Rhesus disease (Rh disease) is a condition that occurs between a mother and her fetus when their blood types are incompatible. This condiiont occurs when an Rh-negative woman conceives a baby with an Rh-positive father and the baby inherits the Rh-positive blood type from the father. Rh-positive means that the protein (D antigen) can be found on the surface of red blood cells (RBCs). If the D antigen is not present, then an individual is considered to be Rh-negative If the mother is Rh-negative and the baby is Rh-positive during pregnancy (mainly during the process of labor and delivery) it is possible that some of the fetus’s Rh-positive RBCs may get into the mother’s bloodstream which is where the problem begins. Because the RBCs are unfamiliar
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Hyperbilirubinemia can be caused by just one or multiple processes including an increase in production of bilirubin, decreased hepatic uptake, decreased conjugation, impaired excretion, impaired bile flow, or an in increase in enterohepatic circulation. The bulk of bilirubin comes from the breakdown of hemoglobin into unconjugated bilirubin. Unconjugated bilirubin binds to albumin in the blood so it can be transported to the liver where it is then taken by the hepatocytes and then conjugated with glucuronic acid by an enzyme so it can become water soluble. The conjugate bilirubin is then excreted in bile and then on into the duodenum. Adults conjugated bilirubin can be reduced by bacteria in the gut to urobilin and then excreted, but infants have less bacteria in their digestive-tracts and in turn, less bilirubin is condensed to urobilin and excreted. Infants also have the enzyme beta-glucuronidase which deconjugates the bilirubin and can then be reabsorbed and recycled into their circulation which is known as enterohepatic circulation of …show more content…
Mildly affected infants can have little to no anemia and may show only hyperbilirubinemia because of the continuing hemolytic effect of the Rh antibodies that have crossed the placenta previously. Moderately affected infants can have a mixture of both anemia and hyperbilirubinemia/jaundice. In severe cases of fetal hyperbilirubinemia, kernicterus develops. Kernicterus is a neurological condition caused by the deposition of bilirubin into central nervous system tissues. Kernicterus typically only occurs several days after the delivery of the infant and is characterized by the loss of their Moro (startle) reflex, posture, poor feeding, inactivity, high-pitched cry or shrilling, and also seizures. Infants who overcome kernicterus may develop hypotonia, hearing loss, and also mental retardation as they grow older. Severe hemolytic anemia and jaundice is another life threatening condition that can be seen in infants affected by Rh disease from erythroblastosis fetalis. Severe forms of erythroblastosis can be characterized by extreme pale pigment of the newborn due to hematocrit levels being below 5, high output cardiac failure, ascites, edema, extramedullary hematopoiesis, and pericardial effusion. Death often occurs just before or after the delivery of the infant due to hydrops fetalis if left
Hyperbilirubinemia can be caused by just one or multiple processes including an increase in production of bilirubin, decreased hepatic uptake, decreased conjugation, impaired excretion, impaired bile flow, or an in increase in enterohepatic circulation. The bulk of bilirubin comes from the breakdown of hemoglobin into unconjugated bilirubin. Unconjugated bilirubin binds to albumin in the blood so it can be transported to the liver where it is then taken by the hepatocytes and then conjugated with glucuronic acid by an enzyme so it can become water soluble. The conjugate bilirubin is then excreted in bile and then on into the duodenum. Adults conjugated bilirubin can be reduced by bacteria in the gut to urobilin and then excreted, but infants have less bacteria in their digestive-tracts and in turn, less bilirubin is condensed to urobilin and excreted. Infants also have the enzyme beta-glucuronidase which deconjugates the bilirubin and can then be reabsorbed and recycled into their circulation which is known as enterohepatic circulation of …show more content…
Mildly affected infants can have little to no anemia and may show only hyperbilirubinemia because of the continuing hemolytic effect of the Rh antibodies that have crossed the placenta previously. Moderately affected infants can have a mixture of both anemia and hyperbilirubinemia/jaundice. In severe cases of fetal hyperbilirubinemia, kernicterus develops. Kernicterus is a neurological condition caused by the deposition of bilirubin into central nervous system tissues. Kernicterus typically only occurs several days after the delivery of the infant and is characterized by the loss of their Moro (startle) reflex, posture, poor feeding, inactivity, high-pitched cry or shrilling, and also seizures. Infants who overcome kernicterus may develop hypotonia, hearing loss, and also mental retardation as they grow older. Severe hemolytic anemia and jaundice is another life threatening condition that can be seen in infants affected by Rh disease from erythroblastosis fetalis. Severe forms of erythroblastosis can be characterized by extreme pale pigment of the newborn due to hematocrit levels being below 5, high output cardiac failure, ascites, edema, extramedullary hematopoiesis, and pericardial effusion. Death often occurs just before or after the delivery of the infant due to hydrops fetalis if left