Haemolytic Disease of the Newborn

[Audio] Haemolytic Disease of the Newborn is a clinically important condition that illustrates key physiological principles related to red blood cell antigens, maternal–fetal immunology, placental transfer of antibodies, and neonatal adaptation..

[Audio] Haemolytic Disease of the Newborn (HDN), also known as erythroblastosis fetalis, is a condition where the red blood cells (RBCs) of a fetus or newborn are destroyed by maternal antibodies. This occurs when there is an incompatibility between the blood groups of the mother and the fetus, most commonly involving the Rh system and occasionally the ABO system. The maternal immune system recognizes fetal RBC antigens as foreign and produces antibodies that cross the placenta, leading to hemolysis. HDN can range from mild anemia to severe complications such as hydrops fetalis and even fetal death. Understanding its pathophysiology is essential for early diagnosis and management..

[Audio] Red blood cells express specific antigens on their surface, which determine blood group classification. The ABO system consists of A, B, and O antigens, while the Rh system primarily involves the D antigen. Individuals with Rh-positive blood have the D antigen, whereas Rh-negative individuals lack it. These antigens are genetically determined and play a crucial role in transfusion compatibility and maternal-fetal interactions. Normally, maternal and fetal blood do not mix significantly during pregnancy, preventing immune reactions. However, during delivery or trauma, fetal RBCs may enter maternal circulation, potentially triggering an immune response if incompatibility exists..

Maternal-fetal blood group incompatibility occurs when the mother lacks an antigen present on fetal RBCs, such as Rh D antigen. During events like childbirth, miscarriage, or invasive procedures, fetal RBCs can enter maternal circulation. The maternal immune system recognizes these cells as foreign and mounts an immune response, producing IgG antibodies against the antigen. These antibodies persist and can cross the placenta in subsequent pregnancies, attacking fetal RBCs. Sensitization is more common in Rh-negative mothers carrying Rh-positive fetuses, and preventive measures like Rh immunoglobulin administration are critical to avoid this immune activation..

[Audio] IgG antibodies are unique in their ability to cross the placenta via Fc receptors. This transfer begins in the second trimester and increases as pregnancy progresses. When maternal IgG antibodies target fetal RBC antigens, they bind and mark these cells for destruction by the fetal reticuloendothelial system. This mechanism underlies the pathogenesis of HDN, as the fetus becomes progressively anemic and vulnerable to complications. The efficiency of IgG transfer explains why HDN severity often increases in subsequent pregnancies after sensitization has occurred..

[Audio] Once maternal IgG antibodies bind to fetal RBCs, these cells undergo destruction primarily in the spleen and liver. The continuous hemolysis leads to severe anemia, which stimulates extramedullary hematopoiesis and causes hepatosplenomegaly. Breakdown of hemoglobin produces bilirubin, resulting in hyperbilirubinemia and jaundice after birth. In severe cases, the fetus develops hydrops fetalis, characterized by generalized edema, ascites, and effusions due to heart failure from profound anemia. These physiological consequences highlight the importance of early detection and intervention to prevent irreversible damage or death..

[Audio] Finally,this table summerized the previously described Mechanism of fetal and neonatal haemolysis..

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