Definition & Overview

Despite careful planning and meticulous preparation, pregnancy and childbirth carry a certain risk, not just for the mother but also for the baby. There are certain diseases that may endanger the unborn child and threaten its life even after birth. An example is the hemolytic disease of the newborn (HDN), a condition that occurs when the blood type of the mother is incompatible with the blood type of the baby. Basically, the fetal red blood cells (RBC’s) carry an antigen that the mother doesn’t have. When they cross the placenta and into the mother’s bloodstream, they are considered anomalies, and this triggers the mother’s body to produce antibodies. The antibodies eventually find their way back to the fetal bloodstream and result in the destruction of the baby’s RBC’s.

It was as early as the 1600s when the theory of HDN was first explored after a French midwife delivered twins who both died, one who was swollen while the other was jaundiced. There were many similar cases resulting in fetal and newborn mortality during this time. It took more than 300 years to fully understand the cause of HDN.

Once the cause was definitive, prevention and treatment programs were initiated especially in mothers whose pregnancies were at high risk of HDN. This action led to a dramatic decrease in the occurrence of HDN.

Cause of Condition

The two common causes of HDN are the following:

  • Rhesus factor (Rh) incompatibility - To better understand, the Rhesus factor (Rh Factor) is a type of protein on the surface of red blood cells. If the protein is present in the RBCs, then you are RH positive. Otherwise, you are Rh negative. An expectant mother is usually tested to identify her Rh factor. HDN occurs when an Rh negative mother has an Rh positive baby. The mother’s body will detect the baby’s RBCs as foreign because they’re different. Antibodies against this “threat” will be produced. The first pregnancy with this incidence will not have a problem since it is only at this point that the antibodies are triggered but not activated. The mother, at this point, is simply Rh sensitized. It is only during the second pregnancy, with another Rh positive baby, that the antibodies will be activated. It is a certainty that the antibodies will find themselves crossing the placenta and attacking and destroying the baby’s red blood cells.

  • ABO incompatibility - People have different blood types (A, B, AB and O) and the immune system is triggered when one blood type mixes or reacts with a different blood type. In general, people with Type O blood can donate to other blood types but only a Type O blood can donate to another Type O. It is in the same manner that mothers with an O blood type can cause HDN if they have a baby with a type A or type B blood type. However, unlike Rh incompatibility, HDN through ABO incompatibility is possible during the first pregnancy because anti-A and anti-B antibodies are found and activated early on in life as A- or B-like antigens are present in food and bacteria.

Key Symptoms

HDN is diagnosed upon the detection of the following key symptoms during pregnancy and after birth. Symptoms may vary per child but these are the most common ones:

During pregnancy

  • When tested through the amniocentesis process, the amniotic fluid may have a yellow coloring and contain bilirubin (a fluid made by the liver)
  • During ultrasound, the fetus may show enlarged liver, spleen or heart. It may also show fluid buildup in the baby’s abdomen, lungs or scalp

After birth

  • The baby may be pale and suffering from anemia
  • Jaundice may be present due to the yellow coloring of the amniotic fluid
  • Enlarged liver and spleen
  • Severe edema (swelling under the skin)

Who to See and Types of Treatments Available

Treatment protocols for HDN do not only involve the baby but also the mother especially when the condition is diagnosed during pregnancy. Both the mother and fetus need to be monitored and protected by performing the following procedures:

During pregnancy

  • When a mother is tested to be Rh negative and the baby is Rh positive, the mother must be checked through an indirect Coombs test to see if she has been “sensitized” - if her body has produced the antibody against the Rh positive antigen. If there are no antibodies yet, the mother will be injected with Rh immune globulin that prevents the body from producing the antibodies that can kill the fetal RBC’s during pregnancy. Additional injections of Rh immune globulin are necessary whenever the mother’s blood come in contact with the baby’s blood.
  • If the fetus has HDN, intrauterine blood transfusion of red blood cells through the mother’s uterus and into the abdominal cavity of the fetus will be initiated.This procedure may be repeated as necessary.
  • If the condition worsens, early delivery may be necessary.

    After birth

  • If the baby is suffering from severe anemia (from the loss of the RBCs), blood transfusions may be required for as long as necessary

  • Intravenous fluids may also be prescribed to combat low pressure
  • Breathing support may be provided for respiratory distress
  • If the bilirubin levels are high, an exchange transfusion is done. This requires alternating giving and withdrawing small amounts of blood. This raises the RBC count too.
  • Intravenous immunoglobin (IVIG) may be given to the baby to strengthen his immune system, reduce the breakdown of RBCs and lower bilirubin levels.

    Conditions for the type of treatment for the disease are contingent on the following:

  • The baby’s gestational age, overall health, and medical history

  • Extent of the disease
  • The baby’s tolerance for medications and procedures
  • Expectations for the outcome during the course of the treatment
  • The parents’ opinion

  • Gruslin AM, Moore TR. Erythroblastosis fetalis. In: Martin R, Fanaroff A, Walsh M, eds. Neonatal-Perinatal Medicine. 9th ed. Philadelphia, Pa: Mosby Elsevier; 2011.

  • Cohen DW. Hemolytic disease of the newborn: RBC alloantibodies in pregnancy and associated serologic issues. UpToDate [online]. Waltham, Ma: Nov 2009.
Share This Information: