Maternal antibodies produced in response to paternally derived D antigens on fetal red blood cells are the leading cause of severe hemolytic disease of the fetus and newborn (erythroblastosis fetalis).
Effective immunoprophylaxis of rhesus D-negative at-risk mothers is key to primary prevention.
Intrauterine fetal transfusion is a lifesaving treatment for severely affected fetuses.
Survival rates are more than 90%.
Rhesus (Rh) incompatibility is caused by destruction of fetal red blood cells (RBCs) from transplacental passage of maternally derived immunoglobulin G (IgG) antibodies. IgG antibodies are produced by the maternal immune system, usually against the RhD antigen. These antibodies can freely cross the placenta, binding to and destroying RBCs. More than 50 known RBC antibodies potentially cause Rh incompatibility. The consequence is progressive fetal anemia, which, untreated, may ultimately lead to hydrops fetalis (collection of fluid in serous compartments) and death.
History and exam
Key diagnostic factors
- presence of risk factors
- maternal RhD-negative status
- fetomaternal hemorrhage
- invasive fetal procedures
- placental trauma
- omission of Rh immunoprophylaxis
- external cephalic version
- molar pregnancy
- ectopic pregnancy
1st investigations to order
- maternal blood type
- maternal serum Rh antibody screen
Investigations to consider
- maternal serum antibody titer
- paternal blood type
- paternal zygosity
- fetal ultrasound
- Doppler velocimetry of fetal middle cerebral artery (peak systolic velocity)
- fetal blood typing (from amniocentesis or maternal circulation)
- direct assessment of fetal anemia
- rosette test
- Kleihauer-Betke test/flow cytometry
neonate with erythroblastosis
- Nonimmune fetal hydrops
- Parvovirus infection
- Non-RhD hemolytic disease
- ACOG practice bulletin no. 192: management of alloimmunization during pregnancy
- ACOG practice bulletin no. 181: prevention of Rh D alloimmunization
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