The sensitized mother produces IgG anti-D (antibody) that crosses the placenta and coats D-positive fetal red cells which are then destroyed in the fetal spleen.
Mild to moderate hemolysis (red cell destruction) manifests as increased indirect bilirubin (red cell pigment).
Severe hemolysis leads to red blood cell production by the spleen and liver.

• Subsequently, hepatic circulatory obstruction (portal hypertension) with placental edema interferes with placental perfusion and ascites develops.[5]
• Hepatomegaly, increased placental thickness, and polyhydramnios often precede the development of hydrops (fetal heart failure).[5]
• As liver damage progresses decreased albumin production results in the development of anasarca, and effusions.