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Anaemia - iron deficiency

SNOMED: 234340006Updated 03/03/2026
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Exam Tips

  • In OSCE/viva, always pair confirmation of iron deficiency (ferritin) with a plan to identify cause; do not stop at prescribing iron.
  • In men and postmenopausal women, treat iron deficiency anaemia as possible occult GI blood loss until proven otherwise.
  • A normal or high ferritin does not exclude iron deficiency when inflammation is present.
  • Response to oral iron supports diagnosis in selected groups (for example premenopausal women with menorrhagia), but this approach is not a substitute for cancer-exclusion pathways in higher-risk groups.
  • Classic film description for exams: microcytic hypochromic cells with pencil cells (see blood-film figure in standard haematology texts).

Definition

Iron deficiency anaemia is reduced haemoglobin production caused by inadequate body iron stores, usually after prolonged negative iron balance from blood loss, reduced absorption, or increased requirements. It is the commonest cause of a microcytic, hypochromic anaemia in UK practice, and is typically confirmed biochemically by low ferritin (commonly <30 micrograms/L in adults) alongside compatible blood count findings.

Pathophysiology

Body iron is first depleted from storage pools (falling ferritin), then circulating iron supply becomes insufficient for marrow erythropoiesis (low transferrin saturation), causing iron-restricted haem synthesis. Red cells become progressively smaller and paler (low MCV, low MCH; microcytosis and hypochromia), with anisopoikilocytosis and pencil cells on film in established disease. Chronic inflammation can mask deficiency by raising ferritin, so interpretation must consider clinical context and inflammatory markers. In pregnancy, plasma-volume expansion causes physiological haemodilution, which can coexist with true iron deficiency.

Risk Factors

  • Heavy menstrual bleeding (most common in premenopausal women)
  • Pregnancy and postpartum iron depletion
  • Occult or overt gastrointestinal blood loss (for example colorectal or gastric cancer, peptic ulceration, angiodysplasia)
  • Use of aspirin, NSAIDs, antiplatelets, SSRIs, or corticosteroids increasing GI bleeding risk
  • Coeliac disease, previous gastrectomy/bariatric surgery, or Helicobacter pylori-associated malabsorption
  • Frequent blood donation
  • Endurance training
  • Low dietary iron intake (usually contributory rather than sole cause in adults)
  • Parasitic infection risk after tropical travel (for example hookworm)

Clinical Features

Symptoms

  • Fatigue and reduced exercise tolerance
  • Exertional dyspnoea
  • Headache
  • Dizziness or light-headedness
  • Palpitations
  • Cognitive difficulty, poor concentration, irritability
  • Restless legs
  • Pica (for example ice craving)
  • Sore tongue, dysgeusia
  • Syncope or angina in severe anaemia

Signs

  • Pallor (can be present even in mild disease)
  • Atrophic glossitis
  • Angular cheilitis
  • Dry skin and hair; diffuse alopecia
  • Nail changes (ridging, koilonychia)
  • Flow murmur or tachycardia
  • Features of cardiac decompensation in severe cases (for example ankle oedema, signs of heart failure)
  • May be no obvious signs despite significant anaemia

Investigations

Full blood count (FBC):Low Hb for age/sex, usually low MCV (<80 fL in adults) and low MCH; MCV <95 fL is sensitive for iron deficiency in anaemic patients
Serum ferritin:Low ferritin supports iron deficiency; <30 micrograms/L is strongly confirmatory in most adults
Blood film:Microcytic, hypochromic red cells with anisopoikilocytosis; pencil cells may be seen (see figure in a haematology blood film atlas)
Reticulocyte count:Often low/normal before treatment; should rise after effective iron replacement
CRP (or other inflammation marker):Helps interpret ferritin because ferritin can be falsely normal/high during inflammation
Coeliac serology (tTG-IgA with total IgA):Positive test suggests malabsorptive cause requiring gastroenterology follow-up
B12 and folate (selected patients):Alternative or mixed deficiency if response to iron is poor or indices are not clearly microcytic
Urinalysis and renal tract assessment if indicated:May identify haematuria as an uncommon blood-loss source
GI investigation (urgent referral/endoscopy pathway in men and postmenopausal women with IDA):Detects occult gastrointestinal bleeding lesions including malignancy

