Raise your hand if you know a baby who died of erythroblastosis fetalis.
Not too long ago, there would have been a lot of raised hands. Before 1968, approximately 10,000 babies died each year of erythroblastosis fetalis, also known as hemolytic disease of the newborn (HDN). Then Rhogam was introduced.
It is fashionable in homebirth midwifery circles to determine what the scientific evidence shows and then reflexively recommend the opposite. Therefore, many homebirth midwives and advocates are now suggesting that women forgo Rhogam without having any understanding of what Rhogam is, what it does, and the nature, incidence and mortality rate of the disease that it prevents.
What is hemolytic disease of the newborn (HDN) It is a relatively common condition in which a mother produces antibodies that cross the placenta and destroy the baby’s red blood cells. The baby becomes profoundly anemic, develops severe jaundice and heart failure. The mortality rate used to be approximately 50%.
Why would a mother make antibodies to her baby’s blood cells? It happens when the mother and baby’s blood type differ in an important way. Usually the difference is that the baby is Rh+ (has the RhoD antigen on its red cells) and the mother is Rh-. The baby of an Rh- mother will be Rh+ only if its father is also Rh+, but not all babies of Rh+ fathers will be Rh+.
How does the mother make antibodies against the baby’s blood if the placenta prevents the mother’s blood from mixing with the baby’s blood? The answer is there are often small leaks of fetal blood into the maternal circulation, particularly at the time of birth. They are not large enough to have any impact on the baby, but only a small amount of Rh+ fetal red cells are needed to produce an immune response in the mother.
When such a response develops, the results are often devastating to the baby, not in the current pregnancy (especially if the sensitization occurs at delivery) but in subsequent pregnancies. What happens in future pregnancies?
… [M]aternal anti-D antibodies cross the placenta into fetal circulation and attach to Rh antigen on fetal RBCs … These antibody-coated RBCs are [destroyed] by lysosomal enzymes released by macrophages and natural killer lymphocytes …
… Tissue hypoxia develops as fetal anemia becomes severe… Hydrops fetalis … starts as fetal ascites and evolves into pleural effusions and generalized edema…
… Destruction of RBCs releases heme that is converted to unconjugated bilirubin. Hyperbilirubinemia becomes apparent only in the delivered newborn because the placenta effectively metabolizes bilirubin…
This is an unmitigated disaster for the baby:
Before any interventions were available, the perinatal mortality rate was 50%. Wallerstein introduced exchange transfusion in 1945 and reduced the perinatal mortality rate to 25%. Later, Chown suggested the early delivery of those severely affected nonhydropic fetuses by 34 weeks’ gestation followed by prompt exchange transfusion helped improve survival. The introduction of intraperitoneal transfusion by William Liley in 1963 and intravascular transfusion (IVT) by Rodeck in 1981 reduced the perinatal morbidity and the mortality rate was further reduced to the current rate of 16%.
Treatment for HDN has clearly improved dramatically, but a death rate of 16% is still extraordinarily high. Imagine if you could prevent your baby from ever getting HDN in the first place, and all it took was two small injections. Since 1968, when Rhogam was introduced, there has been no need to imagine.
Rhogam is human antibody to the Rh antigen. If any fetal blood cells escape into the maternal circulation, Rhogam binds to the Rh antigen and makes it “invisible” to the mother’s immune system. One dose at 28 weeks, and another at the time of delivery is enough to prevent the mother becoming sensitized. Additional injections are given whenever there is any other chance of fetal cells leaking into the maternal circulation, such as at the time of miscarriage, ectopic pregnancy, or episodes of significant vaginal bleeding.
Rhogam has dramatically reduced the incidence of HDN. The incidence is still not zero, however, because there are other less common antigens that can also cause sensitization.
What are the side effects of Rhogam? Sometimes there is a localized skin reaction and occasionally, in people who are sensitive to blood products, there can be an allergic reaction to Rhogam itself.
So why are homebirth midwives suggesting that women refuse Rhogam? Because, as usual, they have no idea what they are talking about.
They are motivated by their insistence that nature is perfect and technology is harmful. First, they insist, bizarrely, that the no fetal blood cells will ever find their way into the maternal circulation unless “interventions” occur during birth. Ignorant of history, they are apparently unaware that HDN was first reported by a French midwife in 1609.
Ignorant of the scientific facts, as always, they are unaware of the Kleihauer-Betke test, a that allows us to quantify exactly how many fetal cells are in the maternal circulation at any given time. That’s how we KNOW that small quantities of fetal cells often slip into the maternal circulation.
Then there is their pathological fear of technology. They are absolutely sure that Rhogam might cause some damage of some kind to babies who never needed it the first place since they had a perfect placenta. They offer no scientific facts to support this claim, since there is no evidence that it is true.
What about the benefits? They don’t appear to understand that nearly 10,000 babies are saved from death by Rhogam each and every year. They have apparently forgotten, if they ever knew, about hemolytic disease of the newborn.
This is yet another example of how modern obstetrics is often stymied by its own success. A dread infant killer is easily prevented by a simple injection, so easily that homebirth midwives have no idea that the risk of death is very real and still exists.