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Interpretation of the full blood count

Red blood cells 

Constituents of the red cell count
  • Haemoglobin (Hb): concentration of haemoglobin within the blood. Hb is the protein in red blood cells which carries oxygen. It is the first value you should look at. Low haemoglobin = ‘anaemia’.
  • Mean corpuscular volume (MCV): mean volume of the red blood cells (‘-cytic’). This is the main method used to classify anaemia (macrocytic = large cells; normocytic = normal cells; microcytic = small cells). 
  • Reticulocyte count: the number of immature red blood cells. Increased in blood loss and haemolytic anaemia because the bone marrow works harder to replace lost cells. Decreased if there is impaired red blood cell production in the bone marrow.
  • Red cell count (RCC): the concentration of red blood cells within the blood
    • It may be increased due to: reduced plasma volume (e.g. dehydration), or increased red blood cell production (e.g. polycythaemia rubra vera)
    • It may be decreased due to: increased plasma volume (e.g. pregnancy), or reduced red blood cell production/red blood cell loss (e.g. bone marrow failure, bleeding, anaemias)
  • Haematocrit (HCT)/packed cell volume (PCV): percentage of the total volume of blood accounted for by red blood cells. Causes of abnormalities are similar to the RCC but the haematocrit is based on volume so is also affected by the red cell volume (MCV). 
  • Mean corpuscular haemoglobin (MCH)/haemoglobin concentration (MCHC): the mean quantity/concentration of haemoglobin within the red bloods cells. This affects the colour of the cells (‘-chromic’: hypochromic = pale; normochromic = normal red).
    • Most normocytic and macrocytic anaemias are normochromic
    • Most microcytic anaemias are hypochromic (except anaemia of chronic disease)
  • Red blood cell distribution width (RDW): measure of the variation of red blood cell volumes. It is used in conjunction with MCV to determine if anaemia is due to a mixed cause or a single cause. Raised red cell distribution width = ‘anisocytosis’.


Anaemia = a reduced concentration of haemoglobin within the blood.

Other relevant tests:

  • WCC and platelet count: if both are also abnormal, a bone marrow cause is likely
  • Reticulocyte count: if raised, the cause is blood loss or haemolytic anaemia
  • Mean corpuscular volume (MCV):
Tests for specific causes
  • Haematinics: B12, folate and ferritin (NB: ferritin is also an acute phase protein so may be falsely elevated due inflammation)
  • Iron studies: see table below
  • TFTs
  • Bilirubin (unconjugated bilirubin is raised in haemolysis)
  • Blood film ± bone marrow biopsy (if bone marrow cause/sideroblastic anaemia suspected)
  • Hb electrophoresis (if haemoglobinopathy suspected)
NB. A low ferritin is consistent with iron-deficiency but a normal ferritin cannot exclude iron-deficiency if there is acute/chronic inflammation because ferritin is an acute phase reactant.
Commonest causes

Iron-deficiency anaemia

  • Physiology: iron is found in meats and fish as haem iron, and in cereals, green vegetables and beans as non-haem iron. In humans, 2/3 is stored as haem, 2/9 as ferritin and 1/9 as haemosiderin.
  • Causes:
    • Chronic blood loss (from GI tract, e.g. malignancy/inflammation/ulcers/varices/haemorrhoids; or menorrhagia)
    • ↑ demand (pregnancy, growth)
    • ↓ absorption (coeliac disease, gastrectomy, achlorhydria)
    • Poor intake
  • Investigations if no clear cause: OGD + colonoscopy, coeliac screen, urine dip
  • Treatment: treat cause, iron supplementation (infusion/ferrous sulphate/fumarate tablets), transfusion if Hb<70

B12-deficiency anaemia

  • Physiology: vitamin B12 is found in meat and dairy products. The stomach produces intrinsic factor which binds to B12, allowing it to be absorbed in the terminal ileum. Body stores last up to 4 years.
  • Causes: pernicious anaemia/atrophic gastritis, malabsorption (e.g. after gastrectomy or terminal ileal disease/resection), strict veganism, chronic alcoholism, drugs (proton pump inhibitors, metformin)
  • Investigations for pernicious anaemia: parietal cell antibodies, intrinsic factor antibodies, Schilling’s test (rarely used)
  • Treatment: treat cause; hydroxocobalamin (B12) injections 3-monthly, or oral vitamin B12 may be used if dietary deficiency

