Why does a newborn develop hyperbilirubinemia after birth but not in utero during hemolytic disease of the newborn (HDN)?

In cases of hemolytic disease of the newborn (HDN), hyperbilirubinemia arises primarily because the normal physiological mechanisms that manage bilirubin levels are disrupted after birth. In utero, the placenta plays a crucial role in the clearance of unconjugated bilirubin by allowing it to be transported from the fetal circulation into the maternal bloodstream, where it is subsequently processed and eliminated.

After birth, this placental connection is severed, and the newborn's liver must take on the responsibility of processing bilirubin independently. At this point, any excess unconjugated bilirubin produced, particularly due to the hemolysis of red blood cells, cannot be excreted via the placenta anymore. As a result, unconjugated bilirubin accumulates in the newborn’s system, leading to hyperbilirubinemia.

While the immaturity of the liver does contribute to difficulties in processing bilirubin, it is the immediate cessation of placental excretion that directly leads to the buildup of bilirubin after birth. The substantial destruction of erythrocytes that also continues post-delivery further exacerbates the situation. Therefore, the correct rationale for why hyperbilirubinemia develops after birth but not in utero during HDN centers on the loss