Chapter 37. Fetal-maternal Incompatibility - Review of Medical Embryology Book

Introduction: the disease caused by fetal-maternal incompatibility begins in the fetus and manifests itself after birth. It results from incompatibility of the blood between the fetus and mother and involves immunization of the mother against a blood group antigen carried by the fetus. It occurs in 1 in 150 births and is the most frequent fetal disease. The most common cause is Rhesus or Rh immunization
Mechanism in Rh immunization

Rh is a blood group carried by the red blood cells in about 85% of individuals and is referred to as Rh+. An Rh- subject can be immunized against the Rh+ antigen if Rh+ red blood cells are introduced into his or her body (e.g., by transfusion). Immunization is manifested by the appearance of anti-Rh antibodies

Immunization of the Rh- woman who has an Rh+ husband can occur during pregnancy. Fetal red blood cells may cross placenta and enter the maternal circulation. If the fetus is Rh+, Rh+ antigen is introduced into the Rh- maternal bloo

The mother is immunized against the Rh+ antigen, and in her blood one sees anti-Rh+ antibodies. The latter, like most antibodies, easily cross the placental barrier and pass into the fetal blood
The maternal antibodies attach themselves to the red blood cells of the fetus, resulting in their destruction in the spleen, causing hemolytic perinatal disease

If the father is homozygous, all the children will be Rh+. The first pregnancy will be normal. Maternal immunization can appear from the second pregnancy on and will become progressively greater with each pregnancy
If the father is heterozygous, some children will be Rh- and be born completely normal, since the maternal antibody will have no effect on their red cells. In contrast, the Rh+ children will be affected as previously described

Blood incompatibility affects only couples in which the mother is Rh- and the father is Rh+. Even in these cases, however, only 5% are affected

Maternal antibodies are fixed on the fetal red blood cells and cause their destruction in the spleen which, as a result, hypertrophies (enlarges), resulting in hemolytic anemia and the release of hemoglobin pigment (from destroyed RBCs). The latter is immediately denatured to yellow bilirubin
The pigment crosses the placenta and is eliminated by the maternal organism
The fetus reacts to the anemia by the formation of new red blood cells in the liver, resulting in an erythropoiesis and liver hypertrophy

As a result of the increased red cell production, some of the red blood cells in the blood are young, nucleated, immature forms or erythroblasts, resulting in an intense erythroblastosis at birth

AT BIRTH severe anemia with erythroblastosis and an enlarged liver and spleen are seen

Icterus (yellow skin color) occurs very rapidly since the pigments are no longer being eliminated by the mother in her circulation

AFTER BIRTH: if the infant is not treated, it is threatened with death as a result of the anemia or by specific complications, such as nuclear icterus, caused by the accumulation and toxic action of bilirubin in the gray nuclei of the brain
IN CERTAIN VERY SERIOUS FORMS, in addition to the symptoms described above, generalized fluid infiltration results in a fetal-placental hydrops, which can produce fetal death in the last months of pregnancy. The placenta becomes exceedingly large and can be more than twice the size of a normal placenta