Exposure to another individual’s RBC antigens resulting in antibody production against those antigens. These antibodies can cross the placenta and cause fetal red cell hemolysis, thus fetal anemia.
Fetus is Rh + (has Rh antigen) and mother is Rh – (lacks Rh antigen) à 15%
Not generally a problem in a woman’s first pregnancy – in subsequent pregnancies even minute exposure can result in an anamnestic response of maternal antibody production.
IgM too large to cross placenta. IgG can easily cross (most antibodies produced are IgG)
Antibodies attach to Rh+ RBC and hemolyze them – producing bilirubin which is transferred back across placenta to be metabolized. At first pregnancy infant may develop elevated bilirubin levels as hemolysis continues after birth and immature liver must metabolize bilirubin. Subsequent pregnancies – accelerated antibody production – fetal liver produces excess RBC but at the cost of protein thus decreasing oncotic pressure (edema and ascites). Hydrops fatalis can result if severe fetal anemia leads to high output cardiac failure as well.
Situations in which a woman may develop antibodies
- threatened/spontaneous/therapeutic abortion
- ectopic pregnancy
- bleeding – placenta previa/abruption
- abdominal trauma
- external version
Indications for 300 mcg RhIg administration
- 28wks GA
- Within 3 days of delivery of an Rh positive baby
- Positive Kleihauer-Berke test