anaemia
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"anaemia" OR "anemia"[MeSH Terms] AND "classification"
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Here is a thorough overview of anaemia drawn from Harrison's Principles of Internal Medicine (22nd ed.), Robbins & Kumar Pathologic Basis of Disease, Frameworks for Internal Medicine, and Bailey & Love's Short Practice of Surgery.
Anaemia
Definition
Anaemia is defined as blood counts (haemoglobin/haematocrit) below the normal for a given population. In practice, common WHO thresholds are:
- Adult men: Hb < 13 g/dL
- Adult women: Hb < 12 g/dL
- Pregnant women: Hb < 11 g/dL
It results in reduced oxygen delivery to tissues, triggering compensatory haemodynamic responses.
Classification
There are two major approaches to classifying anaemia:
1. By Red Cell Size (MCV-based) - Harrison's 22E
| Category | MCV | Key Causes |
|---|---|---|
| Microcytic | < 80 fL | Iron deficiency, thalassaemia, anaemia of chronic disease (sometimes), sideroblastic anaemia |
| Normocytic | 80-100 fL | Aplastic anaemia, renal disease, haemolysis (acute), endocrinopathies, marrow infiltration, myeloma |
| Macrocytic | > 100 fL | B12/folate deficiency, hypothyroidism, liver disease, alcohol use, myelodysplasia, medications |
Peripheral blood smear comparison of microcytic vs macrocytic RBCs:
(Top: microcytic RBCs - note small size and large central pallor compared to lymphocyte nucleus. Bottom: macrocytic RBCs - note large, oval cells)
2. By Mechanism (Pathophysiologic Classification) - Robbins & Kumar
| Mechanism | Examples |
|---|---|
| Blood Loss | Acute (trauma), Chronic (GI lesion, menorrhagia) |
| Increased Destruction (Haemolysis) | |
| - Intrinsic/inherited | Hereditary spherocytosis, G6PD deficiency, pyruvate kinase deficiency, sickle cell disease, thalassaemia |
| - Acquired/extrinsic | Autoimmune haemolytic anaemia, microangiopathic (TTP, HUS, DIC), PNH, drug-induced, malaria |
| Decreased Production | |
| - Nutritional deficiency | Iron, B12, folate, copper deficiency |
| - Erythropoietin deficiency | Chronic kidney disease |
| - Marrow failure | Aplastic anaemia, Fanconi anaemia |
| - Marrow replacement | Metastatic tumour, granulomatous disease |
| - Inflammation | Anaemia of chronic disease (hepcidin-mediated iron sequestration) |
The reticulocyte count is the key first step to distinguish mechanism:
- Elevated reticulocytes → blood loss or haemolysis (hyperproductive response)
- Low/normal reticulocytes → underproduction (bone marrow problem)
Clinical Features
The severity of symptoms depends on chronicity and rate of onset. Even severe anaemia may be well tolerated if it develops gradually.
Symptoms:
- Fatigue, loss of stamina
- Dyspnoea on exertion
- Palpitations
- Dizziness, headache
Physical signs:
- Pallor (mucous membranes, palmar creases, nail beds, conjunctivae)
- Tachycardia, wide pulse pressure, bounding pulses
- Forceful heartbeat, systolic flow murmur
- In severe cases: cardiac decompensation
Key Anaemia Types in Detail
Iron Deficiency Anaemia (most common worldwide)
- Affects ~10% in high-income countries; 25-50% in low-income countries (Robbins & Kumar Basic Pathology)
- Causes: poor intake, chronic blood loss (GI, menstrual), malabsorption
- Labs: low serum ferritin (best initial test), low serum iron, high TIBC (300-350 µg/dL normal), transferrin saturation ~33% normal
- Smear: hypochromic, microcytic RBCs with increased central pallor
Megaloblastic Anaemia (B12 / Folate Deficiency)
- Mechanism: impaired DNA synthesis → nuclear-cytoplasmic asynchrony → ineffective haematopoiesis
- Often presents with pancytopenia (anaemia + thrombocytopenia + granulocytopenia)
- Earliest smear finding: hypersegmented neutrophils (5+ lobes)
- MCV typically > 110 fL; macro-ovalocytes on smear
- B12 deficiency also causes subacute combined degeneration of the spinal cord
Anaemia of Chronic Disease / Inflammation
- Mediated by hepcidin (released by liver in response to IL-6)
- Hepcidin degrades ferroportin → blocks iron release from macrophages → iron-restricted erythropoiesis
- Labs: low serum iron, low TIBC (unlike IDA), elevated ferritin
- Often normocytic, can be microcytic in long-standing cases
Hereditary Spherocytosis
- Defect in RBC membrane skeleton proteins (ankyrin, spectrin, band 3)
- Spherocytes trapped and destroyed in the spleen
- Triad: anaemia + splenomegaly + jaundice
- Coombs test negative (distinguishes from autoimmune haemolytic anaemia)
- Splenectomy corrects the anaemia
Investigations / Diagnostic Approach
- FBC with RBC indices (MCV, MCH, MCHC)
- Reticulocyte count - key to mechanism (high vs. low)
- Peripheral blood smear - morphology
- Iron studies: serum iron, ferritin, TIBC
- B12 and folate levels
- Renal function (CKD-related)
- LFTs, TFTs as indicated
- Direct Coombs test if haemolysis suspected
- Bone marrow biopsy if aplasia or infiltration suspected
Treatment Principles (Surgical Context)
From Bailey & Love's / Pye's Surgical Handicraft:
- A Hb of ≥ 10 g/dL without myocardial disease is generally acceptable for surgery, as increased cardiac output can compensate
- Below this threshold, urgency of the procedure determines whether iron supplementation or blood transfusion is used
- Stored red cells are poor oxygen transporters immediately post-transfusion; transfusion restores volume but not immediate O2 delivery
- In bowel surgery, blood transfusion increases wound infection risk and may worsen prognosis
Sources: Harrison's Principles of Internal Medicine 22E, p. 492 | Robbins & Kumar Basic Pathology | Frameworks for Internal Medicine, p. 330 | Bailey and Love's Short Practice of Surgery 28E | Pye's Surgical Handicraft 22E
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