Folate-deficiency anaemia

  • Physiology: folate is found in green vegetables and fortified cereals. Body stores only last 4 months and deficiency develops earlier in malabsorption/pregnancy.
  • Causes:
    • Dietary (alcoholism, neglect, poor diet)
    • ↑ requirements (pregnancy, haematopoiesis)
    • Malabsorption in small bowel (coeliac disease, pancreatic insufficiency, Crohn’s disease, tropical sprue)
    • Drugs that interfere with metabolism (phenytoin, methotrexate, trimethoprim)
  • Treatment: treat cause, oral folic acid supplements
  • NB: in coexistent B12 and folate deficiency, always treat B12 first to prevent subacute combined degeneration of the cord. (Treat in alphabetical order!)

Anaemia of chronic disease

  • See iron studies table above
  • Physiology: inflammatory cytokines reduce the ability of bone marrow to respond to erythropoietin, leading to anaemia. They also reduce cellular iron release, which reduces the serum iron level and also results in lower transferrin saturation. Ferritin (intracellular iron store) is still normal/high, and transferrin and cellular soluble transferrin receptors are not upregulated because overall body iron stores are normal.
  • Causes: any chronic disease
  • Treatment: treat cause, transfuse if Hb<70

Haemolytic anaemia

  • Physiology:
    • Normally, red cells are destroyed extravascularly by macrophages with the following effects:
      • Hb → globulin (which is broken down into amino acids) + haem (which is broken down into bilirubin)
      • Bilirubin is then conjugated by the liver (a rate-limited process), and released as bile into the bowel, where it is converted to urobilinogen
      • Some urobilinogen is passed in stool; the rest is reabsorbed and excreted in urine as urinary urobilinogen
    • However, if red cells are destroyed intravascularly (pathological), free Hb follows one of three pathways:
      • Some binds to haptoglobin (and is removed by liver)
      • Some is filtered by the glomerulus and passed as haemoglobinuria or haemosiderinuria
      • Some is oxidised to methaemoglobin which dissociates into globin + ferriheme (most ferriheme then binds to albumin → methaemalbuminaemia)
  • Inherited causes:
    • Haemoglobinopathies: sickle cell, thalassaemia
    • Membrane defects: hereditary spherocytosis, elliptocytosis
    • Enzyme defects: G6PD deficiency, pyruvate kinase deficiency
  • Acquired causes:
    • Immune-mediated: autoimmune haemolytic anaemia, drug-induced haemolytic anaemia (e.g. due to cephalosporins, penicillins, levofloxacin, dapsone, levodopa), alloimmune haemolytic anaemia
    • Non-immune-mediated: disseminated intravascular coagulation*, thrombotic thrombocytopenic purpura*, haemolytic uraemic syndrome*, physical damage (e.g. by metallic valves), toxins (e.g. lead/uraemia/drugs), infections (e.g. malaria), paroxysmal nocturnal haemoglobinuria
  • Investigations to confirm haemolysis:
    • Increased Hb breakdown: ↑ unconjugated bilirubin, ↑ lactate dehydrogenase (from red cells), ↑ urinary urobilinogen (on urine dipstick)
    • Increased Hb production: ↑ reticulocytes
    • Intravascular haemolysis: ↓ free haptoglobin, haemoglobinuria (on urine microscopy), ↑ urinary haemosiderin, red cell fragments on blood film
  • Investigations to find cause:
    • Blood film: sickle cells, schistocytes (microangiopathic haemolytic anaemia*), inclusion bodies (malaria), spherocytes/elliptocytes (hereditary spherocytosis/elliptocytosis), Heinz bodies (G6PD), bite/blister cells (G6PD), distorted prickle cells (pyruvate kinase deficiency)
    • Direct antiglobulin/‘Coombs’ test (for autoimmune haemolytic anaemia)
    • Osmotic fragility testing (for membrane abnormalities)
    • Hb electrophoresis (for haemoglobinopathies)
    • Enzyme assays, e.g. G6PD, pyruvate kinase (for enzyme defects)


Polycythaemia = increased volume percentage of red blood cells within the blood.

