RH Incompatibility

Introduction

• Description: Isoimmunization to any fetal blood group not possessed by the mother is possible. The most common example is the Rh (D) factor. What was once a common cause for intrauterine fetal death has been largely eradicated by prophylactic administration of immunoglobulins to those at risk. When mothers develop antibodies against fetal blood antigens, the fetus is at risk for developing hemolytic disease of the fetus and newborn, with serious morbidity or mortality risks. (Roughly 14% of affected fetuses are stillborn; 50% of live-born infants suffer neonatal death or brain injury.) Though isoimmunization to the Rh(D) factor is the prototype for this type of immune problem, alloimmunization to other antibodies (eg, Lewis, Kell) can result in significant morbidity. These are much less common and no prophylaxis against them is available.

• Prevalence: Uncommon in developed countries because of the routine use of D immunoglobulin therapy (with routine antepartum prophylaxis 0.14%–0.2% of pregnancies). Roughly 15%–17% of non-Hispanic Whites are Rh (d) negative; 5%–8% of the Black population and 1%–2% of Asians and Native Americans. Among Whites, an Rh-negative woman has an approximate 85% chance of mating with an Rh-positive man (60% are heterozygous; 40% are homozygous at the D locus).

• Predominant Age: Reproductive age.

• Genetics: Mothers who are Rh (D) negative. The genes for the CDE blood groups are separately inherited from the ABO groups and are located on the short arm of chromosome 1.

Etiology and Pathogenesis

• Causes: Antibody formation against the D antigen.

• Risk Factors: Any process that exposes the woman to blood carrying the D antigen including blood transfusion, miscarriage, ectopic or normal pregnancy, trauma, amniocentesis, and others.

Signs and Symptoms

• Elevated maternal serum titers of anti-D immunoglobulin (IgM)

• Fetal hydrops, erythroblastosis fetalis, hemolytic disease of the newborn

• Intrauterine fetal demise

Diagnostic Approach