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Hemolytic disease of the newborn or fetal erythroblastosis


A disease caused by Rh factor is fetal erythroblastosis or haemolytic disease of the newborn, characterized by destruction of the red blood cells of the fetus or the newborn. The consequences of this disease are severe and may lead to death.

During pregnancy, only the plasma passes from the mother to the child through the placenta and vice versa, due to the so-called blood-placental barrier. However, vascular accidents can occur in the placenta, allowing the passage of red blood cells from the fetus to the maternal circulation.

In cases where the fetus has Rh-positive blood, antigens on its red blood cells will stimulate the maternal immune system to produce anti-Rh antibodies, which will be in the maternal plasma and may, because they are of the IgG class, pass through BHP, causing lysis. in the fetal red blood cells.

Antibody production follows a cascade of events, and therefore antibody production is slow and the amount small at first. From the second pregnancy or after blood transfusion sensitization, if the child is Rh + again, the maternal organism will already contain antibodies to that antigen and the fetus may develop fetal DHPN or erythroblastosis.

The diagnosis can be made by the mother's and father's blood typing early and during pregnancy, the Coombs test, which uses human anti-antibody, can detect if the mother is producing antibody and steps can be taken.

A transfusion, receiving Rh - blood, can be done even intrauterine. Rh - blood does not have Rh - factor red blood cells and cannot be recognized as foreign and destroyed by antibodies received from the mother. After about 120 days, the red blood cells will be replaced by others produced by the individual himself. The blood will again be Rh +, but the fetus will no longer be in danger.

After the birth of the child a prophylactic measure is taken by injecting the mother Rh- , serum containing anti Rh. Application soon after delivery destroys fetal red blood cells that may have passed through the placenta at or before birth. This avoids the production of antibodies by “zeroing the scoreboard”. Each time a conceptus is born and is Rh +, a new application should be made, as new antibodies will be formed.

Symptoms in the newborn that can be observed are anemia (due to red cell destruction by antibodies), jaundice (increased red blood cell destruction will lead to increased indirect bilirubin production, which cannot be converted into the liver) and, after its persistence, the onset of a disease called Kernicterus, which corresponds to the deposition of bilirubin in the nuclei of the brain base, which will generate a delay in the newborn.