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Rh disease (also known as Rh (D) disease, Rhesus disease, RhD Hemolytic Disease of the Newborn, Rhesus D Hemolytic Disease of the Newborn or RhD HDN) is one of the causes of hemolytic disease of the newborn (also known as HDN). The disease ranges from mild to severe. When the disease is mild the fetus may have mild anaemia with reticulocytosis. When the disease is moderate or severe the fetus can have a more marked anaemia and erythroblastosis (erythroblastosis fetalis). When the disease is very severe it can cause morbus haemolyticus neonatorum, hydrops fetalis, or stillbirth.
During any pregnancy a small amount of the baby’s blood can enter the mother’s circulation. If the mother is Rh negative and the baby is Rh positive, the mother produces antibodies (including IgG) against the Rhesus D antigens on her baby’s red blood cells. During this and subsequent pregnancies the IgG is able to pass through the placenta into the fetus and if the level of it is sufficient, it will cause a Rhesus D positive fetus to develop Rh disease. The mechanism is maternal anti-D IgG passing through the placenta to the fetus causing destruction of fetal red blood cells. Generally Rhesus disease becomes worse with each additional Rhesus incompatible pregnancy.
The main and most frequent sensitizing event is child birth (about 86% of sensitized cases), but fetal blood may pass into the maternal circulation earlier during the pregnancy (about 14% of sensitized cases)[1]. Sensitizing events during pregnancy include miscarriage, therapeutic abortion, amniocentesis, ectopic pregnancy, abdominal trauma and external cephalic version.
The incidence of Rh disease in a population depends on the proportion that are rhesus negative. Many non-caucasian peoples have a very low proportion who are Rhesus negative, so the incidence of Rh disease is very low in these populations. In Caucasian populations about 1 in 10 of all pregnancies are of a Rhesus negative woman with a Rhesus positive baby. It is very rare for the first Rhesus positive baby of a Rhesus negative woman to be affected by Rh disease. The first pregnancy with a Rhesus positive baby is significant for a rhesus negative woman because she can be sensitized to the Rh positive antigen. In Caucasian populations about 13% of Rhesus negative mothers are sensitized by their first pregnancy with a rhesus positive baby. If it were not for modern prevention and treatment, about 5% of the second Rhesus positive infants of Rhesus negative woman, would result in still births or extremely sick babies and many babies who managed to survive would be severely ill. Even higher disease rates would occur in the 3rd and subsequent Rhesus positive infants of rhesus negative woman. By using anti-RhD immunoglobulin (Rho(D) Immune Globulin) the incidence is massively reduced .
Rh disease sensitization is about 10 times more likely to occur if the fetus is ABO compatible with the mother than if the mother and fetus are ABO incompatible.
Most Rh disease can be prevented by treating the mother during pregnancy or promptly (within 72 hours) after childbirth. The mother has an intramuscular injection of anti-Rh antibodies (Rho(D) Immune Globulin), so that the fetal Rhesus D positive erythrocytes are destroyed before her immune system can discover them. This is passive immunity and the effect of the immunity will wear off after about 4 to 6 weeks (or longer depending on injected dose) as the anti-Rh antibodies gradually decline to zero in the maternal blood.
It is part of modern antenatal care to give all Rhesus D negative pregnant women an anti-RhD IgG immunoglogbulin injection at about 28 weeks gestation (with or without a booster at 34 weeks gestation). This reduces the effect of the vast majority of sensitizing events which mostly occur after 28 weeks gestation. Anti-RhD immunoglobulin is also given to non-sensitized Rhesus negative women immediately (within 72 hours – the sooner the better) after potentially sensitizing events that occur earlier in pregnancy.
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