Red cells and marrow
Anaemia
Approach
Confirm anaemia, assess severity and classify by MCV and marrow response (reticulocytes). Think blood loss, reduced production or increased destruction.
- Iron deficiency is the most common cause of anaemia and always needs a cause found (1)(2).
- Quick sort: low MCV (iron deficiency, thalassaemia trait, anaemia of chronic disease), normal MCV (acute blood loss, chronic disease, CKD, marrow failure, early haemolysis), high MCV (B12/folate deficiency, alcohol, drugs, MDS).
- Reticulocytes separate under-production (low) from bleeding or haemolysis (high).
Assessment
Fatigue, dyspnoea, chest pain, bleeding, diet, menstruation, GI symptoms, pregnancy, medicines, alcohol, chronic disease and family/ethnic history. Examine for instability, pallor, jaundice, bleeding, nodes and organomegaly.
- Causes of iron deficiency to ask about: low dietary intake (e.g. vegan diet), malabsorption (gastrectomy, duodenal bypass, Crohn disease), chronic GI blood loss (peptic ulcer, colorectal cancer, angiodysplasia), heavy menstrual loss, NSAIDs, PPIs and glucocorticoids (1).
- Pica supports iron deficiency (2).
Urgent features
Haemodynamic instability, active major bleeding, chest pain/ischaemia, syncope, severe hypoxia, rapidly falling haemoglobin or haemolytic/transfusion reaction requires immediate escalation.
- Transfusion is not triggered by haemoglobin alone: assess the patient, give a single unit then reassess (3).
- Australian PBM practice points: Hb under 70 g/L, transfusion is likely appropriate (may not be needed if well compensated or other specific therapy exists); 70-100 g/L, transfuse only to relieve symptoms/signs of anaemia; over 100 g/L, usually inappropriate. In ACS, Hb under 80 g/L likely appropriate and over 100 g/L not advisable (3).
- Heart failure raises the risk of transfusion-associated circulatory overload (3).
Investigations
FBC/film, reticulocytes, ferritin/iron studies, B12/folate, UEC/LFT, CRP and haemolysis tests as indicated. Investigate the source of iron deficiency—especially GI blood loss—rather than replacing iron alone.
- Iron studies (serum iron, ferritin, transferrin, transferrin saturation) are the first-line test for iron deficiency (1). Ferritin under 30 ng/mL is specific for iron deficiency, but it is an acute-phase reactant and rises with inflammation, so a normal ferritin does not exclude it (2). Iron-binding capacity rises and transferrin saturation falls in iron deficiency (2).
- Also request reticulocyte count, RDW and blood film (2).
- Mnemonic, macrocytic anaemia: "Macrocytic Anaemia Leaves Big Fat Reticulocytes" = Myxoedema, Alcohol, Liver disease, B12 deficiency, Folate deficiency, Reticulocytosis.
- Mnemonic, target cells: "HOT LIPS" = Haemoglobinopathy, Obstructive jaundice, Thalassaemia, Liver abscess, Iron deficiency, Polycythaemia, Sideroblastic anaemia.
Management
Treat cause. Oral or IV iron based on indication/tolerance; replace B12/folate appropriately. Red-cell transfusion is guided by symptoms, instability, comorbidity and local thresholds, with reassessment after each unit when appropriate.
- Oral iron first-line for most (1). Therapeutic Guidelines (as quoted in Australian Prescriber) suggests ferrous sulfate 325-650 mg daily (105-210 mg elemental iron) (1). Merck gives 65 mg elemental iron every other day as a typical start; alternate-day dosing is used to improve tolerability (2).
- IV iron if oral iron fails or is not tolerated, or rapid repletion is needed. Ferric carboxymaltose (up to 1000 mg, repeat a week later if required) is the usual outpatient choice in Australia; all IV iron needs resuscitation facilities because of anaphylaxis risk (1). Hb should rise within 2-3 weeks after IV iron (1).
- Treat iron deficiency even if a transfusion is given (3). In heart failure, treat iron deficiency to improve functional status (3).
- Do not give iron without looking for the source: a bleeding site should be sought even in mild anaemia (2).
Last updated from Sen’s notes on 9 October 2026.