Hemolytic Anemia

Introduction   

The red blood cells require certain physical characteristics for attaining maturity and thereafter they can carry out their primary function of keeping hemoglobin in a form suitable for transportation of oxygen and carbon dioxide to and from tissues throughout the body.

The normal RBCs will survive in circulation for 120 days. Factors that upset the physical characteristics of the RBCs will lead to the shortening of the life of the RBCs and these will be defects within the cell itself or alteration in the environment of the cells.

Hemolytic Anemia

Occurrence of HA                

Anemia occurs as as result of hemolysis (breakdown of the red blood cells) when bone marrow is unable to compensate for the increased destruction of RBCs. The adult bone marrow can increase production of cells by an increase in cellularity and the conversion of fatty marrow to red marrow. Anemia results when the survival of red blood cells is reduced below 20 days. Production of RBCs in the bone marrow may be increased about 6 times but several days are necessary for the marrow to reach maximum capacity. In the meantime, acute shortage of RBCs may result in profound anemia.

According to Bishop et al (1964), "In children, the red marrow is already less than in adults so compensation occurs by expansion of the marrow space at the expense of cortical bone" [1]. 

Symptoms and Characteristics of HA  

The characteristic symptoms of HA result from the degree of anemia, the sites of destruction of the red cells and complications associated with increased marrow activity. At birth, HA usually produces a more marked jaundice than in later life because the liver function is less efficient at this time. Cholicystitis and pigment stones are often indicative of chronic hemolysis. The spleen is frequently palpable in chronic hemolytic anemia. Leg ulcers are a complication of various hereditary hemolytic anemias. The urine contains various substances which depend on the site of destruction of the RBCs. Urobilinogen , produced in the gastro-intestinal tract by bacterial breakdown of bilirubin (the pigment present in the bile juices) and reabsorbed, is always present. Hemoglobin sometimes appears in the urine though it may be caused by other conditions not related to HA.

In the diagnosis of HA, the blood count and blood film are most important [2]. There is an increase of the proportion and absolute numbers of reticulocytes. Vitamin deficiency, particularly of folic acid, is also held responsible for appearance of HA.

References

1. Bishop, C. and Sergenor, D.M. (1964) The Red Blood Cell: A Comprehensive Treatise, New York.

2. Dacey, J.V. (1960) Blood Pictures and Methods of Investigations of Haemolytic Anemias , in The Haemolytic Anaemias , Congenital and Acquired , Vol. 1, P.1, London