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Hemolytic Diseases of the Newborn occur when maternal antibodies are present naturally or form in response to an antigen from the fetal blood crossing the placenta and entering the maternal circulation. Maternal antibodies of the immunoglobulin G (IgG) class, in turn, cross the placenta, causing hemolysis of the fetal red blood cells (RBCs), resulting in possible hyperbilirubinemia, jaundice, and anemia.Hemolytic disease of the newborn occurs most often when the blood groups of the mother and baby are different.The most common cause of hemolytic disease of the fetus and newborn is ABO incompatibility, followed by Rh(D) incompatibility.
Rh incompatibility, or isoimmunization (also known as alloimmunization), occurs when an Rh-negative mother has an Rh-positive fetus who inherits the dominant Rh-positive gene from the father. Severe Rh incompatibility results in marked fetal hemolytic anemia because the fetal erythrocytes are destroyed by maternal Rh-positive antibodies. In extreme cases fetal bilirubin levels increase, resulting in fetal jaundice, also known as icterus gravis. The fetus compensates for the anemia by producing large numbers of immature erythrocytes to replace those hemolyzed, resulting in erythroblastosis fetalis.
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This can lead to hydrops fetalis, in which the fetus has:
Marked anemia
Cardiac decompensation
Cardiomegaly
Hepatosplenomegaly
The severe anemia leads to hypoxia.
Because of the decreased intravascular oncotic pressure, fluid leaks out of the intravascular space, leading to:
Generalized edema
Effusions into the peritoneal (ascites), pericardial, and pleural (hydrothorax) spaces
Possible intrauterine or early neonatal death
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This occurs when the fetal blood type is A, B, or AB and the maternal type is O.
It occurs rarely in infants with type B blood born to mothers with type A blood.
Exchange transfusions are required only occasionally.
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Galactosemia
Crigler-Najjar disease
Hypothyroidism
Gilbert syndrome
Pyruvate kinase deficiency
Spherocytosis
Events that can cause a woman to develop antibodies to the Rh factor:
Previous pregnancy with an Rh-positive fetus
Transfusion with Rh-positive blood, which causes immediate sensitization
Ectopic pregnancy, miscarriage, or induced abortion after 8 or more weeks of gestation or fetal death at any time
Chorionic villus sampling or amniocentesis
Placental abruption
External cephalic version
Trauma
The nurse checks the woman's medical record to determine whether she has received Rh immune globulin. For an Rh-negative pregnant woman, the risk of the fetus being Rh-positive must be determined. The first assessment is a paternal zygosity test to determine the father's Rh factor. If the father is Rh-positive, the infant is more likely Rh-positive. An indirect Coombs test is repeated at 28 weeks. If the result remains negative, the woman is given an intramuscular injection of Rho(D) immune globulin. If the result is positive, the injection is repeated every 2 to 4 weeks to monitor the maternal antibody titer until a critical value is reached. Once a critical value is noted, an assessment of fetal hemolytic process is needed.
Dean, L. (2005). Chapter 4: Hemolytic Diseas of the Newborn. Blood Groups and Red Cell Antigens [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK2266/
Hall, V. Avulakunta, I.D., (2022, November 22). Hemolytic Disease of the Newborn. NIH StatPearls: https://www.ncbi.nlm.nih.gov/books/NBK557423/