- Make fresh blood smear.
- Take blood in EDTA.
- Hemolytic anemia is due to RBC hemolysis.
Definition of hemolytic anemia
- These are defined as when there is an increased destruction of the red blood cells.
- Because of the compensation from the bone marrow anemia appears, when the destruction of RBCs becomes a several time more than this compensatory mechanism.
The causes of RBC hemolysis may be:
- Hereditary is due to intrinsic red cells defects.
- Acquired are due to environmental changes.
- Intravascular hemolysis when the destruction of the RBCs takes place in the blood vessels and hemoglobin is released.
- Hemoglobin in the blood gives rise to hemoglobinuria.
- Extravascular hemolysis when the destruction of the RBCs takes place in the mononuclear phagocytic system.
Hereditary Causes of hemolytic anemia:
- RBC cell membrane defect:
- Abnormality in the cell membrane cytoskeleton leads to spherocytosis and elliptocytosis.
- Abnormal lipid synthesis like an increase in the membrane lecithin.
- Red cell enzyme deficiency:
- G-6-PD deficiency.
- Pyruvate kinase deficiency.
- Hexokinase deficiency
- Glutathione synthetase deficiency
- Disorders of hemoglobin synthesis:
- Hemoglobin synthesis defect like Thalassemia.
- Abnormal structure of the hemoglobin-like Sickle cell anemia, Hb E.
Acquired Causes of hemolytic anemia:
- Antibody-mediated cytotoxic reaction (Type II) like ABO incompatibility.
- Hemolytic autoimmune anemia is seen with cold antibody and warm antibody.
- Drug-induced hemolytic anemia seen in Methyldopa, penicillin,
- Microangiopathic hemolytic anemia is seen due to the trauma of RBCs in the cardiac prosthetic valve, and fibrin deposition in the microvasculature.
- Infections: Hemolytic anemia due to toxins like a malarial parasite, septicemia, Clostridium welchii, pneumococci, staphylococci, and lead poisoning.
- Hemolytic anemia due to snake venom and spiders bite.
- Hemolytic anemia due to lead poisoning and copper toxicity.
- Hemolytic anemia due to extensive burns.
- Hemolytic anemia in splenomegaly.
- Paroxysmal nocturnal hemoglobinuria.
- Anemia due to acquired RBCs membrane abnormality.
- Secondary to liver and kidneys diseases.
Clinical presentation of hemolytic anemia:
- There is pallor of the mucous membrane which can be judged from the tongue.
- There is fluctuating of jaundice. In some patients, bilirubin will very high and may need blood transfusion exchange.
- Urine shows no bilirubin but there is the presence of the urobilinogen.
- Gallstones are common in these patients.
- The patients with sickle cell disease may develop ulcers around the ankle.
- Aplastic crises may be seen in these patients.
- Rarely folate deficiency causes aplastic crises.
The Hemolytic anemia shows the following lab changes:
- Hb is reduced and may be mild to moderate decreased from 6 to 10 G/dl.
- Reticulocytes are increased from 5 to 20 % (Reticulocytosis).
- MCV is normal or slightly increased,
- MCHC is increased.
- Bone marrow shows erythroid hyperplasia.
- Normal myeloid: erythroid ratio of 2:1 to 12:1 is reduced to 1:1 or much more reduced.
- Coombs test direct is negative which differentiate it from autoimmune hemolytic anemia.
- Peripheral blood smear shows poikilocytosis and polychromatophilia due to reticulocytes.
- There are elliptocytes and fragmented RBCs.
- There is normochromic and normocytic anemia picture.
- RDW is increased due to anisocytosis and poikilocytosis. Unlike other normochromic and normocytic anemias.
- Increased reticulocytes lead to increased MCV but not like megaloblastic anemias.
- Serum bilirubin is raised.
- Urine urobilinogen is positive.
- Stercobilinogen is increased
- Serum haptoglobin is absent.
||Decreased 6 to 10 g/dL
||Increased 5 to 20%
||Normal or mild increase
||Direct is negative
Possible References Used
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