglutaminase while eating gluten; select stool and inflammatory tests from symptoms rather than screening indiscriminately.
06Reference-standard marrow iron assessment
Why
Demonstrate absent marrow iron only in exceptional complex diagnostic circumstances.
Interpretation and limitations
Absent stainable marrow iron is a reference standard, but invasiveness makes it inappropriate for routine childhood nutritional deficiency.
Investigate chronic inflammation, renal disease, coeliac disease and occult blood loss from clinical clues.
3Arrange haemoglobin analysis and specialist advice before repeated empirical iron when a trait is possible.
03Poor responseAudit treatment before escalationEscalationHaemoglobin fails to rise after a documented therapeutic trial.+
1Confirm current weight, elemental dose, formulation strength, dispensing, timing and actual adherence.
2Recheck FBC, reticulocytes, ferritin and inflammation and look for continued loss or malabsorption.
3Discuss paediatric or haematology referral and intravenous replacement only after the cause is clarified.
04Clinical compromiseEscalate severe anaemiaEscalationCardiovascular symptoms, shock, major bleeding or critical anaemia is present.+
1Stabilise with ABCDE, establish access and obtain urgent senior paediatric and haematology support.
2Investigate severity and cause while avoiding excessive phlebotomy in a small child.
3Use carefully volume-calculated red-cell transfusion only under specialist direction and monitor for overload.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
First-line replacement for confirmed uncomplicated childhood iron-deficiency anaemia while dietary and pathological causes are corrected.
Oral elemental iron
Give elemental iron 3 to 6 mg/kg/day orally in 2 to 3 divided doses, maximum 200 mg elemental iron daily, using the current weight and stated elemental content of the local preparation.
Check formulation strength carefully; nausea, pain, constipation, dark stools and tooth staining affect adherence. Separate from milk, calcium and antacids where practical, reduce in significant renal or hepatic uncertainty with specialist advice, and store securely because overdose can be fatal.