Hemolytic Anaemias Classification Diagnosis And Treatment

hemolytic anaemia
Hemolytic Anaemia


  • The loss of red cells by hemolysis or destruction are main causes hemolytic anaemia. The life span of RBCs is 90 to 120 days in circulation.
  • The destroyed RBCs are re­placed by new red cells formed by the bone marrow. If the rate of destruction of RBCs is more than the rate of replenishment, then anaemia occurs.
  • There is jaundice due to rise in bilirubin generated by destruction of RBCs. There are symptoms of anaemia like fatigue and dyspnoea.
hemolytic anaemia diagnosis
Hemolytic Anaemia jaundice


  • There is passage of red brown urine (hemoglobin­uria).
  • There is history of exposure to drugs or toxins. Usually there is splenomegaly.

Lab tests

  • There is evidence of hemolysis on examination of blood smears.
  • Reticulocyte count is elevated due to erythroid hy­perplasia of the bone marrow.
  • Reticulocytes are also elevated in patients with blood loss, myelophthisis, decrease of red blood cells in cir­culation due to any cause.

Red blood cell morphology IS altered as follows

  • · Spherocytes in hereditary spherocytosis.
  • · Target cells in hemoglobin disorders ­thalassemias, hemoglobin Sand C.
  • · Schistocytes in microangiopathy, intravascular prosthesis.
  • · Sickle cells in sickle cell syndromes.
  • · Acanthocytes and spur cells in severe liver dis­ease.
  • · Agglutinated cells in cold agglutinin disease.
  • · Heinz bodies in oxidant stress.

Classification of hemolytic anaemias

  • Hemolytic anaemia may be due to intracorpuscular defect or extracorpuscular factors.
  • The intracorpuscular (defect is within the RBC) causes are enzyme defects, hemoglobinopathies, hereditary spherocytosis.
  • The extracorpuscular factors are liver disease – spur cell .anaemia, hypersplenism, immune complexes, in­fections, toxins, microangiopathy.

Treatment of Hemolytic Anaemia

  • Splenectomy reduces the hemolysis and im­proves RBC survival.
  • Splenectomy is done by laparoscopy for low risk. Folic acid 1 mgjday is given before splenectomy.


  • When RBC’s are exposed to a drug or toxin which generates free radicals, then glucose metabolism via hexose monophosphate shunt starts to occur. This protects the RBC membrane from oxidation and de­struction.
  • In G6PD deficiency the hexose monophosphate shunt becomes defective and hemoglobin precipitates within the RBC forming Heinz bodies.
  • There is no treatment but the disease is self remit­ting.
  • Oxidant drugs, infections, and Fava beans should be avoided.
  • Drugs causing hemolysis in G6PD deficiency patientPrimaquine, Sulphonamides, Nitrofurantoin, Nalidixic aCid, Furazolidone, Vitamin K, dapsone, doxorubicin etc.


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