Management

Lifestyle Modifications

  • Address reversible causes (for example heavy menstrual bleeding, NSAID exposure, low dietary iron intake)
  • Dietary advice: increase iron-rich foods (red meat, pulses, leafy greens) and vitamin C with meals; reduce tea/coffee around iron dosing
  • Safety-net for red-flag symptoms (weight loss, altered bowel habit, melaena, dysphagia, persistent abdominal pain)

Pharmacological Treatment

Oral iron replacement

  • Ferrous sulfate 200 mg tablet (about 65 mg elemental iron) once daily
  • Ferrous fumarate 210 mg tablet (about 68 mg elemental iron) once daily
  • Ferrous gluconate 300 mg tablet (about 35 mg elemental iron) once daily

First-line for most stable patients. Continue for about 3 months after Hb normalization to replenish stores. If adverse effects occur (nausea, constipation, abdominal pain), reduce frequency (for example alternate-day dosing) or switch salt. Counsel on black stools and interactions: reduced absorption with antacids/calcium, levothyroxine, tetracyclines, quinolones, and bisphosphonates (separate dosing times).

Parenteral iron (IV) when oral iron fails/is unsuitable

  • Ferric carboxymaltose IV (dose by weight and Hb deficit; commonly up to 1000 mg per infusion, maximum 20 mg/kg)
  • Iron derisomaltose IV (dose by calculated iron deficit; can deliver large total-dose infusion)

Use for intolerance, malabsorption, ongoing blood loss, need for rapid repletion, or late pregnancy when clinically indicated. Administer where anaphylaxis management is available; monitor during and after infusion. Avoid IV iron in active systemic infection; use pregnancy-specific guidance (generally avoid in first trimester unless benefits clearly outweigh risks).

Red cell transfusion (selected severe cases)

  • Packed red blood cells, dose individualized to symptoms/comorbidity

Reserve for haemodynamic instability, ongoing bleeding, or severe symptomatic anaemia (especially cardiovascular compromise). Transfusion does not replace need for iron repletion and cause investigation.

Surgical / Interventional

  • Definitive treatment of bleeding source where identified (for example endoscopic therapy of GI lesions, colorectal cancer surgery, fibroid-directed procedures)
  • Gynaecological interventions for refractory heavy menstrual bleeding when indicated

Complications

  • Reduced physical performance and exercise tolerance
  • Cognitive and behavioural effects (especially in children)
  • High-output heart failure in severe anaemia
  • Worsening angina or existing cardiopulmonary disease
  • Increased susceptibility to infection
  • Pregnancy complications: preterm birth risk, lower birthweight, maternal fatigue/depressive symptoms, infant iron deficiency

Prognosis

Prognosis is usually good when the underlying cause is identified and iron stores are adequately replenished, with symptomatic improvement often preceding full haematological recovery. Delayed diagnosis or failure to investigate occult blood loss (particularly in men and postmenopausal women) worsens outcomes by missing serious pathology such as gastrointestinal malignancy.

Sources & References

💊BNF Drug References(12)

✅NICE Guidelines(1)

📖Textbook References(20)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 656)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 714)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1327)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1808)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1801)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1801)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 820, 821)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 820)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1826)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1560)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1366)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 819, 820)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1758)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 668, 669)[context]
  • Emergencies in - Obstetrics and Gynaecology, Second Edition (Stergios K. Doumouchtsis, S. Arulkumaran) (Z-Library).pdf(pp. 360, 361)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 583, 584)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 583, 584)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 387, 388)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 394)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 81)[context]

Sources

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