  • Relative polycythaemia (i.e. ↓ plasma volume)
    • Acute dehydration
    • Chronic (associated with obesity, hypertension, alcohol excess, smoking)
  • Absolute polycythaemia (i.e. ↑ red blood cells)
    • Primary = polycythaemia rubra vera
    • Secondary = due to increased erythropoietin because of chronic hypoxaemia (e.g. COPD, altitude, congenital cyanotic heart disease) or erythropoietin-secreting tumours (e.g. renal cell carcinoma) 
  • WCC and platelet count (both also raised in primary absolute polycythaemia, but not in secondary absolute polycythaemia)
  • Erythropoietin level
  • If polycythaemia rubra vera suspected: request JAK-2 mutation testing and consider bone marrow biopsy 

White blood cells 




  • Decreased production: bone marrow infiltration, aplastic anaemia, vitamin B12/folate deficiency, myelosuppression
  • Increased destruction/consumption
    • Non-immune: disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), haemolytic uraemic syndrome (HUS), heparin induced thrombocytopenia (HIT), sequestration in hypersplenism (including portal hypertension, e.g. in liver cirrhosis)
    • Primary immune: idiopathic thrombocytopenic purpura (ITP)
    • Secondary immune: SLE, chronic lymphocytic leukaemia, viruses, drugs, alloimmune
Possible investigations

  • Blood film ± bone marrow biopsy
  • Infection screen, e.g. HIV, hepatitis C 
  • LFTs
  • Lactate dehydrogenase (increased in haemolysis and lymphoproliferative disorders)
  • Serum vitamin B12 and folate
  • Coagulation screen including fibrinogen and D-dimer (if DIC suspected) 
  • Acute phase proteins (look for evidence of infection)
  • Special tests: von Willebrand factor-cleaving protease (ADAMTS-13) activity (if TTP suspected), heparin induced thrombocytopenia antibodies (if HIT suspected)

  • Treat cause, for example:
    • ITP: observation, or corticosteroids ± IVIg ± platelet concentrate transfusion ± thrombopoietin receptor agonists
    • TTP: plasma exchange + immunosupression (e.g. corticosteroids, rituximab) ± anti-von Willebrand factor monoclonal antibody (Caplacizumab) ± renal replacement therapy 
    • HUS: plasma exchange ± renal replacement therapy 
    • HIT: stop heparin + use non-heparin anticoagulant
  • Give platelet concentrate transfusion if platelets <10×109/L, or if <50×109/L and bleeding (although not for TTP/HUS/HIT – increases thrombosis)
  • Splenectomy may be considered



  • Primary: essential thrombocythaemia, other myeloproliferative disorders
  • Secondary (reactive): bleeding, inflammation, infection, malignancy, post-splenectomy
Possible investigations

  • Blood film ± bone marrow biopsy
  • Acute phase proteins (look for evidence of infection)
  • JAK2 mutation (myeloproliferative diseases)
  • Ferritin (to look for chronic bleeding)

  • Aspirin (to prevent thromboembolic disease)
  • Hydroxycarbamide (if primary cause)



  • Bone marrow infiltration: acute leukaemia, myeloma, lymphoma, myelofibrosis, metastatic carcinoma, TB
  • Myelosuppression: drugs (e.g. chemotherapy, herbal, antibiotics), lead, irradiation, infection (e.g. HIV, parvovirus B19, sepsis)
  • Impaired haematopoiesis: vitamin B12/folate deficiency, aplastic anaemia, myelodysplastic syndrome
  • Peripheral destruction of blood cells: hypersplenism, paroxysmal nocturnal haemoglobinuria, autoimmune disorders
Possible investigations

  • Blood film ± bone marrow biopsy
  • Lactate dehydrogenase (increased in haemolysis and lymphoproliferative disorders)
  • Serum vitamin B12 and folate
  • Reticulocytes
  • Electrophoresis and immunoglobulins (myeloma)
  • Viral serology (HIV/EBV/CMV/Parvovirus)
  • Autoimmune profile
  • Serum direct antiglobulin test

Test your knowledge!

What are the indications for intravenous iron in iron-deficiency anaemia?

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What are the cautions for using intravenous iron?

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Which patients require a gastroenterology referral for OGD/colonoscopy in iron-deficiency anaemia?

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