Lucan · Conditions

Iron deficiency anaemia

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Australian guidance: BloodSafe eLearning + RACGP Iron Deficiency in Adults

1. Definition and epidemiology

Iron deficiency anaemia (IDA) is the most common nutritional deficiency worldwide and the leading cause of anaemia in Australia. It results from a negative iron balance sufficient to impair haemoglobin synthesis, producing a microcytic hypochromic anaemia. In Australia, IDA disproportionately affects women of reproductive age, infants, adolescents, pregnant women, and individuals with gastrointestinal pathology including coeliac disease and colorectal cancer. Aboriginal and Torres Strait Islander peoples carry an elevated burden due to both dietary and hookworm-related losses in some remote communities.

2. Pathophysiology

Iron is an essential element required for haemoglobin and myoglobin formation. Depletion proceeds in three stages. First, iron stores are exhausted as serum ferritin falls below the reference range. Second, iron-limited erythropoiesis develops as transferrin saturation falls and free erythrocyte protoporphyrin rises, reflecting inadequate iron delivery to erythroblasts. Third, frank IDA emerges: haemoglobin synthesis is curtailed, producing small red cells (microcytosis) with reduced haemoglobin content (hypochromia) visible on the peripheral blood film. Robbins (Ch 14) emphasises that the bone marrow shows normocellular to hyperplastic erythroid activity with absent stainable iron on Prussian blue staining, and that serum ferritin remains the most sensitive single marker of depleted stores, though it is elevated as an acute-phase reactant in infection, inflammation, malignancy, hepatic disease, and in the elderly, potentially masking true deficiency. In such cases, transferrin saturation below 16% and an elevated soluble transferrin receptor support the diagnosis.

The major mechanisms of negative iron balance are:

3. Clinical presentation and diagnostic criteria

Symptoms reflect both anaemia and tissue iron depletion. Fatigue, dyspnoea on exertion, decreased effort capacity, and lethargy are the predominant anaemic symptoms. Tissue depletion produces glossitis, angular cheilitis, koilonychia (spoon nails), and in severe cases dysphagia from a Plummer-Vinson web. Pica (craving for non-food substances such as ice or clay) is a characteristic though non-universal feature. Examination may reveal pallor of the conjunctivae and palmar creases, tachycardia, and a flow murmur in significant anaemia.

Diagnostic criteria are not formally codified in a single AU instrument but a diagnosis requires:

  1. Haemoglobin below the sex-specific reference range
  2. Evidence of iron depletion: low serum ferritin OR low transferrin saturation in the appropriate clinical context
  3. Exclusion of haemoglobinopathy and other causes of microcytosis (thalassaemia trait, anaemia of chronic disease) when clinically indicated

4. Investigations and AU-specific cutoffs

Perform investigations in this order:

  1. Full blood count: haemoglobin, MCV (microcytosis typical but absent early), MCH, red cell distribution width (elevated, reflecting anisocytosis)
  2. Blood film: hypochromic microcytes, pencil cells, target cells in established IDA
  3. Serum ferritin: the most specific test for iron stores. A level below 30 micrograms/L confirms depleted stores in most adults. In the presence of inflammation, a ferritin up to 100 micrograms/L may still be consistent with IDA and should prompt assessment of transferrin saturation
  4. Transferrin saturation: below 16% supports iron-limited erythropoiesis
  5. Serum iron and total iron-binding capacity: supportive, less specific than ferritin
  6. Reticulocyte count and reticulocyte haemoglobin content: useful to assess early response to therapy

Cause-directed investigations are mandatory. All men, all postmenopausal women, and any patient without an obvious explanation require colonoscopy and gastroscopy to exclude gastrointestinal malignancy. Coeliac serology (tTG-IgA with total IgA) should be requested in any patient with malabsorptive features or unexplained IDA. Urine dipstick is indicated if haematuria is suspected.

5. Management

The AMH 2026 guidance is that oral iron is first-line treatment for most patients. Dietary advice alone is insufficient to treat established IDA, though encouraging increased intake of haem iron (red meat, chicken, fish) and non-haem iron (legumes, grains, vegetables) with vitamin C co-ingestion to enhance non-haem absorption is appropriate as an adjunct.

Do not delay initiating oral iron while awaiting investigations such as colonoscopy. Iron can be temporarily stopped during the bowel preparation period.

Parenteral iron is indicated when:

Blood transfusion is reserved for symptomatic severe anaemia or anaemia destabilising cardiovascular function. Iron replacement must continue after transfusion to replenish stores.

Treat the underlying cause concurrently. Address heavy menstrual bleeding, eradicate H. pylori if found, and initiate coeliac management as appropriate.

6. Pharmacology and AU PBS notes

Oral iron (first-line)

The AMH 2026 table of PBS-listed oral iron products includes:

Brand (form) Salt and dose Elemental iron
Ferro-grad tablet Ferrous sulfate 325 mg 105 mg
Ferro-grad C / Ferro-Max C / Ferrovance-C tablet Ferrous sulfate 325 mg + ascorbic acid 500 mg 105 mg
Ferro-tab tablet (RPBS) Ferrous fumarate 200 mg 65.7 mg
Ferro-F tablet (RPBS) Ferrous fumarate 310 mg + folic acid 350 mcg 100 mg
Ferropods capsule Ferrous fumarate 304 mg + ascorbic acid 20 mg 100 mg
Ferro-grad F tablet Ferrous sulfate 250 mg + folic acid 300 mcg 80 mg
Fefol capsule Ferrous sulfate 270 mg + folic acid 300 mcg 87.4 mg
Ferro-Liquid oral liquid (PBS) Ferrous sulfate 30 mg/mL 6 mg/mL
Maltofer tablet Iron polymaltose 370 mg 100 mg
Maltofer oral liquid Iron polymaltose 37 mg/mL 10 mg/mL

Standard adult dose is 100 mg elemental iron once daily. Alternate-day dosing (eg 100 mg on alternate days) may reduce gastrointestinal adverse effects and can be used for non-symptomatic IDA without anaemia. Ferrous salts are more bioavailable than ferric polymaltose. Oral iron should be taken on an empty stomach 1 hour before or 2 hours after food; if gastric intolerance occurs it may be taken with or shortly after food, at the cost of reduced absorption. Avoid taking with tea, coffee, or calcium-rich foods. Maltofer (iron polymaltose) liquid may be diluted in water or juice and drunk through a straw to prevent tooth staining.

PBS streamlined authority: Iron preparations are listed on the PBS under streamlined authority (code varies by product) for IDA in Aboriginal and Torres Strait Islander patients and for iron deficiency anaemia in haemodialysis patients.

Parenteral iron (second-line)

Iron polymaltose IV (Ferrosig, Monofer) is the preferred parenteral route per AMH. IV iron administration resources are available at BloodSafe eLearning. Resuscitation equipment must be available; staff must be trained in anaphylaxis management. Monitor the patient closely for at least 30 minutes after each infusion.

7. Complications and monitoring

Anticipated treatment response is a rise in haemoglobin of approximately 20 g/L over 3 to 4 weeks. If no response is detected after 3 to 4 weeks, reassess the diagnosis and consider non-compliance, malabsorption, ongoing occult bleeding, renal impairment, or chronic inflammation as confounders.

Continue oral iron for at least 3 months (2 to 3 months in children) after haemoglobin normalises in order to replenish iron stores. Avoid prolonged unnecessary iron use.

Surveillance schedule:

Key complications to monitor for:

Practise this in Lucan

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.